ANAESTHETIC MANAGEMENT OF A
PATIENT WITH ISCHAEMIC HEART
DISEASE UNDERGOING NON
PRESENTOR: DR.RAJESH CHOUDHURI
PGT, DEPARTMENT OF ANAESTHESIOLOGY
AGMC & GBP HOSPITAL, AGARTALA
• IHD/CAD -- a group of closely related syndromes resulting from myocardial
ischemia—an imbalance between the supply (perfusion) and demand of the heart
for oxygenated blood.
The most common form of heart disease.
5% of patients over 35 years of age have asymptomatic ischaemic heart
May be present in up to 30% of older pts undergoing surgery.
The overall incidence of CAD in surgical patients is estimated to be between
Cardiac dysrhythmias[VF] are a major cause of sudden death.
RISK FACTORS FOR DEVELOPMENT OF ISCHEMIC HEART DISEASE
• Male gender
• Increasing age
• Cigarette smoking
• Diabetes mellitus
• Sedentary lifestyle
• Genetic factors
• Family history of premature ischemic heart disease (male <55 yrs of age,
female <65 yrs)
SPECTRUM OF IHD
• 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 stable angina refers to chest pain or discomfort that does not change
appreciably in frequency or severity over 2 months or longer.
-precipitated by physical activity or emotional upset, relieved by rest or
nitroglycerine with in few minutes.
-develops in the setting of partial occlusion or significant (>70%) chronic
narrowing of a segment of coronary artery.
- Atherosclerosis is the most common cause .
-Temporary depression of ST segment with no myocardial damage.
-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
- Generally responds promptly to vasodilators.
-Transient shifts of ST segment – ST elevation.
- defined as angina at rest, angina of new onset, or an increase in the
severity or frequency of previously stable angina without an increase in
levels of cardiac biomarkers.
-is induced by disruption of an atherosclerotic plaque with
superimposed partial (mural) thrombosis and possibly embolization or
vasospasm (or both). of subsequent acute MI.
- lies between stable angina on the one hand and MI on the other
MYOCARDIAL INFARCTION (MI)
• Focal disruption of an atheromatous plague triggers the coagulation cascade with
subsequent generation of thrombin and partial or complete occlusion of the
• Region of myocardial necrosis due to prolonged cessation of blood supply
• Typical symptoms of myocardial infarction include:SuddenChest Pain, Shortness Of
Breath, Nausea,Vomiting, Palpitations, Sweating,Weakness, Light-headedness,Collapse/syncope .
Diagnosis of Acute MI:
At least 2 of the following
• Ischaemic symptoms.
• Diagnostic ECG changes.
• Serum cardiac marker elevations.
Pre-operative Screening & 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.
PRE-OPERATIVE SCREENING & EVALUATION
• 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
• 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.
SPECIALIZED PREOPERATIVE TESTING
• 12-lead ECG: may show no abnormality, old MI, AMI, ST depression, non specific changes.
• Echocardiography: global cardiac function , LV dysfunction, regional wall motion abnormalities , valvular ds, LV thrombus
• Exercise electrocardiography:C/I- Severe AS, Severe hypotension, Acute myocarditis, Uncontrolled
HF, Infective Endocarditis.
• Stress echocardiography : used with pharmacologic induction of cardiac stress (dobutamine) or
exercise to look at LV segmental wall function at rest & with stress.
• Nuclear stress imaging: Dipyridamole-thallium testing mimics the coronary vasodilator response
associated with exercise.
• Positron emission tomography:to demonstrate regional myocardial blood flow & metabolism, &
• Coronary angiography : Provides information about the coronary anatomy & the extent & location of
the lesions. indicated in pts w/ unstable angina despite maximal therapy.
• Cardiac enzyme elevation: Troponin is more specific than CK-MB ; increases within 4 hours after AMI
& remains elevated up to 1 wk.
• 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.
• Lee’s Revised Cardiac Risk Index:
• The ACC/AHA guidelines integrate risk stratification according to:
1. Clinical risk factors & ECG review.
2. Functional Capacity.
3. Surgery specific risk factors.
CLINICAL PREDICTORS OF INCREASED PERIOPERATIVE
• Unstable coronary syndromes
• Acute / Recent MI
• Unstable/ Severe Angina
• Decompensated Heart Failure
• High grade AV-block
• SymptomaticVentricular Dysrhythmias
• SevereValvular Heart Disease
• Stable Angina
• Previous MI (history/ECG)
• Compensated or previous heart failure
• DM/Renal Insufficiency
• ECG: LVH,LBBB ST-T abnormalities
• Low functional capacity
• H/O CVA/HTN
• The ability to exercise is an excellent indicator of “ cardiovascular fittness”.
• Usually expressed in metabolic equivalents of task ( METs) on a scale defined by the
Duke Activity Status Index.
• One MET is the resting oxygen consumption of a 40 yr old 70 kg male ( 3.5 ml/kg/min).
• Patients who can not sustain 4 METs of physical activity frequently have adverse
outcomes following high-risk surgery.
High/ intermediate risk surgery + Moderate-minor clinical risk factors
No change in medical
DES <12 months
Dual anti platelet
High/intermediate risk surgery+ moderate clinical risk factors
Consider risk of coronary
revascularization vs surgery
PREOPERATIVE MANAGEMENT AFTER RISK STRATIFICATION
• CABG: Indications are the same as those in the non-operative setting.
• PERCUTANEOUS CORONARY INTERVENTION: Poses its own unique set of
problems that need to be considered before elective non cardiac surgery.
• PHARMACOLOGIC MANAGEMENT:
Perioperative beta-blocker therapy: Patients already on beta blockers chronically (I)
In patients with intermediate- or high-risk preoperative tests (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
Perioperative statin therapy: To be continued in patients already taking statins (I)
Patients with vascular disease should receive statins regardless of the need of
Should be started 1-4 weeks prior to surgery and continued perioperatively.
Alpha-2 agonists: may be considered in patients who can not tolerate beta blockers.
ACE inhibitors: discontinued on the morning of surgery. Restart as soon as clinically feasible
postoperatively (IIa ).
Antiplatelet agents: Aspirin may be continued throughout the perioperative period. Clopidogrel
should however be discontinued for a week prior to surgery…restart as soon as possible after surgery/
removal of epidural catheter.
• Anaesthetic Goals : 1.Prevent myocardial ischaemia by optimising myocardial O2
delivery and reducing the O2 demand.
2.To monitor for ischaemia.
3.To institute appropriate measures to treat ishaemia if and
when it develops.
• Causes Of Myocardial O2 Imbalance
DecreasedO2 supply IncreasedO2 demand
Decreased coronary flow
•tachycardia (decreased diastolic
•hypotension (esp diastolic BP)
•hypocapnia (coronary vaso
constriction) coronary vasospam
Decreased O2 content & availability
•reduced release from Hb i.e ODC
shift to left
•2. increased wall tension
•3. increased preload
•4. increased after load
•5. increased myocardial
ANAESTHETIC CONSIDERATIONS DURING INTRAOPERATIVE PERIOD
• Avoid tachycardia: Increases O2 demand , also shortens diastolic filling
• Avoid persistent and excessive changes in BP: Keep the HR and BP within 20
% of the normal awake value.
• Avoid hyperventilation: as hypocapnia can cause coronary artery
• Maintain normothermia: Intraoperative hypothermia may predispose to
shivering on awakening, leading to abrupt and dramatic increases in
myocardial oxygen requirements.
• Correct Anaemia : Blood loss to be taken care of – anaemia can cause
critical reduction in myocardial oxygen supply in IHD pt.
• PRE-MEDICATION: Morphine, scopolamine, and benzodiazepine , alone or in combination –for
sedation and amnesia without causing deleterious myocardial depression, hypotension, or
➣ Continuation or administration of beta blockers .
➣ all pre-medicated patients should receive supplemental oxygen.
• INDUCTION OF ANAESTHESIA: can be accomplished with an intravenous induction drug.
➣ Etomidate is a good choice for patients with poor cardiac reserve.
➣Ketamine is to be avoided as it increases myocardial oxygen demand by
increasing HR and BP.
• INTUBATION:To be facilitated by the use of succinyl choline or a NDMR.
Blunting of haemodynamic response to tracheal intubation by-
1. Keeping the duration short (<15s).
2.Use of laryngotracheal Lidocaine, intravenous lidocaine, esmolol, fentanyl,
• 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.
• 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
• Pancuronium should be avoided to due to its sympathomimetic activity.
• For patients with severely impaired LV function: opioids may be selected as the principal anaesthetic.
• REVERSAL: with an anticholinesterase/anticholinergic drug combination can be safely
Early extubation is possible and desirable in many patients as long as they fulfill the
criteria for extubation.
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 &
• 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
• ECG: 3 lead monitoring II,V4 &V5 orV3V4&V5 is recommended.
Simplest and most cost-effective method for detecting perioperative myocardial ischaemia.
• PULMONARY ARTERY CATHETER : may be considered when underlying medical conditions
that significantly affect hemodynamics cannot be corrected before surgery (IIa).
Intra operative myocardial ischaemia can manifest as an acute increase in pulmonary artery
• 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).
POST OPERATIVE AND LONG-TERM MANAGEMENT
• 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.
• pain control.
• Continuous ECG monitoring with ST-segment analysis .
• Supplemental O2 .
• Avoid & treat shivering.
• Prevent hypoxemia, hypercarbia hypovolaemia, hypotension in postoperative period.
PERIOPERATIVE MYOCARDIAL ISCHAEMIA
• The risk of perioperative death due to cardiac causes is less than 1% for patients who
do not have ischemic heart disease .
The incidence of perioperative MI in patients who undergo elective high-risk
vascular surgery is between 5% and 15%.
PERIOPERATIVE MYOCARDIAL ISCHAEMIA
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.
Intraoperative Management of Myocardial Ischemia
• Delay the procedure,- if not possible, expedite surgery 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 325mgAspirin 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.
Hypotension : treated with sympathomimetic drugs / fluid infusion to restore blood
In an unstable hemodynamic situation, circulatory support with inotropes or an
intra-aortic balloon pump may be necessary.