Congestive Heart Failure (CHF): Causes,Signs and Treatment Guidelines
Congestive heart failure is also known as congestive cardiac failure. Heart failure (HF) is defined as a syndrome of ventricular dysfunction. This occurs when the ventricles fail to pump blood effectively throughout the circulation. In Left ventricular failure, there is shortness of breath and fatigue, and in right ventricular failure, peripheral and abdominal fluid accumulation(congestion) is present. It can involve one ventricle or both ventricles
Congestive cardiac failure (CCF/CHF) is a clinical syndrome characterized by dyspnea and fatigue and features of circulatory congestion like elevated jugular venous pressure (JVP) and pulmonary edema.
Pathophysiology Of Congestive Heart Failure
In heart failure, the heart can no longer meet the metabolic demands of the body tissues at normal physiologic venous pressures. Elevation of pulmonary or systemic venous pressures by the heart may result in organ congestion. This can result from systolic or diastolic dysfunction or both.
As it evolves, the compensatory mechanism takes over throughout the body. This involves changes in vascular function, blood volume, and neurohumoral status. All these mechanisms try to maintain cardiac output and arterial blood pressure. However, these compensatory changes over time can worsen cardiac function.
Cardiac changes during heart failure include
- Reduced ejection fraction(EF) indicating systolic dysfunction;
- Increased end-diastolic volume (EDV);
- Decreased stroke volume and cardiac output(CO);
- Ventricular dilatation or hypertrophy or;
- Impaired filling indicating diastolic dysfunction.
What are these compensatory mechanisms during heart failure?
- Cardiac: Frank-Starling mechanism, tachycardia, and ventricular dilatation.
- Neuronal changes: increased sympathetic adrenergic activity, reduced cardiac vagal activity
- Hormonal: activation of the angiotensin-aldosterone system (RAAS) with Na retention and ECV expansion, catecholamines, vasopressin, and natriuretic peptides
Congestive heart failure is commonly categorized by whether the abnormality is due to contraction(systole) or relaxation (diastole) of the heart. Let's start with systolic dysfunction.
In systolic dysfunction, the ventricle contracts poorly because of loss of contractile strength of the myocardium and empties inadequately due to ventricular dilatation. This leads to increased diastolic volume and pressure and decreased ejection fraction (EF).
This type is also accompanied by a decrease in normal ventricular emptying (usually ejection fraction <45%). Examples of systolic HF include ischemic cardiomyopathy and dilated cardiomyopathy.
Predominant systolic dysfunction is common in heart failure secondary to myocardial infarction, myocarditis, and dilated cardiomyopathy. It may affect primarily the left ventricle or the right ventricle; LV failure often leads to RV failure.
Heart failure with preserved ejection fraction also known as diastolic dysfunction or HF with preserved EF occurs when the filling of one or both ventricles is impaired while the emptying capacity is normal.
This result in reduced ventricular end-diastolic volume, increased end-diastolic pressure, or both. Contractility and ejection fraction(EF) remain normal.
This dysfunction results from an increased ventricular stiffness, impaired ventricular relaxation, valvular disease, or constrictive pericarditis.
Diastolic dysfunction is common among the elderly probably due to myocyte loss and increased interstitial collagen deposition.
Typical examples include hypertensive heart disease and the infiltrative cardiomyopathies.
Left Ventricular failure:
In heart failure secondary to left ventricular dysfunction, cardiac output decreases and pulmonary venous pressure increases.
When pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins, fluid leaks out from the capillaries into the interstitial space and alveoli. This reduces pulmonary compliance and increases the work of breathing. Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid.
Marked fluid accumulation in alveoli alters ventilation-perfusion (V/Q) relationships to a large extent: Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation (PaO2)leading to dyspnea.
Right Ventricular failure:
Here, systemic venous pressure increases, causing fluid extravasation and consequent edema, primarily in dependent tissues such as feet and ankles and abdominal viscera.
Fluid accumulation in the peritoneal cavity (ascites) can occur. Right Ventricular failure commonly causes moderate hepatic dysfunction, with usually modest increases in conjugated and unconjugated bilirubin, and hepatic enzymes like alkaline phosphatase, aspartate aminotransferase (AST), alanine aminotransferase (ALT). The impaired liver breaks down less
aldosterone, further contributing to fluid accumulation.
The kidneys retain salt and water, worsening the EVC expansion. When the rate of fluid accumulation exceeds the rate of absorption by the lymphatics pulmonary edema ensues. It is characterized by audible crackles on auscultation, increased jugular venous pressure and edema on examination, a chest x-ray can also show features of pulmonary edema.
Decompensated HF denotes the worsening of symptoms and clinical findings in pre-existing HF. This can be due to precipitating factors such as non-adherence to medication, an increase in dietary salt, acute ischemia, tachycardia, or pulmonary infection.
Precipitating factors for congestive heart failure
CHF manifests for the first time when a precipitating factor places an additional burden on the heart. These factors include:
- Uncontrolled hypertension.
- Cardiac ischemia and myocardial infarction.
- Arrhythmias- atrial fibrillation.
- Excessive dietary salt.
It may occur as a consequence of most causes of heart disease most common is ischemic heart disease, hypertensive heart disease, cardiomyopathies, and valvular heart disease and congenital heart diseases.
Signs and symptoms of congestive heart failure
Symptoms of heart failure usually differ depending on the ventricle affected. They include dyspnea suggesting pulmonary congestion, orthopnea as heart failure advances, paroxysmal nocturnal dyspnea, and fatigue/weakness due to low CO.
Dyspnea usually occurs during exertion and is relieved by rest. In severe cases, it can occur at night causing nocturnal cough.
In paroxysmal nocturnal dyspnea, dyspnea awakens patients several hours after they lie down and is relieved only after they sit up for 15 to 20 min. It is associated with pulmonary congestion and Cheyne-Stokes respiration with low cardiac output.
In right ventricular failure, the most common symptoms are ankle swelling and fatigue. Sometimes patients feel a sensation of fullness in the abdomen or neck. Right upper quadrant abdominal discomfort due to hepatic congestion, and stomach and intestinal congestion can cause anorexia and abdominal bloating.
On examination, you may realize features of the precipitating factors such as anemia, hemochromatosis, hyperthyroidism, etc..
Tachycardia and tachypnea may be present in LV failure. Patients with severe LV failure may be visibly dyspneic or cyanotic, hypotensive, and confused or agitated because of hypoxia and poor cerebral perfusion.
Central cyanosis reflects severe hypoxemia.
- Check cardiac enzymes to exclude myocardial ischemia or infarction
- Do a chest x-ray to exclude infection
- Inspiratory basilar crackles that do not clear with coughing,
- Pulmonary rales
- Non-tender peripheral pitting edema, Severe edema in multiple areas is known as anasarca.
- Hepatojugular or abdominojugular reflux may be detected
- Jugular venous distension with large a or v waves
- Palpable S3 and S4
- Diffuse sustained, and laterally displaced apical impulse (systolic HF)
The severity of heart failure is commonly classified by using an HF staging system.
New York Heart Association(NYHA) Classification of Heart Failure
Functional Classification (NYHA staging system) relates symptoms to everyday activities and the patient’s quality of life:
Class I: These are patients who have no limitation of activity; they suffer no symptoms from ordinary daily activities.
Class II: Patients in this class have a slight, mild limitation of activity; they are comfortable and relieved with rest or with mild exertion.
Class III: These are patients with marked limitation of activity; they are comfortable and relieved only at rest.
Class IV: patients in class IV are confined to bed or chair; any physical activity brings on discomfort and symptoms occur even at rest.
Diagnosis of congestive heart failure.
Diagnosis starts all the way from history and clinical examination findings of the patient, therefore, a good history taking and clinical examination is key.
The best test to confirm the diagnosis of HF and classify the type is echocardiogram. It helps you to determine ejection fraction(EF) and identify valvular heart disease as well as other cardiac anomalies like dilated ventricle, thickened ventricle, etc. It can also help to evaluate chamber dimensions, valve function
Radionuclide imaging to systolic and diastolic function, previous myocardial infarction, or myocardial hibernation.
A chest x-ray is also used the diagnosis of heart failure; it may show cardiomegaly (enlarged cardiac silhouette), vascular redistribution, Kerley B-lines ( horizontal lines in the periphery of lower posterior lung fields), or interstitial edema, pleural effusion,
An electrocardiogram is used to identify ventricular hypertrophy and/or the presence of ischemic heart disease, arrhythmias, or conduction delays which may cause or precipitate HF.
Brain natriuretic peptide (BNP) (or type B natriuretic peptide) is a type of polypeptide that is secreted by the heart in response to excessive stretching of the muscle cell (myocytes).
BNP is best used for ruling out HF, and a normal BNP generally excludes CHF as the cause of dyspnea. It is almost always elevated (97% sensitivity) in patients with decompensated HF. The only exception is obesity, where BNP can be falsely low. BNP lacks specificity (renal failure can lead to elevated BNP). A positive BNP warrants a follow-up echocardiogram.
A complete blood workup including CBC, creatinine, BUN, electrolytes (Mg and Ca), glucose, albumin, and liver function tests are also recommended. Thyroid function tests (TFTs) are important for patients with atrial fibrillation and elderly patients.
Treatment of congestive heart failure
Management of systolic heart failure
Treatment goals in HF are to diagnose and treat the cause, improve hemodynamics, relieve symptoms, and prolong survival.
Non-pharmacologic treatment includes diet modification by primarily reducing salt intake.
Monitoring of patients with HF includes calculation of fluid intake and excretion as well as monitoring body weight.
Appropriate weight and fitness levels
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.
ACE inhibitors through vasodilation reduce preload and afterload, thereby reducing right atrial, pulmonary arterial, and pulmonary capillary wedge pressures.
Angiotensin receptor blockers (ARB) are acceptable alternatives if the patient is unable to tolerate ACE inhibitors (cough, angioedema).
Combination drug valsartan-sacubitril, an angiotensin receptor neprilysin inhibitor (ARNI). Valsartan is an ARB, while sacubitril inhibits the degradation of natriuretic peptide.
Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides (ANP, BNP) and bradykinin. Inhibition of neprilysin increases levels of these substances, which then counteract the effects of neurohormonal activation such as vasoconstriction and sodium retention. They work by blocking the RAAS system and lead to natriuresis and decrease cardiac hypertrophy and fibrosis.
Ivabradine, used for heart failure and tachycardia unresponsive to beta-blockers, is an inhibitor of the If or “I-funny” channel, which contributes to normal sinus node function. Its effect is to slow the heart rate by decreasing sinus node automaticity.
Diuretic therapy, especially loop diuretics, is the treatment of choice for the relief of acute pulmonary edema symptoms. Furosemide is the most commonly used.
Thiazide diuretics such as hydrochlorothiazide(HCTZ) are useful only in mild cases. 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.
Along with ACE inhibitors, beta-blockers have been demonstrated to decrease mortality, reduce hospitalizations, improve functional class, and improve ejection fraction. Start patients on beta-blockers after stabilization of symptoms with diuretic and ACE inhibitor therapy when blood pressure is normal or high.
Other vasodilators such as combination hydralazine/isosorbide may be used when ACE inhibitors and ARBs are not tolerated or contraindicated.
In severe HF and especially if there is no improvement of symptoms while the patient is on standard therapy of a diuretic, ACE inhibitor, and beta-blocker, the addition of spironolactone may be of benefit.
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 to prevent hyperkalemia. Eplerenone is an alternative to spironolactone that does not cause gynecomastia.
The addition of inotropic agents to patients with severe HF improves symptoms and quality of life and reduces hospitalizations. 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 in systolic dysfunction 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 glycosides
Digitalis will increase both the force and the velocity of the myocardial contraction. It will also promote a more complete emptying of the ventricles.
Digitalis should only be added after all drugs that reduce mortality have been tried. Then it can be used for the treatment of systolic HF, atrial fibrillation/flutter, and paroxysmal atrial tachycardia/SVT.
The serum potassium should be carefully monitored in all patients taking digitalis. Remember that K+ and digitalis compete for myocardium binding sites.
Hyperkalemia will decrease digitalis action, whereas hypokalemia increases digitalis toxicity.
Toxic effects of digitalis include nausea and vomiting; gynecomastia; blurred vision; yellow halo around objects; arrhythmias (commonly paroxysmal atrial tachycardia) with block PVCs (premature ventricular contractions), and bradycardia.
Treatment for intoxication is to stop the drug, add lidocaine and phenytoin (for arrhythmia). Digibind is used only for an acute overdose.