WHAT IS AN HEART FAILURE?
Heart failure (HF), also known as congestive heart failure is not a disease but a syndrome, a combination of signs and symptoms caused by the impairment of the heart’s function as a pump to support the circulatory system at rest or during exercise. It develops when the heart fails properly to fill up with blood during diastole, leading to an decrease in intracardiac pressures or in ejection during systole, thereby reducing cardiac output to the rest of the body. Filling dysfunction and high intracardiac pressure may result in the buildup of fluid in the veins and tissues. This manifests as water retention and swelling due to the buildup of liquid (edema), collectively referred to as congestion. Impaired ejection can cause inadequate perfusion of the body tissues with blood leading to ischemia.
WHAT ARE THE PATHOPHYSIOLOGY?
Heart failure is caused by any condition that reduces the efficiency of the heart muscle, through damage or overloading. Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin–angiotensin system and the sympathoadrenal system, lead to fibrosis, dilation, and structural changes in the shape of the left ventricle from elliptical to spherical.
The heart of a person with heart failure may have a reduced force of contraction due to overloading of the ventricle. In a normal heart, increased filling of the ventricle results in increased contraction force by the Frank–Starling law of the heart, and thus a rise in cardiac output. In heart failure, this mechanism fails, as the ventricle is loaded with blood to the point where heart muscle contraction becomes less efficient. This is due to reduced ability to cross-link actin and myosin myofilaments in over-stretched heart muscle.
WHAT ARE THE SIGNS AND SYMPTOMS?
Heart failure can be ongoing (chronic), or it may start suddenly (acute).
Signs and symptoms may include:
- Shortness of breath with activity or when lying down
- Fatigue and weakness
- Swelling in the legs, ankles and feet
- Rapid or irregular heartbeat
- Reduced ability to exercise
- Persistent cough or wheezing with white or pink blood-tinged mucus
- Swelling of the belly area (abdomen)
- Very rapid weight gain from fluid build-up
- Nausea and lack of appetite
- Difficulty concentrating or decreased alertness
- Chest pain if heart failure is caused by a heart attack
WHAT ARE THE CAUSES?
Since heart failure is a syndrome and not a disease, establishing the underlying cause is vital to diagnosis and treatment. Heart failure is the potential end stage of all heart diseases.
Common causes of heart failure include;
- Coronary artery disease, including a previous myocardial infarction (heart attack)
- High blood pressure
- Atrial fibrillation
- Valvular heart disease
- Excess alcohol use
- Cardiomyopathy of an unknown cause.
In addition, viral infections of the heart can lead to inflammation of the muscular layer of the heart and subsequently contribute to the development of heart failure. Genetic predisposition plays an important role. If more than one cause is present, progression is more likely and prognosis is worse.
WHEN TO SEE A DOCTOR
See your doctor if you think you might be experiencing signs or symptoms of heart failure. Call 911 or emergency medical help if you have any of the following:
- Chest pain
- Fainting or severe weakness
- Rapid or irregular heartbeat associated with shortness of breath, chest pain or fainting
- Sudden, severe shortness of breath and coughing up white or pink, foamy mucus
Although these signs and symptoms may be due to heart failure, there are many other possible causes, including other life-threatening heart and lung conditions. Don’t try to diagnose yourself. Emergency room doctors will try to stabilize your condition and determine if your symptoms are due to heart failure or something else. If you have a diagnosis of heart failure and if any of the symptoms suddenly become worse or you develop a new sign or symptom, it may mean that existing heart failure is getting worse or not responding to treatment. This may also be the case if you gain 5 pounds (2.3 kilograms) or more within a few days. Contact your doctor promptly.
HOW DO WE DIAGNOSE HEART FAILURE IN ALTH?
1. ULTRASOUND: An echocardiogram (ultrasound of the heart) is commonly used to support a clinical diagnosis of heart failure. This can determine the stroke volume (SV, the amount of blood in the heart that exits the ventricles with each beat), the end-diastolic volume (EDV, the total amount of blood at the end of diastole), and the SV in proportion to the EDV, a value known as the ejection fraction (EF). In pediatrics, the shortening fraction is the preferred measure of systolic function. Normally, the EF should be between 50 and 70%; in systolic heart failure, it drops below 40%. Echocardiography can also identify valvular heart disease and assess the state of the pericardium (the connective tissue sac surrounding the heart). Echocardiography may also aid in deciding specific treatments, such as medication, insertion of an implantable cardioverter-defibrillator, or cardiac resynchronization therapy. Echocardiography can also help determine if acute myocardial ischemia is the precipitating cause, and may manifest as regional wall motion abnormalities on echo.
2. CHEST XRAY: Chest X-rays are frequently used to aid in the diagnosis of CHF. In a person who is compensated, this may show cardiomegaly (visible enlargement of the heart), quantified as the cardiothoracic ratio (proportion of the heart size to the chest). In left ventricular failure, evidence may exist of vascular redistribution (upper lobe blood diversion or cephalization), Kerley lines, cuffing of the areas around the bronchi, and interstitial edema. Ultrasound of the lung may also be able to detect Kerley lines.
3. ELECTROPHYSIOLOGY: An electrocardiogram (ECG/EKG) may be used to identify arrhythmias, ischemic heart disease, right and left ventricular hypertrophy, and presence of conduction delay or abnormalities (e.g. left bundle branch block). Although these findings are not specific to the diagnosis of heart failure, a normal ECG virtually excludes left ventricular systolic dysfunction.
4. BLOOD TESTS: Blood tests performed include electrolytes (sodium, potassium), measures of kidney function, liver function tests, thyroid function tests, a complete blood count, and often C-reactive protein if infection is suspected. An elevated brain natriuretic peptide 32 (BNP) is a specific test indicative of heart failure. Additionally, BNP can be used to differentiate between causes of dyspnea due to heart failure from other causes of dyspnea. If myocardial infarction is suspected, various cardiac markers may be used.
WHAT ARE THE PREVENTIONS?
Heart failure can be prevented by lowering high blood pressure and high blood cholesterol, and by controlling diabetes. Maintaining a healthy weight, and decreasing sodium, alcohol, and sugar intake, may help. Additionally, avoiding tobacco use has been shown to lower the risk of heart failure. Diabetes is a major risk factor for heart failure. For women with Coronary Heart disease (CHD), diabetes was the strongest risk factor for heart failure. Diabetic women with depressed creatinine clearance or elevated body mass index (BMI) were at the highest risk of heart failure.
MANAGEMENT OF HEART FAILURE
The goals of the treatment for people with chronic heart failure are the prolongation of life, prevention of acute decompensation, and reduction of symptoms, allowing for greater activity. Heart failure can result from a variety of conditions. In considering therapeutic options, excluding reversible causes is of primary importance, including thyroid disease, anemia, chronic tachycardia, alcohol use disorder, hypertension, and dysfunction of one or more heart valves. Treatment of the underlying cause is usually the first approach to treating heart failure. In the majority of cases, though, either no primary cause is found or treatment of the primary cause does not restore normal heart function. In these cases, behavioral, medical and device treatment strategies exist that can provide a significant improvement in outcomes, including the relief of symptoms, exercise tolerance, and a decrease in the likelihood of hospitalization or death. Breathlessness rehabilitation for chronic obstructive pulmonary disease and heart failure has been proposed with exercise training as a core component. Rehabilitation should also include other interventions to address shortness of breath including psychological and educational needs of people and needs of caregivers. Iron supplementation appears useful in those with iron deficiency anemia and heart failure.
First line medications
First-line therapy for people with heart failure due to reduced systolic function should include angiotensin-converting enzyme (ACE) inhibitors (ACE-I), or angiotensin receptor blockers (ARBs) if the person develops a long-term cough as a side effect of the ACE-I. Use of medicines from these classes is associated with improved survival, fewer hospitalizations for heart failure exacerbations, and improved quality of life in people with heart failure.
Beta-adrenergic blocking agents (beta blockers) also form part of the first line of treatment, adding to the improvement in symptoms and mortality provided by ACE-I/ARB. The mortality benefits of beta blockers in people with systolic dysfunction who also have atrial fibrillation is more limited than in those who do not have it.If the ejection fraction is not diminished (HFpEF), the benefits of beta blockers are more modest; a decrease in mortality has been observed, but reduction in hospital admission for uncontrolled symptoms has not been observed.
In people who are intolerant of ACE-I and ARBs or who have significant kidney dysfunction, the use of combined hydralazine and a long-acting nitrate, such as isosorbide dinitrate, is an effective alternate strategy. This regimen has been shown to reduce mortality in people with moderate heart failure.
SGLT2 inhibitor is the newest medicine for heart failure.
Second-line medications for CHF do not confer a mortality benefit. Digoxin is one such medication. Its narrow therapeutic window, a high degree of toxicity, and the failure of multiple trials to show a mortality benefit have reduced its role in clinical practice. It is now used in only a small number of people with refractory symptoms, who are in atrial fibrillation, and/or who have chronic hypotension.
Diuretics have been a mainstay of treatment against symptoms of fluid accumulation, and include diuretics classes such as loop diuretics (such as furosemide), thiazide-like diuretics, and potassium-sparing diuretics. Although widely used, evidence on their efficacy and safety is limited, with the exception of mineralocorticoid antagonists such as spironolactone.Mineralocorticoid antagonists in those under 75 years old appear to decrease the risk of death.
Anemia is an independent factor in mortality in people with chronic heart failure. Treatment of anemia significantly improves quality of life for those with heart failure, often with a reduction in severity of the NYHA classification, and also improves mortality rates.
The decision to anticoagulate people with HF, typically with left ventricular ejection fractions <35% is debated, but generally, people with coexisting atrial fibrillation, a prior embolic event, or conditions that increase the risk of an embolic event such as amyloidosis, left ventricular noncompaction, familial dilated cardiomyopathy, or a thromboembolic event in a first-degree relative.
Vasopressin receptor antagonists can also be used to treat heart failure. Conivaptan is the first medication approved by US Food and Drug Administration for the treatment of euvolemic hyponatremia in those with heart failure.In rare cases hypertonic 3% saline together with diuretics may be used to correct hyponatremia.
Ivabradine is recommended for people with symptomatic heart failure with reduced left ventricular ejection fraction who are receiving optimized guideline-directed therapy (as above) including the maximum tolerated dose of beta-blocker, have a normal heart rhythm and continue to have a resting heart rate above 70 beats per minute. Ivabradine has been found to reduce the risk of hospitalization for heart failure exacerbations in this subgroup of people with heart failure.
Proper treatment can improve the signs and symptoms of heart failure and may help some people live longer. Lifestyle changes — such as losing weight, exercising, reducing salt (sodium) in your diet and managing stress — can improve your quality of life. However, heart failure can be life-threatening. People with heart failure may have severe symptoms, and some may need a heart transplant or a ventricular assist device (VAD).
FOR MANAGEMENT/CONSULTATIONS KINDLY CONTACT US VIA OUR EMAIL/HOTLINES.