Cardiac disease increases surgical risk: ischaemia, arrhythmias, heart failure, valve disorders.
Anaesthesia and surgical stress increase myocardial oxygen demand.
Cardiac suppression may occur with anaesthetic agents.
Pre-op: Cardiac assessment (METs, ECG, medications, cardiac history).
Intra-op: Monitor ECG, BP, SpO2, ETCO2, fluid balance.
Post-op: Watch for MI, arrhythmias, hypotension, fluid overload.
Right heart: pumps to lungs (pulmonary circulation).
Left heart: pumps to body (systemic circulation).
Coronary arteries perfuse the heart during diastole.
Cardiac output = HR × Stroke Volume.
Determinants of function: preload, afterload, contractility, heart rate.
Conduction pathway: SA node → AV node → Bundle of His → Bundle branches → Purkinje fibres.
Normal ECG values:
PR interval: 0.12–0.20 sec
QRS: ≤ 0.12 sec
QT: 0.36–0.44 sec
Common arrhythmias:
AF: Irregular, no P waves, stroke risk (anticoagulation).
VT: Wide QRS, fast rate, may cause collapse.
Bradycardia: Can cause syncope or hypotension.
STEMI: ST elevation = myocardial infarction → emergency.
Class | Examples | Purpose | Periop Advice |
---|---|---|---|
Beta-blockers | Metoprolol, Atenolol | Reduce HR and BP | Continue unless bradycardic or hypotensive |
ACE inhibitors | Enalapril, Perindopril | BP control, HF, IHD | Hold on surgery day (risk: hypotension) |
ARBs | Losartan, Candesartan | Same as ACEIs, less cough | Hold on day of surgery |
Diuretics | Furosemide, Spironolactone | Manage fluid overload (HF) | Monitor K+ and hydration |
Antiplatelets | Aspirin, Clopidogrel | Prevent thrombotic events | Continue or stop depending on procedure |
Anticoagulants | Warfarin, DOACs | Prevent stroke in AF or VTE | May need bridging or temporary hold |
Nitrates | GTN, Isosorbide | Treat angina (vasodilation) | Use with caution: risk of hypotension |
Statins | Atorvastatin | Cholesterol, plaque stability | Continue perioperatively |
CCBs | Amlodipine, Diltiazem | BP/HR control | Usually continued |
AF on warfarin: Check INR, stop 5 days pre-op, may require LMWH bridging.
HF patient: On diuretics → monitor K+, fluid status closely.
STEMI patient: Chest pain, ST elevation → urgent cardiology, ECG, troponin.
Aortic stenosis: High surgical risk; avoid BP drops and over-sedation.
Use RRRIP method:
Rate
Rhythm (regular or irregular)
P waves: present, upright, 1:1 with QRS?
PR interval
QRS width
ECG findings & meanings:
AF: Irregular, no P waves. Risk: thromboembolism.
VT: Wide QRS, tachycardia. Emergency!
STEMI: ST elevation in 2+ contiguous leads.
Bradycardia: Rate <60 bpm. Check perfusion.
Mechanism of Action:
Block alpha-1 adrenergic receptors on smooth muscles in blood vessels.
Leads to vasodilation (widening of blood vessels).
Lowers blood pressure by reducing vascular resistance.
Common Uses:
Hypertension (high blood pressure)
Benign prostatic hyperplasia (BPH) (to ease urination)
Heart failure (in some cases)
Examples of Alpha Blockers:
Prazosin (Minipress)
Doxazosin (Cardura)
Terazosin (Hytrin)
Mechanism of Action:
Regulate the electrical activity of the heart.
Control or prevent abnormal heart rhythms (arrhythmias) by affecting the ion channels in heart cells that regulate electrical impulses.
Classifications:
Class I (Sodium Channel Blockers):
Slow conduction speed in the heart.
Example: Quinidine, Procainamide
Class II (Beta Blockers):
Reduce heart rate and force of contraction.
Example: Propranolol, Metoprolol
Class III (Potassium Channel Blockers):
Prolong repolarization, stabilizing heart rhythm.
Example: Amiodarone
Class IV (Calcium Channel Blockers):
Slow conduction through the AV node.
Example: Verapamil, Diltiazem
Common Uses:
Atrial fibrillation
Ventricular arrhythmias
Tachycardia (fast heart rate)
Mechanism of Action:
Inhibit calcium ions from entering heart and smooth muscle cells.
Leads to vasodilation (relaxation of blood vessels) and decreased heart rate.
Lowers blood pressure, reduces heart rate, and relaxes coronary arteries.
Common Uses:
Hypertension
Angina (chest pain)
Certain types of arrhythmias (e.g., supraventricular tachycardia)
Examples of Calcium Channel Blockers:
Amlodipine (Norvasc)
Diltiazem (Cardizem)
Verapamil (Calan)
Mechanism of Action:
Block beta-1 adrenergic receptors on the heart.
Reduces heart rate, myocardial contractility, and the heart's oxygen demand.
Lowers blood pressure, prevents arrhythmias, and protects the heart after a heart attack.
Common Uses:
Hypertension
Angina
Post-myocardial infarction (post-heart attack)
Arrhythmias (e.g., atrial fibrillation)
Heart failure
Examples of Beta Blockers:
Atenolol (Tenormin)
Metoprolol (Lopressor, Toprol XL)
Propranolol (Inderal)
Carvedilol (Coreg)
Mechanism of Action:
Help the body get rid of excess sodium and water by increasing urine output.
Reduces fluid volume in the body.
Lowers blood pressure and reduces swelling (edema) caused by heart failure or kidney disease.
Common Uses:
Hypertension
Heart failure (to reduce fluid retention)
Edema (fluid retention)
Chronic kidney disease
Examples of Diuretics:
Furosemide (Lasix) – Loop diuretic
Hydrochlorothiazide (HCTZ) – Thiazide diuretic
Spironolactone (Aldactone) – Potassium-sparing diuretic
Mechanism of Action:
Cardiac glycoside that increases the force of heart contractions (positive inotropic effect) and slows the heart rate (negative chronotropic effect).
Inhibits the sodium-potassium ATPase pump, leading to increased intracellular calcium levels, improving cardiac output.
Common Uses:
Heart failure (especially in atrial fibrillation)
Atrial fibrillation (to control heart rate)
Examples:
Digoxin (Lanoxin)
Mechanism of Action:
Inhibit the enzyme HMG-CoA reductase, which plays a key role in cholesterol production in the liver.
Reduces cholesterol levels, statins help decrease the risk of atherosclerosis (plaque buildup in arteries), lowering the chances of heart attack, stroke, and other cardiovascular events.
Common Uses:
Hyperlipidemia (high cholesterol)
Prevention of heart attack and stroke
Atherosclerosis (to reduce plaque buildup)
After heart surgery or myocardial infarction (to reduce recurrence)
Examples of Statins:
Atorvastatin (Lipitor)
Simvastatin (Zocor)
Rosuvastatin (Crestor)
Pravastatin (Pravachol)
Medications preventing blood clots or their growth.
Used for thromboembolic disorders:
Deep Vein Thrombosis (DVT)
Pulmonary Embolism (PE)
Atrial Fibrillation Stroke
Prevention and treatment of blood clots.
Caution: Increased bleeding risk with other anticoagulants and drugs.
Mechanism: Binds to antithrombin III, inhibiting thrombin (IIa) and factor Xa.
Contraindications: Severe liver or kidney disease.
Side Effects: Alopecia and bleeding.
Use: DVT/PE, MI, perioperative.
Monitor: aPTT (activated Partial Thromboplastin Time).
Reversal agent: Protamine sulfate.
Treatment of venous thrombosis, pulmonary embolism, thromboembolism associated with Atrial Fibrillation
Prophylaxis of systemic embolism post myocardial infarction.
Mechanism: Inhibits vitamin K epoxide reductase, reducing synthesis of clotting factors II, VII, IX, X (vitamin K–dependent factors).
Effect: Slower onset, longer duration.
Use: Atrial fibrillation, mechanical heart valves, DVT/PE.
Monitor: INR.
Reversal agent: Vitamin K, fresh frozen plasma.
Main concern: bleeding risk.
Complications:
Spinal/epidural hematoma (can cause paralysis if untreated)
Uncontrolled surgical bleeding
Delayed wound healing or hematoma formation
Oral anticoagulant.
Treatment of deep vein thrombosis + prevention of stroke + systemic embolism in patients with non-valvular atrial fibrillation.
Mechanism: Direct thrombin (factor IIa) inhibitor.
Should NOT be discontinued; use Praxbind in case of bleeding.
Contraindications: Active bleeding, severe renal impairment, liver disease.
Side Effects: Nausea, allergic reactions, or anemia (due to bleeding).
Reversal agent: Idarucizumab (Praxbind).
Oral anticoagulant.
Treatment of deep vein thrombosis (DVT), pulmonary embolism (PE), and prevention of stroke + systemic embolism in patients with non-valvular atrial fibrillation.
Should NOT be discontinued abruptly – may increase risk of thrombotic events.
Mechanism: Direct Factor Xa inhibitor.
Route: Oral.
Contraindications: Active bleeding, severe renal impairment.
Side Effects: Bleeding (including GI bleeding), dizziness, and headache.
Reversal agent: Andexanet alfa (Andexxa) (for life-threatening or uncontrolled bleeding).
Prevent platelet aggregation (clumping).
Act on the platelet phase of clot formation.
Used in:
Cardiovascular disease (e.g., MI, stroke, stent placement).
Peripheral artery disease.
Secondary prevention of thrombotic events.
Increase bleeding risk, particularly during:
Regional anesthesia (e.g., spinal/epidural) → risk of epidural hematoma.
Surgical procedures → bleeding complications, poor wound healing.
Key considerations:
Know the type of antiplatelet and how long it was held before surgery.
Assess bleeding risk vs thrombosis risk when stopping drugs.
Guidelines recommend specific timing for stopping each agent before neuraxial blocks
Aspirin: Often continued (unless high bleeding risk).
Clopidogrel: Hold for 5–7 days.
Example: Aspirin
Mechanism: Irreversibly inhibits cyclooxygenase-1 (COX-1) → reduces thromboxane A2 → ↓ platelet activation.
Duration: Effect lasts for the lifespan of the platelet (~7–10 days).
Irreversible cyclooxygenase (COX-1 and COX-2) inhibitor, leading to decreased production of thromboxane A₂ – a molecule that promotes platelet aggregation.
Contraindications: Aspirin allergy, severe liver disease, children with viral illness (risk of Reye’s syndrome)
Use: Antiplatelet agent commonly prescribed for the prevention of thrombotic cardiovascular events, including myocardial infarction (MI) and ischemic stroke, especially in patients with known atherosclerotic cardiovascular disease. Also used after stent placement or acute coronary syndromes. Should not be stopped suddenly in patients with established cardiovascular disease due to risk of thrombotic events.
Side Effects: GI irritation or bleeding, hypersensitivity reactions
Reversal strategy: No specific antidote. Stop the drug, supportive care, platelet transfusion may be considered in severe bleeding.
Block ADP receptors on platelets → prevent activation.
Examples: Clopidogrel (Plavix)
Medications used to lower high blood pressure (hypertension) to reduce the risk of:
Stroke
Myocardial infarction
Heart failure
Kidney damage
Selective beta-1 blocker used for rate control in atrial fibrillation, management of hypertension, angina, and secondary prevention after myocardial infarction.
Mechanism: Selective β₁-adrenergic blocker – decreases heart rate and contractility, reducing myocardial oxygen demand.
Route: Oral or IV
Contraindications: Bradycardia, second/third-degree heart block, severe asthma or COPD, acute decompensated heart failure.
Side Effects: Bradycardia, hypotension
Reversal strategy: Stop drug; glucagon may be used in overdose; supportive care (fluids, atropine, pacing).
Combined alpha and beta-blocker used IV for hypertensive emergencies, including pre-eclampsia/eclampsia, and oral for chronic hypertension.
Route: Oral or IV
Contraindications: Asthma/COPD, bradycardia, heart block, cardiogenic shock
Ultra short-acting beta-1 selective blocker used IV for rapid rate control in supraventricular tachycardias, intraoperative hypertension, or aortic dissection.
Ideal for titration in acute settings due to short half-life (~9 minutes).
Mechanism: Selective β₁-adrenergic blocker – decreases heart rate and myocardial oxygen consumption.
Route: IV infusion
Contraindications: Bradycardia or AV block, cardiogenic shock, hypotension
Side Effects: Bradycardia, Hypotension.
Reversal strategy: Discontinue infusion – effects wear off quickly due to short half-life; supportive care.
Centrally acting antihypertensive used for resistant hypertension, hypertensive urgency, opioid withdrawal, and sometimes ADHD.
Mechanism: α₂-adrenergic agonist in the brainstem – reduces sympathetic outflow, lowering blood pressure and heart rate.
Route: Oral or transdermal (patch)
Contraindications: Bradyarrhythmias
Side Effects: Bradycardia, hypotension
Reversal strategy: Supportive care. For rebound hypertension, restart clonidine or use short-acting antihypertensive (e.g., labetalol).
Medications that increase blood pressure by causing vasoconstriction. Some also increase cardiac output.
Typically used in:
Hypotension during anesthesia or shock
Sepsis
Cardiogenic shock
Spinal/epidural-induced hypotension
Key part of anesthetic management when BP drops due to:
Induction agents (e.g., propofol, thiopental)
Spinal/epidural anesthesia (sympathetic blockade → vasodilation)
Intraoperative blood loss
Sepsis or anaphylaxis
Vasopressor + bronchodilator + inotrope used in anaphylaxis, cardiac arrest, severe asthma, and shock unresponsive to fluids.
Contraindications: Hypersensitivity to adrenaline (rare), use caution in hypertension, ischemic heart disease
Side Effects: Tachycardia, arrhythmias, hypertension
Reversal strategy: Supportive; short half-life. Beta-blockers may be used in severe overdose.
Potent vasopressor used in septic shock and hypotension refractory to fluid resuscitation. First-line agent in ICU for vasodilatory shock.
Contraindications: Hypovolemic shock without fluid resuscitation, mesenteric or peripheral vascular thrombosis
Side Effects: Hypertension, reflex bradycardia, ischemia to extremities or gut (from intense vasoconstriction)
Reversal strategy: Supportive, reduce infusion rate; phentolamine (α-blocker) if extravasation occurs.
Indirect sympathomimetic used to raise blood pressure in anesthesia (e.g., spinal-induced hypotension) and for mild bronchodilation.
Contraindications: Severe hypertension, tachyarrhythmias
Reversal strategy: Supportive; effects are short-acting.
Inotrope and vasopressor used in cardiogenic or septic shock, sometimes in bradycardia unresponsive to atropine.
Contraindications: Uncorrected tachyarrhythmias
Side Effects: Arrhythmias, nausea, peripheral ischemia
Reversal strategy: Stop infusion, supportive; phentolamine for extravasation.
Vasopressor used to treat hypotension, especially in perioperative settings or spinal anesthesia-induced hypotension.
Contraindications: Severe hypertension, peripheral vascular disease
Side Effects: Reflex bradycardia, hypertension
Reversal strategy: Supportive; phentolamine may be used for extravasation.
Drugs used to prevent or treat abnormal heart rhythms (arrhythmias).
Work on different phases of the cardiac action potential, targeting specific ion channels or receptors.
Used for: Atrial fibrillation/flutter, supraventricular tachycardia (SVT), ventricular tachycardia/fibrillation
Antiarrhythmic used for treatment of life-threatening ventricular arrhythmias (e.g., VT, VF), and also atrial fibrillation (especially in critically ill or post-operative patients).
Mechanism: Class III antiarrhythmic – prolongs repolarization by blocking potassium channels. Also has Class I, II, and IV properties (sodium channel blockade, beta-blockade, calcium channel blockade).
Route: IV or oral
Contraindications: Severe sinus node dysfunction or AV block (without pacemaker), thyroid dysfunction
Side Effects: Hypotension (IV form), bradycardia, long-term: pulmonary fibrosis, thyroid dysfunction, liver toxicity, corneal deposits, skin photosensitivity
Reversal strategy: No specific antidote. Discontinue drug; supportive care. Monitor thyroid, liver, lungs long-term.
Used IV in ventricular arrhythmias, especially post-MI or during cardiac arrest when amiodarone is not available.
Mechanism: Sodium channel blocker – decreases depolarization and automaticity in ventricular cells.
Route: IV (for arrhythmias), subcutaneous or topical (for anaesthesia)
Contraindications: Severe heart block without pacemaker, known hypersensitivity
Side Effects (IV): CNS toxicity: confusion, seizures, dizziness, bradycardia, hypotension, high doses: respiratory arrest, cardiac arrest
Reversal strategy: Stop infusion, supportive care; benzodiazepines for seizures. Intralipid therapy in severe toxicity.
Ultra-short acting antiarrhythmic used to acutely terminate paroxysmal supraventricular tachycardia (SVT). First-line agent for stable, narrow-complex tachycardia.
Mechanism: Activates A1 adenosine receptors in the AV node → transiently blocks AV nodal conduction → interrupts re-entrant circuits.
Route: Rapid IV push (followed immediately by saline flush)
Contraindications: Second/third-degree AV block (unless pacemaker present), asthma (can cause bronchospasm).
Side Effects: Chest discomfort, shortness of breath, bronchospasm in asthmatics
Reversal strategy: Very short half-life (~10 seconds); effects self-limit quickly. Supportive care only.
Vasodilators used primarily to treat angina, heart failure, and myocardial infarction.
Work by releasing nitric oxide (NO), which leads to smooth muscle relaxation in blood vessels.
Sublingual (SL) - Route of administration where the drug is placed under the tongue for absorption through the mucous membranes, bypassing the gastrointestinal tract and first-pass liver metabolism.
Commonly used for: Nitroglycerin (for angina)
Drugs that block acetylcholine (ACh).
Block the parasympathetic nervous system.
Reduce secretions: Less saliva and mucus = easier intubation and less risk of aspiration.
Prevent slow heart rate: Some anesthetic drugs or vagal stimulation can slow the heart → anticholinergics fix that.
Help breathing: Can relax airways (bronchodilation) — good for asthma or reactive airways.
Reverse side effects: When we reverse muscle relaxants (like with neostigmine), anticholinergics stop the unwanted side effects (e.g., bradycardia, more secretions).
Tertiary Amines — Can enter the brain
Atropine:Speeds up heart rate.
Used in emergencies for bradycardia
Scopolamine: Nausea, motion sickness
Can make you sleepy or forgetful
Cardiac glycoside used to treat heart failure and certain types of abnormal heart rhythms (like atrial fibrillation).
Increases the force of the heartbeat (positive inotrope)
Slows down the heart rate (by affecting the AV node)
It helps the heart pump more effectively while also controlling rhythm.
Important for the anesthesia team to know if a patient is taking Digoxin.
Slow heart rate (bradycardia): Digoxin slows the heart — anesthetic drugs can add to this effect.
Risk of arrhythmias: If Digoxin levels are too high, it can cause dangerous heart rhythms.
Electrolyte imbalance: Digoxin toxicity is more likely with low potassium (K⁺) — anesthesia can affect electrolytes.
Interactions with other drugs: Some anesthetic drugs (like suxamethonium, calcium, or beta-blockers) can worsen Digoxin’s effects.
Reduced AV node conduction: Can increase the risk of heart block, especially when combined with other cardiac depressants.