Cardiology Core Curriculum - part 9 doc

bypass surgery would have been performed if the angioplasty had been complicated by acute closure. There are no data from prospective trials that support or undermine this plan; for this reason, the physicians considered discussion of potential strategies before performance of the non-invasive test for ischemia to be particularly important. Answer to question 4 Hemodynamic monitoring with a pulmonary artery catheter and a radial arterial line can be used to minimize hemodynamic shifts. Hypovolemia due to blood loss can be rapidly detected and treated using such monitoring, and hypertension can be reduced with intravenous vasodilator therapy. Case 15.3 A 76-year-old female with lumbar spinal stenosis was considered for surgery because of intractable pain. The patient had a long history of exertional dyspnea and leg edema. She also had about one episode per week of an epigastric and substernal chest burning that was not associated with exertion. Prior echocardiographic studies had shown a markedly hypertrophied left ventricle with a normal ejection fraction. She had been treated for pulmonary congestion due to presumed diastolic dysfunction with verapamil 240 mg/day orally, furosemide 180 mg/day orally, and potassium 20 mEq orally three times daily. Other medical problems included diabetes, for which she took daily insulin, and restrictive lung disease that was believed to be due to obesity. Examination. Physical examination: the patient was obese and in a wheelchair, unable to stand. Respiratory rate: 18/min. Pulse: 70 beats/min, normal character. Blood pressure: 130/80 mmHg in right arm. Jugular venous pulse: not visible. Cardiac impulse: normal. First heart sound: normal. Second heart sound: split normally on inspiration. Grade 2/6 murmur at the left sternal border that did not change with handgrip or Valsalva. Chest examination: bilateral basal rales. Abdominal examination: soft abdomen, no tenderness and no masses. Normal liver span. Moderate edema of lower extremities. Investigations. Electrocardiogram: sinus rhythm, left ventricular hypertrophy with non-specific ST-T-wave abnormalities. An echocardiographic study showed mild dynamic obstruction in the left ventricular outflow track, and abnormal, diffuse upper septal thickening. Right heart structures were normal in size and function. There was mild tricuspid regurgitation consistent with a right heart systolic pressure of 35–40 mmHg. Cardiology Core Curriculum 500 Questions 1. Should this patient undergo a non-invasive test for ischemia, such as a dipyridamole thallium scintigraphy? 2. Should this patient receive general or spinal/epidural anesthesia? 3. What might be the consequences of postoperative tachyarrhythmias in this patient? Answers Answer to question 1 Even if a non-invasive test for ischemia suggested that the patient had myocardium in jeopardy as the cause of her chest discomfort, the basic management plan would not have been altered. Major elective orthopedic surgery is associated with a low cardiovascular complication rate, and even if the patient had known coronary disease the physicians would have been unlikely to recommend coronary angiography and coronary revascularization, or to have suggested hemodynamic monitoring for this low risk procedure. Had the patient been scheduled for a higher risk procedure, such as major vascular surgery, then the physicians would have considered a non-invasive test for ischemia because the patient’s poor functional status made her history of chest pain unreliable. Answer to question 2 In general, the risks for major complications associated with spinal, epidural, and general anesthesia are similar. However, spinal and epidural anesthesia are relatively contraindicated in patients with hypertrophic cardiomyopathies because venodilatation can rapidly reduce venous return to the heart. Because this patient’s hypertrophied left ventricle is especially dependent on high filling pressures, this reduction in venous return could lead to abrupt severe falls in cardiac output. Answer to question 3 Although this patient’s dynamic outflow obstruction was not severe, she was at risk for hypotension due to reduced cardiac output if she developed a tachycardia because of an arrhythmia or sinus tachycardia resulting from pain or blood loss. Patients with hypertrophic cardiomyopathy require longer filling times for their left ventricle in order to achieve a normal volume. Faster heart rates decrease the amount of time between each systole during which the ventricle can fill. If this patient developed atrial fibrillation, then she would also have lost her “atrial kick” – the augmentation in left ventricular filling that occurs with each atrial contraction. Therefore, tachyarrhythmias were an especially serious potential problem for her. Non-cardiac surgery in patients with heart disease 501 References 1 Mangano DT, Goldman L. Preoperative assessment of patients with known or suspected coronary disease. N Engl J Med 1995;333:1750–6. 2 Mason JJ, Owens DK, Harris RA, Cooke JP, Hlatky MA. The role of coronary angiography and coronary revascularization before noncardiac vascular surgery. JAMA 1995;273:1919–24. 3 ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery. ACC/AHA Guideline Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery: Executive Summary. Circulation 2002;105: 1257–67. 4 Lee TH. Reducing cardiac risk in noncardiac surgery [editorial]. N Engl J Med 1999;341:1838–40. 5 Rao T, El-Etr A. Myocardial infarction following anesthesia in patients with recent myocardial infarction. Anesth Analg 1981;60:271–2. 6 Mangano DT, Layug EL, Wallace A, Tateo I, for the Multicenter Study of Perioperative Ischemia Research Group. Effect of atenolol on mortality and cardiovascular morbidity after noncardiac surgery. N Engl J Med 1996;335: 1713–20. 7 Poldermans D, Boersma E, Bax JJ, et al. The effect of bisoprolol on perioperative mortality and myocardial infarction in high-risk patients undergoing vascular surgery. N Engl J Med 1999;341:1789–94. 8 Weitz H, Goldman L. Noncardiac surgery in the patient with heart disease. Med Clin North Am 1987;71:413–32. 9 Foster E, Davis K, Carpenter J, et al. Risk of noncardiac operation in patients with defined coronary disease: the Coronary Artery Surgery Study (CASS) Registry experience. Ann Thorac Surg 1986;41:42–50. 10 Goldman L, Caldera D, Southwick F, et al. Cardiac risk factors and complications in non-cardiac surgery. Medicine 1978;57:357–70. 11 Katz J, Cronan L, Barash P, et al. Pulmonary artery flow guided catheters in the perioperative period. JAMA 1977;237:2832–4. 12 Kearon C, Hirsh J. Management of anticoagulation before and after elective surgery. N Engl J Med 1997;336:1506–11. 13 Thompson R, Liberthson R, Lowenstein E. Perioperative anesthetic risk of noncardiac surgery in hypertrophic obstructive cardiomyopathy. JAMA 1985;254:2419–21. 14 Vanik P, Davis H. Cardiac arrhythmias during halothane anesthesia. Anesth Analg 1968;47:299–307. 15 Goldman L, Caldera DL, Nussbaum SR, et al. Multifactorial index of cardiac risk in noncardiac surgical procedures. N Engl J Med 1977;297:845–50. 16 Goldman L. Multifactorial index of cardiac risk in noncardiac surgery: ten-year status report. J Cardiothorac Anesth 1987;1:237–44. 17 Zeldin R. Assessing cardiac risk in patients who undergo noncardiac surgical procedures. Can J Surg 1984;27:402–4. 18 Detsky A, Abrams H, Forbath N, Scott J, Hilliard J. Cardiac assessment for patients undergoing noncardiac surgery. A multifactorial clinical risk index. Arch Intern Med 1986;146:2131–4. 19 Jeffrey C, Kunsman J, Cullen D, Brewster D. A prospective evaluation of cardiac risk index. Anesthesiology 1983;58:462–4. 20 Kennedy H, Whitlock J, Sprague M, et al. Long term follow up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med 1985; 312:193–7. 21 Sprung C, Pozen R, Rozanski J, et al. Advanced ventricular arrhythmias during bedside pulmonary artery catheterization. Am J Med 1982;72:203–8. 22 Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for prediction of cardiac risk of major noncardiac surgery. Circulation 1999;100:1043–9. Cardiology Core Curriculum 502 23 Ashton C, Petersen N, Wray N, et al. The incidence of perioperative myocardial infarction in men undergoing noncardiac surgery. Ann Intern Med 1993;118: 504–10. 24 Eagle K, Coley C, Newell J, et al. Combining clinical and thallium data optimizes preoperative assessment of cardiac risk before major vascular surgery. Ann Intern Med 1989;110:859–66. 25 Raby K, Goldman L, Creager M, et al. Correlation between preoperative ischemia and major cardiac events after peripheral vascular surgery. N Engl J Med 1989; 321:1296–300. Non-cardiac surgery in patients with heart disease 503 504 16: Heart disease in pregnancy JOHN D RUTHERFORD During a normal pregnancy there are major changes in blood volume, total body water and sodium, and cardiovascular hemodynamics, in part because of increases in steroid hormones, including estrogens. Cardiac output (the product of stroke volume and heart rate) increases by 40–50%, reaches a peak in mid-pregnancy, and is either maintained or declines slightly at term. There is an inverse relationship between this increase in cardiac output and a significant fall in peripheral arterial resistance (and mean arterial blood pressure), with diastolic blood pressure falling more than systolic blood pressure and pulse pressure increasing. In addition, red blood cell mass increases progressively during pregnancy by 30–40%, with a greater increase in plasma volume resulting in the “physiological anemia of pregnancy”. Total body water and exchangeable body sodium increase with activation of the renin–angiotensin system and lowering of the osmotic thresholds for thirst stimulation and vasopressin release. This results in a fall in plasma sodium and osmolality, and clinical edema is found in up to 80% of healthy pregnant women. Because resting cardiac output is increased the maximal cardiac output induced by exercise is achieved at a lower level of work, and as pregnancy advances there is a gradual increase in resting oxygen consumption. Serial echocardiography shows that the cardiac adaptation to normal pregnancy is a gradual increase in all cardiac dimensions that is more pronounced on the right side of the heart, and that mild, transient tricuspid and mitral regurgitation are normal findings. 1 Because of the changes in hemodynamics associated with pregnancy, particularly the major increase in cardiac output and the fall in systemic vascular resistance, certain cardiac conditions will be well tolerated and others poorly tolerated (Table 16.1). Peripartum cardiomyopathy Peripartum cardiomyopathy is a rare and poorly understood condition that is defined clinically as the development of cardiac failure in the last month of pregnancy, or within 5 months of delivery, in the absence of either recognizable heart disease before the last month of pregnancy or an identifiable cause for the heart failure. 2 Echocardiographic demonstration of left ventricular systolic dysfunction is an important component of the diagnosis. Among a large series of patients with cardiomyopathy, the women with peripartum cardiomyopathy appeared to have a better survival (94% at 5 years) than did patients with other etiologies. 3 After the diagnosis is made some patients’ cardiac function can rapidly revert to normal, whereas others have persistent evidence of cardiac dysfunction beyond 6–12 months of diagnosis. The persistence of cardiac dysfunction beyond 6–12 months often indicates a long-term problem and almost always supports an absolute contraindication to a repeat pregnancy. Even in patients who appear to have “recovered” from peripartum cardiomyopathy, and who have normal resting ventricular function, there may be impaired contractile reserve. Finally, a few patients may rapidly deteriorate, fail medical therapy, and require cardiac transplantation. Valvular heart disease In pregnant patients who are asymptomatic or who have mild cardiac symptoms, the lesions of mild or moderate mitral or aortic valve regurgitation are usually well tolerated. The reduced peripheral vascular resistance (or afterload) of pregnancy tends to diminish the degree of regurgitation and, provided the patient maintains sinus rhythm, the increased hemodynamic load of pregnancy is usually well tolerated. For patients with overt cardiac symptomatology, or major degrees of aortic or mitral regurgitation, the hemodynamic Heart disease in pregnancy 505 Table 16.1 Prognosis of cardiac conditions Well versus poorly tolerated Cardiac condition Well tolerated Asymptomatic patients – those NYHA functional class I Valvular regurgitation: mild and moderate mitral and aortic regurgitation Left to right shunt (without pulmonary hypertension): ASD, VSD, PDA Poorly tolerated Breathless at rest – NYHA functional class IV Valvular stenoses: moderate to severe mitral and aortic stenosis Right to left shunt: Eisenmenger’s syndrome Pulmonary hypertension: moderate to severe Marfan’s syndrome Myocardial infarction ASD, atrial septal defect; NYHA, New York Heart Association; PDA, patent ductus arteriosus; VSD, ventricular septal defect changes of pregnancy may impose an excessive load and lead to hemodynamic compromise. In marked contrast, mitral and aortic valve stenosis are generally poorly tolerated during pregnancy. The severity of the fixed stenosis is accentuated by the increase in cardiac output of pregnancy, and in patients with mitral stenosis the increase in heart rate during pregnancy shortens diastole and increases left atrial pressure. Mitral stenosis Mitral stenosis is the commonest and most important rheumatic cardiac lesion seen in pregnancy. The dominant symptom is breathlessness, and the onset of atrial fibrillation may be associated with marked decompensation and should be considered a medical emergency. In patients with mitral stenosis both diuretics and β-blockers can safely be used during pregnancy. New onset arrhythmias, such as atrial fibrillation or supraventricular tachycardia, should be treated promptly. The use of β-blockers, or perhaps digitalis, may be appropriate for controlling the ventricular response; however, acute pulmonary edema may ensue rapidly if the ventricular rate is not controlled and sinus rhythm regained. Therefore, for rapid atrial fibrillation associated with symptoms, prompt cardioversion is recommended. If a patient in sinus rhythm, with mitral stenosis, becomes pregnant and has symptoms during the first trimester of pregnancy, despite diuretic therapy, then it is doubtful that the patient and/or fetus will tolerate the lesion hemodynamically throughout pregnancy, labor, delivery, and the puerperium. In such patients, with symptomatology of greater than New York Heart Association functional class II, consideration should be given to either surgical intervention or mitral balloon valvuloplasty in appropriate candidates. Generally, pregnancy does not influence the maternal surgical results, but there is a fetal mortality of approximately 10%, and surgery early in pregnancy may be associated with abortion and later in pregnancy with premature labor. With severe mitral valve stenosis, there is a pregnancy-related mortality of up to 5%. Labor, delivery, and especially the immediate postpartum period appear to be the times of greatest risk. In patients with severe symptoms, a rise in pulmonary capillary wedge pressure of approximately 10 mmHg may be anticipated immediately postpartum. Clark et al. 4 recommended that such patients should have oxygen administration in labor in the recumbent position; a pulmonary artery wedge catheter should be placed to monitor hemodynamics during early labor induction, and reduction in Cardiology Core Curriculum 506 pulmonary capillary wedge pressures to approximately 14 mmHg is a desired goal. They recommend epidural anesthesia during the active phase of labor, careful monitoring during the puerperium, and use of cesarean section for obstetric indications alone. Valve replacements Both valve surgery during pregnancy and pregnancy in patients who have had a valve replacement are hazardous to the mother and to the fetus. 5 Mechanical prosthetic valves carry a risk for thromboembolic events, patients require lifelong anticoagulation, and associated pregnancy carries an estimated maternal mortality of up to 4%. Biologic prostheses may structurally deteriorate, especially during the second and third decades of life, although some suggest that these valves may be the preferred replacement in women who are anticipating having a child in an attempt to avoid the deleterious effects of anticoagulation. Anticoagulation Pregnant patients with rheumatic mitral valve disease (and associated paroxysmal or chronic atrial fibrillation), with heart valve replacements, and with a history of recurrent pulmonary thromboembolism may require anticoagulants during pregnancy. Warfarin crosses the placenta, is teratogenic, and its use during the first trimester of pregnancy carries a significant risk to the fetus. Exposure in the weeks 6–9 of gestation may produce the fetal warfarin syndrome, and spontaneous abortions, stillbirths, and neonatal deaths may occur. In a review of anticoagulant use in pregnant women with prosthetic heart valves, 6 use of oral anticoagulation throughout pregnancy was associated with warfarin embryopathy in 6·4% of live births, which was eliminated with substitution of heparin at or before 6 weeks of gestation. When heparin was used between weeks 6 and 12, in place of continued warfarin therapy, the risk for valve thrombosis increased from 4% to 9%. The estimated risk for maternal hemorrhage in a woman taking anticoagulants is 2·5%, with the majority of episodes occurring at the time of delivery. Unfractionated heparin is often used during pregnancy and its complications include hemorrhage, thrombocytopenia, and symptomless bone loss (osteopenia). Low molecular weight heparins and heparinoids are increasingly being used during pregnancy. They do not appear to cross the placenta, are less likely to cause heparin-induced thrombocytopenia, may result in a lower risk for Heart disease in pregnancy 507 heparin-induced osteopenia, and have the potential for once daily administration. Because of the current uncertainty of adequate protection of patients with the use of full dose heparin, the optimal management of women with mechanical heart valves may involve the use of warfarin throughout pregnancy except for two time periods, namely between 6 and 12 weeks gestation (in order to eliminate the risk for warfarin embryopathy) and after 36 weeks of gestation (in order to minimize the risk for maternal hemorrhage at the time of labor and delivery). 6 During these periods, adjusted dose unfractionated heparin should be used to maintain a therapeutic mid-interval activated partial thromboplastin time of 2·0–2·5 times control. Planned pregnancy in patients on long-term anticoagulants In women of childbearing age who require long-term anticoagulants, the risks for anticoagulant therapy during pregnancy must be explained before conception. If pregnancy is desired, then a reasonable approach is to perform frequent pregnancy tests and to substitute heparin for warfarin when pregnancy is achieved. This assumes that warfarin is safe during the first 4–6 weeks of gestation, 7 and after 12 weeks warfarin therapy is reinstituted. Coronary artery disease With increasing age and duration of fertility of mothers, and with more than half of the total births occurring in women aged 30–44 years, coronary artery disease during pregnancy is likely to be encountered with increasing frequency. In pregnancy, coronary artery disease presenting as angina has been associated with smoking alone, vasospastic angina, pre-eclampsia, homozygous familial hypercholesterolemia, and diabetes mellitus. Acute myocardial infarction presenting during pregnancy is very rare (incidence 0·1%) but is potentially lethal for both the mother and the fetus. 8 Usually, women who have a myocardial infarction before the age of 40 years have either insulin requiring diabetes mellitus, a strong family history of premature coronary artery disease, and/or hypertension and hyperlipidemia. Cocaine abuse should also be considered and spontaneous coronary artery dissection is a rare entity, usually reported in women. The latter condition occurs one-third of the time during pregnancy or the puerperium, and presents with sudden death or an unstable coronary syndrome. The left anterior Cardiology Core Curriculum 508 descending coronary artery is usually involved, and if the patient survives the initial event long-term survival is possible. 9 It is important to realize that, during the peripartum period (whether or not acute myocardial infarction has occurred), total creatine phosphokinase and creatine kinase-MB increase markedly during normal vaginal deliveries. They reach a peak of two to four times baseline levels 24 hours postpartum. 10 Evolving electrocardiographic changes, coupled with echocardiographic evidence of regional wall motion abnormalities, are essential in making a diagnosis of acute myocardial infarction during this period. Thrombolytic agents used during pregnancy for venous thrombosis, pulmonary embolism, and thrombosed prosthetic heart valves are associated with a maternal mortality of 1–2%, a fetal mortality of 6%, and hemorrhagic complications in 8%. Such risks may outweigh any potential benefits. Successful percutaneous transluminal coronary angioplasty has been performed during pregnancy. Any management plan of a patient with an acute coronary syndrome requires close consultation between the cardiologist, the obstetric service, and the anesthesiology service in order to coordinate and plan an elective labor or provide optimal management of an unexpected premature labor. In addition, the team needs to develop a strategy to provide a greater chance of prompt and effective rescue of the fetus in the event of sudden maternal demise. Because the course of events can change dramatically and rapidly, it is important that the goals of therapy and the alternatives be explained simply and clearly to the patient and her relatives. Intracardiac shunts The most common left to right cardiac shunts encountered in women of childbearing age are atrial or ventricular septal defects. In the absence of significant cardiac symptomatology or pulmonary hypertension, the outcome of pregnancy is usually normal and uncomplicated because the normal, major fall in systemic vascular resistance during pregnancy tends to diminish the magnitude of the left to right shunting. However, serious and fatal maternal and fetal problems can occur during pregnancy in patients with shunts associated with cardiac arrhythmias, right heart failure, or pulmonary hypertension. Pulmonary hypertension Pulmonary hypertension is associated with substantially increased maternal mortality. Maternal mortality approaches 50% in Heart disease in pregnancy 509 [...]... early puerperium Acta Obstet Gynecol Scand 199 6;75:255–60 521 Cardiology Core Curriculum 11 Weiss BM, Zemp L, Seifert B, Hess OM Outcome of pulmonary vascular disease in pregnancy: a systematic overview from 197 8 through 199 6 J Am Coll Cardiol 199 8;31:1650–7 12 Gleicher N, Midwall J, Hochberger D, et al Eisenmenger's syndrome and pregnancy Obstet Gynecol Surv 197 9;34:721–41 13 Rossiter JP, Repke JT, Morales... pregnancy Chest 199 8;114(suppl):524S–30S 8 Hands M, Johnson MD, Saltzman DH, Rutherford J The cardiac, obstetric, and anesthetic management of pregnancy complicated by myocardial infarction J Clin Anesth 199 0;2:258–68 9 Madu EC, Kosinski DJ, Wilson WR, Burket MW, Fraker TD, Ansel GM Two-vessel coronary artery dissection in the peripartum period Case report and literature review Angiology 199 4;45:8 09 16 10 Abramov... ventricular 36/8, pulmonary arterial 36/21 (24/12), left atrial 18 (7), left ventricular 92 /7 (95 /7), aorta 92 /64 (95 /67) Cardiac index: 2 9 l/min per m2 (2 9 l/min per m2) Mitral valve gradient 9 mmHg (< 2·0 mmHg) Mitral valve area: 1·6 cm2 (>3·0 cm2) Left ventricular angiogram: no mitral regurgitation 517 Cardiology Core Curriculum Before After 40 mmHg a LA v 20 10 0 LV TM 6602858 Figure 16.2 Pressures... the Marfan syndrome Am J Obstet Gynecol 199 5;173:1 599 –606 14 Elkayam U, Ostrzega E, Shotan A, Mehra A Cardiovascular problems in pregnant women with the Marfan syndrome Ann Intern Med 199 5;123:117–22 15 Shores J, Berger KR, Murphy EA, Pyeritz RE Progression of aortic dilatation and the benefit of long-term β-adrenergic blockade in Marfan's syndrome N Engl J Med 199 4;330:1335–41 16 Page RL Treatment of... Heart J 199 5;130:871–6 17 Anonymous Guidelines for cardiopulmonary resuscitation and emergency cardiac care Emergency Cardiac Care Committee and Subcommittees, American Heart Association Part IV Special resuscitation situations JAMA 199 2;268:2242–50 18 Dajani AS, Taubert KA, Wilson W, et al Prevention of bacterial endocarditis Recommendations by the American Heart Association JAMA 199 7;277:1 794 –801 522... produce vasodilation via β-adrenergic pathways (and vasoconstriction via α-adrenergic pathways) β-Adrenergic agonists modulate the renal production of renin, and via the renin–angiotensin–aldosterone system they modulate blood pressure (see Chapter 4) β-Adrenergic blockers (antagonists) partly or completely block the agonist effects In the human heart there is a mixture of β 1- and β2-adrenergic receptors,... in the liver by the 5 29 Cardiology Core Curriculum glutathione–organic nitrate reductase system Tachyphylaxis in response to the hemodynamic effects of nitroglycerin occur with prolonged use and is improved by lower doses of nitrates or by an 8–10 hour nitrate-free period every day Tachyphylaxis is thought, in part, to be secondary to depletion of sulfhydral groups; this nitrate-free period permits... plasminogen activator (t-PA), which is synthesized and released by endothelial cells These agents have been shown to lower mortality of patients with ST-segment elevation acute myocardial infarction when administered within 12 hours of the 533 Cardiology Core Curriculum onset of symptoms .9 There are numerous pharmacologic activators of plasminogen used clinically, including t-PA, streptokinase, retaplase,... ventricular pressure of 100 mmHg while her systolic blood pressure is approximately 90 mmHg The patient probably has Eisenmenger’s syndrome; maternal mortality approaches 50%, and fetal (or neonatal) mortality is around 10–15% There is no 5 19 Cardiology Core Curriculum I II II aVR aVL aVF V1 V2 V3 V4 V5 V6 Figure 16.3 This is a 12-lead electrocardiogram (from left to right and top to bottom the leads displayed... ratio of about 65%/35%, respectively There is a large number of β-adrenergic blocking drugs clinically available, with some or little selectivity for β 1- and β2-receptors; pure antagonism for the receptor or partial agonism; different degrees of lipophilicity; and highly varying pharmacokinetics, with half-lives varying from 8 min to 30 hours β-Adrenergic blockers are commonly used to treat angina pectoris . vascular surgery. N Engl J Med 199 9;341:17 89 94 . 8 Weitz H, Goldman L. Noncardiac surgery in the patient with heart disease. Med Clin North Am 198 7;71:413–32. 9 Foster E, Davis K, Carpenter J,. index for prediction of cardiac risk of major noncardiac surgery. Circulation 199 9;100:1043 9. Cardiology Core Curriculum 502 23 Ashton C, Petersen N, Wray N, et al. The incidence of perioperative. (24/12), left atrial 18 (7), left ventricular 92 /7 (95 /7), aorta 92 /64 (95 /67). Cardiac index: 2 9 l/min per m 2 (2 9 l/min per m 2 ). Mitral valve gradient 9 mmHg (< 2·0 mmHg). Mitral valve area: