This document discusses the anaesthetic management of patients with ischemic heart disease undergoing non-cardiac surgery. It begins by defining ischemic heart disease and outlining its various manifestations including stable angina, unstable angina, and myocardial infarction. It then discusses preoperative evaluation and risk stratification of these patients, including medical history, physical exam, ECG, stress testing, and coronary angiography. Intraoperative management focuses on minimizing myocardial ischemia through beta-blockers, tight blood pressure control, and avoidance of tachycardia or hypotension.

1. 
Presented by:
Dr. Md. Zareer Tafadar
Post Graduate Student
Deptt. Of Anaesthesiology & Critical Care
Silchar Medical College & Hospital.
Anaesthetic Management Of A Patient With
Ischaemic Heart Disease Undergoing Non
Cardiac Surgery

2.  Ischaemic heart disease (IHD) also known as coronary artery
disease (CAD) is the generic designation for a group of closely
related syndromes resulting from myocardial ischemia—an
imbalance between the supply (perfusion) and demand of the heart
for oxygenated blood. Ischemia comprises not only
insufficiency of oxygen, but also reduced availability of nutrient
substrates and inadequate removal of metabolites
 Coronary heart disease (CHD) is the most common form of
heart disease.
 5% of patients over 35 years of age have asymptomatic
ischaemic heart disease.
 May be present in up to 30% of older pts undergoing surgery
 Cardiac dysrhythmias[VF] are a major cause of sudden death.
Introduction

3.  Male gender
 Increasing age
 Hypercholesterolemia
 Hypertension
 Cigarette smoking
 Diabetes mellitus
 Obesity
 Sedentary lifestyle
 Genetic factors
 Family history of premature ischemic heart disease
(male <55 yrs of age, female <65 yrs)
Risk Factors for Development of Ischemic
Heart Disease

4. 
IHD
Angina
Pectoris
Stable angina,
Prinzmetal angina,
Unstable angina—
Acute MI
STEMI
NSTEMI
Chronic IHD
with Heart
Failure
Sudden
Cardiac Death
Spectrum Of IHD

5. Angina Pectoris: symptom complex of IHD characterized by paroxysmal and usually
recurrent attacks of substernal or precordial chest discomfort (variously described as
constricting, squeezing,choking, or knifelike) caused by transient (15 seconds to 15
minutes) myocardial ischemia
 Stable Angina
 Chronic pattern of transient angina pectoris precipitated by
physical activity or emotional upset, relieved by rest with in
few minutes.
 caused by the reduction of coronary perfusion to a critical level by
chronic stenosing coronary atherosclerosis; this renders the heart
vulnerable to further ischemia whenever there is increased cardiac
workload.
 Typical angina pectoris is usually relieved by rest (thereby
decreasingdemand) or nitroglycerin, a strong vasodilator
 Temporary depression of ST segment with no permanent
myocardial damage.
Angina Pectoris

6.  Variant Angina/Prinzmetal Angina
 Typical anginal discomfort usually at rest.
 Develops due to coronary artery spasm rather than increase
myocardial oxygen demand.
 The anginal attacks are unrelated to physical activity,heart
rate, or blood pressure. Generally responds promptly to
vasodilators.
 Transient shifts of ST segment – ST elevation.

7.  Unstable Angina
 Refers to a pattern of pain that occurs with progressively
increasing frequency, is precipitated with progressively less
effort, often occurs at rest, and tends to be of more
prolonged duration.
 In most patients, unstable angina is induced by disruption
of an atherosclerotic plaque with superimposed partial
(mural) thrombosis and possibly embolization or
vasospasm (or both). of subsequent acute MI.
 Thus this syndrome is sometimes referred to as
preinfarction angina, and in the spectrum of IHD, unstable
angina lies between stable angina on the one hand and MI
on the other.

8.  MI, also known as "heart attack," is the death of cardiac muscle
resulting from ischemia.
 Region of myocardial necrosis due to prolonged cessation of
blood supply
 Results from acute thrombus at side of coronary atherosclerotic
stenosis
 Typical symptoms of myocardial infarction include
• Sudden Chest Pain,
• Shortness Of Breath,
• Nausea, Vomiting,
• Palpitations, Sweating
• Weakness, Light-headedness
• Collapse/syncope
Myocardial Infarction (MI)

9. 
Diagnosis of Acute MI:
 At least 2 of the following
• Ischaemic symptoms
• Diagnostic ECG changes
• Serum cardiac marker elevations

10. 

11. 
Screening & Evaluation
Goals
• Identify the risk for heart disease based on risk factors.
• Identify the presence and severity of heart disease from
symptoms, physical findings, or diagnostic tests .
• Determine the need for preoperative interventions.
• Modify the risk for perioperative adverse events.

12. 
 History:
 Aim: To elicit severity progression and functional
limitations imposed by IHD
 Chest discomfort (pain, pressure, tightness), the
duration of the discomfort, precipitating factors,
associated symptoms, and methods of relief.
 Exercise tolerance: In the absence of significant lung
disease limitation indicates decreased cardiac reserve.
 If a patient can climb two to three flights of stairs
without symptoms, it is likely that cardiac reserve is
adequate.

13.  Risk factors : Smoking, hypertension, age, male
gender, hypercholesterolemia, and family history.
 H/O MI
 Acute MI: 1-7 days
 Recent MI: 8- 30 days
 H/O cardiac revascularisation- PCI/CABG
 Co-Existing Noncardiac Diseases: CVA, COPD, DM,
Renal insufficiency
 Current Medications: Anti-hypertensives, Anti
platelet agents, Anticoagulants, Others.

14.  Physical Examination
• Abnormal physical findings are often absent and non-specific.
• Quick assessment of patients vital signs
• Signs of right and left ventricular dysfunction must be sought.
• Jugular venous distention and peripheral edema are signs of
right ventricular failure.
• Auscultation of the chest may reveal evidence of left
ventricular dysfunction such as an S3 gallop or rales.
• A carotid bruit may indicate cerebrovascular disease.
• Orthostatic hypotension may reflect attenuated autonomic
nervous system activity due to treatment with
antihypertensive drugs.

15. 12-lead ECG:
 Preoperative resting 12-lead ECG is reasonable for patients
with known coronary heart disease or other significant
structural heart disease, except for low-risk surgery (IIa)
 May not show any abnormalities at rest or with no symptoms,
or may show evidence of old MI (Q waves) in 2 or more leads
& >1/3 of the QRS complex length)
• May reveal ST segment depression >1 mm from baseline in case
of angina pectoris or ST-segment elevation in association with
AMI or variant angina
• Other changes with symptoms of angina pectoris: reversible T-
wave inversion
• Other findings with AMI: increased T-wave amplitude,
followed by ST elevation, followed by Q-wave development &
resolution of ST elevation
Specialised Preoperative Testing

16. 
• Exercise ECG is useful for detecting signs of
myocardial ischaemia as well as for evaluation of
exercise capacity
Contraindications:
• Severe AS
• Severe hypotension
• Acute myocarditis
• Uncontrolled HF
• Infective Endocarditis

17. 
ECG Changes in Stable Angina: Transient ST depression

18. 
 ECG Changes in Unstable Angina: Transient ST
depression / T wave inversion

19. 
ECG Changes in Myocardial Infarction

20. 

21. 
Echocardiography
• Ventricular wall motion
abnormalities can help to
localise the obstructive coronary
lesions.
• Can be used to assess global
cardiac function. Major
determinant of long-term
prognosis.
• It can also be used to assess
regional wall motion
abnormalities & detect the
presence of previous
myocardial injury.
• It is also used to diagnose LV
thrombus in case of apical &
anterior wall MI.

22. 
 Stress echocardiography: This is used with
pharmacologic induction of cardiac stress
(dobutamine) or exercise to look at LV segmental
wall function at rest & with stress. This can be also
used to differentiate between viable (hibernating,
stunned) & nonviable (infarcted) myocardial
segments

23. Nuclear Stress Imaging
• Thallium scan and technetium scan shows areas of
reduced uptake of radioactive isotope by the
myocardium. Useful for assessing coronary perfusion
• A perfusion defect present during stress but not all
rest indicates reversible myocardial ischemia,
whereas a persistent perfusion defect on scan during
both phases (rest and stress) usually indicates
previous myocardial infarction.
• Thallium scanning is positive in 75-90% of patients
with significant coronary disease. False positive test
may occur in women due to breast tissue.

24. 
Coronary Angiography
•Provides information about the
coronary anatomy & the extent &
location of the lesions.
• It is indicated in pts with
unstable angina despite maximal
therapy.
• It can provide a road map to
coronary revascularization & the
feasibility of percutaneous
angioplasty or surgical treatment
depending on the characteristics
& location of the lesions.

25. 
Positron Emission Tomography:
 May be used to
demonstrate regional
myocardial blood flow
& metabolism, & hence
viability.

26. 
Cardiac Markers:
CK-MB isoenzyme Troponin ( T, I )
Positive if CK/MB > 5% of
total CK and 2 times
normal
Very specific and more sensitive
than CK
Rises 4-6 hours after injury and
peaks at 24 hours
Rises 4-8 hours after injury
Remains elevated 36-48 hours May remain elevated for up
to two weeks
Elevation can be predictive of
mortality
Can provide prognostic
information

27. 

28. 
AIM: Identify patients at increased risk so as to
manage them with pharmacological and other
perioperative interventions that can lessen the risk
and severity of perioperative cardiac events.
Risk Stratification

29. 
Lee’s Revised Cardiac Risk Index:
Uses 6 independent predictors of major cardiac complications for
patients undergoing elective non cardiac surgery.

30. 
 The ACC/AHA guidelines integrate risk stratification
according to:
1. Clinical risk factors & ECG review.
2. Functional Capacity.
3. Surgery specific risk factors.

31. 
Clinical Predictors of Increased Perioperative
Cardiovascular risk
 Major
• Unstable coronary
syndromes
• Acute / Recent MI
• Unstable/ Severe Angina
• Decompensated Heart Failure
• High grade AV-block
• Symptomatic Ventricular
Dysrhythmias
• Severe Valvular Heart
Disease
 Intermediate
• Stable Angina
• Previous MI
(history/ECG)
• Compensated or previous
heart failure
• DM/Renal Insufficiency
 Minor
• Age>70
• ECG: LVH,LBBB ST-T
abnormalities
• Low functional capacity
• H/O CVA/HTN

32. 
Functional Capacity
• Exercise tolerance is a major determinant of perioperative risk.
• It is usually evaluated by the estimated energy requirement for
various activities, and graded in metabolic equivalents (MET)
on a scale defined by the Duke Activity Status Index .
• One MET represents the oxygen consumption of a resting adult
• High-risk group : Ischaemia at low-level exercise (<5 MET or
heart rate <100 min)
Low-risk group: > 7 MET (or heart rate >130 min) without
ischaemia
• In the absence of valve pathology, the ejection fraction of the
left ventricle can be considered as an adequate measurement of
the myocardial functional reserve.
• Patients with good functional capacity and no symptoms can be
considered free of any severe coronary artery disease.

33. 
Duke Activity Status Index

34. 
Risk Factors Associated With Surgery

35. 
Preoperative Assessment Of Patients
With Ischaemic Heart Disease

36. 
 High /Intermediate risk Surgery + Moderate –
Minor Clinical Risk Factors
Prior Revascularization
CABG
<5yrs
No change in medical
condition
Surgery
PCI
BMS >30days
Minimal anti platelet
therapy
Surgery
DES <12 months
Dual anti platelet
therapy
Cardiology Opinion

37. 

38. 

39. 
High /Intermediate risk Surgery + Moderate Clinical
Risk Factors
No Prior
Revascularization
Stable
CAD
Surgery
Decreased Exercise
Tolerance
Non Invasive
Testing -ve
Surgery
Non Invasive Testing +ve
Coronary Angiography
Significant CAD
Consider risk of coronary
revascularization vs surgery

40. 
Three options
 Revascularization by surgery (CABG)
 Revascularization byPCI
 Optimal Medical Management
Management Prior to Surgery

41. 
Coronary Artery Bypass Grafting
 The benefits of the non-cardiac surgery
must be greater than the combined risks
of coronary catheterization and coronary
revascularization.
 Indications:
• Disease of the LMCA.
• Disease of all three coronary vessels
(LAD, LCX & RCA).
• Diffuse disease not amenable to
treatment with a PCI.
• High-risk patients such as those with
severe ventricular dysfunction .
• Occlusion of grafts from previous
CABGs.

42. 
 Traditional bare-metal stent (BMS) coronary stents provide a
mechanical framework that holds the artery wall open, preventing
stenosis of coronary arteries.
 Newer drug-eluting stents (DES) are traditional stents coated with
drugs, which, when placed in the artery, release certain drugs over
time. These types of stents help revent restenosis of the artery by
suppressing tissue growth at the stent site and local modulation of the
body's inflammatory and immune responses. They may be
susceptible to an event known as "late stent thrombosis“.
 DAPT (DAPT; aspirin plus platelet P2Y12 receptor blocker)
significantly lowers the risk of stent thrombosis.
Percutaneous Coronary Intervention

43. 
• PCI using Bare Metal
Stents or Drug Eluting
Stents are associated
with procedural
complications
• Dual antiplatelet therapy
using aspirin +
P2Y12 receptor blockers
increases the risk of
bleeding.

44.  Pharmacological Management (ACC/AHA + European
Guidelines)
 Perioperative beta-blocker therapy
• Patients already on beta blockers chronically (I)
• In patients with intermediate- or high-risk preoperative tests (IIb)
• In patients with ≥3 RCRI factors (IIb)
• If used for prophylaxis should be initiated atleast 1 week prior to
elective surgery.
 Nitrates: Prophylactic use of niroglycerin has not been shown to
reduce perioperative mortality or morbidity.(III)

45.  Perioperative statin therapy
• To be continued in patients already taking statins (I)
• Patients with vascular disease should receive statins regardless
of the need of surgery (IIa)
• Perioperative initiation of statins may be considered in patients
with a clinical risk factor who areundergoing elevated-risk
procedures (IIb)
• Should be started 1-4 weeks prior to surgery and continued
perioperatively.
 Alpha-2 agonists
• Alpha-2 agonists are not recommended for prevention of
cardiac events (III)

46.  ACE inhibitors
• Continuation of ACE inhibitors or ARBs is reasonable
perioperatively (IIa)
• If ACE inhibitors or ARBs are held before surgery, it is
reasonable to restart as soon as clinically feasible
postoperatively (IIa )
 Antiplatelet agents
• Continue DAPT in patients undergoing urgent non-cardiac
surgery during the first 4 to 6 wk after BMS or DES
implantation, unless the risk of bleeding outweighs the
benefit of stent thrombosis prevention (I).
• In patients with stents undergoing surgery that requires
discontinuation of P2Y12 inhibitors, continue aspirin and
restart the P2Y12 platelet receptor–inhibitor as soon as
possible after surgery (I).

47.  Pathophysiological Considerations During Anaesthetic
Management
 Ischemic heart disease is a condition where the myocardial
demand outstrips the O2 supply from coronary vessels. The
increase in stress during perioperative period causes
1. An adrenergic surge leading to an imbalance in myocardial o2
supply – demand ratio. This in turn causes ischemic
myocardium.
2. Alterations in the balance between prothrombotic and
fibrinolytic factors resulting in hypercoagulability and possible
coronary thrombosis.
3. Fluid shift in the perioperative period add to surgical stress.
 All these increase in perioperative morbidity & mortality
Intraoperative Management

48. 
 Causes Of Myocardial O2 Imbalance
 1) Decreased O2 supply
 Decreased coronary flow
• tachycardia (decreased diastolic perfusion time)
• hypotension (esp diastolic BP)
• hypocapnia (coronary vaso constriction) coronary vasospam
 Decreased O2 content & availability
• anemia
• hypoxemia
• reduced release from Hb i.e ODC shift to left
 2) Increased O2 demand
• 1. tachycardia
• 2. increased wall tension
• 3. increased preload
• 4. increased after load
• 5. increased myocardial contractility

49. 
Anaesthetic Goals
 Prevent myocardial ischaemia by optimising
myocardial O2 delivery and reducing the O2 demand.
 To monitor for ischaemia.
 To institute appropriate measures to treat ishaemia if
and when it develops.

50.  Tachycardia
• Increased O2 demand through increased myocardial work
• Also shortens diastolic filling time thereby reducing time
for optimal coronary perfusion.
 Diastolic BP
• In the absence of left ventricle volume overload , a
diastolic arterial pressure of 60 mmHg should be
sufficient to maintain coronary perfusion in most patients
with CAD .
• Above 90 mmHg is counterproductive as this level
invariably requires a higher left ventricular wall tension,
thereby increasing O2 demand as well.
• The aim should be to avoid persistent changes in BP.
Anaesthetic Considerations During The
Intraoperative Period

51.  Hyperventilation:
• Must be avoided as hypocapnia can cause coronary
artery vasoconstriction
 Maintain normothermia:
• Minimizing body heat loss is vital to avoid postop shivering &
precipitation of ischemic myocardial events. This can be
achieved with warm IV fluids, warm operating room
atmosphere, forced warm air covers & irrigation of the surgical
site with warm fluids.
 Correct Anaemia
 Blood loss to be taken care of – anaemia can cause critical
reduction in myocardial oxygen supply in IHD pt.

52. 
 Pre Medication
 Benzodiazepines –
• Quells anxiety
• Hemodynamic stability
• Extended duration of action
• Potential for hypoxia
 Intravenous narcotics (e.g. Fentanyl)
• Effective control of catecholamine surge
• Respiratory depression
• Prolonged ventilation
General Anaesthesia

53. 
 Induction
 Induction agent:
• Thiopentone: Decreases myocardial contractility, pre-load &
BP and causes slight increase of the heart rate.
• Propofol: Causes dose dependent decrease in myocardial
contractility and produces significant decrease of BP and HR.
Not suitable for patients in whom LV function is
compromised.
• Etomidate: Causes minimal haemodynamic changes and is a
good choice for patients with poor cardiac reserve.
• Midazolam: It produces decrease in the MAP and increase in
the HR.
• Ketamine is to be avoided as it increases myocardial oxygen
demand by increasing HR and BP.

54. 
 Intubation: To be facilitated by the use of succinyl choline or a
NDMR.
 Blunting of haemodynamic response to tracheal intubation by
• Keeping the duration short (<15s)
• Use of laryngotracheal Lidocaine, intravenous lidocaine,
esmolol, fentanyl, dexmedetomidine.

55. 
Maintenance
 Volatile anesthetics
• May be used to achieve controlled myocardial depression to
minimise the intense SNS activity associated laryngoscopy and
surgical stimulation
• Decrease myocardial O2 requirements and pre-condition the
myocardium to tolerate ischaemic events.
• AHA guidelines recommend volatile anaesthetic agents for
maintenance of anaesthesia in patients with IHD in a
haemodynamically stable patient with no evidence of CHF. (IIa)
• Halothane has the disadvantage of myocardial depression and
potential of dysrhythmias.
• Although Isoflurane reduces coronary vascular resistance there is
no evidence o suggest that it increases the incidence of intra-op
myocardial ischaemia.

56.  Nitrous Oxide
• The use of N2O in patients with IHD is questionable since it
increases PVR, and predisposes to diastolic dysfunction and
subsequent myocardial ischaemia.
 Muscle Relaxants
• Vecuronium, rocuronium, cisatracurium are attractive choices for
patients with ischemic heart disease
• Atracurium causes histamine release and subsequently fall in
blood pressure which makes it a less desirable agent
• Pancuronium should be avoided to due to its sympathomimetic
activity.
• Increased sensitivity to muscle relaxants may be seen in pts on
CCBs.

57.  Opioids
• Opioids have an important role in supplementing
anaesthesia. They have the Advantage of providing
stable haemodynamics due to
─ Lack of myocardial depressant effect.
─ Absence of histamine release (fentanyl congeners).
─ Supression of stress response to surgery.
• Opioids may be selected as the primary anaesthetic
in patients with compromised LV function.

58.  Regional anesthesia may be preferred to GA if possible,
as it tends to better block the stress response to surgery.
 Associated hypotension should be corrected by fluids &
sympathomimetic agents
 Benefits
• excellent pain control.
• decreased incidence of deep vein thrombosis.
• postoperative analgesia.
 However, the incidence of postoperative cardiac
morbidity and mortality does not appear to be
significantly different between general and regional
anesthesia.
Regional Anaesthesia

59. 
 The combination of thoracic epidural and GA can be used
for upper abdominal, thoracic and major vascular
surgery.
 Preoperative epidural analgesia may be considered to
decrease the incidence of preoperative adverse cardiac
events (IIb).
 The main advantages of epidural blockade are superior
postoperative analgesia and less diminution of vital
capacity.
 Epidural analgesia by suppressing pain improves
transmural distribution of regional myocardial blood flow
and thus minimises myocardial ischaemia.
Combined Regional-General Anaesthesia

60. • Early extubation is possible and desirable in many patients as
long as they fulfill the criteria for extubation.
• However, patients with IHD can become ischemic during
emergence from anesthesia and/or weaning with an increased
heart rate and blood pressure.
• These hemodynamic alterations must be managed diligently.
Pharmacologic therapy with a β-blocker or combined α- and β-
blockers such as labetalol can be very helpful.
• Proper pain control.
• Continuous ECG monitoring with ST-segment analysis is
important to detect any myocardial ischemic events.
• Supplemental O2 to maintain adequate oxygen saturation is
important.
• Avoid & treat shivering.
• Prevent hypoxemia, hypercarbia hypovolaemia, hypotension.
Post Operative And Long-term Management

61. 
• An important goal when selecting monitors for
patients with IHD is to select those that allow early
detection of myocardial ischemia
• Most myocardial ischemia occurs in the absence of
hemodynamic alterations
• So one should be cautious when endorsing routine
use of expensive or complex monitors to detect
myocardial ischemia
Perioperative Monitoring

62.  ECG
 Simplest and most cost-effective method for detecting
perioperative myocardial ischaemia.
 3 lead monitoring II, V4 & V5 or V3 V4&V5 is recommended
• Lead II, III, aVF- RCA
• Lead I, aVL- CxCA
• Lead V3-V5- LCA

63. 
Pulmonary Artery Catheter
 Intra operative myocardial ischaemia can manifest as an acute increase in
pulmonary artery occlusion pressure.
 Can be used to guide fluid replacement, and to evaluate the efficacy of
vasopressor , vasodilator and inotropic therapy.
 3 variables are particularly important in assessing benefit versus risk of
pulmonary artery catheter use:
─ disease severity,
─ magnitude of anticipated surgery,
─ and practice setting .
 Patients most likely to benefit from perioperative use of a pulmonary artery
catheter
• recent MI complicated by HF,
• significant CAD undergoing procedures associated with significant
hemodynamic stress, systolic or diastolic LV dysfunction, cardiomyopathy,
and/or valvular disease who are undergoing high-risk operations
 Use of pulmonary artery catheterization may be considered when underlying
medical conditions that significantly affect hemodynamics cannot be corrected
before surgery (IIa)

64. Central Venous Pressure Monitoring: CVP may correlate with
PCWP if EF = 0.5 & there is no evidence of LV dysfunction
Transesophageal echocardiography:
• Most sensitive to detect intraoperative myocardial ischemia by
detecting new onset of regional wall motion abnormality
• Emergency use of perioperative TEE in patients with hemodynamic
instability is reasonable in patients undergoing noncardiac surgery
if expertise is readily available (IIa)

65.  Perioperative myocardial ischaemia and infarction
(PMI) is a major cause of short and long term morbidity
and mortalityin the surgical population.
 The incidence of perioperative MI in patients who
undergo elective high-risk vascular surgery is between
5% and 15%.
 The risk is even higher for emergency surgery.
 The incidence of perioperative cardiac injury is a
cumulative result of preoperative medical condition, the
specific surgical procedure, expertise of the surgeon, the
diagnostic criteria used to define MI, and the overall
medical care at a particular institution.
Perioperative Myocardial Ischaemia

66. 
 Pathophysiology
Two distinct mechanisms may lead to PMI:
1.Acute coronary syndrome.
• Occurs when an unstable or vulnerable plaque undergoes
spontaneous rupture, fissuring, or erosion, leading to acute
coronary thrombosis, ischemia, and infarction.
• The sympathetic overactivity induced Tachycardia and
Hypertension, common in the perioperative period, may exert
shear stress, leading to rupture of plaques.
• Increased postoperative procoagulants (fibrinogen, factor VIII
coagulant, von Willebrand factor, α1-antitrypsin), increased
platelet reactivity, decreased endogenous anticoagulants (protein
C, antithrombin III), and decreased fibrinolysis have been
reported.

67. 
2. Myocardial O2 Supply – Demand Imbalance
• Tachycardia is the most common cause of postoperative oxygen
supply-demand imbalance. Heart rates >80 bpm in patients
with significant CAD can lead to prolonged ischemia and PMI.
• Postoperative hypotension (hypovolemia, bleeding, or systemic
vasodilatation), hypertension (elevated stress hormones,
vasoconstriction), anemia, hypoxemia, and hypercarbia
aggravate ischemia.
• Stress-induced and ischemia-induced coronary vasoconstriction
impairs coronary perfusion.

68. Intraoperative Diagnosis
Complicated by lack of symptomatic presentation in about half of
patients with perioperative MI. 75% of Intraop MIs are Silent,
present atypically, without ST changes, Q waves or chest pain.
 Signs:
• instability of HR/BP, desaturation, shock refractory to
vasopressors, poor perfusion, new murmur, skin discolored,
pulmonary edema
 ECG:
• LBBB, arrhythmias, ST changes, T wave inversion, QRS & T
wave axis deviations, and R/U wave changes
• ST depression will be 1mm or less in anaesthetized patients.
 Biochemistry:
• Elevated lactate, CK & Troponin levels.

69.  Prevention
 Avoid tachycardia and hypertension.
• Maintenance of adequate depth of anaesthesia
• Control pain & anxiety
• Measures to attenuate pressor responses to laryngoscopy and
endotracheal intubation.
 Ensure adequate ventilation.
 Adequate pain management.
 Maintain normothermia.

70. 
 Management
 If ischemia is detected early in the intraoperative period before the
surgical incision is made, the procedure should be delayed and
patient stabilized by improving the oxygen supply and demand ratio.
 On the other hand, if surgery cannot be stopped, it should be
expedited while the patient is stabilized by improving coronary blood
flow and oxygen delivery and reducing oxygen demand.
 Discontinue volatile anaesthetic agents & start 100% O2
 Administer 325mg Aspirin via ryles’s tube
 Tachycardia : Treated with beta blockers.
 Nitroglycerine is the drug of choice for accompanying hypertension.
 Morphine is a venodilator that reduces ventricular preload and
oxygen requirements and it is also effective in patients with
pulmonary vascular congestion.

71.  Treatment of cardiac dysrrhythmias
 Hypotension
 Moderate hypotension responds to volume expansion with 300-
500ml of crystalloid
 Severe hypotension: Vasopressors
 Refractory hypotension
• PCWP <12mm Hg – Continue volume expansion
> 12 mm Hg - inotropic support with dopamine 3-5/
dobutamine is considered.
• If hypotension persists, considerepinephrine or milrinone.
 In some patients who don't respond, use of percutaneous IABP is
life saving.

72. 
 Thrombolytic/ reperfusion therapy
• Thromboplastin activator (t-PA) or streptokinase is
recommended to minimize the damage caused by
intraoperative infarct.
• Should be given within 4 hrs (maximum up to 12 hrs).
• Contraindicated in patients with fresh surgical wounds.
• Antithrombotics and antiplatelet drugs can be started to
ensure maximum myocardial salvage.
• Heparin should be started in patients in whom thrombolytic
is not given. Heparin has been shown to reduce morbidity
andmortality from thromboembolism.

73. 

74. 
Anaesthetists must be able to:
 Identify patients with pre-existing IHD or those at
risk for perioperative myocardial ischaemia.
 Apply diagnostic measures and guide medical
management of patients with IHD .
 Optimise patients with pre-existing IHD for surgery.
 Minimize physiologic alterations and stress during
surgery and extend the care upto the post –opeartive
period.
To Sum Up

75. 