Cardiovascular Disorder

For C-I HO Students

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

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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

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 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.

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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

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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…
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 1. CONGESTIVE HEART FAILURE

• CHF is a clinical syndrome in which the heart fails

to pump adequate blood to meet the metabolic
demands of the body.
• It can result from structural or functional disorder
of the heart that impairs the ability of the
ventricle to fill or eject blood.
• It represents an end stage of a number of
different diseases.

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Etiology
ischemic heart disease (IHD)
valvular heart disease(VHD)
Cardiomyopathy(CMP)
hypertensive heart disease(HHD)
congenital heart disease(CHD)
pericardial diseases(PD)

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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

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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

Preload= amount of blood that the heart must

pump with each beat.
Determined by:
• venous return to heart
• accompanying stretch of the muscle fibers
Increasing preload  increase stroke volume in
normal heart
Increasing preload in impaired heart  decreased
SV. Blood is trapped chamber enlargement

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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.
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Pathophysiology

Fig. Pathogenesis of heart failure with a depressed ejection fraction

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1.The frank starling mechanism
Increased preload
Adaptive
increased EDV
stretching of sarcomeres
increased contractility
Maladaptive
excessive stretching of sarcomeres
decreased contractility
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2. Increased after load
Adaptive
hypertrophy
increased contractility
Maladaptive
impaired ventricular filling
3.Neurohormonal mechanisms
Adrenergic nervous system
Adaptive mechanism- increased myocardial
contractility
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 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

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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

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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
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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

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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

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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
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 predominantly systolic abnormality
pulmonary edema or hypotension (cardiogenic
shock ) with out peripheral edema
II. chronic : dCMP, VHD
BP is usually maintained , edema is common

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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
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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

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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
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Physical examination
Signs of reduced CO
tachycardia
cool and pale or cyanotic extremities
diaphoresis
Signs of volume overload
basal rales
peripheral edema

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 ascites, tender hepatomegaly
splenomegaly
raised JVP
hepatojugular reflex
Signs of cardiac enlargement
displaced apical impulse
heaves
Other signs of CHF
 S3 gallop

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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
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• 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
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• 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

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 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
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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

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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

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Major criteria Minor criteria

Paroxysmal nocturnal dyspnea Bilateral leg edema

Orthopnea
Nocturnal cough
Elevated JVP
Dyspnea on ordinary exertion
Third heart sound
Hepatomegaly
Pulmonary rales

Cardiomegally on chest x ray Pleural effusion

Pulmonary edema on chest x ray

Tachycardia ( HR >= 120 bpm)
Weight loss >= 4.5 kg in five days in
response to treatment of presumed CHF Weight loss < 4.5 kg in five days

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NYHA functional classification of CHF severity

Class 1- no limitation of physical activity i.e.

ordinary physical activity doesn’t cause
symptoms.
Class 2-slight limitation of physical activity i.e.
ordinary physical activity results in dyspnea and
fatigue.
Class 3 - marked limitation of physical activity ,
less than ordinary activity causes dyspnea and
fatigue
Class 4- Symptomatic at rest.
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 Staging Of Heart Disease
• Stage A : those who are at high risk to develop
heart failure but with out structural heart
disease ( e.g. DM , HTN )
• Stage B : those who have structural heart
disease but with out symptoms ( e.g. previous
MI )
• Stage C : those who have structural heart
disease and who have developed symptoms
• Stage D : those who have refractory HF
requiring special interventions like cardiac
transplantation
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How to write complete diagnosis of CHF?

The severity of the failure state as NYHA class

The stage of the disease
The failure state as CHF
The underlying etiology
The anatomic abnormality( e.g. Valve)
abnormalities as MR , MS etc
The precipitating factor
E.g.NYHA class-III stage c CHF 2ndry to VHD(?MS)
2ndry to RHD precipitated by IE
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 Management of CHF
Principles of management
1. Identify and treat the precipitating factor
2. Control the congestive state
3. Prevention of deterioration of myocardial
function
4. Treat the underlying cause
5.General measures

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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

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  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

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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

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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

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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

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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

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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.

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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

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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

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 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

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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

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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....
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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

Subcutaneous nodules Erythema marginatum

e. other features
-fever
Laboratory investigations
• CBC : leukocytosis
• ESR and CRP : raised
• ASO titer or anti DNAse β titer
• Throat culture
• Rapid antigen tests for streptococcus antigens
• ECG : PR prolongation
• ECHO : new or worsening regurgitant murmur
: minimal pericardial fluid
WHO(2003/4) criteria for the Dx of RF & RHD
Indolent carditis is the type of carditis which is
slowly evolving
Diagnostic categories Criteria
Primary episode of rheumatic fever 2 major or 1 major + 2 minor + evidence
of GA strept infection

Recurrent attack of rheumatic fever in a 2 major or 1 major + 2 minor + evidence

patient without established RHD of GA strept infection

Recurrent rheumatic fever in a patient 2 minor + evidence of streptococcal

with already established RHD infection

Chorea and indolent carditis No other criteria or evidence of strept

infection is required

Chronic valve lesions of RHD No other thing is needed to diagnose as

RHD
Major Carditis
polyarthritis
chorea
erythema marginatum
subcutaneous nodules

Minor Clinical: fever , arthralgia

lab : increased ESR or CRP , leukocytosis
ECG : prolonged PR interval

Supporting Elevated or rising ASO or other streptococcal

evidence antigens
positive throat culture
Rapid antigen test for strept antigens
Recent scarlet fever
Treatment
No treatment for ARF prevents the
development or severity of RHD
 Antibiotics
amoxicillin 500 mg po tid for 10 days
benzathine penicillin G 1.2 million iu IM
stat
erythromycin 500 mg po Qid for 10 days
for penicillin allergies
Salicylates and NSAIDS
 treatment of arthritis , arthralgia , and fever once
diagnosis is confirmed
no value in treatment of carditis or chorea
Aspirin ( ASA) 80 – 100 mg/kg/day for the first few
days up to 2 weeks
When acute symptoms resolve decrease dose to 60
– 80 mg/kg/day for further 2 – 4 weeks
Carditis
conventional therapy for CHF
prednisolone 1-2 mg/kg/day required for only few
days up to 3 weeks maximum
Chorea
medication does not alter the duration or out come
of chorea but may only be to reduce the frequency
of the abnormal movements
carbamazepine , valproate , haloperidol
Prognosis of ARF
• Untreated ARF stays for 12 weeks
• Weekly or 2 weekly follow up of ESR and CRP(
normalize within 4- 6 weeks)
• Echo after 1 month to see the progression of
carditis
• 60 % of patients with ARF develop rheumatic
heart disease
Prevention
Primary prevention
ideal : eliminating risk factors for strept infection
which are over crowdedness and poor hygiene
if sore throat is treated within 9 days of
commencement ARF will be prevented
Secondary prevention
Long term antibiotic prophylaxis is required for
those patients who have sustained an episode of
rheumatic fever
Patient category Duration of prophylaxis

Patient with out proven For 5 years after last attack or

carditis 18 yrs old which ever comes
late

Patient with mild MR or 10 yrs after last attack or 25

healed carditis yrs which ever comes late

More severe VHD Lifelong

Valve surgery Life long

Antibiotic for prophylaxis
Benzathine penicillin 1.2 million IU every 2- 4
weeks
Erythromycin 500 mg po QID
THANK YOU!!!

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