Left Ventricular Failure

Article Author:
Johnny Chahine
Article Editor:
Heidi Alvey
Updated:
3/15/2019 10:09:50 AM
PubMed Link:
Left Ventricular Failure

Introduction

The heart is comprised of the pericardium, myocardium, and endocardium. Pathology in any of those structures can lead to heart failure. Left ventricular failure occurs when there is dysfunction of the left ventricle causing insufficient delivery of blood to vital body organs. Left ventricular failure can further subdivide into heart failure with preserved ejection fraction (HFpEF with EF over 50%), heart failure with reduced ejection fraction (HFrEF with EF less than 40%), or heart failure with mid-range ejection fraction (EF between 41 and 49 percent).

Etiology

The most common etiologies of left heart failure are coronary artery disease and hypertension. The latter can cause left heart failure through left ventricular hypertrophy (leading to HFpEF), and also serves as a risk factor for coronary artery disease (which can lead to HFrEF). Diabetes, smoking, obesity, male gender, and a sedentary lifestyle are also considered risk factors.[1][2][3] Many of these causes are preventable, and as such risk factor control remains of extreme importance in preventing heart failure.[4]

Epidemiology

Heart failure is more prevalent and has a higher incidence in the elderly population. Approximately 5.7 million people in the United States have diagnosed heart failure. The incidence is around 10 per 1000 in people over 65.[5][6]Approximately 50% of all patients with heart failure are considered to have HFrEF; this diagnosis is becoming more prevalent with time.[7][8] HFpEF, as opposed to HFrEF, is more common in women (79% versus 49%) and also tends to affect an older population.[9]

Pathophysiology

Multiple mechanisms can lead to left heart failure. Chronic or poorly controlled hypertension causes increased afterload and therefore increased cardiac workload, which can lead to hypertrophy of the left ventricle. Initially, this hypertrophy serves as a compensatory mechanism and can help maintain cardiac output, but long-term can inhibit relaxation of the myocardium leading to impaired cardiac filling and decrease left ventricular output. Coronary arterial disease causes direct ischemic damage to the myocardium, leading to remodeling and scar formation, which decreases contractility and cardiac output. Arrhythmias can cause remodeling, but in general, decrease cardiac output by impaired ventricular filling and decreased ventricular relaxation. Cardiomyopathies encompass a diverse pathologic spectrum and have variable mechanisms causing cardiac dysfunction.[10]

History and Physical

Patients with left heart failure may present with complaints of shortness of breath (often on exertion, a sensitivity of 89%), orthopnea (a specificity of 89%), paroxysmal nocturnal dyspnea and/or symptoms of volume overload (e.g., leg swelling, weight gain, increased abdominal girth, or right upper quadrant pain due to liver congestion).[11] Interestingly, some patients with advanced disease might experience weight loss, referred to as "cardiac cachexia."[12]

On physical exam, the most common signs encountered are:

  • Rales on lung auscultation indicative of pulmonary edema
  • Decreased breath sounds on lung auscultation suggestive of pleural effusion
  • S3 gallop on heart auscultation indicative of elevated left ventricular end-diastolic pressure
  • Point of maximal impulse displaced laterally on palpation characteristic of increased heart size
  • Jugular venous distention (jugular venous pressure over 8 cm of water) indicative of elevated right atrial pressure
  • Positive hepatojugular reflux (exerting manual pressure on the congested liver causing increased jugular venous pressures)
  • Increased abdominal girth due to ascites
  • Swelling of the scrotum
  • Low blood pressure and rapid heart rate can occur in severely decompensated failure due to decreased cardiac output

Evaluation

The diagnosis of heart failure is clinical. However, several tests are available for further evaluation:

  • Laboratory tests: brain natriuretic peptide (BNP) or NT-proBNP may be the most helpful as it can differentiate acute heart failure from other causes of shortness of breath. However, this test lacks specificity, and a high level of this hormone is not diagnostic of acute heart failure.[11][13] Other laboratory tests include troponin T (to detect myocardial infarction, although the levels may be high due to heart failure itself), complete blood count, basic metabolic panel (low sodium, in particular, indicates advanced disease) and liver function tests (to detect liver injury due to volume overload).
  • Electrocardiography can show nonspecific findings, like ischemic changes, left ventricular hypertrophy, or arrhythmias.
  • Echocardiography can help distinguish HFrEF from HFpEF by determining the ejection fraction, and diastolic left ventricular function can evaluate associated regional wall motion abnormalities that may be suggestive of an ischemic component, as well as valvular and pericardial pathologies.
  • Coronary angiography is indicated in patients with anginal symptoms and may also be indicated in patients with worsening heart failure symptoms.[14]

Treatment / Management

Patients should receive education on the importance of lifestyle modification for improving the outcome of their disease. This includes reasonable salt consumption and avoidance of alcohol, nicotine, and recreational drugs.

Treating the underlying cause is of extreme importance as some heart failure conditions may be reversible when the precipitating factors are addressed, like cardiomyopathies induced by alcohol, tachycardia or ischemia. Tight control of blood pressure will also help prevent further deterioration.[15]Besides loop diuretics for volume overload, the pharmacologic treatment differs between HFrEF and HFpEF [16][17][18]: -For HFrEF, the mainstay of treatment is the combination of an angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) with a beta blocker (carvedilol, metoprolol or bisoprolol). If the patient remains symptomatic on a maximal dose of ACE inhibitor or ARB, an angiotensin receptor-neprilysin inhibitor may be substituted. Other medications include hydralazine, nitrates, mineralocorticoid receptor antagonists such as spironolactone, ivabradine, and digoxin (as a last resort). Nitrates in combination with hydralazine may be especially efficacious in African American patients. Digoxin, ivabradine and the diuretics have not been shown to offer any mortality benefit.

- For HFpEF, the treatment focuses on the underlying cause or contributing factors: control of blood pressure, revascularization if ischemic cardiomyopathy, and management of arrhythmias. A mineralocorticoid receptor antagonist may be beneficial in these patients.

Severely symptomatic patients with an ejection fraction less than 35% should obtain a referral for implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy (CRT) (depending on QRS width and the type of intraventricular conduction delay) after medical optimization. In advanced cases, mechanical circulatory assist devices such as an LVAD, continuous infusion of inotropic medications such as dobutamine or milrinone (which is still possible in the ambulatory setting), and cardiac transplantation are options.

Differential Diagnosis

  • When approaching a patient with shortness of breath on exertion, a broad differential diagnosis exists. A patient with established left heart failure might have a concomitant disease that might contribute to the patient's presentation, and additional workup for other conditions is warranted in case of atypical presentations. Those conditions include other cardiovascular causes (like primary pulmonary hypertension), pulmonary causes (like chronic obstructive pulmonary disease and interstitial lung disease) and extra-cardiopulmonary causes (like anemia).
  • Isolated lower limb edema is less likely heart failure, and other causes must be ruled out first, like venous insufficiency, cirrhosis, nephrotic syndrome, lymphedema and thrombosis of the veins.

Staging

The "2009 focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults" recommends a staging for heart failure.[[19] Patients with stages A and B are those who are asymptomatic but are prone to develop heart failure in the future, for example, diabetic and hypertensive patients. Stage B differs from stage A by the presence of a structural cardiac abnormality, like ventricular hypertrophy or systolic dysfunction, but again with no symptoms. Stage C and D patients include those who have ever experienced symptoms of heart failure. Stage D patients are those with severe heart failure who require advanced treatment like mechanical support, around-the-clock inotropic agents and heart transplantation.Stage C and D patients can be further classified based on the New York Heart Association (NYHA) Functional Classification: 

  • Class I: symptoms not restricting daily activities.
  • Class II: symptoms occurring at moderate effort slightly restricting daily activities.
  • Class III: symptoms occurring at minimal effort with significant restriction of daily activities.
  • Class IV: debilitating symptoms are occurring at rest.

Prognosis

The mortality rate in heart failure in 2008 was 18.2 per 100,000 for males and 15.8 per 100,000 for females based on the "Morbidity and Mortality: 2012 Chart Book on Cardiovascular, Lung and Blood Diseases". Patients with HFpEF have been known to have a lower mortality rate than those with HFrEF.[20]

Multiple variables have associations with worse outcome in heart failure: male gender, advancing age, low ejection fraction, high NYHA functional class, low hematocrit, and sodium levels, high brain natriuretic peptide, low peak exercise oxygen uptake, wide QRS, renal failure, low blood pressure, elevated heart rate, and volume overload refractory to medical treatment.[19][21]

Complications

Left heart failure can be complicated with severe volume overload leading to respiratory distress and anasarca as well as arrhythmias (tachyarrhythmias or bradyarrhythmias), cardiogenic shock due to pump failure and death. It was also reported that pulmonary embolism, acute coronary syndrome, cerebrovascular accidents and rupture of the myocardium are common causes of sudden death in patients with heart failure.[22] In addition to implantable cardioverter-defibrillators, several medications (stated above) reduce mortality in left heart failure and initiation of therapy should be as soon as indicated.

Deterrence and Patient Education

Compliance with lifestyle modification and pharmacologic treatment and control of precipitating factors (like hypertension and arrhythmias) are crucial to prevent hospitalizations for heart failure exacerbation and improve the quality of life. Many of those precipitating factors are potentially under patient control. That is why patient education is an integral part of a multidisciplinary approach to decrease mortality and morbidity due to heart failure.

Enhancing Healthcare Team Outcomes

A multidisciplinary approach is crucial in patients with advanced heart failure with an increased risk of readmissions.[16][23] In a systematic review of 29 randomized controlled trials, a multidisciplinary approach decreased heart-failure related hospital admissions by 27% and all-cause mortality by around 25%. This approach was also cost-effective. Well-trained nurses are an integral part of this approach since heart failure clinics led by nurses and in coordination with the patients' providers were very successful in enhancing patient outcome. In addition to the availability of heart failure clinics, training personnel in heart failure management and patient education are cornerstones to a successful multidisciplinary approach. Telephone follow up reduced hospital readmissions due to heart failure but not mortality. [level II]


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