perioperative myocardial ischaemia and infarction - a review

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Perioperative Myocardial Ischaemia and Infarction-a ReviewSatinder Gombar1, Ashish Kumar Khanna2, Kanti Kumar Gombar3

Key words Cardiac; Ischaemia; Infarction; Perioperative; Anaesthesia; Complications

Introduction

1. MD, Professor, 2. P.G.Student, 3. MD, Professor& Head, Department Of Anaesthesia & Intensive Care, Government Medical College andHospital,Sector 32, Chandigarh,India Correspondence to: Satinder Gombar #1111,Sector 32 B, Chandigarh,IndiaE mail: [email protected]

Perioperative myocardial ischaemia and infarction(PMI) is a major cause of short and long term morbidity andmortality in the surgical population. It is estimated that morethan one half of postoperative deaths are caused by cardiacevents, most of which are ischaemic in origin. Over 50,000patients each year sustain a perioperative MI at an averageadditional cost to the health infrastructure of $12,000 perpatient.1 Thus prevention of a PMI is important to improveoverall postoperative outcome. However, the exact natureof perioperative myocardial injury remains elusive and anarea of continued debate and controversy.2 The followingreview will address these issues and the nature ofperioperative ischaemia in both the cardiac and non-cardiacsurgeryscenarios alongwith its management, includingbothpreventive and therapeutic aspects of the problem.

Perioperative myocardial ischaemia & infarction(PMI): Defining the problem

Myocardial ischaemia is a dual state composed of in-adequate myocardial oxygenation and accumulation ofanaerobic metabolites and occurs when myocardial oxygendemand exceeds the supply. Myocardial infarction is definedas the death of myocardial myocytes due to prolonged is-chaemia.3 Though perioperative MI was thought to be re-lated to the presence of a perioperative ischaemia, it was notuntil the landmark article by Slogoff and Keats in1985 thatthe association between the two was clearly established.4

Incidence of PMIIn patients with, or at risk of coronary artery dis-

ease (CAD), the reported incidence of perioperative myo-cardial ischaemia is 20 - 63%.Various studies have shownthat postoperative myocardialischaemia was consistentlyfound to occur considerably moreoften than preoperativeand intraoperative ischaemia (ratio approximately 3:1 and5:1 respectively).Reported incidence of postoperative

cardiac events (thecombined incidence of non-fatal myo-cardial infarction, unstableangina, congestive heart fail-ure, cardiac death) is 5.5-53% and that of postoperativemyocardial infarction between 1.4 and 38%. Postopera-tive myocardial infarction increased the odds for long-termcardiac events 20-fold. 5,6,7 Unfortunately, there is noreliable data available on the incidence of perioperativeischaemia & infarction in our country.

Pathophysiology

A. Myocardial ischaemia

Myocardial ischaemia is characterized by an imbal-ance between myocardial oxygen supply and demand. Thetwo most common conditions that predispose to myocardialischaemia are CAD and left ventricular hypertrophy(LVH).Reduced oxygen supply or low-flow ischaemia (coronaryvasoconstriction,intracoronaryplateletaggregation or throm-bus formation) is largely responsible for myocardial infarc-tion and unstable angina. Increased myocardial oxygen de-mand or high-flow ischaemia is mostly responsible forischaemic episodes in chronic stable angina (tachycardia,exercise or emotional stress) in the presence of fixed coro-nary artery stenosis. Often, myocardial ischaemia is a cul-mination of multiple factors and results from both a reduc-tion in supply and an increasein oxygen demand.8

Endothelial function is also impaired in CAD,and isan important cause of myocardial ischaemia. Increases incoronary blood flow secondary to an increase in myocar-dialoxygen demand and sympathetic nervous system ac-tivation (e.g. during exercise, mental stress or increaseinheart rate) induce vasodilatation in normal coronary ar-teries but lead on to paradoxical vasoconstriction in theatherosclerotic vessels9.10.Such limitation of coronary flowand the inability of vessels to dilate near the site of anatherosclerotic plaque may result in regional myocardialsupply- or low-flow ischaemia. In the face of an unfavor-

Indian Journal of Anaesthesia 2007; 51 (4) : 287-302

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able oxygen supply demand ratio, the manifestations ofmyocardial dysfunction progressively set in and subse-quently compromise tissue perfusion and cellular aerobicmetabolism.

The clinical manifestations of myocardial ischaemiarange from asymptomatic or “silent” episodes to angina,arrhythmia, conduction blocks, wall motion abnormalities,pulmonary congestion, infarction, and sudden cardiacdeath. Systolic (contractile) and diastolic (ventricular fill-ing) dysfunction occur first; followed by electrocardio-graphic changes, and finally by chest pain.All these eventsoften occur in a short time course of less than 1 minute(Fig.1).11 An 80% reduction in coronary blood flow causesakinesis, whereas a 95% decrease causes dyskinesis. Ifthe ischaemia becomes severe, the increase in left ven-tricular end-diastolic pressure may lead to pulmonaryoedema. After a brief period of severe ischaemia, con-tractile function can return gradually (stunning).Alterna-tively, severe chronic ischaemia can result in diminishedcontractile performance, such as chronic regional wallmotion abnormalities (hibernation). In stunning normalblood flow and energy metabolism are accompanied byreduced contractility, designated as ‘flow-contractilitymismatch’. Hibernation is characterized by reduced con-tractility accompanied by reduced oxygen consumptionas a consequence of reduced blood flow. Partially dam-aged cardiomyocytes can be rescued to full function af-ter stunning as well as hibernation, provided normal bloodflow is restored after the latter within the critical timeperiod before irreversible cell damage has occurred. De-spite their distinct definition, stunning and hibernation maymerely represent intermediary states in a continuum ex-tending from unimpaired functional myocytes to necro-sis.12

It is worth mentioning here that perioperatively, thesingle most common abnormality that is often associatedwith ischaemia is tachycardia, which by causing both anincrease in demand and reduction in supply can in sus-ceptible patients jeopardize the myocardium and bringabout ischaemic changes.4Perioperative tachycardia canresult from many causes, including light plane of anaes-thesia, endotracheal intubation and extubation, hypov-olemia, fever, anaemia, congestive heart failure(CHF), andpostoperative pain. Similarly hypertension can cause in-creased demand and hypotension can lead to decreasedsupply in the perioperative period.

B. Myocardial infarctionMajority of perioperative infarctions occur in pa-

tients with significant preexisting CAD, however hyper-tensive patients with LVH are also susceptible. The tran-sition from stablecoronary artery disease to an acute coro-nary syndrome and infarction is characterized by coro-nary plaque disruption and subsequent thrombosis, whichconstitute the major pathogenic components of unstableor vulnerableplaques.12

A vulnerable plaque is an inflamed fibroatheromawith a lipid-rich core containing cholesterol crystals andnecrotic debris, a thin fibrous cap with an infiltration ofmacrophages and lymphocytes, and low smooth musclecontent. Inflammatory mediators closely regulate the bal-ance between the synthetic and degradative processescontrolling the strength of the cap, specifically the syn-thesis of collagen.8,13

When intraluminal thrombi attach to a rupturedatheromatous plaque, total occlusion of an epicardial coro-nary artery may occur, resulting in interruption ofnutrientblood flow to the myocardium and death of myocardialmyocytes. The situation may be worsened by distal em-bolization of microthrombi and by coronaryvasoconstric-

Fig.1 Progression of signs of myocardial dysfunction as myocar-dial ischaemia worsens11

CHF (congestive heart failure); EF (ejection fraction);

LVEDP (left ventricular end-diastolic pressure);

LVEDV (left ventricular end-diastolic volume); ST delta (ST segmentdeviation)

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tion induced by local, mediator release-induced or sys-temic sympathetic activation. If coronary blood flow isinterrupted for longer than 30 min, myocardial infarctionmayresult. Loss of functional myocardium results in im-paired left ventricular function, which may impair qualityof life and usually leads to premature death.14 The pres-ence of myocardial ischaemia, nonfatal MI, or both withinthe first 7 postoperative days increases the risk of ad-verse cardiovascular events by 2- to 20-fold in the first 2years after a noncardiac operation.

To put it in simple words , it is a complex and unpre-dictable interaction between the structural (central lipidcore, thin cap) and functional (plaque thrombogenicity,intraplaque inflammatory cell infiltrate) intrinsic plaquefactors as well as the exogenous factors (e.g. mechanicalstress, vasomotor tone, infection, blood viscosityand co-agulability) which leads to the final outcome of myocar-dial ischaemic damage.

Most ischaemic episodes tend to start at the end ofsurgery and during emergence from anaesthesia.Thisperiod is characterized by increases in heart rate (HR),arterial blood pressure (BP), sympathetic tone, andprocoagulant activity. Increased sympathetic tone maylead to increases in coronary vasomotor tone and vascu-lar stress which in turn may trigger coronary vasospasm,plaque disruption and coronary thrombosis. Increases inHR & BP may lead to subendocardial ischaemia by in-creasing myocardial oxygen demand in the presence oflimited coronary vasodilator reserve. Simultaneously, sur-gery induced procoagulant and anti-fibrinolytic activitymay trigger coronary artery thrombosis during low flowconditions even in the absence of acute plaque disruption.

Mechanisms and triggers of perioperative myocar-dial injury

Surgery, with its associated trauma, anaesthesia andanalgesia, intubation and extubation, pain, hypothermia,bleeding and anaemia,and fasting, is analogous to an ex-treme stress test. Fig.2 illustrates how these factors ini-tiate inflammatory, hypercoagulable, stress and hypoxicstate, which is associated with perioperativeelevations introponin levels, arterial thrombosis and mortality. 14

Increasing grades of surgical trauma and generalanaesthesiacan initiate inflammatory and hypercoagulablestates. The inflammatory state involves increases in tu-

mour necrosis factor-alpha, interleukin (IL)-1, IL-6 andC-reactive protein; thesefactors may have a direct role ininitiating plaque fissuringand acute coronary thrombosis.The hypercoagulable state involves increases in plas-minogen activator inhibitor-1, factor VIII and platelet re-activity, as well as decreases in antithrombin III; all ofthese factors can lead to acute coronary thrombosis. Thestress state involves increased levels of catecholamines(epinephrine and norepinephrine) and cortisol.Perioperative catecholamine and cortisol levels increasewith general anaesthesia,anaesthetic reversal, extubation,increasing pain scores, increasinggrades of surgical trauma,anaemia, fasting and hypothermia. Increased stress hor-mone levels result in increases in blood pressure, heartrate, coronary artery sheer stress, relative insulin defi-ciency and free fatty acid levels all increase oxygen de-mand. Coronary artery shear stress may trigger plaquefissuring and acute coronarythrombosis. Factors that caninitiate a hypoxic state include anaemia, hypothermia(through shivering), and anaesthesia and analgesia (throughsuppression of breathing). Perioperative hypoxia can re-sult in myocardial ischaemia in the setting of ahaemodynamically significant coronaryartery stenosis.14

Satinder Gombar et al. Perioperative myocardial ischaemia

Fig.2 Potential triggers of states associated with perioperativeelevations in troponin levels, arterial thrombosis and fatal myo-cardial infarction.14

(TNF-a = tumour necrosis factor-alpha, IL = interleukin, CRP = C-reactive protein, PAI-1 = plasminogen activator inhibitor-1, BP = bloodpressure, HR = heart rate, FFAs = free fatty acids.)

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Making a diagnosis

A. Definition and diagnosis of perioperative myo-cardial ischaemia:

Though there is no accepted gold standard for thediagnosisof myocardial ischaemia, the diagnosis can usu-ally be based on clinical, haemodynamic (pulmonary ar-tery capillary wedge and/or left atrial pressure wave), elec-trocardiographic (ECG), functional (echocardiogram),metabolic (coronary lactate production), biochemical (re-lease of creatine kinase-MB isoenzyme and/or troponin)or regional perfusion (scintigram) parameters.8 All thesetechniques in the setting of ischaemia or infarction detec-tion have considerable limitations, varying sensitivity andspecificity and poor inter technique correlation (Table 1)15.

Chest pain: The onset of new cardiac pain can beextremely important when one is diagnosing myocardialischaemia preoperatively, during surgery under local orregional anaesthesia and in the recovery room. Typicallycardiac pain is a sense of chest constriction and may bereferred to arm, neck, jaw, teeth or even post scapulararea. However diabetics may have silent ischaemia be-cause pain pathways are impaired by diabetic neuropa-thy. In fact, it is reported that 70 % of myocardial ischaemicepisodes in fully awake humans are asymptomatic.

Electrocardiography (ECG): Perioperative myo-cardial ischaemia has predominantly been detected anddefined by ECG. The reported incidence of perioperativemyocardial ischaemia greatly depends on choice and num-ber of precordial leads, on the definition of ischaemic ST-segment change (extent and duration of ST-segmentchange), and on themode of data acquisition (continuousvs intermittent). 16

The standard ECG consists of 12 leads, however,during anaesthesia, monitoring is usually limited to five orseven leads. Blackburn et al demonstrated that 89% ofsignificant ST depression was found in precordial leadV5 . They also demonstrated that 100% of ST segmentchanges can be detected by recording leads V

3–V

6and

leads II and aVF.17 In routine practice, leads II and V5are

continuously monitored, giving views of inferior and lat-eral myocardium. The ECG must be calibrated to give apen deflection of 10mm for 1mV potential. This is impor-tant because excessive gain can give false ST depressionand inadequate gain can mask such depression. Properdiagnosis of ischaemia from ECG depends on the diag-nostic mode which brackets a frequency bandwidth of

Table 1 Strengths and limitations of modalities fordetecting PMI15

Modality

ECG

Biochemical

CK-MB

TroponinI

TroponinT

Imaging

TTE

P e r f u s i o nimaging

Strength

New Q waves,”tombstone” STsegment eleva-tion, horizontalor downslopingST-segment, hy-peracute T waves,deep symmetricalT wave inver-sions, involve-ment of multiplecontiguous leads.

Characteristic riseand fall, shortertime course thant r o p o n i n s , C K /CK-MB ratio>5%, AUC timeactivity curve re-lated to infarctsize

Later peak, moresustained dura-tion, prognosticsignificance oflow-level eleva-tion

Same as TroponinI , only one assayin use, well stan-dardized detec-tion limits

New or worseningof baselineSWMA, akinesia,dyskinesia, reduc-tion in ejectionfraction, is-chemic mitral re-g u r g i t a t i o n ,change from priorTTE.

Q u a n t i t a t i v eanalysis, changesin flow

Limitations

Narrow septal orinferior Q waves,LVH, LBBB,r e p o l a r i s a t i o ntype ST segmenta b n o r m a l i t i e s ,upsloping ST seg-ment depression,baseline ST seg-ment abnormaili-ties, diffuse Twave flattening,asymmetrical Twave inversion

N o n - C A D - r e -lated cardiac andother non-cardiacpathology, sustai-ned elevation,gene expression ininjured skeletalmuscle, renal fail-ureNon CAD relatedcardiac pathol-ogy, long durationof elevation, lackof a baseline mea-surement, mul-tiple assays in use,variable detectionlimits.

Non CAD relatedcardiac pathol-ogy, long durationof elevation, lackof a baseline mea-surement, lowlevel chronic el-evation in ESRD

Small Q wave MI,non Q wave MI,prior MI withbaseline SWMAs,reversible is-chemia, stunninghibernating myo-cardium

Prior MI, revers-ible ischemia,stunning, hiber-nating myocar-dium, technical/anatomic arti-facts

R e c o mme n d a -tions

At the time of thesuspected event ,for several daysduring clinicalresolution, withsuspected reinf-arction

Helpful to detectrecurrent infarc-tion with serialsampling

All patients withsuspected PMI

All patients withsuspected PMI ,Troponin I pref-erable for patientswith ESRD

All patients withsuspected PMI.Document size ofMI, impact onventricular func-tion.

Expensive, notrecommended ex-cept possibly inpatients with poorTTE imaging

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0.05-100 Hz. It is equally important to have a workingknowledge of critical ST segment analysis. Horizontal ordownsloping ST segment depression of 1mm or more in-dicates significant subendocardial ischaemia while STsegment elevation greater than 1mm indicates severetransmural ischaemia. Patients with left ventricular hy-pertrophy, left bundle branch block (LBBB), digitalis ef-fect, ventricular pacing and those not in sinus rhythm arenot suitable forECG-derived diagnosis of myocardial is-chaemia. In addition,perioperative changes in acid–basebalance and electrolytes can affect the ECG in a way thatinterferes with ischaemia detection.16

Pulmonary artery pressure: The quantitative in-crease in pulmonary capillary wedge pressure and char-acteristic changes in its waveform have been suggestedas an ischaemia monitor, but it is believed that the pulmo-nary artery catheter is an insensitive monitor of myocar-dial ischaemia and should not be inserted with this as aprimary indication. In addition, the use of pulmonary ar-tery catheters in the perioperative period may actuallycontribute to increased morbidity.11

Transoesophageal echocardiography (TEE):TEE is a highly sensitive ischaemia monitor and demon-strates development of new regional wall motion abnor-malities, decreased systolic wall thickening, and ventricu-lar dilation as a result of ischaemic events. Usually, atransgastric cross-sectional view of the left ventricle isimaged because this view displays the myocardial perfu-sion territories of the three major coronary arteries. Theuse of TEE has become increasingly common in the op-erating room for cardiac surgery but is less frequentlyused in noncardiac surgery. In addition to cost, significantlimitations exist to the routine use of TEE as an ischaemiamonitor. Pre-intubation events are missed, and the imageplane may miss events in other areas of the myocardium.It has been shown that if the anaesthesiologist has thetraining, experience and equipment to perform TEE, itcan be valuable in the early detection of myocardial is-chaemia.16 However, the incremental value of adding TEEto electrocardiographic monitoring in noncardiac surgeryis unclear at this time.

Myocardial lactate: Although used mainly as a re-search tool, the coronary sinus catheter represents the ac-cepted standard for myocardial ischaemia monitors. How-ever, the coronary sinus catheter requires the use of fluo-roscopy, echocardiography, or both for proper placement.In addition, small areas of ischaemia may not be recog-

nized because the lactate produced from these areas willbe diluted by the blood from nonischaemic regions.18

The use of numerical indices of myocardial oxygenconsumption (MVO2) has been popular in general car-diologic practice. Unfortunately, their theoretical advan-tages have failed validation in anaesthetized patients. Therate-pressure product (RPP = systolic blood pressure ×heart rate) has been shown to be a useful measure ofMVO2 in awake patients, but direct correlation of thisindex to MVO2 measurement in anaesthetized patientshas been unreliable. Other indices developed to overcomethe deficiencies of the rate-pressure product have alsofailed validation in anaesthetized patients, probably be-cause it has been shown that most intraoperative ischaemiais related to decrease supply rather than increased de-mand. Most intraoperative ischaemic events occur withrelatively normal haemodynamic parameters. Thus, theindices that are based on increased demand have littlesensitivity for intraoperative ischaemia. Although heartrates above 110 beats/minute double the incidence ofmyocardial ischaemia, ischaemia frequently occurs evenwith heart rates between 60 and 80 beats/minute.11

In summary, there is no single best indicator ofintraoperative myocardial ischaemia. Use of an array ofmonitoring modalities may facilitate the highest yield ofischaemic episodes.

B. Definition and diagnosis of perioperative myo-cardial infarction

According to the definition of the World Health Or-ganization (WHO), at least two of three criteria must befulfilled to diagnose myocardial infarction: typicalischaemic chest pain; increased serum concentration ofcreatine kinase-MBisoenzyme; and typical electrocardio-graphic findings, includingdevelopment of pathological Q-waves.19 This definitionprovides adequate specificity butlacks high sensitivity.

Clinical presentation: Patients receiving GA ob-viously will not complain of chest pain but may have hy-potension, arrhythmias, and signs of congestive heart fail-ure. Most postoperative myocardial infarctions occur earlyafter surgery and are asymptomatic.

ECG: ECG may show changes of subendocardialor transmural ischaemia (ST elevation >1mm).The vastmajority of perioperative myocardial infarctions are of thenon-Q-wave type and preceded by episodes of ST-seg-ment depression and T wave inversion.2 Long-duration

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(single duration >20–30 min or cumulativeduration >1–2h) ST-segment change, rather than merely the presenceof postoperative ST-segment depression, seems to be as-sociated with adverse cardiac outcome. 4,18

The development of assays for the cardiac troponinsT and I,which are highly specific and sensitive for myocar-dial injury,formed the basis of a revised definition of myo-cardial infarctionproposed by the European Society of Car-diology and theAmericanCollege of Cardiology.19The fol-lowing two criteria satisfythe diagnosis of an acute, evolv-ing or recent myocardial infarction: (i) a typical increaseand gradual decrease in troponin concentrations or morerapid increase and decrease in creatine kinase-MB con-centrationin combination with at least one of the following:(a) typicalischaemic symptoms, (b) development of patho-logical Q-waves in the ECG, (c) ECG changes indicative ofmyocardial ischaemia(ST-segment elevation or depression),and (d) coronary artery intervention; and (ii) pathologicalfindings of an acute myocardialinfarction.

Biochemical markers: Increased concentration ofCPK-MB is not useful intraoperatively because the leak-age of these enzymes into the circulation can occur 8-24hours after an MI. Because of the inherent limitations ofCPK-MB concentration and lack of specificity, MI maybe best detected with cardiac TnT concentrations. TnTbinds to tropomyosin, troponin C binds to Ca++,and tropo-nin I (TnI) binds to actin and inhibits actin-myosin inter-actions. While CPK-MB concentrations may rise only10-20 times of normal during infarction and return to nor-mal within 72 hrs, TnT and TnI levels may rise more than20 times above the reference range within 3 hrs afteronset of chest pain and may persist for up to 10-14 days(Fig. 3).This may assist in late diagnosis of infarction.16

Evidence is accumulating that other biochemicalmarkers may further enhance sensitivity or improve riskstratification in patients with ACS including myoglobin(earliest rise after MI), C-reactive protein( a marker ofinflammation that is increasingly appreciated as the pri-mary acute physiological process leading to plaque rup-ture and thrombosis) and B-type natriuretic peptide ( sen-sitive but non-specific response to left ventricular pres-sure or volume overload caused by severe ischaemia orheart failure)20,21

TEE: The sudden appearance of severe wall mo-tion abnormalities in patients being monitored by TEE mayalso indicate MI, though it may be difficult to distinguishevolving infarction, stunned myocardium and hibernatingmyocardium using TEE.16

The question remains whether a reported incidenceof perioperativemyocardial injury based on the traditionaldefinition underestimates the true incidence of clinicallyrelevant myocardial injuryor whether a reported incidencebased on serum concentrations of troponins overestimatesit. When using exclusively biochemical markers, specific-ity may be sacrificed for sensitivity. Given accumulatingevidence that even low levels of troponin elevation in oth-erwise asymptomatic patients are associated with higherlong term (6months -1 year) morbidity and mortality, itappears that they are accurate in detecting perioperativemyocardial injury. At present there is a paucity of formalguidelines on this topic which clearly specify the idealdiagnostic criteria for perioperative infarction.18

Despite widespread use of the TEE and the PAcatheter, the ECG is still the best validated tool for detec-tion of ischaemic episodes postoperatively.

The ACC/AHA Guidelines (Table 2) onperioperative evaluation provide specific recommenda-tions for perioperative surveillance and evaluation of suchpatients that is applicable in most settings.22 We needmore intensive investigations to determine whether thiswarrants a change in the current patterns of perioperativecare.

Preoperative risk assessment

Non cardiac surgery

The fundamental purpose of ascertaining the pres-ence of coronary artery disease, myocardial ischaemia, orboth preoperatively is (1) to determine which patients areat risk and whether any further preoperative treatment is

Fig.3 Biochemical markers re lease, peak and duration ofe leva t io n

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necessary, (2) to design an intraoperative management planto reduce the incidence and consequences of ischaemia inpatients at risk, and (3) in these at risk patients attempt toreduce the risk of adverse outcome by implementing ag-gressive preventive and treatment modalities. Interventionsbased on this assessment may include preoperative medi-cal optimization, coronary revascularization or both. His-tory and physical examination can identify variables asso-ciated with postoperative ischaemia: LVH, hypertension,diabetes mellitus, definite coronary artery disease, smokingand use of digoxin or any other medications. The incidenceof postoperative ischaemia increases from 22% in patientswith none of these variables to 77% in patients with fourvariables present.11

Table 2 Recommendations of the ACC/AHA 2002guidelines on perioperative cardiovascular evalua-tion for non cardiac surgery22

Surveillance should be restricted to patients who develop signs of car-

diovascular dysfunction.

For patients with high or intermediate clinical risk undergoing high or

intermediate risk surgical procedures obtaining an ECG at baseline,

immediately after surgery, and daily for the first 2 days postopera-

tively appears to be the most cost effective strategy.

Troponin measurements should be obtained 24 hours post operatively

and on day 4 or hospital discharge (whichever comes first) for PMI

detection.

Patients who sustain PMI should have evaluation of ventricular func-

tion before hospital discharge and receive therapy as defined by the

ACC/AHA AMI guidelines.

The Goldman Cardiac Risk Index (1977) 23 first identi-fied the importance of surgery-specific risks, which wasvalidated in large prospective series of general surgerypatients. Subsequently, Detsky et al in large prospectivestudies in the 1980s confirmed and refined the originalGoldman index by adding categories of angina and priorhistory of congestive heart failure.24 An alternate clini-cal risk prediction tool, the Revised Cardiac Risk Index(RCRI)25 may equally predict risk. It involves the pres-ence or absence of six clinical risk factors. Zero, one,two, or three (or more) risk factors are categorized intoClass I, II, III, or IV respectively. The correspondingpostoperative cardiac complication rates range from lessthan 1% to over 10%.

American Heart Association/American College ofCardiology (AHA/ACC) published a guideline for

perioperative cardiovascular evaluation for noncardiacsurgery in 1996.This guideline has been recently updatedin 2002 and offers the most comprehensive approach topreoperative cardiac evaluation for noncardiac surger-ies.22 It focuses clinicians’ attention on three major areas:

clinical risk predictors,

surgery-specific risks, and

functional capacityTheguidelinestratifiesclinicalriskpredictors intominor,

intermediate, or major based on estimated risk of postop-erative cardiac events. Minor risk factors are not known tobe associated with postoperative cardiac events, while thepresence of major risk predictors warrants prompt andaggressive investigation and treatment. (Table 3).22

Table 3 Clinical predictors of perioperative cardiacrisk22

Major Intermediate Minor

Acute or recent MI Mild angina Advanced age

Unstable angina Prior MI Abnormal ECG

Decompensated CHF Compensated CHF Rhythm other than sinus

Significant arrhythmias Diabetes mellitus History of stroke

Severe valvular disease Renal insufficiency Uncontrolled hypertension

MI, myocardial infarction; CHF, congestive heart failure; ECG,electrocardiogram

Table 4 Surgery-specific cardiac risks22

High (5%) Intermediate (<5%) Low (1%)

Emergent surgery Carotid endarterectomy Endoscopic procedures

Aortic or major Head and neck surgery Superficial proceduresvascular surgery

Periphral vascular Intraperitoneal Cataract surgerysurgery intrathoracic procedures

Large fluid shifts Orthopaedic surgery Breast surgeryand blood loss

The duration of the procedure, site of operation, andamount of tissue handling combine to confer different risksassociated with various types of surgeries. The AHA/ACC guideline included a more detailed estimate of sur-gery-specific risks based on postoperative cardiac eventsfor each type of surgery based on the Coronary ArterySurgery Study (CASS) registry.26 Surgeries were thencategorized into low, intermediate, and high-risk surgicalgroups.(Table 4) A patient with minor clinical predictorshas an overall low risk except for high risk or urgent/emergent surgeries. Conversely, a patient with major clini-cal predictors who is in stable condition has an accept-able overall risk if the proposed procedure is a low risk


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procedure. The final major component of this evaluationis an assessment of current functional capacity. This as-sessment is based on metabolic equivalents (METs)

(1 MET= O2 consumption at rest- 3.5ml.kg-1.min-1)

Functional capacity of less than 4 METs of activityconfers a 4% risk of postoperative cardiac events,whereas the risk is as low as 0.7% in patients with greaterthan 4 METS of capacity. Examples of exercise equal to4 METs being, climbing a flight of stairs/walking up a hill/walking on level ground at 4mph/running a short distance

Careful consideration of all three aspects, includingclinical characteristics, functional capacity, and surgery-specific risk in accordance with the publishedAHA/ACCguideline, form the basis for informed decision makingregarding further diagnostic testing and/or risk reductioninterventions.26

Cardiac surgeryIn patients undergoing CABG, myocardial ischaemia

that occurs during the intraoperative period has the stron-gest correlation with perioperative MI. Looking at thecardiac patient in the cardiac surgical setting, it is impor-tant to realize that the lesion causing ischaemic changesin the pre operative period is usually remedied in the post-operative period thus outcomes are favourable as com-pared to the non cardiac surgery patient who has to gothrough the post operative vulnerable period with anischaemic myocardium.

Various studies in the cardiac surgery population haveidentified certain factors namely, NYHAfunctional class,urgency of surgery, valvular lesions secondary toischaemia,mean PAP>30mmHg,ejection fraction <40%and a low cardiac index as being predictors of poor out-comes after cardiac surgery.27,28

Preoperative evaluationWhile clinical assessment of risk is necessary for

every patient, in populations deemed to be at high risk weneed a more definitive assessment in the form of preop-erative non-invasive testing. Although a battery of suchtests are now available, recent guidelines by the AHA/ACC clearly state the class I indications for pre operativeevaluation in the cardiac patient and limit testing only tothe population groups deemed to be at the highest risk(e.g, patients undergoing vascular operations). A numberof non invasive tests have been used and studied.

The standard 12-lead electrocardiogram is an in-sensitive test of the risk for myocardial ischaemia. It isnormal in up to 50% of patients with CAD, and somepatients have conduction defects that render the electro-cardiogram uninterpretable for ischaemia. When furtherworkup is required cardiac stress testing is used. Thepurpose of a stress test is to determine The status of ventricular function,

The amount of myocardium at risk for ischaemia,and

The need for further interventions, e.g., medication,angioplasty, or coronary artery bypass grafting, be-fore the proposed surgical procedure.Stress testing can be subdivided into exercise and

pharmacologic testing. Each test method stresses the com-ponents of myocardial oxygen consumption (contractility,heart rate, and afterload) to varying degrees.29

Exercise stress testing assesses a patient’s func-tional capacity. The ability to achieve a target heart rateof >100/min or 85% of the maximum predicted HR pre-dicts a low complication rate. ST segment depressiongreater than 0.1 mV on a preoperative exercise stresstest is an independent predictor of perioperative cardiaccomplications.

When exercise testing is contraindicated (LBBB,significant arrhythmias, CHF) or if patient is unable toexercise because of claudication , pharmacologic andother testing is substituted which include ischaemia moni-toring by ambulatory ECG (AECG),ejection fraction esti-mation by radionuclide ventriculography (RNV), dipy-ridamole thallium scintigraphy (DTS),and dobutaminestress echocardiography. The dipyridamole-thallium stresstest reduces after load and thereby alters supply; whereasdobutamine stress echocardiography test increases de-mand. Mantha et al believe that DSE may show the great-est promise in predicting cardiac events.29

AHA/ACC guidelines also try and answer a ques-tion that so often comes up in the mind of everyperioperative physician “Should patients with signifi-cant coronary artery disease undergo ‘prophylactic’coronary artery bypass grafting or percutaneouscoronary intervention before non-cardiac surgery?”Patients with a severe pattern of coronary disease, suchas a critical left main stem stenosis or severe proximalthree vessel coronary disease have a poor prognosis and,irrespectiveof planned surgery, should be urgently con-

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sidered for coronary revascularization. This interventionsignificantly improvesprognosis especially where an ex-ercise test is strongly positiveor left ventricular functionis impaired. Preoperative percutaneous coronary inter-vention with angioplasty and stenting, on the other hand,exposes destabilized plaque and coronary stent to theprothrombotic post-operative milieuwith potentially cata-strophic consequences and thus its role as a prophylacticintervention to tide over a high risk non cardiac surgery isquestionable if not worth condemning.22

The underlying theme of these guidelines is that anyintervention in the form of prophylactic revascularizationprocedures should be reserved for those who warrantsuch therapy independent of their surgicalprocedure.22Otherwise medical optimization is needed.

Preoperative interventions for prevention ofperioperative MI

Two principal strategies used in an attempt to re-duce the incidence of PMIs and other cardiac events are

A. Preoperative coronary revascularization- PCI orCABG

B. Pharmacological interventionsThe decision for or against preoperative coronary

revascularization- PCI or CABG, should be based entirelyon universally accepted medical indications for coronaryrevascularization. The philosophy of performing preop-erative coronary revascularization merely ‘to get thepatient through surgery’ is contrary to all availableevidence. If the decision for preoperative coronaryrevascularization is made, then timing with respect to thesubsequent surgery appears crucial.18

Coronary artery stenting – challenges and contro-versies

The advent of coronary artery stenting adds furthercomplexity to perioperative management. Since placementof coronary stents denudes the arterial endothelial sur-face, the risk of intrastent thrombosis is high for the firstseveral weeks after the procedure. The use of aspirinand clopidogrel decreases this risk, but if surgery mustoccur in the first several weeks after stent placement, therisk of intrastent thrombosis is high, and may occur evenwhen aspirin and clopidogrel are continued. This is likelydue both to the activation of the sympathetic nervous sys-tem and to the hypercoagulable state which occurs

perioperatively. Current guidelines advocate continuingcombination anti platelet therapy for a minimum of 2-3weeks and ideally for 3 months post stent placement toallow for complete re-endothelialization of the stent.26 Theadvent of drug-eluting stents may further complicateperioperative care. These stents prolong the re-endothelialization of coronary arteries, thus increasing theperiod of thrombotic risk for surgical patients with newstents. Initial guidelines recommended 3 months of com-bination antiplatelet therapy for patients with the sirolimus-eluting stent and 6 months for those with the paclitaxel-eluting stent which have now been extended for upto oneyear uniformly and continuation of aspirin upto the day ofthe planned surgical procedure has also been made man-datory, unless the risks of bleeding are significantly morethan those of perioperative stent thrombosis30. Ifangioplasty must occur before the surgical procedure,some authors recommend either plain angioplasty with-out a stent, or use of a bare metal stent followed by 2weeks of aspirin and clopidogrel before proceeding tononcardiac surgery, since the highest risk of stent throm-bosis appears to occur in the first two weeks.18 Closepreoperative consultation between the interventionalist andanaesthetist is required to minimize the risk of perioperativecardiac morbidity and mortality.

Pharmacological interventionsSeveral classes of drugs have been proposed in or-

der to reduce the risk of ischaemic complications of ana-esthesia and surgery. However, based on current clinicaldata, only aspirin, beta-blockers,alpha2-adrenoceptor ago-nists, and statins may have the potential to affectperioperative cardiovascular outcome.

1.ß-blockersThese drugs, at present, occupy centre stage both

for cardiac prophylaxis and treatment following an ACS.Several studies have shown a reduction in the incidenceof cardiac complications of anaesthesia and surgery inpatientsdeliberately given beta-blockers prophylactically.Cardio protective effects of -blockers are attributed tonumerous cardiovascular and other effects (anti-arrhyth-mic, anti-inflammatory, altered gene expression, protec-tion against apoptosis etc).31 Randomized trials in at riskpatients having non-cardiac surgery32and high-risk patientshaving vascular surgery33 have supported the use ofperioperative beta-blockade. According to the recent up-


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date by the AHA/ACC unless there is a clear contrain-dication, perioperative beta-blocker therapy should be givento all patients who are to have vascular surgery and tomost patients with cardiovascular disease who are to un-dergo major non-cardiac surgery and also those group ofpatients who test positive for inducible ischaemia in amyocardial stress test. Withdrawal of chronic beta-blockertherapy may have seriousadverse effects.34,35 It is impor-tant that beta-blocker therapy is maintained perioperativelyin at risk patients anda rebound ‘withdrawal syndrome’must be avoided. Beta-blockers may be given intrave-nously during or after surgery in patients unable to takeoral drugs.

2.Antiplatelet therapy (APA)-aspirin, clopidogreland glycoprotein IIb/IIIa inhibitors

Aspirin forms an integral part of the acute therapynot only after an ACS but also in patients not known tohave a pre existing CAD. It eliminates the diurnal varia-tion in plaque rupture. Apart from reducing platelet ag-gregation, its anti-inflammatory effect may be additive toits antithrombotic effect in patients with plaque instabil-ity.18 Perioperative antiplatelet therapy presents both ben-efits and risks. For elective surgery the practice of with-drawing all forms of APA has been challenged becauseof fear of an unopposed and even increased risk ofischaemic events. Most experts recommend surgery whilecontinuing APA for most vascular procedures and in set-tings where bleeding risk is likely to be low.36 French So-ciety of anaesthesiology and intensive care (SFAR) rec-ommends that “aspirin can be discontinued in theperioperative period only when, compared with benefits,the specific haemorrhagic risks inherent to the interven-tion is definitely greater than the cardiovascular risk as-sociated with discontinuation”.37 For those patients whoare on combination of two APA, the anaesthesiologistneeds to discuss the risk benefit ratio with the surgicalteam and preferably put the patient on monotherapy atleast 5 days preoperatively.

3.Alpha 2-adrenoceptor agonistsAlpha-2 adrenoceptor agonists improve cardiovas-

cular morbidity and mortality following cardiac and non-cardiac surgery.38 These drugs attenuate perioperativehaemodynamic instability,inhibit central sympatheticdischarge,reduce peripheral norepinephrine release,anddilate post-stenotic coronary vessels.39

4. StatinsHydroxymethylglutaryl coenzyme A (HMGCoA)

reductase inhibitors or statin therapy is associated withmajor benefits in patients with vascular disease. ‘Pleio-tropic’ effects of statins independent of their lipid lower-ing action have been proposed as the mechanism of theirbeneficial effects.18 These benefits are now recognizedtooccur not only in patients with coronary artery disease,butalso in patients with peripheral vascular disease, cere-brovascular disease, and those with multiple risk fac-tors.40,41 These benefits may, in part, relate to the stabili-zation of the atherosclerotic plaque surface andcap, makingplaque rupture less likely and enhancing plaque remodel-ling. All patients with vascular disease should be estab-lished on a statin, given the powerful evidence providedby the Heart Protection Study, statin therapy may be evenmore critical in the perioperative period.40 In a recentmeta analysis Biccard et al concluded that statin therapyis not only preventive but also is of proven benefit in theearly stabilization of patients following the occurrence ofan ACS in the perioperative period.42

5. NitroglycerineWhile nitroglycerine is used successfully in the treat-

ment ofmyocardial ischaemia, there is no evidence that itsprophylacticadministration before anaesthesia and surgerydecreases therisk of perioperative cardiac complications.39

6. MiscellaneousThough effective in the management of ischaemic

heart disease, Ca2+ channel blockers have never beenshown to offer any protection against perioperative car-diac complications of anaesthesia and surgery.39,43

ACE inhibitors have a proven benefit in patients witha recent ACS and also in patients with vascular diseaseand normal left ventricular function.44 These benefitsex-tend to patients with diabetes mellitus where there is theadded advantage of a reduction in progression tomicroalbuminuria.Patients with vascular disease or dia-betes mellitus should be maintained on angiotensin con-verting enzyme inhibitor therapy perioperatively.ACE in-hibitors have anti-ischaemic actions with a 20% relativereduction for myocardial infarction.44,45

The balance of benefits and risks ofACE inhibition inthe perioperative period is uncertain. Inhibition of both thesympathetic nervous system with a beta-blocker and therenin-angiotensin system with an ACE inhibitor removes

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the major protective reflexesfor intravascular volume regu-lation and homeostasis. Such combination therapy may re-sult in a greater risk of hypotension and may necessitatemore detailed and invasive haemodynamic monitoring andmore frequent intervention. In the presence ofACE inhibi-tion,acute renal failure can be precipitated by hypotension,hypovolaemia,radiocontrast, or NSAID administration.46

Antithrombin therapy (Heparin) has been used effec-tively in the management of unstable angina or acute PMI,both as a single agent or as a part of combination therapywith aspirin and thrombolytics. These patients are high riskcandidates for perioperative embolic events and are often onsubcutaneous low molecular weight heparin (LMWH) toreduce the risk of deep vein thrombosis and pulmonary em-bolism. Low dose heparin has been shown to reduce hyper-coagulability after elective abdominal aortic surgery.47

Adenosine modulators facilitate the release of thecoronary vasodilatoradenosine by the ischaemic myocar-dium, thereby improving collateral blood flow toward thecompromised area. Promising results have been obtained,48

with the only agent tested in clinical trials, acadesine.

Nicorandil is both a nitrate and a KATP

channel opener.It iseffective in the management of ischaemic heart dis-ease and itsassociated dysrhythmias. It may prove usefulin the perioperative prevention of cardiac complications.In clinical practice,nicorandil, a K

ATPchannel opener and

nitrate, is widely used in the treatment of angina. It ap-pears to protect by openingK

ATPchannels and to interact

with ischaemic preconditioning and appears to offer addi-tional protection when administered with isoflurane, interms of functional recoveryof the stunned myocardium.49

Preoperative medication: High risk patients ben-efit from optimal preoperative antiischaemia and antihy-pertensive therapy which should be continued inperioperative period. Pharmacological and psychologicalattempts should be made to allay anxiety, the goals beingto produce maximum sedation without undesirable circu-latory and ventilatory depression.

Intraoperative managementThe basic challenge during the perioperative period

is to prevent myocardial ischaemia, this goal is logicallyachieved by maintaining the balance between myocardialoxygen delivery and demand. Table 5 summarizes thevarious intraoperative events that can adversely influencethis balance, and hence should be avoided.

Choice of anaesthetic techniqueInduction of anaesthesia in patient with IHD should

be smooth and attempts should be made to minimize pressorresponse to laryngoscopy and intubation. Various drugslike lidocaine, nitroprusside,esmolol,fentanyl,nitroglycerineetc. have been used for this purpose.

Choice of drugs for maintenance depends on leftventricular function as determined by preoperative evalu-ation. In patients with normal LV function, a combinationof N

2O-opioid with addition of volatile agent (isoflurane,

desflurane, sevoflurane) is acceptable. In patients withseverely impaired LV function,a high dose opioid (fenta-nyl 50-100g.kg-1IV )may be utilized as sole anaesthetic.50

Opioid-based anaesthetics have become popular becauseof the cardiovascular stability associated with their use.The use of high doses, however, is associated with theneed for postoperative ventilation. Because weaning fromthe ventilator in an intensive care setting has been associ-ated with myocardial ischaemia, this feature is importantin the overall risk-benefit equation.

Neuraxial anaesthetic techniques can result insympathetic blockade, resulting in decreases in bothpreload and afterload. The decision to use neuraxial ana-esthesia for the high-risk cardiac patient may be influ-enced by the dermatomal level of the surgical procedure.

Table 5 Intraoperative events that influence thebalance between myocardial oxygen delivery andmyocardial oxygen requirements50

Decreased oxygen delivery

Decreased coronary blood flow

Tachycardia

Diastolic hypotension

Hypocapnia ( coronary artery vasoconstriction)

Coronary artery spasm

Decreased oxygen content

Anaemia

Arterial hypoxaemia

Shift of the oxyhaemoglobin dissociation curve to the left

Increased oxygen requirements

Increased preload (wall tension)

Sympathetic nervous system stimulation

Tachycardia

Systemic hypertension

Increased myocardial contractility

Increased afterload


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Infrainguinal procedures can be performed under spinalor epidural anaesthesia with minimal haemodynamicchanges if neuraxial blockade is limited to those der-matomes. Abdominal procedures can also be performedusing neuraxial techniques; however, high dermatomallevels of anaesthesia may be required and may be associ-ated with significant haemodynamic effects. High der-matomal levels can potentially result in hypotension andreflex tachycardia if preload becomes compromised orblockade of the cardioaccelerators occurs. Studies thathave evaluated regional vs. general anaesthesia for high-risk patients undergoing noncardiac surgery found no dif-ference in outcome in terms of cardiac morbidity.22

Monitored anaesthesia care by an anaesthesiacaregiver includes the use of local anaesthesia supple-mented with intravenous sedation/analgesia and is believedby some to be associated with the greatest safety margin.Although this technique can eliminate some of the unde-sirable effects of general or neuraxial anaesthesia, it pro-vides poor blockade of the stress response unless the lo-cal anaesthetic provides profound anaesthesia of the af-fected area. If the local anaesthetic block is less thansatisfactory or cannot be used at all, monitored anaesthe-sia care could result in an increased incidence of myocar-dial ischaemia and cardiac dysfunction compared withgeneral or regional anaesthesia. To achieve the desiredeffect, excess sedation can occur. Therefore, there maybe no significant difference in overall safety with moni-tored anaesthesia care, and general or regional anaesthe-sia may be preferable.

Perioperative pain managementFrom the cardiac perspective, pain management may

be a crucial aspect of perioperative care. Because themajority of cardiac events in noncardiac surgical patientsoccur postoperatively, the postoperative period may bethe time during which ablation of stress, adversehaemodynamics, and hypercoagulable responses is mostcritical.Although no randomized, controlled study specifi-cally addressing analgesic regimens has demonstratedimprovement in outcome, patient-controlled analgesia tech-niques are associated with greater patient satisfaction andlower pain scores. Epidural or spinal opiates are becom-ing more popular and have several theoretical advantages.The patients having epidural anaesthesia/analgesia havedemonstrated lower opiate dosages, better ablation of thecatecholamine response, and a less hypercoagulable state.Most importantly , an effective analgesic (i.e., one that

blunts the stress response) regimen must be included inthe perioperative plan.51,52

Maintenance of body temperatureHypothermia is common during the perioperative

period in the absence of active warming of patients. Sev-eral methods of maintaining normothermia are availablein clinical practice, the most widely studied being forced-air warming. Perioperative morbid cardiac events havebeen found to occur less frequently in the normothermicpopulation than in the hypothermic group.

Treatment of perioperative myocardial ischaemia1. Prevention of myocardial ischaemia: Careful

attention to prevention of tachycardia during anaesthesiais extremely important. Maintenance of adequate depthof anaesthesia along with judicious use of ultra short act-ingblockers can be very useful in preventing tachycar-dia. Apart from this, one should take adequate measuresto attenuate pressor responses to laryngoscopy and en-dotracheal intubation. If haemodynamic aberrations areassociated with myocardial ischaemia, they may precedeand be the cause of ischaemia ;or ischaemia may pre-cede and may cause haemodynamic aberrations. For ex-ample if an anaesthetized patient has normal ST segmentand then develops tachycardia followed by ST depres-sion, one should assume tachycardia as the cause of is-chaemia, so efforts should be made to reduce the rate.However, if hypovolemic hypotension precedes the onsetof ST depression, perhaps the hypotension and conse-quent decrease in myocardial oxygen supply is the cause,which should be managed accordingly.16

2. Treatment of myocardial ischaemia withoutaccompanying haemodynamic alterations: In suscep-tible patients, myocardial ischaemia often occurs withoutattendant haemodynamic alterations. In these patients ni-troglycerine (sublingual or intranasal) can be useful. Ni-troglycerine decreases preload and wall tension, dilatesepicardial coronary arteries, and increases subendocar-dial blood flow.

3. Treatment of myocardial ischaemia accompa-nied by tachycardia and hypertension: A combinationof tachycardia and hypertension can precipitate myocar-dial ischaemia by disturbing the myocardial oxygen demandand supply balance. After ensuring adequate ventilation,oxygenation and anaesthetic depth,blockers (esmolol ormetoprolol) may be administered in a titrated manner pro-vided there is no evidence of CHF or bronchospasm.

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4. Treatment of myocardial ischaemia accom-panied by tachycardia and hypotension: A combina-tion of tachycardia and hypotension (mostly due to hypo-volemia) can precipitate myocardial ischaemia becauseboth can drastically reduce myocardial oxygen supply.Apart from volume replacement, it is important to restorecoronary perfusion pressure and slow the rate.

5. Severe resistant myocardial ischaemia: Oc-casionally one may come across severe myocardial is-chaemia, which is resistant to all antianginal drugs. Hereintraaortic balloon pump (IABP) can be useful; it acutelydecreases myocardial oxygen requirements and may in-crease myocardial oxygen supply.

Treatment of perioperative myocardial infarctionCardiologists usually do treatment of an acute pre

or postoperative MI; however, in the intraoperative set-ting the anaesthesiologist has a major role to play. Oncethe diagnosis of acute MI is made, it is important to moni-tor the patient carefully: pulse oximetry, automatednoninvasive blood pressure and in selected cases a radialarterial line should be inserted to have a continuous moni-toring. 100% oxygen should be administered and volatileagent discontinued. As soon as PMI is diagnosed, aspirin325 mg is administered orally (through ryle’s tube if un-able to take orally) and is continued thereafter. Promptand aggressive treatment of changes in HR and/or BP isindicated. Tachycardia is treated with IV blockers likeesmolol while nitroglycerine is the drug of choice in thepresence of normal to modestly elevated systemic BP.Class I recommendations for intraoperative nitroglycer-ine include high-risk patients previously taking nitroglyc-erine, who have active signs of myocardial ischaemia with-out hypotension.22

Morphine is a venodilator that reduces ventricularpreload and oxygen requirements. It is the analgesic ofchoice for continuing pain unresponsive to nitrates, and itis also effective in patients with pulmonary vascular con-gestion complicatingACS.

Hypotension should be rapidly treated in order torestore coronary perfusion pressure (CPP). Moderate hy-potension often responds to volume expansion with 300-500ml of crystalloid. If severe hypotension (60-80mmHgsystolic) persists despite volume expansion, vasoactive orinotropic drugs may be given to elevate CPP above criti-cal value.

In the presence of significant left ventricular dys-function, CVP monitoring may not be a good guide forfluid therapy so more invasive haemodynamic monitoring(pulmonary artery catheterization) is indicated in patientswith refractory hypotension (unresponsive to volume ex-pansion), hypotension in the presence of CHF orhaemodynamic deterioration severe enough to requirevasopressors, vasodilators or an IABP. If PCWP is12mmHg or less, volume expansion with crystalloid shouldcontinue. If PCWP is high, use of an inotropic agent likedopamine 3-5g.kg-1.min-1 or dobutamine 2.5-20 g.kg-

1.min-1 is considered. If hypotension persists, considerepinephrine or milrinone. Milrinone is a class III cAMPphosphodiesterase inhibitor, 10 times more potent thanamrinone, shorter half-life and less potential for thromb-ocytopenia. After a bolus of 25-50g.kg-1 and infusion of0.375 to 0.75g.kg-1 .min-1, cardiac output and blood pres-sure increase in a few minutes. In some patients whodon’t respond, use of percutaneous IABP is life saving.16

Treatment of cardiac dysrrhythmias50:Apart from attempts to increase the cardiac output,

one should look for and correct metabolic acidosis (due tolow cardiac output), electrolyte imbalance (esp hypokale-mia), ensure good oxygenation and treat arrhythmias. Si-nus bradycardia is common following acute MI especiallyinferior wall infarctions reflecting acute ischaemia of SA/AV node. Treatment with atropine and a temporary pace-maker is needed when there is haemodynamic compro-mise. Some patients with severe bradycardia may requireemergency cardiac pacing (transcutaneous or transvenousas appropriate).

Atrial fibrillation (AF) occurs in > 10 % of patientsfollowing acute MI and may result from an acute increasein left atrial pressure caused by LV dysfunction. WhenAF is haemodynamically significant, cardioversion shouldbe promptly done however if AF is well tolerated, -blocker therapy is indicated.

Ventricular tachycardia (VT) is common followingacute MI. Sustained or haemodynamically significant VTis treated with electrical defibrillation while asymptom-atic VT is treated with lidocaine, procainamide, oramiodarone.

Ventricular fibrillation (VF) occurs in 3-5% of pa-tients with acute MI. Prophylactic lidocaine is no longerrecommended because of an increased incidence ofbradydysrhythmias and associated asystole. When VF


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occurs, rapid defibrillation with 120-200 Joules biphasicor 360 Joules monophasic current should be administered.Mortality is high when VF occurs in patients with hy-potension and/or CHF.

Thrombolytic or reperfusion therapy usingthromboplastin activator (t-PA) or streptokinase is rec-ommended to minimize the damage caused by intraop-erative infarct. To be effective, they should be preferablygiven within 4 hrs (maximum up to 12 hrs).The majorlimitation is a predisposition for bleeding so it is contrain-dicated in patients with fresh surgical wounds however itmay be useful in patients who have suffered PMI afterprocedures like cystoscopy or direct laryngoscopy.

In addition to thrombolytics, medical therapy with blockers, antithrombotics and antiplatelet drugs can bestarted to ensure maximum myocardial salvage. Heparinshould be started in patients in whom thrombolytic is notgiven. Heparin has been shown to reduce morbidity andmortality from thromboembolism and reinfarction.Earlyadministration of blockers may decrease the size ofinfarct, so all patients should receive intravenousblockersunless contraindications like CHF or large anterior wallMI with EF <40% exist. Such patients should receiveACE inhibitors.

Intra-aortic balloon counterpulsation devicePlacement of an intra-aortic balloon counterpulsa-

tion device has been suggested as a means of reducingperioperative cardiac risk in noncardiac surgery.Althoughthe rate of cardiac complications is low compared withother series of patients at similarly high risk, there are norandomized trials to assess its true effectiveness. Thereis currently insufficient evidence to determine the ben-efits vs. risks of prophylactic placement of an intra-aorticballoon counterpulsation device for high-risk noncardiacsurgery.

ConclusionsPerioperative myocardial infarction is a significant

issue in patients undergoing not only high risk surgery butalso those with clinical predictors that put them at a higherrisk even with minor surgical interventions. Though theunderstanding of the pathophysiology and managementof ischaemia in the perioperative period has increasedtremendously over the last decade but lot of questions stillremain unanswered. In view of the poor positive predic-tive value of non-invasivecardiac stress tests, the empha-

sis is on a combination of selective non-invasive testing(to reliably identify those patients who truly benefit frompreoperative intervention such as preoperative coronaryrevascularization, initiationor optimization of cardio pro-tective medication, aggressiveperioperative pharmacologi-cal therapy or cancellationof surgery).The perioperativeperiod induces large, unpredictable and unphysiologicalchanges in sympathetic tone, cardiovascular performance,coagulation andinflammatory response which in turn leadto alterations in plaque morphology and function. The im-portance of sympathetic activation in ischaemic syndromesleading to plaque rupture and secondary insults have tar-geted therapy towards stabilization of the so called vul-nerable plaque by pharmacological means (statins, aspi-rin,blockers)which may be as important in the preven-tion of PMI as an increase in myocardial oxygen supply(by coronary revascularization), or a reduction in myocar-dial oxygen demand (by blockers or 2-agonists).

Having said that, there is still some way to go be-fore we can have formal strategies and guidelines forpreventing, identifying and managing perioperative subclinical myocardial injury and further research in this areais the need of the hour.

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perioperative myocardial ischaemia and infarction - a review

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