Effects Of Anaesthesia And Drugs On Cardiovascular System

Foundations and mechanisms

Haemodynamic framework

The cardiovascular effects of anaesthesia are best analysed using the coupled determinants of arterial pressure, venous return and myocardial oxygen balance. Mean arterial pressure is approximated by MAP = CO × SVR + CVP, where cardiac output is the product of heart rate and stroke volume. Normal adult values are: cardiac output 4–6 L min⁻¹, cardiac index 2.5–4.0 L min⁻¹ m⁻², MAP 70–100 mmHg, SVR 800–1200 dyn s cm⁻⁵, and central venous pressure 2–6 mmHg. Anaesthetic drugs perturb one or more of preload, afterload, contractility, lusitropy, chronotropy, dromotropy and autonomic reflex gain.

Coronary perfusion pressure is approximated by aortic diastolic pressure − LVEDP; hence tachycardia, hypotension, raised LVEDP and reduced diastolic time are particularly deleterious. Myocardial oxygen demand is driven by wall stress, heart rate and contractility; wall stress follows Laplace’s relationship, σ = Pr/2h, explaining the vulnerability of dilated or hypertrophied ventricles during vasodilatation, tachycardia or hypertension.

Autonomic and vascular mechanisms

General anaesthesia reduces sympathetic outflow, impairs baroreflex-mediated tachycardia and venoconstricts less effectively. Normal arterial baroreflex buffering operates over a pressure range centred around MAP 90–100 mmHg; cerebral autoregulation is classically maintained between MAP 60–150 mmHg, but is shifted rightward in chronic hypertension. Perioperative outcome studies consistently associate organ injury with MAP <65 mmHg, particularly when prolonged; pragmatic perioperative targets commonly aim for MAP ≥65 mmHg or within 20% of baseline, with higher targets in chronic hypertension, cerebrovascular disease or severe coronary disease.

Venous capacitance is critical: approximately 60–70% of blood volume resides in the venous system. Anaesthetic venodilatation reduces stressed volume, mean systemic filling pressure and venous return. Positive-pressure ventilation compounds this by increasing intrathoracic pressure, reducing right ventricular preload, and increasing pulmonary vascular resistance when lung volume is high or hypoxic pulmonary vasoconstriction is inhibited.

Drug class effects: mechanistic classification

Class/drug	Typical dose	Dominant cardiovascular mechanisms	Exam-relevant features
Propofol	Induction 1.5–2.5 mg kg−1; elderly/frail 0.5–1 mg kg−1	Arterial and venous vasodilatation; reduced sympathetic tone; mild negative inotropy	MAP commonly falls 25–40%; SVR falls 15–30%; blunted baroreflex. Context-sensitive decrement remains short after brief infusion but accumulates with duration.
Thiopental	3–5 mg kg−1	Venodilatation; myocardial depression; reflex tachycardia if baroreflex intact	Greater haemodynamic instability in hypovolaemia; histamine release uncommon but possible.
Etomidate	0.2–0.3 mg kg−1	Minimal effect on SVR, contractility and baroreflex	Useful in limited cardiac reserve; inhibits 11β-hydroxylase, suppressing cortisol synthesis after single dose for 6–24 h.
Ketamine	IV induction 1–2 mg kg−1; analgesic 0.1–0.3 mg kg−1	Indirect sympathomimetic effect via catecholamine reuptake inhibition; direct myocardial depression unmasked in catecholamine depletion	Increases HR, BP and CO; may worsen ischaemia, pulmonary hypertension or severe tachyarrhythmia.
Volatile agents	Approximately 0.5–1.3 MAC clinically	Dose-dependent myocardial depression, vasodilatation and autonomic attenuation	At 1 MAC, MAP typically falls 20–30%. Sevoflurane MAC ≈2.0%, isoflurane ≈1.15%, desflurane ≈6.0%, nitrous oxide ≈104%.
Opioids	Fentanyl 1–5 micrograms kg−1; remifentanil infusion 0.05–0.3 micrograms kg−1 min−1	Reduced sympathetic tone; vagal predominance; histamine release with morphine	Bradycardia and hypotension, especially with propofol or hypovolaemia. Remifentanil context-sensitive half-time ≈3–5 min due to ester hydrolysis.
Dexmedetomidine	0.2–0.7 micrograms kg−1 h−1; loading often avoided	Central α2-agonism reduces sympathetic outflow; peripheral α2B vasoconstriction with bolus	Bradycardia, reduced CO; transient hypertension with loading dose 0.5–1 microgram kg−1.

Volatile anaesthetics and myocardial electrophysiology

Volatile agents reduce calcium influx through L-type channels, alter sarcoplasmic reticulum calcium handling and reduce myofilament calcium sensitivity, producing negative inotropy. Isoflurane and desflurane predominantly reduce SVR; sevoflurane has smoother sympathetic responses. Rapid increases in desflurane above approximately 1 MAC may provoke sympathetic activation, tachycardia and hypertension via airway and central mechanisms. Halothane, now largely historical in UK practice, sensitises the myocardium to catecholamines and depresses sinoatrial and atrioventricular conduction.

Vasoactive pharmacology: receptor-level classification

Drug	Receptor profile	Usual bolus/infusion	Primary haemodynamic effect
Phenylephrine	α1	50–100 micrograms IV; infusion 0.1–1 microgram kg−1 min−1	Raises SVR and diastolic pressure; reflex bradycardia; may reduce stroke volume.
Metaraminol	Indirect and direct α activity	0.25–1 mg IV bolus; infusion 0.5–5 mg h−1	Vasoconstriction with modest β effect; common first-line perioperative vasopressor.
Ephedrine	Indirect sympathomimetic; α and β	3–9 mg IV bolus	Increases HR, contractility and BP; tachyphylaxis with catecholamine depletion.
Noradrenaline	α1 > β1	0.02–0.5 micrograms kg−1 min−1	Restores vascular tone while supporting coronary perfusion; first-line in vasodilatory shock.

Neuromuscular blocking drugs may produce cardiovascular effects independent of paralysis: suxamethonium can cause bradycardia, junctional rhythms and hyperkalaemia; pancuronium is vagolytic; atracurium and mivacurium can release histamine causing vasodilatation and tachycardia. Local anaesthetic systemic toxicity reflects sodium-channel blockade: early CNS toxicity may precede myocardial conduction delay, QRS widening, negative inotropy and ventricular arrhythmia. Bupivacaine is particularly cardiotoxic because of avid, slow dissociation from inactivated myocardial sodium channels.

Clinical assessment and investigations

Clinical presentation and immediate clinical framing

Cardiovascular effects of anaesthesia and perioperative drugs most commonly present as hypotension, hypertension, bradycardia, tachycardia, arrhythmia, myocardial ischaemia, low cardiac output, or cardiac arrest. In examination terms, interpretation should be mechanistic rather than descriptive: determine whether the dominant abnormality is preload failure, afterload reduction/increase, myocardial depression, chronotropic/conduction disturbance, or obstructive physiology. Anaesthetic drugs often produce mixed phenotypes: propofol causes venodilatation, arterial vasodilatation and negative inotropy; volatile agents reduce systemic vascular resistance and depress contractility dose-dependently; neuraxial blockade produces sympathectomy with venous pooling and, if high, cardioaccelerator fibre blockade; opioids may cause vagally mediated bradycardia; ketamine may increase sympathetic tone but depress myocardium in catecholamine-depleted patients.

Clinically significant intraoperative hypotension is usually defined as MAP <65 mmHg, SBP <90 mmHg, or a >20–30% fall from baseline. Observational perioperative datasets consistently associate MAP <65 mmHg, particularly when sustained for >10–20 minutes, with myocardial injury, acute kidney injury and mortality. Hypertension is commonly treated when SBP is >180 mmHg, DBP >110 mmHg, or there is end-organ risk, although perioperative thresholds are context-dependent.

Differential diagnosis of peri-anaesthetic cardiovascular instability

Phenotype	Likely mechanisms	Drug-related causes	Key discriminators
Hypotension with low SVR	Vasodilatation, sympathectomy, anaphylaxis, sepsis	Propofol, volatile agents, neuraxial local anaesthetic, ACE inhibitors/ARBs, anaphylaxis to NMBAs/antibiotics/chlorhexidine	Warm peripheries, low diastolic pressure, wide pulse pressure; rash/bronchospasm in anaphylaxis but may be absent
Hypotension with low cardiac output	Negative inotropy, myocardial ischaemia, cardiomyopathy, severe bradycardia	Volatile agents, propofol, beta-blockers, calcium-channel blockers, amiodarone, local anaesthetic systemic toxicity	Narrow pulse pressure, cool peripheries, raised filling pressures, poor contractility on echo
Hypotension with low preload	Hypovolaemia, venodilatation, positive-pressure ventilation, haemorrhage	Propofol, neuraxial blockade, nitrates	Low pulse pressure, small collapsible IVC, PPV/SVV elevated if valid
Obstructive shock	Tension pneumothorax, tamponade, pulmonary embolism, dynamic LVOT obstruction	Positive-pressure ventilation may precipitate; inotropes may worsen LVOT obstruction	High airway pressures, raised JVP, echo diagnosis, severe hypoxaemia or acute RV dilation
Arrhythmia/conduction disturbance	Autonomic imbalance, electrolyte abnormality, ischaemia, drug toxicity	Suxamethonium, anticholinesterases, atropine/glycopyrrolate, volatile agents, QT-prolonging antiemetics/antipsychotics	12-lead ECG, potassium/magnesium, QTc, relationship to drug timing

Monitoring, investigations and interpretation

The minimum assessment is simultaneous evaluation of ECG rhythm/ischaemia, arterial pressure, pulse oximetry, capnography, airway pressure, anaesthetic depth, temperature, urine output and recent drug administration. Always exclude artefact: misplaced NIBP cuff, damping or resonance in an arterial line, transducer height error, electrocautery interference, or pulse oximeter failure. Invasive arterial pressure is indicated for major surgery, expected haemodynamic instability, vasoactive infusions, significant cardiac disease, or when beat-to-beat assessment is required.

• ECG: lead II is optimal for rhythm; V5 is most sensitive for left ventricular ischaemia. ST depression ≥1 mm measured 60–80 ms after the J point suggests subendocardial ischaemia; new ST elevation in contiguous leads requires urgent exclusion of coronary occlusion. QTc is prolonged at approximately >450 ms in men and >470 ms in women; QTc ≥500 ms substantially increases torsades risk, especially with hypokalaemia, hypomagnesaemia and bradycardia.
• Capnography: abrupt hypotension with falling ETCO₂ implies reduced pulmonary blood flow/cardiac output; severe bronchospasm, anaphylaxis, pulmonary embolism and cardiac arrest may all present this way. During CPR, ETCO₂ <10 mmHg suggests poor perfusion, whereas abrupt rise indicates ROSC.
• Arterial blood gas: assess pH, PaO₂, PaCO₂, potassium, ionised calcium, haemoglobin and lactate. Lactate >2 mmol/L indicates impaired oxygen delivery/utilisation; persistent lactate ≥4 mmol/L is high risk. Ionised calcium should generally be >1.0 mmol/L during major transfusion.
• Haemoglobin: restrictive transfusion thresholds are commonly 70 g/L in stable patients and 80 g/L in active cardiac disease or ongoing ischaemia; decisions must integrate bleeding, oxygen delivery and physiology.
• Troponin: perioperative myocardial injury is defined by troponin above the assay’s 99th percentile upper reference limit with or without symptoms. The VISION studies established prognostic significance of postoperative troponin elevation; surveillance is recommended in high-risk patients after major non-cardiac surgery by several contemporary perioperative guidelines.

Advanced haemodynamic assessment

Modality	Useful thresholds	Important limitations
Pulse pressure variation / stroke volume variation	PPV or SVV >12–13% suggests fluid responsiveness	Valid only with controlled ventilation, tidal volume usually ≥8 ml/kg, sinus rhythm, closed chest, no marked RV failure or high intra-abdominal pressure
Passive leg raise / mini-fluid challenge	Increase in stroke volume or cardiac output ≥10% predicts fluid responsiveness	Requires real-time cardiac output measurement; less useful during surgical positioning constraints
Central venous oxygen saturation	ScvO2 normally ~70%; low values suggest inadequate oxygen delivery	Non-specific; may be high in sepsis, shunting or impaired extraction
Transthoracic/transoesophageal echocardiography	Qualitative assessment of LV/RV function, filling, tamponade, embolus, valvular lesions, LVOT obstruction	Operator-dependent; TOE often superior intraoperatively but semi-invasive

Preoperatively, risk stratification contextualises drug sensitivity and haemodynamic reserve. Poor functional capacity is <4 METs; Revised Cardiac Risk Index factors include high-risk surgery, ischaemic heart disease, heart failure, cerebrovascular disease, insulin-treated diabetes and creatinine >177 µmol/L. Natriuretic peptides are useful in selected high-risk patients: elevated BNP or NT-proBNP predicts postoperative cardiac complications, although thresholds vary by guideline and assay. Echocardiography is indicated for unexplained dyspnoea, decompensated heart failure, suspected severe valvular disease, or significant change in clinical status—not as routine screening.

Management, pharmacology and procedures

Immediate haemodynamic management during anaesthesia

Management is directed by the physiological diagnosis: inadequate preload, impaired contractility, excessive afterload, inappropriate vasodilatation, bradycardia/tachyarrhythmia, or myocardial ischaemia. A pragmatic target is maintenance of mean arterial pressure (MAP) within 20% of baseline or MAP ≥65 mmHg; sustained intraoperative MAP <55–60 mmHg is associated with acute kidney injury and myocardial injury, with risk increasing with duration. In patients with chronic hypertension, coronary disease, carotid stenosis or raised intracranial pressure, higher targets are often appropriate.

1. Confirm the signal: cuff size/position, arterial transducer levelled at the right atrium, damping assessment, ECG lead integrity, pulse oximeter waveform.
2. Reduce the insult: decrease volatile concentration, pause propofol/remifentanil boluses, treat high neuraxial block, correct hypoxia, hypercarbia, acidosis, hypothermia and electrolyte disturbance.
3. Assess preload and fluid responsiveness: surgical loss, venous return, airway pressures, dynamic indices where valid. Pulse pressure variation or stroke volume variation >12–13% suggests fluid responsiveness only during controlled ventilation, sinus rhythm, tidal volume usually ≥8 ml kg⁻¹, closed chest and no marked right ventricular dysfunction.
4. Choose vasoactive therapy by mechanism: pure vasoconstrictor for vasodilatation with preserved cardiac output; inotrope for pump failure; chronotrope/pacing for symptomatic bradycardia; vasodilator for excessive afterload or hypertensive crisis.

Key cardiovascular drugs used perioperatively

Drug/class	Typical adult dose	Mechanism and examination points	Important adverse effects
Phenylephrine	50–100 micrograms IV bolus; infusion 0.2–1.5 micrograms kg−1 min−1	Selective α1 agonist; increases SVR and venous return; reflex bradycardia may reduce CO. Useful after propofol/volatile/neuroaxial vasodilatation.	Bradycardia, reduced uteroplacental or splanchnic flow if excessive, hypertension.
Metaraminol	0.25–1 mg IV bolus; infusion 1–10 mg h−1	Direct α1 agonism plus indirect noradrenaline release; common UK obstetric/general anaesthetic vasopressor.	Tachyphylaxis, reflex bradycardia, extravasation injury.
Noradrenaline	0.02–1 micrograms kg−1 min−1	α1 predominant with β1 support; first-line vasopressor in septic/distributive shock per Surviving Sepsis Campaign, target MAP 65 mmHg initially.	Ischaemia, arrhythmia, extravasation; requires reliable central or well-sited peripheral access with close monitoring.
Ephedrine	3–9 mg IV bolus	Indirect sympathomimetic with α/β effects; increases HR and CO. Less predictable in catecholamine-depleted patients; crosses placenta more than phenylephrine.	Tachycardia, increased myocardial oxygen demand, tachyphylaxis.
Adrenaline	Inotrope 0.02–0.2 micrograms kg−1 min−1; cardiac arrest 1 mg IV every 3–5 min	β1/β2 at low dose, α at higher dose; indicated in anaphylaxis, profound myocardial depression, arrest.	Lactic acidosis, tachyarrhythmias, hyperglycaemia, increased myocardial oxygen consumption.
Dobutamine	2.5–20 micrograms kg−1 min−1	β1 inotrope with β2 vasodilatation; useful for low-output states with adequate perfusion pressure.	Hypotension, tachycardia, arrhythmias.
Glyceryl trinitrate	5–200 micrograms min−1 IV	NO donor; venodilatation > arteriolar dilatation, reduces preload and coronary spasm; useful in ischaemia with hypertension/pulmonary oedema.	Hypotension, headache, tachyphylaxis, worsened RV infarction.
Esmolol	0.5 mg kg−1 bolus; 50–200 micrograms kg−1 min−1	β1-selective; esterase metabolism, half-life approximately 9 min; blunts intubation response and treats perioperative tachycardia.	Bradycardia, bronchospasm at high dose, heart failure exacerbation.

Management of common perioperative cardiovascular syndromes

Hypotension after induction usually reflects reduced sympathetic tone, venodilatation, myocardial depression and impaired baroreflexes. Propofol should be titrated cautiously in elderly or hypovolaemic patients; etomidate 0.15–0.3 mg kg⁻¹ or ketamine 0.5–1 mg kg⁻¹ may better preserve arterial pressure, although ketamine may depress myocardium in catecholamine-depleted shock. Treat bradycardic hypotension with atropine 0.5–1 mg IV, glycopyrronium 200–400 micrograms IV, or adrenaline increments 10–50 micrograms IV if severe. Consider high spinal, venous gas/air embolism, anaphylaxis, tension pneumothorax, haemorrhage and tamponade when hypotension is abrupt or refractory.

Hypertension and tachycardia require analgesia, depth of anaesthesia, oxygenation and CO₂ correction before antihypertensives. Labetalol 5–20 mg IV increments, esmolol, GTN, nicardipine 1–5 mg h⁻¹, or magnesium sulphate 30–50 mg kg⁻¹ IV may be selected according to mechanism. Avoid precipitous reductions in chronic hypertension; cerebral and renal autoregulation are right-shifted.

Myocardial ischaemia is managed by restoring oxygen supply-demand balance: maintain MAP/diastolic pressure, treat tachycardia, optimise haemoglobin and oxygenation, reduce wall stress, and obtain 12-lead ECG and troponins. Perioperative myocardial injury is often silent; high-sensitivity troponin surveillance is recommended in high-risk patients by several contemporary perioperative guidelines. Continue chronic β-blockers and statins; do not start high-dose β-blockade immediately before surgery, reflecting POISE trial findings of fewer infarctions but more stroke and mortality with aggressive metoprolol initiation.

Procedures, monitoring and follow-up

• Invasive arterial pressure monitoring is indicated for major surgery, vasoactive infusions, severe cardiovascular disease, or anticipated rapid haemodynamic change. It permits beat-to-beat pressure, blood sampling and dynamic indices, but complications include thrombosis, haematoma, infection and distal ischaemia.
• Central venous access facilitates vasopressors and central venous oxygen saturation, but CVP poorly predicts fluid responsiveness; trends and context matter more than absolute values.
• Cardiac output monitoring includes oesophageal Doppler, pulse contour analysis, lithium/thermodilution and echocardiography. Goal-directed therapy using stroke volume optimisation and avoidance of positive fluid balance has evidence for reducing complications in high-risk major surgery, although effect size varies by baseline risk and protocol.
• Echocardiography rapidly differentiates hypovolaemia, LV/RV failure, tamponade, severe valvular disease and pulmonary embolism. Focused perioperative TTE/TOE is a high-yield escalation when shock is unexplained.
• Postoperative care includes HDU/ICU for ongoing vasopressors, significant myocardial injury, arrhythmias or organ hypoperfusion. Follow-up should document haemodynamic events, drug exposure, ECG/troponin results, renal function, medication reconciliation and communication to cardiology/primary teams where myocardial injury or new heart failure/arrhythmia occurred.

Exam controversies and advanced synthesis

Haemodynamic targets: physiology, guidelines and trial evidence

In the Primary FRCA viva, avoid presenting a single “normal blood pressure” target. The relevant endpoint is organ perfusion pressure, which depends on autoregulation, venous pressure and regional vascular tone. Cerebral and renal autoregulation are often impaired in chronic hypertension, sepsis, diabetes and elderly patients, so a MAP of 65 mmHg may be inadequate in some patients despite being a common threshold in trials and guidelines.

Clinical context	Common target	Exam controversy
Non-cardiac surgery	Avoid MAP <65 mmHg or systolic BP <90 mmHg; avoid >20% fall from baseline in high-risk patients	Retrospective data associate even brief MAP <55 mmHg with myocardial injury and AKI, but causality and optimal treatment remain debated.
Septic shock	Surviving Sepsis Campaign: initial MAP ≥65 mmHg	Higher MAP 80–85 mmHg did not improve mortality overall in SEPSISPAM, but reduced renal replacement therapy in chronic hypertensives.
Traumatic brain injury	Maintain CPP usually 60–70 mmHg; avoid hypotension	Increasing MAP with vasopressors may improve CPP but can worsen bleeding, myocardial stress or pulmonary oedema.

POISE-2 is frequently cited: perioperative aspirin did not reduce death or non-fatal myocardial infarction but increased major bleeding; clonidine did not reduce death or myocardial infarction and increased clinically important hypotension and non-fatal cardiac arrest. Thus, haemodynamic “stability” must be judged by outcome, not merely by pharmacological elegance.

Vasopressors and inotropes: receptor theory versus clinical context

A common pitfall is to classify vasopressors simplistically as “good” or “bad”. The relevant variables are receptor profile, ventricular function, pulmonary vascular resistance, heart rate, preload responsiveness and arrhythmogenic substrate.

Drug	Typical perioperative dose	Key cardiovascular effects	Viva nuance
Phenylephrine	50–100 micrograms IV bolus; infusion 0.1–1 microgram/kg/min	Pure α1 vasoconstriction; ↑SVR, reflex bradycardia, often ↓CO	Useful in vasodilated, tachycardic patients; may reduce uteroplacental or right ventricular output if excessive.
Ephedrine	3–9 mg IV bolus	Indirect and direct α/β agonism; ↑HR and contractility	Tachyphylaxis; less predictable in catecholamine-depleted states or with MAOIs. Historically favoured in obstetrics, now often superseded by phenylephrine/noradrenaline strategies.
Noradrenaline	0.02–0.5 micrograms/kg/min IV infusion; dilute peripheral use increasingly accepted short-term via large vein	α predominant with modest β1; ↑MAP with less reflex bradycardia than phenylephrine	Increasingly used for post-induction vasoplegia; may preserve CO better than phenylephrine at equipressor doses.
Adrenaline	0.01–0.5 micrograms/kg/min infusion; cardiac arrest 1 mg IV	Dose-dependent β then α; ↑lactate, ↑arrhythmias, ↑myocardial oxygen demand	Excellent in anaphylaxis and low-output states, but lactataemia may reflect β2-driven glycolysis rather than hypoperfusion.
Dobutamine	2–20 micrograms/kg/min	β1 inotropy, β2 vasodilatation	May worsen hypotension unless vasoplegia is corrected; useful in low cardiac output with high filling pressures.

Anaesthetic technique: cardioprotection, harm signals and overstatement

Volatile anaesthetics produce dose-dependent myocardial depression, reduced SVR and blunting of baroreflexes; they also precondition myocardium through mitochondrial K_ATP channels, reduced calcium overload and attenuation of reperfusion injury. However, extrapolating cellular cardioprotection to hard clinical outcomes is controversial. Large comparative studies in cardiac surgery have not consistently shown mortality superiority of volatile anaesthesia over TIVA. Conversely, propofol causes venodilatation, arterial vasodilatation, impaired sympathetic tone and negative inotropy; hypotension is common after induction, particularly in hypovolaemia, frailty, severe aortic stenosis and β-blockade. Typical induction dosing should be titrated: propofol 1–2.5 mg/kg in healthy adults, but 0.5–1 mg/kg or less in shocked or elderly patients.

Etomidate 0.2–0.3 mg/kg remains haemodynamically attractive because it preserves sympathetic tone and baroreflexes, but it inhibits 11β-hydroxylase and can suppress cortisol synthesis after a single dose for 6–24 hours. Whether this worsens outcomes in sepsis is unresolved; many examiners expect balanced discussion rather than dogma. Ketamine 1–2 mg/kg IV usually increases HR, BP and CO via sympathetic stimulation, but in catecholamine-depleted shock its direct negative inotropy may dominate. Dexmedetomidine, with an elimination half-life of approximately 2 hours, causes central sympatholysis, bradycardia and hypotension; loading doses of 0.5–1 microgram/kg over 10 minutes are often avoided in unstable patients.

Perioperative cardiovascular drugs: guideline-sensitive pitfalls

• β-blockers: continue chronic therapy. Do not start high-dose β-blockade immediately preoperatively. POISE showed metoprolol reduced myocardial infarction but increased stroke and mortality, largely through hypotension and bradycardia.
• ACE inhibitors/ARBs: commonly withheld on the day of surgery for hypertension because of refractory post-induction vasoplegia; continuation may be appropriate in heart failure after individual risk assessment.
• Statins: continue perioperatively; abrupt withdrawal is undesirable in vascular patients.
• Antiplatelets/anticoagulants: decisions depend on stent timing, bleeding risk and neuraxial safety. Recent coronary stents require specialist planning; stopping dual antiplatelet therapy may be more dangerous than surgical bleeding in high-risk windows.

Advanced viva integration

For any drug-induced cardiovascular change, structure the answer around preload, afterload, contractility, heart rate/rhythm, coronary perfusion and autonomic reflexes. Severe aortic stenosis illustrates the synthesis: avoid tachycardia, bradycardia, vasodilatation and myocardial depression; maintain sinus rhythm and coronary perfusion pressure. In hypertrophic obstructive cardiomyopathy, avoid reduced preload, reduced afterload and increased contractility; phenylephrine is often preferable to inotropes. In right ventricular failure, excessive α-mediated pulmonary vasoconstriction and high airway pressures can be catastrophic; consider noradrenaline, vasopressin 0.01–0.04 units/min, inodilators, pulmonary vasodilators and meticulous ventilation. The highest-scoring answers explicitly link receptor pharmacology to ventricular-arterial coupling and patient-specific pathophysiology.