CONGESTIVE HEART FAILURE (CHF)

CONGESTIVE  HEART  FAILURE (CHF)

Case 1:

A 62-year-old man with hypertension and dyslipidemia presents with dyspnea and lower-extremity edema for 2 months. On exam there is jugular venous distention (about 9 cm.), an S3 gallop, and the apical impulse is displaced to the left of the mid-clavicular line at the 6th intercostal space. The chest x-ray shows enlarged cardiac silhouette. The echocardiogram shows a dilated left ventricle with an ejection fraction of 35  .

Case 2:

A 57-year-old man with history of multiple myeloma presents with dyspnea and lower-extremity edema for 2 months. On exam there is jugular venous distention (about 8 cm.), an audible S4, and the apical impulse is non-displaced at the 5th intercostal space. The chest x-ray shows normal cardiac silhouette. The echocardiogram shows a thickened left ventricle with an ejection fraction of 65 .

Heart failure (HF) arises from the inability of the ventricle to efficiently pump blood throughout the circulation. Clinically HF presents with symptoms of breathlessness, exercise intolerance, and fatigue (see below signs and symptoms).

As HF evolves, changes in vascular function, blood volume, and neurohumoral status occur throughout the body. These changes serve as compensatory mechanisms to help maintain cardiac output (primarily by the Frank-Starling mechanism) and arterial blood pressure (by systemic vasoconstriction). However, these compensatory changes over time can worsen car- diac function. Cardiac changes during HF include: increased end-diastolic volume; ventricular dilatation or hypertrophy; decreased stroke volume and cardiac output; reduced ejection frac- tion (systolic dysfunction) or impaired filling (diastolic dysfunction). Compensatory mecha- nisms during HF include:

• Cardiac: Frank-Starling mechanism, tachycardia, ventricular dilatation;

• Neuronal: increased sympathetic adrenergic activity, reduced cardiac vagal activity;

• Hormonal: activation of angiotensin-aldosterone system, vasopressin, catechol- amines, and natriuretic peptides.

In clinical practice, HF is commonly categorized by whether the abnormality is due to contraction or relaxation of the heart. Systolic HF (systolic dysfunction) is due to a loss of contractile strength of the myocardium accompanied by ventricular dilatation. This type of HF is also accompanied by a decrease in normal ventricular emptying (usually ejection frac- tion of less than 45%). Examples of systolic HF include ischemic cardiomyopathy and dilated cardiomyopathy (Case 1 in this section).

Diastolic HF (diastolic dysfunction or HF failure with normal ejection fraction) occurs when the filling of one or both ventricles is impaired while the emptying capacity is normal (echo- cardiogram confirms that the ejection fraction is normal). The infiltrative cardiomyopathies (amyloidosis) are typical examples of diastolic HF (Case 2 in this section).

Congestive HF indicates a clinical syndrome of dyspnea and fatigue as well as evidence of features of circulatory congestion (peripheral edema, elevated jugular venous pressure [JVP]). In heart failure, intravascular congestion occurs with elevation of left ventricular diastolic and pulmonary venous pressures that eventually causes transudation of fluid from the pulmonary capillaries into the interstitial space. Pulmonary edema develops when the rate of fluid accumulation goes above the rate of lymphatic absorption. Pulmonary edema is detected by audible crackles, increased JVP and edema on exam, and chest x-ray findings.

Decompensated HF or exacerbation of HF denotes worsening of symptoms and clinical findings in pre-existing HF. This can be due to precipitating factors such as non-adherance to medication, increase in dietary salt, acute ischemia, tachycardia, or pulmonary infection.

In evaluating patients with HF or worsening of pre-existing HF, it is also important to exclude precipitating factors. Commonly, HF manifests for the first time when a precipitating factor places additional burden on the heart. Such factors include:

• Cardiac ischemia and myocardial infarction

• Infections (especially pulmonary infections)

• Arrhythmias (especially atrial fibrillation)

• Excessive dietary salt (commonly after holiday meals)

• Uncontrolled hypertension (especially after abrupt cessation of anti-hypertensive medication)

• Thyrotoxicosis

• Anemia

HF may occur as a consequence of most causes of heart disease, but ischemic heart disease   is responsible for over 70% of all cases in the western world. Other common causes include: hypertensive heart disease, the cardiomyopathies (idiopathic, alcohol related, etc.), and valvular and congenital heart diseases.

Symptoms of HF include:

• Dyspnea (differentiate from pulmonary dyspnea—See Table 5-4)

• Orthopnea

• Paroxysmal nocturnal dyspnea

• Fatigue, weakness

Table 5-4. Most Common Causes of Acute Pulmonary Edema

Clinical Pearl

In the work-up of patients with new-onset HF, always try to identify potentially reversible causes.

Clinical Pearl

In the work-up of patients with exacerbation of HF, always:

• Check cardiac enzymes to exclude myocardial ischemia or infarction

• Do a chest x-ray to exclude infection

Physical findings in HF:

• Pulmonary rales

• Peripheral edema, ascites

• Hepatomegaly

• Jugular venous distention

• Displaced apical impulse (systolic HF)

The severity of heart failure is commonly classified by using a HF staging system. The New York Heart Association Functional Classification (NYHA staging system) relates symptoms to everyday activities and the patient’s quality of life:

• Class I: patients have no limitation of activity; they suffer no symptoms from ordi- nary activities

• Class II: patients with slight, mild limitation of activity; they are comfortable with rest or with mild exertion

• Class III: patients with marked limitation of activity; they are comfortable only at rest

• Class IV: patients are confined to bed or chair; any physical activity brings on dis- comfort and symptoms occur at rest

Diagnosis. Echocardiography is the test-of-choice to confirm the diagnosis of HF and to classify the type (systolic vs. diastolic). With the echocardiogram, the clinician is able to determine ejection fraction and identify valvular heart disease as well as other cardiac anom- alies (dilated ventricle, thickened ventricle, etc.).

Chest x-rays are also used to aid in the diagnosis of heart failure. They may show cardio- megaly, vascular redistribution, Kerley B-lines, and interstitial edema.

Note

BNP is used acutely if the cause of dyspnea is not clear.

Electrocardiogram is used to identify ventricular hypertrophy and/or the presence of isch- emic heart disease, arrhythmias, or conduction delays which may cause or precipitate HF.

Brain Natriuretic Peptide (BNP) is a polypeptide secreted by the heart in response to excessive stretching of the myocytes. It is a valuable tool in the evaluation of patients with presumed HF or decompensated HF in the acute setting. The BNP is almost always elevated (97% sensitiv- ity) in patients with decompensated HF. Normal BNP excludes CHF as the cause of dyspnea.

Management. The treatment goals in HF are to improve hemodynamics, relieve symptoms (improve quality of life), and prolong survival. Remember, always evaluate for reversible causes at the same time.

Non-pharmacologic treatment includes primarily reduction of salt   intake.

For pharmacologic treatment, ACE inhibitors are the basis of therapy and recommended for all patients with HF (especially systolic HF), irrespective of blood pressure status. They improve survival and reduce ventricular hypertrophy—and eventually, symptoms. ACE inhib- itors through vasodilation reduce preload and afterload, thereby reducing right atrial, pulmo- nary arterial, and pulmonary capillary wedge pressures. All ACE inhibitors have been studied and are considered equal in terms of HF treatment. Angiotensin receptor blockers (ARB) are acceptable alternatives if the patient is unable to tolerate ACE inhibitors (cough, angioedema).

Diuretic therapy, especially loop diuretics, is the treatment of choice for the relief of acute pulmonary edema symptoms. Several classes are used but the loop diuretics (furosemide)

 class is the most commonly used. Thiazide diuretics (hydrochlorothiazide) are useful only in mild HF. Spironolactone and eplerenone (aldosterone antagonists) have been used as add-on therapy to ACE inhibitors in severe heart failure to prolong survival by presumed aldosterone inhibition.

Chronic adrenergic activation has been implicated in the pathogenesis of HF and thus

-adrenergic blocking agents are an important part of HF therapy. Along with ACE inhibi- tors, beta blockers have been demonstrated to decrease mortality, reduce hospitalizations, improve functional class, and improve ejection fraction in several large-scale, randomized, placebo-controlled trials. Patients should be started on beta blockers after stabilization of symptoms with diuretic and ACE inhibitor therapy, irrespective of blood pressure status. The beta blockers that have been demonstrated in trials are carvedilol and  metoprolol.

Other vasodilators, such as a combination of hydralazine and isosorbide, may be used when ACE inhibitors and ARBs are not tolerated or contraindicated (renal failure). There is a reduction in death and a decrease in hospitalization when a combination of hydralazine and isosorbide is used.

In severe HF and especially if there is no improvement of symptoms while the patient is on standard therapy (diuretic, ACE  inhibitor, and beta blocker), the addition of  spironolactone   is of benefit. The addition of spironolactone in patients with severe congestive heart failure significantly reduces (about 30% relative risk) death and hospitalizations among treated  patients. Spironolactone is used in patients with NYHA class III-IV. Once the patient is started on spironolactone, serum potassium levels have to be monitored closely.

Eplerenone is an alternative to spironolactone that does not cause gynecomastia.

Note

Agents which lower mortality in systolic dysfunction

• ACE (ARB)

• Beta blockers

• Spironolactone (or eplerenone)

The addition of inotropic agents to patients with severe HF improves symptoms and quality  of life and reduces hospitalizations but does not improve survival. The most commonly used inotropic agent is digitalis. Digitalis inhibits Na+/K+ - ATPase pump which results in increased intracellular concentration of Na+ and decreased exchanges of intracellular Ca2+. The end result is an increase in intracellular concentration of Ca2+ which results in improved cardiac contractility.

Cardiac glycosides work by inhibition of Na+/K+-ATPase pump, which results in:

• Increased intracellular concentration of Na+

• Decreased exchange of intracellular Ca2+ for extracellular Na+

• The end result is an increase in the intracellular concentration of Ca2+, which gives the (+) inotropic effect characteristic of glycoside

Remember that K+ and digitalis compete for myocardium binding sites. Hyperkalemia will decrease digitalis activity, whereas hypokalemia results in toxicity.

Digitalis will increase both the force and the velocity of the myocardial contraction. It will also promote a more complete emptying of the ventricles.

It is used for the treatment of:

• CHF

• Atrial fibrillation/flutter

• Paroxysmal atrial tachycardia/SVT

Conditions which predispose to digitalis toxicity are:

• Renal insufficiency

• Electrolyte disturbances (hypokalemia, hypercalcemia, hypomagnesemia)

• Advanced age

• Sinoatrial and atrioventricular block

• Thyroid disease, especially hypothyroidism

Note

Agents which decrease symptoms but not mortality

• Digoxin

• Diuretics

 Toxic Effects of Digitalis

• Nausea and vomiting

• Gynecomastia

• Blurred vision

• Yellow halo around objects

• Arrhythmias—commonly paroxysmal atrial tachycardia (PAT) with block, PVCs (premature  ventricular  contractions), and bradycardia

Treatment for Intoxication

• Stop drug

• Lidocaine and phenytoin (for arrhythmia)

• Digibind only for acute overdose

Sympathomimetic amines (dopamine, doputamine) and phosphodiesterase inhibitors (amrinone, milrinone) are sometimes used in the management of severe acute HF (hospi- talized patients). They must be administered by intravenous infusion and need continuous monitoring of the blood pressure and cardiac  rhythm.

Clinical Pearl

Diastolic HF may worsen when diuretics and vasodilators are used excessively. The goal

in diastolic HF is to slow the heart rate with beta blockers and calcium channel blockers (verapamil, diltiazem) in order to allow adequate diastolic filling.

Monitoring of patients with HF includes calculation of fluid intake and excretion (in the hospital) as well as monitoring body weight (in the out-patient  setting).

In refractory HF (defined as progression of HF despite standard treatment), the patient may be considered for: biventricular pacing, implantable defibrillator, and heart transplantation.