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  • PCWP:-PAP-NMean PAWP-slightly incPAWP- abnormal with tall a waves (more than 21 mmhg) due to diastolic dysfunction.
  • Troponin more than 0.1ng/ml at 1 hour after the onset of symptoms makes MI most likely.
  • Transcript

    • 2. INTRODUCTION  Peri-operative myocardial ischemia (PMI) is the single most cardiac risk factor for an adverse cardiac outcome after non- cardiac surgery.  More than half of postoperative deaths are caused by cardiac events most of which are ischemic.  Identification of vulnerable patients and prevention of a PMI is essential to improve the postoperative outcome.
    • 3. PERIOPERATIVE MYOCARDIAL ISCHEMIA (PMI)  Traditional Definition of MI includes 1. Patient symptoms 2. ECG changes 3. Cardiac enzymes  This definition does not hold good under anaesthesia because 1. No symptoms- Deep sedation or Analgesic cover 2. Subtle ECG changes 3. CK-MB has limited sensitivity (Sk. Muscle injury)
    • 4.  The ACC criteria for PMI includes 1. Typical rise and gradual fall in Cardiac Troponin concentration or Rapid rise and fall of CK-MB along with typical ischemic symptoms / pathological q waves in ECG / ST segment depression or elevation in ECG / coronary artery intervention. 2. Pathological findings of acute MI
    • 5. PATHOPHYSIOLOGY 1. Acute Coronary Syndrome {Type I PMI}. 2. Myocardial Oxygen - Supply demand imbalance {Type II PMI}.
    • 6. Acute Coronary Syndrome {Type I PMI}  Plaque rupture can be spontaneous / due to external stresses.  Spont. ACS:-  Intraplaque inflammation  Plaque irritability  Spont. rupture /fissure / erosion  Acute coronary thrombosis / Ischaemia / Infarction.  External stresses:- a) Physiological or emotional stress  sympathetic induced hemodynamic changes, coronary vasospasm, prothrombotic factor release  plaque disruption. {increased cathecholamines}
    • 7. b) Tachycardia and Hypertension:- Shear stress  inward (positive) remodeling or Circumferential Tensile stress outward (negative) remodeling. b) Increased Peri-op Procoagulant Factors:- increased- fibrinogen, factor VIII, vWF, AT increased platelet reactivity decreased- protein C, AT-III, alpha 2 macroglobulin decreased fibrinolysis post op immobilisation (venous stasis)
    • 8. OXYGEN SUPPLY DEMAND IMBALANCE DECREASED OXYGEN DELIVERY INCREASED OXYGEN REQUIREMENT  Decreased CBF  Tachycardia  Diastolic hypotension  Hypocapnia  Coronary artery spasm  Decreased oxygen content  Anemia  Arterial hypoxemia  Shift of ODC to left  Sympathetic nervous system stimulation  Tachycardia  Hypertension  Increased myocardial contractility  Increased afterload  Increased preload
    • 9.  Generally, the diagnosis can be based on:- 1. Electrocardiographic (ECG) 2. Haemodynamic (pulmonary artery capillary wedge and/or left atrial pressure wave) 3. Functional (echocardiogram : Segmental Wall Motion abnormalities, Mitral regurgitation, etc) 4. Metabolic (coronary lactate production) 5. Biochemical (release of creatine kinase-MB isoenzyme and/or troponin) or 6. Reperfusion (scintigram) parameters.
    • 10.  Early recognition of PMI can enable us to prevent morbidity and mortality by employing appropriate pharmacological interventions.  Apart from history and examination, various criteria to establish the diagnosis of PMI include  Electrocardiography (ECG), Exercise Stress Testing, Serum Cardiac Markers, Echocardiography, Nuclear Imaging techniques, Cardiac Computed Tomography (CT), and Magnetic Resonance Imaging (MRI).
    • 11. PRE-OPERATIVE ASSESSMENT OF PATIENTS  HISTORY:-  Elicit the severity, progression, and functional limitations imposed by IHD.  Focus on determining the presence of major, moderate and minor clinical risk factors in a particular patient.  Symptoms such as angina and dyspnoea may be absent at rest, emphasizing the importance of evaluating the patient's response to various physical activities such as walking or climbing stairs.  Limited exercise tolerance in the absence of significant lung disease is very good evidence of decreased cardiac reserve
    • 12.  Previous Myocardial Infarction  Co-Existing Noncardiac Diseases  Current Medications
    • 13. ELECTROCARDIOGRAPHY {ECG}  25 to 50% of patients with CAD will have normal resting ECG.  In 25% of patients ECG is not diagnositc (LBBB/WPW).  Still, ECG is the most important preoperative test for patients with IHD.
    • 14. ELECTROCARDIOGRAPHY {ECG}  Ischemic Manifestations: i) ST SEGMENT CHANGES (most specific) ii) T wave changes (flattening or inversion in high risk groups) iii) Dysrhythmias iv) New conduction abnormalities v) New atrio-ventricular block vi) Heart rate changes
    • 15. ST segment criteria for ischemia  Patients with LVH, LBBB, digitalis effect, ventricular pacing and those not in sinus rhythm are not suitable for ECG-derived diagnosis of MI.
    • 16.  ST Depression: subendocardial ischemia, poor localization 1. Horizontal / downsloping depression > 0.1 mV (1 mm) at 60-80 msec after J point 2. Upsloping depression > 0.15 mV at 80 msec after J point
    • 17.  ST Elevation: transmural ischaemia, good localization > 0.1 mV (>0.2 mV in Men & > 0.15 mV in Women) at 60-80 msec after J point.  Other causes for ST segment elevation are:- 1. Conduction disturbances 2. R wave amplitude changes 3. Autonomic Nervous System changes 4. Hyperventilation 5. Myocardial contusion
    • 18. 6. Electrolyte changes, hypoglycaemia 7. Neurological (trauma, SAH) 8. Hypothermia 9. Acute pericarditis 10. Body position changes/ retractors
    • 19.  Sensitivity of different ECG lead combinations No. of leads Combination Sensitivity (%) 1 lead II, V4, V5 33 61 75 2 leads II /V5 V4/V5 80 90 3 leads V3,V4,V5 II,V4,V5 94 96 4 leads II, V2-5 100
    • 21. EXERCISE STRESS TESTING  Exercise induced ischemia usually occurs in coronary arteries that are moderately or severely obstructed (> 75% of the cross sectional area), or in those that develop vasospasm.  Patients with moderate CAD typically exercise to lower stages before termination of the test because of symptoms or heart rate limitation.  During exercise, and in the recovery period, the principal indicator of myocardial ischemia is ST segment deviation.
    • 22.  A criterion of 2 mm deflection has been conventionally accepted.  ST depression of 1-3 mm is associated with 67% probability of one to three vessel disease.  Changes of 2 mm or more, occurring during stage 1 and 2, are associated with 90% probability of one to three vessel disease.  The occurrence of early ST changes is associated with poor prognosis.  Limitation:- Negative tests do not imply lack of disease.
    • 23. SERUM BIOCHEMICAL MARKERS  Serum biomarkers that are indicative of myocardial damage include  Myoglobin (4 Hrs)  Total Ck(16hrs)  CK-MB Isoenzyme (24 Hrs)  Troponin I And T (24 Hrs)  Lactate Dehydrogenase (76 hrs).
    • 24.  New markers of perioperative cardiac injury include :-  Brain Natriuretic Peptide (BNP)  Soluble CD40 Ligand, And  High Sensitive C-reactive Protein.
    • 25. ECHOCARDIOGRAPHY  Acute MI results in Abnormal Inward Motion and Thickening of the affected myocardial region.  Regional Wall Motion Abnormalities (RWMA) occur within seconds of inadequate blood flow or oxygen supply.  Abnormalities in Diastolic Function usually precede abnormal changes in systolic function.  Diastolic ventricular function can be assessed by monitoring the Rate Of Filling associated with changes in chamber dimensions.
    • 26.  Regional systolic function can be estimated by determination of wall thickening and wall motion during systole in both long and short-axis views of the ventricle.  The short axis view of the left ventricle at the papillary muscle level displays myocardium perfused by three main coronary arteries, and is, therefore, very useful.
    • 27.  RWMA can be assessed by inward movement of endocardium toward the centre of the cavity during systole.  As the myocardial oxygen supply / demand balance worsens, RWMAs progress from mild hypokinesia to severe hypokinesia, akinesia, and finally dyskinesia.  Normal contraction is defined as > 30% shortening of the radius from centre to endocardial border.  Mild hypokinesia refers to radial shortening of 10-30%, and severe hypokinesia is defined as < 10% radial shortening
    • 28.  RWMAs are more sensitive than ECG or PA catheter  Limitation of RWMA analysis:-  It does not differentiate stunned or hibernating myocardium from acute ischemia.  It does not differentiate the cause of ischemia between increased oxygen demand and decreased oxygen supply.
    • 29. TRANSESOPHAGEAL ECHO (TEE)  The most obvious limitation of TEE monitoring is that ischemia cannot be detected during critical periods such as induction, laryngoscopy, intubation, emergence, and extubation.
    • 30. Dobutamine Stress Echocardiography (DSE)  DSE involves the identification of new or worsening RWMAs using 2D Echo during infusion of intravenous dobutamine.  Advantages of DSE as compared to dipyridamole thallium are:  DSE can also assess LV function and valvular abnormalities,  Low cost  No radiation exposure  Shorter duration of study , and  Immediate results.  The sensitivity and specificity of DSE for CAD is 89 and 85% respectively.
    • 31. DIPYRIDAMOLE THALLIUM SCINTIGRAPHY  Dipyridamole works by blocking adenosine receptors and increasing adenosine concentration in the coronary vessels.  Adenosine is a direct coronary vasodilator.  After infusion of the vasodilator, flow is preferentially distributed to area distal to normal coronary arteries, with minimal flow to areas distal to a coronary stenosis.
    • 32.  A radioisotope such as thallium or 99-technetium sestamibi is then injected.  Normal myocardium will show up on initial imaging, while areas of either myocardial necrosis or ischemia distal to a significant coronary stenosis will demonstrate a defect.  After a delay of several hours, or after infusion of second dose of 99-technetium, the myocardium is again imaged.
    • 33.  Those initial defects that remain as defects are consistent with old scars, while those defects that demonstrate normal activity on subsequent imaging are consistent with areas at risk of MI.  Patients at high risk of MI will show increased lung uptake, left ventricular dilatation, increased end-systolic and end-diastolic volumes, stress induced ischemia, and multiple perfusion defects.  Thallium imaging has sensitivity and specificity of around 90% for detection of acute infarct, provides information regarding viability and has prognostic value.
    • 34. Computed Tomography and Magnetic Resonance Imaging  High-speed CT can visualize coronary artery calcification.  Intravenous administration of radiographic contrast medium enhances the clarity of the images.  MRI provides even greater image clarity and can delineate the proximal portions of the coronary arterial circulation.  However, CT and MRI are more expensive and less mobile than other modalities of cardiac evaluation.
    • 35. Radionuclide Ventriculography  Radionuclide ventriculography quantitates left and right ventricular systolic and diastolic function.  The EF determined by this method does not provide information that can be used to accurately predict PMI, but an EF of less than 50% does predict an increased risk of postoperative CHF in patients undergoing abdominal aortic surgery.
    • 36. TREATMENT OF PMI 1. Prevention of myocardial ischaemia:  Attention to prevention of tachycardia (judicious beta blockers) during anaesthesia is extremely important.  Maintenance of adequate depth of anaesthesia  Attenuation of pressor responses to laryngoscopy and endotracheal intubation.  If an anaesthetized patient has normal ST segment and then develops tachycardia followed by ST depression, one should assume tachycardia as the cause of ischaemia, (reduce the heart rate).  If hypovolemic hypotension precedes the onset of ST depression, manage with volume.
    • 37. 2. Treatment of myocardial ischaemia without accompanying haemodynamic disturbances:  In these patients nitroglycerine (sublingual or intranasal) can be useful.  Nitroglycerine decreases preload and wall tension, dilates epicardial coronary arteries increasing the sub-endocardial blood flow
    • 38. 3. Myocardial ischaemia associated with tachycardia and hypertension:  Treat common causes of tachycardia  Beta-blockade (aim for HR < 60 bpm)  I.V. Esmolol - 0.25 - 0.5 mg/kg bolus, 25 - 300 mcg/kg/min infusion  Metoprolol - 0.5 – 1mg titrated bolus over 15 minutes If beta-blockade is contra-indicated  Verapamil - 2.5 mg - repeat as needed. Infuse at 1- 10mg/hr [may be first choice if ST segment elevation (coronary spasm)]  Alpha-2 agonists -: Clonidine, Dexmedetomidine, Mivazerol
    • 39.  Hypertension 1. Initially treat common causes e.g. light anaesthetic depth, CO2 retention, 2. GTN – sublingual (0.3-0.9 mg - works within 3 min) 3. IV NTG infusion (0.25 - 4 mcg/kg/min - titrate to effect) 4. Clonidine (30 mcg every 5 minutes up to 300 mcg) 5. Dexmedetomidine (1mcg/kg load, infuse at 0.2-0.7 mcg/kg/hr)
    • 40. 4. Myocardial ischaemia associated with tachycardia and hypotension:-  Treat cause e.g. hypovolemia (300-500ml of crystalloid)  Reduce anaesthetic depth  Adjust PEEP  Check surgical manipulation (retractors pressing IVC during laparotomy)  Vasopressors are preferred (Metaraminol, Phenylephrine) to increase coronary perfusion pressure  Reduce the heart rate.
    • 41. 5. If ischaemia persists with optimal haemodynamics :- (Persistent MI)  Keep increasing GTN  Combine with vasopressor if there is hypotension  Increase monitoring - CVP, PCWP, TEE  Alter surgical plan
    • 42. 6. Severe resistant Myocardial Ischemia: CONSIDER Acute Coronary Syndrome (unstable angina, myocardial infarct)  Aspirin (Oral / Ryles tube : 325 mg)  Heparin (I.V. 5000 Units bolus, then 1000 U/hr) if surgery permits  Continue beta-blockade if no signs of CCF  Aspirin & beta-blockade reduce risk of infarct and mortality  Watch for complications- dysrhythmias, CCF, myocardial infarction
    • 43.  Obtain Cardiology consultation  Intra Aortic Balloon Counterpulsations (IABP )  PTCA  Thrombolysis is generally contraindicated
    • 44. POSTOPERATIVE MANAGEMENT OF PMI  ICU or CCU postop and/or Cardiology referral  Watch for perioperative Myocardial Infarction  ECG immediately postop and on day 1 and 2  Cardiac troponin at 24 hrs and day 4 (or hosp discharge) (CK-MB of limited use)  PTCA if needed  LONG TERM risk factor management  Aspirin, Statins, Beta-blockade, ACE inhibitors
    • 45. TO CONCLUDE:- TREATMENT OF PMI:  100% Oxygen, stop volatile anaesthetics  Increase monitoring : Arterial line,CVP/PCWP/TEE  Oral/Ryle’s tube :Aspirin 325 mg  NTG  Morphine : Analgesia and also effective in patients with pulmonary vascular congestion complicating ACS.  Hypotension : Volume (300-500ml of crystalloid)  Inotropes, vasopressors.  Heparin  IABP
    • 46.  Thrombolysis :-  Should be done within 4 hrs (maximum 12 Hrs) with t-PA or streptokinase.  The major limitation is bleeding so it is contraindicated in patients with fresh surgical wounds.  Beta blockers : Contraindications are CCF or large anterior wall MI with EF <40%)  Antithrombotics and antiplatelet drugs can be started.  Antiarrhythmic agents, Beta blockers  Emergency cath lab & Percutaneous Coronary Intervention.
    • 47. References : 1. Miller’s Anesthesia 2. Stoeltings coexisting diseases 3. Perioperative Myocardial Ischemia and Infarction- a Review. IJA 2007: 51(4) :287-302 4. Internet
    • 48. THANK YOU