Cardiac Complications Postoperative Hypertension Causes

Transcription

1 Cardiac Complications Postoperative Hypertension Causes Hypertension is a serious problem that can cause devastating complications in the preoperative, intraoperative, and postoperative periods. Perioperative hypertension (or hypotension) occurs in 25% of patients undergoing surgery. The risk of hypertension is related to the type of surgery performed and the presence of perioperative hypertension. Cardiovascular, thoracic, and intra-abdominal procedures are most commonly associated with hypertensive events. Preoperatively, most hypertension is essential hypertension; much less common are cases associated with renovascular causes and, even rarer, vasoactive tumors. Intraoperatively, fluid overload and pharmacologic agents may cause hypertension. Postoperatively, a host of causative factors are associated with hypertension, including pain, hypothermia, hypoxia, fluid overload in the postanesthesia period caused by fluid mobilization from the extravascular compartment, and discontinuation of chronic antihypertensive therapy before surgery. Other causes of postoperative hypertension include intra-abdominal bleeding, head trauma, clonidine withdrawal syndrome, and pheochromocytoma crisis. Presentation and Management Most cases of hypertension are detected during the routine preoperative workup. The observant surgeon will consider hypertension in the preoperative screening of patients, recognizing that failure to detect significant problems with hypertension can lead to needless hypertension-related complications. By definition, any patient who has a diastolic blood pressure higher than 110 mm Hg must be assessed and treated preoperatively if elective surgery is being contemplated. Patients taking chronic antihypertensive medications who are undergoing elective surgery are instructed to continue taking the medication up to the day of surgery. Patients receiving oral clonidine can be switched to a clonidine patch for at least 3 days before surgery. In emergency cases, the medications administered during induction and maintenance of anesthesia will assist in bringing the blood pressure down. Intraoperatively, the anesthesiologist must carefully monitor blood pressure, make certain that it stays within acceptable limits, and avoid fluid overload, hypoxia, and hypothermia. In the postoperative period, the patient is given adequate analgesia for pain control and long-term antihypertensive medications are resumed. In patients who are not able to take oral medications, beta blockers, angiotensin-converting enzyme (ACE) inhibitors, calcium channel antagonists, or diuretics are given parenterally or clonidine is administered as a transdermal patch. Although hypertension in the postoperative period is common, a hypertensive crisis is uncommon, especially after noncardiac surgery. A hypertensive crisis is characterized by severe elevation of blood pressure associated with organ dysfunction cerebral and subarachnoid hemorrhage and stroke, acute cardiac events, renal dysfunction, and bleeding from the operative wound. This particularly appears to be the case in carotid endarterectomy, aortic aneurysm surgery, and many head and neck procedures. Diastolic hypertension (>110 mm Hg) is significantly associated with cardiac complications and systolic hypertension (>160 mm Hg) is associated with an increased risk for stroke and death. In patients with new-onset or severe perioperative hypertension and patients with a hypertensive emergency, treatment with agents that have a rapid onset of action, short half-life, and few autonomic side effects to lower blood pressure is essential. Medications most commonly used in this setting include nitroprusside and nitroglycerin (vasodilators), labetalol and esmolol (beta blockers), enalaprilat (useful for patients receiving long-term ACE inhibitors), and nicardipine (calcium channel blocker). It is crucial in the acute setting not to decrease blood pressure more than 25% to avoid ischemic strokes and hypoperfusion injury to other organs.

2 Perioperative Ischemia and Infarction Cause Approximately 30% of all patients taken to the operating room have some degree of CAD. Older patients, patients with peripheral artery disease, and those undergoing vascular, thoracic, major orthopedic, or upper abdominal procedures are at high risk for an acute coronary syndrome in the postoperative period. Major risk factors for developing CAD are smoking, family history, adverse lipid profiles, diabetes mellitus, and elevated blood pressure. [22] Although management of nonoperative MI has improved, the mortality associated with perioperative MI remains approximately 30%. Perioperative myocardial complications result in at least 10% of all perioperative deaths. In the 1970s, the risk for recurrence of MI within 3 months of an MI was reported to be 30% and, if a patient underwent surgery within 3 to 6 months of infarction, the reinfarction rate was 15%; 6 months postoperatively the reinfarction rate was only 5%. However, improved preoperative assessment, advances in anesthesia and intraoperative monitoring, and the availability of more sophisticated intensive care unit monitoring have resulted in improvement in the outcome of patients at risk for an acute cardiac event. Individuals undergoing an operation within 3 months of an infarction have an 8% to 15% reinfarction rate; between 3 and 6 months postoperatively, the reinfarction rate is only 3.5%. The general mortality associated with MI in patients without a surgical procedure is 12%. Myocardial ischemia and MI result from the imbalance between myocardial oxygen supply and demand. Primary causes that reduce myocardial perfusion and therefore oxygen supply include coronary artery narrowing caused by a thrombus that develops on a disrupted atherosclerotic plaque, dynamic obstruction caused by spasm of an epicardial coronary artery or diseased blood vessel, and severe narrowing caused by progressive atherosclerosis. Secondary causes that increase myocardial oxygen requirements, usually in the presence of a fixed restricted oxygen supply (limited myocardial perfusion), are extrinsic cardiac factors that include fever and tachycardia (increased myocardial oxygen demand), hypotension (reduced coronary blood flow), and anemia and hypoxemia (reduced myocardial oxygen delivery). The increased circulating catecholamines associated with surgical stress further increase myocardial oxygen demand. Presentation and Diagnosis Acute coronary syndrome refers to a constellation of clinical symptoms that are compatible with myocardial ischemia and encompasses MI: ST-segment elevation myocardial infarction (STEMI) and depression (Q wave and non Q wave), and unstable angina (UA)/non ST-segment elevation myocardial infarction (NSTEMI). UA/NSTEMI is defined as ST-segment depression or prominent T wave inversion and/or positive biomarkers of myonecrosis in the absence of ST-segment elevation and in an appropriate clinical setting. The risk for myocardial ischemia and MI is greatest in the first 48 hours after surgery, and it may be difficult to make the diagnosis. The classic manifestation, chest pain radiating into the jaw and left arm region, is often not present. Patients may have shortness of breath, increased heart rate, hypotension, or respiratory failure. Perioperative myocardial ischemia and MI are often silent and, when they occur, are marked by shortness of breath (heart failure, respiratory failure), increased heart rate (arrhythmias), change in mental status, or excessive hyperglycemia in diabetics. Many perioperative MIs are non Q wave NSTEMI. Periprocedural MI is associated with the release of biomarkers of necrosis, such as MB isoenzymes of creatinine kinase (CK-MB) and troponins, into the circulation. The troponin complex consists of three subunits, T (TnT), I (TnI), and C (TnC). TnT and TnI are derived from heartspecific genes and are referred to as cardiac troponins (ctns). ctns are not present in healthy individuals; their early release is attributable to the cytosolic pool and late release to the structural pool. Patients considered to have acute coronary syndrome should have a 12-lead ECG and placed in an environment with continuous electrocardiographic monitoring and defibrillator capability. Biomarkers of myocardial necrosis are measured. CK-MB has a short half-life and is less sensitive and less specific than ctns. Troponins can be detected in blood as early as 2 to 4 hours but elevation may be delayed for up to

3 8 to 12 hours. The timing of elevation of ctns is similar to CK-MB but ctns persist longer, for up to 5 to 14 days. Elevated ctn levels above the 99th percentile of normal in two or more blood samples collected at least 6 hours apart indicates the presence of myocardial necrosis. Equivalent information is obtained with ctni and ctnt, except in patients with renal dysfunction, in whom ctni has a specific role. Each patient should have a provisional diagnosis of acute coronary syndrome with UA (electrocardiographic changes of ischemia and no biomarkers in the circulation), STEMI, or NSTEMI. The distinction has therapeutic implications because patients with STEMI may be considered for immediate reperfusion therapy (fibrinolysis or percutaneous intervention). [22] Treatment Preventing coronary ischemia is a function of identifying patients prospectively at risk for a perioperative cardiac complication. This will allow improvement of the condition of the patient, possibly lowering the risk, selection of patients for invasive or noninvasive cardiac testing, and identifying patients who will benefit from more intensive perioperative monitoring. Preoperative cardiac risk assessment includes adequate history taking, physical examination, and basic diagnostic tests. The history is important to identify patients with cardiac disease or those at risk for cardiac disease, including previous cardiac revascularization, history of MI or stroke, and presence of valvular heart disease, heart failure, arrhythmia, hypertension, diabetes, lung disease, and renal disease. Unstable chest pain, especially crescendo angina, warrants careful evaluation and probable postponing of an elective operation. Physical examination may reveal uncontrolled hypertension, evidence of peripheral artery disease, arrhythmia, or clinical stigmata of heart failure (HF). The CXR may show pulmonary edema, ECG may show an arrhythmia, blood gas analysis may reveal hypercapnia or a low PaO 2, and blood tests may show abnormal kidney function. The patient who is found to have HF on physical examination or by history must have the problem treated before consideration for an elective operative procedure. Guidelines for Perioperative Cardiovascular Evaluation for Noncardiac Surgery, published by the American College of Cardiology (ACA) and American Heart Association (AHA), have stratified clinical predictors of increased perioperative cardiovascular risk leading to MI, CHF, or death into major, intermediate, and minor risks (Table 13-6) and stratified cardiac risk into high, intermediate, and low (Table 13-7). [21] Table Clinical Predictors of Increased Perioperative Cardiovascular Risk Leading to Myocardial Infarction, Heart Failure, or Death LEVEL OF RISK RISK FACTOR Unstable coronary syndromes Major Acute or recent MI with evidence of considerable ischemic risk as noted by clinical symptoms or noninvasive studies Unstable or severe angina (Canadian class III or IV) Decompensated heart failure Significant arrhythmias High-grade atrioventricular block

4 LEVEL OF RISK RISK FACTOR Symptomatic ventricular arrhythmias in the presence of underlying heart disease Supraventricular arrhythmias with an uncontrolled ventricular rate Severe valve disease Intermediate Mild angina pectoris (Canadian class I or II) Previous MI identified by history or pathologic evidence Q waves Compensated or previous heart failure Diabetes mellitus (particularly insulin dependent) Renal insufficiency Minor Advanced age Abnormal electrocardiogram (e.g., left ventricular hypertrophy, left bundle branch block, ST-T abnormalities) Rhythm other than sinus (e.g., atrial fibrillation) Low functional capacity (e.g., inability to climb one flight of stairs with a bag of groceries) History of stroke Uncontrolled systemic hypertension

5 Table Cardiac Risk Stratification for Noncardiac Surgical Procedures LEVEL OF RISK High (cardiac risk often >5%) RISK FACTOR Emergency major operations, particularly in the elderly Aortic and other major vascular surgery Peripheral vascular surgery Anticipated prolonged surgical procedures associated with large fluid shifts and blood loss Intermediate (cardiac risk generally <5%) Carotid endarterectomy Intraperitoneal and intrathoracic surgery Orthopedic surgery Prostate surgery Low (cardiac risk generally <1%) Endoscopic procedures Superficial procedures Cataract surgery Breast surgery From Eagle KA, Berger PB, Calkins H, et al: ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery Executive Summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1996 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 94: , The ACC/AHA guidelines permit more appropriate use of preoperative testing (echocardiography, dipyridamole myocardial stress perfusion imaging, traditional exercise stress test, or angiography) and beta blocker therapy, with probable cancellation of the elective operative procedure. [23] An algorithm for perioperative cardiovascular evaluation is presented in Figure The role of preoperative coronary artery revascularization has yet to be determined. Percutaneous transluminal coronary angioplasty may be beneficial in reducing perioperative cardiac morbidity in a select group of patients.

6 FIGURE 13-1 Algorithm for perioperative cardiovascular evaluation for noncardiac surgery. Patients with major predictors of risk and patients with intermediate predictors of risk and a planned high-risk procedure undergo additional testing and resultant indicated treatment before elective surgery. CHF, Congestive heart failure; MI, myocardial infarction. (Adapted from Eagle KA, Brundage BH, Chaitman BR, et al: Guidelines for perioperative cardiovascular evaluation for noncardiac surgery. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 27: , 1996.) Patients identified as being at high risk for myocardial events in the perioperative period are managed with beta blockers, careful intraoperative monitoring, maintenance of perioperative normothermia and vital signs, and continued postoperative pharmacologic management, including the administration of adequate pain medication. Given several days before surgery and continued for several days afterward, beta blockers (e.g., atenolol) have been shown to reduce perioperative myocardial ischemia by 50% in patients with CAD or CAD risk factors. [24] Patients with chronic stable angina continue with their antianginal medications, and beta blockers are continued to the time of surgery and thereafter. An ECG is obtained before, immediately after, and for 2 days after surgery. Patients are monitored for 48 hours, and

7 in high-risk patients for 5 days, after surgery and cardiac enzyme levels are also checked. Invasive hemodynamic monitoring is appropriate for patients with left ventricular dysfunction, fixed cardiac output, and unstable angina or recent MI. Shortness of breath and chest pain remain the two postoperative symptoms that must always be carefully evaluated and never written off as postoperative discomfort. Subtle changes in the ST segment and T wave hint of possible ischemia or MI. Evaluation of a patient suspected of having an intraoperative or postoperative MI includes immediate assessment by electrocardiography and measurement of biomarkers of myocardial necrosis. Constant electrocardiographic monitoring is required so that the development of any potentially lethal arrhythmia can immediately be treated. If the level of cardiac function is a concern, echocardiography is considered. Cardiac troponin levels identify patients with myocardial necrosis but do not identify the cause of necrosis. Cardiac-specific troponin levels begin to rise by 3 hours after myocardial injury. A troponin I level more than 1 ng/ml is specific, and elevations persist for 7 to 10 days. Troponin T elevations persist for 10 to 14 days after MI. Medical management of myocardial ischemia and MI includes immediate administration of high-flow oxygen, transfer to the intensive care unit, and early involvement of a cardiologist. The goal of management of myocardial ischemia is to preserve the maximal amount of myocardial muscle possible, as well as improve coronary blood flow and decrease myocardial work. Immediate administration of beta blockers (oral or IV, dose-titrated to decrease heart rate to less than 70 beats/min) and aspirin (160 to 325 mg) is essential. Beta blockers are not indicated for patients with bradycardia, hypotension, severe left ventricular dysfunction, heart block, or severe bronchospastic disease. Nitroglycerin (given as a continuous IV infusion after a loading dose) alleviates pain and is beneficial for patients with MI complicated by HF or pulmonary edema. Systemic heparinization (or SC LMWH), if not contraindicated, is administered. In most cases, thrombolytic therapy is contraindicated in the postoperative period and can be used only in the situation in which minor surgery is performed. Studies have shown that emergency stricture dilation and coronary artery stenting may be more effective than thrombolytic therapy. ACE inhibitors may be given early after MI, especially anterior MI or with a low left ventricular ejection fraction, and probably continued as a long-term therapy. Angiography must be strongly considered if the patient has ongoing myocardial ischemia that does not respond to pharmacologic therapy. Cardiogenic Shock Causes Cardiogenic shock is one of the most serious sequelae of acute MI. Presumably, 50% or more of left ventricular muscle mass is irreversibly damaged, leading to a substantial reduction in cardiac output and resulting hypoperfusion. Other possible, less frequent causes of cardiogenic shock include ruptured papillary muscle or ventricular wall, aortic valvular insufficiency, mitral regurgitation, and ventricular septal defect. Cardiogenic shock is a highly lethal condition that results in the death of up to 75% of patients unless immediate management is instituted. Other serious sequelae from acute MI include CHF, arrhythmias, and thromboembolic complications. Presentation and Management Observant physicians will watch a patient with an acute MI closely for evidence of the aforementioned complications. Cardiogenic shock usually develops rapidly over a short period and is marked by hypotension and respiratory failure. Aggressive management is required to save the life of a patient with this devastating condition. Immediate institution of mechanical ventilation with a high FIO 2, and occasional monitoring with a Swan-Ganz catheter, is important. For patients who do not respond to pharmacologic and conservative management, intra-aortic balloon pumps and ventricular assist devices may be lifesaving. For patients who have adequate myocardial reserve, coronary artery bypass may occasionally be indicated. Cardiac transplantation remains the gold standard treatment of end-stage HF.

8 Postoperative Cardiac Arrhythmias Causes Cardiac arrhythmias are common in the postoperative period and are more likely to occur in patients with structural heart disease. Cardiac arrhythmias are classified into tachyarrhythmia, bradyarrhythmia, and heart block. Tachyarrhythmia is further subdivided into supraventricular (sinus, atrial, nodal) and ventricular (premature ventricular contraction [PVC], ventricular tachycardia, ventricular fibrillation). Sustained supraventricular arrhythmia in patients undergoing major noncardiac surgery may be associated with an increased risk for a cardiac event (e.g., heart failure, MI, unstable angina) and cerebrovascular event. [24] Factors associated with increased risk for supraventricular arrhythmias are increasing age, history of heart failure, and type of surgery performed. Sinus tachycardia and atrial flutter or fibrillation are the most common types of tachyarrhythmia. Sinus tachycardia is caused by pain, fever, hypovolemia, anemia, anxiety and, less commonly, heart failure, MI, thyrotoxicosis, and pheochromocytoma. Atrial flutter or fibrillation occurs commonly in patients with electrolyte imbalance, history of atrial fibrillation, and chronic obstructive lung disease. Ventricular ectopy occurs in one third of patients after major noncardiac surgery and risk factors associated with an increased risk for PVCs include the presence of preoperative PVCs, history of CHF, and cigarette smoking. Postoperative risk factors include hypoxia, acute hypokalemia, and hypercapnia. Ventricular arrhythmias consist of largely benign and sustained ventricular tachycardia and fibrillation. Nonsustained ventricular tachycardia commonly occurs during or after major vascular procedures. Presentation The physiologic impact of an arrhythmia depends on its type and duration and the patient's underlying cardiac status and ventricular response. Most arrhythmias are transient and benign and are not associated with symptoms or physiologic changes. Occasionally, sinus tachycardia may precipitate ischemia and PVCs, and unsustained ventricular tachycardia may precipitate ventricular tachycardia. Arrhythmias may also represent a prelude to hemodynamic compromise, especially in patients with severe heart disease or a history of MI or cardiomyopathy. Both bradyarrhythmia and tachyarrhythmia may decrease cardiac output. Symptoms associated with arrhythmias include palpitations, chest pain, shortness of breath, dizziness, loss of consciousness, cardiac ischemia, and hypotension. Treatment The patient's underlying cardiac status is the key to management of arrhythmias. Arrhythmias may signal the presence of reversible causes or precipitating factors that must be sought and dealt with, and treatment is based on the presence of adverse hemodynamic effects of the arrhythmia, not its mere presence. In tachyarrhythmia, control of the ventricular response is essential, and distinction between arrhythmias that traverse the atrioventricular node (atrial fibrillation, ectopic atrial tachycardia) from those that do not (ventricular tachycardia, fibrillation) is paramount. Antiarrhythmics that alter atrioventricular node conduction and control the ventricular rate are indicated in the treatment of arrhythmias that traverse the node and dangerous in those that do not. Beta blockers are avoided in patients with a low ejection fraction and bronchospastic lung disease. The ultimate goal of therapy is to achieve sinus rhythm and, if not possible, prevention of complications associated with arrhythmias must be addressed (e.g., anticoagulants given to patients with atrial fibrillation for more than 48 hours). The management of postoperative arrhythmias is outlined in Box 13-8.

9 Box 13-8 Management of Postoperative Cardiac Arrhythmias Cardiology consultation Monitoring of the patient on a telemetry floor or in the intensive care unit 12-lead ECG and long strip to differentiate between atrial and ventricular arrhythmia Clinical assessment Vital signs Peripheral perfusion Cardiac ischemia and congestive heart failure Level of consciousness Treatment of arrhythmia Tachyarrhythmia Unstable: Cardioversion Stable Bradyarrhythmia Supraventricular tachyarrhythmia: Beta blockers (esmolol), ibutilide, or alternatives (e.g., digoxin, calcium channel blockers, amiodarone) Paroxysmal supraventricular tachyarrhythmia: vagal stimulation or adenosine. Digoxin, amiodarone, or calcium channel blocker if adenosine fails Multifocal atrial tachycardia: Beta blocker, calcium channel blocker, or amiodarone Ventricular tachycardia: Lidocaine, procainamide, or amiodarone Sustained: Atropine or β-adrenergic agonist Transient: No therapy Heart block: Persistent high-grade second- or third-degree block; insertion of a permanent pacemaker

10 Postoperative Heart Failure Causes Heart failure is a clinical syndrome characterized by any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. [25] Several risk factors predispose to the development of heart failure, the most significant of which are CAD, hypertension, and increasing age. Poorly controlled heart failure represents one of the most serious cardiac risk factors for a preoperative patient, whereas patients with well-managed heart failure generally do well during an operation. Many factors can lead to new-onset heart failure or decompensation of preexisting heart failure in the perioperative period, including perioperative myocardial ischemia or MI, volume overload, hypertension, sepsis, occult cardiac valvular disease, PE, and new-onset atrial fibrillation. The risk for heart failure is greatest immediately after surgery and in the first 24 to 48 hours after surgery. Presentation Patients with poorly controlled heart failure or new-onset heart failure suffer from shortness of breath and wheezing. Physical examination often reveals tachycardia, a narrow pulse pressure, low pressure or orthostatic hypotension, jugular venous distention, peripheral edema, rales, and general evidence of poor peripheral perfusion. The ECG may reveal an MI, ventricular hypertrophy, atrial enlargement, or arrhythmias. A CXR may indicate cardiomegaly, pulmonary edema, and pleural effusion. Echocardiography assesses ventricular function and provides information about regional wall motion and valve function. Treatment Management of patients with heart failure is directed at optimizing preload, afterload, and myocardial contractility. Afterload reduction is accomplished by lowering the vascular resistance against which the heart must contract, and ACE inhibitors are a cornerstone of therapy for heart failure. Nitrates (venodilator) and hydralazine (vasodilator) reduce excessive preload and are used as an alternative in patients who cannot tolerate ACE inhibitors. β-adrenergic blockade (selective or nonselective) for heart failure has proved effective in reducing mortality in patients with ischemic and nonischemic heart failure. [26] Digoxin (a sympatholytic agent) has traditionally been used for patients with heart failure in sinus rhythm. Its use has decreased given the superior and definitive beneficial effects of ACE inhibitors and beta blockers. Diuretics are necessary in all patients with heart failure for the management of volume overload and relief of symptoms of congestion. Calcium channel blockers are used only for the treatment of hypertension or angina not adequately controlled with other agents, such as ACE inhibitors or beta blockers. Inotropes increase cardiac contractility and are used in the critically ill and patients with endstage heart failure. Copyright 2013 Elsevier Inc. All rights reserved.