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
11. 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.
12. 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).
13. 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
16. 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.
17. 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
18. 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.
19. 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
20. 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
21. 6. Electrolyte changes, hypoglycaemia
7. Neurological (trauma, SAH)
8. Hypothermia
9. Acute pericarditis
10. Body position changes/ retractors
22. 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
24. 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.
25. 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.
26. 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).
27. New markers of perioperative cardiac injury
include :-
Brain Natriuretic Peptide (BNP)
Soluble CD40 Ligand, And
High Sensitive C-reactive Protein.
28.
29. 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.
30.
31. 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.
32. 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
33. 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.
34. 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.
35. 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.
36. 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.
37. 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.
38. 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.
39. 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.
40. 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.
41. 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.
42. 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
43. 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
44. 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)
45. 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.
46. 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
47. 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
48. Obtain Cardiology consultation
Intra Aortic Balloon Counterpulsations (IABP )
PTCA
Thrombolysis is generally contraindicated
49. 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
50.
51. 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
52. 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.
53.
54. 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
