Ischaemic heart disease & its anaesthetic implications

Ischaemic Heart disease &
its Anaesthetic Management.
Dr. Swadheen kumar Rout
1st
year P.G
Dept. of Anaesthesiology
M.K.C.G College & hospital

Overview:-
• Leading cause of death & health care expenditure.
• 5% of patients over 35 years of age have asymptomatic
ischaemic heart disease.
• May be present in up to 30% of older pts ( >65 yrs)
undergoing surgery.
• ↑ incidence of peri- & post-operative MI in patients with
known coronary disease.

Physiology:- supply & demand
• Oxygen demand is a concept that is closely related
to the oxygen consumption of an organ.
• The two terms are often used interchangeably
although they are not equivalent.
• Demand is related to need ,whereas consumption is
the actual amount of oxygen consumed per minute.
• Under some conditions, demand may exceed
consumption because the latter may be limited by the
supply of oxygen to the organ.

Organ VO2 (ml O2/min/100g)
Brain 3
Kidney 5
Skin 0.2
Resting muscle 1
•Highly oxidative organs such as the heart have a high demand for
oxygen and therefore have a relatively high oxygen consumption.
Physiology:- supply & demand
CARDIAC STATE MVO2 (ml O2/min/100g)
Arrested heart 2
Resting heart 8
Heavy exercise 70
VO2 = O2 consumption/
demand
MVO2 = Myocardial O2
consumption/demand

Physiology:- demand
•In order to support MVO2, particularly during times of increased
oxygen demand (e.g., during exercise), the heart must extract oxygen
from the arterial blood supplying the myocardium.
Myocardial Oxygen Demand
Myocardial LV wall tension
Heart rate
Cardiac contractility
(preload & afterload)

Physiology:-Cont..
Fick’s Principle- (CO)
•States that blood flow to an organ can be calculated using a
marker substance if the following is known:
-Amount of marker substance(Consumption) taken up by the organ per unit time (VO2)
-Concentration of marker substance in arterial blood supplying the organ (Ca)
-Concentration of marker substance in venous blood leaving the organ (Cv)
•Applying Fick’s principle to coronary circulation, myocardial O2 consumption
(MVO2) can be calculated
MV02 = CBF× (CaO2 – CvO2)
• CBF = Coronary blood flow (ml/min)
• CaO2 – CvO2 = Arterio-venous O2 content difference
(ml O2/ml blood)

Physiology:-Supply
MVO2 = (CBF ×CaO2) – (CBF × CvO2)
• In another way
CBF × CaO2 is the oxygen supply (or delivery)
to the myocardium.
CBF × CvO2 is the unextracted oxygen leaving the
heart via the venous circulation.
•The delivery of oxygen(MDO2) to the myocardium (oxygen
supply) is determined by two factors:
• CBF (Coronary blood flow)
• CaO2 (Oxygen content of the arterial blood)
(O2 Delivery) MDO2 = CBF × CaO2

OXYGEN content of blood:-
CaO2 (O2 content) = ( Hgb x 1.36 x SaO2) + (0.0031 x PaO2)
• CaO2: Directly reflects the total number of oxygen molecules in
arterial blood (both bound and unbound to haemoglobin).
• Hgb = haemoglobin
Normal range(Adults): Male: 13-18 g/dl Female: 12-16 g/dl
• SaO2 = % of haemoglobin saturated with oxygen
(Normal range: 93-100%)
• PaO2= Arterial oxygen partial pressure
(Normal range: 80-100 torr)

Myocardial Ischemia :- Aetiology
Demand > Supply
Myocardial hypoxia
↓ Availability of nutrient substrates
•Results due to Imbalance between Myocardial oxygen supply
and demand.
↓ removal of metabolites

Increase in O2 demand may be due to:
• Tachycardia
• Hypertension
• Stress.
• Drugs
• Severe pain
However, 50% or more of the ischemic episodes may be
unrelated to increased demand suggesting that decreased
oxygen supply is the primary cause.

Potential aetiologies for ↓myocardial O2 supply include:
External factors:
• Hypotension ,Tachycardia, Increased filling pressure,
Anaemia, Hypoxemia, and ↓ Cardiac output.
Internal factors:
• Acute coronary artery thrombosis & spasm.
• Myocardial O2 supply/demand mismatch is the main
trigger of myocardial injury.

Risk factors:-
Risk factors
Non-modifiable/irreversible Modifiable/reversible
•Male sex
•Age
•Genes

Myocardial Ischemia:-
•More than 90% of cases, the cause of myocardial ischemia is
reduction in coronary blood flow due to atherosclerotic coronary
arterial obstruction.
•Hence often termed coronary artery disease (CAD).
•Limits normal rise in coronary blood flow in response to↑
myocardial oxygen demand

Clinical manifestation:-
– Myocardial necrosis (infarction)
– Ischaemia (usually angina)
– Arrhythmias (resulting in sudden death)
– Ventricular dysfunction (CHF) – ischemic cardiomyopathy

Clinical manifestation:-
• Patients with IHD can present with chronic stable angina or
with Acute coronary syndrome.
Which includes ST elevation myocardial infarction
(STEMI)/non–ST elevation myocardial infarction (NSTEMI) on
presentation and unstable angina
• Chronic stable angina: Chronic pattern of transient
angina pectoris precipitated by physical activity or
emotional upset, relieved by rest with in few minutes.
• Unstable angina: Increased frequency and duration of
Angina episodes, produced by minimal exertion or at rest
(high frequency of MI if not treated)

Treatment of IHD:-
• The general approach
– Prevent progression of disease by correcting risk factors-
lifestyle modification to prevent stress & improve exercise
tolerance.
– Correction of complicating medical condition like,
HTN, Anemia, Hypoxemia, Thyrotoxicosis, Infection.
– Pharmacological therapy aimed in restoring balance between
myocardial oxygen supply and demand.
– Surgical correction of Coronary lesion
• Percutaneous coronary intervention (PCI).
• Coronary artery bypass surgery (CABG).
• Pharmacological agents
– Calcium channel blockers
– β-blockers
– Nitrates

Anti-ischemic Rx. effect on myocardial O2
Demand Heart Rate Contractility Preload Afterload
Nitrates No ,  No ,   
β-blockers   No ,  No
DHP*  No No 
V / D**  No ,  No 
Supply Regional CBF Diastolic filling time
Nitrates  +/-
β-blockers  
DHP*  
V / D**  
Demand:
Supply:

Anaesthesia :- Pre-operative Assesment
GOALS:
A. Evaluate patient’s current medical status.
B. To estimate peri-operative CV risk.(Risk Stratification)
C. Know when to perform stress testing or special
investigations pre-operatively.
D. Pre-operative management to reduce risk peri-
operatively in those at higher risk

Evaluation of current medical status:-
History:
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.
 If a patient can climb two to three flights of stairs without
symptoms, it is likely that cardiac reserve is adequate.
• Previous Myocardial Infarction.
• Co-Existing Noncardiac Diseases
• Current Medications

Routine investigations:-
• Blood chemistry tests-
• Chest X-RAY - excluding cardiomegaly or pulm. Congestion
secondary to ventricular disfunction.
• Standard ECG - changes of a previous MI – abmormal Q waves.
- loss of R waves.
• Suggest myocardial ischaemia - ST segment depression
- ST elevation (variant angina)
- Flattening of T waves
- Inverted T waves
- Abnormally tall T waves
• Resting ECG may be normal in 50% of patients with IHD
• Also detect conduction defects, ventricular hypertrophy,
& arrhythmias

GOALS:
D. Pre-operative management protocol to reduce risk peri-

Risk Stratification:-Estimate peri-operative CV risk
• Numerous risk indices and predictors have been used over the
years for estimating peri-operative risk .
•The Goldman Index was the first risk stratification method to use
modern statistical methods and identified 9 clinical factors which
correlated with cardiovascular risk and death.
•A weight was assigned to each risk factor based on the strength
of the statistical risk and it was possible, using this method, to
assign a number of points and use this point score, generally to
place a patient in one of four risk categories.
Demerit - underestimate risk in certain populations (elderly,obese)

Detsky modified Index:-
Class Points Cardiac risk
I 0 to 15 Low
II 20 to 30 Moderate
III 31 + high High

Clinical Predictors of Increased
Perioperative Cardiovascular Risk

J Am Coll. Cardiol, 2007; 50:1707-1732
ACC/AHA Guidelines:- (2007)
• Based on - Active cardiac conditions.
- Surgery-Specific Risk
- Functional Capacity
- Cardiac risk factors

Active Cardiac Conditions:- for Which the Patient Should Undergo
Evaluation and Treatment Before Surgery

Functional Capacity :Metabolic Equivalents (METs)
• One MET is the basal oxygen consumption (VO2) of a 70
Kg ,40 yr old man in resting state (3.5 ml/kg/min).
• Multiples of the baseline MET value can be used to
express aerobic demands for specific activities .
• Perioperative cardiac and long-term risks are increased
in patients unable to meet a 4-MET demand during most
normal daily activities.

Functional Capacity : Duke Activity Status Index

Surgery-Specific Risk:-
• Urgency.
• Type/complexity of surgery.

ACC/AHA
Stepwise approach to perioperative cardiac assessment
Cardiology
consultation
Cardiology
consultation

GOALS:
C. Know when to perform stress testing or
special investigations pre-operatively.
D. Pre-operative management protocol to reduce risk peri-

Special Cardiac Investigation :-
• 1) Non-invasive tests.
• 2) Invasive tests
Assesment of LV function
Noninvasive Stress Testing
- Active cardiac conditions.
- 3 or more clinical risk factors & poor
functional capacity (less than 4 METs)
requiring high risk surgery.

Special Cardiac Investigation:-Noninvasive tests
• Holter Monitoring- Continuous ambulatory ECG
monitoring.
• Evaluating the severity and frequency of ischemic episodes &
arrhythmias
• Excellent negative predictive value
for perioperative cardiac complications.

Exercise electrocardiography-
•Contraindications include severe aortic stenosis, severe HTN,
limited exercise tolerance, uncontrolled heart failure and IE.
•Normal test does not necessarily exclude CAD but suggests that
severe disease is not likely.

Echocardiography-
• Can be used to assess global
cardiac function.
• Assess regional wall motion
abnormalities & detect the
presence of previous myocardial
injury.
• LV function assessment is a
major determinant of long-term
prognosis.
• Ejection fraction < 50% (poor
outcome)

Myocardial perfusion scans-
• Nuclear tracers (thallium-201 or technetium-99m) are used to
measure coronary blood flow to myocardium.
• IV dipyridamole or adenosine (coronary dilator) produces a
hyperemic response similar to exercise.
• A significant coronary obstructive lesion causes less blood
flow and thus less tracer activity.
Size of the perfusion abnormality
is the most important indicator
of the significance of CAD.

• Coronary angiography- indicated in patients who continue
to have angina pectoris despite maximal medical therapy/ for
definitive diagnosis.
• Gold standard to evaluate CAD.
• Provides information about the
coronary anatomy & location
the extent & of the lesions.
Determine need of coronary
revascularization & the feasibility
of PCI/CABG depending on the
characteristics & location of the lesions.
Special Cardiac Investigation:- Invasive tests

Supplemental Preoperative Evaluation:
When and Which Test

Other investigations:-
Cardiac enzymes-
 Cardiac-specific Troponins (T or I).
 Creatinine kinase (MB isoenzyme).
 Lactate dehydrogenase (type 1 isoenzyme).
 Myoglobins.

GOALS:
D. Pre-operative management to reduce risk
peri-operatively in those at higher risk.

Preoperative management:-
• At risk patients need to be managed with pharmacologic and
other pre-operative interventions that can ameliorate
perioperative cardiac events.
Optimisation of medical
management.
Coronary revascularization
(PCI / CABG)

Optimisation of medical management:-
• Continue cardiac medications (beta blockers, CCBs, Nitrates)
till morning of surgery.
Sudden withdrawal of antianginal medication can
precipitate a sudden increase in ischemic episodes (rebound).
Prophylactic -adrenergic blockade has been shown to reduce
the incidence of intra-op & post-op ischemic episodes.
■ ACE inhibitors – Severe hypotension.
• Anti platelet therapy-
Aspirin- patient-specific strategy. (Risk/Benefit)
(Risk of perioperative bleeding while continuing aspirin is, as compared with
concomitant thromboembolic risks associated with aspirin withdrawal)
• Stop ticlodipine & clopidrogel

Coronary Artery
Disease
Patient Scheduled for Surgery With
Two Risk Factors:
Age > 65
Hypertension
Diabetes
Cholesterol > 240 mg/dl
Smoking
Beta Blockers:
Atenolol 25 mg po qd to start, if heart rate greater
than 60 and systolic blood pressure greater than
120 mmHg. Titrate dose to effect.
Atenolol or Metoprolol IV on day of surgery.
Atenolol or Metoprolol IV post op until taking PO
then.
Atenolol 100 mg PO qd for at least a week post op
(hold for heart rate less than 55 or systolic blood
pressure less than 100 mmHg)
If known CAD continue beta blocker indefinitely.
If patient has a specific contraindication
(asthma not COPD) to beta blockers:
Clonidine 0.2 mg PO tablet night before
surgery
Clonidine TTS#2 Patch (0.2 mg/24 hours)
night before surgery
Clonidine 0.2 mg PO table morning of surgery.
Hold for systolic blood pressure less than 120.
If Unable to take beta blockers
Proceed with Surgery
Perioperative Cardiac Risk Reduction
Therapy (PCRRT)
α2 agonists by virtue of its
sympatholytic effects is useful
in patients where beta blockers are
contraindicated.

Coronary Revascularization:- PCI/CABG
• Guided by patient's cardiac
condition & potential consequence
of delaying surgery for recovery
after coronary revascularization.
• Patients who underwent coronary
vascularization had better outcome
after noncardiac surgery.
Stent / baloon(per-cutaneous Angioplasty)
Coronary artery bypass graft

Anaesthesia:- Premedication
Goal- Allaying anxiety minimizes the sympathetic system
effects on the myocardium decreasing possibility of ischemic
events perioperatively.
• Benzodiazepine, alone or with opioid are m/c used.
• Excellent results can be obtained by a combination of
morphine (0.1–0.15 mg/kg) and scopolamine (0.2–0.4 mg)
IM.
• Concomitant administration of oxygen helps avoid hypoxemia
following premedication.

Choice of Anesthesia:-
• Regional anesthesia may be preferred to
general anesthesia if possible, as it tends
to better block the stress response to
surgery.
• Hypotension associated can be corrected
by fluids & sympathomimetic agents.
• Potential benefits include excellent pain
control, decreased incidence of deep vein
thrombosis in some patients, and the
opportunity to continue the block into the
postoperative period.
• However, the incidence of postoperative
cardiac morbidity and mortality does not
appear to be significantly different between
general and regional anesthesia.
Anaesthetic management skills
more important than technique

General anesthesia:-
■ Induction :
➣ The main goal during
induction is to avoid haemodynamic alteration (minimize
extreme variation in HR & BP), thereby decreasing drastic
cardiac events.
➣.
Produce reliable loss of consciousness, & provide sufficient
depth of anaesthesia

• In general all agents can be used safely if given slowly in
small increments. However Ketamine due to its indirect
sympathomimetic effects can adversely affect the myocardial
oxygen demand–supply balance.
Intravenous anaesthetics-
1) Thiopentone - Reduces myocardial contractility, preload and
BP & slight increase in HR. It should be administered slowly
and with caution.
2) Propofol - Reduces arterial BP & HR significantly. There is
dose dependent reduction in myocardial contractility. It can be
used in with good ventricular function but is not good induction
agent for patients with CAD.
General anesthesia:-Choice of agent

3) Midazolam - It produces decrease in mean arterial pressure
and increase in heart rate. It provides excellent amnesia and is
widely used for patient with CAD.
4) Etomidate - It causes minimum haemodynamic changes. It is
excellent for induction in patients with poor cardiac reserve.
General anesthesia:-Choice of agent

Intubation : choice of muscle relaxant
• Rocuronium, vecuronium, pipecuronium, and doxacurium
produce minimum haemodynamic alterations & safe in IHD.
• Histamine releasing drugs better avoided.
General anesthesia:-
• Control cardiovascular response to tracheal intubation by
keeping low duration of laryngoscopy(<15sec) or by
pharmacologic means.
• Pharmacologic interventions include lidocaine IV (1.5–2
mg/kg), 1.5 to 2 min before intubation intratracheal lidocaine (2
mg/kg) at the time of laryngoscopy, IV fentanyl ,IV esmolol or
IV nitroprusside.

• Volatile anaesthetics (isoflurane, desflurane & sevoflurane) are
safe in IHD. Volatile agents generally have a favorable effect on
myocardial oxygen balance, reducing demand & increasing suppl
(administered alone or in combination with nitrous oxide.)
• Alternately nitrous oxide – opioid combination with the addition
of a low dose of volatile anesthetic to treat any undesirable
increases in blood pressure can also be used.
Opoids:-
Morphine is the preferred drug for its relative cardiac stability &
very good analgesic effect. It produces arterial and venous
dilatation resulting in reduction of afterload and preload. Newer
agents like fentanyl, alfentanyl and sufentanil also provide
adequate cardiac stability and pain relief.
General anesthesia:- Maintenance

GOALS
• Stable haemodynamics. (A common recommendation is to keep
the heart rate and blood pressure within 20% of the normal awake value)
• Prevent MI by optimizing myocardial oxygen supply and
reducing oxygen demand.
• Monitor for ischaemia.
• Treat ischemia or infarction if it develops.
• Normothermia.
• Avoidance of significant anaemia
Intraoperative management:-

Intraoperative management:-
• Maintenance of balance between myocardial O2 supply &
demand is more important than the specific anaesthetic
technique or drugs selected to produce anaesthesia and
muscle relaxation.
Intraoperative Events That Influence the Balance Between
Myocardial O2 supply & demand

Triggers •Surgical Trauma
•Anesthesia/analgesia
•Intubation/extubation
•Pain
•Hypothermia
•Bleeding/anemia
•Fasting

• BP-invasive & noninvasive
• Pulse oximetry,Temp.
• In addition an important goal
when selecting monitors for
patients with IHD is to select
those allowing early detection
of myocardial ischemia.
• Most myocardial ischemia
occurs in the absence of
hemodynamic alterations.
• One should be cautious when
endorsing routine use of
expensive or complex
monitors to detect myocardial
ischemia.

Monitors used depend on disease severity & operative
procedure complexity
➣ ECG: Simplest & Cost effective. ST-segment changes are
principally used to diagnose myocardial ischaemia.
➣ Pulmonary artery catheter: Ischaemia manifests as a sudden
increase in PCWP (not specific). more useful as a guide in the
treatment of myocardial dysfunction.
➣ Central venous pressure 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.

Intraoperative Management of Myocardial
Ischemia
• If patient is haemodynamically stable-
IV Beta blockers like metoprolol / Esmolol (associated with tachycardia).
IV Nitroglycerine (associated with HTN).
Heparin after consultation with surgeon.
• If patient is haemodynamically unstable-
Support with inotropes.
Use of intraoperative ballon pump may be necessary.
Urgent consultation with cardiologist to plan for earliest possible cardiac
catheterization.

Reversal and recovery:
• Muscle relaxants can be reversed with neostigmine in
combination with glycopyrrolate, as the latter produces less
tachycardia. Nevertheless, atropine can be used with no
adverse effects as long as the pt is adequately beta blocked.
• Early extubation is desirable in many patients as long as they fulfill
the criteria for extubation.
• However, patients with IHD can become ischemic during
emergence from anesthesia 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.

Postoperative Management:-
• The goals are to prevent ischemia, monitor for myocardial
injury, and treat myocardial ischemia/infarction.
• Supplemental oxygen is crucial.
• Adequate Pain control to avoid excessive sympathetic nervous
system stimulation.
• 12-lead ECG as a baseline for detecting ischaemia.
• Prevention of shivering & maintenance of normothermia is
crucial to avoid oxygen desaturation & sympathetic overactivity.
• Maintaining adequate oxygenation & tight pain control for
48 to 72 hr post-op is very important, since this is the period
when the likelihood of developing AMI is highest.

Ischaemic heart disease & its anaesthetic implications

Ischaemic heart disease & its anaesthetic implications

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