Congestive Heart Failure

Dr Muxyi

2. Congestive Heart FailureLearning objectives: at the end of this lesson the student will

be able to :

1. Define congestive heart failure.

2. List the etiologic agents of congestive heart failure.

3. Understand the Epidemiology of congestive heart failure.

4. Describe the pathophysiology of congestive heart failure.

5. Identify the clinical manifestation of congestive heart failure.

6. Understand the diagnostic approach of congestive heart failure.

7. Manage patients with congestive heart failure.

8. Design strategies for prevention of congestive heart failure.

Definition:

Heart failure is a clinical syndrome characterized by inadequate systemic perfusion to meet the body's metabolic demands as a result of abnormalities of cardiac structure or function.

This may be further subdivided into either systolic or diastolic heart failure.

• Systolic heart failure: there is reduced cardiac contractility

• Diastolic heart failure there is impaired cardiac relaxation and abnormal ventricular filling.

• The body, sensing inadequate organ perfusion, activates multiple systemic neurohormonal pathways which compensate initially by redistributing blood flow to vital organs but later exacerbate the patient's symptoms and lead to clinical deterioration.

Etiology:

The most common cause of heart failure is left ventricular systolic dysfunction (about 60% to 70% of patients). The following are some of the underlying causes of heart failure .

1) Decreased contractile functionA. Valvular heart diseaseB. Coronary Heart Disease : Myocardial ischemiaC. Myocardial Disease : Cadiomyopathy , Myocarditis

2) Increased after loada. Acute systemic hypertension

3) Abnormalities in preloadA. Excessive preload

B. Reduced preload

4) Reduced compliance states: Constrictive pericarditis , Restrictive cardiomyopathy

Precipitating factors for heart failure:

• These are relatively acute disturbances that place an additional load on a myocardium that is chronically and excessively burdened.

• In compensated state patients are asymptomatic; however as patients have little additional reserve, they become symptomatic in the presence of these precipitating factors.

• Knowing the precipitating factors is important because most of the time they are treatable and the cardiac function improves when these precipitating factors are treated or avoided.

• The most important precipitating factors may be represented with the mnemonic, HEART FAILES

HEART FAILES

• H- Hypertension (systemic)• E- Endocarditis (infections) • A- Anemia• R- Rheumatic fever and myocarditis• T- Thyrotoxicosis and pregnancy

• F- Fever (infections) • A- Arrhythmia• I- infarction (myocardial) • L- Lung infection• E- Embolism (pulmonary)• S- Stress (emotional, physical, environment, dietary, fluid

excess)

Pathophysiology

In left ventricular systolic dysfunction, regardless of the etiology, cardiac output is low and pulmonary pressures are high, leading to pulmonary congestion. As a result, a series of adaptive mechanisms are activated. Initially, as a direct result of inadequate cardiac output and systemic perfusion, the body activates several neurohormonal pathways in order to increase circulating blood volume.

• With continuous neurohormonal stimulation, the left ventricle undergoes remodeling with left ventricular dilatation and hypertrophy, such that stroke volume is increased without an actual increase in ejection fraction. This is achieved by myocyte hypertrophy and elongation. However, left ventricular chamber dilatation causes increased wall tension, worsens subendocardial myocardial perfusion, and may provoke ischemia in patients with coronary atherosclerosis.

• Furthermore, left ventricular chamber dilatation may cause separation of the mitral leaflets and mitral regurgitation with worsening of pulmonary congestion. Enhanced neurohormonal stimulation of the myocardium also causes apoptosis, or programmed cell death, leading to worsening of ventricular contractility.

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Clinical Manifestations

1. Progressive dyspnea which initially occurs with exertion and later occurs at rest.

• Dyspnea on exertion has been found to be the most sensitive complaint, yet the specificity for dyspnea is less than 60%.

2. Orthopnea and paroxysmal nocturnal dyspnea (PND) are more specific symptoms;

however, sensitivity for orthopnea and PND is only 20-30%.

3. Cough productive of pink, frothy sputum is highly suggestive of CHF. Wheezing may also occur.

4. Peripheral edema and ascites5. Nonspecific complaints include the following: easy

fatigability , light headedness , malaise anxiety abdominal pain , nausea etc

• Past medical history may include the following: rheumatic fever , alcohol use, hypertension , angina , previous history of myocardial infarction and familial history of heart disease

Physical findings:• Tachycardia and Tachypnea and signs of respiratory

distress including use of accessory muscles of respiration

• Jugular venous distention (JVD) frequently is present and engorged neck veins

• Pulsus alternans (alternating weak and strong pulse indicative of depressed left ventricle[LV] function

• Wheezing or rales may be heard on lung auscultation and there may be bilateral basal dullness.

• Apical impulse frequently is displaced laterally

• Cardiac auscultation may reveal aortic or mitral valvular abnormalities, S3 or S4.

• Skin may be diaphoretic or cold, gray, and cyanotic

• Lower extremity edema also may be noted, especially in the subacute process.

• New York Heart Association Heart Failure Classification scheme is used to assess the severity of a patient's functional limitations and correlates fairly well with cardiovascular prognosis.

Table III -2-1: New York Heart Association Heart

Failure Symptom Classification System

Grade Symptoms

I No symptom limitation with ordinary physical activity

IIOrdinary physical activity somewhat limited by dyspnea (i.e.,

long distance walking, climbing 2 flights of stairs)

IIIExercise limited by dyspnea at mild workloads (i.e., short

distance walking, climbing one flight of stairs)

IV Dyspnea at rest or with very little exertion

Diagnostic Workup

1. Chest x-ray: the main findings are cardiomegally, pulmonary edema, and pleural effusion.

2. Echocardiography: may help identify valvularabnormalities, ventricular dysfunction, cardiac temponade, pericardial constriction, and pulmonary embolus.

3. Electrocardiogram (ECG): is a nonspecific tool but may be useful in diagnosing concomitant cardiac ischemia, prior myocardial infarction (MI), cardiac dysrhythmias, chronic hypertension, and other causes of left ventricular hypertrophy.

4. Other laboratory tests : Hemoglobin, Urinalysis, BUN, Creatinine

Management of Heart Failure

Principles of management

1. Identify and treat the precipitating factors

2. Control the congestive state

3. Improve myocardial performance

4.Prevention of deterioration of myocardial function (slowing progression of heart failure )

5. Treat the underlying cause

A. General measures :Dietary sodium restriction should be implemented in all

patients with congestive heart failure to < 3 g/d.

Activity and life style modification :

Meals should be small in quantity but more frequent.

Reduce anxiety and emotional stress

Avoid excess physical exertion ( NB exercise may be advised within the limit of the patient’s cardiac function )

Weight loss in encouraged in obese patients.

Cessation of smoking

Avoid other CVD risk factors

B. Control of the Congestive stateDiuretics: are useful in relieving congestion and

reduce or prevent edema.• Most patients with heart failure have some

degree of symptomatic congestion and benefit from diuretic therapy.

• Usually a loop diuretic is required, with the addition of a Thiazide diuretic in patients refractory to the loop diuretic alone.

1. Furosomide: Initial dose 20-40 mg PO 1-2 X daily or 20 mg IV Maximum dose 400 mg PO/day or 80 mg IV /day

2. Hydrochlorothiazide: Initial dose 25 mg PO/day Maximum dose 100 mg PO/day

• N.B . Loop and thiazide diuretics are useful for symptomatic relief; however they have not been shown to improve survival.

Side effects : Azotemia, hypokalemia, metabolic alkalosis and elevation of neurohormones

3. Spirinolactone: is an aldosterone inhibitor, reduces mortality in patients with advanced heart failure. This drug should be reserved for patients with moderately severe or severe heart failure ( class IV symptoms )

Initial dose: 25 mg PO/day or every other dayMaximum dose: 50 mg PO BID or higher

Side effects

Hyperkalemia is common so monitoring K+ the serum potassium level is essential. As a result, this drug should not be used in patients with a creatinine above 2.5 mg/dl.

Gynecomastia in men is the other side effect of this drug.

C. Enhancement of Myocardial contractility :

1) Digoxin: is a drug which has :• Inotropic effect and acts by inhibiting the

Na+-K+ ATPase and increase intracellular calcium. This increases myocardial contractility.

•Neurohormonal modulation of centrally mediated parasympathomimetic and sympatholytic activity. By doing so it blocks the AV node and delays AV conduction.

Initial dose : 0.125 mg PO/dayMaximum dose : 0.25 mg PO/day

The use of digoxin can improve symptoms, reduce the duration and the need for hospitalization in patients with heart failure,, but has no effect on long term survival.

♦ Digoxin is renally excreted and so dose adjustment is necessary in renal failure.

♦ A low dose of the drug (0.125 mg daily) should be prescribed, especially in women.

♦ Digoxin use is recommended for patients with left ventricular systolic dysfunction, particularly if they have atrial fibrillation.

♦ It is relatively contraindicated in some cardiac disease Cardiac outflow obstruction in MS (in the absence of

atrial fibrillation ) Corpulmonale

Because of it narrow window of safety, digoxin is associated with different Side effects including:

GI : anorexia , nausea, vomiting , weight loss

Neuralgia, delirium

Yellow vision

Gynecomastia

Arrhythmias of different types

2) Vasodilators: may be useful in patients with severe acute heart failure who demonstrate systemic vasoconstriction despite ACE inhibitor therapy. Through vasodilatation they reduce the peripheral resistance and after load and improve cardiac performance.

Hydralazine: Initial dose: 25 mg PO TID Maximum dose: 150 mg PO QID.

Isosorbide dinitrate: Initial dose 10 mg PO TID Maximum dose: 80 mg PO TID

♦ Hydralazine and nitrates in combination are effective afterload reducing agents used in ACE-intolerant patients.

D. Prevention of deterioration of

Myocardial function :

The following drugs prevent deterioration in myocardial function by inhibiting the neurohumeral mechanism which causes cardiac remodelling and progression of heart failure.

1) Angiotensin Converting Enzyme (ACE) InhibitorsAfterload reduction and neurohormonal modulation with ACE

inhibitors ( e.g. Captopril, Enalapril, etc) have been shown to improve mortality, symptoms, and hospitalizations. The dose of ACE inhibitors should be titrated to the maximum that can be tolerated symptomatically or the target dose. .

Initial dose: Captopril 6.25 mg PO/day or every other dayEnalapril 2.5 mg PO BID

Maximum dose: Captopril 50-100 mg PO QIDEnalapril 10- 20 mg PO BID

2) Angiotensin-II Receptor blocker- These drugs are useful in patients who cannot tolerate ACE inhibitors due to different side effects like cough angioedema and lukopenia.

Lasortan: Dose: - 25-50 mg once 0r twice daily

3) Beta Adrenorecepter blockersAdministration of these drugs with

gradually increasing dose has been reported to improve symptoms of heart failure, the need for hospitalization and reduce mortality. They are indicated to moderately severe heart failure.

• They are not indicated in unstable heart failure , hopotensive states , severe fluid overload , sinus bradycardia , AV block and asthma.

Metoprololol: Initial dose 6.25 mg PO BID Maximum dose: 75 mg PO BID