congestive heart failure sagar naik

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CONGESTIVE HEART FAILURE Sagar Naik, PT 1 CONGESTIVE HEART FAILURE Sagar Naik, PT Heart failure is a pathophysiolo gic state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at rate commensurate with the requirements of the metabolizing tissu es or can do so only from an abnormally elevated filling pressure. It can be thought of as a clinical syndrome comprising a constellation of symptoms and signs attributable to cardiac dysfunctio n. Etiology: Heart failure is frequently, but not always, caused by a defect in myocardial contraction. It may result from Primary abnormality in the heart muscle  Cardiomyopathies Extramyocard ial abnormalities  Coronary atheroscler osis Abnormalities of the heart valves  Mitral stenosis A similar clinical syndrome may be present without any detectable abnormality of myocardial function. Acute hypertensive crisis Rupture of aortic valve cusp Massive pulmonary embolism

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8/6/2019 Congestive Heart Failure Sagar Naik

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CONGESTIVE HEART FAILURE Sagar Naik, PT

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CONGESTIVE HEART FAILURE

Sagar Naik, PT

Heart failure is a pathophysiologic state in which an abnormality of 

cardiac function is responsible for the failure of the heart to pump blood 

at rate commensurate with the requirements of the metabolizing tissues

or can do so only from an abnormally elevated filling pressure.

It can be thought of as a clinical syndrome comprising a constellation of 

symptoms and signs attributable to cardiac dysfunction.

Etiology:

Heart failure is frequently, but not always, caused by a defect in myocardial 

contraction.

It may result from

• Primary abnormality in the heart muscle

 Cardiomyopathies

• Extramyocardial abnormalities

 Coronary atherosclerosis

• Abnormalities of the heart valves

 Mitral stenosis

A similar clinical syndrome may be present without any detectable abnormality of 

myocardial function.

• Acute hypertensive crisis

• Rupture of aortic valve cusp

• Massive pulmonary embolism

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In addition, conditions associated with impairment of filling of the ventricles

like tricuspid or mitral stenosis, constrictive pericarditis and endocardial 

fibrosis can lead to heart failure in presence of normal myocardial function.

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 Precipitating Causes:

• Infection

• Anemia

• Thyrotoxicosis, Pregnancy & Obesity

• Arrhythmias

• Rheumatic, viral, & other forms of myocarditis

• Infective endocarditis

• Physical, dietary, fluid, environmental, & emotional excesses

• Systemic hypertension

• Myocardial infarction

• Pulmonary embolism

• Drugs induced

Classification of Heart Failure:

Heart failure can be classified or described in several ways, which are as follows:

 High Output VS Low Output Heart Failure:

 The low output heart failure i.e., heart failure with low cardiac output is

seen in patients with heart failure secondary to

• Ischaemic heart disease

• Dilated Cardiomyopathy

• Valvular & Pericardial diseases

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• Hypertension

 The high output heart failure i.e., heart failure with high cardiac output is

seen in patients with

• Hyperthyroidism

•Anemia

• Pregnancy

• Arteriovenous fistulas

• Beriberi physio4all...

CONGESTIVE HEART FAILURE Sagar Naik, PT

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• Paget’s disease

In clinical practice, however, low-output and high-output HF cannot always be

readily distinguished.

The normal range of cardiac output is wide [2.2 to 3.5 (L/min)/m2]; in manypatients with so-called low-output heart failure, the cardiac output may actually be

 just within the normal range at rest (although lower than it had been previously),

but it fails to rise normally during exertion.

On the other hand, in patients with so-called high-output heart failure, the output

may not exceed the upper limits of normal (although it would have been elevated

had it been measured before heart failure supervened); rather, it may have fallen to

within normal limits.

  Acute VS Chronic Heart Failure:

The acute heart failure is the sudden development of a large myocardial 

infarction or rupture of a cardiac valve in a patient who previously was

entirely well.

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Chronic heart failure is typically observed in patients with dilated 

cardiomyopathy or multivalvular heart disease that develops or 

 progresses slowly.

 Acute heart failure is usually predominantly systolic, and the sudden reduction

in cardiac output often results in systemic hypotension without peripheral 

oedema.

In contrast, in chronic heart failure, arterial pressure is ordinarily well 

maintained until very late in the course, but there is often accumulation of 

oedema.

 Right-Sided VS Left-Sided Heart Failure:

Many of the clinical manifestations of heart failure result from the accumulation of 

excess fluid behind either one or both ventricles.

 This fluid usually localizes upstream to (behind) the ventricle that is initially

affected.

Patients in whom the left ventricle is hemodynamically overloaded (e.g., aortic

stenosis) or weakened (e.g., postmyocardial infarction) develop dyspnoea and 

orthopnoea as a result of pulmonary congestion, a condition referred to as

left-sided heart failure.

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In contrast, when the underlying abnormality affects the right ventricle primarily

(e.g., congenital valvular pulmonic stenosis or pulmonary hypertension secondary

to pulmonary thromboembolism), symptoms resulting from pulmonary 

congestion are uncommon, and edema, congestive hepatomegaly, and 

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systemic venous distention, i.e., clinical manifestations of right-sided heart

failure, are more prominent.

When heart failure has existed for months or years, such localization of excess fluid

behind the failing ventricle may no longer exist.

E.g. – Patients with long-standing aortic valve disease or systemic hypertension may

develop ankle edema, congestive hepatomegaly, and systemic venous distention

late in the course of their disease, even though the abnormal hemodynamic burden

initially was placed on the left ventricle.

 Backward VS Forward Heart Failure:

 The concept of backward heart failure contends that in heart failure, one or the other ventricle fails to discharge its contents or fails to fill normally .

As a consequence, the pressures in the atrium and venous system behind the failing

ventricle rise, and retention of sodium and water occur as a consequence of the

elevation of systemic venous and capillary pressures and the resultant transudation

of fluid into the interstitial space.

In contrast, the proponents of the forward heart failure hypothesis maintainthat the clinical manifestations of heart failure result directly from an

inadequate discharge of blood into the arterial system.

According to this concept, salt and water retention is a consequence of diminished

renal perfusion and excessive proximal tubular sodium reabsorption and of 

excessive distal tubular reabsorption through activation of the renin-angiotensin-

aldosterone (RAA) system.

 Systolic VS Diastolic Heart Failure:

 The distinction between these two forms of heart failure, relates to whether the

 principal abnormality is the inability of the ventricle to contract normally 

and expel sufficient blood (systolic failure) or to relax and/or fill normally 

(diastolic failure).

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 The major clinical manifestations of systolic failure relate to an inadequate

cardiac output with weakness, fatigue, reduced exercise tolerance, and 

other symptoms of hypoperfusion, while in diastolic failure the manifestations

relate principally to the elevation of filling pressures.

Clinical Features:

 Symptoms:

• Dyspnoea on exertion

• Orthopnoea

• Paroxysmal nocturnal dyspnoea

• Cheyne-Stokes respiration (Periodic or cyclic respiration)

• Fatigue & weakness

• Anorexia & Nausea associated with abdominal pain

• Weight loss

• Cerebral Symptoms

 Confusion

 Difficulty in concentration

 Impairment of memory 

 Headache

 Insomnia

  Anxiety 

 Nocturia

 Physical Signs:

• Pulse

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 Pulse pressure may be diminished (Severe)

 Sinus tachycardia

 Pulsus alternans

• Raised Jugular Venous Pressure

• 3rd & 4th heart sounds are often audible but are not specific for heart

failure

• Pulmonary Rales physio4all...

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• Cardiac oedema

• Pleural effusion & ascites

• Congestive hepatomegaly & enlargement of spleen may occur

• Cardiac Cachexia

• Laterally displaced apical impulse

Investigations:

• Chest radiograph

 Pulmonary venous hypertension (left ventricular failure) seen as dilatation and 

engorgement the upper lobe pulmonary veins

 Pleural effusion & interlobal thickening

 Cardiomegaly 

• ECG

• Echocardiogram

• Cardiac catheterization

• Exercise testing with respiratory gas analysis

Differential Diagnosis:

• Non-cardiogenic pulmonary oedema

• Renal insufficiency with fluid overload

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• Hepatic insufficiency

• Anemia

• Thyrotoxicosis

Treatment:

 Medical Management:

 The treatment of heart failure may be divided into four components:

• Removal of the precipitating cause

• Correction of the underlying cause

• Prevention of deterioration of cardiac function

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• Control of the congestive HF state

General therapeutic measures to be taken by the patient of heart failure are as

follows:

• Restrict salt intake

• Recommend regular, moderate exercise

• Avoid antiarrhythmic agents for asymptomatic arrhythmias

• Avoid non-steroidal anti-inflammatory agents (NSAIDs)

• Provide influenzal and pneumococcal immunization

Diuretics are generally prescribed for all patients with symptoms of heart failure

who have fluid retention.

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All patients with heart failure due to left ventricular systolic dysfunction should

receive an ACE inhibitor , unless they have been shown to be unable to tolerate

these drugs.

All patients with heart failure due to left ventricular systolic dysfunction should

receive β-adrenergic receptor blockers, unless they are unable to tolerate

treatment with these drugs or have a contraindication to their use.

Digoxin is recommended to improve the clinical status of patients with heart failure

and should be used in conjunction with diuretics, ACE inhibitors or β blockers.

Other drugs, which can be used, are as follows:

• Hydralazine & Isosorbide Dinitrate

• Angiotensin Receptor Blockers

• Aldosterone Antagonists

• Calcium Antagonists

• Antiarrhythmic & Device Therapy

• Anticoagulant Therapy

• Positive Inotropic Therapy

 Surgical Management:

• Pacemaker

• Heart transplant physio4all...