This document describes the case of a 40-year-old male patient who experienced hypotension, bradycardia, and ST segment changes during a long orthopedic surgery, indicating possible acute coronary syndrome. Biomarkers after surgery confirmed myocardial injury. The patient was treated in the ICU and recovered. The document then reviews risk factors, mechanisms, diagnosis, and management of perioperative myocardial infarction.

1. DR ZIKRULLAH

2.  A 40 years old male diagnosed as a case of GCT Femur
and Supracondylar Fracture Shaft Femur was posted
for ORIF (Nailing and Grafting ).
 He was a chronic bidi smoker.
 He had no H/O H.TN, D.M or any other chronic illness.
 Preoperative blood investigations were normal.
 CXR and ECG were WNL.

3.  SAB with inj. Bupivacaine 12.5 mg(heavy) +
Fentanyl 25mcg administered , and surgery was
started.
 Monitoring consisted of H.R, pulse oxymetry ,
automatic blood pressure measurement, and
ECG.
 Hemodynamics were quiet stable initially.

4.  After around two hours of surgery, the patient
suddenly became hypotensive which was treated
with increased amount of fluids.
 The patient did not responded to this, there was
further hypotension ( SBP = 50-60 mmhg) . So,
Noradrenaline infusion was started.
 Further bradycardia (H.R = 30 bpm) occurred which
was treated with atropine.

5.  12 lead ECG was done which showed ST depression
in lead II and avF.
 O2 flow was increased and Analgesic was
given(Ketorolac).
 The patient developed temporary tachycardia.
Mean arterial pressure (MAP) was elevated to 50-
60 mm of Hg. SpO2 remained 100% throughout
surgery.

6.  Surgery was completed in next 2 hours and patient was
shifted to intensive care unit (ICU) for further
monitoring and management.
 Cardiac enzymes were sent and again a 12 lead ECG was
done.
 Trop.I = 2822.3 ng/L (N<19)
 CK-MB = 8.94ng/ml ( N= 0-5.1)
 ECG = ST depression in II , aVF .
T/T : Ecosprin 300 mg
Clopidogrel 300 mg Medicine ref.
Statin 80mg.

7.  Later ECHO was done which was found to be WNL
with No RWMA.
 Patient remained haemodynamically stable
during 1 day stay of ICU and then shifted to HDU .
 Further, Rosuvastatin 10 mg
and aspirin 75 mg continued. Cardio.ref.

8.  Acute Coronary Syndrome ( Unstable Angina,
NSTEMI, STEMI )
 Pericarditis (ST elevation in all leads)
 Pulmonary embolism (Sinus Tachycardia )

9.  The term acute coronary syndrome (ACS) refers to
any group of clinical symptoms compatible with
acute myocardial ischemia and includes unstable
angina, non-ST-segment elevation myocardial
infarction and ST-segment elevation myocardial
infarction (STEMI).

11.  Elderly
 Cigarette smoking
 Hypertension,
 Obesity
 Sedentary lifestyle
 High cholesterol
 Diabetes mellitus
 Family H/O premature coronary artery disease.
 Chronic kidney disease
 Peripheral arterial disease

12.  Hypoxia
 Hypotension / Hypertension
 Hypothermia
 Pain
 Blood loss causing anaemia
 Arrhythmogenic electrolyte disturbances
 Inflammation
 Blood sugar instability in diabetics
 Acute stress response
 Avoidance of anticoagulation.

15.  Two distinct mechanisms may lead to
PMI(periop. M.I) :
1. Acute coronary syndrome.
2. Prolonged myocardial oxygen supply
demand imbalance in the presence of stable
coronary artery disease (CAD).

16.  Acute coronary syndrome occurs when an
unstable or vulnerable plaque undergoes
spontaneous rupture, fissuring, or erosion, leading
to acute coronary thrombosis, ischemia, and
infarction.
 External stressors may contribute.

17.  The sympathetic induced Tachycardia and
Hypertension, common in the perioperative period,
may exert shear stress, leading to rupture of pIaques .
 Increased perioperative 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.

18.  The oxygen demand is increased perioperatively
due to increased heart rate, heart wall tension,
preload, afterload, and myocardial contractility.
 On the other hand, the oxygen supply is
decreased due to decreased coronary blood flow,
tachycardia, hypotension, hypocapnia,
hypoxemia, anemia, etc.

19.  Tachycardia is the most common cause of
perioperative oxygen supply-demand
imbalance.
 Heart rates >80 bpm in patients with significant
CAD can lead to prolonged ischemia and PMI.

20.  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.

22. The ACC/AHA guidelines on cardiovascular
evaluation for noncardiac surgery concluded that
three elements must be assessed to determine the
risk of cardiac events :
1. Patient specific clinical variables.
2. Exercise capacity.
3. Surgery-specific risk.

23. Acc. To the ACC/AHA guidelines, clinical
predictors of MACE [Major Adverse Cardiac
Events ] are categorized into major,
intermediate, and minor factors as follows :

26. Functional status can be expressed in metabolic
equivalents (MET). Patients with good functional status
have a lower risk of complications.
 1 MET is defined as the oxygen uptake in a sitting
position (3.5 mL O2 uptake/kg per min).
 Perioperative cardiac risk is increased in patients
unable to meet a 4-MET demand during most normal
daily activities.

27. The type and timing of surgery significantly affects
the patient's risk of perioperative cardiac
complications.
 High-risk procedures - Rate of cardiac death or
nonfatal MI is > 5%
 Intermediate-risk procedures – 1% - 5%
 Low-risk procedures - < 1%

29. In 1977 Goldman,et al., developed the first
cardiac index which included 9 variables.
In 1999 Lee et.al. modified it which is k/a RCRI.
RCRI ?

31.  Diagnosis complicated by lack of symptomatic
presentation in about half of patients with
perioperative MI.
 Deveraux et al, proposed the following diagnostic
criteria:
 Rise in troponin (or fall after an elevated value) plus
one or more of following.
 Ischemic signs or symptoms (e.g., SOB)
 New pathologic Q waves on ECG.
 New wall motion abnormality or fixed defect on
echo.

32.  Acc. To ACC, two criteria must met for diagnosis:
 (i) increase or decrease in cardiac enzymes, in
combination with at least one of the following:
(a) typical ischaemic symptoms,
(b) development of pathological Q-waves in the ECG,
(c) ECGchanges indicative of myocardial ischaemia
(ST- segment elevation or depression), and
(d) coronary artery intervention; and
 (ii) pathological findings of an acute myocardial
infarction.

33. Clinical presentation:
Patients receiving GA obviously
 will not complain of chest pain but may have
hypotension,
 arrhythmias,
 and signs of congestive heart failure.

34. ST Elevation
New ST elevation at the J-point in 2 contiguous leads with
cutt off > 0.2 mV in men or > 0.15mV in women in leads
V2-V3 and/or > 0.1mV in other leads.
ST Depression and T wave changes
New horizontal or Down sloping ST depression > 0.05 mV
in 2 contiguous leads ; and/or T-wave inversion >0.1 mv in
2 contiguous leads with prominent R-wave or R/S ratio >1

37.  Biochemical markers: Increased
concentration of CPK-MB is not useful
intraoperatively because the leakage of
these enzymes into the circulation can occur
8-24 hours after an MI.

38.  CPK-MB concentrations may rise only 10-20
times of normal during infarction and return
to normal within 72 hrs, TnT and TnI levels
may rise more than 20 times above the
reference range within 3 hrs after onset of
chest pain and may persist for up to 10-14
days. This may assist in late diagnosis of
infarction.

39. ENZYME ONSET PEAK RETURN TO
NORMAL
Myoglobin 2-6 hrs 24 hrs
CPK MB 2-4 hrs 24 hrs 72 hrs
LDH 24 hrs 4-5 days 10 days
AST Within 12 hrs 48 hrs 4-5 days
Trp I Within 4-8 hrs 7-10 days
Trp T Within 4-8 hrs 10-14 days

40.  TEE: The development of new regional wall
motion abnormalities[RWMA] is considered to be
the first detectable change in the left ventricle
during ischemia.
 TEE changes more predictive of MI than ECG
changes.
 TTE can replace TEE in patients with
contraindication to TEE or patients who are awake.

41.  The management of PMI is different as thrombolytics
cannot be given, and anticoagulant use is with
caution.
 The risk of life-threatening bleeding cancels
thrombolytics as an option, hence a more
conservative approach is recommended.
 So, the mainstay of treatment includes good pain
control, β-blockers, statins, antiplatelets,
nitroglycerine, and unfractionated heparin.

42. As soon as PMI is diagnosed, MONA THERAPY should
be initiated.
 M = Morphine (2-4 mg i.v every 5-15 min.)
 O = Oxygen (SpO2 > 94% )
 N = Nitroglycerin , if SBP>100 ( 0.3 - 0.4 mg S/L
or 1-2 sprays every 5 min for upto 3 doses )
 A = Aspirin (160-325 mg is administered orally or
through ryle’s tube) and is continued
thereafter.[risk-benefit ratio for surgical pts]

45. 1) Ischaemic : Angina, re-infarction, infarct extension.
2) Mechanical : Heart failure, cardiogenic shock, mitral
valve dysfunction, aneurysms, cardiac muscles rupture
3) Arrythmic : Atrial or ventricular arrythmias, SA or AV
node dysfunction.
4) Thrombosis or embolic : Central or peripheral
embolisation.
5) Inflammatory : Pericarditis.
6) Psychosocial : Depression

46. THANKYOU….