Heart Failure (HF)
Heart failure (HF) refers to any abnormality of function or structure in which there is a reduced ability for the ventricle to fill with or eject blood, resulting in impairment of cardiac output. The categories of heart failure are based on a measurement that signifies the efficiency with which the left ventricle ejects blood, called the left ventricular ejection fraction (LVEF). As a percentage, the LVEF is designated as
- Systolic Heart Failure (LVEF ≤ 40%): HF with reduced ejection fraction (HFrEF)
- Diastolic Heart Failure (LVEF >50%): HF with preserved ejection fraction (HFpEF)
Ventricular contractility and its resulting ejection force of its volume depend on the blood that fills the ventricle (“preload”), the contractility stimulation from cardiac fiber stretch, and the resistance from the aorta and stress from the ventricular walls (“afterload”). Thus, ventricular function is in a 3-way relationship among preload, contractility, and afterload. The net result of quality failure in any of these components results in decreased ejection fraction (heart failure) of the left ventricle.
Causes of Heart Failure
Left ventricular hypertrophy is a prominent condition of HF, regardless of whether it emerges as a complication of coronary artery disease, hypertension, diabetes, or valve disease. Causes of heart failure in order of importance:
- Coronary heart disease
- Cigarette smoking
- Valvular heart disease
- Conditions in which the diagnosis is not identifiable
Signs and Symptoms
As HF progresses, the symptoms emerge and worsen dyspnea, fatigue, and exertion intolerance. In advanced HF, walking only one city block, dressing, bathing, and other activities of daily living become difficult. Exercise intolerance increases. Edema from overload can present as pulmonary congestion, peripheral edema, and elevated jugular vein pressure. Renal function can decline.
Complications of Heart Failure
HF is a progressive condition, and eventually patients can have dyspnea at rest. Activities of daily living become impossible. Weight loss and hypotension are signs of advanced HF.
Acute Decompensated Heart Failure (ADHF)
There is a continuum for HF, and when a threshold of compensation is breached, the condition can become life-threatening and portend poorly for survival. In ADHF, the progression from chronic symptoms to acute emergent conditions is accompanied by hypotension, which is commensurate with hypoperfusion of blood, i.e., decreased oxygenation of tissue and subsequent end-organ compromise and/or failure:
- Dyspnea at rest
- Acute coronary syndrome
- Electrolyte disturbances
- Renal failure
HF is approached from a functional standpoint: diuretics, control of blood pressure, medical therapy, mechanical circulatory support (left ventricular assist devices–LVADs), heart transplant, and if treatment fails to the point of end-stage disease, palliative care.
The morbidity from HFpEF and HFrEF is about the same. Mortality rate, annually, is 5%, which is low, considering the pathology. Nevertheless, attempts to lower this percentage by reducing risk factors and comorbidities are important steps in prevention of advanced heart failure.
How Is Heart Failure Diagnosed?
The heart is a mechanical pump, and as such, lends itself to measurement of its functional physiology. Diagnosis of heart failure begins with a history and physical exam to identify dyspnea, fatigue, and exercise intolerance, volume overload and edema, weight loss, or signs of inadequate perfusion (renal compromise).
Blood Tests in the Diagnosis of Heart Failure (HF)
- Kidney evaluation: Serum creatinine, which can indicate the reduction in glomerular filtration rate (GFR–the function of the kidney) seen in HF. Blood Urea Nitrogen (BUN) rises with HF. These parameters can be followed serially as a gauge for HF progression.
- Serum sodium: sodium depletion is due to neurohumoral changes of the body’s perceived decreased volume (from a paradoxical perspective of decreased ejection fraction).
- Serum albumin: the hypoalbuminemia from liver dysfunction and renal and GI losses will present as a low albumin level in the blood.
- Liver function tests and serum bilirubin evaluation: bilirubin can rise and liver function can decline in HF.
- Natriuretic peptide measurement: persistent elevations occur in HF.
Chest X-ray (CXR)
CXR can demonstrate volume overload as pulmonary edema, pleural effusions, and vascular congestion in the lung.
An ECG can demonstrate alterations in the normal wave patterns typically recorded in healthy individuals and how far they deviate from the normal. Although there is no ECG “marker” that is diagnostic for HF, wave abnormalities that indicate prior myocardial infarction or cardiomyopathy can reveal possible causes of HF or its comorbidities. Arrhythmias such as the atrial fibrillation or ventricular tachycardia that contribute to advanced HF can be identified for the purpose of driving therapy decisions.
Diagnosis of Advanced Heart Failure
Much of the diagnostic evaluation on HF patients, since there is a previously established diagnosis of HF, is to diagnose the transition to advanced heart failure, which is based on severity of symptoms and failure to remedy fluid retention or renal failure, along with advancing cardiac dysfunction. Such a transition into the “advanced” category worsens the prognosis and therefore calls for more aggressive surveillance and therapy:
- Blood tests for serum electrolytes (including sodium), blood count (CBC), renal function tests (BUN and creatinine), thyroid function tests, liver function tests (including serum albumin, bilirubin, and liver enzymes), and natriuretic peptide levels
- Chest X-ray to identify any pulmonary edema and rule out other causes for dyspnea (pneumonia, malignancy, etc.)
- Ultrasonography–a transthoracic echocardiogram (TTE) to evaluate ventricular and valve function and if inconclusive, a transesophageal echogram (TEE)
- Limited exercise testing, if feasible
- Right cardiac catheterization for those on mechanical circulatory support (left ventricular assistance devices–LVADs) or who have had cardiac transplantation
Therapeutic Goals in Heart Failure (HF)
Reducing morbidity, progression of disease, and the mortality associated with HF are the three major goals, along with simultaneous improvement of function (activities of daily living) and quality of life.
Management of Co-factors and Co-morbidities
The causes of HF are in interaction with its own complications, often as a vicious cycle of co-dependent conditions. Management includes:
- Lifestyle alteration, including weight management, smoking cessation, strict glycemic control (in diabetics), and supervised exercise.
- Management of hypertension, using a four-part therapy regimen of a 1) beta blocker, 2) ACE inhibitor, 3) an angiotensin II receptor blocker (ARB), and 4) a diuretic (“potassium-sparing” mineralocorticoid receptor antagonist–MRA).
Beta blockers can also relieve angina symptoms. Prior to MRA administration, a serum potassium should be obtained to preclude the risk of hyperkalemia.
- Coronary atherosclerosis: The dominant cause of HF, should be treated with antianginal drugs and lipid-altering statins; revascularization can improve coronary atherosclerosis and with it, heart failure.
- Renovascular disease (renal hypertension): as a complication of coronary artery disease, besides with use of antihypertensive therapy (above), might also benefit from revascularization (coronary stenting or bypass).
- Whether valvular disease is the cause for HF or a complication (mitral and tricuspid regurgitation), surgical correction of valve stenosis or regurgitation will improve heart function, mitigating heart failure.
- Any arrhythmias that accompany HF, such as tachycardia, atrial flutter, or atrial fibrillation, which can prolong and complicate HF, should be resolved. Antiarrhythmic drugs should be used with great caution due to their risk of actually provoking arrhythmia. Reversion to sinus rhythm and slowing down tachycardia can be done via implantable cardiac devices to prevent sudden cardiac death, which has been proven to be superior to antiarrhythmics in reducing mortality.
Since much of the treatment is designed to prevent disease progression, frequent and serial monitoring is part of the therapeutic strategy.
Renal function (via serum creatinine and BUN), surveillance for arrhythmia (via ECG), and identifying worsening volume overload and cardiac dysfunction (via echocardiography and chest X-rays) should be done routinely, based on a schedule individualized for a patient’s particular level of disease and compromise to his or her quality of life and activities of daily living.
How Can I Prevent Heart Failure from Happening?
Prevention of heart failure (HF) is best pursued by identifying those patients at risk so that early detection can allow the treatment of predisposing conditions. If HF is prevented or mitigated, so is the the increased morbidity and morality associated with it. Such a strategy can forestall heart failure (HF).
Major Areas of Focus Is Prevention of or Therapy For:
- Coronary artery disease
- Obesity and metabolic syndrome
- Dyslipidemia (elevated LDL-cholesterol, lower-than-normal HDL-cholesterol, and elevated triglycerides)
- Smoking, if applicable
- Illicit drug abuse, including sympathomimetic substances (cocaine, amphetamines)
Preventative care also includes annual influenza vaccinations and pneumococcal immunization to prevent the infectious complications that result in any further compromise of respiration due to pulmonary congestion and the general debilitation that HF creates.
Crucial in prevention of HF (delay of its onset) is early detection of left ventricular ejection fraction decreases (≤40%) in asymptomatic patients. For those who have already sustained a cardiac arrest, a repeat adverse cardiac event (including sudden cardiac death) is a constant threat. Therefore, implantable cardioverters-defibrillators are necessary in such HF patients. These have been proven to be more effective than antiarrhythmics alone.
Reversible causes of arrhythmias in HF patients, such as the electrolyte disturbances from renal impairment, should be sought, identified, and when present, reversed.
Heart failure may be impossible to prevent, since most patients who are diagnosed arrive with the current pathology attributable to age, genetics, and/or a long-lived life of poor lifestyle choices. The diagnosis of heart failure is not a forgone conclusion of mortality, but a challenge to institute prevention protocols to limit its morbidity.