Which of the following is a compensatory response to decreased cardiac output in myocardial infarction?

Introduction

Chronic heart failure is a syndrome, not a specific disease, and occurs as a final common pathway in multiple disease states.

The pathophysiology of chronic heart failure (HF) exists when either the left ventricle, the right ventricle, or both, require elevated filling pressures to maintain cardiac output. The neurohormonal responses to impaired cardiac function constitute a negative feedback cycle that is an integral part of the HF syndrome and, to date, blockade of that cycle is the most effective pharmacologic approach to management.

HF can be due to the following:

• Systolic dysfunction with reduced ejection fraction - HFrEF
• Diastolic dysfunction abnormal relaxation or impaired filling with preserved ejection fraction - HFpEF
• Valvular heart disease
• Pulmonary hypertension with right HF
• Arrhythmia
• High output HF (ie, severe anemia, arteriovenous malformations)

This section presents a review of systolic HF, currently known as HF with reduced ejection fraction, or HFrEF. Diastolic HF (or HFpEF), valvular heart disease, pulmonary hypertension and right HF, and high output HF are discussed elsewhere.

Chronic HF affects approximately 6 million Americans (approximately 1.8% of the total U.S. population) and despite recent improvements in therapy, it remains one of the most common reasons for hospitalization.

Pathophysiology – Chronic Heart Failure -HFrEF

Chronic HF results in the activation of multiple compensatory mechanisms in an attempt to maintain cardiac output. These frequently suffice in the short term; however, their long-term effects are detrimental to heart function because of negative remodeling. The two primary mechanisms — considered “neurohormonal” responses — are activation of the sympathetic nervous system (SNS) and activation of the renin-angiotensin-aldosterone system (RAAS). Medical therapy is aimed at reducing the activity of these two systems. A third compensatory response occurs via B-type natriuretic peptide and A-type natriuretic peptide — see Figure below.

When the carotid baroreceptors sense a low blood pressure, one response is to activate the SNS increasing epinephrine and norepinephrine levels, which increase heart rate, contractility and, most importantly, increase afterload via peripheral vasoconstriction and increased peripheral resistance. This response has chronic deleterious effects and leads to further left ventricular systolic decline. Beta-blockers are the primary therapy to reduce this SNS activation.

When renal perfusion is decreased, renal homeostatic responses react to correct hypovolemia. However, reduced cardiac output also decreases renal perfusion. The primary renal compensatory mechanism is retention of sodium and water through activation of the renin-angiotensin-aldosterone system. Angiotensin also increases peripheral vascular resistance (afterload) via peripheral vasoconstriction. Activation of the RAAS contributes substantially to negative remodeling of the heart, resulting in cardiac function. The RAAS can be blocked by angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers, and aldosterone antagonists, as described in Treatment below.

Both A-type (ANP) and B-type (BNP) natriuretic peptide have beneficial hemodynamic effects in HF and represent a compensatory pathway. In HF, ANP is released primarily from the atrium and BNP primarily from the ventricles in response to myocyte stretch. They cause vasodilation and increase sodium excretion, resulting in natriuresis. Sacubitril, a neprilysin inhibitor, interferes with the breakdown of natriuretic peptides, increasing the levels of these compensatory cardiac hormones. Sacubitril has recently been approved as part of the combination formulation sacubitril/valsartan (Entresto, Novartis).

Endothelin also promotes remodeling and vasoconstriction; however, clinical trials of endothelin inhibitors have not demonstrated a convincing long-term benefit, and thus the role of endothelin remains unclear.

Etiology – Chronic Heart Failure -HFrEF

There are numerous causes of HFrEF, but one of the most common is coronary artery disease with prior myocardial infarction. HFrEF due to coronary disease is often referred to as “ischemic cardiomyopathy” and it accounts for approximately half of all HFrEF cases.

Dilated cardiomyopathy is the second-leading cause of systolic HF. The term covers a wide variety of pathologic entities, including idiopathic (50% of cases), post-viral, peripartum, chemotherapy-related, stress-induced (Takotsubo), alcohol-related, selenium or thiamine deficiency, tachycardia-mediated, giant cell myocarditis, hyperthyroidism, cocaine use, obstructive sleep apnea and familial cardiomyopathies.

The third-leading cause of systolic HF is valvular heart disease, including aortic and mitral degenerative valve disease. In Central America, Chagas disease, caused by chronic infection by the parasite Trypanosoma cruzi remains common despite public health measures. Chagas heart disease should be considered as a potential cause of heart failure in the growing immigrant population in the U.S.

Recall that right HF and HFpEF are different entities from the left-sided or biventricular HFrEF reviewed here, and that they therefore have distinct etiologies.

Symptoms – Chronic Heart Failure

The symptoms of HF include fatigue, exercise intolerance, dyspnea and eventually edema. The symptoms are similar regardless of the etiology of the heart disease, and reflect either impaired cardiac output or fluid retention. Symptoms are important in differentiating left ventricular failure from right ventricular failure.

Clinical Classification – Chronic Heart Failure

Two HF classification systems are widely used: the New York Heart Association (NYHA) functional classification and the American College of Cardiology and American Heart Association (ACC/AHA) staging system. [Heidenreich 2022;10a(e905)]
The NYHA system categorizes patients into one of four classes based on a health care professional’s subjective assessment of the patient’s symptoms:

• Class I: No symptoms of HF
• Class II: Symptoms of HF with moderate exertion, such as walking two blocks or climbing two flights of stairs
• Class III: Symptoms of HF with minimal exertion such as walking one block or one flight of stairs, but no symptoms at rest
• Class IV: Symptoms of HF at rest

The ACC/AHA staging categorizes patients into one of four stages on the basis of risk factors, cardiac structural abnormalities associated with HF and the presence of symptoms of HF: [Heidenreich 2022:10a]

• Stage A: At high risk for HF but without symptoms, structural heart disease or cardiac biomarkers of stretch or injury
• Stage B: Pre-HF, defined as no signs or symptoms of HF but evidence of one of the following: structural heart disease, evidence of increased filling pressures or risk factors plus increased levels of BNPs or persistently elevated cardiac troponin
• Stage C: Structural heart disease with prior or current symptoms of HF
• Stage D: Marked HF symptoms that interfere with daily life and with recurrent hospitalizations despite attempts to optimize guideline-directed medical therapy (GDMT)

In addition to focusing on different classificatory parameters, the NYHA functional classification differs from the ACC/AHA heart failure staging in that NYHA allows movement from any one class to another while the ACC/AHA system only allows unidirectional progression of stages (A→B→C→D). [Heidenreich 2022:10a]

Diagnosis – Chronic Heart Failure -HFrEF

Patient history and physical examination remain the cornerstone of HF diagnosis, as they allow the detection of HF symptoms and specific signs, including elevated jugular venous pressure, positive abdominojugular reflux, S3 heart sound (gallop rhythm) and laterally displaced apical impulse. [Murphy 2020:2a]

Physical examination of the HFrEF patient may reveal an S3 heart sound if significant left ventricular dysfunction is present. (An S4 heart sound is more common in HFpEF.) The apical impulse (PMI), will be sustained and usually laterally displaced and, occasionally, the S3 can even be palpable. A systolic murmur of “functional” mitral regurgitation is often audible. [Rovai 2007:3a]

Physical examination in patients with right HF may reveal elevated jugular venous pressure, including hepatojugular reflux, lower extremity pitting edema and ascites. Pleural effusions may be present and more prominent on the right compared to the left.

When a diagnosis of HFrEF is suspected, initial testing includes: [Murphy 2020:2c] (1) laboratory analysis, including the measurement of renal function and natriuretic peptides (sensitive but not necessarily specific markers of HF generated by cardiomyocytes in response to myocardial stretch); [Heidenreich 2022:15a(e910)] (2) electrocardiography (a 12-lead ECG); [Heidenreich 2022:15a(e910)] and (3) chest X-ray to assess heart size and pulmonary congestion. [Heidenreich 2022:18a(e913)]
Echocardiography, in particular a 2D Doppler echocardiogram, is indicated in all patients with a new diagnosis of HF to help determine the etiology. [Heidenreich 2022:18a(e913)] The LV systolic function can be assessed, including estimation of LV ejection fraction. Diastolic function assessment can help determine the left heart diastolic pressures. The cardiac valves can be interrogated for significant regurgitant or stenotic lesions.

Cardiac catheterization including coronary angiography is indicated whenever angina symptoms accompany a new onset of congestive HF (Class I). If no angina is present, stress testing to evaluate for ischemia as a contributor is recommended. Alternatively, coronary CT angiography can be done when no angina is present to exclude occlusive coronary artery disease.

Treatment – Congestive Heart Failure - Systolic

Medical Therapy

Lifestyle modification to help decrease the risk for volume overload leading to hospitalization is important. The current ACC/AHA guidelines for the management of HF include a Class I recommendation for exercise training or regular physical activity to improve functional status. [Heidenreich 2022:24a(e919)]; The guidelines also state that an individualized degree of reduction in dietary sodium intake may be considered (Class IIa recommendation) to reduce symptoms in patients with Stage C HF. [Heidenreich 2022:30b(e925)]

Daily weight monitoring at home in order to dose diuretics on an individual basis is recommended. Educating patients on the importance of medication compliance is crucial to prevent decompensated episodes of HF.

There is an abundance of clinical evidence demonstrating mortality reduction and symptom improvement with currently available pharmacotherapies in patients with HFrEF. It is important distinguish the therapies that reduce mortality from those that only relieve symptoms.

Angiotensin Converting Enzyme (ACE) Inhibitors / Angiotensin Receptor Blockers (ARBs)

Angiotensin converting enzyme inhibitors are a class of oral medications that act primarily through blockade of the angiotensin converting enzyme (ACE). This enzyme converts angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction, increasing afterload, and thus increasing systemic blood pressure. Angiotensin contributes to the production of aldosterone, which normally acts to retain sodium and water.

Reducing the activity of the RAAS is crucial in HF, during which it is overactive and contributes to negative remodeling. ACE inhibitors can reduce the symptoms of HF and have been shown in multiple clinical trials to have a mortality benefit in patients with HFrEF. Doses usually start low, with uptitration to a predetermined goal dose if the patient is able to tolerate it. Commonly used ACE inhibitors include lisinopril, captopril, ramipril and enalapril.

Angiotensin receptor blockers (ARBs) are a class of oral medications that act primarily through blockade of the angiotensin receptor. Very similar effects on the RAAS are achieved with ARBs as with ACE inhibitors. ARBs are primarily used when a patient with systolic HF is unable to tolerate an ACE inhibitor, frequently due to a cough.

These drugs have significant mortality benefits, as shown in multiple clinical trials. The current ACC/AHA guidelines provide a Class I recommendation for an angiotensin receptor/neprilysin inhibitor (ARNI) (see below) for all patients with HFrEF, in conjunction with other medications. ACE inhibitors are recommended if the use of an ARNI is not feasible. If ARNI use us not feasible and the patient is intolerant to ACE inhibitors because of cough or angioedema, then an ARB is recommended. [Heidenreich 2022:33b(e928)]

Angiotensin receptor-neprilysin inhibitor (ARNI)

Sacubitril/valsartan is a first-in-class ARNI drug. It combines the ARB valsartan and the neprilysin inhibitor sacubitril. In the PARADIGM-HF trial, which compared the efficacy of sacubitril/valsartan to that of the ARB enalapril in patients with HFrEF and NYHA class II-IV HF, sacubitril/valsartan showed a 20% reduction in cardiovascular death or HF (the primary endpoint of the trial), compared to the ARB. A significant reduction was also noted for cardiovascular death, hospitalization and all-cause mortality in the sacubitril/valsartan group. [Hurst’s The Heart - Section 11:71a]

Based on these results, the current ACC/AHA guidelines provide a Class I recommendation to replace an ACE inhibitor or ARB with an ARNI in patients with chronic symptomatic HFrEF NYHA class II or III in order to further reduce morbidity and mortality [Heidenreich 2022:33b(e928)]

The guidelines also note that ARNIs should not be administered concomitantly with ACE inhibitors or within 36 hours of the last dose of an ACE inhibitor, as their concomitant use can lead to angioedema (Class III: Harm). Furthermore, ARNIs should not be administered to patients with a history of angioedema (Class III: Harm). [Heidenreich 2022:33b(e928)]

Beta-blockers

Beta-blockers antagonize beta-1 and beta-2 receptors — the usual targets of the SNS, epinephrine and norepinephrine. Chronically increased SNS activity has deleterious effects on long-term cardiac function, as described above. Three beta-blockers are approved by the FDA in the United States for the treatment of HF: metoprolol succinate, carvedilol and bisoprolol. These drugs have significant mortality benefits, as shown in multiple clinical trials.

The current ACC/AHA guidelines recommend that a beta-blocker be initiated as soon as HFrEF is diagnosed in all patients except those with contraindications or intolerance to these agents. [Heidenreich 2022:36a(e931)]

Beta-blockers are contraindicated specifically in HFrEF when pulmonary edema is present and when there are signs of cardiogenic shock, severe bradycardia, hypotension or wheezing related to asthma.

Aldosterone Antagonists

Mineralocorticoid antagonists, or aldosterone antagonists (spironolactone, eplerenone) block the action of aldosterone, inhibiting the reuptake of sodium and water. Normally, when sodium is reabsorbed, it is exchanged with potassium, which is excreted. Because aldosterone inhibition decreases sodium reabsorption, it also decreases potassium excretion and may result in higher serum potassium levels.

Spironolactone was investigated in the Randomized Aldactone Evaluation Study (RALES) trial, and a mortality benefit was shown in patients categorized as NYHA functional class III and IV. Significant hyperkalemia did contribute to sudden cardiac death.

The aldosterone antagonist eplerenone was evaluated in the Epleronone Post-Acute Myocardial Infarction Heart Failure Efficacy and Survival Study (EPHESUS) trial, leading to the recommendation for use of the agents with an ACE inhibitor prior to hospital discharge after an acute coronary syndrome if there is LV systolic dysfunction (EF ≤ 40%), either diabetes or symptomatic HF present and no contraindication.

The current ACC/AHA guidelines for the management of HF recommend aldosterone antagonists (spironolactone or eplerenone) in patients with HFrEF and NYHA Class II to IV symptoms to reduce morbidity and mortality if estimated glomerular filtration rate (eGFR) is > 30 mL/min/1.73m2 and serum potassium is < 5.0 mEq/L. [Heidenreich 2022:36b(e931)]

The guidelines also note that inappropriate use of aldosterone receptor antagonists is potentially harmful because of life-threatening hyperkalemia and renal insufficiency (Class III recommendation: Harm). Therefore, patients should be carefully selected for initiation of aldosterone antagonists. The guidelines recommend regular checks for serum potassium and levels and renal function at 1 week, then 4 weeks, then 6 months after initiating or intensifying an aldosterone receptor antagonist. [Heidenreich 2022:37a(e932)]

A class effect is likely present for aldosterone antagonists; therefore, spironolactone is frequently used instead of eplerenone due to cost concerns, though there are no direct data to support this practice. In this population, aldosterone antagonists do give a mortality benefit.

SGLT2 inhibitors

Sodium-glucose co-transporter 2 (SGLT2) inhibitors were developed to treat diabetes but were found to improve cardiovascular-related outcomes in patients with HFrEF. They block the SGLT2 protein located in the proximal convoluted tubule of the nephron, resulting in glycosuria and natriuresis, lowering plasma glucose concentrations. [Joshi 2021:1b]

The current ACC/AHA guidelines list SGLT2 inhibitors as one of the four classes of optimal medical therapy for patients with HFrEF, along with beta-blockers, aldosterone antagonists and ARNIs/ACE inhibitors/ARBs. For patients with symptomatic chronic HFrEF, they are recommended (Class I) to reduce HF hospitalization and CV mortality, regardless of whether the patient has diabetes. [Heidenreich 2022:37b(e932)]

Digitalis

Digitalis is a drug preparation derived from flowering plants of the genus Digitalis (foxgloves) with more than two centuries of history as an HF medication. [Hurst’s the Heart - Section 11:70a] Digoxin is the most commonly prescribed form of digitalis. At the cellular level, digitalis glycosides act by blocking the sodium/potassium ATPase pump. The mechanism by which this decreases atrioventricular (AV) conduction is not clear but may be due to increased vagal tone. Digitalis increases intracellular calcium within the cardiac myocytes, resulting in increased inotropy (contractility); thus, digoxin has been frequently used when atrial fibrillation and left ventricular systolic dysfunction coexist.

The current ACC/AHA guidelines state that digoxin may be considered (Class IIb recommendation) to decrease hospitalizations for HF in patients with HFrEF and no contraindications to its use who are symptomatic despite GDMT or unable to tolerate GDMT. [Heidenreich 2022:45b(e940)] The largest clinical trial of digitalis, the Digitalis Intervention Group (DIG) trial, showed no mortality benefit from treatment, there was improvement in symptoms and fewer hospitalizations for HF in those who received digoxin.

Commonly, if HFrEF is present in combination with atrial fibrillation and an uncontrolled ventricular rate, digoxin therapy is utilized. Digitalis toxicity is a serious concern, and the dose must be adjusted in the setting of renal failure.

Diuretics

The loop diuretics (so called because they act at the loop of Henle) furosemide, bumetanide and torsemide are used to control fluid retention and help maintain euvolemia in patients with heart failure. In hypertensive patients with HF and mild fluid retention, thiazide diuretics (which act at the distant portion of the renal tubule) may be considered because of their longer-persisting antihypertensive effects. [Heidenreich 2022:32b(e927)] The current ACC/AHA guidelines recommend diuretics (Class I recommendation) for patients with HFrEF with fluid retention. [Heidenreich 2022:32b(e927)] These drugs are used for symptom relief only; they have never been shown to provide a mortality benefit. Based on the patient’s lifestyle, including fluid and salt intake, frequent dose adjustments may be required.
Arginine Vasopressin Antagonists

Tolvaptan is a vasopressin receptor antagonist. The antidiuretic hormone (ADH) vasopressin plays a role in water retention by causing water absorption in the collecting ducts of the nephron. Blocking the ADH receptor allows increased water excretion. Many patients with HF present with some degree of hyponatremia from excess water retention. Clinical trials confirm that tolvaptan administration can increase sodium levels; however, mortality and rehospitalization rates were not improved. The role for tolvaptan in HF management is not well defined. Tolvaptan is approved by the FDA for the treatment of euvolemic hyponatremia and hypervolemic hyponatremia.

Ivabradine

Ivabradine is a novel inhibitor of the If ion channel which is associated with slowing of the sinus node depolarization rate in individuals who are in sinus rhythm. In the Systolic Heart Failure Treatment with the If Inhibitor Ivabradine Trial (SHIFT), ivabradine treatment resulted in a significant (18%) reduction in cardiovascular death or HF hospitalization in HF patients with NYHA functional class II to IV, sinus rhythm with a rate of ≥ 70 bpm, and an LVEF ≤ 35% (compared to the placebo). [Hurst’s The Heart - Section 11:71b,72a]

Based on these results, the current ACC/AHA guidelines state that ivabradine can be beneficial (Class IIa recommendation) to reduce HF hospitalization for patients with symptomatic (NYHA class II-III) stable chronic HFrEF (LVEF ≤ 35%) who are receiving GDMT, including a beta-blocker at maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest. [Heidenreich 2022:44b(e939)]

Hydralazine and Nitrates

Hydralazine is a direct-acting arterial vasodilator that decreases afterload. Isosorbide dinitrate is a long-acting oral nitrate that decreases preload. The combination of these two drugs has beneficial hemodynamic effects in HF. The combination of hydralazine and nitrates, however, does not provide the important neurohormonal blockade benefit associated with ACE inhibitors or ARBs. Despite this, a clear mortality benefit has been present with the use of this combination when ACE inhibitors or ARBs are contraindicated, especially in the Black population.

The current ACC/AHA guidelines provide the following two recommendations for the use of hydralazine and isosorbide dinitrate in patients with Stage C HFrEF:

• The combination of hydralazine and isosorbide dinitrate is recommended (Class I recommendation) to reduce morbidity and mortality for patients self-described as Black with NYHA class III–IV HFrEF receiving optimal medical therapy, unless contraindicated [Heidenreich 2022:38b(e933)]
• A combination of hydralazine and isosorbide dinitrate can be useful (Class IIB recommendation) to reduce morbidity or mortality in patients with current or prior symptomatic HFrEF who cannot be given an ARNI, ACE inhibitor or ARB because of drug intolerance or renal insufficiency, unless contraindicated [Heidenreich 2022:38b(e933)]

Mechanical Therapy

The treatment of HF with therapies other than medications, such as the use of devices, is considered mechanical therapy. This includes biventricular pacing, implantable cardioverter defibrillators and left ventricular assist devices.

Biventricular Pacing

Biventricular pacing or cardiac resynchronization therapy (CRT) improves HF symptoms in properly selected patients with QRS prolongation (generally left bundle branch block [LBBB]) and dyssynchronous ventricular contraction. The normal cardiac conduction system delivers the electrical impulse to both the right and left ventricles simultaneously; however, in the presence of left bundle branch block, lateral wall contraction is delayed. The resulting cardiac dyssynchrony results in impairment of left ventricular function.

The current ACC/AHA guidelines include the following recommendations on the use of CRT in patients with Stage C HFrEF: [Heidenreich 2022:46b(e941)]

• CRT is indicated (Class I recommendation) for patients who have LVEF ≤ 35%, sinus rhythm, LBBB with a QRS ≥ 150 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT
• CRT can be useful (Class IIa recommendation) for patients who have LVEF ≤ 35%, sinus rhythm, a non-LBBB pattern with QRS ≥ 150 ms, and NYHA class III/ambulatory class IV symptoms on GDMT
• CRT can be useful (Class IIa recommendation) for patients who have LVEF ≤ 35%, sinus rhythm, LBBB with a QRS 120 to 149 ms, and NYHA class II, III, or ambulatory IV symptoms on GDMT
• CRT can be useful (Class IIa recommendation) in patients with AF and LVEF ≤ 35% on GDMT if:
  
  • a) the patient requires ventricular pacing or otherwise meets CRT criteria and
  • b) AV nodal ablation or rate control allows near 100% ventricular pacing with CRT
• CRT can be useful for patients (Class IIa recommendation) on GDMT who have LVEF ≤ 35% and are undergoing new or replacement device implantation with anticipated ventricular pacing (> 40%)
• CRT may be considered (Class IIb recommendation) for patients who have LVEF ≤ 35%, sinus rhythm, a non-LBBB pattern with a QRS duration of 120 to 149 ms, and NYHA class III/ambulatory class IV on GDMT
• CRT may be considered (Class IIb recommendation) for patients who have LVEF ≤ 30%, ischemic etiology of HF, sinus rhythm, LBBB with QRS ≥ 150 ms, and NYHA class I symptoms on GDMT

CRT is not indicated for patients whose comorbidities and/or frailty limit survival to less than 1 year, for patients with QRS duration < 120 ms or for patients with NYHA Class I or II symptoms and a non-LBBB pattern with QRS < 150 ms. [Heidenreich 2022:47a(e942)]

To maximize benefit, biventricular pacing should occur with 98% of ventricular contractions. In patients with AF, short RR-intervals may occur frequently enough that this threshold is not reached. Thus, patients with permanent AF undergoing biventricular pacing, should undergo AV nodal ablation as well in order to achieve 100% biventricular pacing.

Many patients who are candidates for biventricular pacing receive devices that have the capacity for defibrillation as well (CRT-D).

Implanted Cardioverter Defibrillator

An implantable cardioverter defibrillator (ICD) is a permanent implanted electrical device that until quite recently required a transvenous lead system much like a permanent pacemaker; combination pacemaker-ICDs were often employed. Currently, the introduction of subcutaneous ICDs, and leadless pacemakers, is dramatically changing the landscape of device therapy.

The current ACC/AHA guidelines provide the following two recommendations for the use of ICDs for primary prevention of sudden cardiac death (SCD) in patients with HFrEF: [Heidenreich 2022:46b(e941)]

• ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤ 35% and NYHA class II or III symptoms on chronic GDMT, who are expected to live more than 1 year
• ICD therapy is recommended for primary prevention of SCD in selected patients with HFrEF at least 40 days post-MI with LVEF ≤ 30% and NYHA class I symptoms while receiving GDMT, who are expected to live more than 1 year

ICDs are also indicated for secondary prevention of SCD regardless of the type of underlying structural heart disease. [Epstein 2008: p27A]

Left Ventricular Assist Device

A left ventricular assist device (LVAD), a form of mechanical circulatory support (MCS), is a surgically implanted cardiac assist pump. A cannula in the left ventricle diverts the pulmonary venous return to the pump and the pump delivers blood to the systemic circulation through an outflow cannula in the proximal aorta. These pumps require an external power source connected through the skin by a driveline, a potential source of infection.

An LVAD may be used in the settings listed below:

• Postoperative cardiogenic shock, not able to be weaned from cardiopulmonary bypass
• Back-up in patients undergoing high-risk surgical procedures
• Massive myocardial infarction without other therapeutic options
• Severe cardiac decompensation (regardless of cause), such as progression of a nonischemic cardiomyopathy
• Bridge to transplantation
• Destination therapy for chronic HF with a poor prognosis but not a transplant candidate.

Special Situations – Chronic Heart Failure -HFrEF

Heart Failure Exacerbations

The terms “acute decompensated heart failure” (ADHF) or “heart failure exacerbation” describe new-onset HF or, more commonly, situations when a volume-overloaded HF patient presents with rapid and unexpected symptomatic deterioration.

Determining the precipitating factors for a HF exacerbation will help to direct medical therapy appropriately — not only to improve the current HF symptoms, but to prevent recurrence.

Every patient with HF presenting to the ED or hospital ward should be evaluated for the following:

• Dietary noncompliance: Consuming large amounts of fluids and/or sodium can result in volume overload, causing symptoms of HF and eventual pulmonary edema
• Medication noncompliance: Frequently, diuretics are not taken as prescribed due to the nuisance of increased urine volume. Also, increased peripheral resistance and loss of neurohormonal blockade from not taking other cardiovascular medications may contribute
• Ischemia: Acute coronary syndromes or progression of ischemic heart disease can cause HF exacerbations. Patients with acute decompensated HF should have at least an ECG and cardiac enzymes evaluated
• Arrhythmia: Multiple different arrhythmias, particularly atrial fibrillation, can occur in patients with HF, resulting in worsening volume overload
• Progression of underlying heart disease: Worsening of the primary cause of the patient’s HF, such as worsening valvular heart disease or a further decline in LV function with either ischemic or nonischemic cardiomyopathies, can trigger HF exacerbations
• Noncardiac illness: Fever, pneumonia with hypoxia, severe sepsis with hypotension and anemia due to gastrointestinal bleeding are examples of conditions that require increased cardiac output. In patients with impaired ventricular function, these illnesses can trigger clinical HF

Heart Transplantation

Heart transplantation provides highly effective therapy for end-stage HF in carefully selected individuals. However, the limited availability of donor organs restricts transplantation as an option. HF patients should be referred to an HF program capable of heart transplantation for consultation if cardiopulmonary stress testing shows the maximal oxygen consumption, or VO2 max, is less than 14 mL/kg.
Heart transplantation is contraindicated in patients with severe fixed pulmonary hypertension or significant non-cardiac illness with limited survival.

References:

• Epstein AE, et al. Circulation. 2008;doi:10.1161/CIRCULATIONAHA.108.189742.
• Heidenreich PA, et al. Circulation. 2022;doi:10.1161/CIR.0000000000001063.
• Hurst’s the Heart, 13th Edition (2018). Section 11: Heart Failure.
• Joshi SS, et al. Heart. 2021;doi:10.1136/heartjnl-2020-318060.
• Murphy SP, et al. JAMA. 2020;doi:10.1001/jama.2020.10262.
• Rovai D, et al. Eur J Heart Fail. 2007;doi:10.1016/j.eheart.2007.02.002.

Which of the following is a compensatory response to decreased cardiac output?

What are the 4 compensatory mechanisms of heart failure?

What are the three compensatory mechanism for heart failure?

Which compensatory mechanism is triggered by sympathetic responses to heart failure?