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Summary

Ischemic Heart Disease (IHD)

Pathogenesis of Various Types of IHD

Pathogenesis and subtypes

Factors Contributing to Atherosclerosis

• High Serum LDL: ↑ Availability of lipids that deposit in arterial wall.
• Low Serum HDL: ↓ Removal of LDL from coronary artery walls (transport of LDL to liver is impaired).
• Endothelial Dysfunction: Compromise of endothelial barrier → vessel wall vulnerable to infiltration by LDL and cells of the immune system.

Atherosclerosis

• Arterial wall degeneration, characterized by fat deposition in and fibrosis of the inner layer of arteries.
• Occurs in Coronary Arteries:

Stable Angina

• Stable Atheromatous Plaque:
  • Fibromuscular cap overlying fatty plaque contents remains intact, and plaque contents are not released into the vessel lumen.
  • Plaque serves as a fixed luminal obstruction to blood flow.
  • If vessel stenosis is significant (≥70%), myocardial oxygen demand starts to exceed supply, especially with exertion.
  • Predictable, transient myocardial ischemia.

Unstable Angina

• Unstable Atheromatous Plaque:
  • Fibromuscular cap overlying fatty plaque ruptures.
  • Thrombogenic plaque contents (especially tissue factor) are exposed to coagulation factors in the vessel lumen.
  • Activation of platelets and the clotting cascade at the site of rupture.
  • Thrombus forms over already partially occlusive plaque → occludes lumen → ↓ perfusion of myocardium.
  • Transient ischemia of cardiomyocytes.

Myocardial Infarction (MI)

• Infarction (death) of cardiomyocytes.

Acute Coronary Syndromes (ACS)

• Includes Unstable Angina and Myocardial Infarction.

Myocardial Infarction: Findings on Investigations

Investigations

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Complications

• Tissue Ischemia: Disrupts normal cardiac electrical conduction (detected on serial ECG).
  • ST-Segment Depression: Non-localizing, ischemia of sub-endocardial myocardium.
  • ST-Segment Elevation: Localizes to site of ischemia, acute, trans-mural myocardial ischemia.
  • If ischemia progresses to tissue infarction, Pathologic Q-waves form (localizes to site of ischemia).

Additional Notes

• Both types of ST-segment changes can indicate myocardial infarctions but can also be false positives (e.g., caused by left ventricular hypertrophy, bundle branch blocks, and other non-myocardial ischemic causes).

Complications of MI

Complications of MI

Pathophysiology

Cardiac Contractility Due to Death of Cardiomyocytes

• Inadequate Cardiac Output:
  • Stasis of blood in the ventricle.
  • Formation of mural thrombus on akinetic inflamed wall segments.
  • Embolization of thrombus.
  • Systemic emboli (i.e., stroke, renal infarction, limb infarction).

Necrosis of Ventricular Wall 2° to Infarction

• Transmural Necrosis:
  • Dead tissue disrupts cardiac conduction system (e.g., bundle of His).
  • Causes acquired ventricular septal defect (VSD) and acquired mitral regurgitation (MR).

Irritability by Viable Tissue Adjacent to Area of Infarct

• Myocardial Electrical Instability:
  • Ectopic beats, re-entry circuits.
  • Necrotic tissue irritates and inflames pericarditis.

Complications

Pump Dysfunction

• Profound/Acute Dysfunction:
  • Cardiac output ↓↓↓.
  • Cardiogenic shock: ↓ Systemic & myocardial perfusion.
  • Acidemia, systemic organ failure (renal failure, myocardial damage).
• Less Profound/Acute Dysfunction:
  • Congestive heart failure.
  • Ventricular aneurysm: Atria distend due to stasis, disrupts electrical conduction, atrial fibrillation.

Ventricular Free Wall Rupture

• If pericardial adhesion is covering the rupture, blood from rupture is contained within the adhesion.
  • False aneurysm: If adhesion bursts.
  • Cardiac tamponade: If excess inflammatory fluid/edema accumulates within the pericardial sac.

Arrhythmias

• Myocardial electrical instability, ectopic beats, re-entry circuits

Pericarditis

• Inflammatory process.

Conduct of Anaesthesia for IHD in Non Cardiac Surgery

Goals

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Pre-Operatively

Goals of Pre-Op Assessment

• Current medical status
• Provide clinical risk profiling
• Decide on further testing
• Treat modifiable risk factors
• Plan management of cardiac illness during the peri-operative period

History and Optimization

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Pre-Op Testing

• ECG:
  • Detects myocardial ischemia, MI, cardiac rhythm/conduction disturbances, ventricular hypertrophy, and electrolyte abnormalities.
• Peri-Operative Coronary Angiography:
  1. High risk of adverse outcome based on non-invasive test results.
  2. Angina pectoris unresponsive to medical therapy.
  3. Unstable angina, particularly with intermediate or high-risk non-cardiac surgery.
  4. Equivocal non-invasive test results in high-risk patients undergoing high-risk surgery.

Susceptibility to Perioperative Ischemia

• Patient Factors: Co-morbidities (e.g., cerebrovascular disease, AF, elderly, PFO, IE, DM, male, smoker).
• Surgical Factors: High-risk surgery (vascular, neuro, cardiac).

Intraoperative Adverse Events:

• Arrhythmias, hypotension, CPR, embolic phenomenon.

Risk Stratification

• Type of surgery, presence/type of clinical indicators of coronary artery disease, and patient functional status.
• Low-Risk Procedure: Combined surgical and patient characteristics predict a MACE risk of death or MI of <1%. Procedures with a risk of MACE of ≥1% are considered elevated risk.

Clinical Predictors of Increased Peri-Operative Cardiovascular Risk

• Level of Risk: Major (Cardiac Risk > 5%)
  • Unstable coronary syndromes
  • Decompensated CHF
  • Significant arrhythmias
  • Severe valvular disease
• Level of Risk: Intermediate (Cardiac Risk < 5%)
  • Mild angina pectoris
  • Prior MI
  • Compensated/prior HF
  • Diabetes mellitus (particularly on insulin)
  • Renal insufficiency
• Level of Risk: Minor (Cardiac Risk < 1%)
  • Advanced age
  • Abnormal ECG
  • Rhythm other than sinus
  • Low functional capacity
  • History of stroke
  • Uncontrolled systemic hypertension

Assessment of Functional Capacity: The Duke Activity Index

• 1 MET (Metabolic Equivalent): Oxygen consumption of 3.5 ml/kg/min.

Exercise Level	Equivalent Activity
1-4 METs	Standard light home activities, walk around the house, take care of yourself (eating, bathing, using the toilet).
5-9 METs	Climb a flight of stairs, walk up a hill, walk one or two blocks on level ground, run a short distance, moderate activities (golf, dancing, mountain walk), have sexual relations.
>10 METs	Strenuous sports (swimming, tennis, bicycle), heavy professional/domestic work such as scrubbing floors, lifting or moving heavy furniture.

Cardiac Risk Classification of Non-Cardiac Surgical Procedures

• Elevated Risk (> 1%)
  • Emergent major operations, particularly in the elderly.
  • Aortic and other major vascular surgery.
  • Peripheral vascular surgery.
  • Anticipated prolonged surgical procedures with large fluid shifts and/or blood loss.
  • Carotid endarterectomy.
  • Head and neck surgery.
  • Intraperitoneal and intrathoracic surgery.
  • Orthopedic surgery.
  • Prostate surgery.
• Low Risk (< 1%)
  • Endoscopic procedures.
  • Superficial procedures.
  • Cataract surgery.
  • Breast surgery.

Pre-Operative Interruption and Resumption of Antiplatelet Therapy

Agent	Stop Before Surgery	Resume After Surgery	Dose
Oral
Aspirin	7 days	24 h	80-160 mg daily
Clopidogrel	5 days	24 h	Load with 300-600 mg, then 75 mg/day
Prasugrel	7 days	24 h	Bolus 60 mg, then 10 mg/day
Ticagrelor	5 days	24 h	Bolus 180 mg, then 90 mg bid
Intravenous
Tirofiban	4-8 h	4-6 h	0.1-0.15 µg/kg/min
Eptifibatide	4-6 h	4-6 h	2 µg/kg/min
Cangrelor	60-90 min	4-6 h	0.75 µg/kg/min

Anaesthesia For Ischaemic Heart Disease (IHD)

Factors Affecting Myocardial Oxygen Supply-Demand Balance

Factors Decreasing Supply

• Decreased coronary blood flow.
• Tachycardia.
• Hypotension.
• Increased preload.
• Hypoxia.
• Coronary artery spasm.
• Decreased oxygen content and availability (e.g., anemia, hypoxemia).

Factors Increasing Demand

• Tachycardia.
• Increased wall tension.
• Increased afterload (hypertension).
• Increased myocardial contractility.

Goals

• Avoid tachycardia and extreme blood pressure variations.
• Maintain a balance between myocardial oxygen supply and demand.

Intraoperative Management

Premedication

• Use benzodiazepines to reduce anxiety and blunt the stress response.
• Consider etomidate over propofol for induction in hemodynamically compromised patients.

Induction

• Avoid ketamine (as it increases myocardial oxygen consumption).
• Ensure a blunted intubation response using short-acting opioids or beta-blockers.

Maintenance

• Utilize volatile anaesthetics (e.g., isoflurane, sevoflurane) or total intravenous anaesthesia (TIVA) to maintain haemodynamic stability.

Extubation

• Aim for a blunted extubation response to minimize myocardial stress.
• Ensure optimal analgesia and avoid sudden hemodynamic changes.

Monitoring

1. Standard Monitoring:
   • Pulse oximetry.
   • Capnography.
   • Non-invasive blood pressure (BP).
   • Temperature.
   • Urine output.
2. Continuous ECG Monitoring:
   • Detect myocardial ischaemia and arrhythmias.
   • Use computerized ST-segment analysis with multiple lead monitoring (Leads II, V4, and V5).
3. Advanced Monitoring:
   • Invasive arterial pressure monitoring.
   • Central venous catheters.
   • Pulmonary artery catheters (if needed for hemodynamic assessment).
   • Transesophageal echocardiography (TEE) for ventricular function and regional wall motion abnormalities.

Treatment Of Intraoperative Ischaemia

• Myocardial Oxygen Supply/Demand Balance:
  • Deepen the plane of anaesthesia using inhalational or intravenous agents.
• Beta-Blockers:
  • Esmolol.
  • Metoprolol.
  • Labetalol.
• Vasodilators:
  • Nitroglycerine for coronary perfusion improvement.
• Hypotension Management:
  • Treat with phenylephrine and fluids to maintain coronary perfusion.
• Other Measures:
  • Maintain hemoglobin >8 g/dL.
  • Treat hypothermia.
  • Address arrhythmias promptly.

Postoperative Management

• Cardiac Monitoring:
  • Serial 12-lead ECGs to detect ischaemic events.
  • Troponin measurements to assess myocardial injury.
• Pain Management:
  • Ensure effective analgesia while avoiding significant hemodynamic changes.
  • Avoid COX-2 inhibitors to reduce cardiovascular risk.
• Hemodynamic Stability:
  • Monitor for signs of recurrent ischaemia, arrhythmias, or myocardial dysfunction.

Peri-Operative Myocardial Infarction (MI)

• May be due to myocardial oxygen supply/demand mismatch or acute plaque disruption.
• Prevention of Peri-Operative MI: Pre-operative coronary revascularization and pharmacological intervention.

Coronary Revascularization Indications

1. Acceptable coronary revascularization risk and viable myocardium with left main coronary artery stenosis.
2. Three-vessel coronary artery disease with left ventricular dysfunction.
3. Left main equivalent (high-grade block in left anterior descending and circumflex arteries).
4. Intractable coronary ischemia despite maximal medical therapy.

• Major noncardiac procedures should wait at least 4–6 weeks (possibly 6 months).
• In patients with recent coronary angioplasty and stenting, risk of stent thrombosis and MI increases if dual antiplatelet treatment is stopped; risk of surgical bleeding increases on continuation of drugs.
• Use low-dose aspirin (75 mg/day) based on individual decision considering peri-operative bleeding risk and thrombotic complications.
• ACC/AHA guidelines recommend a delay of at least 6 weeks between bare-metal stent insertion and noncardiac surgery, and 6 months (preferably 1 year) delay for drug-eluting stents for stent reendothelization. In case stent insertion is required before surgery, either bare-metal stent insertion or percutaneous angioplasty is preferable.

Stents

Bridging Therapy

• Drugs for bridging therapy: tirofiban, eptifibatide, and cangrelor.
• Oral antiplatelet drugs are stopped 5–7 days before planned surgical procedures and started on continuous IV infusion of tirofiban or eptifibatide until 4–6 h of procedures. These drugs are restarted postoperatively till DAPT can be reinstituted.

Medical Management

• Peri-Operative Beta-Blockers:
  • Metoprolol, atenolol, and bisoprolol are commonly used.
  • Target HR: 50–70 bpm.
  • ACC/AHA guidelines suggest continuing beta blockers preoperatively and throughout the perioperative period in patients already on them.
  • Beta-blockers should be started at least 24 hours before elective surgery and dose titrated to achieve the target HR of 50–60 bpm without significant hypotension.

Types of MI

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Links

• Cardiac physiology
• Acute coronary syndrome (ACS)
• Anticoagulation|Anticoagulation

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References:

1. The Calgary Guide to Understanding Disease. (2024). Retrieved June 5, 2024, from https://calgaryguide.ucalgary.ca/
2. FRCA Mind Maps. (2024). Retrieved June 5, 2024, from https://www.frcamindmaps.org/
3. Anesthesia Considerations. (2024). Retrieved June 5, 2024, from https://www.anesthesiaconsiderations.com/
4. Lees, H. D. and Charlesworth, M. (2021). Anaesthesia for patients with cardiac disease undergoing non-cardiac surgery. Anaesthesia &Amp; Intensive Care Medicine, 22(5), 297-300. https://doi.org/10.1016/j.mpaic.2021.03.008
5. Hedge, Jagadish; Balajibabu, PR; Sivaraman, Thirunavukkarasu. The patient with ischaemic heart disease undergoing non cardiac surgery. Indian Journal of Anaesthesia 61(9):p 705-711, September 2017. | DOI: 10.4103/ija.IJA_384_17

Summaries:

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© 2025 Francois Uys. All Rights Reserved.

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