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.

Blood supply of heart:-

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 isthe actual amount of oxygen consumed per minute.

• Under some conditions, demand may exceedconsumption because the latter may be limited by thesupply 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 theheart 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

Modifiable factors:-

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 ,

-blockers No , No DHP* No No

V / D** No , No

Supply Regional CBF Diastolic filling time Nitrates +/ -

-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

Physical examination:-

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-operatively in those at higher risk

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)

Goldman Risk Index:- (1977)

Detsky modified Index:- 1986

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

Cardac risk factors:-

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/AHAStepwise approach to perioperative cardiac assessment

Cardiology consultationCardiology

consultation


GOALS:




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

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 > 65HypertensionDiabetesCholesterol > 240 mg/dlSmoking

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 surgeryClonidine TTS#2 Patch (0.2 mg/24 hours) night before surgeryClonidine 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

Delaying surgery after PCI:-

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 supply.(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

Health & Medicine

oxygen content of blood

supply demand oxygen

blood supply of heart

o2 demand

venous blood

myocardial o2consumptiondemand

unextracted oxygen

myocardial o2 consumptionmvo2