2 - Alterations in Oxygenation 1.1
2 - Alterations in Oxygenation 1.1
2 - Alterations in Oxygenation 1.1
OXYGENATION
❖ a.k.a “erythrocytes”
❖ contain the O2 – carrying hemoglobin
❖ live only about 120 days
❖ healthy adult male – 5.4 million RBC
per (ml) of blood
❖ healthy adult female – 4.8 million
RBC
■ function: to transport oxygen from lungs to
tissues
■ RBC production
☛ regulated by erythropoietin
☛ requires iron, vitamin B12, & folate
☛ occurs in the bone marrow
■ lifespan: 120 days
■ heme is converted to bilirubin & removed by
the liver through bile
RBC ANATOMY
♥ RBC’s are biconcave discs with a diameter
of 7.8 mm
♥ RBC’s lack a nucleus
♥ can neither reproduce nor carry on
extensive metabolic activities
♥ are highly specialized for their O2 transport function
♥ lack mitochondria & generate ATP aerobically
♥ each RBC has 280 million hemoglobin molecules
♥ each hemoglobin can carry up to 4 O2 molecules
RBC
Physiology
HEMOGLOBIN
Proerythroblast
Reticulocyte
Mature RBC
Main Stimulus
for
Erythropoeisis:
HYPOXIA
Some stimulus disrupts
Homeostasis by
decreasing
O2 delivery to kidneys
(and other tissues)
Receptors
kidney cells detect low O2 level
Increased erythropoeitin
input secreted into blood
Control center
Proerythroblasts in red bone marrow mature
more quickly into reticulocytes
More reticulocytes enter
output circulating blood
Effectors
Larger # of RBC’s in circulation
►results from:
►excessive loss (blood loss anemia)
►increased destruction (hemolytic anemia)
►impaired production of RBC’s (IDA,
megaloblastic & aplastic anemia)
Manifestations of ANEMIA:
✦ impaired O2 transport
✦ alterations in red cell
structure
✦ s/s associated with the
pathologic process
❖ EXTRINSIC
➢drugs
➢bacterial & other
toxins hemolytic anemia in the
➢ antibodies Microvasculature
physical trauma
Manifestations:
❖ fatigability, palpitations, dyspnea, angina, &
tachycardia
iron deficiency anemia, atrophic glossitis
Treatment:
❖ increasing dietary intake of iron
❖administering supplemental iron
➢ ferrous sulfate
➢iron dextran
♦ exposure to radiation
E
♦ inherited condition
S
S ❖ headache
❖ dizziness
Y ❖ nausea
❖ shortness of breath
M
❖ bruising
❖ lack of energy or tiring easily (fatigue)
❖ abnormal paleness or lack of color of the skin
P ❖ blood in stool
❖ nosebleeds
T
❖ bleeding gums
❖ fevers
❖ sinus tenderness
O ❖ enlarged liver or spleen
❖ oral thrush - white patches on a red, moist,
S
How is aplastic anemia diagnosed?
complete medical
history and physical
examination, diagnostic
procedures for anemia
include additional
blood tests and
a bone marrow
biopsy.
aplastic anemia,
bone marrow
Polycythemia is an increased volume of red blood cells.
The hematocrit is elevated by more than 55% in men or
more than 50% in women.
Symptoms:
elderly
■ underlying neoplasms: may contribute to
anemia
The Cardiovascular
System
Gross Anatomy of the Heart
■ Borders of the Heart:
☛ right border: RA
☛ left border: LVpart of L auricle
☛ superior border: root of great vessels
☛ inferior border: RV, apical LV
■ Cardiac walls:
☛ endocardium
☛ myocardium
☛ epicardium
Chambers of the Heart
■ RA
☛ receives blood from the SVC & the IVC
☛ coronary sinus: blood from walls of the heart
■ RV
☛ pumps blood via the pulmonic valve
☛ wall thicker than RA
☛ crescent-shaped
■ LA
☛ behind the RA
☛ drains into the LV guarded by the bicuspid or
mitral valve
■ LV
☛ circular in shape
☛ pumps blood into the systemic circulation
Prepared by:
Eric B. Panopio, M.D.
ALTERATIONS IN
PULMONARY GAS
EXCHANGE
Pneumothorax
MANIFESTATIONS OF SPONTANEOUS
PNEUMOTHORAX
■ Mediastinal shift
■ Distention of the neck veins
■ Clinical signs of shock
ATELECTASIS
■ Refers to reduction or absence of air in part or
all of a lung, with resulting loss of lung
volume.
■ Pulmonary collapse: secondary atelectasis due
to bronchial obstruction, pleural effusion or
pneumothorax, cardiac hypertrophy, or
enlargement of other structures adjacent to the
lungs.
MANIFESTATIONS OF
ATELECTASIS
■ Tachypnea
■ Dyspnea
■ Cyanosis
■ Signs of hypoxemia
■ Diminished chest expansion
■ Absence of breath sounds
■ Intercostal retractions
■ Fever and other signs of infections
HYPOXEMIA
■ Refers to a reduction in blood oxygen levels.
■ Subnormal oxygenation of arterial blood, short
of anoxia.
Causes of Hypoxemia
■ Inadequate amount of oxygen in the air
■ disease of the respiratory system
■ alterations in circulatory function
MANIFESTATIONS OF HYPOXEMIA
SIGNS AND SYMPTOMS OF HYPOXIA
■ tachycardia ■ Loss of judgement
■ mild BP ■ euphoria
■ cool, moist skin ■ unruly or combative behavior
■ confusion ■ sensory impairment
■ delirium ■ mental fatigue
■ difficulty problem solving ■ drowsiness
■ stupor,coma (late)
■ hypotension(late)
■ Bradycardia (late)
TYPES OF HYPOXIA
■ HYPOXEMIC HYPOXIA
■ CIRCULAORY HYPOXIA
■ ANEMIC HYPOXIA
■ HISTOTOXIC HYPOXIA
HYPOXEMIC HYPOXIA
■ Refers to decrease oxygen level in the blood
resulting in decrease oxygen diffusion into the
tissues.
■ Causes:
CIRCULATORY HYPOXIA
■ Hypoxia resulting from inadequate capillary
circulation.
■ Causes:
ANEMIC HYPOXIA
■ Result of decreased effective hemoglobin
concentration, which causes a decrease in the
oxygen-carrying capacity of the blood.
HISTOTOXIC HYPOXIA
CYANOSIS
- refers to the bluish discoloration of the skin and mucous membranes
that results from excessive concentration of reduced or deoxygenated
hemoglobin in the small blood vessels.
MARKED: lips, nail beds, ears, cheeks.
DEGREES: modified by the amount of cutaneous pigment, skin thickness,
and the state of the cutaneous capillaries.
**Difficult to distinguish in person with dark skin and in areas of the body
with increased skin thickness.
TYPES:
Central Cyanosis – evident in the tongue and lips
- it is caused by an increased amount of deoxygenated
hgb or an abnormal hgb derivative in the arterial blood
Peripheral Cyanosis – occurs in the extremities and on the tip of the nose
or ears.
DIAGNOSIS is based on clinical observation and diagnostic measures of
oxygen level.
TWO NON-INVASIVE METHODS FOR OXYGEN ASSESSMENT
1. Transcutaneous Sensor Method
- uses an oxygen electrode
2. Pulse Oximeter
- cannot distinguish between oxygen-carrying hgb and CO-
carrying hgb.
Central Cyanosis
Peripheral CYANOSIS
Pulse Oximeter
Cyanosis
HYPERCAPNIA
- refers to an increased in the CO2 content of the blood.
- diagnosis is based on physiologic manifestations, arterial pH, and
blood gas levels.
- can occur in a number of disorders that cause hypoventilation or
mismatching of ventilation and perfusion.
- hypoventilation is a cause of hypercapnia in respiratory failure due
to depression of the respiratory.
- due to ventilation-perfusion inequalities is seen most commonly in
persons with COPD.
Hypercapnia
Respiratory Failure
MECHANISM
■ Respiratory failure – is a condition in which the
lungs fall to oxygenate the blood adequately
and to prevent carbon dioxide retention.
■ It is the result of number of condition that
impair ventilation and perfusion, or disrupt
blood flow in the lungs
COMMON MANIFESTATION OF
RESPIRATORY FAILURE:
CAUSES:
▪ cause of SIDS is unknown
SIDS
Factors increase the risk of SIDS:
CLINICAL SYNDROMES
Type A COPD
-- Referred to as pink puffers
-- Predominant emphysema, progressive exertional dyspnea,
weight loss
-- Little improvement with bronchodilators
-- Symptoms show at a relatively old age (>60)
Chronic Obstructive
Pulmonary Disease
Type B COPD
Centri-acinar emphysema
Chronic Bronchitis
Symptoms: Chronic bronchitis may be asymptomatic for years. A
productive cough and exertional dyspnea are typical presenting
signs. The cough becomes increasingly progressive and the
sputum production copious; several attacks a year are common.
Chest retractions, wheezing, tachypnea, and cyanosis may also be
present.
Potential Complications: Cor pulmonale, pulmonary hypertension,
right ventricular hypertrophy, and respiratory failures are
common complications.
Chronic Bronchitis
Diagnostic Tests: Clinical evaluation: History of chronic lung irritation (e.g.,
smoking, occupational exposure); Radiology: Increased markings,
hyperinflation; Pulmonary function: Residual volume increased, forced vital
capacity and forced expiratory volume decreased; compliance and diffusion
normal; Arterial blood gases: PaO2 decreased, PaCO2 increased; Sputum:
Culture of multiple microorganisms and neutrophils.
Prepared by:
Eric B. Panopio, M.D.
Alterations in Cardiac
Output and Heart Failure
■ Dyspnea
➢ most frequently encountered symptom of CHF
➢ the feeling of breathlessness is due to vascular congestion w/c reduces
pulmonary oxygenation
■ Orthopnea
➢ dyspnea that occurs in the recumbent position and is relieved by
elevation of the head
➢ results from volume pooling in the central vasculature during
recumbency
■ Paroxysmal nocturnal dyspnea
➢ sudden dyspnea that awakens the patient from sleep
■ Nocturia
➢ due to ↑ renal blood flow in recumbency during sleep
■ Edema
■ Anorexia
■ Tachycardia
➢ A compensatory mechanism for maintaining cardiac output
in the presence of decreased stroke volume
■ Pulmonary rales
➢ The increased left ventricular filling pressure is referred to
the left atrium and pulmonary veins and the increased
hydrostatic pressure produces transudation of fluid into the
alveoli
■ Ascites
➢ Transudation of fluid into the peritoneal space
■ Cardiac enlargement
■ Ventricular gallop
■ Neck vein distension
■ Edema
Right-Sided Heart Failure
■RH pumps de-O2ated bld from the systemic
circ into the pulmo circ
■ RH Failure: accumulation/damming back of
distress
■ Cyanosis
■ Elevation in peripheral venous pressure
Left-Sided Heart Failure
■ LH pumps bld from the low-pressure
pulmonary circ into the high-pressure arterial
side of the systemic circ
■ LH failure: Dec in CO; Inc in LA and LV
end-diastole pressures; congestion in the
pulmonary circulation
Manifestations of Left-Sided Heart
Failure
■ Exertional dyspnea
■ Orthopnea
■ Paroxysmal nocturnal dyspnea
■ Cough
■ Blood-tinged sputum
■ Cyanosis
■ Elevation in pulmonary capillary wedge
pressure
RIGHT-SIDED vs. LEFT-SIDED HEART
FAILURE
RIGHT-SIDED HEART FAILURE LEFT-SIDED HEART FAILURE
LDL
Pathophysiology
■ Type A personality
■ Obesity
■ Hypertriglyceridemia
■ Serum cholesterol - higher LDL and VLDL
■ Age
■ Sex
■ Smoking
■ Hypertension
■ Diabetes mellitus
■ (+) family history
■ Oral contraceptives
Signs & Symptoms
Angina Pectoris
■ related to exertion, the single most impt feature of
angina is precipitation by exertion
■ symptom quality: feeling a pressure sensation in their
chest
■ radiation of pain: left arm, right arm, jaw, teeth, or
throat
Unstable angina
■ a change in the status of a px’s angina e.g. new-onset
angina, increasing severity, duration or frequency
Variant or Prinzmetal’s Angina
■ usually occurs at rest instead of during exercise
Angina Pectoris
■ “Heart Attack”
■ Means “ death of the myocardium”
■ Blood supply to the heart is significantly reduced
or blocked
■ Part of heart dies
■ Most die 2 hours after signs and symptoms
■ Death due to Cardiogenic Shock , Congestive
Heart Failure – 3-7 days post attack,
Dysrhythmias – irritable heart/problems of
electrical conduction of the heart.
Angina Pectoris Myocardial Infarction
Location Substernal or across Same
of Pain the chest
■ Assume its MI
■ Make patient comfortable, Semi-Fowlers often best
■ Have the patient cease ALL movement, Do not allow to
help self position
■ Loosen clothing
■ Reassure and calm the patient
■ Assist and administer medication (Nitroglycerin) – if not
relieved, chances are suffering from MI
■ Call for assistance, Monitor and record Vital Signs
■ If arrests, do CPR
Diagnosis & Tests
■ Dizziness
■ Syncope
➢ Loss of consciousness and postural tone caused by
diminished cerebral blood flow
Diagnosis & Tests
■ Non-medical intervention
■ Aimed at correcting the reversible causes
■ Assist the client in compensating for the
disorder
■ Prevent falls and injuries
PERICARDITIS
Definition
■ Inflammation of the pericardium
■ Pain occurs as a result of the inflamed pericardium
rubbing against the heart
■ Fluid may accumulate in the pericardial sac
■ Most often affects men ages 20 to 50, usually
following respiratory infections
Classification
■ Bacterial pericarditis: purulent or infectious
pericarditis
■ Constrictive pericarditis
■ Post-MI pericarditis
Causes & Risk Factors
■ Heart failure
■ Pulmonary edema
VALVULAR HEART
DISEASE
Definition
■ A defect or disease in any of the 4 valves that
control the flow of blood will disrupt normal
blood flow
■ 2 types:
➢ stenosis – the valve fails to open fully
➢ insufficiency or regurgitation – the valve does not
close properly
■ HEART VALVES – determines the direction of the blood flow
through the heart chambers
■ VALVULAR HEART DEFECTS – exert their effects by
obstructing flow of blood (stenotic valve disorder) or
allowing backward flow of blood (regurgitant valve disorder)
■ STENOTIC VALVULAR DEFECTS – produce distention of
the heart chamber that empties blood through the diseased valve
& impaired filling of the chamber that receives blood that
moves through the valve
■ REGURGITANT VALVES – allow blood to move back through
the valve when it should be closed . This produce distention and
places increase work demands on the chamber ejecting blood
through the diseased valve
Causes & Risk Factors
■ ECG
■ Echocardiography
■ Cardiac catheterization
➢ measure pressure gradient
Abnormal Heart Sounds
Mitral Stenosis
Medical
■ Diuretics
■ Digitalis
■ Anticoagulants
Surgical
■ Commissurotomy
➢ allows relief of stenosis without valve replacement
■ Valve Replacement
➢ if commissurotomy cannot be performed
End:
Alterations in Cardiac Output and Heart
Failure
Prepared by:
Eric B. Panopio, M.D.
ALTERATIONS IN
CIRCULATION & TISSUE
PERFUSION
• B. Venous diseases
1. Chronic venous insufficiency
2. Varicose veins
3. Acute Venous diseases
4. Thrombophlebitis
5. Thromboembolism
• C. Arteriovenous fistula
• D. Lymphedema
Arteriosclerosis Obliterans (ASO)
TREATMENT:
1. Conservative Program Approach:
- cessation of smoking
- dietary mngt
- Pain control
- Daily walking
2. Medical:
- Low-dose aspirin
3. Bypass graft or Angioplasty
Doppler Sonography
■ US enhanced with Doppler
measurements, which employ
the Doppler effect to assess
whether structures (usually
blood) are moving towards or
away from the probe, and its
relative velocity
■ By calculating the frequency
shift of a particular sample
volume, for example a jet of
blood flow over a heart valve,
its speed and direction can be
determined and visualised
Impedance Plethysmography
■ An instrument for measuring
changes in volume within an
organ or whole body (usually
resulting from fluctuations in
the amount of blood or air it
contains)
■ Air plethysmography
uses a similar principle
but based on an air-filled
long cuff, which is more
convenient but less
accurate
Thromboangiitis Obliterans
• Idiopathic diffuse inflammation in both arteries
and veins and surrounding CT.
• SECOND MOST COMMON chronic @ial d/o 4. Cold sensitivity
• Can affect arteries & veins ( most common in 5. cyanosis
Arteries) 6. decreased/absent posterior tibial &
• MEDIUM sized arteries of legs dorsalis pedis artery
• Syn: BUERGER’S Disease 7. ulceration & gangrene
• 40 y/o men who smoke heavily 8. thin, shiny, hairless skin
• SSx:
pain and tenderness Diagnosis:
Symptoms: Episodic and Segmental Arteriography
Intermittent claudication Histologic exam
- Client instructions:
Avoid: 1. prolonged sitting & standing
2. crossing the legs
3. sitting too high
4. wearing tight clothing above the knee
2. Acute venous diseases
A. Varicose veins:
- abnormal dilation of veins leading to tortuosity of the vessels, incompetence of the valves & propensity
for thrombosis
- in 15% of adults; in women (in pregnancy)
- Etiology & Risk factors:
1. Heavy lifting 4. Obesity
2. heart failure 5. hemorrhoids
3. constipation
Clinical Presentation:
1. Gradual, dull aching heaviness (MOST COMMON Sx)
2. Feeling of fatigue on long standing
3. Lower leg cramps
4. Lower leg ulceration
5. Relieved by leg elevation
6. Dilated tortuous, elongated veins under the skin
(MOST VISIBLE sign)
Diagnosis:
Visual inspection & palpation
Doppler US – used to localize incompetent valves
Treatment:
1. periodic rest; feet elevated
2. Client education in:
1. promoting circulation
2. frequent posture changes
3. performance of simple exercises
4. use of properly fitting elastic stockings
3. Surgery – vein stripping
Thrombophlebitis:
■ Inflammation of a vein with thrombus formation
■ Damage to endothelial lining on which platelets are deposited leading to thrombus formation
■ May affect:
1. deep veins (pelvis & LE)
2. superficial veins (saphenous veins)
• Etiology:
*1. venous stasis
2. hypercoagulability
3. vein wall trauma – direct blow, IV injection, fractures, dislocation
• Clinical presentation:
- asymptomatic during the early stage
- Dull ache, tightness and pain in the calf
- Affected side is warmer
- Cyanotic skin
• Diagnosis: Doppler US
• Treatment:
1. anticoagulants
2. bed rest
3. heat application
4. ambulation with elastic stockings
Clinical feature: Pain & signs of acute Silent with few SSx.
inflam.
Arteriovenous Fistula
• Abnormal communication of artery & vein ■ Anatomic changes:
• TYPES:
1. Congenital or A-V malformation
1. elongated & distended
2. Acquired arterio-venous fistula 2. smooth muscle atrophy
• Etiology: 3. dec. elastic tse
1. penetrating injury 4. atheromatous plaque
2. aneurysmal erosion formation
3. infection & neoplasm
4. surgical construction in dialysis 5. distal vein dilates &
• Clinical presentation: elongates with incompetent
valves
A. Acute phase:
1. (+) pulsating hematoma
2. (+) palpable thrill
3. (+) bruit
B. Chronic phase:
1. heart failure
2. peripheral ischemia
3. gangrene
Arteriovenous Fistula
Lymphedema
■ Abnormal accumulation of water and protein in skin and subcutaneous tse. d/t disruption or occlusion of
lymph channels.
■ TYPES:
A. Primary Lymphedema
- impaired lymphatic flow owing to Congenital malfunction of the lymphatic vessels
1. Congenital lymphedema:
*Agenesis – no formation of lymph sys.
*Aplasia – poorly developed lymph sys.
2. Hereditary lymphedema:
* Milroy’s dse (AD) – lymphedema of 1 or more ext right after
birth.
` - will not impair dev’t & act.
3. Lymphedema Praecox:
- in 2nd & 3rd decade
- pitting & soft edema to non-pitting & firm edema
- no pain, ulceration
- with recurrent infections
4. Lymphedema Tarda:
- Tarda (“late”)
- >35 y/o
- non-pitting & firm edema
- no pain, ulceration
- with recurrent infections
Secondary Lymphedema
dyspnea wheezing
confusion slurred speech
gen. itching nausea, vomiting
abdominal pain skin redness
nasal congesion cough
Septic Shock
■ a serious, abnormal condition that occurs when an
overwhelming infection leads to low blood pressure
and low blood flow
■ SSx:
■ Thirst
■ Increased heart rate
■ Cool and clammy skin
■ Decreased in arterial blood pressure
■ Decreased in urine output
■ Changes in mentation
TREATMENT
■ Supine position
■ Administer oxygen
- Crystalloids
■ TREATMENT modalities
- surgical intervention
* pulmonary embolectomy
* pericardiocentesis ( removal of fluid from the
pericardial sac) for cardial tamponade
* the insertion of a chest tube
■ DISTRIBUTIVE SHOCK
characteristics
- loss of sympathetic vasomotor tone
- presence of vasodilating substances in
the blood
- presence of inflammatory mediators
KINDS OF DISTRIBUTIVE
SHOCK
■ NEUROGENIC SHOCK
- caused by decreased sympathetic control of
blood vessels tone due to a defect in the
vasomotor center in the brain stem or the
sympathetic outflow to the blood vessels.
■ Fainting due to emotional causes is a
transient form of neurogenic shock
■ The term spinal shock is used to describe
the neurogenic shock that occurs in persons
with spinal cord injury.
■ Neurogenic shock often slower than normal,
and the skin is dry and warm.
■ This is rare and usually transitory.
■ ANAPHYLACTIC SHOCK
- characterized by massive vasodilatation,
pooling of blood in the peripheral blood
vessels, and increased permeability
- caused by an immunologically mediated
reaction in which vasodilator substances
such as histamine are released into the
blood.
- frequent causes of anaphylactic shock are
reactions to drugs (penicillin); foods (nuts); and
insect venoms.
■ Fever
■ Vasodilatation
■ Warm, flush skin
Prepared by:
Eric B. Panopio, M.D.