HEART FAILURE
Definition Heart failure is a complex pathophysiologic state described by the inability of the heart to fill with or eject blood at a rate appropriate to meet tissue requirements. The clinical syndrome is characterized by symptoms of dyspnea and fatigue and signs of circulatory congestion or hypoperfusion.
Etiology
Heart failure is a clinical syndrome arising from diverse causes. The principal pathophysiology of heart failure is the inability of the heart to fill or empty the ventricle. Heart failure is most often due to (1) impaired myocardial contractility secondary to ischemic heart disease or cardiomyopathy; (2) cardiac valve abnormalities; (3) systemic hypertension; (4) diseases of the pericardium; or (5) pulmonary hypertension (cor pulmonale). The most common cause of right ventricular failure is left ventricular (LV) failure.Heart failure may be described in various ways: systolic or diastolic, acute or chronic, left sided or right sided, high output or low output. Early in the course of heart failure, the various categories may have different clinical and therapeutic implications. Ultimately, however, all forms of heart failure develop high ventricular end-diastolic pressure due to altered ventricular function and neurohormonal regulation.
SYSTOLIC AND DIASTOLIC HEART FAILURE
Decreased ventricular systolic wall motion reflects systolic dysfunction, whereas diastolic dysfunction is characterized by abnormal ventricular relaxation and reduced compliance. There are differences in both myocardial architecture and function in SHF and DHF. Clinical signs and symptoms do not reliably differentiate systolic dysfunction from diastolic dysfunction.
Systolic Heart Failure
A decreased ejection fraction, the hallmark of chronic LV systolic dysfunction, is closely related to the increase in the diastolic volume of the left ventricle ( Fig. 6-1 ). Measuring the LV ejection fraction via echocardiography, radionuclide imaging or ventriculography provides the quantification necessary to document the severity of ventricular systolic dysfunction.
diastolic Heart Failure
Symptomatic heart failure in patients with normal or near-normal LV systolic function is most likely due to diastolic dysfunction.
Class I DHF is characterized by an abnormal LV relaxation pattern with normal left atrial pressure. Classes II, III, and IV are characterized by abnormal relaxation as well as reduced LV compliance resulting in an increase in LV end-diastolic pressure (LVEDP). As a compensatory mechanism, the pressure in the left atrium increases so that LV filling can occur despite the increase in LVEDP. Factors that predispose to decreased ventricular distensibility include myocardial edema, fibrosis, hypertrophy, aging, and pressure overload.
Ischemic heart disease, long-standing essential hypertension, and progressive aortic stenosis are the most common causes of DHF. In contrast to SHF, DHF affects women more than men. Hospitalization and mortality rates are similar in patients with SHF and DHF. The major differences between SHF and DHF are presented in Table 6-1 .
TABLE 6–1 -- Characteristics of Patients with Diastolic Heart Failure and Patients with Systolic Heart Failure
ACUTE AND CHRONIC HEART FAILURE
Acute heart failure is defined as a change in the signs and symptoms of heart failure requiring emergency therapy. Chronic heart failure is present in patients with long-standing cardiac disease. Typically, chronic heart failure is accompanied by venous congestion, but blood pressure is maintained. In acute heart failure due to a sudden decrease in cardiac output, systemic hypotension is typically present without signs of peripheral edema. Acute heart failure encompasses three clinical entities: (1) worsening chronic heart failure; (2) new-onset heart failure such as with cardiac valve rupture, large myocardial infarction, or severe hypertensive crisis; and (3) terminal heart failure, which is refractory to therapy.
LEFT-SIDED AND RIGHT-SIDED HEART FAILURE
The clinical signs and symptoms of heart failure are produced by increased ventricular pressures and subsequent fluid accumulation upstream from the affected ventricle. In left-sided heart failure, high LVEDP promotes pulmonary venous congestion. The patient complains of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea, which can evolve to pulmonary edema.
Right-sided heart failure causes systemic venous congestion. Peripheral edema and congestive hepatomegaly are the most prominent clinical manifestations. Right-sided heart failure may be caused by pulmonary hypertension or right ventricular myocardial infarction, but the most common cause is left-sided heart failure.
LOW-OUTPUT AND HIGH-OUTPUT HEART FAILURE
The normal cardiac index varies between 2.2 and 3.5 L/min/m2. It may be difficult to diagnose low-output heart failure because a patient may have a cardiac index that is nearly normal in the resting state but does not respond adequately to stress or exercise. The most common causes of low-output heart failure are CAD, cardiomyopathy, hypertension, valvular disease, and pericardial disease.
Causes of high cardiac output include anemia, pregnancy, arteriovenous fistulas, severe hyperthyroidism, beriberi, and Paget's disease. The ventricle fails not only because of the increased hemodynamic burden placed on it but also because of direct myocardial toxicity as caused by thyrotoxicosis and beriberi and myocardial anoxia caused by severe and prolonged anemia.
PATHOPHYSIOLOGY OF HEART FAILURE
Heart failure is a complex phenomenon at both the clinical and cellular levels.
The initiating mechanisms of heart failure are pressure overload (aortic stenosis, essential hypertension), volume overload (mitral or aortic regurgitation), myocardial ischemia/infarction, myocardial inflammatory disease, and restricted diastolic filling (constrictive pericarditis, restrictive myocarditis).
In the failing ventricle, various adaptive mechanisms are initiated to help maintain a normal cardiac output. These include (1) the Frank-Starling relationship; (2) activation of the sympathetic nervous system (SNS); (3) alterations in the inotropic state, heart rate, and afterload; and (4) humoral-mediated responses.
Frank-Starling Relationship
The Frank-Starling relationship describes the increase in stroke volume that accompanies an increase in LV end-diastolic volume and pressure ( Fig. 6-2 ). Stroke volume increases because the tension developed by contracting muscle is greater when the resting length of that muscle is increased. The magnitude of the increase in stroke volume produced by changing the tension of ventricular muscle fibers depends on myocardial contractility. For example, when myocardial contractility is decreased, as in the presence of heart failure, a lesser increase in stroke volume is achieved relative to any given increase in LV end-diastolic pressure. Constriction of venous capacitance vessel shifts blood centrally, increases preload, and helps maintain cardiac output by the Frank-Starling relationship.
Activation of Sympathetic Nervous System
Activation of the SNS promotes arteriolar and venous constriction. Arteriolar constriction serves to maintain systemic blood pressure despite a decrease in cardiac output. Increased venous tone shifts blood from peripheral sites to the central circulation, thereby enhancing venous return and maintaining cardiac output by the Frank-Starling relationship. Furthermore, arteriolar constriction causes redistribution of blood from the kidneys, splanchnic organs, skeletal muscles, and skin to maintain coronary and cerebral blood flow despite overall decreases in cardiac output. The decrease in renal blood flow activates the renin-angiotensin-aldosterone system (RAAS), which increases renal tubular reabsorption of sodium and water, resulting in an increase in blood volume and ultimately cardiac output by the Frank-Starling relationship.
Although heart failure is associated with SNS activation, a down-regulation of β-adrenergic receptors is observed. Plasma and urinary concentrations of catecholamines are increased in patients in heart failure and correlate with worse clinical outcomes. High plasma levels of norepinephrine are directly cardiotoxic and promote myocyte necrosis and cell death, which lead to ventricular remodeling. Therapy with β-blockers attempts to decreases these deleterious effects of catecholamines on the heart.
Alterations in the Inotropic State, Heart Rate, and Afterload
The inotropic state describes myocardial contractility as reflected by the velocity of contraction developed by cardiac muscle. The maximum velocity of contraction is referred to as Vmax. When the inotropic state of the heart is increased, as in the presence of catecholamines, Vmax is increased. Conversely, Vmax is decreased when myocardial contractility is impaired as in heart failure.
Afterload is the tension the ventricular muscle must develop to open the aortic or pulmonic valve. The afterload presented to the left ventricle is increased in the presence of systemic arteriolar constriction and hypertension. The forward LV stroke volume in patients with heart failure can be increased by administering vasodilating drugs.
In the presence of SHF and low cardiac output, the stroke volume is relatively fixed with any increase in CO being dependent on an increase in heart rate. Tachycardia is an expected finding in the presence of SHF with a low ejection fraction and reflects activation of the sympathetic nervous system. However, in the presence of DHF, tachycardia can produce a decrease in CO due to inadequate ventricular filling time. Therefore, heart rate control is a target for therapy of DHF.
Humoral-Mediated Responses and Biochemical Pathways
As heart failure progresses, various neurohumoral pathways are activated in order to maintain adequate cardiac output during exercise and ultimately even at rest.
Generalized vasoconstriction is initiated via several mechanisms including increased activity of the SNS and RAAS, parasympathetic withdrawal, high levels of circulating vasopressin, endothelial dysfunction, and release of inflammatory mediators.
In an attempt to counterbalance these mechanisms, the heart evolves into “an endocrine organ.” This concept emerged more than 20 years ago when Bold and colleagues reported the presence of a potent diuretic and vasodilator in the atria of rats. Atrial natriuretic peptide is stored in atrial muscle and released in response to increases in atrial pressures, such as produced by tachycardia or hypervolemia. More recently, B-type natriuretic peptide (BNP) was discovered. It is secreted by both the atrial and ventricular myocardium. In the failing heart, the ventricle becomes the principal site for BNP production.
The natriuretic peptides promote blood pressure control and protect the cardiovascular system from the effects of volume and pressure overload.
Physiologic effects of the natriuretic peptides include diuresis, natriuresis, vasodilation, antihypertrophy, anti-inflammation, and inhibition of the RAAS and SNS.
Myocardial Remodeling
Myocardial remodeling is the result of the various endogenous mechanisms that the body uses to maintain cardiac output. It is the process by which mechanical, neurohormonal, and genetic factors change the LV size, shape, and function. The process includes myocardial hypertrophy, myocardial dilation and wall thinning, increased interstitial collagen deposition, myocardial fibrosis, and scar formation due to myocyte death. Myocardial hypertrophy represents the compensatory mechanism to chronic pressure overload. This mechanism is limited because hypertrophied cardiac muscle functions at a lower inotropic state than normal cardiac muscle. Cardiac dilation occurs in response to volume overload and increases the CO by the Frank-Starling relationship. However, increased cardiac wall tension produced by the enlarged ventricular radius is also associated with increased myocardial oxygen requirements and decreased cardiac efficiency. The most common cause of myocardial remodeling is ischemic injury, and it encompasses both hypertrophy and dilation of the left ventricle. Angiotensin-converting enzyme inhibitors (ACEIs) have been proven to promote a “reverse-remodeling” process. Therefore, they are first-line therapy for heart failure.
SIGNS AND SYMPTOMS OF HEART FAILURE
Symptoms of Heart Failure
Dyspnea reflects increased work of breathing due to stiffness of the lungs produced by interstitial pulmonary edema. It is one of the earliest subjective findings of LV failure. Initially, this symptom occurs only with exertion. It can be quantified by asking the patient how many flights of stairs can be climbed or the distance that can be walked at a normal pace before dyspnea occurs. Patients experiencing angina pectoris may interpret substernal discomfort as breathlessness. Dyspnea can be caused by many other diseases such as asthma, chronic obstructive pulmonary disease (COPD), airway obstruction, anxiety, and neuromuscular weakness. Dyspnea related to heart failure will be linked to other supporting evidence such as a history of orthopnea, paroxysmal nocturnal dyspnea, a third heart sound, rales on physical examination, and elevated BNP levels.
Orthopnea reflects the inability of the failing left ventricle to handle the increased venous return associated with the recumbent position. Clinically, this will be manifested as a dry, nonproductive cough that develops when in the supine position and that is relieved by sitting up. The orthopneic cough differs from the productive morning cough characteristic of patients with chronic bronchitis and must be differentiated from the cough produced by ACEIs. Paroxysmal nocturnal dyspnea is shortness of breath that awakens a patient from sleep. This symptom must be differentiated from anxiety-provoked hyperventilation or wheezing due to accumulation of secretions in patients with chronic bronchitis. Paroxysmal nocturnal dyspnea and wheezing caused by pulmonary congestion (“cardiac asthma”) are accompanied by radiographic evidence of pulmonary congestion.
A hallmark of decreased cardiac reserve and low cardiac output is fatigue and weakness at rest or with minimal exertion. During exercise, the failing ventricle is unable to increase its output in order to deliver adequate amounts of oxygen to the muscles. These findings, although nonspecific, are very common in patients with heart failure.
Heart failure patients may complain of anorexia, nausea, or abdominal pain related to increased liver congestion and prerenal azotemia. Decreases in cerebral blood flow may produce confusion, difficulty concentrating, insomnia, anxiety, or memory deficits. Nocturia may contribute to insomnia.
Physical Examination
The classic physical findings in patients with LV failure are tachypnea and the presence of moist rales. These rales may be confined to the lung bases in patients with a mild degree of LV failure, or they may be diffuse in those with acute pulmonary edema. Other findings in heart failure include resting tachycardia and a third heart sound (S3 gallop or ventricular diastolic gallop). This heart sound is produced by blood entering and distending a relatively noncompliant left ventricle. Despite peripheral vasoconstriction, severe heart failure may manifest as systemic hypotension with cool and pale extremities. Lip and nail bed cyanosis may be present. A narrow pulse pressure with a high diastolic pressure reflects a decreased stroke volume. Marked weight loss, also known as cardiac cachexia, is a sign of severe chronic heart failure. Weight loss is caused by a combination of factors including an increase in the metabolic rate, anorexia and nausea, decreased intestinal absorption of food caused by splanchnic venous congestion, and the presence of high levels of circulating cytokines.
In the presence of right heart or biventricular failure, jugular venous distention may be present or inducible by pressing on the liver (hepatojugular reflux). The liver is typically the first organ to become engorged with blood in the presence of right or biventricular failure. The hepatic engorgement may be associated with right upper quadrant pain and tenderness or even jaundice in severe cases. Pleural effusions (usually right sided) may be present. Bilateral pitting pretibial leg edema is typically present with right ventricular failure and reflects both venous congestion and sodium and water retention.
DIAGNOSIS OF HEART FAILURE
The diagnosis of heart failure is based on the history, physical examination, and interpretation of laboratory and diagnostic tests. The signs and symptoms of heart failure have already been noted.
Laboratory Diagnosis
The use of serum BNP as a biomarker for heart failure has helped physicians establish the etiology of dyspnea. Plasma BNP levels below 100 pg/mL indicate that heart failure is unlikely (90% negative predictive value); BNP in the range of 100 to 500 pg/mL suggests an intermediate probability for heart failure; levels above 500 pg/mL are consistent with the diagnosis of heart failure (90% positive predictive value). Plasma levels of BNP may be affected by other factors such as sex, advanced age, renal clearance, obesity, pulmonary embolism, atrial fibrillation, and/or other cardiac tachydysrhythmias. Therefore, these factors have an impact on the interpretation of BNP levels.
A complete metabolic profile is indicated in the evaluation of patients with heart failure. Decreases in renal blood flow may lead to prerenal azotemia characterized by a disproportionate increase in blood urea nitrogen concentration relative to the serum creatinine concentration. When moderate liver congestion is present, liver function tests may be mildly elevated, and when liver engorgement is severe, the prothrombin time may be prolonged. Hyponatremia, hypomagnesemia, and hypokalemia may be present.
Electrocardiography
Patients with heart failure usually have an abnormal 12-lead electrocardiogram (ECG). Therefore, this test has a low predictive value for the diagnosis of heart failure. The ECG may show evidence of a previous myocardial infarction, LV hypertrophy, conduction abnormalities (left bundle branch block, widened QRS), or various cardiac dysrhythmias, especially atrial fibrillation and ventricular dysrhythmias.
Chest Radiography
Chest radiography (posteroanterior and lateral) may be useful in the evaluation of a heart failure patient by detecting the presence of pulmonary disease, cardiomegaly, pulmonary venous congestion, and interstitial or alveolar pulmonary edema.
Echocardiography
Echocardiography is the most useful test in the diagnosis of heart failure. A comprehensive two-dimensional echocardiogram coupled with Doppler flow examination can assess whether any abnormalities of the myocardium, cardiac valves, or pericardium are present. This examination addresses the following topics: ejection fraction, LV structure and functionality, the presence of other structural abnormalities such as valvular and pericardial disease and the presence of diastolic dysfunction and right ventricular function. This information can be presented as numerical estimates of ejection fraction, LV size and wall thickness, left atrial size, and pulmonary artery pressure. Assessment of diastolic function provides information about LV filling and left atrial pressure. A preoperative echocardiographic evaluation can serve as a baseline for comparison with perioperative echocardiography if a patient's condition deteriorates
CLASSIFICATION OF HEART FAILURE
Heart failure has been classified in various ways. The most commonly used classification is that of the New York Heart Association and is based on the functional status of the patient at a particular time. Functional status may worsen or improve. These patients have structural heart disease and symptoms of heart failure. There are four functional classes:
Class I: Ordinary physical activity does not cause symptoms
Class II: Symptoms occur with ordinary exertion
Class III: Symptoms occur with less than ordinary exertion
Class IV: Symptoms occur at rest
This classification is useful because the severity of the symptoms has an excellent correlation with survival and quality of life. However, the American College of Cardiology and the American Heart Association published the 2005 Guideline Update for the Diagnosis and Management of Chronic Heart Failure and introduced a new classification based on the progression of the disease. This classification has four stages:
Stage A: Patients at high risk of heart failure but without structural heart disease or symptoms of heart failure
Stage B: Patients with structural heart disease but without symptoms of heart failure
Stage C: Patients with structural heart disease with previous or current symptoms of heart failure
Stage D: Patients with refractory heart failure requiring specialized interventions
This classification is meant to be complementary to the New York Heart Association classification and to be used in guiding therapy.
MANAGEMENT OF HEART FAILURE
Management of Chronic Heart Failure
The current recommended therapy of chronic heart failure is based on results of large, adequately powered, randomized trials and on the American College of Cardiology/American Heart Association and European Society of Cardiology guidelines for the diagnosis and treatment of chronic heart failure. According to these guidelines, treatment options include lifestyle modification, patient and family education, medical therapy, corrective surgery, implantable devices, and cardiac transplantation.
Management of Systolic Heart Failure
The major classes of drugs used for medical management of SHF include inhibitors of RAAS, β-adrenergic blockers, diuretics, digoxin, vasodilators, and statins. Most heart failure patients are managed on a combination of drugs. Therapy with ACEIs and β-blockers favorably influences long-term outcome.
Inhibitors of the Renin-Angiotensin-Aldosterone System
Inhibition of the RAAS can be performed at several levels: by inhibiting the enzyme that converts angiotensin I to angiotensin II, by blocking the angiotensin II receptor, or by blocking the aldosterone receptor.
Angiotensin-Converting Enzyme Inhibitors
ACEIs block the conversion of angiotensin I to angiotensin II. This decreases the activation of the RAAS and decreases the degradation of bradykinin. Beneficial effects include promoting vasodilation, reducing water and sodium reabsorption, and supporting potassium conservation. This class of drugs has been proven to decrease ventricular remodeling and even to potentiate the “reverse-remodeling” phenomenon. In large clinical trials, ACEIs have consistently been shown to reduce morbidity and mortality of patients in any stage of heart failure. For this reason, they are considered the first line of treatment in heart failure. It appears, however, that the African American population does not derive as much clinical benefit from ACEI therapy as the white population. Side effects of ACEIs include hypotension, syncope, renal dysfunction, hyperkalemia, and development of a nonproductive cough and angioedema. Treatment with ACEIs should be started at low doses to avoid significant hypotension. Then the dose can be gradually increased until the target dose defined by clinical trials is reached.
Angiotensin II Receptor Blockers
As their name implies, angiotensin receptor blockers block angiotensin II receptors. These drugs have similar but not superior efficacy compared to ACEIs. Currently, angiotensin receptor blockers are only recommended for patients who cannot tolerate ACEIs. In some patients treated with ACEIs, angiotensin levels may return to normal due to alternative pathways of angiotensin production. Such patients may benefit from the addition of an angiotensin receptor blocker to the medical therapy.
Aldosterone Antagonists
In advanced stages of heart failure, there are high circulating levels of aldosterone. Aldosterone stimulates sodium and water retention, hypokalemia, and ventricular remodeling. Spironolactone, an aldosterone antagonist, may reverse all these effects. There is strong clinical evidence showing reduced mortality and hospitalization rates with the use of a low dose of aldosterone antagonist in New York Heart Association class III and IV patients. During therapy with spironolactone, patients should have renal function and potassium levels monitored and the dose of spironolactone adjusted accordingly.
β-Blockers
β-Blockers are used to reverse the harmful effects of SNS activation in heart failure. Recent clinical trials have consistently shown that these drugs reduce morbidity and the number of hospitalizations and improve both quality of life and survival. β-Blockers improve the ejection fraction and decrease ventricular remodeling. American College of Cardiology and the American Heart Association guidelines recommend β-blockers as an integral part of the therapy for heart failure. Caution should be used when administering β-blockers to patients with reactive airway disease, diabetics with frequent hypoglycemic episodes, and patients with bradydysrhythmias or heart block.
Diuretics
Diuretics can relieve circulatory congestion and the accompanying pulmonary and peripheral edema more rapidly than any other drugs. Symptomatic improvement can be noted within hours. Diuretic-induced decreases in ventricular diastolic pressure will decrease diastolic ventricular wall stress and prevent the persistent cardiac distention that interferes with subendocardial perfusion and negatively affects myocardial metabolism and function. Thiazide and/or loop diuretics are recommended as an essential part of the therapy of heart failure. Potassium and magnesium supplementation may be needed in patients chronically treated with diuretics in order to prevent cardiac dysrhythmias. Excessive doses of diuretics may cause hypovolemia, prerenal azotemia, or an undesirably low cardiac output and are associated with worse clinical outcomes.
Digitalis
Digitalis enhances the inotropy of cardiac muscle and decreases activation of the SNS and the RAAS. These latter effects are related to the ability of digitalis to restore the inhibitory effects of cardiac baroreceptors on central SNS outflow. It is unclear whether digitalis treatment improves survival, but digoxin may impede the worsening of heart failure and result in fewer hospitalizations. Digitalis can be added to standard therapy when patients are still symptomatic despite treatments with diuretics, ACEIs, and β-blockers. Patients with the combination of atrial fibrillation and heart failure present another subgroup that may benefit from digoxin therapy. Caution should be used when administering this drug to elderly patients or to those with impaired renal function since they are particularly prone to development of digitalis toxicity. Manifestations of digitalis toxicity include anorexia, nausea, blurred vision, and cardiac dysrhythmias. Treatment of toxicity may include reversing hypokalemia, treating cardiac dysrhythmias, administering antidigoxin antibodies, and/or placing a temporary cardiac pacemaker.
Vasodilators
Vasodilator therapy relaxes vascular smooth muscle, decreases resistance to LV ejection, and increases venous capacitance. In patients with dilated left ventricles, administration of vasodilators results in increased stroke volume and decreased ventricular filling pressures. African Americans seem to respond very well to vasodilator therapy and show improved clinical outcomes when treated with a combination of hydralazine and nitrates.
Statins
By their anti-inflammatory and lipid-lowering effects, statins have been proven to decrease morbidity and mortality in patients with SHF. Promising studies suggest that DHF patients could derive similar benefits from statin therapy.
Management of Diastolic Heart Failure
The management of SHF is based on the results of large-scale randomized trials, but the therapy of DHF remains mostly empirical. It is generally accepted that the best treatment strategy for DHF is prevention. American College of Cardiology and the American Heart Association guidelines recommend that patients at risk of developing DHF should be preemptively treated. Unfortunately, there are no drugs that selectively improve diastolic distensibility. Current treatment options include a low-sodium diet, cautious use of diuretics to relieve pulmonary congestion without an excessive decrease in preload, maintenance of normal sinus rhythm at a heart rate that optimizes ventricular filling, and correction of precipitating factors such as acute myocardial ischemia and systemic hypertension. Long-acting nitrates and diuretics may alleviate the symptoms of DHF but do not alter the natural history of the disease. Statin therapy early in the course of the disease may play an important role in decreasing ventricular remodeling and reducing disease progression. The general concepts of managing patients with DHF are outlined in Table 6-2 .
TABLE 6–2 -- Management Strategies for Diastolic Heart Failure
Goals | Management Strategies | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Prevent development of diastolic heart failure by decreasing risk factors | |||||||||||||
Allow adequate filling time of left ventricle by decreasing heart rate | β-Blockers, calcium channel blockers, digoxin | ||||||||||||
Control volume overload | Diuretics, long-acting nitrates, low-sodium diet |
Restore and maintain sinus rhythm | Cardioversion, amiodarone, digoxin | ||||||
Decrease ventricular remodeling | Angiotensin-converting enzyme inhibitors, statins | ||||||
Correct precipitating factors |
Management of Acute Heart Failure
Patients may experience acute heart failure as a result of decompensated chronic heart failure or de novo. Anesthesiologists deal with acute heart failure when caring for patients in overt heart failure who present for emergency surgery or patients who decompensate intraoperatively. Acute heart failure therapy has three phases: the emergency phase, the in-hospital management phase, and the predischarge phase. For the anesthesiologist, the emergency phase is of most interest and is the phase that is addressed here.
The hemodynamic profile of acute heart failure is characterized by high ventricular filling pressures, low cardiac output, and hyper- or hypotension. Traditional therapy includes diuretics, vasodilators, inotropic drugs, mechanical assisted devices (intra-aortic balloon pump, ventricular assist device), and emergency cardiac surgery. Newer therapy includes calcium sensitizers, exogenous BNP, and nitric oxide synthase inhibitors.
Diuretics and Vasodilators
Loop diuretics can improve symptoms rapidly, but in high doses, they may have deleterious effects on clinical outcomes. It may be more desirable to use a combination of a low dose of loop diuretic with an intravenous vasodilator. Nitroglycerin and nitroprusside reduce LV filling pressure and systemic vascular resistance and increase stroke volume. However, nitroprusside may have a negative impact on clinical outcome in patients with acute myocardial infarction.
Inotropic Support
Positive inotropic drugs have been the mainstay of treatment for patients in cardiogenic shock. Their positive inotropic effect is produced via an increase in cyclic adenosine monophosphate, which promotes an increase in intracellular calcium levels and, thereby, an improvement in excitation-contraction coupling. Catecholamines (epinephrine, norepinephrine, dopamine, and dobutamine) do so by direct β-receptor stimulation, whereas phosphodiesterase inhibitors (amrinone, milrinone) block the degradation of cyclic adenosine monophosphate. Side effects of inotropic drugs include tachycardia, increased myocardial energy demand and oxygen consumption, dysrhythmias, worsening of DHF, and down-regulation of β-receptors. Long-term use of these drugs may result in cardiotoxicity and accelerate myocardial cell death.
Calcium Sensitizers
Myofilament calcium sensitizers are a new class of positive inotropic drugs that increase contractility without increasing intracellular levels of calcium. Therefore, there is no significant increase in myocardial oxygen consumption or heart rate and no propensity for dysrhythmias. The most widely used medication in this class is levosemindan. It is an inodilator increasing myocardial contractile strength and promoting dilation of systemic, pulmonary, and coronary arteries. It does not worsen diastolic function. Studies have shown that levosemindan may be particularly useful in the setting of myocardial ischemia. Levosemindan is included in the European guidelines for treatment of acute heart failure, but it is not yet available for use in the United States.
Exogenous B-Type Natriuretic Peptide
Nesiritide (Natrecor) is recombinant BNP that binds to both the A- and B-type natriuretic receptors. It promotes arterial, venous, and coronary vasodilation, thereby decreasing LVEDP and improving dyspnea. Nesiritide induces diuresis and natriuresis. It has many effects similar to nitroglycerin but generally produces less hypotension and more diuresis than nitroglycerin.
Nitric Oxide Synthase Inhibitors
The inflammatory cascade stimulated by heart failure results in production of a large amount of nitric oxide in the heart and vascular endothelium. These high levels of nitric oxide have a negative inotropic and profound vasodilatory effect leading to cardiogenic shock and vascular collapse. Inhibition of nitric oxide synthase should decrease these harmful effects. L-NAME (N-nitro-L-arginine methyl ester) is the principal drug in this class under investigation.
Mechanical Devices
If the etiology of acute heart failure is a large myocardial infarction, the insertion of an intra-aortic balloon pump should be considered. The intra-aortic balloon pump is a mechanical device inserted via the femoral artery and positioned just below the left subclavian artery. Its balloon inflates in diastole increasing aortic diastolic blood pressure and coronary perfusion pressure. The balloon deflates in systole creating a “suction” effect that enhances LV ejection. Complications of intra-aortic balloon pump placement include femoral artery or aortic dissection, bleeding, thrombosis, and infection.
In severe cardiogenic shock, emergency insertion of LV and/or right ventricular assist devices may be necessary for survival.
Surgical Management of Heart Failure
Part of the overall management of heart failure includes trying to eliminate the cause of the disease. LV ischemia may be treated with percutaneous coronary interventions or coronary artery bypass surgery. Increasingly severe symptoms in the presence of correctable cardiac valve lesions may be alleviated surgically. Ventricular aneurysmectomy may be useful in patients with large ventricular scars after myocardial infarction. The definitive treatment for heart failure is heart transplantation. However, the limited supply of donors renders this treatment unattainable in most patients.
Ventricular assist devices include extracorporeal membrane oxygenators and implantable pulsatile devices. These mechanical pumps take over function of the damaged ventricle and facilitate restoration of normal hemodynamics and tissue blood flow. These devices may be useful in patients who require ventricular assistance to allow the heart to rest and recover its function and in those who are awaiting cardiac transplantation.
Cardiac resynchronization therapy (CRT) is aimed at patients with advanced stages of heart failure who have a ventricular conduction delay (QRS prolongation on the ECG). Such a conduction delay creates a mechanical dyssynchrony that impairs ventricular function and worsens prognosis. CRT, also known as biventricular pacing, consists of the placement of a dual-chamber cardiac pacemaker but with an additional lead introduced into the coronary sinus/coronary vein until it reaches the dyssynchronous LV wall. With this lead in place, the heart contracts more efficiently and ejects a larger cardiac output. CRT is recommended for New York Heart Association Class II/IV patients with an LV ejection fraction less than 35% and a QRS duration between 120 and 150 milliseconds. Patients undergoing CRT may have fewer symptoms, better exercise tolerance, and improved ventricular function compared to similar patients on pharmacologic therapy alone. The reverse remodeling induced by CRT may also improve survival in these patients. Unfortunately, approximately one third of patients do not respond to this form of therapy.
Implanted cardioverter/defibrillators (ICDs) are used for prevention of sudden death in patients with advanced heart failure. Approximately one half of deaths in heart failure patients are sudden and due to cardiac dysrhythmias. Current recommendations for ICDs in patients at risk of sudden death are listed in Table 6-3 .
TABLE 6–3 -- Indications for Implantable Cardioverter Defibrillator Placement for Prevention of Sudden Death
Cause of Heart Failure | Condition | ||||||
|---|---|---|---|---|---|---|---|
Coronary artery disease | |||||||
All other causes | After first episode of syncope or aborted ventricular tachycardia/ventricular fibrillation |
Cause of Heart Failure
MANAGEMENT OF ANESTHESIA
Preoperative Evaluation and Management
The presence of heart failure has been described as the single most important risk factor for predicting perioperative cardiac morbidity and mortality. In the preoperative period, all precipitating factors for heart failure should be sought and aggressively treated before proceeding with elective surgery.
Patients treated for heart failure are usually on several medications that may affect anesthetic management.
It is generally accepted that diuretics may be discontinued on the day of surgery.
Maintaining β-blocker therapy is essential since many studies have shown that β-blockers reduce perioperative morbidity and mortality.
Due to inhibition of the RAAS, ACEIs may put patients at increased risk of intraoperative hypotension. This hypotension can be treated with a sympathomimetic drug such as ephedrine, an α-agonist such as phenylephrine, or vasopressin or one of its analogues. If ACEIs are being used to prevent ventricular remodeling in heart failure patients and kidney dysfunction in diabetic patients, then stopping the medication for 1 day will not significantly alter these effects. However, if ACEIs are used to treat hypertension, then discontinuing therapy the day of or the day before surgery may result in significant hypertension.
Angiotensin receptor blockers produce profound RAAS blockade and should be discontinued the day before surgery.
Digoxin therapy can be continued until the day of surgery.
Results of recent electrolyte, renal function, and liver function tests and the most recent ECG and echocardiogram should be evaluated.
Intraoperative Management
All types of general anesthetics have been successfully used in patients with heart failure. However, drug doses may need to be adjusted.
Opioids seem to have a particularly beneficial effect in heart failure patients because of their effect on the δ-receptor, which inhibits adrenergic activation. Positive pressure ventilation and positive end-expiratory pressure may be beneficial in decreasing pulmonary congestion and improving arterial oxygenation.
Monitoring is adjusted to the complexity of the operation.
Intra-arterial pressure monitoring is justified when a major operation is required in a patient with heart failure. Monitoring of ventricular filling and fluid status is a more challenging task. Fluid overload during the perioperative period may contribute to the development or worsening of heart failure. Intraoperative use of a pulmonary artery catheter may help in evaluation of optimal fluid loading, but in patients with DHF and poor ventricular compliance, accurate assessment of LV end-diastolic volume may be quite difficult.
Transesophageal echocardiography may be a better alternative, allowing not only monitoring of ventricular filling but also ventricular wall motion and valvular function. However, transesophageal echocardiography requires trained personnel to perform and interpret the study and may not be readily available in all circumstances.
Regional anesthesia is acceptable for suitable operations in heart failure patients. In fact, the modest decrease in systemic vascular resistance secondary to peripheral SNS blockade may increase cardiac output. However, the decreased systemic vascular resistance produced by epidural or spinal anesthesia is not always predictable or easy to control. The pros and cons of regional anesthesia must be carefully weighed in heart failure patients.
Postoperative Management
Patients who have evidence of acute heart failure during surgery should be transferred to an intensive care unit where invasive monitoring can be continued postoperatively. Pain should be aggressively treated since its presence and hemodynamic consequences may worsen heart failure. Patients should have their usual medications restarted as soon as possible.
management of patients with decompensated heart failure
In general patients in decompensated HF are not candidates for elective procedures. Waiting
a few days to optimize cardiac performance is indicated. In emergent circumstances invasive
monitoring (arterial line, pulmonary artery catheter) is indicated to guide fluid therapy and
assess response to anesthetic agents and inotropic or vasodilator therapy. Transesophageal
echocardiography is extremely helpful to evaluate the effect of the fluid therapy on the heart,
measure stroke volume and CO, and evaluate systolic and diastolic function
anesthetic agents can be used in decompensated heart failureAvoiding myocardial depression still remains the goal of anesthetic management. The
barbiturates and propofol generally produce the most profound depression of cardiac function
and blood pressure when used for induction of general anesthesia. Etomidate produces few
aberrations in cardiovascular status, although hypotension may occur in the setting of
hypovolemia. Ketamine administration may result in elevated CO and blood pressure secondary
to increased sympathetic activity. However, in patients with increased sympathetic activation
from decompensated HF, ketamine acts as a negative inotropic agent and can cause severe
hypotension and cardiac failure. Cardiovascular side effects (decreasing blood pressure) are
mild when benzodiazepines are given in sedative doses but become moderate when induction
doses are given or when administered in combination with opioids. All of the potent volatile
anesthetic agents are myocardial depressants, but low doses are usually well tolerated.
For the patient with severely compromised myocardial function, narcotic-based anesthesia
with or without low-dose volatile agent is useful. Remifentanil, a short-acting opioid, can
be well suited especially to short surgical procedures.
Regional anesthesia
Regional anesthesia, when prudently administered, is an acceptable anesthetic technique.
In fact, modest afterload reduction may enhance CO. Continuous regional techniques (spinal or
epidural) are preferable because they are associated with gradual loss of sympathetic tone,
which may be treated with titration of fluids and vasoactive drugs. Invasive monitoring is
necessary during regional anesthesia. An arterial line is important to keep the blood pressure
in an appropriate range, and pulmonary artery catheter can be helpful in selected cases.
Support of the heart in decompensated heart failure during anesthesia
Patients with HF often require circulatory support intraoperatively and after surgery. After
optimization of preload and afterload, inotropic drugs such as dopamine or dobutamine have
been shown to be effective in low output states and produce modest changes in systemic
vascular resistance at lower doses. In severe failure more potent drugs such as epinephrine
may be required. Phosphodiesterase III inhibitors such as milrinone, with inotropic and
vasodilating properties, may improve hemodynamic performance. Stroke volume is inversely
related to afterload in the failing ventricle, and the reduction of LV afterload with vasodilating
drugs such as nitroprusside and nesiritide is also effective to increase CO.
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