Diagnostic examinations

o Chest x-ray
o ECG
o Echocardiography
o Cardiac catheterization
o Laboratory tests
 CARDIOVASCULAR DISEASES

 Coronary heart disease

 Valvular heart disease

 Septal heart defects

 Patent ductusarteriosus

 Pericardial effusion

 Cardiac tumor and trauma

 Cardiac tumor

 Myocardial rupture

 Cardiac arrest
• Aortic aneurysm
• Thrombophlebitis
• Arteriovenus fistula
• Varicose veins
• Gangrene
• Dissecting Aorta
• DVT
 EYE & EAR

• Assessment of head
• Assessment of Eye
• Assessment of the Ear
• Physical examination
 EYE DISORDERS
• Cataract
• Trichiasis
• Benign and malignant tumors of Eye and related
structures
• Trauma of Eye and surrounding structures
• Glaucoma
• Retinal detachment
• Transplant of eye, Corneal lens
• chalazion
• hordeolum/stye
 DISORDERS OF EAR
Disorder of the Ear [2 hrs]
o Outer ear: Mass/tumors/lump
o -abscess
o - Foreign bodies in the ear
o - middle ear:

o Perforation of the tympanic membrane

o Otosclerosis
o Mastoiditis
o -Inner ear: menierre’s disease
-labrynthitis
CARDIOVASCULAR
SYSTEM
OVERVIEW OF ANATOMY & PHYSIOLOGY
Normal Heart:

 Size of fist.
 300 gm.
 6000 litres/d

Suchitra Rathod 9
Shape, Location
of the Heart

• Size of a closed fist

• Shape
– Apex: Blunt rounded
point of cone
– Base: Flat part at
opposite of end of
cone
• Located in thoracic
cavity in
mediastinum
20-10
• RESTS ON THE DIAPHRAGM
• NEAR THE MIDLINE OF THE THORACIC CAVITY
 PERICARDIUM
• CONFINES HEART TO THE
MEDIASTINUM
• ALLOWS SUFFICIENT
FREEDOM OF MOVEMENT.
• CONSISTS OF TWO
PARTS:THE FIBROUS AND
SEROUS.
Pericardium

20-13
LAYERS OF THE HEART WALL
 Heart Wall

• Three layers of tissue

– Epicardium: This serous membrane of smooth
outer surface of heart
– Myocardium: Middle layer composed of
cardiac muscle cell and responsibility for heart
contracting
– Endocardium: Smooth inner surface of heart
chambers

20-15
CHAMBERS OF THE HEART
External Anatomy
• Four chambers
– 2 atria
– 2 ventricles

• Major veins
– Superior vena cava
– Pulmonary veins
• Major arteries
– Aorta
– Pulmonary trunk

20-17
HEART VALVES AND CIRCULATION
OF BLOOD
ATRIOVENTRICULAR &
SEMILUNAR VALVES
 Blood supply through the heart
• SVC & IVC

• Right atrium

• Right ventricle (via Rt AV valve)

• Pulmonary artery(de o2 blood)

• Lt pulmonary artery Rt pulmonary artery

• Co2 excreted o2 absorbed

• Pulmonary veins (o2 blood)

• Lt atrium

• Lt ventricle (via Lt AV valve)

• Aorta
20-23
Systemic and Pulmonary Circulation

20-24
 Blood supply to the heart
Arterial supply

• Heart is supplied with Rt & Lt coronary arteries

• These are branch of aorta
• Coronary arteries receives 5% of blood
pumped from heart
Venous drainage

• venous blood collected into small veins that

join to form coronary sinus which opens into
Rt atrium.
Coronary Circulation

20-27
 Cardiac cycle
• The function of the heart is to maintain a
constant circulation of blood throughout the
body
• The heart act as a pump and its action
consists of series of events known as cardiac
cycle.
• During the heartbeat heart contracts and
relaxes
Contraction systole
Relaxation diastole
CARDIAC CYCLE
 Stages
Cardiac cycles 60 to 80 per minute
• Atrial systole (0.1 sec)
• Ventricular systole (0.3 sec)
• Complete cardiac diastole (0.4sec)
Total period of 1 cycle 0.8 sec.
 CARDIAC OUTPUT

• CO = SV X HR
mL/min mL/beat (Beats/min)

• FOR A RESTING ADULT

CO = 70mL/beat x75beats/min
= 5250 mL/min
= 5.25 L/min
CONDUCTION SYSTEM

Chapter 18, Cardiovascular System 35

Figure 18.14a
 Heart Physiology: Sequence of Excitation

• Sinoatrial (SA) node generates impulses about

75 times/minute
• Atrioventricular (AV) node delays the impulse
approximately 0.1 second

Chapter 18, Cardiovascular System 36

 Heart Physiology: Sequence of Excitation

• Impulse passes from atria to ventricles via

the atrioventricular bundle (bundle of His)
– AV bundle splits into two pathways in the
interventricular septum (bundle branches)
1. Bundle branches carry the impulse toward the
apex of the heart
2. Purkinje fibers carry the impulse to the heart
apex and ventricular walls

Chapter 18, Cardiovascular System 37

Heart Excitation Related to ECG

Figure 18.17
Chapter 18, Cardiovascular System 38
 HEART SOUNDS
• PRODUCED FROM BLOOD
TURBULENCE CAUSED BY CLOSING
OF HEART VALVES
• S1 – ATRIOVENTRICULAR VALVE
CLOSURE
• S2 – SEMILUNAR VALVE CLOSURE
• S3 – RAPID VENTRICULAR FILLING
• S4 – ATRIAL SYSTOLE
 PRELOAD
• STRETCH OF CARDIAC MUSCLE
PRIOR TO CONTRACTION.
 AFTERLOAD
• THE PRESSURE THAT MUST BE OVERCOME
BEFORE A SEMILUNAR VALVE CAN OPEN IS
TERMED THE AFTERLOAD.
• HTN AND AHTEROSCLEROSIS INCREASES THE
AFTERLOAD.
• Circulation
– Coronary circulation – the circulation of blood
within the heart.
– Pulmonary circulation – the flow of blood
between the heart and lungs.
– Systemic circulation – the flow of blood
between the heart and the cells of the body.
 Functions of the Heart
• Generating blood pressure
• Routing blood
– Heart separates pulmonary and
systemic circulations
• Ensuring one-way blood flow
– Heart valves ensure one-way flow
• Regulating blood supply
– Changes in contraction rate and force
match blood delivery to changing
metabolic needs
Suchitra Rathod 20-43
Coronary Arteries of the heart

Suchitra Rathod 44
ASSESMENT OF CARDIOVASCULAR
SYSTEM
 History
• Family
• Personal
– Social History: work, stress, smoking, age, diet, gender,
race, life style, exercise
– Past Medical History: angina, MI, CHF, hypertension,
diabetes, renal disease, congenital disorders
• Chief Complaint: pain, palpitations, syncope
• Associated Symptoms: diaphoresis, N/V, fatigue,
orthopnea, syncope
 Pain Assessment
“PQRST”
• P = Provocation
• Q = Quality
• R = Region & Radiation
• S = Severity, and
associate Symptoms
• T = Timing
 Physical examination
• The examination which proceeds logically
from head to toe, can be performed in about
10 minutes with practice and covers the
following areas:
 Sequence in CVS assesment:
• General appearance
• Cognition
• Skin
• BP
• Arterial pulses
• Jugular venous pulsations and pressures
• Heart
• Extremities
• Lungs
• Abdomen
 INSPECTION
• Inspect and Note General Overall
Appearance

“ You see only what you look for

and you recognize only what you
know”
 General appearance
• Level of distress
 Cognition
• Level of consciousness
• Thought process(cerebral perfusion)
• Anxiety
 Weight management
• Weight
• Height
• Body mass index
• Waist circumferance
 WEIGHT MANAGEMENT

• Measure the client’s weight, height, and waist

circumference, and calculate body mass index
(BMI).
• The desirable weight, defined as BMI range of
21 to 25 kg/rn2.
• A desirable waist circumference for women is
no more than 35 inches or 88 cm and for men
is less than 40 inches or 102 cm.
 HEAD, NECK, NAILS, AND SKIN

• When examining the head, pay particular

attention to the eyes, ear lobes, lips, and
buccal mucosa
 Premature Corneal Arcus
• Premature Corneal Arcus: Grayish white ring
surrounding the sclera. Normal in elderly.
Premature development indicative of
hyperlipidemia.
 Exopthalmus
• Exopthalmus: Fixed stare with bulging eyes is
indicative of hyperthyroidism.
• Exophlathmos – Check Thyroid Studies
 Early Cataracts
• Early Cataracts: seen in diabetes , Marfan’s
and Down’s, all of which increase the risk for
cardiovascular disease.
 INSPECTION OF EAR
– Diagonal ear lobe creases, if not congenital, are
suggestive of hyperlipidemia. 77% increased risk
of CAD if bilateral. 33% if unilateral.
• Preauricular crease
 Pulsatile Earlobes:
• Pulsatile Earlobes: Pulsation of the earlobes,
corresponding with the patient’s heart beat, may be
seen in severe tricuspid insufficiency.
 Inspection of skin
Skin color
 Pallor (paleness, whiteness)
 Jaundice
 Peripheral cyanosis
 Central cyanosis
 Scar

 Temperature

 Texture

 Ecchymosis

 Purpura

 Petechiae

 Edema

 Skin turgor
 Scars:
• Look for obvious scars indicating
cardiovascular surgery or trauma. Patients
may be poor historian regarding such
procedures.
– Legs: from bypass grafts?
– Chest: mediastinum from bypass surgery?
– Shoulders: from pacemaker insertion?
– Scars indicative of cardiovascular trauma ie:
previous car accidents.
 Pallor
• Is caused by lack of oxyhemoglobin
• Pallor is observed around the fingernails, lips,
and oral mucosa.
• In patients with dark skin, the nurse observes
the palms of the hands and soles of the feet.
 Jaundice

Test Normal Range Comments

Total Bilirubin 0.3 to 1.9 mg/dL Discoloration of skin and the sclera of the eye occurs when
bilirubin accumulates in the blood at a level greater than
approximately 2.5 mg/dL.

Direct (conjugated) 0 - 0.3 mg/dL Elevated direct (or conjugated) bilirubin or urobilogen (post
Bilirubin hepatic problem – i.e. obstruction)

Indirect 0.1 - 1.0 mg/dl Elevated indirect (or unconjugated) bilirubin (pre-hepatic
(unconjugated) Bilirubin problem – i.e. hemolysis or intra-hepatic problem)
Jaundice
 Peripheral cyanosis
• A bluish tinge, most often of the nails and skin
of the nose, lips, earlobes, and extremities –
suggests decreased flow rate of blood to a
particular area.
• This may be normal in periferal
vasoconstriction associated with a cold
environment, in patients with anxiety or in
disease states such as HF.
 Central cyanosis
• A bluish tinge observed in the tongue and
buccal mucosa – denotes serious cardiac
disorders (pulmonary edema and congestive
heart disease) in which venous blood passes
through the pulmonary circulation without
being oxygenated.
 Xanthelasma
• Yellowish slightly raised plaques in the skin-
may be observed along the nasal portion of
one or both eyelids and may indicate elevated
cholesterol levels
 Tuberous Xanthomas
Striated Xanthomas
• Tuberous Xanthomas (soft yellowish tumor
like deposits) & Striated Xanthomas
( yellowish streaks along palmar creases) are
due to increased lipid levels in the vascular
system.
• Hyperlipidemia Suspected-check lipid panel
 Lab Normal Value Comments

Total Cholesterol < 200 mg/dl Essential for the production of bile salts and steroid
hormones, but excess increase atherosclerotic plaque. 0.5-
1.0% of the population have hyperlipidemia that is familial.
The remainder is caused by DIET, liver disease with biliary
obstruction, corticosteroids, hypothyroidism, and pancreatic
disfunction.
HDLs > 45 mg/dl

LDLs < 100 mg/dl

Triglycerides <150 mg/dl Elevated due to diet, but also can be elevated due to
nephrotic syndrome, pancreatic dysfunction, diabetes and
hypothyroidism.
 Ecchymosis
• A purplish blue color fading to green, yellow or
brown over time – is associated with blood
outside of the blood vessels and is usually caused
by trauma.
• Pts who are receiving anticoagulant therapy
should be carefully observed for unexplained
ecchymosis. In these pts excessive bruising
indicates prolonged clotting times(PT OR PTT)
caused by an anticoagulant dosage that is too
high.
 Petechiae:
• Pinpoint hemorrhages into the skin usually around
hair follicles. Can be due to hypertension. White
centered petechiae of infective endocarditis.
• Rashes: Especially the brownish colored rash
that appears on the feet and ankles of
persons with vascular insufficiency (stasis
dermatitis)
 Varicose Veins

• Dilated and swollen

 Evaluate venous incompetence
• Trendelenburg test
• person is supine
• Lift the leg above the level of the heart until
the veins empty
• Then lower the leg quickly
• An incompetent system will allow rapid filling
of the veins(normally fill within 30-35
seconds)
 Homan’s sign
• Dorsiflexion of the foot with the knee slightly
bent
• Positive sign is calf pain
• This is usually an abnormal sign indicating
thrombosis (“blood clot”)
 EDEMA

• Inspect dependent areas for edema. In the

mobile client, edema is best seen in the feet,
ankles, and lower legs.
• In the bedridden client, edema may be
palpated over the sacrum, abdomen, or
scapula.
• Assess the severity of edema by pressing a
thumb or finger carefully into the area. A
depression that does not rapidly resume its
original contour is noted as pitting, edema.
 Pitting Edema Score:

• 0 Absent
• +1 2mm; disappears rapidly
• +2 4mm; disappears in 10-15 sec
• +3 6mm; disappears in 1 or 2 min
• +4 8 mm; may be seen after 5 min
 Does the Skin Appear Glossy/Shiny:

– Frequently due to edema creating taunt skin.

– Anasarca- Check Albumin & LFTs
 Liver studies
Test Normal Value Comments

Albumin 3.3-4.6 g/dL Major protein present within the blood. Synthesized by the liver.
(Alb) Malnutrition can also cause low albumin (hypoalbuminemia) with
no associated liver disease.

Alanine transaminase 0- 50 U/L Level of ALT abnormality is increased in conditions where cells of
(ALT or SGPT) the liver or heart have been inflamed or undergone cell death.

Aspartate transaminase 0-45 U/L Enzyme elevation reflects damage to the hepatic or cardiac cells.
(AST or SGOT) It is less specific for liver disease. May be elevated in other
conditions such as an MI.
Alkaline phosphatase 100-250 U/L Not specific to the biliary tract (also found in bone and the placenta).
(ALP) If the alkaline phosphatase is elevated, biliary tract damage and
inflammation should be considered. May be renal or GI too.

Ammonia level 35-45 µg/dL The liver normally convert NH3 (ammonia), a byproduct of protein
metabolism into urea to be excreted by kidneys. In severe liver failure
ammonia levels increase. Elevated ammonia levels will cause s/s of
hepatic encephalopathy.
 skin turgor (elasticity)
• Assess skin turgor (elasticity) by lifting a fold of
skin over the sternum or lower arms and
releasing it.
• Normal skin immediately returns to the baseline
position, but skin with decreased turgor stays
pinched (tenting) for up to 30 seconds.
• Decreased skin turgor occurs with dehydration,
volume depletion, rapid weight loss, and
advanced age.
 Temperature and moistness
• Are controlled by autonomic nervous system. Normally the
skin is warm and dry. Under stress, the hands may become
cool and moist.
• In cardiogenic shock, SNS stimulation causes
vasoconstriction, and the skin becomes cold and clammy.
• During MI diaphoresis is common.
• The temperature of the skin may reflect cardiac disease.
Severe anemia, beriberi, and thyrotoxicosis tend to make
the skin warmer; intermittent claudication (leg pain related
to peripheral vascular disease) is associated with coolness
of the lower extremity compared with the upper extremity.
 capillary refill (circulation)
• Assess capillary refill (circulation) by putting
slight pressure on a nail bed until it blanches.
Quickly release the pressure. When circulation
is adequate, nail color returns to baseline in
less than 2 seconds.
• Always check capillary refill before using pulse
oximetry; if capillary refill is abnormal, pulse
oximetry findings are inaccurate.
 Clubbing
• Check fingers for clubbing, in which the distal
tips of the fingers become bulbous and the
angle between the base of the nail and the
skin next to the cuticle increases from the
normal 160 to 180 degrees or more. In
addition, the nails feel soft and spongy. Finger
clubbing is associated with pulmonary and
cardiovascular disease.
 Splinter hemorrhages
• Splinter hemorrhages of the nail are
classically associated with subacute bacterial
endocarditis.
 Assessment of Blood Pressure
• Always measure in both arms sitting
• Then take BP standing
 Blood pressure
• Accurate reading.
• Avoid using a hand in which
• Iv infusion
• AV shunts
• Arm nearest a radical mastectomy
 Pulse pressure
• Normal 30 – 40 mm of hg
• Increases in condition that elevates the stroke
volume(anxiety, exercise, bradycardia)
• Decreased pulse pressure is an abnormal
condition reflecting reduced stroke volume
and ejection velocity(shock, hypovolemia)
 Orthostatic hypotension
• Occurs when the BP drops significantly after the patient
assumes an upright posture. It is usually accompanied by
dizziness, lightheadedness or syncope.
• A drop in systolic BP of 20 mmHg or more when standing
is orthostatic

• The three most causes are

• reduced volume of fluid or blood in the circulatory system
• Inadequate vasoconstrictor mechanisms
• Insufficient autonomic effect on vascular constriction.
 PULSE

• The pulse characteristics can vary.

• If the pulse is irregular, assess for a pulse

deficit by taking apical and radial pulses
simultaneously, noting difference in rate.

• Assess the peripheral pulses, comparing both

the extretimities
• Pulse rate
• Rhythm
• Quality: absent, diminished, normal or
bounding.
• Scales can be used to rate the strength of the
pulse. The following is an example of 0 – 4
scale
• 0 pulse not palpable or absent
• +1 : weak thready pulse difficult to palpate;
obliterated with pressure
• +2 : diminished pulse, cannot be obliterated
• +3 : easy to palpate, full pulse, cannot be
obliterated
• +4: strong, bounding pulse, may be abnormal.
 Peripheral Pulses

• Carotid
• Apical
• Brachial
• Radial
• Femoral
• Popliteal
Posterior Tibial
Dorsalis Pedis
 Allen’s Test:
Evaluating arterial supply in arms
• Occlude the radial artery by firm pressure.
Ask patient to clinch his fist, then open the fist
and observe the color of the palm
• Then compress ulnar artery, clinch fist, and
observe color of palm
• Pallor of the palm during compression of one
artery indicates occlusion of the OTHER
artery!
 Acute Arterial Occlusion:
The Five P’s
• Pain
• Pallor
• Paresthesia
• Paralysis
• Pulselessness
 Assessment of the Arterial Pulse
• Grasp both radial arteries, count for 30
seconds, and multiply by 2
• Determine rhythm. The slower the rate, the
longer you should palpate.
 Arterial Pulse, con’t

• Palpate the carotid artery by standing at the

patients’ right side with him resting on his
back. Listen first for possible bruit and do not
palpate if you hear one
 Arterial Pulse, con’t
• Never palpate both carotids at the same time
Examination of the carotid arteries:
• A bruit may be heard by listening to the
carotid arteries with the diaphragm of a
stethoscope.
• A bruit generally indicates that the carotid
artery has narrowed.
• Note whether a bruit (a blowing sound) is
present by listening with the diaphragm of a
stethoscope over the arteries while the client
holds the breath.
• A bruit generally indicates that the carotid
artery has narrowed. Bruits typically result
from atherosclerosis or radiation of sounds
from an aortic valve murmur.
 Hepatojugular Reflex
• A useful test for assessing high jugular venous
pressure (also called abdominal compression)
• By applying pressure over the liver, you can
grossly assess RV function. People with RV
failure have dilated sinusoids in the liver.
Pressure over right upper quadrant pushes
blood out and increases JV pressure
How to Check for Hepatojugular Reflex
• Have patient lie in bed, mouth open, breathe
normally .
• Place right hand over RUQ and apply firm
pressure for 10 seconds
• Normally there will be a short increase in
venous dilation followed by fall to baseline
 How to Check for Hepatojugular Reflex –
Cont.
• If there is RV failure, neck veins will stay
elevated during entire time of compression
 Hepatojugular Reflux (HJR):
• Hepatojugular Reflux (HJR): is performed to
assess for right heart failure leading to liver
congestion.
– Place a patient in a 45o angle, then raise or lower
the HOB until the highest point of the internal
jugular vein is visible.
– Compress upper right abdomen for 30 to 45
seconds.
– If the neck vein distention rises by > 1 cm or more,
it is abnormal (+ HJR)
 Jugular venous pulsations
• An estimate of right sided heart function can be
made by observing the pulsations of the jugular
veins of the neck.
• Are most commonly assessed
• If they are difficult to see pulsations of the
external jugular veins may be noted.
• These veins are more superficial and are visible
just above the clavicles, adjacent to the sterno
cleido mastoid muscle.
• External jugular veins are frequently distended
while the pt lies supine on the examining
table. As the pt head is elevated the distention
of the veins disappears.
• Obvious distention of the veins with the pts
head elevated 45 degrees to 90 degrees
indicates an abnormal increase in the volume
of the venous system. This is associated with
right sided HF.
JUGULAR VENOUS DISTENTION
JVD
CHEST EXAMINATION
Chest Landmarks

Manubrium

Manubrial junction –
Angle of Louis

Costal angle
 Precordium

• Perform INSPECTION AND PALPATION of the

precordium together to determine the presence of
normal and abnormal pulsations.

• Ideally, the client should be supine with the chest

exposed.

• Stand at the client’s right side and observe the

anterior chest for size, shape, symmetry of
movement, and any evident pulsations.
• The point of maximum intensity (PMI) or apical
impulse is usually seen at the apex.

• The PMI is associated with left ventricular

contraction and should appear at the fifth
intercostal space medial to the left midclavicular
line.

• It may be prominent in thin people and obscured in

those who are obese or have large breasts.
• Right ventricular enlargement can produce an abnormal pulsation
that may be seen as a sustained thrust along the left sternal border.
Termed “heaves” or “lifts,” these pulsations may be found with
various disorders, such as valvular disease and pulmonary
hypertension.

• Thrills represent turbulent blood flow through the heart, especially

across abnormal heart valves. Use the heel or ulnar surface of the
hand to palpate over each of the five cardiac landmarks. Thrills are
perceived as a rushing vibration. Thrills are associated with
significant heart murmurs.

• They may also be palpated over partially obstructed blood vessels.

 “Have you ever felt a thrill?”
• Thrills are superficial vibratory sensations felt
on the skin overlying an area of turbulence
• The presence of a thrill indicates that you will
hear a loud murmur (grade 4-6)
• Simply an indication of what you will hear
when you listen.
 Asymmetry

• Pectus excavatum is a condition in which the

"breast bone" (sternum) appears sunken and
the chest concave. It is sometimes called
"funnel chest".
Inspection & Palpation: Thorax
• Observe for:
– Breathing patterns
– Visible point of maximal impulse (PMI)
– Heaves, or lifts (thrusts)
 Point of Maximal Impulse (PMI)
• Stand on the right side of the patient with him
sitting. Place fingertips at 5th ICS, MCL and
you should feel PMI
• PMI is usually within 10 cm of the midsternal
line and no larger than 2-3 cm diameter
• PMI that is lateral or displaced suggests
cardiomegaly
 PMI, con’t
• About 70% of the time you will be able to feel
PMI with patient sitting. If you can’t, turn
patient to his left side, lying down.
• A PMI that is over 3 cm diameter indicates left
ventricular hypertrophy and is 86% predictive
of increased left ventricular end diastolic
pressure
 PERCUSSION
• Not helpful in CV assessment
• CXR shows heart size and borders very
accurately
AUSCULTATION
Chest Landmarks

Aortic
Pulmonic

Right
Ventricle
Mitral/PMI
 Cardiac Areas
• All Aortic
• People Pulmonic
• Enjoy Erb’s point (2nd pulmonic)
• Their Tricuspid
• Meals Mitral (Apical)
 Cardiac Areas
• Aortic
– 2nd RICS @ RSB
• Pulmonic
– 2nd LICS @ LSB
• Erb’s point (second pulmonic)
– 3rd LICS @ LSB
• Tricuspid
– 4th or 5th LICS @ LSB
• Mitral
– 5th LICS in LMCL
 HOW TO AUSCULTATE

• Position yourself on the client's right side.

• The client should be supine with the upper trunk elevated 30 degrees.

• Use the diaphragm of the stethoscope to auscultate all areas of the precordium for
high-pitched sounds.

• Use the bell of the stethoscope to detect (differentiate) low-pitched sounds or

gallops.

• The diaphragm should be applied firmly to the chest, whereas the bell should be
applied lightly.

• Focus on one sound at a time as you auscultate each area of the precordium. Start
by listening to the heart's rate and rhythm.
 Heart Sounds
• Heart sounds are characterized by location,
pitch, intensity, duration, and timing within the
cardiac cycle
 Heart Sounds
• High-pitched sounds such as S1 and S2,
murmurs of aortic and mitral regurgitation,
and pericardial friction rubs are best heard
with the diaphragm.
• The bell is preferred for low-pitched sounds
such as S3 and S4.
 Heart Sounds – S1…(Lub)…
• S1: Closure of AV valves (mitral and tricuspid
valves: M1 before T1)
• Correlates with the carotid pulse
• Loudest at the cardiac apex
 Heart Sounds – S2…(Dub)…
• S2: Closure of Semilunar valves (aortic &
pulmonic)
• Loudest at the base of the heart
 Heart Sounds – S2…(Dub)…
• S1 and S2 assessed in all four sites in upright
and supine position
 Extra Heart Sounds
S3… S4…
• Due to volume overload • Due to pressure overload
• Due to Rapid ventricular • Due to slow ventricular
filling: ventricular gallop contraction: atrial gallop
• S1 -- S2-S3 (Ken--tuc-ky) • S4-S1 — S2 (Ten-nes—see)
 Third Heart Sound
• When AV valves open, the period of rapid
filling of ventricles occurs. 80% of ventricular
filling occurs now. At the END of rapid filling, a
3rd heart sound may be heard
• S-3 is normal in children and young adults,
but not in people over age 30. It means there
is volume overload of ventricle
 What an S3 Sounds Like...
• SLOSH-ing-in, Slosh-ing-in, Slosh-ing-in
• Or Ken-tuck-y
 Fourth Heart Sound
• At the end of diastole, atrial contraction
contributes to the additional 20% filling of the
ventricle
• If the left ventricle is stiff and non-compliant,
you will hear an S4.
• It sounds like this: a-STIFF-wall, a-STIFF-wall,
a-STIFF-wall
• Or sounds like TEN-ne-see
 Gallop Rhythms
• The presence of an S3 and an S4 creates a
cadence resembling the gallop of a horse.
• Hence the term “gallop rhythm”
 Murmurs
• They are produced when there is turbulent
blood flow within the heart
• Turbulence may be due to a narrowed
opening of a valve (stenosis) or a valve that
does not close completely, allowing blood to
slosh backwards (regurgitation or
insufficiency)
 Murmurs

• Listen for murmurs in the same auscultatory sites

APETM
• Systolic b/w S1 & S2
• Diastolic b/w S2 & S1
 Systolic Murmurs
• These are ejection murmurs
• May be caused by turbulence across the aortic
or pulmonic valves if they are stenosed
• May be caused by turbulence across the
mitral or tricuspid valves if they are
incompetent (regurgitant)
 Systolic Murmurs, con’t
• The murmur falls between S1 and S2
• Sounds like, LUB-shhh-dub
 Diastolic Murmurs
• Mitral and tricuspid stenosis can cause a
diastolic murmur
• Aortic or pulmonic regurgitation can cause a
diastolic murmur
• Sounds like this: Lub-dub-shhh
 Describing Murmurs
• When in the cardiac cycle do you hear the
murmur? Systole? Diastole? Pan-systolic?
• Location (in which of the 4 cardiac areas do
you hear it the loudest?)
• Radiation (does the sound travel throughout
the chest?)
• Duration of the murmur
 The Intensity of Murmurs
• Grade I = lowest intensity, not heard by
inexperienced listener
• Grade II = low intensity, usually audible to
everyone
• Grade III = medium intensity but no palpable
thrill
• Grade IV = medium intensity with a thrill
 Intensity of murmurs, con’t
• Grade V = loudest murmur audible when
stethoscope is on the chest. Has a thrill
• Grade VI = loudest intensity, audible when
stethoscope is removed from the chest. Has a
thrill
 Murmurs

• Grade I :barely audible

• Gr II : audible but quiet and soft
• Gr III : moderated loud, without thrust or thrill
• Gr IV : loud, with thrill
• Gr V : louder with thrill, steth on chest wall
• Gr VI : loud enough to be heard before steth on chest
 Murmurs
• Thrill:
– a palpable murmur
• Bruits:
– Vascular murmur
– sounds made by turbulent blood flow
– Heard over blood vessels with constricted lumens.
– Carotid and femoral are routinely assessed for bruits
– Sometimes found over the vertebral, subclavian and abdominal arteries
 LUNGS

• Because the cardiovascular and respiratory systems are

intimately related, assessment of the cardiovascular system
must include evaluation of the respiratory system.
• Common respiratory findings related to CVD are as follows.

• Tachypnea. Tachypnea, or rapid respirations, is often

associated with pain and anxiety accompanying myocardial
ischemic pain. Tachypnea is also a common compensatory
mechanism in heart failure and pulmonary edema.
•
Note the rate, rhytm, depth, and quality of the
breath. Variations in the respiratory rate and
characteristics may indicate heart failure or
pulmonary edema.
• Auscultate the lungs for the presence of crackles,
rhonchi or other abnormal breath sounds.
• Severe left ventricular failure may produce
pulmonary congestion and resultant frothy sputum
.
• Crackles. Crackles frequently signal left ventricular failure and usually occur just after the
onset of an S3 gallop. As pulmonary capillary pressure increases because of the
backward pressure of left ventricular failure, fluid shifts into the intra-alveolar spaces
and crackles can be auscultated. Crackles may also result from atelectasis (incomplete
lung expansion) related to limited chest wall excursion during prolonged bed rest, chest
splinting from pain, and the effects of sedatives and opioids. Crackles are high-pitched,
noncontinuous sounds. Crackles are best heard at the lung bases (because of
gravitational effects on the fluid) during late inspiration.
•
• Blood-Tinged Sputum. Pink, frothy sputum may indicate acute pulmonary edema. This
manifestation accompanies diffuse pulmonary crackles and denotes serious left
ventricular failure. Frank hemoptysis may be associated with pulmonary embolus. A
cough frequently occurs with hemoptysis.
•
• Cheyne-Stokes Respirations. Cheyne-Stokes respirations are characterized by abnormal
periods of deep breathing alternating with periods of apnea. They are a common finding
in heart failure, anemia, and brain damage.
 Pericardial Friction Rub
• These are extra-cardiac sounds of short
duration that have a sound like scratching on
sandpaper
• May result from irritation of the pericardium
from infection, inflammation, or after open
heart surgery
• Best heard when patient sits and holds breath
 Friction Rub, con’t
• A rub that disappears when the patient holds
his breath does NOT come from the heart.
This is probably a pleural friction rub
 ABDOMEN

Inspection and Palpation

Inspection may reveal abdominal distention.

Palpation may confirm the presence of ascites and an enlarged liver.

these findings indicate liver failure, which can be result of chronic right
ventricular failure.

In addition, you may elicit a hepatojugular reflex. After assessing for

jugular vein distention, apply pressure with one hand over the liver for 1
min. An increase in jugular vein distention during and immediately after
liver compression indicates chronically elevated right ventricular pressure.
Auscultation
Loud bruits, heard with the bell over or above
the umbilicus, may indicate an aortic obstruction
or aortic aneurysm. Bruits heard over the upper
midline or toward the back typically from renal
arterial stenosis.
 CARDIOVASCULAR DIAGNOSTIC
PROCEDURES
• Chest x-ray
• ECG
• Echocardiography
• Cardiac catheterization
• Laboratory tests
 Chest X-ray
• Chest X-Ray

• A chest x-ray is obtained to determine the size, contour, and

position of the heart.

• It reveals cardiac and pericardial calcifications and demonstrates

physiologic alterations in the pulmonary circulation.

• Although it does not help diagnose acute MI, it can help diagnose
some complications (eg, HF). Correct placement of cardiac
catheters, such as pacemakers and pulmonary artery catheters, is
also confirmed by chest x-ray.
 Densities
The big two densities are:

(1) WHITE - Bone

(2) BLACK - Air

The others are:

(3) DARK GREY- Fat

(4) GREY- Soft tissue/water

And if anything Man-made is on the film, it is:

(5) BRIGHT WHITE - Man-made

ELECTROCARDIOGRAP
HY
ELECTROCARDIOGRAM
 INTRODUCTION
• The ECG is a diagnostic tool used in assessing the
cardiovascular system. It is a graphic recording of the
electrical activity of the heart.
• The ECG is obtained by placing disposable electrodes in
standard positions on the skin of the chest wall and
extremities.
• The heart's electrical impulses are recorded on special graph
paper, with 12, 15, or 18 leads, showing the activity from
those different reference points.
 DEFENITION
• An electrocardiogram is a graphic record of
the electrical impulses that are generated by
depolarization and repolarization of the
myocardium.
These impulses are conducted to
the external surface of the body where they are
detected by electrodes and measured by
galvanometer.
 Objectives
• To diagnose the presence of MI.
• To diagnose the presence of cardiac dysrrhythmias.
• To diagnose the presence of cardiac enlargement and
size of cardiac champers.
• To detect the electrolyte abnormalities especially K
and Ca.
• To evaluate the effect of therapeutic interventions on
the heart ( e.g. drugs, fluid, and mechanical support)
Electrocardiogram(ECG)
• The SA node(pacemaker of the heart) initiates each
heartbeat by discharging an electrical impulse.
• As this electrical impulse spreads over the atria and
ventricles, the atria contracts and is followed by
ventricular contraction(depolarization).
• As the wave of contraction passes off, atria and
ventricles relax(repolarization).
• This process normally takes place with each heart
beat(60 to 100times per minute.)
The Normal Conduction System
RECALL THE EVENTS IN CARDIAC CYCLE

The impulse is generated

in the SA node.
It spreads through both
atria and cause both atrial
contraction.
It crosses the atrio
ventricular node and is
passed down to the
bundle of His.
• It decends down through
right and left bundle
branches, and finally
reaches the terminal
purkinje fibres.
• Ventricular contraction
takes place.
(systole/depolarization)
• After contraction, the
muscle relax and recover
while the ventricles are
filled with blood
(Diastole/repolarization)
 Pacemakers of the Heart
• SA Node - Dominant pacemaker with an
intrinsic rate of 60 - 100 beats/minute.
• AV Node - Back-up pacemaker with an intrinsic
rate of 40 - 60 beats/minute.
• Ventricular cells - Back-up pacemaker with an
intrinsic rate of 20 - 45 bpm.
Impulse Conduction & the ECG
Sinoatrial node

AV node

Bundle of His

Bundle Branches

Purkinje fibers
RELATIONSHIP

190
 NORMAL ECG
• To understand an ECG record, note the
following points.
• The electric activity of the cardiac cycle is
characterized by five primary wave deflections
• These are designated by the letters “P , Q , R ,
S , T.
Waveforms
 ECG paper
• The ECG paper is divided into large squares
and small squares.
• Each small square is 1mm and one large
squares is 5mm(5 small squares).
• Each small square signifies the passage of 0.04
second and each large square signifies the
passage of the 0.20 seconds.
The Normal ECG
CARDIAC CYCLES

196
 LEAD PLACEMENT
• A lead is an electrical picture of the heart.
Sometimes it is used to mean the pieces of wire
that connect the patient to the ECG recorder.
• The electrical signal from the heart is detected at
the surface of the body through electrodes,
which are joined to the ECG recorder by wires.
• The ECG recorder compares the electrical activity
detected in the different electrodes, and the
electrical picture so obtained is called a “Lead”
 EKG Leads
The standard EKG has 12 leads:

 3 Standard bipolar leads (I,II,III)

 3 Unipolar limb leads.
 6 Unipolar chest leads.
 LIMB LEADS
• The limb leads view the electrical activity of
the heart along a frontal plane, from the top
of the heart to bottom of the heart, or from
the right to left of the heart.
 CHEST LEADS
• Chest leads (V1 to V6)/ Precordial leads view
the heart along the horizontal plane or cross
section from front to back of the body.
• There are three major planes of electric activity detected with electrodes
placed on the right arm, left arm, and the left leg. These are standard limb
leads(leads I, II, III) that measure the difference between the two
points(bipolar).
• Lead I connects the two arms at the wrist.
• Lead II connects the right arm with the left leg.
• Lead III connects the left arm with the left leg.
• Most arrythmias and most types of heart blocks are easily diagnosed from
these leads alone.
• In addition to these three leads, there are three augmented unipolar
leads(AVR, AVL, AVF) that record the differences in potential between the
limbs and the Centre of the heart and six chest leads(VI-V6) that provides
views of the heart from different angles and are used to determine how
far anteriorly or posteriorly the electrical forces are directed.
 The 12 lead ECG
• The six “standard” leads, which are recorded
from the electrodes attached to the Limbs, can
be thought of as looking at the heart in a
vertical plane(ie from the sides or the feet)
• Leads I,II and VL look at the lateral surface
• Leads III, VF at the inferior surface
• Lead VR look at the right atrium.
• The six V leads look at the heart in a horizontal
plane, from the front and the left side.
• Thus V1 & V2 look at the right ventricle
• V3 & V4 look at the septum between the
ventricles and the anterior wall of the left
ventricle.
• V5 & V6 look at the anterior and lateral walls
of the left ventricle.
EINTHOVENS TRIANGLE

204
Lead Placement

aVF
 LIMB LEADS

• Bipolar leads
I II III

• Augment leads
Avr Avl Avf

206
STANDARD BIPOLAR LIMB LEADS
• Lead I-Records the difference of electrical
potential between the left arm(LA) and
right arm.
• Lead II-Records the difference of electrical
potential between the left leg (LL) and the
right arm.
• Lead III-Records the difference of electrical
potential between the Left leg(LL)and left
arm(LA)
 STANDARD LIMB LEADS
• Each of the leads are bipolar; i.e., it
requires two sensors on the skin to make a
lead.
• There will be a positive end at one
electrode and negative at the other.
 UNIPOLAR LIMB LEADS (AUGMENTED)

• Unipolar leads use the center of the heart as their

negative electrode
• aVR-Records the difference of electrical potential
between the right limb and the central terminal.
• aVL-Records the difference of electrical potential
between left arm and the central terminal.
• aVF-Records the difference of electrical potential
between the left leg and the central terminal.
Precordial Leads

Adapted from: www.numed.co.uk/electrodepl.html

 PLACEMENT OF THE CHEST LEADS
• VI-4TH intercostal space to the right of the
sternum.
• V2-4th intercostal space to the left of the
sternum.
• V3-Half way between V2 and V4.
• V4-Fifth intercostal space in the midclavicular
line.
• V5-Fifth intercostal space in the anterior axillary
line.
• V6-Fifth intercostal space in the midaxillary line
• Lead V1 and aVR represents the right side of
the heart.
• Lead V3, V4 represents the anterior
portion of the heart.
• Leads V5, V6, I, aVL represents the left side of
the heart.
• Leads II, III, aVF represent inferior part of the
heart.
 EKG Distributions

• Anteroseptal: V1, V2, V3, V4

• Anterior: V1–V4
• Anterolateral: V4–V6, I, aVL
• Lateral: I and aVL
• Inferior: II, III, and aVF
• Inferolateral: II, III, aVF, and V5
and V6
 Summary of Leads

Limb Leads Precordial Leads

Bipolar I, II, III -

(standard limb leads)

Unipolar aVR, aVL, aVF V1-V6

(augmented limb leads)
COMPONENTS OF ELECTROCARDIOGRAM

ECG consists of waves,complexes,segments and

intervals.
1. Waves or complexes: It is a deflexion that can
be positive,negative,or both .
Waves - P Q R S T U.
Complexes - QRS
 CONTD..
• 2. Segment - A segment is the period of time
between a wave or complex and another
wave or complex ;
• Normally,it is a straight line(Iso electric line)
Eg S-T,

3. Interval -An interval is the period of time

between two points on the ECG that includes
a wave, a complex or both. Eg ; P-R,Q-T,R-R
WAVEFORMS AND INTERVALS
 P WAVE
• 1st positive deflection seen
on the ECG.
• It is smoothly rounded.
• It appears just before the
QRS complex.
• Presence of P wave indicates
that stimulus began in the SA
node (Pacemaker) and
subsequently spreads
through both atria causing
atrial contraction.
 CONTD..
• It represents the time taken
by the atria to empty the
blood into the ventricles
through the open AV valves.
• Normally , p wave has a
duration of less than 0.11
(0.08)second and a height of
less than 2.5 .(3 small
squares width and 3 small
sqaures height.)
 ABNORMALITIES OF P WAVE
• P wave may be hidden ,absent, inverted or
there may be more than one P wave.
• An abnormal p wave indicates that the
excitation impulse is in a pacemaker other
than SA node or atrial depolarization is
abnormal.
• When there are more P waves then QRS
complexes it indicates atrio-ventricular
conduction block.
 CONTD..
• P wave is considered enlarged ,if it is more
than 3 small squares tall and / or 3 small
squares wide, indicative of atrial enlargement.
• If the p-wave is enlarged, the atria are
enlarged.
• If the P wave is inverted, it is most likely an
ectopic atrial rhythm not originating from the
sinus node.
 ABSENT P WAVE
• Atrial fibrillation-P waves are replaced by
numerous small,irregularly occuring fibrillatory
waves.
• Atrial flutter-P waves are re placed by flutter
waves,giving a saw-toothed appearance.
• VT-Difficult to identify as they lie buried in the
wide QRS complexes.
• Hyperkalemia-Reduced in amplitude or
absent.Associated with tall T waves and wide
QRS complexes.
ABSENT P WAVE
 Tall P wave
• If the right atrium is
enlarged ,the deflection of
the right atrium is
superimposed on the left
atrial deflection resulting
in a tall P wave in L III,
aVF.
• Tall P wave - Right atrial
enlargement, Pulmonary
hypertension
 BROAD P WAVE
• If the left atrium is
enlarged , the
deflection of the of the
left atrium is further
delayed after the right
atrial deflection .
• Also a notch appears in
the P wave between its
right and left atrial
components.
 PR INTERVAL
• Measured from the beginning of P wave to the
beginning of the QRS complex.
• It represents the time during which the wave of
contraction passes through the entire conduction
system from the AV node to the purkinje fibers in
the myocardium (‘P-R’ interval represents the time it
takes for the impulse to spread from the atria to the
ventricles).
• During the PR interval ,the filling of the ventricles is
completed.
• Normally it measures less than 0.20 second (5 small
squares )
• Since the P wave represent atrial
depolarization and QRS complex represents
ventricular depolarization, the PR interval is a
measure of atrioventricular conduction time.
 ABNORMALITIES OF P-R INTERVAL

• P-R interval more than o.20 s and less than

0.12 s are considered abnormal.
• If prolonged beyond 0.20 s, it indicates first
degree atrio ventricular block.
• P-R interval less than0.12 s indicates a
pacemaker in the atria other than S.A node
or in the A.V node.
PROLONGED P-R INTERVAL
SHORT PR INTERVAL
CARDIAC CYCLES

236
3.QRS COMPLEX
• Q wave-Initial
downward
deflection.
• R wave-A large
upward deflection.
• S wave-A second
downward
deflection.
 CONTD..

• It represents the depolarization of ventricles.

• It represents the time required for the impulse
to spread through the ventricles to complete
the ventricular contraction.
• Normal QRS complex is narrow with a sharply
pointed wave.
• It measures 0.08 to 0.11 s or less than 3 small
squares in width
ABNORMALITIES OF QRS COMPLEX
• QRS complex more than 0.11 s in width and
often with a bizarre appearance indicate that
depolarization is proceeding in abnormal
sequence and direction.
• Widened QRS complex is indicative of bundle
branch block.
 LOW VOLTAGE QRS COMPLEX
• If the voltage of the tallest R wave in the
limb leads is less than 5mm and that in the
precordial leads is less than 10 mm – low
voltage graph.
Causes
1. Due to low voltage generation.
• Hypothyroidism.
• Constrictive pericarditis.
• Diffuse myocardial disease
 CONTD
2. Due to intervening substance
 Adipose tissue in obesity.
 Muscles in thick chest wall.
 Fluid in pericardial effusion.
 Air in pulmonary emphysema
 ALTERNATING QRS VOLTAGE
• If the voltage of QRS complexes
alternates between high and low in
successive beats.
Causes
Pericardial effusion.
Ischemic cardiomyopathy
QRS Complex

Q waves
CARDIAC CYCLES

245
 Q-T INTERVAL
• From the onset of the Q wave to the
termination of the T wave.
• The duration of the QRS complex , the length
of the ST segment , and the width of the T
wave are included in the measurement of Q-T
interval.
• Normal Q-T interval-0.35-0.43sec.
 SHORTENED Q-T INTERVAL
• Less than .35 sec
Causes
• Hyperkalemia.
• Hypercalcemia.
• Digitalis effect.
 PROLONGED Q-T INTERVAL
Greater than 0.43 sec.
Causes
• Electrolyte deficiency
• Mitral valve prolapse syndrome.
• Coronary disease
• Intracranial event.
 S-T SEGMENT
• S-T segment begins at the end of the S wave
and terminates at the beginning of the t wave.
• It correlate with the period between the
ventricular depolarization and repolarization.
• Normally ST segment lies on the iso electric
line.
• Duration-.08 - .12 Sec
 ABNORMALITIES
• If the ST segment is more than 1 mm
above or below the baseline , it
indicates possible myocardial
ischemia or infarction.
 ST SEGMENT DEPRESSION

• NONSPECIFIC CAUSES
Physiological states
 Anxiety
 Tachycardia.
 Hyperventilation
Extracardiac disorders
 Systemic-Hemorrhage,shock.
 Cerebral-vascular accident
 Abdominal-Pancreatitis,cholecystitis.
 Respiratory-Pulmonary embolism
 SPECIFIC CAUSES
Primary abnormality.
 Pharmacological-Digitalis , quinidine.
 Metabolic-Hypokalemia , Hypothermia.
 Myocardial-Cardiomyopathy , Myocarditis.
 Ischemic-Coronary insufficiency , infarction.
Secondary abnormality
Ventricular hypertrophy.
 ST SEGMENT ELEVATION
Causes
• CAD
• Acute pericarditis.
• Ventricular aneurysm.
• Early repolarization
LOCATION OF INFARCTION DETERMINED FROM ECG
LEADS

ST elevation in Location of
infarction
V1-v4 Anterioseptal
V3-v6,L1,aVL Anteriolateral
v3-,v4 Anterior
V5-v6,L1,aVL Lateral
LII,LIII,aVF Inferior
RELATIONSHIP

258
 Ischemia
• Usually indicated by ST changes
– Elevation = Acute infarction
– Depression = Ischemia
• Can manifest as T wave changes
• Remote ischemia shown by q waves
 What is the diagnosis?
Acute inferior MI with ST elevation in leads
II, III, aVF
 What do you see in this EKG?

ST depression II, III, aVF, V3-V6 = ischemia

 5.T wave
 T wave represents the electrical recovery
of ventricles (repolarization).
 Normally it appears upright and
measures less than 0.20 s in width and
not more than 5mm in height.
 ABNORMALITIES OF T WAVE
• Flat T waves indicate Myocardial ischemia
• Inverted t waves indicate myocardial
infarction.
• Tall t waves indicate elevated serum
potassium.
 TALL T WAVE
• The T wave exceeding a voltage of 5 mm in
the standard leads and 10 mm in precordial
leads is considered tall.
CAUSES
• Hyperkalemia
• Myocardial ischemia/injury
 T wave
• T wave represents the return of the ventricles
to a resting state following
contraction(repolarization of the ventricles).
• Alterations in the direction height or shape of
the “T” wave may be indicative of muscle
injury or electrolyte imbalance.
• T wave: 0.16 seconds
 Hyperkalemia

Tall, narrow and symmetric T waves

 Hypokalemia

U waves
Can also see PVCs, ST depression, small T waves
 6 U WAVE
• Small upright wave of
low voltage, sometimes
seen following T wave.
• Produced by slow and
late repolarization of the
intraventricular purkinje
system.
• Significance is not known.
• Difficult to notice the U
wave but when seen ,it is
best appreciated in the
precordial leads v2-v4.
 PROMINENT U WAVE

• A U wave that is exaggerated and

approximates the size of the T wave is
considered to be a prominent U waves are:
CAUSES
Hypokalemia.
Cardiovascular drugs.
Psychotropic drugs (phenothiazines,tricyclics)
 INVERTED U WAVE

• Represents myocardial
ischemia or ventricular strain.
 U wave
• In some ECGs an extra wave can be seen on
the end of the T wave, and this is called a “U”
wave.
• Its origin is uncertain, though it may represent
repolarization of the papillary muscles.
• If a U wave follows a normally shaped T wave
it can be assumed to be normal. If it follows a
flattened shaped T wave, it may be
pathological.
 SUMMARY OF ECG AND THEIR
SIGNIFICANCE

WAVE SIGNIFICANCE TIME PERIOD ABNORMALITIES

P wave Depolarization of Less than 0.12 Abnormal or absent p wave
atria second indicate that an area other than
S.A node is acting as a
pacemaker.

P-R Time for the Less than0.20 Prolonged P-R interval indicate
interval impulse to reach second first degree heart block.
the ventricles

QRS Depolarization of Less than 0.12 Prolonged QRS complex indicates

complex ventricles. second abnormal sequence of
conduction through the
ventricles(Bundle branch block)
ST segment Completion of Less than 0.20 Elevation or
depolarization of second depression of ST
ventricles segment
represents
ischemia or
infarction of
cardiac muscles

T wave Complete electrical Less than 0.20 Flat T wave

recovery of ventricles. second indicates
ischemia
Inverted T wave
indicates
Myocardial
infarction.
Tall and spiky T
wave indicates
elevated
potassium
The “PQRST”

• P wave - Atrial

depolarization
• QRS - Ventricular
depolarization
• T wave - Ventricular
repolarization
 WHAT TO LOOK FOR IN ECG
• Heart rate - Normal, Tachycardia,
Bradycardia.
• Cardiac rhythm - Regular, Irregular.
• P waves - Regularity, Shape, Duration,
Relationship with QRS complex.
• P-R interval - Duration.
• QRS complex- Duration, R-R interval.
• S-T segment - Elevation, Depression
• T wave - Flat, Inverted, Tall
Criteria's of a normal heart rhythm

1. Presence of one upright and consistent-

appearing P wave before each QRS
complex.
2. P-R interval between 0.12-0.20 seconds
3. A consistent appearing QRS complex of
less than 0.12 seconds.
4. Consistent R-R interval
5. A heart rate between 60-100
beats/minute
identification of heart rate from ECG
• Count the number of
large squares between
consecutive R waves on
the ECG and divide 300
by this figure.
• Alternatively count the
number of small
squares between R-R
interval and divide 1500
by this figure.
What is the heart rate?

www.uptodate.com

(300 / ~ 4) = ~ 75 bpm
What is the heart rate?

www.uptodate.com

(300 / 6) = 50 bpm
 The Rule of 300
It may be easiest to memorize the following table:

# of big Rate
boxes
1 300
2 150
3 100
4 75
5 60
6 50
RHYTHM OR REGULARITY OF THE HEART BEAT

• Determined by comparing the duration of

the R-R interval in an ECG strip.
• If all the R-R intervals are equal ,the rhythm
is considered to be regular.
• If one or more R-R intervals are not equal
to each other, the rhythm is said to be
irregular.
The Normal ECG
12-LEAD ECG LAYOUT

284
ECG IN HEART DISEASES
 Ischemic Heart Disease

• Is most commonly due to atherosclerosis

in coronary arteries
• Often accompanied by angina pectoris
• Detectable by changes in S-T segment of ECG
 Arrhythmias Detected on ECG
• Arrythmias are
abnormal heart
rhythms
• Heart rate
<60/min is
bradycardia;
>100/min is
tachycardia
 cont
• In flutter contraction rates can be
200-300/min
• In fibrillation contraction of
myocardial cells is uncoordinated &
pumping ineffective
–Ventricular fibrillation is life-
threatening
• A V node block occurs when node is damaged
• First degree A V node block is when
conduction thru AV node > 0.2 sec
– Causes long P-R interval
• Second degree AV node block is when only 1
out of 2-4 atrial APs can pass to ventricles
– Causes P waves with no QRS
• In third degree or complete AV node block , no atrial
activity passes to ventricles
– Ventricles are driven slowly by bundle of His or Purkinjes
 MI- Changes
• Sequence of ECG changes
• Normal ECG
• Raised ST segments
• Appearance of Q waves
• Normalization of ST segements
• Inversion of T waves.
 Types
• Anterior infarction – changes classically in
leads v3 v4, but often also in leads v2 & v5
• Inferior infarction : changes in leads III and VF
• Lateral infarction : Changes in leads I, VL, V5-
V6.
• True posterior infarction : dominant R wavesin
lead V1.
 NURSING IMPLICATIONS
• No special patient preparation.
• Explain procedure.
• Ask the patient to lie flat and as relaxed as
possible.
• Keep the bystanders away from the patient.
• Check the functioning of the machine.
• Check for standardization.
• The machine should be properly grounded.
 cont
• Make sure that the electrodes are placed in
the proper place and manner.
• There should be good contact between the
patients skin and the electrodes.
• While selecting a site select a flat and fleshy
site instead of bony surface and muscular
areas.
• After each use the electrode plates should be
thoroughly cleansed with soap and water.
 CAUSES OF POOR ECG SIGNAL
• Oily ,dirty and scaly skin.
• Dirty electrodes.
• Improper application of electrodes.
• Loose or dislodged electrodes.
• Patients movement.
• Muscle tremor.
• Broken cable wire.
• Faulty grounding
• Faulty equipment.
 Echocardiography

• Echocardiography is a noninvasive ultrasound test that is used to examine

the size, shape, and motion of cardiac structures.
• It is particularly useful for diagnosing pericardial effusions, determining
chamber size and the etiology of heart murmurs, evaluating the function
of prosthetic heart valves, and evaluating ventricular wall motion.
• It involves transmission of high-frequency sound waves into the heart
through the chest wall and recording of the return signals.
• The ultrasound is generated by a hand-held transducer applied to the front
of the chest. The transducer picks up the echoes, converts them to
electrical impulses, and transmits them to the echocardiography machine
for display on an oscilloscope and recording on a videotape.
• An ECG is recorded simultaneously to assist with interpreting the
echocardiogram.
• Two-dimensional or cross-sectional echocardiography, an enhancement of
the technique, creates a sophisticated, spatially correct image of the heart.
• Other techniques, such as Doppler and color flow imaging echocardiography,
show the direction and velocity of the blood flow through the heart.
• Echocardiography may be performed with an exercise or pharmacologic stress
test; resting and stress images are obtained.
• Myocardial ischemia from decreased perfusion during stress causes
abnormalities in ventricular wall motion and is easily detected by
echocardiography.
• A stress test using echocardiography is considered positive if abnormalities in
ventricular wall motion are detected during stress but not during rest.
• These findings are highly suggestive of CAD and require further evaluation,
such as a cardiac catheterization.
 Nursing Interventions

• Before echocardiography, the nurse informs the patient about

the test, explaining that it is painless.
• Echocardiographic monitoring is performed while a transducer
that emits the sound waves is moved on the surface of the
chest wall. Gel applied to the skin helps transmit the sound
waves.
• Periodically, the patient will have to turn onto the left side or
hold a breath. The test takes about 30 to 45 minutes.
• If the patient is to undergo an exercise or pharmacologic stress
test with echocardiography, information on stress testing is
also reviewed with the patient.
 Transesophageal Echocardiography (TEE)

• A significant limitation of traditional echocardiography has been the

poor quality of the images produced. Ultrasound loses its clarity as it
passes through tissue, lung, and bone. Another echocardiographic
technique involves threading a small transducer through the mouth
and into the esophagus. This technique, called transesophageal
echocardiography (TEE), provides clearer images because
ultrasound waves are passing through less tissue.

• The high-quality imaging obtained during TEE makes this technique

an important first-line diagnostic tool for evaluating patients with
many types of CVD, including those with HF, valvular heart disease,
and intracardiac thrombi.
• It is frequently used during cardiac surgery to continuously
monitor the response of the heart to the surgical procedure (eg,
valve replacement or coronary artery bypass).

• Complications are uncommon during TEE, but if they do

occur they are serious. These complications are caused by
sedation and impaired swallowing resulting from the topical
anesthesia (respiratory depression and aspiration) and by
insertion and manipulation of the transducer into the
esophagus and stomach (vasovagal response or esophageal
perforation).
 Nursing Interventions

• The patient must fast for 6 hours before the study.

• An IV line is started for administering a sedative and any
pharmacologic stress testing medications.
• The patient is maintained on moderate sedation, defined as a state
of depressed consciousness during which time the patient responds
appropriately to commands and can maintain a patent airway .
• The patient's throat is anesthetized before the probe is inserted.
The patient is then asked to swallow the probe until it is correctly
positioned in the esophagus.
• BP, ECG, respiration, and oxygen saturation (SpO2) are monitored
throughout the study.
• During recovery from moderate sedation,
frequent assessments of the parameters
previously identified are made as well as the
patient's level of consciousness.
• The patient must continue to fast until fully alert
and the effects of the topical anesthetic are
reversed, usually 2 hours after the procedure.
• The patient may have a sore throat for the next
24 hours.
 Cardiac Catheterization

• Cardiac catheterization is an invasive diagnostic procedure in

which radiopaque arterial and venous catheters are introduced
into selected blood vessels of the right and left sides of the
heart.

• Catheter advancement is guided by fluoroscopy. Most

commonly, the catheters are inserted percutaneously through
the blood vessels, or via a cutdown procedure if the patient has
poor vascular access.

• Pressures and oxygen saturation levels in the four heart

chambers are measured.
 Indications
 Cardiac catheterization is most frequently used to diagnose CAD,

 Assess coronary artery patency

 Determine the extent of atherosclerosis based on the percentage of

coronary artery obstruction.
 These results determine whether revascularization procedures, including
pci or coronary artery bypass surgery, may be of benefit to the patient .
 Cardiac catheterization is also used to diagnose pulmonary arterial
hypertension
 To treat stenotic heart valves via percutaneous balloon valvuloplasty.
• During cardiac catheterization, the patient has an IV line in
place for the administration of sedatives, fluids, heparin, and
other medications.
• Noninvasive hemodynamic monitoring that includes BP and
multiple ECG tracings is necessary
 NURSING RESPONSIBILITY

• The myocardium can become ischemic and trigger dysrhythmias as catheters

are positioned in the coronary arteries or during injection of contrast agents.
Resuscitation equipment must be readily available during the procedure.

• Staff must be prepared to provide advanced cardiac life support measures as

necessary.

• Radiopaque contrast agents are used to visualize the coronary arteries. Some
contrast agents contain iodine, and the patient is assessed before the
procedure for previous reactions to contrast agents or allergies to iodine-
containing substances (eg, seafood).

• If the patient has a suspected or known allergy to the substance,

antihistamines or methylprednisolone (Solu-Medrol) may be administered
before the procedure.
• In addition, the following blood tests are performed to identify
abnormalities that may complicate recovery:
 Blood urea nitrogen (BUN)
 creatinine levels
 International normalized ratio (INR)
 Prothrombin time (PT)
 Activated thromboplastin time (aptt)
 Hematocrit and hemoglobin values
 Platelet count
 Electrolyte levels.
• Diagnostic cardiac catheterizations are commonly performed on an
outpatient basis and require 2 to 6 hours of bed rest after the procedure
before the patient ambulates.

• Variations in time to ambulation are related to the size of the catheter used
during the procedure, the site of catheter insertion (femoral or radial
artery), the anticoagulation status of the patient, and other patient variables
(eg, advanced age, obesity, bleeding disorder).

• The use of smaller (4 or 6 French) catheters, which are associated with

shorter recovery times, is common in diagnostic cardiac catheterizations.
• Several options to achieve arterial hemostasis after catheter
removal, including

• manual pressure,

• mechanical compression devices such as the FemoStop

(placed over puncture site for 30 minutes),

 The latter devices are positioned at the femoral arterial puncture site
after completion of the procedure. They deploy a saline-soaked
gelatin sponge (QuickSeal), collagen (VasoSeal), sutures (Perclose,
Techstar), or a combination of both collagen and sutures (Angio-
Seal).

 Other newer products that expedite arterial hemostasis include

external patches (Syvek Patch, Clo-Sur PAD). These products are
placed over the puncture site as the catheter is removed and manual
pressure is applied for 4 to 10 minutes. Once hemostasis is achieved,
the patch is covered with a dressing that remains in place for 24
hours.
• Patients hospitalized for angina or acute MI who require
cardiac catheterization usually return to their hospital rooms
for recovery.

• In some cardiac catheterization laboratories, an angioplasty

may be performed immediately during the catheterization if
indicated.
 Angiography

 Cardiac catheterization is usually performed with angiography, a

technique in which a contrast agent is injected into the vascular system

to outline the heart and blood vessels.

 When a specific heart chamber or blood vessel is singled out for study,

the procedure is known as selective angiography.

 Angiography makes use of cineangiograms, a series of rapidly changing

films on an intensified fluoroscopic screen that record the passage of

the contrast agent through the vascular site or sites.

 Common Sites

Common sites for selective angiography are

The aorta,

The coronary arteries,

The right and left sides of the heart.

 Aortography

An aortogram is a form of
angiography that outlines the lumen of the
aorta and the major arteries arising from it. In
thoracic aortography, a contrast agent is used
to study the aortic arch and its major
branches. The catheter may be introduced
into the aorta using the translumbar or
retrograde brachial or femoral artery
approach.
 Coronary Arteriography

In coronary arteriography, the catheter is introduced

into the right or left brachial or femoral artery, then passed into
the ascending aorta and manipulated into the right and left
coronary arteries.
• Coronary arteriography is used to evaluate the degree of
atherosclerosis and to determine treatment.
• It is also used to study suspected congenital anomalies of the
coronary arteries.
 Nursing Interventions

• Nursing responsibilities before cardiac catheterization include the following:

• The patient is instructed to fast, usually for 8 to 12 hours, before the procedure.

• The patient is informed of the expected duration of the procedure and advised
that it will involve lying on a hard table for less than 2 hours.

• The patient is reassured that mild sedatives or moderate sedation will be given IV.

• The patient is informed about certain sensations that will be experienced during
the catheterization. Knowing what to expect can help the patient cope with the
experience. The nurse explains that an occasional pounding sensation
(palpitation) may be felt in the chest because of extrasystoles that almost always
occur, particularly when the catheter tip touches the myocardium.
• The patient may be asked to cough and to breathe deeply,
especially after the injection of contrast agent. Coughing may
help disrupt a dysrhythmia and clear the contrast agent from the
arteries. Breathing deeply and holding the breath help lower the
diaphragm for better visualization of heart structures.

• The injection of a contrast agent into either side of the heart may
produce a flushed feeling throughout the body and a sensation
similar to the need to void, which subsides in 1 minute or less.

• The patient is encouraged to express fears and anxieties. The

nurse provides teaching and reassurance to reduce apprehension.
CARDIAC LABORATORY TESTS
 LABORATORY TESTS

Laboratory tests may be performed for the

following reasons:
• To assist in identifying the cause of cardiac-related signs and
symptoms
• To identify abnormalities in the blood that affect the prognosis of a
patient with CVD
• To assess the degree of inflammation
• To screen for risk factors associated with CAD
• To determine baseline values before initiating therapeutic
interventions
• To ensure that therapeutic levels of medications (eg, antiarrhythmic agents
and warfarin) are maintained
• To assess the effects of medications (eg, the effects of diuretics on serum
potassium levels)
• To screen generally for abnormalities
 Cardiac Biomarker Analysis

• Enzymes are released from injured cells when the cell membranes rupture.
certain isoenzymes come only from myocardial cells and are released when
those cells are damaged by sustained hypoxia or trauma that results in
infarction. The isoenzymes leak into the interstitial spaces of the
myocardium and are carried into the general circulation by the lymphatic
system and the coronary circulation, resulting in elevated serum enzyme
concentrations.

• Creatine kinase (CK) and its isoenzyme CK-MB are the most specific enzymes
analyzed in acute MI, and they are the first enzyme levels to increase.
• Lactic dehydrogenase and its isoenzymes may also be analyzed but only in
select patients who have delayed seeking medical attention, because the
blood levels of these substances peak in 2 to 3 days, much later than CK
levels.
• Other important cardiac biomarkers that are
assessed include the myoglobin and troponin
T or I.
 CARDIAC ISOENZYMES
• CK-MB
– Specific to myocardium
– Enzyme found in heart, skeletal, and brain muscle
cells. Enzyme is released with injury to cells
– Increases with acute MI, myocarditis , post-CABG,
cardioversion
– May also elevate with chronic renal failure
– With acute MI, MB occurs in serum in 6-12 hrs. &
remains for 18-32 hrs.
– Presence is diagnostic of MI
 Myoglobin
• Myoglobin,early marker of MI, is a heme protein with a small
molecular weight.
• Oxygen-binding protein of striated muscle. Released with
injury to muscle.
• This allows it to be rapidly released from damaged myocardial
tissue and accounts for its early increase, within 1 to 3 hours
after the onset of an acute MI.
• Myoglobin peaks in 4 to 12 hours and returns to normal in 24
hours.
• Myoglobin is not used alone to diagnose MI, because
elevations can also occur in patients with renal or
musculoskeletal disease.
 Troponin T and I
• Troponin T and I are laboratory tests that have several
advantages over traditional enzyme studies such as CK-
MB.
• Troponin t and i are proteins found only in cardiac muscle.
• After myocardial injury, elevated serum troponin t and i
concentrations can be detected within 3 to 4 hours;
• They peak in 4 to 24 hours and remain elevated for 1 to 3
weeks.
• These early and prolonged elevations make very early
diagnosis of mi possible or allow for late diagnosis if the
patient has delayed seeking treatment.
 TROPONIN I and T
• Troponin I more specific
• Unique to heart muscle
• Released with very small amounts of damage
as early as 1-3 hrs. after injury
• Peaks in 12-48 hrs.
• Levels return to normal in 7-10 days.
• Useful in delayed diagnosis of MI also
 Blood Chemistry, Hematology, and Coagulation Studies

Cholesterol Levels
• Cholesterol (normal level is less than 200 mg/dL) is a lipid
required for hormone synthesis and cell membrane
formation. It is found in large quantities in brain and nerve
tissue.
• Two major sources of cholesterol are diet (animal products)
and the liver, where cholesterol is synthesized. Elevated
cholesterol levels are known to increase the risk of CAD.
• Factors that contribute to variations in cholesterol levels
include age, gender, diet, exercise patterns, genetics,
menopause, tobacco use, and stress levels.
• LDLs (normal level is less than 160 mg/dL) are the primary transporters
of cholesterol and triglycerides into the cell. One harmful effect of LDL
is the deposition of these substances in the walls of arterial vessels.
Elevated LDL levels are associated with a greater incidence of CAD. In
people with known CAD or diabetes, the primary goal for lipid
management is reduction of LDL levels to less than 70 mg/dL.
• HDLs (normal range in men is 35 to 70 mg/dL; in women, 35 to 85
mg/dL) have a protective action. They transport cholesterol away from
the tissue and cells of the arterial wall to the liver for excretion.
Therefore, there is an inverse relationship between HDL levels and risk
of CAD. Factors that lower HDL levels include smoking, diabetes,
obesity, and physical inactivity. In patients with CAD, a secondary goal
of lipid management is the increase of HDL levels to more than 40
mg/dL.
 Triglycerides

• Triglycerides (normal range is 100 to 200 mg/dL),

composed of free fatty acids and glycerol, are
stored in the adipose tissue and are a source of
energy.
• Triglyceride levels increase after meals and are
affected by stress.
• Diabetes, alcohol use, and obesity can elevate
triglyceride levels.
• These levels have a direct correlation with LDL and
an inverse one with HDL.
 B-type NATRIURETIC PEPTIDE
(BNP)
• Hormone produced by ventricles of the heart
that increases in response to ventricular
volume expansion and pressure overload.
• Marker of ventricular systolic and diastolic
dysfunction
• Useful in diagnosing CHF
• Normal is less than 100 ng/L
 C-Reactive Protein

• High-sensitivity assay for C-reactive protein

(hs-CRP) is a venous blood test that measures
levels of CRP, a protein produced by the liver
in response to systemic inflammation.
• Inflammation is thought to play a role in the
development and progression of
atherosclerosis. Therefore, hs-CRP is used as
an adjunct to other tests to predict CVD risk.
• People with high levels of hs-CRP (3.0 mg/dL)
are at greatest risk for CVD compared to
people with moderate (1.0 to 3.0 mg/dL) or
low (less than 1.0 mg/dL) levels of hs-CRP.
• In addition, an elevated hs-CRP places patients
with ACS at high risk for recurrent cardiac
events, including unstable angina and acute
MI, higher mortality, and increased risk of
restenosis of coronary arteries after PCI
 Sodium (Na ) +

Hyponatremia: Decreased sodium levels

indicate fluid excess and can be caused by
heart failure or administration of thiazide
diuretics.
Hypernatremia: Increased sodium levels
indicate fluid deficits and can result from
decreased water intake or loss of water
through excessive sweating or diarrhea.
 Potassium has a major role in cardiac
electrophysiologic function.
•
Hypokalemia: Decreased potassium levels due to administration of
potassium-excreting diuretics can cause many forms of dysrhythmias,
including life-threatening ventricular tachycardia or ventricular
fibrillation, and predispose patients taking digitalis preparations to
digitalis toxicity.
•
Hyperkalemia: Increased potassium levels can result from an increased
intake of potassium (eg, foods high in potassium or potassium
supplements), decreased renal excretion of potassium, use of
potassium-sparing diuretics (eg, spironolactone), or use of angiotensin-
converting enzyme inhibitors (ACE inhibitors) that inhibit aldosterone
function. Serious consequences of hyperkalemia include heart block,
asystole, and life-threatening ventricular dysrhythmias.
 Calcium is necessary for blood coagulability, neuromuscular
activity, and automaticity of the nodal cells (sinus and
atrioventricular nodes).
•
Hypocalcemia: Decreased calcium levels slow nodal function
and impair myocardial contractility. The latter effect
increases the risk for heart failure.
•
Hypercalcemia: Increased calcium levels can occur with the
administration of thiazide diuretics because these
medications reduce renal excretion of calcium.
Hypercalcemia potentiates digitalis toxicity, causes increased
myocardial contactility, and increases the risk for varying
degrees of heart block and sudden death from ventricular
fibrillation.
• Magnesium is necessary for the absorption of calcium, maintenance of
potassium stores, and metabolism of adenosine triphosphate. It plays a
major role in protein and carbohydrate synthesis and muscular
contraction.
•
Hypomagnesemia: Decreased magnesium levels are due to enhanced
renal excretion of magnesium from the use of diuretic or digitalis
therapy. Low magnesium levels predispose patients to atrial or
ventricular tachycardias.
•
Hypermagnesemia: Increased magnesium levels are commonly caused
by the use of antacids containing magnesium. Increased magnesium
levels depress contractility and excitability of the myocardium,
causing heart block and, if severe, asystole.
 Blood urea nitrogen (BUN)
• BUN and creatinine are end products of
protein metabolism excreted by the kidneys.
 Creatinine
• Elevated BUN reflects reduced renal perfusion
from decreased cardiac output or intravascular
fluid volume deficit as a result of diuretic therapy
or dehydration.
Both laboratory values are used to assess
renal function, although creatinine is a more
sensitive measure. Renal impairment is detected
by an increase in both BUN and creatinine. A
normal creatinine level and an elevated BUN
detect an intravascular fluid volume deficit.
 GLUCOSE
• Glucose levels are elevated in stressful
situations, when mobilization of endogenous
epinephrine results in conversion of liver
glycogen to glucose. Serum glucose levels are
drawn in a fasting state.
 Glycosylated hemoglobin
• Glycosylated hemoglobin (hemoglobin A1C) is
monitored in people with diabetes. It reflects
the blood glucose levels over 2 to 3 months.
The glycemic goal is to maintain the
hemoglobin A1C below 7% (normal range 4%–
6%), reflecting consistent near-normal blood
glucose levels.
Hematologic Studies
 CBC
• The CBC identifies the total number of white
and red blood cells and platelets, and
measures hemoglobin and hematocrit. The
CBC is carefully monitored in patients with
cardiovascular disease.
 WBC
• WBC counts are monitored in
immunocompromised patients, including
patients with heart transplants or in situations
where there is concern for infection (eg, after
invasive procedures or surgery).
 The hematocrit
• The hematocrit represents the percentage of
red blood cells found in 100 mL of whole
blood. The red blood cells contain
hemoglobin, which transports oxygen to the
cells. Low hemoglobin and hematocrit levels
have serious consequences for patients with
cardiovascular disease, such as more frequent
angina episodes or acute myocardial
infarction.
 Platelets
• Platelets are the first line of protection against bleeding. Once
activated by blood vessel wall injury or rupture of
atherosclerotic plaque, platelets undergo chemical changes
that form a thrombus. Several medications inhibit platelet
function, including aspirin, clopidogrel (Plavix). When these
medications are administered, it is essential to monitor for
thrombocytopenia (low platelet counts).
 CARBON DIOXIDE
• Measures bicarbonate level of blood
• Measures metabolic state
 BLOOD UREA NITROGEN
(BUN)
• Increased level (azotemia) with impaired renal
function caused by:
– CHF, Dehydration, Shock, Stress, Acute MI
• Increased levels also with renal disease and GI
bleed
 LIVER FUNCTION TESTS
• AST, ALT, Alkaline Phosphatase
• May elevate in CHF due to hepatic congestion
• Will elevate in low perfusion states causing
“shock liver” due to ischemia. Common with
cardiac arrest S/P resuscitation, prolonged
hypotension, shock states, embolic event.
 MISCELLANEOUS LABS
• Amylase & Lipase
– Increases with pancreatitis or GB disease
– May order if suspect GI source of chest pain
• Magnesium
– Decreased levels cause arrhythmias
– Always check in atrial & ventricular arrhythmias
and QT prolongation
 MISCELLANEOUS
• Thyroid Function Tests
– Thyroid abnormalities can cause:
• Arrhythmias
• Fatique
• Anemia
– Usually start by checking TSH. If abnormal, check
full thyroid panel
CARDIOVASCULAR
DISORDERS
CORONARY ARTERY DISEASE
 Introduction
• The epidemic of cardiovascular diseases (CVDs) is

accelerating globally over all regions and social classes.

356
Percentage Breakdown of Deaths from Cardiovascular
Disease in the United States, 2001
 Coronary Artery Disease (CAD)
• Coronary artery disease (CAD) /Coronary
heart disease (CHD) occurs due to
atherosclerosis/arteriosclerosis.

358
 Coronary Artery Disease:
Occurs when the coronary arteries
that supply the heart muscle
become blocked.

• Partially blocked it causes angina.

• Fully blocked it causes a myocardial

infarction or a heart attack!
Suchitra Rathod 359
 Coronary Artery Disease
• Atherosclerosis:- The term
atherosclerosis is derived from two
Greek words: athere meaning “fatty
mush”, and skleros meaning “hard”,
This word combination indicates
that atherosclerosis begins as soft
deposits of fat that harden with
age.
• Atherosclerosis referred to as
“hardening of the arteries’.
Suchitra Rathod 360
 Contd..
• Define: thickness and hardening of
the arteries caused by deposits of
fat and fibrin which harden.

• Leads to decreased lumen and

decreased blood flow and ischemia
and death of the tissue

Suchitra Rathod 361

 Coronary Atherosclerosis

•Left Coronary Artery. LCx

• Anterior Descending (LAD)
• Left Circumflex (LCx)
•Right Coronary Artery. LAD

Suchitra Rathod 362

• Arteriosclerosis:
– Define: loss of elasticity and
abnormal thickening or hardening of
the walls of the arteries which can be
due to accumulation of lipids,
cholesterol, calcium or thrombus.
– May also lead to occlusion of the
lumen of the vessel, usually at the
bifurcation of the vessels
– May develop collateral circulation if
develops slowly
Suchitra Rathod 363
Suchitra Rathod 364
Suchitra Rathod 365
Common Blood Vessel Disorders

• Thrombus – blood
clot
• Embolus – free
flowing clot
• Aneurysm – bulging
or burst blood vessel

367
Fig. Atherosclerosis

368
369
Consequences of Atherosclerosis

370
 Risk Factors for CAD
1. Modifiable risk factors:
- Cholesterol levels
- Cigarette smoking
- Hypertension
-Diabetes mellitus
-Sedentary life style
2. Non-modifiable risk factors:
- Age
- Gender
- Family history
- Race 371
 Risk Factors
Nonmodifiable Risk Factors
• Gender (men yr of age) women until 60
• Ethnicity (whites Americans) African
• Genetic predisposition and family history of
heart disease
 Modifiable Risk Factors

Major Contributing
• Serum lipids: elevated • Diabetes mellitus
triglycerides, and LDL • Fasting blood sugar >110
cholesterol mg/dl*
• Hypertension • Psychologic states
• Obesity: • Homocysteine levels
• Physical inactivity
• Tobacco use
 1. Non modifiable risk factors
a. Age: With ↑ing age, there is
progressive atherosclerosis. The
risk over 40 yrs, even in their 30s,
20s.
b. Sex: Women of childbearing age
display ¼ the risk compared with
men of the same age (influence of
oestrogen)
Women who take oral contraceptives.
Suchitra Rathod 374
 Contd..
- After menopause, the incidence
tends to become equal in two sex
groups
- Women with an early menopause
have three times the risk as women
with a normal or late menopause.

Suchitra Rathod 375

b. Heredity: There is a strong familial
or genetic predisposition towards
CAD.
- Family history of premature CAD,
in Ist degree relatives. Among
sibling is almost 1:5

Suchitra Rathod 376

c. Race: In 1992, the death rate for black
males was 2.4% higher than that for
white males, while the death rate for
black females was 33% higher than
white females
2. Modifiable risk factors:
a. Environment: CAD is seven times more
prevalent in North America, Australia,
Europe and Newzealand
- Urban population have higher
incidence than rural population
Suchitra Rathod 377
- In developing countries, is most
prevalent in the affluent
- Environmental factors like nutrition
& socio economical status
b. Cigarette smoking: A third major
risk factor in CAD.
- Male adult smokers have a 70%
higher morality rate than do male
non smokers.(risk for CAD is 2 to 6
times higher)
Suchitra Rathod 378
- They have two or four times the
risk of sudden cardiac death
- The risk infarction is correlated
with the number of cigarettes
smoked daily.
 The three substances increase the
prevalence of CAD.
1.Tar, 2.Nicotin, 3. Carbon monoxide.
1. Tar: Contains hydrocarbons and
other carcinogenic substances.
Suchitra Rathod 379
2. Nicotine: ↑es the release of
epinephrine and nor
epinephrine, which results in
peripheral vasoconstriction,
elevated blood pressure & heart
rate, greater oxygen
consumption & ↑
dysarrhythmias. Diminishes
available oxygen by ↑ing the
level of carbon monoxide
Suchitra Rathod 380
- Lowers the HDL and ↑es LDL, ↑es
myocardial oxygen demand
- Nicotine activates platelets &
stimulates smooth muscle cell
proliferation in the arterial walls
3.Carbon monoxide: reduces the
amount of blood available to the
intima of the vessel wall & ↑es the
permeability of the endothelium.
Suchitra Rathod 381
 Contd..
• Smoking causes an increase in
myocardial oxygen consumption,
heart rate and blood pressure,
which is mediated through increase
in blood catecholamine.
• The carbon monoxide inhaled also
decreases the oxygen-carrying
capacity of the blood, and produces
direct damage to the arterial
endothelium.
Suchitra Rathod 382
 Contd..
c. Hypertension: The second major
risk factor in CAD and premature
death.
- Elevated BP increases the rate of
atherosclerotic development.
- Vasoconstriction & increase
myocardial oxygen demand

Suchitra Rathod 383

 Contd..
d. Elevated lipid levels: ↑es the risk
of developing CAD.
e. Physical inactivity: Is a 4th major
modifiable risk factor. By increasing
weight & blood pressure & ↓the
protective HDL and increasing LDL.
↑ myocardial oxygen demand. ↓
functional capacity of
cardiovascular system.
Suchitra Rathod 384
d. Excessive alcohol use- Increase bl.
Pressure leading to heart failure,
↑triglycerides, cause irregular heart
beats.
3. Obesity: Increase an extra heart
workload (Increase requiring the
muscle to work harder to pump
enough blood to support added
tissue mass) & risk of hypertension,
diabetes, hyperlipidemia
Suchitra Rathod 385
. g. Diabetes: ↑es the risk of HPN,
obesity & elevated blood lipids. The
incidence is ↑ed 4 times in DM.
Stress: ↑es heart workload & risk
for HPN.
Stress: Chronic stress is defined as
a persistence feeling of fatigue,
lack of energy, increased
irritability and demoralization,
and depression
Suchitra Rathod 386
e. Oral Contraceptives: It ↑ BP, faster
clotting time, glucose level etc.

Suchitra Rathod 387

f. Type A personality (coronary prone
behavior): Have twice the risk of
CAD as compared to Type B
personality. Type A is urgency,
hostility, aggression, ambition,
impatience, competitiveness,
frustration etc. These behavior
elevate the level of cholesterol &
triglycerides in blood, enhanced
platelet aggregation, faster clotting
time etc. Suchitra Rathod 388
 Type ”A” Personality
• Highly Competitive
• Strong Personality
• Restless when
inactive
• Seeks Promotion
Punctual
• Thrives on deadlines
• Maybe jobs at once
Suchitra Rathod 389
Type “B” Personality
• Works methodically
• Rarely competitive
• Enjoys leisure time
• Does not anger easily
• Does job well but
doesn’t need
recognition
• Easy-going
Suchitra Rathod 390
 Developmental Stages of CAD

Fatty Streak.
• Fatty streaks, the earliest lesions of atherosclerosis,
are characterized by lipid-filled smooth muscle
cells.
Fibrous Plaque.
• The fibrous plaque stage is the beginning of
progressive changes in the endothelium of the
arterial wall.
• The fatty streak is eventually covered by collagen
forming a fibrous plaque.
• The result is a narrowing of the vessel lumen and a
reduction in blood flow
 CONTI..
Complicated Lesion.
• As the fibrous plaque grows, continued
inflammation can result in plaque instability,
ulceration, and rupture.
• Platelets accumulate in large numbers, leading
to a thrombus.
• The thrombus may adhere to the wall of the
artery, leading to further narrowing or total
occlusion of the artery.
Progression of atherosclerosis
 Progression of Heart Disease

High Blood Pressure

High Cholesterol Levels
Myocardial Infarction

Atherosclerosis Necrosis

Ischemia

394
 CAD-Atherosclerosis—Treatment
• Decrease cholesterol and LDL
• Decrease sodium ion intake
• Control primary disorders
• Quit smoking
• Oral anticoagulant
• Surgical interventions
– Percutaneous transluminal coronary angioplasty (PTCA)
– Cardiac catheterization
– Laser beam technology
– Coronary artery bypass grafting (CABG)
395
• Most heart disease is the result of atherosclerotic
obstruction of the coronary arteries
• Depending on the degree & character of the
obstruction CAD can be:
– Angina pectoris(AP)
– Myocardial infraction (MI),
– Sudden cardiac death
396
 Angina (Angina Pectoris)-AP

• Resulting from narrowing of blood vessels to the

coronary artery,
• secondary to arteriosclerosis,

• Atherosclerotic heart disease occurs when there is

a buildup of plaque within the coronary arteries.

397
 Comparison of types of Angina pectoris
Stable Unstable Prinzmetal’s
Angina Angina Angina

Etiology Myocardial Rupture of Coronary

ischemia, thickened vasospasm
usually to plaque,
atherosclero exposing
sis thrombogeni
c surface

Suchitra Rathod 398

Characteri Episodic pain New-onset of Occurs
stics lasting 5 – 15 angina primarily at
min. Angina of ↑ rest
Provoked by frequency, Triggered by
exertion duration or smoking
Relieved by severity May occur in
rest or Occurs at rest presence or
nitroglycerin or minimal absence of
e exertion CAD
Pain
refractory
To nitrogen

Suchitra Rathod 399

 SIGNS AND SYMPTOMS
• Chest pain lasting 3 to 5 minutes—not all
patients get substernal pain; it may be
described as pressure, heaviness, squeezing, or
tightness.
• Use the patient’s words.

400
 S/S…
• Can occur at rest or after exertion, excitement,
or exposure to cold—due to increased oxygen
demands or vasospasm.
• Usually relieved by rest—a chance to re-
establish oxygen needs.

401
 S/S…

• Pain may radiate to other parts of the body such as

the jaw, back, or arms—angina pain is not always

felt in the chest.

• Ask if the patient has had similar pain in the past.

• Sweating (diaphoresis)—increased work of body to

meet basic physiologic needs; anxiety.

402
 S/S…
• Tachycardia—heart pumping faster trying to meet

oxygen needs as anxiety increases.

• Difficulty breathing, shortness of breath (dyspnea)

—increased heart rate increases respiratory rate and

increases oxygenation.

• Anxiety—not getting enough oxygen to heart muscle,

the patient becomes nervous.

403
 INTERPRETING TEST RESULTS
 Electrocardiogram(ECG) during episode:

• T-wave inverted with initial ischemia, which is reduced

blood flow due to an obstructed vessel, usually first sign.

• ST-segment changes occur with injury to the

myocardium (heart muscle).

• Abnormal Q-waves due to infarction of myocardium.

404
• Labs: troponins, CK-MB, which is an enzyme released

by damaged cardiac tissue 2 to 6 hours following an

infarction, electrolytes.

• Chest x-ray to determine signs of heart failure.

• Coronary arteriography to determine plaque build-up

in coronary arteries.

405
• Cardiac PET (positron emission tomography) to

determine plaque build-up in coronary arteries.

• Stress testing to determine symptoms when at exercise

or under pharmacologic stress.

• Echocardiogram or stress-echo to determine any

abnormality of wall motion due to ischemia.

• Cardiology consult.

406
• Complete Blood Count (CBC) used to determine the

general health status of the patient,

• chemistry (provides information about the status of

eletrolytes, kidneys, acid/base balance, blood sugar

and calcium levels),

407
• Prothrombin Time (PT/INR), Activated Partial

Throboplastin Time (PTT) (helps to detect and

diagnose bleeding disorders and the effectiveness of

anticoagulants), (BNP) measures the presence and

severity of heart failure.

408
 Cholesterol panel to evaluate risk.

• Increased risk for coronary artery disease with

increased total cholesterol,

• increased low-density lipoproteins (LDL), increased

triglycerides and decreased high-density lipoproteins.

(HDL).

409
Chronic Stable Angina : Manifestation of Coronary Artery
Disease
 Chronic stable angina
• Chronic stable angina refers to chest pain that
occurs intermittently over a long period with
the same pattern of onset, duration, and
intensity of symptoms
• Angina is rarely sharp or stabbing, and it usually
does not change with position or breathing.
• The pain usually lasts for only a few minutes (3
to 5 minutes) and commonly subsides when
the precipitating factor is relieved
 Etiology and Pathophysiology

• Angina, or chest pain, is the clinical

manifestation of reversible myocardial
ischemia.
• Either an increased demand for oxygen or a
decreased supply of oxygen can lead to
myocardial ischemia
 PATHOLOHY OF ANGINA
• coronary occlusion

• contractility ceases after several minutes

• myocardial cells deprived of oxygen and glucose for

aerobic metabolism.

• Anaerobic metabolism begins and lactic acid

accumulates

• Increased lactic acid irritate the myocardial nerve fibers

• Transmit a pain message to the cardiac nerves and

 Types
• Nocturnal angina occurs only at night but not
necessarily when the person is in the recumbent
position or during sleep.
• Angina decubitus is chest pain that occurs only while
the person is lying down and is usually relieved by
standing or sitting.
• Prinzmetal's angina
usually in response to spasm of a major coronary artery
• Coronary spasm can be described as a strong
contraction of smooth muscle in the coronary artery
caused by an increase in intracellular calcium.
MANAGEMENT: CHRONIC STABLE ANGINA- Drug Therapy

Short-Acting Nitrates
• Dilating coronary arteries and collateral
vessels.
• Dilating peripheral blood vessels
Sublingual Nitroglycerin.
• The recommended dose is 1 tablet taken
sublingually
 CONTI..
Long-Acting Nitrates.
Nitroglycerin Ointment.
• 2% nitroglycerin topical ointment is placed on the
skin, over a flat muscular area that is free of hair
and/or scars
Transdermal Controlled-Release Nitrates.
• Reservoir and Matrix.
• The reservoir system delivers the drug using a rate-
controlled permeable membrane.
• The matrix system provides for a slow delivery of the
drug through a polymer matrix.
 CONTI..
β-Adrenergic Blockers.
• These drugs decrease myocardial contractility, HR,
SVR, and BP, all of which reduce the myocardial
oxygen demand
EG. propranolol , metoprolol
Calcium Channel Blockers.
• (1) systemic vasodilation with decreased SVR,
• (2) decreased myocardial contractility, and
• (3) coronary vasodilation.
Angiotensin-Converting Enzyme Inhibitors.
 Unstable Angina

• Chest pain that is new in onset, occurs at rest,

or has a worsening pattern is called unstable
angina.
• Unlike chronic stable angina, UA is
unpredictable and represents an emergency.
• It will occur with increasing frequency and is
easily provoked by minimal or no exertion,
during sleep, or even at rest.
 Medical management
Prevention, rather than treatment,
is the goal for clients with CAD.
- Cessation of cigarette smoking,
- Controlling diet and dietary
modification is an initial step.
- Managing diabetes & HPN can
also decrease the risk of CAD.
Suchitra Rathod 420
•Get regular medical checkups.
•Control blood pressure.
•Check cholesterol.
•Don’t smoke.
•Exercise regularly.
•Maintain a healthy weight.
•Eat a heart-healthy diet.
•Manage stress.
Suchitra Rathod 421
 How can You Stop CVD?
• Diet and Nutrition, there are several
guidelines listed by the American
Heart Association:
• Eat a variety of fruits and vegetables
every day. ( 5 servings - they are
naturally low in fat and high in
vitamins and minerals)
• Eat a variety of grain products ( 6 a
day) Suchitra Rathod 422
 Diet and Prevention of CVD
• Choose non-fat or low-fat
products.
• Use lean meats- choose chicken,
fish, turkey and lean cuts of beef
and pork.
• Switch to fat-free milk- gradually
reduce the fat content of the milk
you drink.
Suchitra Rathod 423
 Dietary Guidelines
• Choose fats with 2 gms or less of
saturated fats per serving canola oil
and olive oil.
• Balance the # of calories you eat
with the number of calories you
use each day.
• Maintain a level of physical activity
that keeps you fit and matches the
# of calories you eat.
Suchitra Rathod 424
 Dietary Guidelines
• Limit your intake of foods high
in calories and low in nutrition,
including foods like soft drinks
and candy.
• Limit foods high in saturated fat,
and cholesterol
• Eat less than 6 gms of salt a day
• Have no more than one
alcoholic drink a day.
Suchitra Rathod 425
 Exercise and CVD
• Serves several functions in
preventing and treating those at
high risk.
• Reduces incidence of obesity.
• Increases HDL
• Lowers LDL and total cholesterol
• Helps control diabetes and
hypertension
• Those at high risk should take part in
a specially supervised program.
Suchitra Rathod 426
 Medical management
1. Opiate analgesic- Morphine
Sulphate 2-10 mg for q 5-15 min of
nitroglycerine
2. Vasodilators- Nitrate
3. Calcium channel blockers-
Nifedipine
4. Beta Blockers- propranolol
5. Thrombolytic therapy: streptokines,
Urokinase.Suchitra Rathod 427
 Nitrates
Mechanisms of Action
• Nitric oxide has been identified
as endothelium-derived relaxing
factor
• Organic nitrates are therapeutic
precursors of endothelium-
derived relaxing factor
Suchitra Rathod 428
 Nitrates
Mechanisms of Action
Venous vasodilatation /pre-load
reduction
• Arterial dilation/after-load reduction
• Coronary arterial vasodilatation
• Prevention of coronary
vasoconstriction
• Enhancement of coronary collateral
flow
• Antiplatelet and antithrombotic effects
Suchitra Rathod 429
 Nitrates
Reducing Tolerance
• Smaller doses
• Less frequent dosing
• Avoidance of long-acting
formulations unless a prolonged
nitrate-free interval is provided
• Build-in a nitrate-free interval of
8-12 hours Suchitra Rathod 430
 Nitrates
Side Effects
• Headache
• Flushing
• Palpitations
• Tolerance

Suchitra Rathod 431

 Nitrates
Common Available Agents
• Isorbide dinitrate
• Isorbide mononitrate
• Long-acting transdermal patches
• Nitroglycerin sl

Suchitra Rathod 432

 Beta-Blockers
• Decrease myocardial oxygen
consumption
• Blunt exercise response
• Beta-one drugs have theoretical
advantage
• Try to avoid drugs with intrinsic
sympathomimetic activity
• First line therapy in all patients with
angina if possible
Suchitra Rathod 433
 Beta Blockers: Side Effects
• Bronchospasm
• Diminished exercise capacity
• Negative inotropy
• Sexual dysfunction
• Bradyarrhythmia
• Masking of hypoglycemia
• Increased claudication
• Hair loss
Suchitra Rathod 434
 Beta Blockers
Common Available Agents
• Propranolol
• Atenolol
• Metoprolol
• Nadolol
• Timolol

Suchitra Rathod 435

 Calcium Channel Blockers
Mechanisms of Action
• Arterial dilation/after-load reduction
• Coronary arterial vasodilation
• Prevention of coronary
vasoconstriction
• Enhancement of coronary collateral
flow
• Improved subendocardial perfusion
• Slowing of heart rate with diltiazem,
verapamil Suchitra Rathod 436
Calcium Channel Blockers
Mechanisms of Action

Suchitra Rathod 437

Calcium Channel Blockers
Mechanisms of Action

Suchitra Rathod 438

 Calcium Channel Blockers
Side Effects
• Palpitations
• Headache
• Ankle edema
• Gingival hyperplasia

Suchitra Rathod 439

 Calcium Channel Blockers
Available Agents
• Verapamil
• Diltiazem
• Nifedipine
• Nicardipine
• Amlodipine
• Felodipine
• Nisoldipine
• Bepridil
Suchitra Rathod 440
 Surgical Management:
- Percutaneous Transluminal
Coronary Angioplasty (PTCA)
- Coronary Atherectomy
- Coronary Artery stents.
- Laser Ablation
- Coronary Artery Bypass Graft
(CABG)

Suchitra Rathod 441

Treatment (continued)
•a) Angioplasty a balloon catheter is
passed through the guiding catheter to
the area near the narrowing.
•A guide wire inside the balloon catheter
is then advanced through the artery
until the tip is beyond the narrowing.
The angioplasty catheter is moved over
the guide wire until the balloon is within
the narrowed segment.
Suchitra Rathod 442
 Contd…
• Balloon is inflated, compressing the
plaque against the artery wall.
• Once plaque has been compressed
and the artery has been sufficiently
opened, the balloon catheter will
be deflated and removed.

Suchitra Rathod 443

Coronary Angioplasty:

Suchitra Rathod 444

Suchitra Rathod 445
Treatment (continued)
•
a stent is introduced into a blood
vessel on a balloon catheter and
advanced into the blocked area of
the artery
• the balloon is then inflated and
causes the stent to expand until it fits
the inner wall of the vessel,
conforming to contours as needed
Suchitra Rathod 446
• The balloon is then deflated and
drawn back
•The stent stays in place
permanently, holding the vessel
open and improving the flow of
blood.

Suchitra Rathod 447

Suchitra Rathod 448
Suchitra Rathod 449
 Synchronization of cardiac assist devices

• Left ventricular assist

device (LVAD)
• Intra-aortic balloon pump
• Implantable Cardioverter
Defibrillator

Suchitra Rathod 450

 Treatment (continued)
By pass surgery healthy blood vessel
removed from leg, arm or chest
• blood vessel is used to create new blood
flow path in your heart
• the “bypass graft” enables blood to reach
your heart by flowing
Around (bypassing) the blocked portion
of the diseased artery. The increased
blood flow reduces angina and the risk
of heart attack.
Suchitra Rathod 451
Suchitra Rathod 452
Suchitra Rathod 453
Suchitra Rathod 454
Coronary Bypass Surgery:

Suchitra Rathod 455

 CABG

Suchitra Rathod 456

CABG

Suchitra Rathod 457

 Results of CABG
• 65% remain symptom-free at ten
years
• 85% remain free of fatal/nonfatal
MI at ten years
• Mortality of 2-3% yearly over ten
years
• 2.5% incidence of preoperative MI

Suchitra Rathod 458

 PROGNOSIS
• Patients can often be managed with lifestyle
modifications and medications to control symptoms of
angina.

• The most important factor is patient education.

• Patients need to understand the importance of their

symptoms and when to seek medical attention.

• The pain must be evaluated initially and whenever a

change in pattern or lack of response to treatment occurs.
459
• Percutaneous transluminal coronary angioplasty(PTCA).

• This is a nonsurgical procedure in which a long tube with a

small balloon is passed through blood vessels into the

narrowed artery.

• The balloon is inflated, causing the artery to expand.

• Coronary artery stent (CAS):-This is a small, stainless steel

mesh tube that is placed within the coronary artery to keep it

open.

• The balloon is inflated, causing the artery to expand.

460
 Coronary artery bypass graph (CABG).

• This is a surgical procedure in which a vein from

a leg or an artery from an arm or the chest is
removed and graphed to coronary arteries,
bypassing the blockage and restoring free flow of
blood to heart muscles.
• Low-cholesterol, low-sodium, and low-fat diet.

461
CABG

462
 NURSING DIAGNOSES
• Anxiety
• Decreased cardiac output
• Acute pain

463
 NURSING INTERVENTION
• Monitor vital signs—look for change in BP, P, R;

irregular pulse; pulse deficit; when a discrepancy is

found between an atrial rate and a radial rate, when

measured simultaneously; pulse oximetry.

• Notify physician if systolic blood pressure is less than 90

mmHg.

464
• Nitrates dilate arteries to the heart and increase blood

flow.

• You may have an order to hold nitrates if SBP < 90

mmHg to reduce risk of patient passing out from lack

of blood flow to brain.

• Notify physician if heart rate is less than 60 beats per

minute.

465
• Beta-adrenergic blockers slow conduction through the AV
node and reduce the heart rate and contractility.

• You may have an order to hold beta blockers if heart rate

goes below 60;

• you should continuously monitor the patient’s pulse rate.

• Assess chest pain each time the patient reports it.

• Remember PQRST (an acronym for a method of pain

assessment) as follows.

466
Describe AP ‘s pain as:-
• Place,(chest,shoulder, back…)

• Quality (describe as—stabbing, squeezing, etc.),

• Radiation (does the pain travel anywhere else?),

• Severity (on a scale of 1 to 10), and

• Timing (when it started and how long it lasts and

what preceded the pain).
467
• Monitor cardiac status using a 12-lead
electrocardiogram (EKG) while the patient is
experiencing an angina attack.

• Each time the patient has pain, a new 12-lead

EKG is done to assess for changes, even if one
was already done that day.

468
• Record fluid intake and output.

• Assess for renal function.

• Place patient in a semi-Fowler's position

(semi-sitting with knees flexed).

469
 Explain to patient:

• Rest when pain begins to decrease oxygen demands.

• Take nitroglycerin when any pain begins—it helps

dilate coronary arteries and get more oxygen to heart

muscle.

• Avoid stress and activities that bring on an angina

attack.

470
• Stop smoking! Smoking is associated with heart
disease.
• Adhere to the prescribed diet and exercise plan.

• Lower cholesterol and fat intake to decrease further

plaque build-up, and decrease excess salt intake to
help BP control.
• Slowly increase exercise to build up activity tolerance.

• Possibly exercise with cardiac rehabilitation.

471
• How to recognize the symptoms of a
myocardial infarction:
• Pay attention to chest pains as well as changes
in patterns of pain and response to treatment.
• Be aware of changes in respiratory patterns,
increase in shortness of breath, swelling, and
general feelings of malaise.

472
Suchitra Rathod 473
Beta-Blockers

Suchitra Rathod 474

Don’t be so busy in work that you
forget to exercise
– Prevent the production of the chemicals that
causes blood vessels to narrow
– Resulting in blood pressure decreasing and the
heart pumping easier

Suchitra Rathod 476

 Myocardial Infarction (MI)
• MI occurs when blood supply to the

myocardium is interrupted for a prolonged time

due to the blockage of coronary arteries or by

complete blockage of one of the coronary

arteries

477
• This results in insufficient blood/oxygen

reaching cardiac muscle, causing cardiac

muscles/cells become ischemic, die, and form

an infarct

• MI may result in sudden death, or the infarct

undergoes a healing process and is replaced with

connective tissue
478
• MI is commonly known as a heart attack.

• After an MI the heart may be weakened and

develop congestive failure or cardiac arrhythmias
• The area of infarction is often due to build-up of
plaque over time (atherosclerosis).

479
• It may also be due to a clot that develops in

association with the atherosclerosis within the

vessel.

• Patients are typically (not always) symptomatic,

but some patients will not be aware of the event;

they will have what is called a silent MI.

480
Myocardial Infarction

481
 MI—Complications
• Arrhythmias
– 25% pts sudden death after MI
• Due to ventricular arrhythmias and fibrillation

– Heart block

– Premature ventricular contraction (PVCs)

• Cardiogenic shock

• CHF
482
 Complications of Myocardial Infarction

• Dysrhythmias.
• Heart Failure.
• Cardiogenic Shock.
• Papillary Muscle Dysfunction - causes mitral
valve regurgitation,
• Ventricular Aneurysm.
• Pericarditis.
• Dressler Syndrome – It is characterized by
pericarditis with effusion and fever that develops
4 to 6 weeks after MI.
 PROGNOSIS
• The outcome depends on site/size of infarct of
the coronary artery affected and time elapsed
before treatment
• The earlier the person enters the healthcare
system, the better the prognosis is, because
emergency measures will be available for
otherwise fatal arrhythmias.
484
• There is a better outcome for patients who
receive adequate medical attention and make
appropriate lifestyle changes post-myocardial
infarction.
• Mortality rate in 1st year30-40% due to
complications, recurrences
• Cardiac rehabilitation can help patients make
these changes safely.
485
 Signs & Symptoms of MI
• Chest pain that is unrelieved by rest or nitroglycerin,

• Pain that radiates to arms, jaw, back and/or neck

• Shortness of breath, especially in the elderly or

women
• Nausea or vomiting possible

• Maybe asymptomatic, known as a silent MI, which is

more common in diabetic patients

486
487
• Heart rate >100 (tachycardia) rapid and weak pulse
(low CO)because of sympathetic stimulation, pain
• Variable blood pressure
• Anxiety
• Restlessness
• Pale, cool, clammy skin; sweating (diaphoresis)
• Sudden death due to arrhythmia usually occurs within
first hour

488
 INTERPRETING TEST RESULTS
• EKG.
• T-wave inversion—sign of ischemia.
• ST-segment elevated or depressed—sign of
injury.
• Significant Q-waves—sign of infarction.
• Decreased pulse pressure because of
diminished cardiac output.
• Increased white blood count (WBC) due to
inflammatory response to injury.
489
Blood chemistry:

• Elevated creatine kinase MB (CK-MB)—usually done

serially, the numbers will rise along a predetermined
curve to signify myocardial damage and resolution.

• Elevated troponin I- and troponin T-proteins elevated

within one hour of myocardial damage.

• Less than 25 ml/hr of urine output due to lack of renal

blood flow.
490
Serum cardiac markers in the blood after
myocardial infarction
 TREATMENT
• Treatment is focused on reversing and
preventing further damage to the myocardium.

• Early intervention is needed to have the best

possible outcome.

• Thrombolytic therapy is instrumental in

reducing mortality.
492
• A three-hour time window is ideal for

maximizing benefit.

• Medications are used to enhance blood flow

to the heart muscle while reducing the
workload of the heart.

• Supplemental oxygen is used to help meet

myocardial oxygen demand.
493
• Following the acute management, the patient
will have to make lifestyle changes.

• Life style changes—altering diet and exercise,

stopping smoking, and so on.

• Administer oxygen, aspirin.

494
Administer antiarrhythmics because

arrhythmias are common as are conduction

disturbances.

• Amiodarone.

• Lidocaine.

• Procainamide.

495
Administer thrombolytic therapy within 3 to 12
hours of onset because it can re-establish blood
flow in an occluded artery, reduce mortality, and
halt the size of the infarction.
• Alteplase.
• Streptokinase.
• Anistreplase.
• Reteplase.
• Heparin following thrombolytic therapy.

496
Administer calcium channel blockers as they
appear to prevent reinfarction and ischemia, only
in non–Q-wave infarctions.
• Verapamil.

• Diltiazem.

497
Administer beta-adrenergic blockers because
they reduce the duration of ischemic pain and
the incidence of ventricular fibrillation;
decreases mortality.
• Propranolol.

• Nadolol.

• Metroprolol.
498
Administer analgesics to relieve pain, reduce
pulmonary congestion, and decrease
myocardial oxygen consumption.
• Morphine.
Administer nitrates to reduce ischemic pain by
dilation of blood vessels; helps to lower BP.
• Nitroglycerin.
499
 NURSING DIAGNOSES

• Ineffective tissue perfusion

• Decreased cardiac output

500
 NURSING INTERVENTION
Monitor:

• Cardiovascular—look for changes or instability

in pulse, heart sounds, murmur.

• Respiration—look for changes, fluid in lung

fields, shortness of breath.

501
 NURSING INTERVENTION….

• EKG during attack—12-lead during any episode

of pain.

• EKG continuous monitoring for arrhythmias.

• Vital signs—check for changes in BP, pulse

quality, peripheral pulses.

• Pulse-oximetry monitoring.
502
 NURSING INTERVENTION…
 Explain to the patient:

• Change to a low-fat, low-cholesterol, low-sodium

diet.
• The difference between angina pain and myocardial
infarction pain.
• When to take nitroglycerin.

503
 NURSING INTERVENTION…

• Smoking cessation.

• Limit activities.

• Need for cardiac rehabilitation.

• Stress reduction.

• Lifestyle changes such as increase in exercise,

diet changes.
504
Coronary Artery Bypass Graft Surgery.
 CABG

• CABG surgery consists of the construction of

new conduits (vessels to transport blood)
between the aorta, or other major arteries,
and the myocardium distal to the obstructed
coronary artery (or arteries).
• The procedure involves one or more grafts
using the internal mammary artery,
saphenous vein, radial artery, gastroepiploic
artery, and/or inferior epigastric artery.
 Procedure
• CABG surgery requires a sternotomy (opening
of the chest cavity) and the use of
cardiopulmonary bypass (CPB).
• CPB involves diverting (bypassing) the
patient's blood from the heart to the CPB
machine.
• Here blood is oxygenated and returned (via a
pump) to the patient.
• In this way, vital organs are perfused while the
surgeon operates on a nonbeating, bloodless
 Conti.
• The internal mammary artery (IMA) is the most
common artery used for bypass graft.
• The left and/or right IMA is dissected from the chest
wall.
• It is then anastomosed (connected with sutures) to
the coronary artery distal to the stenosis.

• The saphenous vein is also used for bypass grafts.

• It is removed from one or both legs and sections
are anastomosed proximally to the ascending aorta
and to a coronary artery distal to the blockage
Minimally Invasive Direct Coronary Artery Bypass.

• MIDCAB is a new technique that offers the patient with

single-vessel disease
• Its an approach to surgical treatment that does not
involve a sternotomy and CPB.
• The technique requires several small incisions between
the ribs.
• A thoracoscope is used to dissect the IMA.
• The heart is slowed using a β-adrenergic blocker (e.g.,
esmolol) or stopped temporarily with adenosine,
• A mechanical stabilizer is used to immobilize the
anastomosis site.
• The IMA is then sutured to the left anterior descending or
 Off-Pump Coronary Artery Bypass

• The off-pump coronary artery bypass (OPCAB)

procedure uses full or partial sternotomy to
enable access to all coronary vessels.
• OPCAB is also performed on a beating heart
using mechanical stabilizers and without CPB.
 Transmyocardial Laser Revascularization.
• Transmyocardial laser revascularization (TMR) is an
indirect revascularization procedure used for patients
with advanced CAD who are not candidates for
traditional bypass surgery
• The procedure involves the use of a high-energy laser
that is triggered electrocardiographically to create
channels between the left ventricular cavity and the
coronary microcirculation
• The channels allow blood to flow into ischemic areas.
• The procedure may be performed during cardiac
catheterization as a percutaneous TMR or during
surgery using a left anterior thoracotomy incision.
 Nursing Diagnosis
• Acute pain related to myocardial ischemia as evidenced by
severe chest pain and tightness, radiation of pain to the neck
and arms
• Ineffective tissue perfusion (cardiac) related to myocardial
injury as evidenced by peripheral edema, and pulmonary
edema
• Anxiety related to perceived or actual threat of death, pain,
possible lifestyle changes as evidenced by restlessness,
agitation, and verbalization
• Ineffective therapeutic regimen management related to lack
of knowledge of risk factors, disease process, rehabilitation,
home activities, and medications as evidenced by frequent
questioning about illness
• Activity intolerance related to fatigue secondary to decreased
cardiac output and poor lung and tissue perfusion as
evidenced by fatigue with minimal activity
STRESS TEST
 An exercise test on a bicycle or treadmill
helps the doctor measure your exercise
capacity.
 This test will also give you confidence to
resume physical tasks at home. It involves
pedalling a stationary bike or walking on a
treadmill while you’re attached to an ECG
monitor. This records your heart’s
response to exercise.
 Your blood pressure will be taken regularly
and you’ll be asked if you’re feeling any
chest discomfort.
Coronary Angioplasty:

Suchitra Rathod 519

 Treatment (continued)
A stent is introduced into a blood
vessel on a balloon catheter and
advanced into the blocked area of
the artery
The balloon is then inflated and
causes the stent to expand until it fits
the inner wall of the vessel,

Suchitra Rathod 520

• The balloon is then deflated and
drawn back
•The stent stays in place
permanently, holding the vessel
open and improving the flow of
blood.

Suchitra Rathod 521

Suchitra Rathod 522
Sudden cardiac death
 Definition
• Sudden cardiac death is unexpected death from
cardiac causes
 Incidence
• CAD is the most common cause of SCD and
accounts for 80% of all SCDs. The affected
person may or may not have a known history
of CAD, and SCD may be the first sign of illness
for 25% of those who die of heart disease.
 ETIOLOGY
 Acute ventricular dysrhythmias(eg. Ventricular
tachycardia, ventricular fibrillation)

 Primary left ventricular outflow obstruction(eg:

aortic stenosis, hypertrophic cardiomyopathy

 CAD
 RISKFACTORS
• Left ventricular dysfunction and ventricular
dysrhythmias following MI
• Male gender
• Family history of premature atherosclerosis
• Tobacco use
• Diabetes mellitus
• Hypercholesterolemia
• Hypertension
• Cardiomyopathy
 Diagnostic measures
• Cardiac markers
• ECGs
• Cardiac catheterisation
• PCI
• CABG
 PREVENTION
• Use of implantable Cardioverter-Defibrillator
• Use of Amiodarone with ICD
 MANAGEMENT
• CPR
• DEFIBRILLATOR
• PACEMAKER
PLEURAL EFFUSION
 INTRODUCTION
• Pleural fluid normally seeps continually into
the pleural space from the capillaries lining
the parietal pleura and is reabsorbed by the
visceral pleural capil­laries and lymphatic
system. Any condition that inter­feres with
either secretion or drainage of this fluid leads
to pleural effusion. It is not a disease but
rather a sign of a serious disease.
 DEFINITION
• Pleural effusion is an accumulation of fluid in
the pleural space.
ETIOLOGY
• Increased systemic hydrostatic pressure (e.g.,
heart failure)
• Reduced capillary oncotic pressure (e.g., liver or
renal failure)
• Increased capillary permeability (e.g., infections
or trauma)
• Impaired lymphatic function (e.g.,
lymphatic ,;: obstruction caused by tumor)
• TYPES
• Pleural effusion is frequently classified as
• Transudative
• Exudative
According to whether the
protein content of the effusion is low or high,
respec­tively.
• A transudate occurs primarily in noninflammatory condi­
tions and is an accumulation of protein-poor, cell-poor
fluid.
• Tran­sudative pleural effusions are caused by
• (I) increased hydrostatic pressure found in heart failure
(HF), which is the most common cause of pleural effusion,
• (2) de­creased oncotic pressure (from hypoalbuminemia)
found in chronic liver or renaldisease.
• In these situations, fluid movement is facili­tated out of the
capillaries and into the pleural space.
• An exudative effusion is an accumulation of
fluid and cells in an area of inflammation.
• An exudative pleural effusion results from
increased capillary permeability characteristic
of the inflammatory reaction.
• This type of effusion occurs secondary to
conditions such as pulmonary malignancies,
pulmonary infections, pulmonary
embolization.
 DIFFERENCE
• The type of pleural effusion can be determined by a
sample of pleural fluid obtained via thoracentesis (a
procedure done to re­move fluid from the pleural space).

• Exudates have a high protein content, and the fluid is

generally dark yellow or amber.

• Transudates have a low protein content or contain no

protein, and the fluid is clear or pale yellow. The fluid can
also be analyzed for RBCs and WBCs, malignant cells,
bacteria, and glucose.
• An empyema is a pleural effusion that
contains pus. It is caused by conditions such as
pneumonia, TB, lung abscess, and infection of
surgical wounds of the chest.
• A complication of empy­ema is fibrothorax, in
which there is fibrous fusion of the visceral
and parietal pleurae .
• CLINICAL MANIFESTATIONS AND DIAGNOSTIC
MEASURES
• Clinical manifestations depend on the amount of
fluid present and the severity of lung
compression.
• If the effu­sion is small (i.e., 250 ml), its presence
may be discov­ered only on a chest radiograph.
• With larger effusions, expansion may be
restricted, and the client may experience
• dyspnea, primarily on exertion, and
• a dry, nonproductive cough caused by
bronchial irritation
• Tactile fremitus may be decreased or absent,
and percussion notes dull or flat.
• Common clinical manifestations of pleural effusion are

• progres­sive dyspnea

• decreased movement of the chest wall on the af­fected side.

• There may be pleuritic pain from the underlying dis­ease.

• Physical examination of the chest will indicate dullness to percussion and

absent or decreased breath sounds over the affected area.
• The chest x-ray will indicate an abnormality if
the effusion is greater than 250 ml.

• Manifestations of empyema include the mani­

festations of pleural effusion, as well as fever,
night sweats, cough and weight loss.

• A thoracentesis reveals an exudate containing

thick, purulent material
• THORACENTESIS
• If the cause of the pleural effusion is not known, a diagnostic tho­
racentesis is needed to obtain pleural fluid for analysis .

• If the degree of pleural effusion is severe enough to impair breathing,

a therapeutic thoracentesis is done to improve breathing and to
remove fluid for analysis.

• A thoracentesis is performed by having the patient sit on the edge of a

bed and lean forward over a bedside table.

• The puncture site is determined by chest x-ray, and percussion of the

chest is used to assess the maximum degree of dullness.
• The skin is cleaned with an antiseptic solution
and anesthetized locally.

• The thoracentesis needle is inserted into the

intercostal space. Fluid can be aspirated with a
syringe, or tubing can be connected to allow
fluid to drain into a sterile collecting bottle.
• After the fluid is re­moved, the needle is withdrawn, and a
bandage is applied over the insertion site.

• Usually only 1000 to 1200 ml of pleural fluid are removed

at one time. Because high volumes are removed, rapid
removal can result in hypotension, hypoxemia, or
pulmonary edema.

• A follow-up chest x-ray should be done to detect a possible

pneumothorax that could have been induced by
perforation of the visceral pleura
• During and after the procedure, vital signs and
pulse oximetry are monitored, and the patient
should be observed for any manifesta­tions of
respiratory distress.

• The removed fluid is analyzed determine

whether it is transudate or exudate.
• Pleural fluid may be
• (1) hemorrhagic (or bloody), as when a tumor is
present or after trauma or pulmonary embolus with
infarction;
• (2) chylous (or thick and white), such as after
lymphatic obstruction or trauma to the thoracic
duct; or
• (3) rich in cholesterol, such as in chronic, recurrent
effusions caused by tuber­culosis or rheumatoid
arthritis.
• If there is high WBC count and the pleural fluid is purulent, the
effusion is called an empyema.

• An empyema of any volume requires drainage and treatment of

the infection.
•
• If the pus is not drained, it may become thick and almost
solidified or loculated (containing cavities), a condition called
fibrothorax.

• Fibrothorax may signifi­cantly restrict lung expansion and may

require surgical intervention.
• The procedure, known as decortication, involves removal
of the restrictive mass of fibrin and inflammatory cells.
Decortication is usually not per­formed until the fibrothorax
is relatively solid, so it can be easily removed.

• After the thoracentesis, closed-chest drainage with suction

is used to reexpand the lung rapidly and fill the pleural
space. If the fibrous material has restricted the lung for
some time, the lung may not reexpand effec­tively and
further intervention (usually thoracoplasty/ may be needed
 MANAGEMENT
• The main goal of management of pleural effusions is to treat the underlying cause.

• For example, adequate treatment of HF with di­uretics and sodium restriction will
result in decreased pleural effu­sions.

• The treatment of pleural effusions secondary to malignant disease represents a

more difficult problem. These types of pleural effusions are frequently recurrent
and accumulate quickly after thoracentesis.

• Chemical pleurodesis may be used to sclerose the pleural space and prevent
reaccumulation of effusion fluid.

• Al­though doxycycline (Vibramycin) and bleomycin (Blenoxane) have been used for
sclerosing with good results, talc appears to be the most effective agent for
pleurodesis."
• Thoracoscopy can be used to perform talc pleurodesis after
inspection of
• the pleural space.

• After instillation of the sclerosing agent, patients may be

instructed to rotate their positions to spread the agent uniformly
throughout the pleural space. The decision to rotate the patient
from side to side to back depends on physician preference and
the patient's ability to tolerate turning.

• Chest tubes are left in place after pleurodesis until fluid drainage
is less than 150 ml/day and no air leaks are noted.
• Treatment of empyema is generally with chest tube
drainage
• . Appropriate antibiotic therapy is also needed to
eradicate the causative organism.
• A condition called trapped lung can occur with
effusions and empyemas. This is a fibrous peel
around the pleura that can cause severe pulmonary
restriction.
• A decortica­tion surgical procedure to remove the
pleural peel may need to be performed.
• RECURRENT PLEURAL EFFUSIONS
• In some cases, pleural effusions may recur
despite repeated thoracenteses (e.g.,
malignancy-induced effu­sions), with resultant
compromise of lung function or persistent
pleural pain. Treatment of recurrent effusions
is accomplished through obliteration of the
pleural space. Methods of obliterating the
pleural space are as follows:
• Pleurectomy (pleural stripping): Surgical strip­ping of the parietal pleura
away from the visceral pleura, which produces an intense inflammatory
reaction that promotes adhesion formation between the two layers
during healing.
• Pleurodesis: Instillation of a sclerosing substance (e.g., unbuffered
tetracycline, bleomycin) into the pleural space via a chest tube to create
an inflam­matory response that causes the pleitra to adhere and sclerose
to each other. During the instillation, the client is rolled side to side to
spread the sub­stance throughout the pleural space.
• Because pleural space obliteration creates permanent changes, the
client's existing and predicted postproce­dure respiratory status must be
carefully evaluated. If a large area is involved, significant alterations in
ventila­tory mechanics (e.g., deep breathing, coughing) may occur, leading
to compromised respiratory function.
• After the procedure, closely monitor lung
function, including respiratory rate and
ventilation pattern. Docu­ment alleviation or
persistence of pleural pain and watch for
indications of a return of the pleural effusion.
•
CONGENITAL
 Introduction
• Cardiovascular disorder in children are divided
in two major groups
1. Congenital heart disease
2. Acquired cardiac disorders
 Congenital heart disease
• It is the anatomical abnormalities present at
birth that result in abnormal cardiac function .
• The clinical consequences of congenital heart
disease fall in to two broad categories,
– Congestive heart failure
– hypoxemia
 Etiology and risk factors
• Exact cause is unknown . The major risk
factors are:
• 1) maternal factors
– Chronic illness
– Alcohol conception
– Prenatal viral infections
– Poor nutritional status
– Maternal age
– Drugs such as anticonvulsants, lithium etc.
 Etiology and risk factors
2) hereditary
– Family history of cardiac defect especially from
first degree relatives.

3) Chromosomal abnormalities
- down syndrome
 Classification of CHD
• It is classified in to two
• 1) acyanotic heart disease
• 2) cyanotic heart disease
 1) a cyanotic heart disease

• Defect with increased • Obstruction to flow

pulmonary blood flow from ventricles
– Atrial septal defect – Coarctation of
– Ventricular septal Aorta
defect – Pulmonary
– Patent ductus stenosis
arteriosis
– Aortic stenosis
– Atrio-ventricular
canal defect
 2) cyanotic heart disease

• Decreased • Mixed blood flow

pulmonary blood – Trans position of
flow great vessels
– Tricuspid atresia – Hypo plastic left
– Tetralogy of fallot heart syndrome
Arterial septal defect
ventricular septal defect
Arterioventricular canal defect
Patent ductus arteriosis (PDA)
Coarctation of aorta (COA)
Aortic stenosis
Pulmonary stenosis
Tetrology of fallot
Tricuspid atresia
Transposition of great vessels
Hypo plastic left heart syndrome
VALVULAR HEART DISEASE
 Valvular Heart Diseases (VHD)

• When any of the heart valves do not close or open

properly, blood flow is affected.
1. Stenosis:- When valves do not open completely, results
reduced flow of blood through the valve.
2. Regurgitation:- When valves do not close completely,
blood flows backward through the valve,
3. Valve Prolapse :- Stretching of the valve leaflet into
the atrium during systole
577
 The Cardiovascular System (cont.)

• The Heart (cont.)

– Bicuspid (mitral)
valve.
– Tricuspid valve.
– Pulmonary valve.
– Aortic valve.
• Valvular heart disease from chronic rheumatic fever is
still the commonest cardiac disease in the developing
world, occurring at the younger age.
• It causes significant morbidity and mortality due to lack
of appropriate preventive and therapeutic intervention.
• It accounts for 42 % of cardiac patients attending
hospitals in Ethiopia.

579
• Generally, patients with stenotic valvular lesions can
be monitored clinically until symptoms appear.
• In contrast, patients with regurgitate valvular lesions
require careful echocardiographic monitoring for left
ventricular function and may require surgery even if
no symptoms are present

580
• Aside from antibiotic prophylaxis, very little medical
therapy is available for patients with
• valvular heart disease; surgery is the treatment for most
symptomatic lesions or for lesions causing left
ventricular dysfunction even in the absence of
symptoms.
• However surgical management is unavailable for most
patients who are suffering from valvular heart diseases
in Ethiopia.
581
 Valvular heart disease(VHD) includes:-

Aortic Stenosis (AS)

Aortic Regurgitation (AR)

Mitral Stenosis (MS)

Mitral Regurgitation (MR)

Tricuspid Regurgitation (TR)

Mitral Valve Prolapse(MVP)

582
• Valvular heart disease is defined according to
the valve or valves affected and the type of
functional alteration: stenosis or regurgitation.
 Anatomy and physiology
• The heart contains
• Two atrioventricular valves,
• The Mitral and the Tricuspid
• Two semilunar valves
• The aortic
• The pulmonic
• Which are located in four strategic locations to
control undirectional blood flow.
• The atrioventricular valves separate the atria
from the ventricles and include
• the tricuspid valve
• which seperates the right atrium from the
right ventricle,
• and the mitral valve which seperates the left
atrium from the left ventricle. The tricuspid
valve has three leaflet and the mitral valve has
two.
• Both valves has chordate tendinae that anchor
the valve leaflets to the papillary muscles of
the ventricles.
• The semilunar valve are located between the
ventricles and their corresponding arteries.
• The pulmonic valve lies between the right
ventricle and pulmonary artery.
• The aortic valve lies between the left
ventricle and the aorta.
• When any of the heart valves do not close or
open properly, blood flow is affected. When
valves do not close completely blood flows
backward through the valve, a condition
called regurgitation .
• when valves do not open completely a
condition called stenosis, the flow of blood
through the valve is reduced
MITRAL VALVE STENOSIS
 DEFINITION

• MITRAL STENOSIS IS AN OBSTRUCTION OF

BLOOD FLOWING FROM THE LEFT ATRIUM IN
TO THE LEFT VENTRICLE.
 ETIOLOGY

• Most cases of adult mitral valve stenosis result

from rheumatic heart disease.
• Less common causes are congenital mitral
stenosis.
• rheuma­toid arthritis
• systemic lupus erythematosus.
• Rheumatic endo­carditis
• Endocarditis causes scarring of the valve
leaflets and the chordae tendineae.
• Contractures and adhesions develop between
the com­missures (the junctional areas).
• The stenotic mitral valve takes on a "fish
mouth" shape because of the thickening and
shortening of the mitral valve structures .
• These structural deformities cause obstruction of
blood flow and create a pressure difference be­
tween the left atrium and the left ventricle during
diastole.
• Left atrial pressure and volume elevations cause
increased pulmonary vascula­ture pressure and
subsequent hypertrophy of the pulmonary vessels.
• In chronic mitral stenosis, pressure overload occurs
in the left atrium, the pulmonary bed. and the right
ventricle.
 CLINICAL MANIFESTATIONS

• The primary symptom of mitral stenosis is exertional

dyspnea due to reduced lung compliance .

• Fatigue and palpitations from atrial fibrillation may

also occur.

• Less frequently, patients may have hoarseness (from

atrial enlargement pressing on the laryn­geal nerve)
• hemoptysis (from pulmonary hypertension),
• chest pain (from decreased CO)
• and seizures or a stroke (from emboli). Em­boli
can arise from blood stasis in the left atrium.
 DIAGNOSTIC MEASURES
• History and physical examination
• Chest Xray
• Electrocardiogram
• Echocardiography
• Cardiac catheterization.
 MANAGEMENT

Medical management
patients with mitral stenosis may benefit from
anticoagulants to decrease the risk for
developing atrial thrombus
may also require treatment for anemia.
Patient with mitral stenosis are advised to avoid
straneous activity.
 MITRAL VALVE REGURGITATION
DEFINITION
Mitral regurgitation (MR) is
defined as an abnormal reversal of blood flow
from the left ventricle to the left atrium.
 ETIOLOGY

• degenerative changes of the mitral valve (eg,

mitral valve prolapse)
• ischemia of the left ventricle
• rheumatic heart disease
• MI,
• chronic rheumatic heart disease
• mitral valve prolapse
• ischemic papillary muscle dysfunction
• IE.
 PATHOPHYSIOLOGY
• MR allows blood to flow backward from the
left ventricle to the left atrium due to
incomplete valve closure during systole.
• The left ventricle and left atrium both work
harder to preserve an adequate CO.
• In chronic MR, the additional volume load
results in atrial enlargement, ventricular
dilation, and eventual ventricu­lar hypertrophy.
• In acute MR, the left atrium and ventricle do
not abruptly dilate. The sudden increase in
pressure and volume is transmitted to the
pulmonary bed, resulting in pulmonary edema
and shock.
 CLINICAL MANIFESTATIONS

• thready, pe­ripheral pulses and cool, clammy

extremities.
• Patients with chronic MR may remain asymptomatic
for many years.
• Initial symptoms of left ventricular failure may
include weak­ness, fatigue, palpitations, and dyspnea
that gradually progress to
• or­thopnea, paroxysmal nocturnal dyspnea, and
peripheral edema.
• Dyspnea on exertion
• hemoptysis; fatigue; palpitations
 MEDICAL MANAGEMENT

• Management of mitral regurgitation is the same as

that for heart failure.
• Patients with mitral regurgi­tation and heart failure
benefit from afterload reduction (ar­terial dilation)
by treatment with
• angiotensin-converting enzyme (ACE) inhibitors,
such as captopril (Capoten), enalapril (Vasotec),
lisinopril (Prinivil, Zestril), ramipril (Altace), or
hydralazine (Apresoline);
•
• angiotensin receptor blockers (ARBs), such as
losartan (Cozar) or valsartan (Dio-van); and
• beta-blockers, such as carvedilol (Coreg).
• Once symptoms of heart failure develop, the
patient needs to re­strict his or her activity level
to minimize symptoms.
• Surgi­cal intervention consists of mitral
valvuloplasty (ie, surgical repair of the valve) or
valve replacement.
 MITRAL VALVE PROLAPSE
• Mitral valve prolapse (MVP) is an abnormality
of the mitral valve leaflets and the papillary
muscles or chordae that allows the leaflets to
prolapse, or back into the left atrium during
sys­tole
 ETIOLOGY

• Unknown
• results from a connective tissue defect
affecting only the valve, or as part of Marfan's
syndrome or other hereditary conditions that
affect the structure of collagen in the body.
 Pathophysiology
• In mitral valve prolapse, a portion of one or both
mitral valve leaflets balloons back into the atrium
during systole.
• Rarely, the ballooning stretches the leaflet to the
point that the valve does not remain closed during
systole (ie, ventric­ular contraction).
• Blood then regurgitates from the left ven­tricle back
into the left atrium.
• eventually experience heart enlargement, atrial
fibrillation, pulmonary hypertension, or heart failure .
 CLINICAL MANIFESTATIONS

• Most patients are asymptomatic and remain

so for their entire lives.
• A characteristic of MVP is a murmur from
regurgitation that gets more intense through
systole
• Patients may or may have chest pain. The
cause of the chest pain is not known, but it
may be due to abnormal tension on the
papillary muscles.
• Dyspnea, palpitations, and syncope may
occasionally accompany the chest pain and do
not respond to antianginal treatment (e.g.,
nitrates).
 DIAGNOSTIC FINDINGS

• History collection
• physical examination
• Doppler echocardiography may be used to
diagnose and monitor the progression of
mitral valve prolapse
 Medical management
• Medical management is directed at controlling symptoms.
• If dysrhythmias are documented and cause symptoms, the
patient is advised to eliminate caffeine and alcohol from the
diet and to stop smoking.
• Most patients do not require any medications; prophylactic
antibiotics are no longer recom­mended prior to dental or
invasive procedures although antiarrhythmic medications may
be prescribed.
• Chest pain that does not respond to nitrates may respond to
calcium channel blockers or beta-blockers.
• In advanced stages of disease, mi­tral valve repair or
replacement may be necessary
 AORTIC VALVE STENOSIS
DEFINITION
Aortic stenosis is the obstruction of blood flow
across the aortic valve.

Aortic valve stenosis is narrowing of the orifice

between the left ventricle and the aorta.
 ETIOLOGY

• Congenital
• In older pa­tients, aortic stenosis is a result of
rheumatic fever or senile fibro-calcific
degeneration
• In rheumatic valvular disease, fusion of the
commissures and secondary calcification
cause the valve leaflets to stiffen and retract,
resulting in stenosis.
• In adults, the stenosis is often a result of
degenerative calcifications. Calcifications may
be caused by inflammatory changes that occur
in response to years of normal mechanical
stress. Diabetes mellitus, hyper­
cholesterolemia, hypertension, and low levels
of high-density lipoprotein cholesterol may be
risk factors for degenerative changes of the
valve.
 PATHOPHYSIOLOGY

• Aortic stenosis causes obstruction of

flow from the left ventri­cle to the aorta during
systole. The effect is left ventricular hyper­
trophy and increased myocardial oxygen
consumption because of the increased
myocardial mass. As the disease progresses
and compensatory mechanisms fail, reduced
CO leads to pulmonary hypertension and HF.
 CLINICAL MANIFESTATIONS

• Symptoms include the classic triad of angina,

syncope, and exertional dyspnea, reflecting
left ventricular failure.
• Auscultation of aortic stenosis typically reveals
a normal or soft Si; a diminished or absent S2
• murmur
• a prominent fourth heart sound (S4).
 DIAGNOSTIC MEASURES

• On physical examination, a loud, rough systolic

murmur may be heard over the aortic area.
• Doppler echocardiography is used to diagnose
and mon­itor the progression of aortic stenosis
• Evidence of left ventricular hypertrophy may
be seen on a 12-lead ECG and an
echocardiogram.
 MEDICAL MANAGEMENT

• Medications are prescribed to treat

dysrhythmia or left ven­tricular failure
• Definitive treat­ment for aortic stenosis is
surgical replacement of the aortic valve.
Patients who are symptomatic and are not
surgical candidates
• may benefit from one-balloon or two-balloon
percutaneous valvuloplasty procedures.
AORTIC VALVE REGURGITATION
• DEFINITION
• Aortic regurgitation is the flow of blood back
into the left ventricle from the aorta during
diastole.
 ETIOLOGY

• Acute aortic re­gurgitation (AR) is caused by IE,

trauma, or aortic dissection
• Chronic AR is generally the result of rheumatic
heart disease, a congenital bicuspid aortic
valve, syphilis, or chronic rheumatic conditions
 PATHOPHYSIOLOGY

• AR causes retrograde blood flow from the

ascending aorta into the left ventricle during
diastole, resulting in volume overload. The left
ventricle initially compensates by dilation and
hypertrophy.
• Myocardial contractility eventually declines
and blood volumes increase in the left atrium
and pulmonary bed. This results in pulmonary
hypertension and right ventricular failure.
 CLINICAL MANIFESTATIONS

• The patient develops severe dyspnea, chest pain, and

hypotension indicating left ventricular failure and shock
that constitute a medical emergency.

• Patients with chronic, severe AR develop a water-hammer

pulse (a strong, quick beat that collapses immediately).

• Heart sounds may include a soft or absent Si, presence of

S3 or S4, and a soft, decrescendo high-pitched diastolic
murmur.
• A systolic ejec­tion click may also be heard, as well as
a low-frequency diastolic murmur known as an
Austin-Flint murmur.

• The patient with chronic AR generally remains

asymptomatic for years and is seen with exertional
dyspnea, orthopnea, and par­oxysmal nocturnal
dyspnea only after considerable myocardial
dysfunction has occurred. Angina occurs less
frequently than in aortic stenosis
 DIAGNOSTIC FINDINGS

• A diastolic murmur is heard as a high-pitched, blowing sound at

the third or fourth intercostal space at the left ster­nal border.
• The pulse pressure (ie, difference between sys­tolic and diastolic
pressures) is considerably widened in pa­tients with aortic
regurgitation.
• One characteristic sign of the disease is the water-hammer
(Corrigan's) pulse, in which the pulse strikes the palpating finger
with a quick, sharp stroke and then suddenly collapses.
• The diagnosis may be confirmed by Doppler echocardiography
(preferably transesophageal), radionuclide imaging, ECG,
magnetic resonance imaging (MRI), and cardiac catheterization.
• Waterhammer pulse is the medical sign which
describes a pulse that is bounding and
forceful, rapidly increasing and subsequently
collapsing.
• This is associated with increased stroke
volume of the left ventricle and decrease in
the peripheral resistance leading to the
widened pulse pressure of aortic
regurgitation.
• Systolic murmurs occur between S1 and S2
• Aortic and pulmonic valve stenosis
• Mitral and tricuspid regurgitation.
• Diastolic murmurs occur after S2 and before
S1.they are assoc with ventricular relaxation
anf filling.
• Aortic and pulmonic valve regurgitation
• Mitral or tricuspid valve stenosis
click
 MEDICAL MANAGEMENT

• The patient is advised to avoid physical exertion, competi­tive

sports, and isometric exercise.

• . The medications usually prescribed first for patients with symp­

toms of aortic regurgitation are vasodilators such as calcium
channel blockers (eg, nifedipine )

• ACE inhibitors (eg, captopril, enalapril, lisinopril, ramipril), or

hydralazine.
• The treatment of choice is aortic valvulo­plasty or valve
replacement, preferably performed before left ventricular
failure occurs.
TRICUSPID AND PULMONIC VALVE DISEASE
• TRICUSPID AND PULMONIC VALVE DISEASE
• Diseases of the tricuspid and pulmonic valves
are uncommon, with stenosis occurring more
frequently than regurgitation.
• ETIOLOGY
• Tricuspid valve stenosis occurs almost
exclusively in patients with rheumatic fever
• In IV drug abusers
• Pulmonary stenosis is al­most always
congenital
• PATHOPHYSIOLOGY
• Tricuspid and pulmonic stenosis both result in
an increase in blood volume in the right
atrium and right ventricle, respectively.
• Tricuspid stenosis results in right atrial
enlargement and elevated systemic venous
pressures. Pulmonic stenosis results in right
ven­tricular hypertension and hypertrophy .
• DIAGNOSTIC STUDIES FOR VALVULAR HEART DISEASE
•
• Diagnosis of valvular heart disease is generally based on
the re­sults of
• History,
• Physical examination,
• Echocardiogram, and
• Car­diac catheterization (especially if surgery is
considered.
• Chest x-ray results,
 MANAGEMENT

• Goal
• An important aspect of conservative management of valvular heart
disease is prevention of recurrent rheumatic fever and IE .

• It focuses on preventing exacerbations of HF, acute pulmonary edema,

thromboembolism, and recurrent endo­carditis.

• Treatment depends on the valve involved and the sever­ity of the

disease. If manifestations of HF develop, vasodilators, positive in­
otropes
• (3-adrenergic blockers, diuretics, and a low-sodium diet are
recommended .
• Anticoagulant therapy is used to prevent and treat
systemic or pulmonary embolization and is also
used prophylactically in pa­tients with atrial
fibrillation.

• Dysrhythmias, especially atrial dys­rhythmias, are

common and are treated with digoxin, antidysrhyth­
mic drugs, or electrical cardioversion.
• Beta Adrenergic blockers may be used to slow the
ventricular rate in patients with atrial fibrilla­tion.
 SURGICAL MANAGEMENT

• Valvuloplasty
The repair, rather than replacement, of a
cardiac valve is re­ferred to as valvuloplasty.
• Commissurotomy
The most common valvuloplasty procedure
is commissuro­tomy. Each valve has leaflets; the site
where the leaflets meet is called the commissure. The
leaflets may adhere to one another and close the
commissure (ie, stenosis). A commissurotomy is the
procedure performed to separate the fused leaflets.
• Closed commissurotomies do not require
cardiopulmonary bypass, in which a surgical
technique is u a midsternal incision is made, a
small hole is cut into the heart, and the
surgeon's finger or a dilator is used to open
the commissure.
• OPEN COMMISSUROTOMY
Open commissurotomies are
performed with direct visuali­zation of the valve.
The patient is under general anesthesia.
A midsternal or left thoracic incision is made.
Cardiopul­monary bypass is initiated and an
incision is made into the heart.
• ANNULOPLASTY
• Annuloplasty is the repair of the valve
annulus (ie,-junc­tion of the valve leaflets and
the muscular heart wall).
• CHORDOPLASTY is repair of the chordae
tendineae
• VALVE REPLACEMENT
When valvuloplasty is not a
viable alternative valve replacement is
performed. (eg, when the annulus or leaflets of
the valve are immobilized by cal­cifications,
severe fibrosis or fusion of the chordate
tendineae, papillary muscles, and leaflets below
the valve).
• MECHANICAL VALVES
• Mechanical valves are of the bileaflet,
• ball-and-cage, or tilting-disk design
• are thought to be more durable than tissue prosthetic
valves; therefore, they are often used for younger
patients.
• these valves are made of strong durable material.
• They are the most long lasting type or replacement valve.
• this will last throughout the entire of life of the patient.
• life time blood thinning medication
• TISSUE (BIOLOGIC) VALVES
• Tissue (ie, biologic) valves are of three types:
xenografts, homografts, and autografts.
• Are created from animal donors. Can last 10-
20yrs
• Not require the long term use of medications.
• Xenografts
A tissue graft or organ transplant
from a donor of a different species from the
recipient
• Homografts
• Homografts, or allografts (ie, human valves),
are obtained from cadaver tissue donations
and are used for aortic and pulmonic valve
replacement.
• Homografts are not always available and are
very expensive. They last for about 10 to 15
years, somewhat longer than xenografts. They
are resistant to infectious endocarditis.
• A graft of tissue between individuals of the
same species . Types of donors are
cadaveric,living related
Cadaver/corpse/dead body
• Autografts
• Autografts (ie, autologous valves) are
obtained by excising the patient's own
pulmonic valve and a portion of the pul­
monary artery for use as the aortic valve.
 Preload
• Preload , also known as the left ventricular
end diastolic pressure, is the amount of
ventricular stretch at the end of diastole.
Think of it as the heart loading up for the next
big squeeze of the ventricles during systole.
 Afterload
• Also known as systemic vascular
resistance(SVR) , is the amount of resistance
the heart must overcome to open the aortic
valve and push the blood volume into the
systemic circulation.
• If u think about the balloon analogy afterload
is representd by the knot at the end of the
balloon. To get the air out, the balloon must
work against that knot.
 Cardiac output
• Is the volume of blood the heart pumps per
minute. It is calculated by multiplyingthe
stroke volume by the heart rate. 4 to 8 L/min.
• Cardiac index is a calculation of the cardiac
output divided by the persons body surface
area.
• Septal Repair
• The atrial or ventricular septum may have an abnormal opening between the right and left
sides of the heart (ie, septal defect). Although most septal defects are congenital and are
repaired during infancy or childhood, adults may not have undergone early repair or may
develop septal defects as a result of myocardial infarctions or diagnostic and treatment
procedures.
• Repair of septal defects requires general anesthesia and cardiopulmonary bypass. The
heart is opened, and a pericardial or synthetic (usually polyester or Dacron) patch is used
to close the opening. Atrial septal defect repairs have low morbidity and mortality rates.
When the mitral or tricuspid valve is involved, however, the procedure is more complicated
because valve repair or replacement may be required and the heart failure may be more
severe. Generally, ventricular septal defect repairs are uncomplicated, but close proximity
of the defect to the intraventricular conduction system and the valves may make this repair
more complex. (See Chapter 28, Chart 28-13, which presents a plan of nursing care for a
patient recovering from cardiac surgery.) Patients should be taught the importance of
infective endocarditis antibiotic prophylaxis for 6 months after the repair. If minimal or no
hemodynamic abnormality is evident by Doppler echocardiography after 6 months,
antibiotic prophylaxis may be discontinued.
Sudden cardiac death
VASCULAR DISORDERS
 RAYNAUD’S DISEASE
• Raynaud’s disease is an episodic vasospastic disorder
of small cutaneous arteries, most frequently
involving the fingers and toes.

• Raynaud’s phenomenon is used to refer to localized,

intermittent episodes of vasoconstriction of small
arteries of the feet and hands that cause colour and
temperature changes.
 Etiology
• Exact reason is unknown
• One popular theory is that the vasospasm
results from an exaggerated response to
sympathetic nervous system stimulation.
• Occupationally related trauma and pressure to
the fingertips as noted in typists, pianists and
those who use handheld vibrating equipment.
• Exposure to heaavy metals(eg: lead)
 pathophysiology
• Vasoconstriction is regulated by alpha-2 receptors.
• Sympathetic stimulation or cold exposure causes
the release of noradrenalin which activates the
alpha 2 receptors and cause vasoconstriction and
vasospasm.
• Person’s with Raynau’s disease may have increased
number of alpha 2 receptors.
• They may also have decreased in beta receptors and
calcitonin which are responsible for vasodilation.
 Clinical features
• Raynauds phenomenon is charecterised by vasospasm induced color
changes of the fingers, toes, ears and nose(white, blue and red).

• Decreased perfusion results in pallor,

• The digits then appear cyanotic

• These changes are followed by rubor(red) caused by hyperemic

response that occurs when perfusion is restored

• The patient usually describes coldness and numbness in the

vasoconstrictive phase followed by throbbing, aching pain, tingling and
swelling in the hyperemic phase.
• After frequent prolonged attacks the skin may
become thickened and nail brittle

• Punctuate(small hole) lesions of the fingertips

and superficial gangrenous ulcers in advanced
stages
 Management
• Patient teaching:

• Loose warm clothing should be worn as protection from the cold including
gloves when the refrigerator or freezer is used or when cold objects are
being handled.

• The pt should be stop using all tobacco products and avoid caffeine and
other drugs with vasoconstrictive effects.

• If symptoms are exacerbated by stress the pt needs to develop coping

strategies for anxiety producing situations(biofeedback, relaxation training,
stress management)

• Immersing hands in warm water often decreases the vasospasm.

• Calcium channel blockers such as nifedipine
and diltiazem relax smooth muscles of the
arterioles by blocking the influx of calcium into
the cells, thus reducing the number of
vasospastic attacks.

• Sympathectomy is considered only in

advanced cases.
 Thromboangitis obliterans
• Thromboangitis obliterans
(Buerger’s disease) is a rare nonatherosclerotic, segmental,
recurrent inflammatory vasoocclusive disorder of the small
and medium sized arteries, veins and nerves of the upper and
lower extrmities.

• Buergers disease is a rare disease of the

arteries and veins in the arms and legs. Buergers disease is
charecterised by a combination of inflammation and clots in the
blood vessels, which impairs blood flow.
 Varicose veins

• Varicose veins or varicosities are dilated, tortuous

subcutaneous veins most frequently found in the saphenous system.

• They may be small and innocuous or large and

bulging.
 Primary varicose veins
• Primary varicose veins ,
• idiopathic,
• which are more common in women and
• patients with a strong family histoty are
probably caused by congenital weakness of
the veins
 Secondary varicose veins
• Typically result from a previous DVT or
another identifiable obstruction.
• Secondary varicose veins may also occur in the
esophagus(esophageal varices),
• in the anorectal area(hemorrhoids), and as
• abnormal arteriovenous connections(AV
fistulas and malformations).
 Risk factors
• Congenital weakness of the vein structure
• Female gender
• Use of hormones(oral contraceptives)
• Increasing age
• Obesity
• Pregnancy
• Venous obstruction resulting from thrombosis or
extrinsic pressure by tumors
• Occupations that require prolonged standing
 pathophysiology
• As the veins enlarge
• The valves are stretched and become incompetent
• Allowing venous blood flow to be reversed
• As back pressure increases and the calf muscle
pump(muscle movement that squeezes venous blood
back towards the heart) fails
• Further venous distention
• The increased venous pressure is transmitted to the
capillary bed
• Edema develops
 Clinical manifestations
• Discomfort
• Ache and pain after prolonged standing, which
is relieved by walking or elevating the limb.
• Patients feel pressure or cramplike sensation
in the legs
• Swelling
• Nocturnal leg cramps
 complications
• Superficial thrombophlebitis
• Rupture of the varicose veins from weakening
of the vessel wall
• Ulceration of the skin
 Diagnostic measures
• History collection
• Superficial varicose veins(appearance)
• A duplex ultrasound can detect obstruction
and reflux in the venous system
 prevention
• The pt should avoid activities that cause venous stasis, such as wearing tight
socks or a constricting panty girdle
• Crossing the legs at the thighs
• Sitting or standing for a long period.

• Changing position frequently

• Elevating the legs when they are tired.

• Getting upto walk for several minutes of every hour promote circulation

• Encouraged walking to 1 or 2 miles

• Swimming
• Elastic compression stockings
• Knee high stockings
• The overweight pt should reduce their weight.
 Management
• Goal :
• To improve circulation
• Relieve pain
• Avoid complications
• Elastic compression stockings
• Injection sclerotherapy or lasers
• Surgical intervention : radiofrequency ablation
stripping to remove incompetent valves.
 sclerotherapy
• The injection of a substance that obliterates venous
telangiectasis(spider veins)
• Two sclerotherapy techniques are available

1. Injection of a sclerosing agent alone

2. Injection of a mixture containing a sclerosing and foaming agent

• Commonly used sclerosing agents include hypertonic saline, saline

plus hypertonic dextrose
• Morrhuate sodium
• Ethanolamine oxalate
 sclerotherapy
• Direct iv injection of a sclerosing agent
induces inflammation and results in eventual
thrombosis of the vein.
• After inj the leg is wraped with an elastic
bandage for 24 to 72 hrs to maintain pressure
over the vein.
• After removal of the elastic bandage
compression stockings are recommended for
2 – 3 weeks to minimize complications.
 Laser therapy
• Vascular lasers work by heating the
hemoglobin in the vessels, which injures the
endothelium resulting in vessel sclerosis.
 Pulsed light therapy
• Is similar to laser therapy but uses a spectrum
of light rather than a single wavelenth.
 surgery
• Ligation of the entire vein and dissection and
removal of its incompetent tributaries.
• An alternative, but time consuming technique is
ambulatory phlebectomy which involves pulling the
varicosity through a “stab” incision followed by
excision of the vein.
• Transilluminated powered phlebectomy involves the
use of a powered tissue resector to destroy the
varices and removes the pieces via aspiration.
 DEEP VEIN THROMBOSIS
• Deep vein thrombosis refers to thrombophlebitis
of the deep veins.

• Veins and valves permanently damaged by deep

vein thrombosis increase the risk for another
deep vein thrombosis, pulmonary embolism and
venous stasis ulcers.
• DVT is a disorder involving a thrombus in a deep
vein, most commonly iliac and femoral veins.
 incidence
• DVT is a common disorder , more so in women
than in men, and more in adults than in
children. It is particularly common among
hospitalized patients.
 etiology
• Venous stasis
• Hypercoagubility
• Injury to the venous wall
• This is known as “Virchow’s triad”

• It is thought that at least two of the three

conditions must be present for thrombi to
form.
 Venous stasis
• Action of the muscles in the extrmities and the funtional
adequacy of venous valves which allow unidirectional flow.
Venous stasis occurs when the valves are dysfunctional or
the muscles of the extremities are inactive.
• Immobilization
• Surgery
• Obesity
• Pregnancy
• Paralysis
• Congestive heart failure
 HYPERcoagubility
• Occurs in many of the hematologic disorders,
particularly polycythemia
• Severe anemia
• Malignancies
• Elevated lipoprotein
• Sepsis (release endotoxins- hypercoagulable
state)
• Pregnant women
• Women in postpartum period
 Endothelial damage
• Vein may be caused by trauma or external pressure
and occurs any time a venipuncture is performed.
• Damaged endothelium has decreased fibrinolytic
properties
• Predisposing to thrombus development
• Increased endothelial damage is sustained when
pts on potassium, chemotherapeutic agents, or
hypertonic solutions such as parenteral nutirition.
• Other causes: prolonged presence of IV catheter
 R I CO S E V E I N
VA
 INTRODUCTION:
Veins are blood vessels that return
deoxygenated blood from the outer part of the
body back to the heart and lungs .Veins have
pairs of leaflet valve to prevent blood from
flowing backwards .When veins becomes
abnormally thick , full of twists and turns , are
enlarged they are called varicose vein .This
happens most commonly in the veins in the legs
and thighs .
 DEFINITION:
Varicose veins or varicosities ,are
dilated ,tortuous subcutaneous veins most
frequently found in the saphenous system .
 INCIDENCE:
1) This condition is most common after age
50 .
2) Women is having 3-4 times more than
men .
 CAUSES:
AGE: As you get older, your veins can loss
elasticity, causing them to stretch. Blood pools
in your veins ,and enlarge and become
varicose.
PREGNANCY: Some pregnant women
develop varicose veins.Pregnancy increases
the volume of blood in your body,but
decreases the flow of blood from your legs to
your pelvis.
 RISK FACTORS:
1) Congenital weakness of the vein structure.
2) Female gender.
3) Use of hormones{ oral contraceptives or
HRT}.
4) Increasing age.
5) Obesity.
6) Pregnancy.
7) Occupations that requires prolonged
standing.
 SIGNS AND SYMPTOMS:

1) Aching ,heavy legs{ often worse at night and after

exercise.}
2) Appearance of spider veins[ telangiectasia] in the affected
leg.
3) Ankle swelling,especially in evening.
4) A brownish – yellow shiny skin discolouration near the
affected veins.
5) Redness, dryness and itchiness of the areas of the skin.
6) Cramp like sensation in the legs.
7) Minor injuries to the area may bleed or take long time to
heal.
 PATHOPHYSIOLOGY:
As the veins enlarge, the valves are streched.

Become incompetent, allowing venous blood flow to be

reversed
as back pressure increases and calf muscle pump{muscle
movement that squeezes venous blood back toward
heart}fails
Result in the venous distention .
Increased venous pressure is transmitted to capillary bed
Edema develops.
 DIAGNOSTIC STUDIES:
• Trendelenburg test: To determine the site of venous
reflux and the nature of the sapheno femoral junction
• Multiple tournique test :To more accurately localize
the site of the venous reflux
• Fegan test:To assess the nature of any perforating
vein blow outs
• Perthes test: To check the patency of the deep veins
• Lower limbs venous ultrasonography.
 STAGES:
According to the CEAP classification:
•C0- no visible or palpable signs of venous
disease.
•C1- Telangectasia or reticular veins.
•C2- varicose veins .
•C3- edema.
•C4a –pigmentation of eczema
•C4b- lipodermatosclerosis, atrophie,
blanche.
•C5- healed venous ulcer.
C6- active venous ulcer.

PREVENTION AND MANAGEMENT:

1) Elevating the legs often provides temporary
symptomatic relief.
2) Advice about regular exercise. It sounds
sensibile .
3) The wearing of graduated compression
stocking with variable pressure gradient.
has been shown to correct the swelling ,
nutritional exchange, and improve the
microcirculation in legs affected by varicose
vein.
4) Wearing of intermittent pneumatic
compression devices have been shown to
reduce swelling and increase circulation.
5) Topical gel application ,helps in managing
symptoms related to varicose vein such as
inflammation, pain, swelling, itching, dryness.
 MANAGEMENT:
SURGICAL:
 Sclerotherapy: In this procedure, your doctor
injects small and medium sized varicose vein
with a solution that scars and closes those
veins.
 Foam sclerotherapy of large veins: Injection of
a large vein with a foam solution is also a
possible treatment to close a vein and seal it.
 Laser surgeries: It works by sending stong
bursts of light into the vein, which makes the
vein slowly fade and disappear.
Catheter-assisted procedures using
radiofrequency or laser energy: In one
of these treatments, your doctor inserts a thin
tube {catheter} into an enlarged vein and
heats the tip of the catheter using either
radiofrequency or laser energy.
High ligation and vein stripping: This
procedure involves tying off a vein before it
join a deep vein and removing the vein
through small incisions.
Ambulatory phlebectomy: Your doctor
removes smaller varicose veins through a series
of tiny skin punctures.
Endoscopic vein surgery:Your surgeon
uses a thin video camera inserted in your
leg to visualize and close varicose veins
and then removes the veins through small
incisions.
NURSING MANAGEMENT:
Nurse should instruct the patient to avoid
sitting or standing for long periods of time.
Maintain ideal body weight, and take
precautions against injury to the extremities.
Avoid wearing constrictive clothing, and
participate in a daily walking program.
Encourage for deep breathing , which helps to
promote venous return to the right side of the
heart.
Postoperatively, the legs are elevated at 15
angle to prevent edema.
Compression stockings are applied and
removed every 8 hours for short periods and
then reapplied.
The patient with an occupation that require
prolonged period of standing or sitting needs
to change position frequently.
 COMPLICATION:
 Pain, tenderness.
 Dermatitis.
 Skin ulcers near the ankle.
 Development of carcinoma , sarcoma in long
standing venous ulcers.
 Thrombophlebitis.
 Acute fat necrosis.
 AORTIC ANEURYSM
Aneurysm
• An aneurysm is a localized sac or dilation
formed at a weak point in the wall of the
artery.
 Etiology / Classification of Arterial
Aneurysms
• Congenital: Primary connective tissue disorders (Marfan's syndrome)

• Mechanical (hemodynamic): Poststenotic and arteriovenous fistula

• Traumatic (pseudoaneurysms): Penetrating arterial injuries, blunt arterial injuries

• Inflammatory (noninfectious): Associated with arteritis , systemic lupus erythematosus,

periarterial inflammation (ie, pancreatitis)

• Infectious (mycotic): Bacterial, fungal, spirochetal infections

• Pregnancy-related degenerative: Nonspecific, inflammatory variant

• Anastomotic and graft aneurysms: Infection, arterial wall failure, suture failure, graft
failure
 TYPES
• It may be classified by its shape or form.

• The most common forms of aneurysms are saccular and

fusiform. A saccular aneurysm projects from one side of the
vessel only.

• f an entire arterial segment becomes dilated, a fusiform

aneurysm develops.

• Very small aneurysms due to localized infection are called

mycotic aneurysms.
 Thoracic Aortic Aneurysm

• Approximately 85% of all cases of thoracic

aortic aneurysm are caused by
atherosclerosis.
• They occur most frequently in men between
the ages of 40 and 70 years.
• The thoracic area is the most common site for
a dissecting aneurysm. About one third of
patients with thoracic aneurysms die of
rupture of the aneurysm (Rutherford, 2005).
 Clinical Manifestations

• Some patients are asymptomatic.

• In most cases, pain is the most prominent symptom. The pain is usually
constant and boring but may occur only when the person is supine.
• Other conspicuous symptoms are dyspnea, the result of pressure of the
aneurysm sac against the trachea, a main bronchus, or the lung itself;
• Cough, frequently paroxysmal;
• Hoarseness
• Stridor
• Weakness or complete loss of the voice (aphonia) resulting from
pressure against the laryngeal nerve
• Dysphagia (difficulty in swallowing) due to impingement on the
esophagus by the aneurysm.
 Assessment and Diagnostic Findings

• When large veins in the chest are compressed by

the aneurysm, the superficial veins of the chest,
neck, or arms become dilated
• Edematous areas on the chest wall and cyanosis are
often evident.
• Pressure against the cervical sympathetic chain can
result in unequal pupils.
• Diagnosis of a thoracic aortic aneurysm is principally
made by chest x-ray, transesophageal
echocardiography (tee), and ct.
 Medical Management

• General measures such as controlling blood

pressure and correcting risk factors may be helpful.
• It is important to control blood pressure in patients
with dissecting aneurysms. Systolic pressure is
maintained at about 100 to 120 mm Hg with
antihypertensive medications (eg, hydralazine
[Apresoline], or a beta-blocker such as esmolol
[Brevibloc] or metoprolol [Lopressor]). Sodium
nitroprusside (Nipride) may be used by continuous
IV drip to emergently lower the blood pressure.
 In most cases, an aneurysm is treated
by surgical repair.

• The goal of surgery is to repair the aneurysm and restore vascular continuity with a
vascular graft

• Intensive monitoring is usually required after this type of surgery, and the patient is
cared for in the critical care unit.

• Repair of thoracic aneurysms using endovascular grafts implanted (deployed)

percutaneously in an interventional suite (eg, interventional radiology, cardiac
catheterization laboratory) or an operating room may decrease postoperative
recovery time and decrease complications compared with traditional surgical
techniques.

• These endovascular grafts are inserted into the thoracic aorta via various vascular
access routes, including the femoral or iliac artery. Because a large operative incision
is not necessary to gain vascular access, the overall patient recovery time tends to be
shorter than if the patient had open surgical repair.
 Abdominal Aortic Aneurysm

• The most common cause of abdominal aortic

aneurysm is atherosclerosis.
• The condition, which is more common among
Caucasians, affects men four times more often
than women and is most prevalent in elderly
patients.
• Most of these aneurysms occur below the
renal arteries (infrarenal aneurysms).
 Clinical Manifestations

• Only about 40% of patients with abdominal aortic aneurysms

have symptoms.
• Some patients complain that they can feel their heart beating
in their abdomen when lying down
• they may say they feel an abdominal mass or abdominal
throbbing.
• If the abdominal aortic aneurysm is associated with thrombus,
a major vessel may be occluded or smaller distal occlusions
may result from emboli.
• Small cholesterol, platelet, or fibrin emboli may lodge in the
interosseous or digital arteries, causing cyanosis and mottling
of the toes.
 Assessment and Diagnostic Findings
• The most important diagnostic indication of an
abdominal aortic aneurysm is a pulsatile mass
in the middle and upper abdomen.
• About 80% of these aneurysms can be
palpated.
• A systolic bruit may be heard over the mass.
• Duplex ultrasonography or CT is used to
determine the size, length, and location of the
aneurysm.
• Most abdominal aortic aneurysms occur in patients
between 60 and 90 years of age.
• Rupture is likely with coexisting hypertension and with
aneurysms more than 6 cm wide.
• In most cases at this point, the chances of rupture are
greater than the chance of death during surgical repair.
• If the elderly patient is considered at moderate risk of
complications related to surgery or anesthesia, the
aneurysm is not repaired until it is at least 5.5 cm (2
inches) wide.
 Medical Management
Pharmacologic Therapy
• If the aneurysm is stable in size based on serial
duplexultrasound scans, the blood pressure is closely
monitored over time, because there is an association
between increased diastolic blood pressure (above 100
mm Hg) and aneurysm rupture .
• Antihypertensive agents, including diuretics, beta-
blockers, ACE inhibitors, angiotensin II receptor
antagonists, and calcium channel blockers, are
frequently prescribed to maintain the patient's blood
pressure within acceptable limits .
 Surgical Management

• An expanding or enlarging abdominal aortic aneurysm is likely to

rupture.
• Surgery is the treatment of choice for abdominal aortic aneurysms
more than 5.5 cm (2 inches) wide or those that are enlarging; the
standard treatment has been open surgical repair of the aneurysm by
resecting the vessel and sewing a bypass graft in place.
• The mortality rate associated with elective aneurysm repair, a major
surgical procedure, is reported to be 1% to 4%.
• The prognosis for a patient with a ruptured aneurysm is poor, and
surgery is performed immediately .
• An alternative for treating an infrarenal abdominal aortic aneurysm is
endovascular grafting, which involves the transluminal placement and
attachment of a sutureless aortic graft prosthesis across an aneurysm .
• This procedure can be performed under local or regional anesthesia.
• Endovascular grafting of abdominal aortic aneurysms may be
performed if the patient's abdominal aorta and iliac arteries are not
extremely tortuous and if the aneurysm does not begin at the level of
the renal arteries.
• Clinical trials are being conducted to evaluate endograft treatment of
abdominal aortic aneurysms at or above the level of the renal arteries
and the thoracic aorta.
• Potential complications include bleeding, hematoma, or wound
infection at the femoral insertion site; distal ischemia or
embolization; dissection or perforation of the aorta; graft thrombosis
or infection; break of the attachment system; graft migration;
proximal or distal graft leaks; delayed rupture; and bowel ischemia.
 Nursing Management

• Before surgery, nursing assessment is guided by anticipating a rupture

and by recognizing that the patient may have cardiovascular, cerebral,
pulmonary, and renal impairment from atherosclerosis.
• The functional capacity of all organ systems should be assessed.
Medical therapies designed to stabilize physiologic function should be
promptly implemented.
• Signs of impending rupture include severe back or abdominal pain,
which may be persistent or intermittent.
• Abdominal pain is often localized in the middle or lower abdomen to
the left of the midline.
• Low back pain may be present because of pressure of the aneurysm
on the lumbar nerves. This is a significant symptom, usually indicating
that the aneurysm is expanding rapidly and is about to rupture.
• Indications of a rupturing abdominal aortic aneurysm include constant, intense back
pain; falling blood pressure; and decreasing hematocrit.
• Rupture into the peritoneal cavity is rapidly fatal.
• A retroperitoneal rupture of an aneurysm may result in hematomas in the scrotum,
perineum, flank, or penis.
• Signs of heart failure or a loud bruit may suggest a rupture into the vena cava.
• If the aneurysm adheres to the adjacent vena cava, the vena cava may become
damaged when rupture or leak of the aneurysm occurs.
• Rupture into the vena cava results in higher-pressure arterial blood entering the lower-
pressure venous system and causing turbulence, which is heard as a bruit.
• The high blood pressure and increased blood volume returning to the right side of the
heart from the vena cava may cause right-sided heart failure. The overall surgical
mortality rate associated with a ruptured aneurysm is 50% to 75%.
• Postoperative care requires intense monitoring of pulmonary, cardiovascular, renal, and
neurologic status. Possible complications of surgery include arterial occlusion,
hemorrhage, infection, ischemic bowel, renal failure, and impotence
 Medical Management

• Surgical repair is performed with replacement

grafts or endovascular repair using a stent-
graft or wall graft, which is a Dacron or PTFE
graft with external structures made from a
variety of materials (nitinol, titanium, stainless
steel) for additional support.
 Nursing Management

• The patient who has had an endovascular repair must lie supine for 6 hours; the
head of the bed may be elevated up to 45 degrees after 2 hours.
• The patient needs to use a bedpan or urinal while on bed rest, or an indwelling
urinary catheter may be used.
• Vital signs and Doppler assessment of peripheral pulses are performed every 15
minutes for four times, then every 30 minutes for four times, then every hour for
four times, and then as directed by the physician or agency policy.
• The access site (usually the femoral or iliac )is assessed when vital signs and pulses
are monitored.
• The nurse assesses for bleeding, pulsation, swelling, pain, and hematoma formation.
• Skin changes of the lower extremity, lumbar area, or buttocks that might indicate
signs of embolization, such as extremely tender, irregularly shaped, cyanotic areas,
as well as any changes in vital signs, pulse quality, bleeding, swelling, pain, or
hematoma, are immediately reported to the physician.
• The patient's temperature should be monitored every 4 hours, and any signs of
postimplantation syndrome should be reported.
• Postimplantation syndrome typically begins within 24 hours of stent-graft placement and
consists of a spontaneously occurring fever, leukocytosis, and, occasionally, transient
thrombocytopenia.
• The exact etiology is unknown, but the symptoms are thought to be related to the activation of
cytokines, which results from thrombosis in the repaired aneurysm that occurs because of the
release of coagulation proteins and platelets.
• These symptoms can be managed with mild analgesics or anti-inflammatory agents, such as
acetaminophen or ibuprofen, and usually subside within a week.
• Because of the increased risk for hemorrhage, the physician is also notified of persistent
coughing, sneezing, vomiting, or systolic blood pressure greater than 180 mm Hg.
• Most patients can resume their preprocedure diet and are encouraged to drink fluids.
• An IV infusion may be continued until the patient can drink normally.
• Fluids are important to maintain blood flow through the arterial repair site and to assist the
kidneys with excreting IV contrast agent and other medications used during the procedure.
• Six hours after the procedure, the patient may be able to roll from side to side and may be able
to ambulate with assistance to the bathroom.
• After the patient can take adequate fluids orally, the IV infusion may be discontinued and the IV
access converted to a saline lock.
 Dissecting Aorta

• Occasionally, in an aorta diseased by

arteriosclerosis, a tear develops in the intima
or the media degenerates, resulting in a
dissection.
• Arterial dissections are three times more
common in men than in women and occur
most commonly in the 50- to 70-year-old age
group .
 Pathophysiology

• Arterial dissections (separations) are commonly associated with poorly controlled

hypertension, blunt chest trauma, and cocaine use.
• The profound increase in sympathetic response caused by cocaine use creates an increase in
the force of left ventricular contraction that causes heightened shear forces upon the aortic
wall .
• Dissection is caused by rupture in the intimal layer. A rupture may occur through adventitia
or into the lumen through the intima, allowing blood to re-enter the main channel and
resulting in chronic dissection (eg, pseudoaneurysm) or occlusion of branches of the aorta.
• As the separation progresses, the arteries branching from the involved area of the aorta
shear and occlude.
• The tear occurs most commonly in the region of the aortic arch, with the highest mortality
rate associated with ascending aortic dissection.
• The dissection of the aorta may progress backward in the direction of the heart, obstructing
the openings to the coronary arteries or producing hemopericardium (effusion of blood into
the pericardial sac) or aortic insufficiency, or it may extend in the opposite direction, causing
occlusion of the arteries supplying the gastrointestinal tract, kidneys, spinal cord, and legs.
 Clinical Manifestations

• Onset of symptoms is usually sudden.

• Severe and persistent pain, described as tearing or ripping, may be reported.
• The pain is in the anterior chest or back and extends to the shoulders, epigastric
area, or abdomen.
• Aortic dissection may be mistaken for an acute myocardial infarction, which
could confuse the clinical picture and initial treatment.
• Cardiovascular, neurologic, and gastrointestinal symptoms are responsible for
other clinical manifestations, depending on the location and extent of the
dissection.
• The patient may appear pale.
• Sweating and tachycardia may be detected.
• Blood pressure may be elevated or markedly different from one arm to the other
if dissection involves the orifice of the subclavian artery on one side.
• Because of the variable clinical picture associated with this condition, early
diagnosis is usually difficult.
 Assessment and Diagnostic Findings

• Arteriography, CT, transesophageal

echocardiography, duplex ultrasonography,
and MRI aid in the diagnosis.
 Medical Management

• The medical or surgical treatment of a

dissecting aorta depends on the type of
dissection present and follows the general
principles outlined for the treatment of
thoracic aortic aneurysms.
 Nursing Management

• A patient with a dissecting aorta requires the

same nursing care as a patient with an aortic
aneurysm requiring surgical intervention, as
described earlier in this chapter.
 DVT
• Venous Thrombosis, Deep Vein Thrombosis,
Thrombophlebitis, and Phlebothrombosis
• Although the terms venous thrombosis, deep
vein thrombosis (DVT), thrombophlebitis, and
phlebothrombosis do not necessarily reflect
identical disease processes, for clinical
purposes they are often used interchangeably.
 Pathophysiology

• Superficial veins, such as the greater saphenous, lesser saphenous, cephalic,

basilic, and external jugular veins, are thick-walled muscular structures that lie
just under the skin.
• Deep veins are thin-walled and have less muscle in the media.
• They run parallel to arteries and bear the same names as the arteries.
• Deep and superficial veins have valves that permit unidirectional flow back to
the heart.
• The valves lie at the base of a segment of the vein that is expanded into a
sinus.
• This arrangement permits the valves to open without coming into contact with
the wall of the vein, permitting rapid closure when the blood starts to flow
backward.
• Other kinds of veins are known as perforating veins. These vessels have valves
that allow one-way blood flow from the superficial system to the deep system.
• Although the exact cause of venous
thrombosis remains unclear, three factors,
known as Virchow's triad, are believed to play
a significant role in its development:
 Stasis of blood (venous stasis),
 Vessel wall injury,
 Altered blood coagulation.
• Venous stasis occurs when blood flow is reduced, as in heart failure or
shock; when veins are dilated, as with some medication therapies; and
when skeletal muscle contraction is reduced, as in immobility, paralysis of
the extremities, or anesthesia.
• Moreover, bed rest reduces blood flow in the legs by at least 50% (Porth,
2005). Damage to the intimal lining of blood vessels creates a site for clot
formation.
• Direct trauma to the vessels, as with fractures or dislocation, diseases of
the veins, and chemical irritation of the vein from IV medications or
solutions, can damage veins.
• Increased blood coagulability occurs most commonly in patients for
whom anticoagulant medications have been abruptly withdrawn.
• Oral contraceptive use and several blood dyscrasias (abnormalities) also
can lead to hypercoagulability.
• Formation of a thrombus frequently accompanies
thrombophlebitis, which is an inflammation of the vein
walls.
• When a thrombus develops initially in the veins as a
result of stasis or hypercoagulability but without
inflammation, the process is referred to as
phlebothrombosis.
• Venous thrombosis can occur in any vein, but it occurs
more in the veins of the lower extremities.
• The superficial and deep veins of the extremities may be
affected.
• Upper extremity venous thrombosis is not as common as lower
extremity thrombosis. Upper extremity venous thrombosis is more
common in patients with IV catheters or in patients with an
underlying disease that causes hypercoagulability.
• Internal trauma to the vessels may result from pacemaker leads,
chemotherapy ports, dialysis catheters, or parenteral nutrition lines.
• The lumen of the vein may be decreased as a result of the catheter
or from external compression, such as by neoplasms or an extra
cervical rib.
• Effort thrombosis of the upper extremity is caused by repetitive
motion (as in competitive swimmers, tennis players, and
construction workers) that irritates the vessel wall, causing
inflammation and subsequent thrombosis.
• Venous thrombi are aggregates of platelets attached to the vein wall that have a
tail-like appendage containing fibrin, white blood cells, and many red blood cells.
• The “tail” can grow or can propagate in the direction of blood flow as successive
layers of the thrombus form.
• A propagating venous thrombosis is dangerous because parts of the thrombus
can break off and produce an embolic occlusion of the pulmonary blood vessels.
• Fragmentation of the thrombus can occur spontaneously as it dissolves naturally,
or it can occur in association with an elevation in venous pressure, as occurs
when a person stands suddenly or engages in muscular activity after prolonged
inactivity.
• After an episode of acute DVT, recanalization (ie, reestablishment of the lumen
of the vessel) typically occurs. The time required for complete recanalization is
an important determinant of venous valvular incompetence, which is one
complication of venous thrombosis.
 Clinical Manifestations

• A major problem associated with recognizing

DVT is that the signs and symptoms are
nonspecific.
• The exception is phlegmasia cerulea dolens
(massive iliofemoral venous thrombosis), in
which the entire extremity becomes massively
swollen, tense, painful, and cool to the touch.
 Deep Veins

• With obstruction of the deep veins comes edema and swelling of the
extremity because the outflow of venous blood is inhibited.
• The amount of swelling can be determined by measuring the circumference of
the affected extremity at various levels with a tape measure and comparing
one extremity with the other at the same level to determine size differences.
• If both extremities are swollen, a size difference may be difficult to detect.
• The affected extremity may feel warmer than the unaffected extremity, and
the superficial veins may appear more prominent.
• Tenderness, which usually occurs later, is produced by inflammation of the
vein wall and can be detected by gently palpating the affected extremity.
• Homans' sign (pain in the calf after the foot is sharply dorsiflexed) is not
specific for DVT because it can be elicited in any painful condition of the calf.
• In some cases, signs and symptoms of a pulmonary embolus are the first
indication of DVT.
 Superficial Veins

• Thrombosis of superficial veins produces pain or

tenderness, redness, and warmth in the involved
area.
• The risk of the superficial venous thrombi
becoming dislodged or fragmenting into emboli is
very low because most of them dissolve
spontaneously.
• This condition can be treated at home with bed
rest, elevation of the leg, analgesics, and possibly
anti-inflammatory medication.
 Assessment and Diagnostic Findings

• Careful assessment is invaluable in detecting early signs of

venous disorders of the lower extremities.
• Patients with a history of varicose veins, hypercoagulation,
neoplastic disease, cardiovascular disease, or recent major
surgery or injury are at high risk.
• Other patients at high risk include those who are obese or
elderly and women taking oral contraceptives.
• When performing the nursing assessment, key concerns
include limb pain, a feeling of heaviness, functional
impairment, ankle engorgement, and edema; differences
in leg
• circumference bilaterally from thigh to ankle;
• increase in the surface temperature of the leg,
particularly the calf or ankle;
• and areas of tenderness or superficial
thrombosis (ie, cord-like venous segment).
• Although Homans' sign has been used
historically to assess for DVT, it is not a reliable
or valid sign and has no clinical value in
assessment for DVT .
 Prevention

• Venous thrombosis, thrombophlebitis, and DVT can be

prevented, especially if patients who are considered at high
risk are identified and preventive measures are instituted
without delay.
• Preventive measures include the application of elastic
compression stockings, the use of intermittent pneumatic
compression devices, and special body positioning and
exercise (discussed later in the section on nursing
management).
• An additional method to prevent venous thrombosis in
surgical patients is administration of subcutaneous
unfractionated or low-molecular-weight heparin (LMWH).
 Medical Management

• The objectives of treatment for DVT are to prevent the

thrombus from growing and fragmenting (risking
pulmonary embolism) and to prevent recurrent
thromboemboli.
• Anticoagulant therapy (administration of a medication
to delay the clotting time of blood, prevent the
formation of a thrombus in postoperative patients, and
forestall the extension of a thrombus after it has
formed) can meet these objectives, although
anticoagulants cannot dissolve a thrombus that has
already formed.
 Pharmacologic Therapy

• Measures for preventing or reducing blood

clotting within the vascular system are
indicated in patients with thrombophlebitis,
recurrent embolus formation, and persistent
leg edema from heart failure.
• They are also indicated in elderly patients with
a hip fracture that may result in lengthy
immobilization.
 Unfractionated Heparin

• Unfractionated heparin is administered

subcutaneously to prevent development of DVT, or
by intermittent or continuous IV infusion for 5 to 7
days to prevent the extension of a thrombus and the
development of new thrombi. Oral anticoagulants,
such as warfarin (Coumadin), are administered with
heparin therapy. Medication dosage is regulated by
monitoring the activated partial thromboplastin
time (aPTT), the international normalized ratio (INR),
and the platelet count.
 Low-Molecular-Weight Heparin

• Subcutaneous LMWHs that may include medications such as

dalteparin (Fragmin) and enoxaparin (Lovenox) are effective
treatments for some cases of DVT. These agents have longer half-
lives than unfractionated heparin, so doses can be given in one or
two subcutaneous injections each day. Doses are adjusted according
to weight. LMWHs prevent the extension of a thrombus and
development of new thrombi, and they are associated with fewer
bleeding complications and lower risks of heparin-induced
thrombocytopenia (HIT) than unfractionated heparin. Because there
are several preparations, the dosing schedule must be based on the
product used and the protocol at each institution. The cost of LMWH
is higher than that of unfractionated heparin; however, LMWH may
be used safely in pregnant women, and patients who take it may be
more mobile and have an improved quality of life.
 Thrombolytic Therapy

• Unlike the heparins, thrombolytic (fibrinolytic) therapy lyses and

dissolves thrombi in 50% of patients. Thrombolytic therapy (eg,
t-PA [Alteplase, Activase], reteplase [r-PA, Retavase],
tenecteplase [TNKase], staphylokinase, urokinase, streptokinase)
is given within the first 3 days after acute thrombosis. Therapy
initiated beyond 5 days after the onset of symptoms is
significantly less effective (Moore, 2002). The advantages of
thrombolytic therapy include less long-term damage to the
venous valves and a reduced incidence of postthrombotic
syndrome and chronic venous insufficiency. However,
thrombolytic therapy results in a threefold greater incidence of
bleeding than heparin. If bleeding occurs and cannot be
stopped, the thrombolytic agent is discontinued.
 Factor Xa Inhibitor

• Fondaparinux (Arixtra) selectively inhibits factor Xa.

This agent is given daily subcutaneously at a fixed
dose, has a half-life of 17 hours, and is excreted
unchanged via the kidneys (and therefore must be
used with caution in patients with renal insufficiency).
Fondaparinux has no effect on routine tests of
coagulation, such as the aPTT or activated clotting
time (ACT), so routine coagulation monitoring is
unnecessary (Weitz, 2004). Fondaparinux is approved
for prophylaxis during major orthopedic surgery, such
as hip or knee arthroplasties.
 Oral Anticoagulants

• Warfarin (Coumadin) is a vitamin K antagonist that is

frequently used for extended therapy. Routine coagulation
monitoring is essential to ensure that a therapeutic response
is obtained and maintained over time. Interactions with a
range of other medications can reduce or enhance the
anticoagulant effects of warfarin, as can variable intake of
foods containing vitamin K (see Chapter 33, Chart 33-15, for a
review of agents that interact with warfarin). Warfarin has a
narrow therapeutic window, and there is a slow onset of
action. Treatment is initially supported with concomitant
parenteral anticoagulation with heparin until the warfarin
demonstrates anticoagulant effectiveness.
 Surgical Management

• Surgery is necessary for DVT when anticoagulant or

thrombolytic therapy is contraindicated (see Chart 31-8),
the danger of pulmonary embolism is extreme, or the
venous drainage is so severely compromised that
permanent damage to the extremity is likely. A
thrombectomy (removal of the thrombosis) is the
procedure of choice. A vena cava filter may be placed at the
time of the thrombectomy; this filter traps large emboli and
prevents pulmonary emboli (see Chapter 23). Balloon
angioplasty and stent placement are being used in the iliac
veins of patients with acute and chronic venous disease.
 Nursing Management

• If the patient is receiving anticoagulant therapy,

the nurse must frequently monitor the aPTT,
prothrombin time (PT), INR, ACT, hemoglobin
and hematocrit values, platelet count, and
fibrinogen level, depending on which medication
is being given. Close observation is also required
to detect bleeding; if bleeding occurs, it must be
reported immediately and anticoagulant therapy
discontinued the INR is 2.0 to 3.0).
 Assessing and Monitoring Anticoagulant Therapy

• To prevent inadvertent infusion of large volumes of

unfractionated heparin, which could cause hemorrhage,
continuous IV infusion by an electronic infusion device is
the preferred method of administering unfractionated
heparin. Dosage calculations are based on the patient's
weight, and any possible bleeding tendencies are
detected by a pretreatment clotting profile. If renal
insufficiency exists, lower doses of heparin are required.
Periodic coagulation tests and hematocrit levels are
obtained. Heparin is in the effective, or therapeutic,
range when the aPTT is 1.5 times the control.
• Oral anticoagulants, such as warfarin
(Coumadin), are monitored by the PT or the
INR. Because the full anticoagulant effect of
warfarin is delayed for 3 to 5 days, it is usually
administered concurrently with heparin until
desired anticoagulation has been achieved (ie,
when the PT is 1.5 to 2 times normal or