Cardiovascular HO Final GROUP2
Cardiovascular HO Final GROUP2
Cardiovascular HO Final GROUP2
Dr Siraj Sh.
Introduction
• Cardiovascular diseases (CVDs) is accelerating
globally over all regions and social classes.
• Most global burden is attributable to the change in
the life style of people.
Why CVDs is rising in developing countries?
An overall increase in the population
Improved life expectancy
2
Lifestyle transition:-increase urbanization,
industrialization, globalization and change in
nutritional habit.
Past or current nutrition deprivation in utero and
early childhood.
• Causes of cardiovascular diseases in developing
countries include:
Rheumatic heart disease
3
Hypertensive heart disease
Cardiomyopathies
Congenital heart disease
Ischemic heart disease
Ethiopia
very few studies about CVDs
the prevalence of rheumatic heart disease
is 6/1000 in school children.
4
One study at Tikur Anbessa Hospital has showed
that acute myocardial infraction (AMI) was the
third cause of ICU admission, and AMI annual
admission increased consistently.
DDX of dyspnea
Cardiovascular causes
congestive heart failure
constrictive pericarditis
5
Systemic causes
high out put states : anemia, thyrotoxicosis
metabolic disorders: DKA, hepatic failure,
uremia
drug over dose: salicylates
anxiety
Pulmonary diseases: TB, Pneumonia…
Marked obesity, abdominal mass, ascites…
6
1. CONGESTIVE HEART FAILURE
7
Etiology
ischemic heart disease (IHD)
valvular heart disease(VHD)
Cardiomyopathy(CMP)
hypertensive heart disease(HHD)
congenital heart disease(CHD)
pericardial diseases(PD)
8
Precipitating factors
• These are relatively acute disturbances which
place additional work load on the myocardium
which is chronically and excessively burdened
• They usually don’t cause CHF by themselves but
unmask an asymptomatic cardiac dysfunction and
make patients symptomatic
• Knowing these factors is important because most
are treatable and cardiac function improves when
they are relieved
9
Represented with the mnemonic, ‘HEART FAILES’
H – Hypertension A – Arrhythmia
E – Infective Endocarditis I – Infarction
A – Anemia L – Lung Infection
R – Recurrent Rheumatic Fever And E – Embolism (Pulmonary)
Myocarditis S – Stress (Psychological
T – Thyrotoxicosis ,Physical ) ,Salt
F – Fever (Infections),fetus(pregnancy)
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Important Terminologies
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Afterload
• The pressure that must be overcome for the
heart to pump blood into the arterial
system.
• Dependent on the systemic vascular
resistance
• With increased afterload, the heart muscles
must work harder to overcome the
constricted vascular bed chamber
enlargement
• Increasing the afterload will eventually
decrease the cardiac output.
12
Pathophysiology
13
1.The frank starling mechanism
Increased preload
Adaptive
increased EDV
stretching of sarcomeres
increased contractility
Maladaptive
excessive stretching of sarcomeres
decreased contractility
14
2. Increased after load
Adaptive
hypertrophy
increased contractility
Maladaptive
impaired ventricular filling
3.Neurohormonal mechanisms
Adrenergic nervous system
Adaptive mechanism- increased myocardial
contractility
15
Maladaptive-increases afterload and work load
on the ventricles
The rennin angiotensin aldosterone
system(RAAS)
increased salt and water retention maintains
cardiac out put
this in the long run results in increased preload to
the heart and contributes to CHF
16
also contributes to the occurrence of edema
Angiotensin is also vasoconstrictor and it
contributes to the increase in the afterload
These neurohormonal mechanisms are
initially adaptive responses to the cardiac
dysfunction which results from any of the
etiologic agents
17
But in the long run these adaptive mechanisms
further increase the cardiac work load to increase
the cardiac output.
These results in hypertrophy ,dilatation and
remodeling of the ventricles which finally
damages the myocytes and worsens the failure
state
Treatment to prevent progression of CHF is
directed in antagonizing these neurohormonal
mechanisms
18
Forms of CHF
Systolic vs Dystolic failure
a. Systolic failure
inability of ventricles to pump sufficient blood
e.g. dCMP , IHD
presents primarily with weakness and
decreased exercise tolerance
b.Dystolic failure
inability of ventricles to relax normally during
diastole and decreased filling of blood
19
e g. hCMP , rCMP , constrictive pericarditis , IHD
primarily present with edema
NB. Most CHF results from combination of the two
forms
Right sided vs left sided heart failure
1.Right sided failure-usually results from left sided
failure
isolated right sided failure which results from
pulmonary hypertension is called cor pulmonale
20
peripheral edema,hepatomegally,ascites
2. left sided failure
dyspnea , orthopnea , PND
High output vs low out put failure
high output : thyrotoxicosis , anemia , AR
low out put : IHD , dCMP , rCMP
Acute vs chronic failure
I. Acute: extensive MI , rupture of valves ,
myocarditis , massive PE
21
predominantly systolic abnormality
pulmonary edema or hypotension (cardiogenic
shock ) with out peripheral edema
II. chronic : dCMP, VHD
BP is usually maintained , edema is common
22
Approach to patients with CHF
Cardiac Symptoms
progressive exertional dyspnea
Orthopnea
paroxysmal nocturnal dyspnea
cough productive of pink frothy sputum
wheezing (cardiac asthma)
peripheral edema , abdominal distension (ascites)
right upper quadrant abdominal pain (congested
liver)
non specific symptoms : fatigue , light headedness ,
malaise
23
Risk factors suggestive of etiology
history of rheumatic fever : sore throat ,
migratory joint pain , abnormal body movement
history of HTN and DM
history of angina and intermittent claudication
smoking and alcoholism
family history of heart disease, and sudden
death
24
Risk factors suggestive of precipitating
factors
tooth extraction,GIT&GUT instrumentation,
fever, reddish urine (for IE)
new onset palpitation (for arrhythmia)
symptoms of anemia
symptoms of thyrotoxicosis
Pregnancy
drug discontinuation
25
Physical examination
Signs of reduced CO
tachycardia
cool and pale or cyanotic extremities
diaphoresis
Signs of volume overload
basal rales
peripheral edema
26
ascites, tender hepatomegaly
splenomegaly
raised JVP
hepatojugular reflex
Signs of cardiac enlargement
displaced apical impulse
heaves
Other signs of CHF
S3 gallop
27
Signs of underlying etiology
-murmurs of VHD
-distant heart sounds in pericardial
effusion or pericardial friction rub or knock in
pericarditis
Signs of precipitating factors
anemia , arrhythmias , thyrotoxicosis
Severe resp. distress
• Evidenced by orthopnea, dyspnea
• Hx of paroxysmal nocturnal dyspnea
28
• Severe apprehension, agitation, confusion
Resulting from hypoxia
Feels like he/she is smothering
• Cyanosis
• Diaphoresis
Results from sympathetic stimulation
• Pulmonary congestion
• Often present
• Rales-especially at the bases
29
• Rhonchi-associated with fluid in the larger
airways indicative of severe failure
• Wheezes-response to airway spasm
• Jugular Venous distention-not directly
related to LVF.
comes from back pressure building from
right heart into venous circulation
• Vital Signs
significant increase in sympathetic
discharge to compensate
30
BP-elevated
Pulse rate-elevated to compensate for
decreased stroke volume.
Respirations-rapid and labored
• LOC
• may vary.
• Depends on the level of hypoxia
• Chest Pain
• May in the presence of MI
• Can be masked by the RDS
31
Investigations
Chest x ray : findings suggestive of CHF
- cardiomegally (cardiothoracic ratio >
50%)
- cephalization
- pulmonary edema
- pleural effusion
ECG ( electrocardiogram) : shows findings that
suggest specific etiologies
- identifies arrhythmia
32
Echocardiography : provides important
information about ventricular size , function and
valvular abnormalities
Other investigations to identify precipitating
factors should also be done.
Modified Framingham's criteria for diagnosis
of CHF
Diagnosis requires 2 major or 1 major and two
minor criteria not attributed to other medical
conditions
33
Major criteria Minor criteria
Orthopnea
Nocturnal cough
Elevated JVP
Dyspnea on ordinary exertion
Third heart sound
Hepatomegaly
Pulmonary rales
34
NYHA functional classification of CHF severity
38
A.General measures
Dietary sodium restriction : less than 3gm per
day.
Activity and life style modifications.
small and frequent meals
reduce anxiety and emotional stress
avoid excess physical exercise
weight loss for obese patients
39
cessation of smoking
drugs like NSAIDs
avoid other CVD risk factors
B. Control of the congestive state
1.Reduction of cardiac work load
those general measures stated.
2.Control of excess fluid
salt restriction
40
Diuretics
a. Loop diuretics : furosemide( lassix)
potent diuretics useful in all forms of CHF
started at lower dose like 20-40 mg po or
20 mg iv and increased if there is no
response to doses as high as 400 mg po
daily or 160 mg iv per day
Side effects : hypokalemia , hypovolemia ,
hyperuricemia, hyperglycemia
41
b. thiazides : hydrochlorthiazide , chlorthiazide
weaker diuretic agents useful in mild CHF alone
or used in combination with loop diuretics in CHF
which doesn't respond to high dose lassix.
Dose- hydrochlorthiazide 25 mg per day increased
up to 100 mg per day.
Side effects : hypotension , hypokalemia
42
c. potassium sparing diuretics :spironolactone
are aldosterone antagonists.
weak diuretics , usually used with other
diuretics for their potassium sparing property
Dose: spironolactone 25 mg po per day
increased up to 100 mg BID
Side effects- hyperkalemia , gynecomastia
spironolactone is contraindicated in
patients with renal failure
43
3. Enhancement of myocardial contractility(Inotropic
agents)
Cardiac glycosides : digoxin and digitoxin
digoxin is less toxic than digitoxin.
it is the commonly used glycosides.
Effects-positive inotropic effect(increase
myocardial contractility)
increased automaticity(arrhythmia)
delays AV node conduction
44
Uses
in systolic heart failure not responding to
diuretic therapy
particularly when atrial fibrillation coexists with
CHF
Dose:0.25 mg per day
it is excreted via the kidneys and therefore
dose should be reduced to 0.125 mg per day
in patients with renal failure and elderly.
45
Toxicity of digoxin
early non cardiac : anorexia ,nausea, vomiting
chronic toxicity : weight loss , neuralgia ,
worsening of CHF, intractable vomiting
Treatment of toxicity
-discontinue digoxin
-treat the arrhythmia
-supplement potassium if hypokalemic
-anti digoxin antibodies
46
C. Prevention of deterioration of myocardial
function
The following drugs prevent deterioration in
myocardial function by antagonizing the
neurohormonal mechanisms which cause cardiac
remodeling and progression of failure state.
1.Angiotensin converting enzyme inhibitors
(ACEIs) : captopril , enalapril
inhibit the RAAS
47
start at low dose : captopril 6.25 mg po per day,
enalapril 2.5 mg per day and increase dose
to maximum of captopril 50 – 100 mg po qid
and enalapril 20 mg po bid
Side effects : angioedema , cough ,acute renal
failure , hyperkalemia ,hypotension
contraindications : angioedema ,renal failure,
hypotension, pregnancy
48
2. Angiotensin receptor blockers(ARBs)
given to patients who are intolerant to ACEIs
Losartan : 25-50 mg once or twice daily
3.Aldosterone antagonists-spironolactone
4.Beta adrenergic receptor blockers
Metoprolol-initial dose 6.25 mg po bid to 75 mg
po bid has shown to decrease mortality from CHF
Contraindicated : in unstable heart failure ,
hypotension , bradycardia , AV block and asthma
49
D. Treatment of the underlying cause
• Surgery for valvular heart disease
• Implantation of cardiac prosthesis
• Cardiac transplantation
E. Treatment of precipitating factors
• Anaemia
• Arrhythmia
• Thyrothoxicosis
• HTN
• Infection....
50
Follow Up
• V/S
• Input & Out Put
• Wt
• Rft
• Serum Electrolyte
• Drug Side Effects
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2. ACUTE RHEUMATIC FEVER
Introduction
• Multi system disease resulting from autoimmune
reaction to infection with group A streptococcus
• Crowdedness and poor hygiene leads to increased
transmission of the bacteria
• Mainly disease of children(5-14yrs),rare after 30
yrs
• In adult the risk of developing of RF is about 3%
following GAS pharyngitis with a recurrence rate
of 1/6.
• Adolescents and adults affected by recurrence rather
than primary episode
Pathogenesis
Etiology : infection of the URT with group A, β hem
olytic streptococcus
M serotypes (types 3, 5, 6, 14, 18, 19, 24, and 29) were
implicated in outbreaks of rheumatic fever
repeated pharyngitis is required to prime the
immune system before the development of ARF
• Immune reaction : autoimmune reaction leads to
damage of host tissue because of cross reactivity
between antigens of the organism and host tissue.
Clinical features
• Latent period : 3 wks( 1- 5 wks )
• Most preceding pharyngeal infection are
subclinical
A. Heart Involvement (Pancarditis):50-60%
• 60% of patients with ARF develop rheumatic
heart disease
• Damage of heart valves is the hallmark
• Mitral valve is almost always affected
• Aortic valve may be involved with the mitral
valve but isolated aortic valve involvement is
rare
• Early valve damage leads to regurgitant
murmur
• With recurrent episode leaflet thickening,
scarring, calcification and valvular stenosis may
develop
• Pericarditis , friction rub , small effusion on
echocardiography
• Rarely pleuritic chest pain from adjacent
involvement of the pleura
• Myocardial involvement is almost never responsible
by itself for cardiac failure but can affect electrical
conduction pathways leading to PR interval
prolongation and softening of S1.
B. Joint Involvement : 60-75%
to qualify as a major manifestation joint
involvement must be arthritic (with evidence of
inflammation)
it is a migratory arthritis moving from one joint
to the other in period of hours
it involves large joints (ankle , knee , hip ,
elbow)
arthralgia with out signs of inflammation may
occur with similar pattern as arthritis but only
qualify as minor criteria
• Highly responsive to NSAIDS : joint involvement
that stays more than one to two days after starting
salicylates is unlikely to be due to ARF
C. Sydenhams Chorea(5-10%)
usually occur in the absence of other
manifestations
abrupt purposeless nonrhythmic involuntary
abnormal body movement which ceases during
sleep
usually occurs in females
abnormal body movement e.g. darting movement
of the tongue and extremity
usually resolve in 6 weeks
d. Skin
Erythema marignatum-classic rash of ARF
which starts as pink macule that clears centrally
leaving serpinginous border
Subcutaneous nodules-are small painless
swellings occurring under the skin overlying bony
promineneces
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