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Coronary Circulation

          Myocardial blood supply is derived entirely from the right and left coronary arteries (Figs 5.4 and 5.5). Blood flows from epicardial to endocardial vessels. After perfusing the myocardium, blood returns to the right atrium via the coronary sinus and the anterior cardiac veins. A small amount of blood returns directly into the chambers of the heart by way of the thebesian veins. The right coronary artery (RCA) normally supplies the right atrium, most of the right ventricle, and a variable portion of the left ventricle (inferior wall). In 85% of persons, the RCA gives rise to the posterior descending artery (PDA), which supplies the superior–posterior interventricular septum and inferior wall—a right dominant circulation; in the remaining 15% of persons, the PDA is a branch of the left coronary artery—a left dominant circulation.

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        The left coronary artery normally supplies the left atrium and most of the interventricular septum and left ventricle (septal, anterior, and lateral walls). After a short course the left main coronary artery bifurcates into the left anterior descending artery (LAD) and the circumflex artery (CX); the LAD supplies the septum and anterior wall and the CX supplies the lateral wall. In a left dominant circulation, the CX wraps around the AV groove and continues down as the PDA to also supply most of the posterior septum and inferior wall.

        The arterial supply to the SA node may be derived from either the RCA (60% of individuals) or the LAD (the remaining 40%). The AV node is usually supplied by the RCA (85–90%) or, less frequently, by the CX (10–15%); the bundle of His has a dual blood supply derived from the PDA and LAD. The anterior papillary muscle of the mitral valve also has a dual blood supply that is fed by diagonal branches of the LAD and marginal branches of the CX. In contrast, the posterior papillary of the mitral valve is usually supplied only by the PDA and is therefore much more vulnerable to ischemic dysfunction.

      The unique features of coronary blood flow are given below:

  1. Unlike all the other organs where the blood flow occurs constantly, the left ventricle gets blood supply only during diastole as the coronary arteries are compressed during myocardial contraction.

  2. The absence of anastomoses between the left and right coronary arteries means that the critical occlusion ofany segment of the coronary vasculature cannot be compensated by the other sided vessels.

  3. The heart extracts 70% of the arterial oxygen content at rest resulting in a coronary venous oxygen saturation of about 30%. This is in contrast to the rest of the body where the oxygen extraction is only 25% of the oxygen delivery. The implication of this is that there is very little reserve for the heart to increase its oxygen extraction in times of increased oxygen requirement. The only way by which oxygen delivery can be increased is by increasing the blood supply by coronary vasodilation. However, an increase in coronary blood flow can independently increase myocardial oxygen consumption (Gregg effect). This may be explained by full coronary arteries splinting the heart and increasing the end-diastolic fiber length and contractility

Coronary Autoregulation

       Autoregulation is an intrinsic mechanism to keep the organ blood flow constant despite changes in the arterial perfusion pressure. For a given myocardial oxygen demand, the coronary blood flow (CBF) will remain relatively constant between mean arterial pressures of 60–140 mm Hg (Fig. 5.6). The exact mechanism of coronary autoregulation is not known although myogenic, tissue pressure and metabolic factors have been hypothesized.

        When coronary perfusion pressure (CPP) is 60 mm Hg there will be maximal autoregulatory vasodilatation to maintain coronary blood flow. Further decreases in coronary perfusion pressure will result in decrease in coronary blood flow. The reserve provides the increased coronary blood flow necessary to meet increases in myocardial oxygen consumption such as those induced by exercise, strain, etc. (Coronary perfusion pressure-CPP refers to the pressure gradient that drives coronary blood pressure.

       CPP = AODP – LVEDP where

                  AODP - Aortic Diastolic Pressure; LVEDP - Left Ventricular End-Diastolic Pressure).

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Ischemic heart disease - Etiology & Pathophysiology

        Atherosclerosis of epicardial arteries is the most common cause of myocardial ischemia. The precursor lesions of atherosclerosis are believed to be the fatty streak and diffuse intimal thickening. The typical advanced lesion is the fibrous plaque, which compromises blood flow. The plaque is often complicated by thrombosis, hemorrhage, and/or calcification. Fissures may develop, with consequent thrombosis, embolism, or aneurysmal dilatation, which may increase the dimension of the plaque with worsening of obstruction.

       A fixed coronary lesion is not always necessary to produce ischemia. Subendocardial ischemia may occur whenever the supply-demand ratio is reduced beyond the compensatory ability of the vasculature. The common conditions (many of which may coexist) are enumerated below:

  • Abnormally matched oxygen demand-supply (hypertensive ventricular hypertrophy, aortic stenosis, idiopathic hypertrophic subaortic stenosis)

  • Congenitalabnormalities(arteriovenousfistulas,ductus arteriosus) 

  • Reduced oxygen carrying capacity of blood (anemia, carboxyhemoglobin)

  • Coronary artery embolism (infective, thrombotic)

  • Coronary spasm

  • Arteritis (leutic aortitis, polyarteritis nodosa)

  • Hematologic thrombosis (polycythemia vera, thrombocytosis)

      There is a tight coupling between the coronary flow and myocardial oxygen demand. The heart is an aerobic organ, and, thus, it can tolerate only a small oxygen debt. Oxygen supply is provided by coronary blood flow. Coronary blood flow depends on:

  • Coronary perfusion pressure

  • Coronary vascular resistance (controlled by autoregulation and sympathetic factors)

  • Duration of diastole.

       The subendocardium is most susceptible for ischemia. It has limited vasodilation reserve and a higher metabolic demand than the subepicardium. Normal coronary vessels have the ability to reduce the flow resistance to 20% of the basal levels as a response to increases in myocardial oxygen demand. A vessel stenosis of greater than 40% will result in poststenotic dilatation to maintain flow. An 80% reduction in the vessel diameter will produce maximal dilatation with maintenance of adequate perfusion at rest. Any degree of increase in myocardial oxygen demand superimposed on this stenotic lesion will result in ischemia.

      The clinical squeal of myocardial ischemia may be the consequence of either an increase in myocardial oxygen demand in the face of fixed obstruction or a reduction in myocardial oxygen supply resulting from coronary spasm or transient platelet aggregation. In the involved areas, the metabolism switches from aerobic to anaerobic, with consequential loss of metabolic substrates and calcium entrapment. In addition, the perfusion impairment causes inadequate removal of metabolic by products (inosine and hypoxanthine) along with potassium ions, prostaglandins, kinins, and acetate—which may lead to further vasodilatation and worsening hypoperfusion. Persistent ischemia will result in tissue death accompanied by paradoxical motion of the central ischemic area (dyskinesia), reduction of contractility of adjacent areas (hypokinesia), and compensatory hyperfunction of uninvolved myocardium, resulting from local release of catecholamines and the Frank-Starling mechanism.

        The functional effects of the injury are related to the extent of the lesion. Diastolic function becomes abnormal in the early phase of the ischemic event. If the loss of activity involves critical or large areas, the ventricular compliance is reduced with a rise in end diastolic volume and end diastolic pressure further compromising coronary perfusion. This is followed by impairment of systolic function, with decrease of contractility and depression of stroke volume, cardiac output, and ejection fraction. Eventually cardiac failure will be the result if the regional abnormalities overwhelm the compensatory activity of the uninvolved myocardium.


Chronic Stable Angina

        Angina pectoris has been defined as discomfort in the chest or adjacent areas caused by transient myocardial ischemia without necrosis. The typical angina pain is usually described as a sensation of tightness, squeezing, burning, pressing, choking, aching, bursting, “gas,” indigestion, or an ill-characterized discomfort. It is often characterized by clenching a fist over the mid chest. The distress of angina is rarely sharply localized and is not spasmodic. The location of the referred pain may be variable: ulnar surface of left arm, right arm, neck, jaw, throat, head, or epigastrium. Frequently associated symptoms are nausea, vomiting, sweating, and sometimes palpitations. Exertion and emotional stress are usual precipitating factors along with conditions increasing oxygen demand such as cold exposure, fever and hypoglycemia. Prompt improvement or relief of symptoms with rest or nitroglycerine administration, or both, provides useful diagnostic information. Indeed, pain lasting less than 5 minutes or more than 20 to 30 minutes is usually not of anginal origin.

       In typical stable angina, the increase in myocardial oxygen demand or the sudden fall of oxygen supply, results in ischemia of the area supplied by the obstructed epicardial coronary artery. The effects are related to the degree of the anatomic obstruction, to the effectiveness of the collateral layer (if present), and to the number and degree of vessels involved.


Unstable Angina

         Unstable angina is defined as angina pectoris or equivalent ischemic discomfort with at least one of three features:

(1) it occurs at rest (or with minimal exertion), usually lasting >10 min;

(2) it is severe and of new onset (i.e., within the prior 4–6 weeks); and/or

(3) it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

         The pain is qualitatively similar to the typical angina pain, but is prolonged, and nitroglycerine does not provide lasting relief. Unstable angina usually represents the acute worsening of the atherosclerotic heart disease and carries a more grave prognosis if it is untreated. Events such as platelet aggregation, thrombosis, and spasm probably contribute to the precipitation of the ischemic episodes. Unstable angina of new onset can also be attributable to a vasoconstrictive component associated with a preexistent fixed obstruction of a single vessel.


Prinzmetal's Angina

       Prinzmetal (variant) angina is a clinical syndrome in which chest pain occurs without the usual precipitating factors and is associated with ST segment elevation rather than depression. It often affects women under 50 years of age. It characteristically occurs in the early morning, awakening patients from sleep, and is apt to be associated with arrhythmias or conduction defects. It may be diagnosed by challenge with ergonovine (a vasoconstrictor), although the results of such provocation are not specific and it entails risk. The pain is usually experienced at night and can result in syncope, acute myocardial infarction, severe arrhythmias, and sudden death. The leading event is coronary artery spasm. The transient dramatic reduction of the diameter of an epicardial artery results in ischemia, even in the absence of increased myocardial oxygen demand. Usually the spasm is focal, often close to the atheromatous plaques.

Myocardial Infarction

       Myocardial infarctions are the result of total or near-total coronary artery occlusion. ST segment elevation myocardial infarction (STEMI) results, in most cases, from an occlusive coronary thrombus at the site of a preexisting (though not necessarily severe) atherosclerotic plaque. More rarely, infarction may result from prolonged vasospasm, inadequate myocardial blood flow (eg, hypotension), or excessive metabolic demand. Very rarely, myocardial infarction may be caused by embolic occlusion, vasculitis, aortic root or coronary artery dissection, or aortitis. Cocaine is a cause of infarction, which should be considered in young individuals without risk factors.

      Acute transmural infarctions are often caused by coronary thrombi close to the atherosclerotic plaque or may be precipitated by coronary artery embolism. In subendocardial infarction, the necrosis involves only the subendocardium or the intramural myocardium, or both, without extension through the entire ventricular wall. The pathogenesis is often related to conditions that increase oxygen demand (pulmonary embolism, hypertension, hypotension, anemia) superimposed on narrowed but still patent vessels. In other instances, the cause is a thrombotic occlusion followed by early spontaneous thrombolysis.

       The extent and the functional consequences of the acute myocardial infarction depend on anatomic and pathophysiologic factors. The result is necrosis of the myocardium and loss of functional activity. Acutely, left ventricular pump function is depressed, with decrease in cardiac output, stroke volume, and blood pressure. Myocardial cell dropout is a consequence of not only the infracted area of the tissue but also infarction expansion during postinfarction remodeling. This can result in larger volumes of injured tissue.


Hibernating and Stunned myocardium

        Hibernating myocardium is a state when some segments of the myocardium exhibit abnormalities of contractile function. These abnormalities can be visualised during echocardiography or ventriculography. The phenomenon is highly significant clinically because it usually manifests itself in setting of chronic ischemia, that is potentially reversible by revascularization via cardiac catheterization. The regions of myocardium are still viable and can restore its function. There develops a new steady state between myocardial blood flow and myocardial function—myocardial blood flow is reduced and in consequence function is reduced too. The clinical situations where one can expect hibernating myocardium are: chronic stable angina, unstable angina, silent ischemia, after acute myocardial infarction.

       Stunned myocardium is a state when some section of the myocardium (corresponding to area of a major coronary occlusion) shows a form of contractile abnormality. This is a segmental dysfunction which persists for a variable period of time, about two weeks, even after ischemia has been relieved (by, for instance, angioplasty or coronary artery bypass surgery). In this situation, while myocardial blood flow returns to normal, function is still depressed for a variable period of time. Clinical situations of stunned myocardium are: acute myocardial infarction, after percutaneous transluminal coronary angioplasty (PTCA) and after cardiac surgery.

Coronary Steal Phenomenon


      A hypothetical framework for understanding coronary steal is presented in figure 5.7. Stenoses in the nonligated arteries provide sites for pressure gradient development. Under resting conditions there may be no pressure drop or only a small gradient across a stenosis, but after dipyridamole a pressure gradient may appear or become accentuated. Even if aortic pressure is maintained, coronary pressure may decrease markedly distal to the stenosis. Reduction in downstream pressure in turn causes a decrease in driving pressure for collateral flow; i.e., there is a narrowing of the pressure difference between the bed originating collateral flow and the bed receiving it. Decreased driving pressure causes a diminution in collateral flow and an augmentation of ischemia. In contrast, when the arteries providing collateral flow are normal, dipyridamole does not produce a significant fall in downstream pressure. Distal coronary pressure remains within a few mm Hg of the aortic pressure, and as long as aortic pressure is maintained, collateral driving pressure is also maintained. In this setting, collateral flow may increase if collateral resistance (either the vascular or extravascular components) is reduced sufficiently.

      In the schematic diagram, coronary artery divides into two branches—one completely occluded, the other stenosed but providing collaterals to the first. In the control situation on the left, distal pressure is low in the occluded arterial bed and there is a small gradient in mean pressure across the stenosis. Flow in the ischemic region (shaded area) is 20 ml/min/100 g and is determined by the collateral driving pressure, or the difference between distal pressures in the bed supplying collaterals (80 mm Hg) and the ischemic bed (20 mm Hg). Flow in the distribution of the stenotic vessel is normal at 70 ml/min/100 g and is evenly distributed between subendocardium (lower value in bracket) and subepicardium (upper value). During dipyridamole, with blood pressure maintained constant by phenylephrine, flow increases in the nonischemic bed to 200 ml/min/100 g but becomes maldistributed between subendocardium and subepicardium. In addition, pressure distal to the stenosis falls to 50 mm Hg, causing a reduction in collateral driving pressure. As a result, flow to the ischemic region decreases to 10 ml/min/100 g, interpreted as a coronary steal.


        The purpose of the preoperative diagnostic evaluation is to delineate the extent of ischemic heart disease and to assess its functional implications.

Physical examination

The physical examination often provides little information, lacking both in specificity and sensitivity. However some physical findings can be of predictive value.

  • Dyspnea on mild exertion or at rest—Poor ventricular function

  • Dependent edema, hepatojugular reflux, and hepato- megaly—Congestive heart failure

  • A displaced cardiac apex/jugular venous distention

  • S3 and S4 heart sounds—Decreased diastolic compliance; prior myocardial infarction

  • New apical holosystolic murmur—Papillary muscle dysfunction or valvular incompetence

  • Basal crepitations—Congestive heart failure.

Biochemical tests

      Although biochemical findings are usually not specific, they can provide information about risk factors; high levels of low density lipoproteins, increased cholesterol levels, and elevated platelet aggregation are often related to underlying coronary artery disease. None of the typical markers of the myocardial infarction (creatine phosphokinase-MB [CPK-MB], lactic dehydrogenase, etc.) are detectable two weeks after the ischemic injury. Thus, unless an acute event is witnessed, laboratory blood testing provides little in evaluation of ischemic heart disease.

Chest X-ray

Look for the following features:

  • Enlarged cardiac silhouette

  • Signs of pulmonary congestion

  • Calcium deposits within the coronary artery and in the aorta.

Electrocardiogram (ECG)

       The ST-T segment, representing myocardial repolarization, is the component of the ECG most sensitive to acute myocardial ischemia. ST elevation, which may be accompanied by tall positive (hyperacute) T waves, indicates transmural ischemia and is most often the result of acute coronary artery occlusion caused by either coronary thrombosis or vasospasm (Prinzmetal’s variant angina). Reciprocal ST depression may appear in the contralateral leads. Ischemia confined to the subendocardial area is usually denoted by ST-segment depression. Subendocardial, ST depression—type ischemia typically occurs during episodes of symptomatic or asymptomatic (“silent”) stable angina pectoris. It is characteristic of ischemia occurring during exercise, tachycardia, or a pharmacologic stress test in patients with significant but stable coronary artery disease (CAD).

       With prolonged ischemia, there is a risk of developing myocardial necrosis or myocardial infarction (MI). The electrocardiographic manifestation of MI includes decreased R-wave amplitude and pathologic Q waves (> 1 mm in depth and > 40 msec in duration), which may develop as a result of loss of electromotive forces in the infarcted area. Transmural infarctions are more likely to culminate in pathologic Q-waves, whereas subendocardial (nontransmural) infarcts are less likely to produce Q-waves. However, pathologic studies have shown such a wide overlap between the two entities and their electrocardiographic expression that “Q-wave” or “non-Q-wave” infarction is not synonymous with transmural or nontransmural infarction. Pathologic Q waves usually develop days after the onset of acute MI, and once they develop, they infrequently disappear and serve as an indicator of the location of the infarction. Persistent T-wave inversion may also be the only sign of chronic ischemia and recent or old MI. Pathologic Q waves with ST elevation that persists for weeks or longer after MI correlate strongly with severe myocardial mechanical dysfunction, akinesis, or ventricular aneurysm.

       Electrocardiographic leads demonstrating ST-T changes or Q waves may help define the location and the coronary artery responsible for the ischemia or MI. For example, precordial leads V1 to V3 correspond to the anteroseptal or apical walls of the left ventricle; leads V4 to V6 to the apical or lateral LV walls; leads II, III, and aVF to the inferior LV wall; and the right-sided leads to the right ventricle. Posterior wall infarction induces ST elevation or Q-waves in leads placed over the left side and back (V7 to V9), and

reciprocal ST depression or tall R-waves may develop in leads V1 to V3.

       The resting ECG is normal in 25-50% of patients with stable angina. Premature ventricular contractions (VPCs) are the most common arrhythmias occurring in patients with chronic ischemic heart disease. The arrhythmias that carry the greatest risks of sudden death include R on T phenomena, multiform repetitive VPCs, ventricular tachycardia, and fibrillation. Ventricular arrhythmias in the presence of a ventricular aneurysm markedly raise the mortality. Other conduction abnormalities that can predispose to perioperative events include complete heart block, Mobitz type II second-degree heart block, and bundle branch blocks.

exercise electrocardiography

        Exercise electrocardiography is useful for detecting signs of myocardial ischemia and establishing their relationship to chest pain. The appearance of a new murmur of mitral regurgitation or a decrease in blood pressure during exercise adds to the diagnostic value of this test. Exercise testing is not always feasible either because of the inability of a patient to exercise or the presence of conditions that interfere with interpretation of the exercise ECG (paced rhythm, left ventricular hypertrophy, digitalis administration, or preexcitation syndrome). Contraindications to exercise stress testing include severe aortic stenosis, severe hypertension, acute myocarditis, uncontrolled heart failure, and infective endocarditis.

       The underlying logic of this form of testing is that major determinants of myocardial oxygen consumption are affected by exercise, i.e. increases in heart rate, wall tension and contractility. This oxygen demand is met primarily by increases in coronary artery flow, and only secondarily by increases in oxygen extraction. Coronary flow can increase by 400% during vigorous exercise, whereas oxygen extraction may only increase by upto 25–30%.

        The exercise ECG is most likely to indicate myocardial ischemia when there is at least 1 mm of horizontal or down-sloping ST-segment depression during or within 4 minutes after exercise. The greater the degree of ST segment depression, the greater the likelihood of significant coronary artery disease. When the ST segment abnormality is associated with angina pectoris and occurs during the early stages of exercise and persists for several minutes after exercise, significant coronary artery disease is very likely. Exercise electrocardiography is less accurate but more cost effective than imaging tests for detecting ischemic 

heart disease. A negative stress test does not exclude the presence of coronary artery disease, but it makes the likelihood of three-vessel or left main coronary disease extremely low.

         All exercise ECG programmes increase myocardial oxygen demand in a progressive controlled manner. The Bruce programme consists of 3-min stages in which both treadmill gradient and speed are altered to increase the load incrementally (Fig. 5.8). Stage I has a speed of 1.7mph with a 10% slope, and stage 5 has a speed of 5.0 mph with an 18% slope. Most people are exhausted by the end of stage 5 (15 min). The ECG is continually monitored, and serial recordings of 12-lead ECGs and blood pressure are made. Oxygen consumption may also be measured.

Three main groups of ST segment responses have been described during and after exercise.

  • ST depression occurring during the exercise period and reverting to normal during the postexercise period. This is considered severe if the magnitude of ST depression is greater than 2mm; if ST depression occurs during stages 1-3; or if hypotension occurs during the exercise period, with or without ST segment changes.

  • ST depression continues into and may worsen during postexercise period. Associated with particularly poor prognosis.

  • Characterized by ST elevation (transmural ischemia) which may be due to coronary artery spasm.

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Perioperative ECG monitoring

         During the perioperative period, electrocardiographic monitoring most commonly identifies stress-induced, ST-segment depression–type ischemia. Such electrocar- diographic changes do not provide information about the location of the ischemic myocardial area. In contrast, ST-segment elevation indicating transmural ischemia, seen particularly during cardiac surgery, provides useful information about the myocardial segment and coronary perfusion territory responsible for the ischemic episode. Because the majority of modern patient-monitoring systems do not monitor all 12 electrocardiographic leads simultaneously, selecting which chest leads to monitor is of great importance, particularly in noncardiac surgery.

        During exercise stress testing, investigators have identified leads V4 and V5 as the most sensitive leads to detect exercise-induced ischemia (90% to 100% sensitivity). In high-risk patients undergoing noncardiac surgery, the greatest sensitivity for ischemia was obtained with lead V5 (75%), followed by lead V4 (61%). Combining leads V4 and V5 increased the sensitivity to 90%, whereas with the standard lead II and V5 combination, the sensitivity was only 80%. If three leads (II, V4, and V5) could be examined simultaneously, the sensitivity would rise to 98%.

        For patients with acute coronary syndromes (e.g., those with atherosclerotic plaque disruption), the recommendation is to monitor limb lead III and leads V3 and V5 as the most sensitive combination for detection of ischemia. Monitoring of a right-sided precordial lead (V4R) may be of benefit in patients with occlusive disease of the right coronary artery, as might inspection of posterior leads (V7 to V9) in patients with suspected posterior ischemia.


Non-invasive Imaging Tests

       Many patients who are at increased risk of coronary events cannot exercise because of peripheral vascular or musculoskeletal disease, deconditioning, or dyspnea on exertion. Noninvasive imaging tests for the detection of ischemic heart disease are usually recommended when exercise electrocardiography is not possible or interpretation of ST-segment changes would be difficult. Administration of atropine, infusion of dobutamine, or institution of artificial cardiac pacing produces a rapid heart rate to create cardiac stress. Alternatively, cardiac stress can be produced by administering a coronary vasodilator such as adenosine or dipyridamole. These drugs dilate normal coronary arteries but evoke minimal or no change in the diameter of atherosclerotic coronary arteries. After cardiac stress is induced by these interventions, either echocardiography to assess myocardial function or radionuclide tracer scanning to assess myocardial perfusion is performed.


        Historically the order of development echocardiography has determined the modalities available: M-mode, two- dimensional, Doppler and colour-flow Doppler examination. Transesophageal and transtracheal echocardiography have been developed recently.

M-mode echocardiography gives a one-dimensional view of cardiac events. This image can be very useful for assessing the timing of events. Two-dimensional echocardiography enables the user to develop a real-time, cross-sectional view of the heart. This enables one to assess the structure and function of heart valves, chamber size, ventricular wall thickness, wall motion, and estimate end-systolic and end- diastolic chamber areas. It can also give valuable information on the effects of myocardial ischemia. Segmental or regional wall motion abnormalities which occur in the presence of ischemia, may be described qualitatively or quantitatively. Qualitative descriptions include hyperkinetic, normal, hypokinetic or dyskinetic (paradoxical motion). Various quantitative methods have been described, which allow scoring of ventricular function.

        Doppler echocardiography makes use of the change in frequency of ultrasound reflected from moving red cells. Pulsed-wave Doppler allows simultaneous two-dimensional imaging, thus improving simultaneous good anatomical localization of the sampling, but does not quantify flow as accurately as continuous-wave Doppler, but here no simultaneous two-dimensional image is available for reference and so the operator needs to be highly skilled. More recently colour-flow Doppler has become available. Its main advantage is that it is able to superimpose areas of abnormal flow as colours (red and blue) on the two- dimensional image of the heart, thus allowing further interrogation using Doppler. These colours depend on the direction of flow with respect to the transducer.

In practice, all four methods are used in conjunction. The main limitation of trans-thoracic echocardiography is that it is not always possible to obtain useful images, for example in the presence of emphysema or in certain environments. Trans-esophageal echocardiography circumvents these problems, but is semi-invasive and requires additional skills.

       Echocardiographic wall motion analysis is performed immediately after stressing the heart. An intravenous echocardiographic contrast dye can improve the accuracy of stress echocardiography. The ventricular wall motion abnormalities induced by stress correspond to the site of myocardial ischemia, thereby localizing the obstructive coronary lesion. In contrast, exercise electrocardiography can indicate the presence of ischemic heart disease but does not reliably predict the location of the obstructive coronary lesion. Dipyridamole and dobutamine stress echocardiography have been described. They have very high sensitivity and specificity for perioperative cardiac events. Dipyridamole and dobutamine produce totally different kinds of stress – the former an acute coronary vasodilator that may exaggerate steal-prone anatomy, and the latter an increase in myocardial work that may mimic perioperative conditions.

Nuclear Stress Imaging

      Nuclear stress imaging is useful for assessing coronary perfusion. It has greater sensitivity than exercise testing for detection of ischemic heart disease. It can define vascular regions in which stress-induced coronary blood flow is limited and can estimate left ventricular systolic size and function. Tracers (e.g., thallium, technetium) can be detected over the myocardium by single-photon emission computed tomography techniques. A significant coronary obstructive lesion causes less blood flow and thus less tracer activity.

      Exercise increases the difference in tracer activity between normal and underperfused regions because coronary blood flow increases markedly with exercise except in those regions distal to a coronary artery obstruction. Imaging is carried out in two phases: first immediately after cessation of exercise to detect regional ischemia and then 4 hours later to detect reversible ischemia. Areas of persistently absent uptake signify old MI. The size of the perfusion abnormality is the most important indicator of the significance of the coronary artery disease detected.

Electron Beam Computed Tomography

        Calcium deposition occurs in atherosclerotic vessels. Coronary artery calcification can be detected by electron beam computed tomography. Although the sensitivity of electron beam computed tomography is high, it is not a very specific test and yields many false-positive results. Its routine use has not been recommended.

Coronary Angiography

         Coronary angiography provides the best information about the condition of the coronary arteries. It is indicated in patients who continue to have angina pectoris despite maximal medical therapy, in those who are being considered for coronary revascularization, and for the definitive diagnosis of coronary disease in individuals whose occupations could place others at risk (e.g., airline pilots). Coronary angiography is also useful for establishing the diagnosis of nonatherosclerotic coronary artery disease such as coronary artery spasm. Surgical coronary bypass is most effective when a diseased coronary artery is of reasonable size, has a high-grade proximal stenosis, and is free of significant distal plaques. The most suitable atherosclerotic lesion for coronary angioplasty is discrete, concentric, proximal, noncalcified, and less than 5 mm in length.

Pharmacological Stress Tests

(a) Inotropes

  • Commonly used inotropes include dobutamine and the newer agent arbutamine. These drugs increase myocardial oxygen demand through inotropic stimulation

  • They can often achieve coronary blood flows greater than with exercise but not as great as with adenosine or dipyridamole

  • They tend to be used in patients with asthma who cannot tolerate vasodilators

  • Dobutamine is best avoided in patients with serious arrhythmias and severe hypertension or hypotension.

(b) Coronary Vasodilators

      These agents produce non-physiological and sometimes supra-physiological increases in coronary flow without altering the metabolic demands of the heart.

  • Adenosine is a breakdown product of ATP metabolism and is a potent coronary vasodilator. In conditions of oxygen starvation rising adenosine levels result in coronary vasodilation linking coronary blood flow to myocardial oxygen demand.

  • Dipyridamole inhibits the breakdown of free adenosine causing levels to rise and thereby produces coronary vasodilatation as described above.

  • Methylxanthines (e.g. caffeine) are competitive inhibitors of adenosine at purinergic receptors and patients are advised to avoid these for at least 6–8 h prior to testing achieve maximal coronary vasodilator effect.

      All these agents can induce or exacerbate bronchospasm, and their use is relatively contraindicated in asthmatics. Unexpected severe bronchospasm can be readily antagonised with intravenous aminophylline. Dipyridamole should also be avoided in patients with critical carotid disease. Other adverse effects include headaches, flushing and hypotension.

      Examples of some non-invasive tests that employ pharmacological stressors include:

Dobutamine Stress Echocardiography

  • Provides an opportunity to assess both LV and valvular function.

  • Can be performed safely and with acceptable patient tolerance.

  • Very accurate in identifying patients with significant angiographic coronary disease.

  • The published experience of dobutamine stress echocardiography to assess perioperative risk before vascular and nonvascular surgery is relatively small compared with the published literature on exercise testing or intravenous dipyridamole myocardial perfusion imaging.

  • Adding atropine to those patients who fail to meet the target heart rate improves sensitivity.

       Several studies suggest that the degree of wall motion abnormalities and/or wall motion change at low infusion rates of dobutamine is especially important.


Goldman's Cardiac Risk Index

This landmark paper was published in the New England Journal of Medicine (NEJM) 1977, and is a well-known method for stratifying risk (Table 5.12).

Its limitations are few but include:

  • The index overestimated the incidence of cardiac morbidity in Class IV patients undergoing non-cardiac surgery.

  • The index underestimated risk in Class I and II patients undergoing aortic surgery.

  • The study group included elective non-emergent cases only.

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Revised Cardiac Risk Index (RCRI)

       The Revised Cardiac Risk Index is a recent scoring systems and was introduced by Lee et al in 1999 (Table 5.13). The index was derived from a population of 4000 patients, and identified the risk of major cardiac complications in a population undergoing major non-emergent non-cardiac surgery.

       Major cardiac complications included MI, pulmonary edema, ventricular fibrillation or primary cardiac arrest, or complete heart block.

     Its advantages over the earlier scoring systems include:

  • only six prognostic factors,

  • simple variables,

  • dependent on presence or absence of conditions rather than estimating disease severity,

  • less reliance on clinical assessment and judgment,

  • could easily be incorporated on preoperative evaluation forms.

The shortcomings of the system are that:

  • It is not applicable to emergency surgery,

  • It is not applicable to lower-risk populations,

  • It may not be as reliable for preselected high-risk populations such as patients undergoing major vascular surgery.


Modified ECG Leads

         The same three electrodes are used but with change in position on the body. MCL (Modified Chest Leads), CS5, CM5, CB5 and CC5 are in this group. They offer the advantage of maximizing ‘P’ waves for dysrhythmia monitoring and increase the sensitivity of the three electrode system for anterior wall ischemia monitoring. Out of these MCL1 in ICU and CS5 in the operating room are most commonly used. The electrode positions and their polarity are given in Table 5.14.