This document discusses the arterial supply of the heart, control of coronary circulation, determinants of myocardial oxygen supply and demand, ischemic heart disease, risk factors and pathophysiology of IHD, and evaluation and management of cardiac patients undergoing non-cardiac surgery. Key points include: - The left coronary artery supplies the left side of the heart and the right coronary artery supplies the right side. - Coronary blood flow is regulated by metabolic demands and weakly by the autonomic nervous system. - Ischemic heart disease results from an imbalance between myocardial oxygen supply and demand. - Risk factors for IHD include age, smoking, hypertension, diabetes, and family history. - Evaluation of cardiac patients for

1. Presented by : Dr. Amit Prasad
Moderator : Dr. Panna Jain

2. Arterial supply of heart
1. Left Coronary Artery –
A) Anterior descending branch
-Right bundle branch
-Left bundle branch
-Anterior & posterior papillary muscles
-Anterolateral left ventricle
B) Circumflex branch
-Lateral left ventricle
2. Right coronary artery
-SA and AV nodes
-Right atrium and ventricle
-Posterior interventricular septum
-Posterior fascicle of left bundle branch
-Interatrial septum

4. Control of coronary circulation
 Normal coronary blood flow is 225 ml/min at rest (5% of
cardiac output)
 Autoregulation is the intrinsic capability of the heart to
maintain coronary blood flow in the presence of changes in
coronary perfusion pressures
 Autoregulation of blood flow occurs between coronary
perfusion pressure of 50 – 120 mmHg beyond which blood
flow becomes pressure dependent because of maximal
vasoconstriction or vasodilation

5.  Coronary arterial tone is controlled
Strongly by metabolic demands (O2,CO2, adenosine,
nitric oxide, endothelin, prostaglandins)
Weakly by autonomic nervous system
Direct effects - Ach causes vasodilation in normal
vessels.
Indirect effects - Sympathetic & parasympathetic
mediated

6. A. SYMPATHETIC STIMULATION 
α1 mediated vasoconstriction
β1 mediated vasodilation (resulting from ↑ in HR &
contractility)
B. PARASYMPATHETIC STIMULATION
Release of Ach from vagus  ↓ in HR & contractility  ↓
in myocardial O2 consumption  ↓ in blood flow locally by
coronary vasoconstriction

7. Myocardial O2 supply determinants-
-HR (diastolic time)
-Coronary perfusion pressure
(aortic diastolic blood pressure)
-Arterial O2 content (Pa O2, Hb)
-Coronary vessel diameter
Myocardial O2 demand determinants-
-Basal requirement
-HR
-Wall tension (preload , afterload)
-Contractility

8. Ischaemic Heart Disease
 Ischemic heart disease (IHD) is the generic designation
for a group of closely related syndromes resulting from
myocardial ischaemia – an imbalance between the supply
(perfusion) and demand of the heart for oxygenated blood.
 Ischaemia comprises not only insufficiency of oxygen ,
but also reduced availability of nutrient subtrates and
inadequate removal of metabolites

9.  Supply
 Atheroma, thrombosis, spasm, embolus
 Demand
 Exercise,Anaemia, hypertension, high cardiac output
(thyrotoxicosis, myocardial hypertrophy)

10. Manifestations of IHD
 Angina pectoris
 Acute myocardial infarction
 Sudden death
 Pts. with IHD can present with :
- Chronic stable angina
- Acute coronary syndrome

12. Risk factors for development of IHD
 Male gender
 Increasing age
 Hypertension
 Hypercholesterolemia
 Cigarette smoking
 Diabetes mellitus
 Obesity
 Sedentary lifestyle
 Genetic factors / family history

13. Pathophysiology of IHD
 In more than 90% of cases , the cause of myocardial
ischaemia is reduction in coronary blood flow due to
atherosclerotic coronary arterial obstruction.
 Disruption of atherosclerotic plaques with large areas of
foam cells and extracellular lipid , thin fibrous caps , few
smooth muscle cells ( vulnerable plaques ) – intraplaque
haemorrhage , erosion or ulceration , or rupture or fissuring.
 Exposed to subendothelial collagen and necrotic plaque
contents, platelets undergo adhesion, aggregation ,
activation and release of potent aggregators like
thomboxane A2, serotonin and platelet factors 3 and 4.

14.  Vasospasm occurs
 Activation of coagulation – adding to bulk of thrombus
 Thrombus evolves to completely occlude the lumen of the
coronary vessel.
 A fixed obstructive lesion of 75% of more generally
causes sympyomatic ischaemia induced by exercise.
 A 90 % stenosis can lead to inadequate coronary blood
flow even at rest.

15. Management of Ischemic Heart Disease:
A. Lifestyle modification –
- maintenance of an ideal body weight
- low fat, low cholesterol diet
- regular exercise
- cessation of smoking

16.  B. Medical treatment –
1. Beta Blockers
Act either selectively or non-selectively on Beta receptors:
 Beta 1 cardiac muscle  increase rate and contraction
 Beta 2 dilates bronchial smooth muscle
2. Ca++ Channel Blockers
Acts on vasculature blocking Ca++ and causing vasodilation
3. Nitrates
Vasculature vasodilation
4. Anti-Hypercholesterolemic drugs (statins)
HMG CoA Reductase Inhibitors  reduction in cholesterol thus
helping to reduce atheroma formation

17. 5. Antiplatelet drugs:
- Clopidogrel
- Aspirin
6. Angiotensin – Converting Enzyme inhibitors -
angiotensin II promotes inflammatory responses and
atheroma formation.
C. Revascularization –
- Percutaneous coronary intervention
- Coronary artery bypass grafting

18. Evaluation of cardiac patient undergoing non
cardiac surgery
The goals of preoperative evaluation -
• 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

19.  In patients with known CAD, as well as those with
previously occult coronary disease, the questions become
1) What is the amount of myocardium in jeopardy?
2) What is the ischemic threshold, ie, the amount of stress
required to produce ischemia?
3) What is the patient’s ventricular function? and
4) Is the patient on his or her optimal medical regimen?
Clarification of these questions is an important goal of the
preoperative history and physical examination .

20.  Preoperative cardiac evaluation must be carefully tailored to
the circumstances that have prompted the evaluation and to
the nature of the surgical illness.
 Given an acute surgical emergency, preoperative evaluation
might have to be limited to simple and critical tests.
 Only the most essential tests and interventions are
appropriate until the acute surgical emergency is resolved.
 A more thorough evaluation can be conducted after surgery.
 Under less urgent circumstances, the preoperative cardiac
evaluation may lead to a variety of responses, including
cancellation of an elective procedure.

21.  Preoperative tests for additional diagnostic cardiac
evaluation are recommended only if the information
obtained will result in
- a change in the surgical procedure performed,
- a change in medical therapy or monitoring during or
after surgery, or
- a postponement of surgery until the cardiac condition
can be corrected or stabilized.

22. History :
 A history is crucial to the discovery of cardiac and/or comorbid
diseases that would place the patient in a high surgical risk
category.
 The history should seek to identify serious cardiac conditions
such as unstable coronary syndromes, prior angina, recent or
past MI, decompensated HF, significant arrhythmias, and
severe valvular disease.
 Many patients without cardiac symptoms may have severe
double- or triple-vessel disease that is not clinically obvious
because the patients may present atypically or are functionally
limited by severe arthritis or peripheral vascular disease.
 Whether the patient has a prior history of a pacemaker or
implantable cardioverter defibrillator (ICD) or a history of
orthostatic intolerance.

23.  Modifiable risk factors for coronary heart disease (CHD)
should be recorded, along with evidence of associated
diseases, such as -
- peripheral vascular disease, cerebrovascular disease,
diabetes mellitus, renal impairment, and chronic
pulmonary disease.
 In patients with established cardiac disease, any recent
change in symptoms must be ascertained.
 Accurate recording of current medications used.
 Use of alcohol, tobacco should be documented.

24. The history should also seek to determine the patient’s
functional capacity
1 MET
Can you
Take care of yourself?
Eat, dress, or use the toilet?
Walk indoors around the house?
Walk a block or 2 on level ground at 2 to 3 mph (3.2 to 4.8 kph)?
4 METs
Do light work around the house like dusting or washing dishes?
Climb a flight of stairs or walk up a hill?
Walk on level ground at 4 mph (6.4 kph)
Run a short distance?
Do heavy work around the house like scrubbing floors or lifting or
moving heavy furniture?
Participate in moderate recreational activities like golf, bowling,
dancing, doubles tennis, or throwing a baseball or football?
> 10 METs
Participate in strenuous sports like swimming, singles tennis,
football, basketball, or skiing?

25.  1 MET = consumption of 3.5 mL O2/min/kg of body
weight
10 MET – excellent
7-10 MET – good
4-7 MET – moderate
< 4 MET – poor

26.  Prior cardiac evaluation (noninvasive test,
angiography)
 CABG , balloon angioplasty or stenting (BMS or
DES)
 Angina pectoris
NYHA classification
Grade I – angina with strenuous exercise only
Grade II – angina with ordinary physical activity
Grade III – angina with minimal activity
Grade IV – angina at rest
Risk is moderate to severe in grade III &IV

27. Physical examination
 A cardiovascular examination should include an assessment
of vital signs –
- Blood pressure in both arms,
- Carotid pulse contour and bruits,
- Jugular venous pressure and pulsations,
- Auscultation of the lungs,
- Precordial palpation and auscultation,
- Abdominal palpation, and
- examination of the extremities for edema and vascular
integrity.
- The presence of associated vascular disease should heighten
suspicion of occult CAD.

28. Multivariable Indices to Predict Preoperative
Cardiac Morbidity - Revised cardiac risk index
 The basic clinical evaluation obtained by history,
physical examination, and review of the ECG
usually provides the consultant with sufficient data
to estimate cardiac risk.
 - Six independent risk correlates were identified
1) Ischaemic heart disease-defined as
-history of MI
-history of positive treadmill test
-use of nitroglycerin
-current complaints of chest pain thought to be
secondary to coronary ischemia
-ECG with abnormal Q waves

29. 2) Cerebral vascular disease –defined as
-history of TIA or stroke
3) Congestive heart failure-defined as
-history of HF
-pulmonary edema
-paroxysmal nocturnal dyspnea
-peripheral edema
-bilateral rales
-S3
-X-ray with pulmonary vascular redistribution
4) High risk surgery-abdominal aortic aneurysm or other
vascular, thoracic, abdominal, or
orthopaedic
surgery
5) Preoperative insulin treatment for DM
6) Preoperative creatinine greater than 2 mg /dL.

30. Clinical assessment according to ACC / AHA
guidelines 2007
 A group of active cardiac conditions that when present
indicate major clinical risk. The presence of 1 or more of
these conditions mandates intensive management and may
result in delay or cancellation of surgery unless the surgery is
emergent
 These include
● Unstable coronary syndromes,
- unstable or severe angina,
- recent MI,
● Decompensated HF,
● Significant arrhythmias, and
● Severe valvular disease.

31. Clinical risk factors include
 ● history of ischemic heart disease,
 ● history of compensated or prior HF,
 ● history of cerebrovascular disease,
 ● diabetes mellitus, and
 ● renal insufficiency

32.  A history of MI or abnormal Q waves by ECG is listed as a
clinical risk factor, whereas an acute MI (defined as at least
1 documented MI 7 days or less before the examination) or
recent MI (more than 7 days but less than or equal to 1 month
before the examination) with evidence of important ischemic
risk by clinical symptoms or noninvasive study is an active
cardiac condition.
 If a recent stress test does not indicate residual myocardium at
risk, the likelihood of reinfarction after noncardiac surgery is
low.
 Although there are no adequate clinical trials on which to base
firm recommendations, it appears reasonable to wait 4 to 6
weeks after MI to perform elective surgery.

33.  Minor predictors are recognized markers for cardiovascular
disease that have not been proven to increase perioperative
risk independently, for example, -
- Advanced age (greater than 70 years),
- Abnormal ECG (LV hypertrophy,left bundle-branch block,
ST-T abnormalities),
- Rhythm other than sinus, and
- Uncontrolled systemic hypertension.
 The presence of multiple minor predictors might lead to a
higher suspicion of CAD but is not incorporated into the
recommendations for treatment.

34. Cardiac Risk stratification for Noncardiac
surgeries (ACC / AHA 2007)
Vascular surgery (cardiac risk >5%)
 Aortic & other major vascular surgeries
 Peripheral vascular surgery
Intermediate risk procedure (cardiac risk 1-5%)
 Intraperitoneal & intrathoracic surgery
 Carotid endarterectomy
 Head & neck surgery
 Orthopaedic surgery
 Prostate surgery
Low risk procedure (cardiac risk <1%)
 Endoscopic procedure
 Superficial procedure
 Breast surgery
 Cataract surgery
 Ambulatory surgery

35. Cardiac evaluation and care algorithm
for noncardiac surgery based on active
clinical conditions, known
cardiovascular disease, or cardiac risk
factors for patients 50 years of age or
greater.

36. Step 1
Step 2
Step 3
Need for
emergency
non cardiac
surgery
O.R.
Perioperative
surveillance &
postoperative
risk stratification
& risk factor
management
Active
cardiac
condition
Evaluate &
treat as per
ACC/AHA
guidelines
Consider
O.R.
Low risk
surgery
Proceed
with
planned
surgery
Yes
No
No
Yes
Yes

37. No
Functional Capacity ≥ 4 MET
Without symptoms
Step 4 Yes Proceed with planned
surgery
Step 5
No or
unknown
≥ 3 clinical risk factors 1 or 2 clinical risk factors No clinical risk factors
Vascular
surgery
Intermediate
Risk
surgery
Vascular
surgery
Intermediate
Risk
surgery
Proceed with
planned
surgery
Proceed with planned surgery with HR control
or consider noninvasive testing if
it will change management
Consider testing if it will
change management

38. ACC / AHA guidelines 2007
 The recommendations for various interventions are
graded from class I to III
 Class I “is recommended”
 Class IIa “is probably recommended”
 Class IIb “might be considered”
 Class III “is not recommended”

39.  Level of evidence is graded A to C
 Level A evidence – multiple (3- 5) population risk strata
evaluated (gender, age, H/O DM, H/O previous MI, H/O heart
failure & previous aspirin use)
 Level B evidence – limited (2-3) population risk strata
evaluated
 Level C evidence – very limited (1-2) population risk strata
evaluated
Level B & C does not imply that the recommendation is weak

40. Recommendations for Preoperative Resting 12-
Lead ECG
Class I – At least 1 clinical risk factor; for vascular
surgery (Level of Evidence: B)
- Known CAD, peripheral arterial disease or
cerebrovascular disease; for intermediate
risk surgery (Level of Evidence: C)
Class IIa – No clinical risk factors ;for vascular surgery
(Level of Evidence: B)
Class IIb – At least 1 clinical risk factors; for
intermediate risk surgery (Level of Evidence :B)
Class III – Asymptomatic patients; for low risk surgery
(Level of Evidence: B)

41. Resting echocardiography – for evaluation of LV
function
Class IIa - Patients with dyspnoea of unknown origin
(Level of Evidence: C)
- Patients with current or prior HF with worsening
dyspnoea or other change in clinical status to undergo preoperative
evaluation of LV function if not performed within 12months. (Level
of Evidence: C)
Class IIb - Reassessment of LV function in clinically
stable patients with previously documented
cardiomyopathy is not well established. (Level of Evidence: C)
Class III - Routine perioperative evaluation of LV
function in patients is not recommended. (Level of Evidence: B)

42. Noninvasive stress testing (exercise stress test, dobutamine
stress echocardiography, dipyridamole thallium
scintigraphy)
 Class I - Active cardiac conditions in whom noncardiac
surgery is planned (Level of Evidence: B)
Class IIa – 3 or more clinical risk factors and poor functional
capacity (less than 4 METs) who require vascular
surgery if it will change management (Level of Evidence:B)
Class IIb - At least 1 to 2 clinical risk factors and poor functional
capacity (less than 4 METs) who require intermediate-
risk or vascular surgery. (Level of Evidence: B)
Class III – No clinical risk factors undergoing intermediate- risk
noncardiac surgery. (Level of Evidence: C)
- Patients undergoing low-risk noncardiac
surgery. (Level of Evidence: C)

43. Preoperative coronary revascularisation (CABG or PCI)
Class I - Stable angina who have significant left main
coronary artery stenosis.
- Stable angina who have 3-vessel disease.
(Survival benefit is greater when LVEF is less than 0.50.)
- Stable angina who have 2-vessel disease with
significant proximal LAD stenosis and either EF less than
0.50 or demonstrable ischemia on noninvasive testing.
- High-risk unstable angina or non–ST-segment
elevation MI.
- Acute STelevation MI.

44. Class IIa - In patients in whom coronary
revascularization with PCI is appropriate for
mitigation of cardiac symptoms and who need elective
noncardiac surgery in the subsequent 12 months, a
strategy of balloon angioplasty or bare-metal stent
placement followed by 4 to 6 weeks of dual-
antiplatelet therapy is probably indicated.
- In patients who have received drug-eluting coronary
stents and who must undergo urgent surgical
procedures that mandate the discontinuation of
thienopyridine therapy, it is reasonable to continue
aspirin if at all possible and restart the thienopyridine
as soon as possible.

45. Class IIb - The usefulness of preoperative coronary
revascularization is not well established in
high-risk ischemic patients (e.g.abnormal dobutamine
stress echocardiograph with at least 5 segments of
wall-motion abnormalities).
- The usefulness of preoperative coronary
revascularization is not well established for low risk
ischemic patients with an abnormal dobutamine stress
echocardiograph (segments 1-4).

46. Class III - It is not recommended that routine prophylactic
coronary revascularization be performed in
patients with stable CAD before noncardiac surgery.
- Elective noncardiac surgery is not recommended
within 4 to 6 weeks of bare-metal coronary stent
implantation or within 12 months of drug-eluting coronary
stent implantation in patients in whom thienopyridine
therapy, or aspirin and thienopyridine therapy, will need to
be discontinued perioperatively.
-Elective noncardiac surgery is not recommended
within 4 weeks of coronary revascularization with balloon
angioplasty.

47. Perioperative Management of Patients With Prior
PCI Undergoing Noncardiac Surgery
 Assessment of the patient’s surgical and haemorrhagic risk
 What is the precise nature of the planned operation and
anaesthetic, and the possible complications?
 How high is the perceived haemorrhagic risk?
 Are there any other individual haemorrhagic risk factors?
 What are the consequences of excessive bleeding?
 How necessary is the surgery?
 What is the urgency of the surgery—can the surgery be
delayed?
 Are there any possible alternatives to surgical treatment?

48.  Assessment of the patient’s thrombotic risk
 When was the stent inserted?
 What type of stent does the patient have?
 How many stents were inserted and where are they located?
 Was the revascularization complete?
 Is there a history of stent thrombosis previously?
 What antiplatelet regimen is being followed and what duration of
therapy has been recommended?
 Does the patient suffer from other associated risk factors for stent
thrombosis including:
- Diabetes?
- Renal impairment?
- Low cardiac ejection fraction?
 Are there any other individual thrombotic risk factors?

49.  Duration of antiplatelet therapy and recommended
delays for non-cardiac surgery after PCI –
 Dilatation without stenting: 2–4 weeks
- Surgery postponed for 2–4 weeks (vital surgery only)
 PCI and BMS: 4–6 weeks
- Vital surgery postponed for 6 weeks
- Elective surgery postponed for 3 months
 PCI and DES: 12 months
- Elective surgery postponed for 12 months
 Aspirin: lifelong therapy, whichever is the
revascularization technique

50. Approach to the management of patients with previous
PCI who require non cardiac surgery
After CABG, non-cardiac surgery should be delayed by at
least 30 days. Previous PCI
Balloon angioplasty BMS DES
Time
since
PCI
<14 days > 14 days
>
30-45 days
<
30-45 days
< 365 days > 365 days
Delay for
elective or
nonurgent surgery
Proceed to the OT
with aspirin
Delay for elective or
nonurgent surgery
Proceed to the
OT with
aspirin

51. Algorithm for preoperative management of
patients receiving antiplatelet therapy

52. Proposed scheme for management of patients taking
antiplatelet therapy and requiring surgery.
 Cerebro- and cardiovascular risk
 Low -
>6 months after MI, PCI,BMS, CABG, stroke >12 months
if complications
 Intermediate –
6–24 weeks after MI, PCI+BMS,CABG, or stroke;
>12 months after DES; high-risk stents (long,
proximal, multiple,overlapping, small vessels,
bifurcation); low EF, diabetes

53.  High –
< 6 weeks after MI, PCI, BMS,CABG; ,
<6 months after same if complications;
<12 months after high-risk DES;
<2 weeks after stroke
Surgical haemorrhagic risk
 . Low risk
- Transfusion normally not required; peripheral,
plastic, and general surgery, biopsies; minor
orthopaedic, ENT, and general surgery; endoscopy;
eye anterior chamber; dental extraction and surgery

54.  Intermediate risk -
 Transfusions frequently required;
- visceral surgery; cardiovascular surgery; major
orthopaedic, ENT, reconstructive surgery; endoscopic
urology
 High risk
- Possible bleeding in a closed space;
intracranial neurosurgery; spinal canal surgery; eye
posterior chamber surgery

55. Surgical
haemorrhagic risk
Cerebro- and
cardiovascular risk
Low Intermediate High
Low risk Elective surgery: OK;
maintain aspirin
Elective surgery: OK;
maintain aspirin,
clopidogrel (if
prescribed)
Elective surgery:
postpone; vital or
emergency surgery:
OK; maintain
aspirin and
clopidogrel
Intermediate risk Elective surgery: OK;
maintain aspirin
Elective surgery:
postpone; surgery
absolutely required:
OK; maintain
aspirin, clopidogrel
(if prescribed)
Elective surgery:
postpone; vital or
emergency surgery:
OK; maintain
aspirin and
clopidogrel
High risk Elective surgery: OK;
maintain statin;
withdraw
aspirin (maximum 7
days)
Elective surgery:
postpone; surgery
absolutely required:
OK; maintain
aspirin, or replace
aspirin by
ibuprofen; stop
clopidogrel
OK only for vital or
emergency
surgery; maintain
aspirin Bridge
with
tirofiban/eptifibatide
and
heparin

56.  Possible substitutes
 An anti-thrombin agent such as a heparin does not mimic
the effect of antiplatelet agents such as clopidogrel
oraspirin.
 There are no data to support that maintenance of aspirin
and replacement of clopidogrel by heparin is an efficient
protection in high-risk coronary situations.
 Nevertheless, heparin is routinely prescribed as a
substitute because it has been proven efficient in the
treatmentof unstable angina and non-ST-elevation MI.
 Non-steroidal anti-inflammatory drugs (NSAIDs) as does
ibuprofen or indobufen inhibit COX-1 such as aspirin, but
their blocking action on platelet activity is reversible.

57.  As platelet function is completely recovered within 24 h
after NSAID withdrawal, these drugs can be used to
maintain an efficient antiplatelet activity during the week
between aspirin cessation and surgery.
 This might be useful in situations such as intracranial
surgery.
 Replacing a long-acting antiplatelet agent such as
clopidogrel by a shorter-acting GP-IIb/IIIa inhibitor such
as tirofiban or eptifibatid has been suggested empirically
as a bridge across the period between clopidogrel
discontinuation and re-initiation.

58. The problem of regional and neuraxial blockade
 Clopidogrel with aspirin during the week preceding an
operation is an accepted contra-indication to any form of
regional anaesthesia
 The guidelines produced in 2003 by ASRA suggest that
without prior platelet transfusion, clopidogrel should be
stopped for a minimum of 7 days and ticlopidine for a
minimum of 14 days.
 Aspirin and NSAIDs do not represent an added risk for the
development of spinal haematoma in patients receiving
epidural or spinal anaesthesia.

59.  The protective effect of antiplatelet agents is more
efficacious than the effects of RA on arterial thrombosis
and on the reduction of MI and cardiac death rates.
 Moreover, the intraoperative sympatholysis of epidural
anaesthesia can be achieved with agents such as b-
blockers, a2-agonists, and higher dosages of opioids given
i.v.
 Risk/benefit ratio of preoperative withdrawal of
antiplatelet drugs in order to perform a regional or
neuraxial blockade is not justified.
 Similar caution is required for the placement and removal
of central venous lines, particularly using the subclavian
route, in patients on dual antiplatelet therapy.

60. Proposed treatment for patients requiring percutaneous
coronary intervention (PCI) who need subsequent
surgery.

61.  If the non-cardiac operation must be performed within 24–48
hrs., the patient should be put on maximal medical therapy (β-
blocker, aspirin, and clopidogrel).
 It is useless to perform a coronary angiogram, because the
results will not modify the therapeutic choice.
 If necessary, transthoracic echocardiography will determine
the ventricular function and rule out associated valvular
disease.

62. Restarting antiplatelets after operation
 After the operation, antiplatelet agents should be resumed
within the first 12–24 hrs.
 Thienopyridines should be restarted as soon as is practicable
and safe after surgery. The precise timing should be discussed
between the surgeon, anaesthetist, and cardiologist.
 Following initiation of therapy, clopidogrel reaches its
maximum platelet aggregation inhibition after 3–5 days, with
the bleeding time reaching a maximum of 1.5–3 fold of
baseline at 3–7 days.
 Restarting clopidogrel with a loading dose is routine in
interventional cardiology, and the licensed loading dose after
PCI is 300 mg, but cardiologists are increasingly using a
loading dose of 600 mg with the aim of shortening the time to
maximal platelet inhibition.

63. Perioperative Medical Therapy
 Perioperative Beta-Blocker Therapy –
 Recommendations for Beta-Blocker Medical Therapy
 CLASS I
 1. Beta blockers should be continued in patients
undergoing surgery who are receiving beta blockers to
treat angina, symptomatic arrhythmias, hypertension,
(Level of Evidence: C)
 2. Beta blockers should be given to patients undergoing
vascular surgery who are at high cardiac risk owing to the
finding of ischemia on preoperative testing. (Level of
Evidence: B)

64.  CLASS IIa
 1. Beta blockers are probably recommended for patients
undergoing vascular surgery in whom preoperative
assessment identifies CHD. (Level of Evidence: B)
 2. Beta blockers are probably recommended for patients in
whom preoperative assessment for vascular surgery
identifies high cardiac risk, as defined by the presence of
more than 1 clinical risk factor. (Level of Evidence: B)
 3. Beta blockers are probably recommended for patients in
whom preoperative assessment identifies CHD or high
cardiac risk, as defined by the presence of more than 1
clinical risk factor, who are undergoing intermediate-risk
or vascular surgery. (Level of Evidence: B)

65.  CLASS IIb
 1. The usefulness of beta blockers is uncertain for patients
who are undergoing either intermediate-risk procedures or
vascular surgery, in whom preoperative assessment
identifies a single clinical risk factor. (Level of Evidence:
C)
 2. The usefulness of beta blockers is uncertain in patients
undergoing vascular surgery with no clinical risk factors
who are not currently taking beta blockers. (Level of
Evidence: B)
 CLASS III
 1. Beta blockers should not be given to patients
undergoing surgery who have absolute contraindications
to beta blockade. (Level of Evidence: C)
 Effective heart rate control with beta blockers should be
targeted at less than 65 bpm.

66.  Recommendations for Statin Therapy
 CLASS I
 1. For patients currently taking statins and scheduled for
noncardiac surgery, statins should be continued. (Level of
Evidence: B)
 CLASS IIa
 1. For patients undergoing vascular surgery with or
without clinical risk factors, statin use is reasonable.
(Level of Evidence: B)
 CLASS IIb
 1. For patients with at least 1 clinical risk factor who are
undergoing intermediate-risk procedures, statins may be
considered. (Level of Evidence: C)

67.  Alpha-2 Agonists
 CLASS IIb
 1. Alpha-2 agonists for perioperative control of
hypertension may be considered for patients with known
CAD or at least 1 clinical risk factor who are undergoing
surgery. (Level of Evidence: B)
 CLASS III
 1. Alpha-2 agonists should not be given to patients
undergoing surgery who have contraindications to this
medication. (Level of Evidence: C)
 Perioperative Calcium Channel Blockers
- a large-scale trial was needed to define the value of these
agents.

68. Anesthetic Considerations and Intraoperative
Management
 Choice of Anesthetic Technique and Agent –
 Recommendations for Use of Volatile Anesthetic
Agents
 CLASS IIa
 1. It can be beneficial to use volatile anesthetic agents
during noncardiac surgery for the maintenance of general
anesthesia in hemodynamically stable patients at risk for
myocardial ischemia. (Level of Evidence: B)

69.  Randomized clinical trials in patients undergoing CABG
surgery indicate that volatile anesthetics decrease troponin
release and enhance LV function compared with propofol,
midazolam, or balanced anesthesia techniques with
opioids.
 These data can likely be generalized to patients with CAD
who are undergoing noncardiac surgery.

70.  Neuraxial anesthetic techniques , spinal and epidural
approaches can result in sympathetic blockade, resulting
in decreases in both preload and afterload.
 The decision to use neuraxial anesthesia for the high-risk
cardiac patient may be influenced by the dermatomal level
of the surgical procedure.
 High dermatomal levels of anesthesia may be required and
may be associated with significant hemodynamic effects.

71. “Monitored anesthesia care” includes the use
of local anesthesia supplemented with intravenous
sedation/analgesia.
 Although this technique can eliminate some of the
undesirable effects of general or neuraxial anesthesia, it
provides poor blockade of the stress response unless the
local anesthetic provides profound anesthesia of the
affected area.
 If the local anesthetic block is less than monitored
anesthesia care could result in an increased incidence of
myocardial ischemia and cardiac dysfunction compared
with general or regional anesthesia.
 To achieve the desired effect, excess sedation can occur.
Therefore, there may be no significant difference in
overall safety with monitored anesthesia care, and general
or regional anesthesia may be preferable.

72.  Perioperative Pain Management –
 From the cardiac perspective, pain management may be a
crucial aspect of perioperative care.
 An effective analgesic regimen must be included in the
perioperative plan.
 Prophylactic Intraoperative Nitroglycerin
 CLASS IIb
 1. The usefulness of intraoperative nitroglycerin as a
prophylactic agent to prevent myocardial ischemia and cardiac
morbidity is unclear for high-risk patients undergoing
noncardiac surgery, particularly those who have required nitrate
therapy to control angina.
 The recommendation for prophylactic use of nitroglycerin must
take into account the anesthetic plan and patient hemodynamics
and must recognize that vasodilation and hypovolemia can
readily occur during anesthesia and surgery. (Level of
Evidence: C)

73.  Use of TEE
 CLASS IIa
 1. The emergency use of intraoperative or perioperative
TEE is reasonable to determine the cause of an acute,
persistent, and life-threatening hemodynamic abnormality.
(Level of Evidence: C)
 Currently, there is insufficient evidence to determine the
cost-effectiveness of TEE for its use as a diagnostic
monitor or to guide therapy during noncardiac surgery;
therefore, the routine use of TEE in noncardiac surgery
does not appear warranted.

74.  Maintenance of Body Temperature
 Recommendations for Maintenance of Body
Temperature
 CLASS I
 1. Maintenance of body temperature in a normothermic
range is recommended for most procedures other than
during periods in which mild hypothermia is intended to
provide organ protection (eg, during high aortic cross-
clamping). (Level of Evidence: B)
 Perioperative morbid cardiac events (unstable
angina/ischemia, ventricular tachycardia, cardiac arrest,
and MI) occurred less frequently in the normothermic
group than in the hypothermic group.

75.  Intra-Aortic Balloon Counterpulsation Device –
 There is currently insufficient evidence to determine
the benefits versus risks of prophylactic placement of
an intra-aortic balloon counterpulsation device for
high-risk noncardiac surgery.

76. Perioperative Surveillance
 Recommendations for Perioperative Use of PACs
 CLASS IIb
 1. Use of a PAC may be reasonable in patients at risk for
major hemodynamic disturbances that are easily detected
by a PAC. However, the decision must be based on 3
parameters: patient disease, surgical procedure (ie,
intraoperative and postoperative fluid shifts), and practice
setting (experience in PAC use and interpretation of
results), because incorrect interpretation of the data from a
PAC may cause harm. (Level of Evidence: B)
 CLASS III
 1. Routine use of a PAC perioperatively, especially in
patients at low risk of developing hemodynamic
disturbances, is not recommended. (Level of Evidence: A)

77. Intraoperative and Postoperative Use of ST-
Segment Monitoring
 CLASS IIa
 1. Intraoperative and postoperative ST-segment
monitoring can be useful to monitor patients with known
CAD or those undergoing vascular surgery, with
computerized ST-segment analysis, when available, used
to detect myocardial ischemia during the perioperative
period. (Level of Evidence: B)
 CLASS IIb
 1. Intraoperative and postoperative ST-segment
monitoring may be considered in patients with single or
multiple risk factors for CAD who are undergoing
noncardiac surgery. (Level of Evidence: B)

78. Surveillance for Perioperative MI
 CLASS I
 1. Postoperative troponin measurement is recommended in
patients with ECG changes or chest pain typical of acute
coronary syndrome. (Level of Evidence: C)
 CLASS IIb
 1. The use of postoperative troponin measurement is not
well established in patients who are clinically stable and
have undergone vascular and intermediate-risk surgery.
(Level of Evidence: C)
 CLASS III
 1. Postoperative troponin measurement is not
recommended in asymptomatic stable patients who have
undergone low-risk surgery.(Level of Evidence: C)

79. Preoperative preparation
 Nil per orally
 Written informed consent
 Anxiety reduction by both psychological &
pharmacological means
 Explaining the anaesthetic sequence in detail
 The goal of drug administration is to produce sedation and
amnesia without undesirable degrees of circulatory &
ventilatory depression.
 Options –
BZD + opioid (morphine) 1 hr prior to OT

80.  H2 blockers do not seem to produce adverse effects , although
there is theoretical risk of H1 mediated coronary artery
vasoconstriction
 All antianginal, antihypertensive or antiarrhythmic medications
should be continued upto and including the day of the surgery

81. Anaesthetic goals
 Stable haemodynamics
 Prevent MI by optimizing myocardial O2 supply &
reducing O2 demand
 Monitor for ischaemia
 Treat ischaemia or infarction if it develops
 Normothermia
 Avoidance of significant anaemia
 Maintain HR & systemic BP within 20% of the normal
awake value.

82. Monitoring
 ECG –
V4 – 61% sensitive
V5 – 75% sensitive
II, V5 – 80% sensitive
V4, V5 – 90% sensitive
II, V4,V5 – 98% sensitive

83.  Pulse oximetry
 Noninvasive blood pressure
 Urine output
 Temperature
 Capnography
 CVP & intra-arterial BP – where large fluid shifts are
anticipated
 Pulmonary artery catheter (Class IIb) in patients EF <
0.4, pulmonary HTN, combined coronary stenosis &
valvular disease & complex cardiac lesion

84.  TEE (not routinely) Class IIa
Demonstrates - New regional wall motion abnormality
- Decreased systolic wall thickening
- Ventricular dilation as a result of
ischaemic events.
Transgastric cross sectional view of LV is imaged
Limitations – high cost & inability to detect preintubation
events & events in other areas of myocardium

85. General anaesthesia
 Preoxygenation
 Attenuation of sympathetic response to laryngoscopy &
intubation
 I/V fentanyl 1- 3µg/kg slowly or morphine 0.1-0.2mg/kg
 I/V lidocaine 1.5 mg/kg 90 seconds before D/L
or
 I/V nitroprusside 1-2 µg/kg 15 seconds before D/L
or
 I/V esmolol 100-300 µg/kg/min before & during D/L

86.  Induction
 I/V thiopentone or propofol or etomidate in titrated doses
 Muscle relaxation
 I/V vecuronium or rocuronium or cisatracurium (newer agents
like pipecuronium, mivacurium, doxacurium ) Atracurium
avoided

87. Maintenance
 Normal LV function
 Controlled myocardial depression using volatile anaesthetic
(isoflurane, desflurane, sevoflurane) (Class IIa)
 With or without nitrous oxide
 Opioids
Impaired LV function
 High dose opioid (fentanyl 50-100 µg/kg I/V) as a sole
anaesthetic intermittently
 Nitrous oxide, benzodiazepines or low dose volatile
anaesthetic can be added if total amnesia cannot be assured
with opioid alone.

88.  Obtundation of extubation response
 To prevent tachycardia & hypertension associated with
extubation & emergence, patient is given low dose of
lignocaine or esmolol 2 minutes before extubation
 Reversal
 Neostigmine + glycopyrrolate

89. Regional anaesthesia
 Patient should be nicely premedicated without any
apprehension
 Spinal / graded epidural / combined spinal epidural
 High dose of LA may cause myocardial toxicity & depression
 A drop in blood pressure by 20% of the preblock value should
not be permitted to persist & should be promptly treated with
intravenous fluids & sympathomimetic drugs (phenylephrine,
ephedrine,

90. Intraoperative ischaemia
 Diagnosis by ECG
 ST segment depression
 Upsloping ST segment
 Horizontal ST segment
 Downsloping ST segment
 ST segment elevation
 T wave inversion

91. Treatment
 Sinus tachycardia –
- Beta blockade (propanolol 1 mg at a time or esmolol
100 – 500 µg/kg as intermittent bolus or
continuous infusion
 Hypertension –
- Deepening of anaesthesia
- Vasodilator (NTG 1 µg/kg/min or a bolus of 2µg/kg)
- Labetalol intermittent bolus of 5 – 10mg

92.  Hypotension-
- Vasoconstrictors (when reduced vascular tone)
- Volume infusion
- Inotropes like dopamine and dobutamine(when ↑ in
PAOP & ↓ in stroke volume)
- Intraaortic balloon pump

93. Postoperative monitoring
 In patients at high risk of stent thrombosis in the perioperative
period, who have stopped clopidogrel prematurely, the risk of
an ischaemic event may be as high as 45%.
 Consequently, these patients should be managed in a high
dependency unit (HDU) setting with continuous ECG
monitoring and regular review by cardiologists.
 The optimum duration of HDU stay is not known, as, although
stent thrombosis appears to occur in the early postoperative
period, there are reported cases of later presentation
 The perioperative hypercoagulable state lasts for several days
and it is probably appropriate to monitor these patients
intensively until antiplatelet therapy has been reinstated and the
antiplatelet action confirmed.
 The most appropriate length of stay may vary according to the
individual patient risk of complications.

94.  Oxygen supplementation
 Continuous ECG monitoring
 Pulse oximetry
 B.P. Monitoring
 Urine output
 Temperature maintenance
 Pain control - I/V PCA or PCEA
 Resuming antiplatelet therapy as soon as possible

95. Postoperative PCI
 As the greatest risk of ischaemia and infarction occurs
during the first days after surgery, the treatment of chronic
CAD (b-blocker, calcium antagonist, and antihypertensive
agent) or unstable coronary syndrome (aspirin,
clopidogrel, and heparin) must be restarted as soon as
possible after the operation.
 Routine monitoring of cardiac enzymes is useful to detect
silent ischaemia, which is frequent during the
postoperative period, and predicts long-term mortality.

96.  ST elevation on the ECG is an indication for coronary
angiogragraphy and PCI. Dilatation is mandatory, but
stenting may be a problem because of early postoperative
acute systemic inflammatory syndrome and blood
hypercoagulability.
 It is not possible to use thrombolysis or GP IIb/IIIa
inhibitors in the first 24–48 h after surgery, because of the
risk of major bleeding.
 In such a case, it may therefore be safer to avoid stenting
and proceed to a simple dilatation.

97. Conclusions
 Successful perioperative evaluation and management of
highrisk cardiac patients undergoing noncardiac surgery
requires careful teamwork and communication between
surgeon, anesthesiologist, the patient’s primary caregiver,
and the consultant.
 In general, indications for further cardiac testing and
treatments are the same as in the nonoperative setting, but
their timing is dependent on several factors, including the
urgency of noncardiac surgery, patient-specific risk factors,
and surgery-specific considerations.


98.  The use of both noninvasive and invasive preoperative
testing should be limited to those circumstances in which
the results of such tests will clearly affect patient
management.
 Future research should be directed at determining the
value of routine prophylactic medical therapy versus more
extensive diagnostic testing and interventions.

99. Thank you