SECTION I. Cardiovascular System
A Cardiomyopathy
DEFINITION
Cardiomyopathies are diseases of the myocardium that are characterized by myocardial dysfunction. They ultimately affect contractile function, and life-threatening congestive heart failure (CHF) is common to all cardiomyopathies.
ETIOLOGY
Cardiomyopathies can be classified according to their pathophysiologic basis in the categories of dilated (congestive), restrictive, and hypertrophic.
DILATED CARDIOMYOPATHY
The cause of dilated cardiomyopathies can be inflammatory or noninflammatory. The inflammatory type or myocarditis usually results from infection. The noninflammatory variety results from idiopathic, toxic, degenerative, or infiltrative processes in the myocardium. The primary clinical symptom is myocardial failure, which presents as ventricular dilation, elevated filling pressures, and pulmonary edema. Dilated cardiomyopathies can be acute or chronic and can lead to a decrease in myocardial contractility, often involving both ventricles. Alcoholic cardiomyopathy is an example of noninflammatory cardiomyopathy that is associated with tachycardia, premature ventricular contractions which progresses left ventricular failure and valvular disease.
Clinical symptoms are characterized as “forward” failure or “backward” failure. Symptoms of forward failure may include fatigue, hypotension, and oliguria due to a decreased organ perfusion.
Symptoms of backward failure may include elevated filling pressures and ventricular failure. The left ventricular (LV) dilation and mitral regurgitation results in orthopnea, paroxysmal nocturnal dyspnea and pulmonary edema. Symptoms of right-sided failure include hepatomegaly, jugular venous distention and peripheral edema.
TREATMENT
Patients with dilated cardiomyopathy must avoid unnecessary physical activity and must exhibit total abstinence from alcohol. CHF is treated with digoxin and diuretics. Vasodilator treatment or an inotrope with vasodilator properties (amrinone or milrinone) may also be helpful. Ventricular arrhythmias are treated with procainamide or quinidine. Because of the increased risk of pulmonary embolism, these patients may be treated with anticoagulants (not proved to be of benefit). Patients with associated collagen vascular disease, sarcoidosis, or inflammation on endocardial biopsy are treated with corticosteroids preoperatively. Tachyarrhythmias can be treated with β-blockers. Patients with coronary artery disease and dilated cardiomyopathy may benefit from coronary revascularization to improve LV function. With advanced CHF, these patients may be candidates for heart transplantation, provided pulmonary hypertension does not exist.
ANESTHETIC CONSIDERATIONS
• Avoid myocardial depression.
• Maintain normovolemia.
• Prevent increases in afterload.
• Invasive monitoring may be necessary if manipulation of pulmonary and systemic vascular resistances is needed.
Excess cardiovascular depression on induction of anesthesia in patients with a history of alcohol abuse may reflect undiagnosed dilated cardiomyopathy; however, failure of this expected response to intravenous induction agents may reflect a slow circulation time.
During maintenance, myocardial depression produced by volatile agents must be considered. Opiates exhibit benign effects on cardiac contractility but may not produce unconsciousness. In addition, an opioid, nitrous, benzodiazepine technique may cause unexpected cardiac depression. Increases in heart rate associated with surgical stimulation may be treated with β-blockers. Nondepolarizing muscle relaxants that exhibit few cardiovascular effects are advised.
Cardiac filling pressures should guide intravenous fluids; therefore, a pulmonary artery catheter aids in early recognition of the need for inotropes or vasodilators. Prominent “v” waves reflect mitral or tricuspid regurgitation.
Intraoperative hypotension is treated with ephedrine. Phenylephrine could adversely affect afterload as a result of increased systemic vascular resistance (SVR).
Regional anesthesia may be used in selected patients, although caution is indicated in avoiding abrupt sympathetic blockade as seen in spinal or epidural anesthesia.
PROGNOSIS
Prognosis of dilated cardiomyopathy is poor, with a 5-year survival rate of 25% to 40%. The cause of death in 75% of these patients is CHF. Pulmonary embolism or sudden death from arrhythmia is found in more than 50% of these patients on autopsy.
RESTRICTIVE CARDIOMYOPATHY
This condition manifests as impaired diastolic filling that produces increased filling pressures and decreased CO mimicking constrictive pericarditis. Restrictive cardiomyopathy causes a greater impairment of LV filling than right ventricular (RV) filling. LV filling pressures are usually greater than RV filling pressures, and the left ventricle becomes less compliant. There is no effective treatment for this disease, and death is often the result of cardiac arrhythmia or intractable CHF. Anesthetic management follows the same principles used in cardiac tamponade.
HYPERTROPHIC CARDIOMYOPATHY
DEFINITION
A genetically transmitted disorder that is a form of myocardial dysfunction, which can cause coronary artery disease, valvular dysfunction, ventricular remodeling, and hypertension. The incidence in the adult population is approximately 1 in 500 persons. Obstructive hypertrophic cardiomyopathy has previously been referred to as idiopathic hypertrophic subaortic stenosis. Currently the preferred term is hypertrophic cardiomyopathy with or without left ventricular outflow obstruction. This disease is an autosomal dominant hereditary condition. The peak incidence is in patients 50 to 70 years of age. Most elderly patients diagnosed with this condition are female.
ETIOLOGY
The myocardial defect that is associated with hypertrophic cardiomyopathy is related to the contractile mechanism. An increase in the density of calcium channels appears to lead to myocardial hypertrophy. Asymmetric hypertrophy of the interventricular septum of the LV occurs. The asymmetric hypertrophy of the intraventricular septum causes a left outflow tract obstruction, and therefore the hemodynamic consequences are similar to those that are characteristic of aortic stenosis (AS). Hypertrophic cardiomyopathy is the most common cause of sudden death in the pediatric and young adult populations.
Myocardial hypertrophy is the pathophysiologic abnormality that precipitates the hemodynamic derangements associated with hypertrophic cardiomyopathy and is caused by left ventricular outflow obstruction.
PATHOPHYSIOLOGY
The pathophysiologic abnormalities related to hypertrophic cardiomyopathy include the presence of systolic and diastolic dysfunction. A loss of diastolic compliance results in an abnormally elevated left ventricular end-diastolic pressure (LVEDP) in the presence of low-normal end-diastolic volume. Loss of left ventricular diastolic compliance requires a greater contribution of volume from atrial contraction. As a result, CHF may ensue as left atrial pressures continue to increase.
Hypertrophic cardiomyopathy with obstruction is characterized by its dynamic nature. Three basic hemodynamic parameters can affect the degree of outflow obstruction. Manipulation of these parameters can exacerbate or ameliorate the hemodynamic consequences of outflow obstruction. These three parameters include preload, afterload, and contractility. Increasing myocardial contractility in patients with dilated cardiomyopathy exacerbates the obstruction by increasing septal wall contraction and decreasing CO. Increased blood flow velocity causes a greater degree of systolic anterior motion of the mitral valve’s anterior leaflet, creating further obstruction. Decreased preload changes left ventricular geometry and thereby brings the anterior leaflet of the mitral valve into closer proximity of the hypertrophied septum. Increases in left ventricular contractility cause the LV to empty more completely and increase the degree of septal contractility, which results in a greater degree of obstruction.
In hypertrophic cardiomyopathy with obstruction, conditions that impair ventricular function under normal physiologic conditions improve cardiac function. This implies that factors that normally impair contractility, such as myocardial depression, increased end-diastolic volume, and increased SVR, improve forward flow and diminish the degree of obstruction.
TREATMENT
The goal of treatment in these patients is to relieve the obstruction to LV outflow. This is often achieved with β-blockers to lower the heart rate and decrease contractility. Calcium channel antagonists may also help. Caution should be taken to prevent drug-induced hypotension and negative inotropic effects; therefore, nitroglycerin should be avoided in these patients who present with angina. Should CHF also exist, treatment becomes more difficult. Diuretics can lead to hypovolemia, and digoxin can increase cardiac contractility, both of which may worsen the obstruction. Cardioversion may be necessary to maintain normal sinus rhythm. Patients with atrial fibrillation require anticoagulant treatment to prevent embolization. These patients are at risk for infective endocarditis and should receive prophylactic antibiotic treatment for dental or surgical procedures. Myotomy or myomectomy under cardiac bypass may be needed in 10% to 15% of patients. Mitral valve replacement may also be needed.
ANESTHETIC CONSIDERATIONS
Anesthetic management should focus on strategies that alleviate and do not increase left ventricular outflow obstruction. It is imperative that adequate or slightly elevated left ventricular volume be maintained. Measures that decrease venous return and interfere with adequate ventricular preload should be avoided. Factors that increase myocardial contractility should be avoided. Inadequate depth of anesthesia that causes sympathetic nervous system stimulation may be detrimental. In the event that hypotension occurs, adequate perfusion pressure should be maintained by increasing preload with fluid administration and increasing SVR with phenylephrine. Pharmacologic therapy used to treat hypertrophic cardiomyopathy (including β-blockers and calcium channel blockers) should be continued until the time of surgery.
| Preload | Increase |
| Afterload | Increase |
| Contractility | Decrease |
| Heart rate | Maintain |
| Heart rhythm | Normal sinus rhythm |
Anesthetic management must focus on increasing left ventricular preload, decreasing myocardial contractility, controlling HR, and maintaining or increasing afterload. Regional anesthesia is not contraindicated in patients with dilated cardiomyopathy. Decreases in blood pressure must be treated immediately. Hypovolemia must be avoided and expeditiously treated if it occurs. Deep general anesthesia with a volatile agent is preferred in patients with hypertrophic cardiomyopathy and obstruction.
The potential for hemodynamic deterioration because of increasing subaortic obstruction along with secondary mitral regurgitation (MR) necessitates aggressive hemodynamic monitoring. Invasive monitoring via a pulmonary artery catheter allows for maintenance of adequate left ventricular end-diastolic volume (LVEDV). Because of reduced diastolic compliance associated with hypertrophic cardiomyopathy, pulmonary capillary wedge pressure (PCWP) does not correlate directly with LVEDV. The PCWP should be maintained at approximately 18 to 25 mm Hg. If hemodynamic status deteriorates and exacerbation of outflow obstruction is suspected, β-blocking drugs (propanolol or esmolol) should be administered. In addition, vasoconstrictors such as phenylephrine should be used in order to increase SVR.
B Congestive Heart Failure
DEFINITION
Congestive heart failure (CHF) is the failure of the myocardium to function properly, causing pulmonary congestion and ultimately pulmonary edema. CHF may involve one or both sides of the heart.
ETIOLOGY
CHF is usually caused by impaired myocardial contractility (secondary to ischemic heart disease or cardiomyopathy), cardiac valve abnormalities, systemic hypertension, or pulmonary hypertension (cor pulmonale). CHF in the preoperative period is the most important contributor to postoperative cardiac morbidity and mortality.
DIAGNOSTIC AND LABORATORY FINDINGS
• Cardiac index is less than 2.5 L/min in severe CHF.
• Ejection fraction is often less than 0.50 (50%).
• LVEDP parallels the end-diastolic volume and is increased in the presence of CHF. LVEDP is normally less than 12 mm Hg, and right ventricular end-diastolic pressure is normally less than 5 mm Hg.
CLINICAL MANIFESTATIONS
Left Ventricular Failure
• Fatigue
• Dyspnea resulting from interstitial pulmonary edema
• Orthopnea
• Paroxysmal nocturnal dyspnea
• Acute pulmonary edema
• Tachypnea and rales
• Tachycardia and peripheral vasoconstriction
• Oliguria
• Pleural effusion
Right Ventricular Failure
• Systemic venous congestion: jugular venous distention
• Hepatomegaly
• Ascites
• Peripheral edema: dependent and pitting edema
TREATMENT
Treatment of CHF includes the use of digitalis, diuretics, angiotensin-converting enzyme inhibitors, vasodilators, and/or inotropes.
Digitalis
Digitalis is the only orally effective positive inotropic agent currently in use. Digoxin is excreted mainly by the kidneys, and its elimination parallels creatinine clearance. In the perioperative period, sensitivity to digoxin can be increased if there are decreases in renal function or hypokalemia. Prophylaxis with digitalis is controversial in those patients with CHF undergoing elective surgery. Digitalis may be continued in the preoperative period, especially if it is used to control heart rate. Toxicity should be suspected if the patient complains of nausea and vomiting, if cardiac arrhythmias are present, and if the serum digitalis level is greater than 3 ng/mL. Treatment of digitalis toxicity includes correction of hypokalemia, treatment of arrhythmias, and insertion of a temporary pacemaker if complete heart block ensues. If surgery cannot be delayed in the patient with digitalis toxicity, it is important to avoid sympathomimetics (ketamine) and hyperventilation (leading to hypokalemia).
Diuretics
Loop diuretics (e.g., furosemide) are often given to patients with CHF. Long-term administration of these drugs can lead to hypovolemia, orthostatic hypotension, and hypokalemia. Monitoring serum electrolytes (i.e., potassium) is essential, especially if the patient is treated with digitalis preparations.
Vasodilators
Vasodilators are the mainstay in the treatment of CHF because they decrease the impedance against which the left ventricle must work. Hypotension can result, however, and is a limiting factor in treating CHF with these drugs. Invasive monitoring (arterial and pulmonary artery catheters) may become necessary when information regarding CO; filling pressures; and systemic, pulmonary, and peripheral vascular resistances are needed to treat these patients effectively.
Inotropes
Inotropic therapy is used cautiously because β-agonists can increase myocardial oxygen demand and can also increase heart rate via β 1 stimulation. Intravenous dopamine and dobutamine are used perioperatively to improve myocardial contractility. The combination of these two drugs provides beneficial renal effects (from dopamine) and β effects (from dobutamine) at doses that are unlikely to increase afterload. A phosphodiesterase inhibitor such as milrinone (Primacor) may also be used as an inotropic agent. The advantage of this drug is increased inotropic action with afterload reduction. Epinephrine is also a drug of choice for inotropic support secondary to its β effects. A pulmonary artery catheter should be used to monitor the effects of these drugs on CO, cardiac index, and filling pressures.
ANESTHETIC CONSIDERATIONS
If surgery is absolutely necessary, the goal is to optimize CO. Ketamine, etomidate, and midazolam, given slowly and sparingly, have all been used successfully to induce anesthesia in the patient with CHF. Volatile anesthetics must be used with caution because of their propensity to cause myocardial depression. Severe CHF requires careful titration of all anesthetic agents for maintenance. Positive-pressure ventilation may help by decreasing pulmonary congestion and improving arterial oxygenation but may also reduce venous return and lower blood pressure. Therefore, invasive monitoring should strongly be considered in these patients. CO can be supported with dopamine, dobutamine, or both as needed. Regional anesthesia may be used for extremity surgery in the patient with CHF. Anesthetic technique and agents should be individualized for each patient, with consideration of the medical history and surgical procedure.
C Hypertension
INCIDENCE
Hypertension affects approximately 60 million people in the United States, and the frequency at which it occurs increases with age. Nearly two thirds of people over the age of 65 years have hypertension.
ETIOLOGY
Hypertension is classified on the basis of its causes. Essential (primary) hypertension, which has no identifiable cause, accounts for 95% of all cases of the disease, and its diagnosis is determined on the basis of exclusion. Remedial (secondary) hypertension has an identifiable and potentially curable cause. Sources of secondary hypertension include pheochromocytoma, coarctation of the aorta, renal artery stenosis, primary renal diseases (e.g., pyelonephritis, glomerulonephritis), primary aldosteronism (Conn’s disease), and hyperadrenocorticism (Cushing’s disease).
The classification of hypertension is listed below.
The risk of cardiovascular disease doubles with each increment of 20/10 mm Hg above 115/75 mm Hg. It is estimated that the implementation of antihypertensive therapy is associated with a 25% decrease in cardiovascular complications and a 38% decrease in stroke.
PATHOPHYSIOLOGY
Systemic blood pressure is regulated by interactive feedback mechanisms involving the sympathoadrenal axis and baroreceptors in the heart and great vessels. It is accepted that some degree of sympathetic dysfunction is responsible for essential hypertension. Dysfunction of the sympathetic nervous system leads to a state of chronic vasoconstriction. In an attempt to maintain normal intravascular volume, the renal juxtaglomerular apparatus secretes renin. All the vascular and hormonal effects of renin are caused by its conversion of angiotensin I to angiotensin II. Angiotensin II is the major stimulus for the secretion of aldosterone by the adrenal cortex.
TREATMENT
When DBP is greater than 90 mm Hg, drug treatment is usually employed, although isolated systolic HTN may respond to diet modification and weight loss. Patients with borderline HTN can decrease their BP with exercise and weight loss. If DBP exceeds 105 mm Hg, aggressive treatment is needed to decrease morbidity and mortality from myocardial infarction, congestive heart failure, cerebrovascular accident, and renal failure.
Drugs used to treat HTN include diuretics, angiotensin-converting enzyme inhibitors, calcium antagonists, β-blockers, and vasodilators. A combination of two antihypertensives is often used to minimize the undesirable physiologic responses to any one particular drug (e.g., a compensatory increase in renin activity). Serum potassium levels should be monitored, because hypokalemia or hyperkalemia may be a side effect.
ANESTHETIC CONSIDERATIONS
Preoperative
The most important issues to be addressed in the preoperative evaluation are the identification and the adequacy of treatment. If perioperative diastolic blood pressure is maintained below 110 mm Hg, the risk of perioperative cardiac morbidity does not increase significantly. Reviewing the patient’s medication and determining adequacy of BP control is essential.
An individualized anesthetic plan must be created by taking into account the type and extent of cardiac pathophysiology, other disease states, and the surgical procedure. In order to maintain a stable intraoperative course, administration of antihypertensive medications should be continued on schedule until the time of surgery. Tachycardia, hypertension, angina, and myocardial infarction can result from interruption of therapy with β-blockers and calcium channel–blocking agents. These drugs should be discontinued with caution and only after utmost discretionary review of the patient’s physiologic status.
Determining whether to proceed with elective surgery in a patient in whom hypertension is untreated or poorly controlled remains controversial. Patients with diastolic blood pressures greater than 110 mm Hg have a significantly increased risk of perioperative cardiac morbidity. This caveat may be modified in patients with hypertension in whom diastolic blood pressures greater than 110 mm Hg occur frequently despite aggressive antihypertensive drug therapy (e.g., patients with end-stage renal disease).
Preoperative sedation may be indicated for patients with hypertension in order to attenuate sympathetic responsiveness. Establishing control of the blood pressure before induction should result in a more stable hemodynamic course during the induction, maintenance, and emergence from anesthesia. A fluid bolus and incremental titration of anesthetic induction agents may help to decrease the degree and duration of hypotension.
INDUCTION OF ANESTHESIA
• Patients with hypertension react in an exaggerated manner to induction agents and the stimulation associated with laryngoscopy and tracheal intubation. This response is highly variable and may result in hypertension or hypotension.
• Hypertensive patients are hypovolemic, either as a result of renal-compensatory mechanisms, extreme vasoconstriction, or pharmacologic therapy (diuretics). Increased vasoconstriction as a consequence of hypertension results in volume contraction and a greater susceptibility to hypotension from the vasodilating and cardiac depressant effects of anesthetic agents.
• Etomidate, propofol, or sodium pentothal induction agents can be used in patients with hypertension.
• The stimuli of laryngoscopy and tracheal intubation can result in an exaggerated hypertensive response despite postinduction hypotension. Administration of adjunct medications before induction such as blocker or arterial dilators can reduce the hyperdynamic sympathetic response to tracheal intubation.
• Hypotensive episodes can be treated with fluid administration, decrease in anesthetic depth, and administration of vasoconstrictors. The pressor response to laryngoscopy and intubation can be significantly reduced by laryngotracheal or intravenous administration of lidocaine, reducing the duration of airway manipulation to 15 seconds or less and the administration of a β-blocker before induction. Administration of fentanyl (2 to 3 mcg/kg) just before induction also helps attenuate the pressor response.
• The maintenance of an adequate depth of anesthesia at induction that produces extreme hypotension may be more detrimental to both coronary and cerebral perfusion than the hypertensive response it was intended to prevent. Because the hypertensive patient is frequently hypovolemic as compared with the normotensive patient, adequate hydration before induction may help to prevent post-induction hypotension.
MAINTENANCE OF ANESTHESIA
• The goal of anesthetic management of the hypertensive patient undergoing general anesthesia is to maintain blood pressure stability within 20% of the normal mean pressure. Intraoperative events that cause wide fluctuations in blood pressure should be anticipated and treated immediately.
• The most common event precipitating intraoperative hypertension is the painful stimulus of surgery. This induces increased sympathetic tone via a neurohormonal reflex and represents the stress-induced response of surgical stimulation. Volatile and opioid agents given alone and in combination have the ability to attenuate this response.
The adjunct use of drugs such as β-antagonists, nitroprusside, angiotensin-converting enzyme inhibitors (e.g., enalapril), α 2-agonists (e.g., clonidine), calcium-channel blockers (e.g., nifedipine), and α 1-blockers (e.g., droperidol) may be necessary for achieving control.
The onset of profound hypotension during anesthesia maintenance should be immediately recognized, diagnosed, and treated. Treatment of hypotension may require reduction of the amount of volatile agent used and infusion of adequate volume. Should these measures prove inadequate or untimely, a rapid-acting vasopressor such as phenylephrine or ephedrine may be administered as a temporizing measure until the cause of the hypotension can be diagnosed. It is important to realize that hypertensive patients may have exaggerated responses to vasopressor agents.
POSTOPERATIVE CONSIDERATIONS
• Termination of anesthesia results in hyperdynamic, hypertensive responses, even in patients with well-controlled hypertension. Intraoperative control of blood pressure should continue into the immediate postoperative period.
• Initiation of adjunct administration of antihypertensive medications should be anticipated early in the postoperative period. Adequate control of pain represents a primary antihypertensive consideration. The hypertensive patient is more susceptible to perioperative cardiac morbidity than the normotensive patient during the postoperative period. Adequate control of blood pressure in the postoperative period reduces the incidence of cardiovascular complications.
D Ischemic Heart Disease
DEFINITION
Ischemic heart disease (IHD) describes the condition in which atherosclerotic plaque is present in the coronary arteries, giving way to coronary artery disease (CAD).
INCIDENCE
More than 10 million adults in the United States have IHD, and it is the leading cause of death (500,000 deaths/year). The first manifestation of IHD is often acute myocardial infarction resulting in sudden death.
The overall prognosis of patients with IHD is dependent on the frequency and severity of cardiac arrhythmias, myocardial infarction, and LV dysfunction. About 40 million people in the United States undergo anesthesia and operations each year; of these, 30% are considered to be at high risk because of the presence of IHD.
ETIOLOGY
IHD results from the presence of atherosclerotic plaque in the coronary arteries that causes narrowing and subsequently impedes blood flow. Angina pectoris is the presenting complaint of the patient experiencing a reduction in coronary artery blood flow. Dyspnea that occurs after the onset of angina indicates acute LV dysfunction, which can lead to congestive heart failure (CHF) from myocardial ischemia. The most important risk factors are advanced age and male gender. Other risk factors include hyperlipidemia, hypertension, cigarette smoking, diabetes, obesity, sedentary lifestyle, familial history of premature development of IHD, and other psychosocial characteristics. There are three types of angina: stable, variant, and unstable. Stable angina is chest pain that occurs predictably when there is an increase in cardiac work. As the heart rate increases (usually more than 100 beats/min), demand exceeds supply, and angina becomes evident. Variant angina is due to coronary artery spasm of unknown cause that gives way to ischemia and ultimately chest pain. Unstable angina is a combination of stable and variant angina and usually represents an advanced degree of CAD. These patients may have angina at rest.
DIAGNOSTIC AND LABORATORY FINDINGS
Cardiac Evaluation
A complete history and physical examination, chest x-ray study, and electrocardiogram (ECG) should be performed in the patient with known or suspected IHD. If the initial evaluation suggests IHD, stress testing may be indicated. An exercise ECG with or without concomitant administration of intravenous radionuclide (i.e., thallium) or pharmacologic echocardiography is usually performed. If the stress test is suggestive of IHD, cardiac catheterization may then be indicated. In addition, dobutamine stress echocardiography is also available to evaluate overall cardiac function further (see the following box).
Evaluation of Left Ventricular Function
Poor Function
1. History
a. Multiple MI
b. Symptoms of CHF
2. Cardiac catheterization
a. EF <40%
b. LVEDP >18 mm Hg
c. Multiple areas of ventricular dyskinesia
d. Decreased CO
e. Ventricular septal defect
f. MI in progress
g. Extreme age
Good Function
1. History
a. Angina
b. Hypertension and obesity
c. No symptoms of CHF
2. Cardiac catheterization
a. EF >50%
b. LVEDP <12 mm Hg
c. No areas of ventricular dyskinesia
d. Normal CO
CHF, Congestive heart failure; CO, cardiac output; EF, ejection fraction; LVEDP, left ventricular end-diastolic pressure; MI, myocardial infarction.
History
The clinician should elicit the severity and functional limitations imposed by IHD. Evaluation of symptoms as they relate to exercise tolerance, dyspnea, angina, and peripheral edema will give a qualitative estimate of the degree of impairment. Symptoms in some patients may not be present at rest, so the patient’s response to physical activity should be elicited through careful, appropriate questioning (e.g., Can the patient climb a flight of stairs?). One must be able to identify borderline CHF because the stress of anesthesia and operation may elicit overt heart failure perioperatively.
CLINICAL MANIFESTATIONS
Angina
Angina pectoris is substernal chest pain that often radiates to the neck, jaw, left shoulder, or left arm and is frequently precipitated by exertion. It may be relieved with rest or sublingual nitroglycerin (see the following table).
Classic
• The symptom is precipitated by exertion and is relieved by rest.
• It is a specific predictor for identification of patients with CAD, placing them at a higher risk for cardiac complications.
Atypical
• Signs and symptoms are different in type, location, precipitating events, or character.
Unstable
• The progression of coronary stenosis is occurring more rapidly than the development of collateral circulation.
TREATMENT
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