3 Describe the classification of heart failure

Stage A: Patients with coronary artery disease, hypertension, or diabetes mellitus who do not yet demonstrate impaired left ventricular (LV) function, LV hypertrophy, or geometric chamber distortion

Stage B: Patients who are asymptomatic but demonstrate LV hypertrophy, geometric chamber distortion, and/or impaired LV systolic or diastolic function

Stage C: Patients with current or past symptoms of HF associated with underlying structural heart disease

Stage D: Patients with HF refractory to medical therapy that might be eligible for specialized advanced treatment strategies such as mechanical circulatory support, procedures to facilitate fluid removal, continuous inotropic infusions, cardiac transplantation, or end-of-life care.

This classification system recognizes that there are established risk factors and structural prerequisites for the development of HF (stages A and B) and that therapeutic interventions introduced even before the appearance of LV dysfunction or symptoms can reduce the morbidity and mortality of HF.

4 How is the severity of heart failure classified?

Typically the status of patients with heart failure can be classified on the basis of symptoms, impairment of lifestyle, or severity of cardiac dysfunction. The New York Heart Association (NYHA) classification is used to assess symptomatic limitations of heart failure and response to therapy:

Class I: Ordinary physical activity does not cause symptoms. Dyspnea occurs with strenuous or prolonged exertion at work or with recreation.

Class II: Ordinary physical activity results in symptoms. Dyspnea is occurring while walking or climbing stairs rapidly or walking uphill. Walking more than two blocks on the level and climbing more than one flight of ordinary stairs at a normal pace results in symptoms.

Class III: Less than ordinary activity results in symptoms. Dyspnea occurs with walking one to two blocks on the level or climbing one flight of stairs at a normal pace.

Class IV: Dyspnea occurs at low level of physical activity or at rest.

The NYHA classification describes the functional status of patients with stages C or D heart failure. The severity of symptoms characteristically fluctuates even in the absence of changes in medications, and changes in medications can have either favorable or adverse effects on functional capacity in the absence of measurable changes in ventricular function. Some patients may demonstrate remarkable recovery associated with improvement in structural and functional abnormalities. Usually sustained improvement is associated with drug therapy, and that therapy should be continued indefinitely.

5 What major alterations in the heart occur in patients with heart failure?

LV dysfunction begins with some injury to, or stress on, the myocardium and is generally a progressive process. The principal manifestation of such progression is a change in the geometry and structure of the left ventricle such that the chamber dilates and/or hypertrophies and becomes more spherical—a process referred to as cardiac remodeling. Specific patterns of ventricular remodeling occur in response to the imposed augmentation in workload. With pressure overload, the increased wall tension during systole initiates parallel addition of new myofibrils, causing wall thickening and concentric hypertrophy. With volume overload the wall tension increases during diastole, initiating series addition of new sarcomeres, resulting in chamber enlargement and eccentric hypertrophy. Ventricular dilation allows the chamber to eject an adequate stroke volume with less muscle shortening, but wall stress is increased as described by the Laplace relationship:

where P = intracavity pressure, R = the radius of the chamber, and h = the thickness of the chamber wall.

Increasing wall tension requires higher oxygen demand for the same performance. Myocardial hypertrophy with increasing wall thickness allows the heart to overcome pressure overload with decreased wall tension.

6 What is the Frank-Starling law?

The Frank-Starling law states that the force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched. In a clinical situation, when increased quantities of blood flow into the heart (increasing preload), the walls of the heart stretch. The cardiac muscle then contracts with increased force and, within limits, empties the expanded chambers with increasing stroke volume. There is an optimal sarcomere length and thus an optimal fiber length from which the most forceful contraction occurs. The left ventricle normally operates at an LV end-diastolic volume with less than optimal fiber lengths. The clinical implication of this is that stroke volume increases with increasing preload until the optimal fiber length of the myocardium is reached. Increasing the preload further causes a decrease in stroke volume.

7 How is cardiac output calculated? What is a normal cardiac output and index?

Cardiac output (CO) is the amount of blood that the heart can pump during 1 minute. The main determinants of CO:

where CO = arterial pressure/ total peripheral resistance, SV = stroke volume and HR = heart rate.

CO varies widely with the level of activity of the body. The average value for resting adults is about 5 L/min. For women this value is 10% to 20% less. CO increases in proportion to the surface area of the body. To compare the CO of different-size people to each other, the term of cardiac index (CI) was introduced, which is the CO per square meter of body surface area. The normal average CI for adults is about 3 L/min/m². There are definite limits to the amount of blood the heart can pump. The normal heart, functioning without any excess nervous stimulation, can pump an amount of venous return up to about 2.5 times the normal venous return, which is about 13 L/min CO. Nervous stimulation increases HR and contractility. These two effects can raise the CO up to 25 L/min.

8 What is the connection between exercise and cardiac output?

Oxygen delivery is the product of CO and arterial blood oxygen content. Exercise increases the oxygen consumption of the body. This increased oxygen demand is covered by increasing CO. Heart failure results in a mismatch between tissue oxygen consumption and tissue perfusion based on the generated CO at a certain exercise level. The mismatch creates tissue hypoxemia, acidosis, and the inability to hold the exercise at the level at which the mismatch occurs.

9 What is systolic dysfunction?

The symptoms and signs of heart failure can be caused by either an abnormality in systolic function that leads to diminished ejection fraction (EF) or an abnormality in diastolic function that leads to altered ventricular filling.

Systolic dysfunction leads to decreased ejection of blood from the left ventricle. The EF is diminished, the end-systolic and end-diastolic volume are enlarged, and the left ventricle is dilated. The stroke volume can be normal, but it is generated by a dilated ventricle with higher wall tension and oxygen consumption. In this pathologic condition the left ventricle has less reserve capacity to overcome pressure or volume load, which manifests in decreased exercise capacity (Figure 34-1, Loop 3).

Figure 34-1 Left ventricular (LV) pressure-volume loops illustrating normal performance (loop 1), diastolic (loop 2), and systolic dysfunction (loop 3). AB, Diastolic filling; BC, isovolumic contraction; CD, = ejection; DA, isovolumic relaxation. In diastolic dysfunction one of the problems can be the impaired LV compliance, which manifests in high LV end-diastolic pressure. The stroke volume and ejection fraction are normal. This loop can represent diastolic dysfunction in hypertension or aortic stenosis with LV hypertrophy (loop 2). In systolic dysfunction the LV is dilated, the stroke volume is normal or less than normal; the left ventricular end-diastolic and end-systolic volumes are enlarged. The end-diastolic pressure can be normal or higher than normal, depending on the compliance of the LV. This loop may represent dilated cardiomyopathy (loop 3).

10 What is diastolic dysfunction?

Diastolic dysfunction can occur with normal LV EF in many patients. Impaired LV relaxation or compliance or both are the major characteristic features of LV diastolic dysfunction. Early diastolic filling depends on the rapidity of ventricular relaxation, characterized by an energy-dependent reuptake of calcium from the cytosol into the sarcoplasmic reticulum of the myocytes. Late diastolic filling (atrial contraction) depends on LV compliance, which is the ratio of change in ventricular volume to change in ventricular diastolic pressure. In diastolic dysfunction the size of the LV cavity can be normal but ischemia, myocardial hypertrophy, pericardial constriction, fibrosis, or myocardial diseases alter the diastolic filling process. Systolic dysfunction with dilated left ventricle and high LV end-diastolic pressure accompanies significant diastolic dysfunction because of decreased LV relaxation and compliance (see Figure 34-1, Loop 2).

11 Do the neurohumoral responses in heart failure have therapeutic significance?

Although several factors can accelerate the process of LV remodeling, there is substantial evidence that the activation of endogenous neurohumoral systems plays an important role in cardiac remodeling and thereby in the progression of HF. Patients with HF have elevated circulating or tissue levels of norepinephrine, angiotensin II, aldosterone, endothelin, vasopressin, and cytokines, which can adversely affect the structure and function of the heart. These neurohumoral factors not only increase the hemodynamic stresses on the ventricle by causing sodium retention and peripheral vasoconstriction but may also exert direct toxic effects on cardiac cells and stimulate myocardial fibrosis, which can further alter the architecture and impair the performance of the failing heart.

β-Blockers and angiotensin-converting enzyme inhibitors (ACEIs) are cornerstones in the management of heart failure because they attenuate the deleterious effects of the neurohumoral mediators on the performance of the heart.

12 What are the presenting symptoms of heart failure?

Exertional dyspnea and fatigue are most often the primary complaints. Paroxysmal nocturnal dyspnea, nocturia, coughing, wheezing, right upper quadrant pain, anorexia, and nausea and vomiting also may be complaints. Although HF is generally regarded as a hemodynamic disorder, many studies have indicated that there is a poor relation between measures of cardiac performance and the symptoms produced by the disease. Patients with a very low EF may be asymptomatic (stage B), whereas patients with preserved LVEF may have severe disability (stage C). The apparent discordance between EF and the degree of functional impairment is not well understood but may be explained in part by alterations in ventricular distensibility, valvular regurgitation, pericardial restraint, cardiac rhythm, conduction abnormalities, and right ventricular function. In addition, in ambulatory patients many noncardiac factors may contribute substantially to exercise intolerance. These factors include but are not limited to changes in peripheral vascular function, skeletal muscle physiology, pulmonary dynamics, neurohumoral and reflex autonomic activity, and renal sodium handling.

13 What physical signs suggest heart failure?

Cardiac palpation may reveal an expanded impulse area (ventricular dilation) or a forceful sustained impulse with LV hypertrophy. Auscultation reveals a gallop rhythm with S₃ or S₄ secondary to impaired LV filling or forceful atrial contraction, respectively. Murmurs of valvular diseases should be looked for. Severe failure may result in cyanosis.

Pulmonary examination often reveals rales located most prominently over the lung bases. Decreased breath sounds secondary to pleural effusions occur more often in patients with chronic heart failure.

Jugular venous distention >4 cm above the sternal angle with the patient recumbent at a 45-degree angle is considered abnormal.

14 What laboratory studies are useful in evaluating the patient with heart failure?

The posteroanterior and lateral chest radiograph may detect cardiomegaly or evidence of pulmonary vascular congestion, including perihilar engorgement of the pulmonary veins, cephalization of the pulmonary vascular markings, or pleural effusions.

The electrocardiogram is often nonspecific, but ventricular or supraventricular dysrhythmias; conduction abnormalities; and signs of myocardial hypertrophy, ischemia, or infarction are present frequently.

Echocardiography characterizes chamber size, wall motion, valvular function, and LV wall thickness. Stroke volume can be measured using Doppler methods. EF can be calculated by measuring the end-diastolic and end-systolic volumes. Diastolic function can be evaluated by studying the flow pattern through the mitral valve and the left upper pulmonary vein using Doppler technique. Radionuclide angiography provides a fairly reproducible and accurate assessment of left and right ventricular ejection fraction.

Serum electrolytes, arterial blood gases, liver-function tests (LFTs), and blood cell counts are frequently evaluated. Many patients with heart failure are hyponatremic from activation of the vasopressin system or from the treatment with ACEI. Treatment with diuretics may lead to hypokalemia and hypomagnesemia. Some degree of prerenal azotemia, hypocalcemia, and hypophosphatemia is often present. Hepatic congestion may result in elevated bilirubin levels and elevated LFTs. Elevated brain natriuretic peptide levels may help in suspected diagnosis of HF or trigger consideration of HF when the diagnosis is unknown but should not be used in isolation to confirm or exclude the presence of HF.

15 What treatment strategies are used in the different stages of heart failure?

Stage A: Patients at high risk for developing HF

In patients at high risk for developing HF, systolic and diastolic hypertension, lipid disorders, thyroid disorders, and diabetes mellitus should be controlled. Patients should be counseled to avoid smoking, excessive alcohol consumption, and illicit drug use that may increase the risk of HF. Patients who have known atherosclerotic vascular disease should be followed for secondary prevention. ACEIs or angiotensin II receptor blockers can be useful to prevent HF in patients who have a history of atherosclerotic vascular disease, diabetes mellitus, or hypertension.

Stage B: Patients with cardiac structural abnormalities or remodeling who have not developed HF symptoms

All recommendations for stage A should apply to patients with cardiac structural abnormalities who have not developed symptoms. β-Blockers and ACEIs should be used in all patients with a recent or remote history of myocardial infarction (MI) regardless of EF or presence of HF. β-Blockers and ACEIs are indicated in all patients without a history of MI who have a reduced LVEF with no HF symptoms.

Stage C: Patients with current or prior symptoms of HF

Patients with Reduced LVEF:

Measures listed as recommendations for patients in stages A and B are also appropriate for patients in stage C. Diuretics and salt restriction are indicated in patients with current or prior symptoms of HF and reduced LVEF who have evidence of fluid retention. ACEIs and/or β-blockers (using one of the three proven to reduce mortality [i.e., bisoprolol, carvediol, and sustained release metoprolol succinate]) are recommended for all patients with current or prior symptoms of HF and reduced LVEF unless contraindicated. Addition of an aldosterone antagonist is reasonable in selected patients with moderately severe–to-severe symptoms of HF and reduced LVEF. Implantable cardioverter-defibrillator therapy and cardiac resynchronization therapy can be instituted in high-risk patients.

Patients with Normal LVEF:

Systolic and diastolic hypertension should be controlled in patients with HF and normal LVEF. Ventricular rate should be controlled in patients with atrial fibrillation. Diuretics should be used to control pulmonary congestion and peripheral edema. Coronary revascularization is reasonable in patients with coronary artery disease in whom symptomatic or demonstrable myocardial ischemia is judged to be having an adverse effect on cardiac function.

Stage D: Patients with refractory end-stage heart failure

16 What should be considered in preparing to conduct an anesthetic on patients with heart failure?

Patients with stages A or B heart failure have good functional status; thus they can go for surgery after routine preoperative evaluation.

In stage C heart failure the NYHA functional status should be evaluated, and signs of decompensated HF should be checked. Patients with dyspnea, worsening dyspnea, or other change in clinical status are reasonable candidates to undergo preoperative noninvasive evaluation of LV function and postpone elective surgery until compensation.

Stage D heart failure represents patients in NYHA class IV who are refractory to standard medical therapy. They can be on intravenous inotropic medications or assist device therapy and need special anesthetic management for noncardiac surgery.

17 How would you manage a patient 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.

18 Which anesthetic agents can be used in decompensated heart failure?

Avoiding 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.

19 Is regional anesthesia contraindicated in patients with heart failure?

No. 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.

20 How would you support 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.