Cardiopulmonary bypass: principles and physiology

11 min read Last updated April 8, 2026

Surgical approach (typical steps in cardiac surgery using CPB)

  • Median sternotomy (most common) or minimally invasive thoracotomy (selected cases)
  • Systemic heparinisation → confirm adequate anticoagulation (ACT target set by unit)
  • Cannulation
    • Venous: right atrial (single 2-stage) or bicaval (SVC/IVC) cannulae
    • Arterial: ascending aorta (commonest); alternatives: femoral/axillary (redo/aortic pathology)
    • Optional: LV vent (via pulmonary vein/LA/LV) to prevent distension; aortic root vent
  • Commence CPB: venous drainage to reservoir → pump → oxygenator/heat exchanger → arterial return
  • Aortic cross-clamp (for arrested-heart surgery) and cardioplegia delivery
    • Cardioplegia routes: antegrade (aortic root/coronary ostia) ± retrograde (coronary sinus)
    • Temperature strategy: normothermic, mild/moderate hypothermia; deep hypothermic circulatory arrest in selected aortic cases
  • Surgical repair/replacement (CABG/valve/aortic) while perfusion maintained by CPB
  • Rewarming, de-airing, remove cross-clamp, reperfusion; restore rhythm (pacing/defib as needed)
  • Wean from CPB with optimisation of preload/afterload/contractility; remove cannulae; protamine reversal; haemostasis and closure

Anaesthetic management (overview)

  • Type of anaesthesia: General anaesthesia with invasive monitoring; TEE commonly used
  • Airway: cuffed ETT (almost always); lung isolation rarely needed (selected minimally invasive cases)
  • Duration: typically 3–6 hours (case dependent; redo/aortic procedures longer)
  • Analgesia: moderate–severe postoperative pain (sternotomy); multimodal + regional options (e.g., parasternal blocks/ESP) depending on anticoagulation and local practice
  • Monitoring/lines: arterial line pre-induction if unstable; large-bore IV; central line; temperature; urinary catheter; cerebral oximetry where available
  • Key anaesthetic phases: pre-CPB (induction/sternotomy), on-CPB (perfusion management), separation from CPB (inotropes/vasopressors, ventilation), haemostasis and ICU transfer

Aims of CPB and core concepts

  • Purpose: provide systemic perfusion and gas exchange while heart (and often lungs) are excluded from circulation
  • Key physiological differences vs native circulation: non-pulsatile (usually), haemodilution, hypothermia, altered microcirculation, blood–artificial surface interaction
  • Perfusion is typically flow-targeted with pressure as a surrogate of vascular tone and organ perfusion

CPB circuit: components and function

  • Venous drainage: gravity siphon or vacuum-assisted venous drainage (VAVD)
    • Determinants: cannula size/position, height differential, intrathoracic pressure, blood viscosity, VAVD level
  • Reservoir: collects venous return; allows volume buffering; risk of air entrainment if level low
  • Pump: roller or centrifugal
    • Roller: fixed stroke volume; risk of tubing wear/spallation; can generate high line pressures if occluded
    • Centrifugal: flow depends on afterload and preload; lower risk of massive overpressure; can entrain air if not managed
  • Oxygenator: membrane oxygenator provides O2 uptake and CO2 removal; includes heat exchanger
    • Gas flow (“sweep”) primarily controls CO2 removal; FiO2 controls PaO2 (within limits)
  • Arterial line filter and bubble trap: reduce particulate and gaseous microemboli
  • Cardiotomy suction/cell salvage: returns shed blood but increases lipid/air/activated mediator load; may worsen coagulopathy/inflammation
  • Prime: crystalloid ± colloid ± blood; causes haemodilution and reduced oncotic pressure

Anticoagulation and monitoring (heparin/ACT/protamine)

  • Unfractionated heparin: potentiates antithrombin → inhibits thrombin (IIa) and Xa; prevents circuit thrombosis
  • Typical dosing: 300–400 units/kg IV before cannulation (unit-dependent) + additional doses guided by ACT/heparin concentration
  • Monitoring: ACT baseline then post-heparin; target commonly ≥ 480 s for CPB (varies with equipment/strategy)
  • Heparin resistance: failure to achieve target ACT after adequate heparin
    • Causes: antithrombin deficiency (common), prior heparin exposure, high factor VIII/fibrinogen, sepsis/inflammation, thrombocytosis
    • Management: additional heparin; antithrombin concentrate or FFP; consider alternative anticoagulation in HIT (e.g., bivalirudin) with specialist protocol
  • Protamine reversal: positively charged protein binds heparin; dose often based on heparin dose/concentration; avoid over-reversal (anticoagulant effect)
  • Protamine reactions: hypotension (rapid infusion), anaphylactoid/anaphylaxis, pulmonary hypertension/right heart failure, complement activation
    • Risk factors: prior protamine exposure, NPH insulin use, fish allergy, prior vasectomy (association described)
    • Management: stop/slow infusion, vasopressors, treat anaphylaxis, consider inhaled pulmonary vasodilators for PHT, return to CPB if severe

Perfusion targets and oxygen delivery (DO2)

  • Flow: commonly 2.2–2.6 L/min/m² (cardiac index equivalent), adjusted for temperature, metabolic demand, anaemia, and patient factors
  • Pressure: MAP often targeted 50–80 mmHg (individualised: chronic hypertension, cerebrovascular disease, carotid disease may need higher)
  • Oxygen delivery: DO2 = Flow × CaO2; CaO2 depends mainly on Hb and SaO2
    • CaO2 ≈ (1.34 × Hb × SaO2) + (0.003 × PaO2)
    • Critical DO2 concept: below a threshold, VO2 becomes supply-dependent → anaerobic metabolism, rising lactate, organ injury (AKI risk)
  • Indicators of adequacy: mixed/venous saturation (SvO2), lactate, NIRS (regional), urine output (imperfect), acid–base status

Temperature management and acid–base strategies

  • Hypothermia reduces metabolic rate (CMRO2 falls ~6–7% per °C) and provides organ protection but increases viscosity and impairs coagulation
  • Rewarming: avoid rapid gradients and hyperthermia; aim for controlled rewarming and normothermia at separation
  • Acid–base management during hypothermia
    • Alpha-stat: interpret gases at 37°C without temperature correction; maintains intracellular charge neutrality; preserves autoregulation (common in adults)
    • pH-stat: correct gases to patient temperature and add CO2 to maintain pH 7.40 at that temperature; increases CBF via hypercapnia; used in deep hypothermia/paediatrics to improve cooling uniformity

Haemodilution, viscosity, and microcirculation

  • Haemodilution from prime reduces Hb and oncotic pressure → tissue oedema; lowers viscosity which may improve microcirculatory flow but reduces O2 carrying capacity
  • Transfusion strategy varies; balance DO2, bleeding risk, and transfusion harms; consider ultrafiltration/modified ultrafiltration (esp. paediatrics) to concentrate blood and remove inflammatory mediators

Inflammatory and coagulation effects of CPB

  • Blood contact with non-endothelial surfaces → complement activation, cytokines, leukocyte activation, endothelial dysfunction → SIRS-like picture
  • Coagulopathy mechanisms
    • Dilution of clotting factors/platelets; platelet activation/dysfunction; hypothermia; fibrinolysis; consumption; residual heparin; protamine excess
    • Shed mediastinal blood reinfusion increases activated factors and fibrinolysis; cell salvage preferred over unprocessed cardiotomy suction where feasible
  • Point-of-care testing (TEG/ROTEM) guides targeted therapy: fibrinogen, platelets, PCC/FFP, antifibrinolytics

Organ physiology on CPB

  • Brain: risks from emboli (air/particulate), hypoperfusion, impaired autoregulation, hyperthermia; delirium and stroke are key complications
    • Maintain adequate MAP/flow, avoid hyperthermia, meticulous de-airing, consider NIRS and prompt correction of desaturation
  • Heart: myocardial protection via cardioplegia and hypothermia; reperfusion injury and stunning can occur; risk of air in coronaries
  • Lungs: largely unperfused during CPB → atelectasis, inflammatory lung injury; post-CPB increased shunt and pulmonary vascular reactivity
  • Kidneys: AKI risk from low DO2, haemolysis, inflammation, emboli, venous congestion; urine output may be misleading on CPB
  • Liver/GI: splanchnic hypoperfusion and endotoxin translocation contribute to inflammation; maintain perfusion and avoid prolonged low-flow states
  • Endocrine/metabolic: stress response, insulin resistance; glucose control important but avoid hypoglycaemia

Gas management and ventilation around CPB

  • On CPB: lungs often not ventilated; oxygenation/CO2 controlled by oxygenator; consider CPAP/low ventilation strategy per local practice to reduce atelectasis
  • Pre-separation: recruit lungs, resume ventilation, check ETT position, manage pulmonary hypertension and RV function
  • V/Q changes post-CPB: increased shunt and dead space; treat with recruitment, PEEP, optimisation of haemodynamics, and addressing pulmonary oedema

Weaning from CPB: physiology and practical sequence

  • Prerequisites: normothermia (or planned target), adequate ventilation/oxygenation, rhythm control, corrected electrolytes (K+, Ca2+), Hb/volume status, surgical haemostasis reasonable
  • Gradually reduce pump flow while heart fills and ejects; adjust preload, afterload, and inotropy/chronotropy
  • Common issues and responses
    • Low cardiac output: check rhythm, ischaemia, ventricular function (TEE), preload, tamponade, graft/valve issues; start inotrope (e.g., adrenaline/dobutamine) ± mechanical support (IABP/VA-ECMO)
    • Vasoplegia (low SVR): vasopressors (noradrenaline/vasopressin), optimise Ca2+, consider methylene blue/hydroxocobalamin per protocol
    • RV failure/pulmonary hypertension: optimise oxygenation/ventilation, avoid acidosis, consider inhaled NO/prostacyclin, inotropes, reduce PVR

Complications specific to CPB

  • Air embolism: from venous line entrainment, low reservoir, surgical field; can cause stroke/MI
  • Atheroembolism: aortic manipulation/cannulation/cross-clamp; higher risk in atheromatous aorta
  • Haemolysis: high negative pressures (VAVD), suction, small cannulae, high shear; leads to pigment nephropathy and hyperkalaemia
  • Systemic inflammatory response/vasoplegia: capillary leak, hypotension, organ dysfunction
  • Coagulopathy and bleeding: multifactorial; may require targeted blood products and surgical haemostasis
  • Electrolyte/acid–base disturbances: K+ shifts (cardioplegia), hypocalcaemia (citrate), metabolic acidosis/alkalosis
Describe the cardiopulmonary bypass circuit and the function of each major component.

Structure your answer: venous drainage → reservoir → pump → oxygenator/heat exchanger → arterial filter → patient; plus suction/venting and monitoring.

  • Venous cannulae and drainage (gravity/VAVD): returns systemic venous blood to circuit
  • Reservoir: volume buffer; allows removal of air; risk if level low (air entrainment)
  • Pump (roller or centrifugal): generates forward flow; centrifugal flow depends on afterload/preload
  • Oxygenator: membrane gas exchange; sweep controls CO2; FiO2 controls oxygenation; includes heat exchanger for temperature control
  • Arterial line filter/bubble trap: reduces particulate and gaseous microemboli before arterial return
  • Cardiotomy suction/vents: return shed blood and decompress heart; contributes to inflammatory/coagulopathic burden
What perfusion targets would you use on CPB and how would you judge adequacy of perfusion?

Give flow and pressure ranges, then link to oxygen delivery and monitoring surrogates.

  • Flow: typically 2.2–2.6 L/min/m²; increase if anaemia, warming, high metabolic demand, rising lactate, low SvO2
  • MAP: often 50–80 mmHg; individualise (higher targets for chronic HTN, carotid disease, cerebrovascular disease)
  • Adequacy markers: SvO2, lactate trend, acid–base, NIRS, urine output (limited), temperature, haemoglobin/DO2
  • DO2 concept: DO2 = Flow × CaO2; optimise Hb/SaO2/flow to avoid supply-dependent VO2 and organ injury (AKI)
Explain alpha-stat and pH-stat strategies during hypothermic CPB. When might you choose each?

Define each, then discuss cerebral blood flow/autoregulation and typical adult vs deep hypothermia use.

  • Alpha-stat: blood gases analysed at 37°C; no temperature correction; maintains protein ionisation; preserves cerebral autoregulation (common adult strategy)
  • pH-stat: temperature-corrected gases; add CO2 to keep pH 7.40 at patient temperature; increases CBF (hypercapnia) and improves cooling uniformity
  • Use pH-stat more often in deep hypothermia/circulatory arrest (and paediatrics) where enhanced cooling and uniform cerebral temperature may be advantageous; accept potential increased embolic load due to higher CBF
Outline heparin anticoagulation for CPB, how you monitor it, and how you manage heparin resistance.

Include mechanism, dosing, ACT targets, causes of resistance, and management options.

  • UFH mechanism: potentiates antithrombin → inhibits thrombin (IIa) and Xa
  • Dose: commonly 300–400 units/kg IV pre-cannulation; confirm ACT response; top-up as required
  • Monitoring: ACT baseline and after heparin; typical target ≥ 480 s (unit-dependent); consider heparin concentration assays where available
  • Heparin resistance causes: antithrombin deficiency, high factor VIII/fibrinogen, prior heparin, inflammation
  • Management: additional heparin; give antithrombin concentrate or FFP; if HIT/contraindication consider direct thrombin inhibitor (e.g., bivalirudin) with specialist protocol
Describe protamine reversal and the adverse reactions to protamine. How would you manage a severe reaction?

Define mechanism, dosing principle, then classify reactions and immediate management including return to CPB.

  • Mechanism: protamine binds heparin to form inactive complex; dose often based on heparin dose/concentration; avoid excess protamine (can anticoagulate)
  • Adverse effects: hypotension (rapid infusion), anaphylaxis/anaphylactoid, pulmonary hypertension with RV failure, complement activation
  • Risk factors: NPH insulin, prior protamine exposure, fish allergy, prior vasectomy (association)
  • Management: stop/slow protamine; treat anaphylaxis (adrenaline, fluids, vasopressors); manage PHT with inhaled NO/prostacyclin; consider returning to CPB if cardiovascular collapse
What are the main causes of coagulopathy after CPB and how would you approach ongoing bleeding post-bypass?

Separate surgical bleeding from medical coagulopathy; use temperature, calcium, and point-of-care testing.

  • Causes: dilution of clotting factors/platelets, platelet dysfunction, hypothermia, fibrinolysis, residual heparin, protamine excess, inflammation, cardiotomy suction effects
  • Immediate checks: surgical source, temperature, ionised calcium, ACT (residual heparin), full blood count and fibrinogen
  • Use TEG/ROTEM to guide targeted therapy: fibrinogen replacement, platelets, PCC/FFP, antifibrinolytic if hyperfibrinolysis
  • Avoid iatrogenic contributors: excessive crystalloid, hypothermia, uncontrolled hypertension, protamine overdose
Discuss the physiological consequences of non-pulsatile flow and haemodilution during CPB.

Focus on microcirculation, oxygen delivery, renal/cerebral perfusion, and viscosity/oncotic pressure effects.

  • Non-pulsatile flow: may reduce microcirculatory shear and alter autoregulation; clinical significance debated; MAP becomes key surrogate for perfusion pressure
  • Haemodilution: reduced Hb → reduced CaO2 and DO2; reduced viscosity may improve flow but risks critical DO2; reduced oncotic pressure → tissue oedema
  • Practical response: optimise flow, Hb, temperature, and SVR; consider ultrafiltration to concentrate blood and reduce oedema
How does CPB affect the lungs and how do you optimise respiratory function when coming off bypass?

Mention atelectasis, inflammatory lung injury, shunt, and a practical ventilation plan.

  • During CPB: lungs often unventilated and underperfused → atelectasis; inflammatory mediator release contributes to increased permeability and pulmonary dysfunction
  • Post-CPB: increased shunt and dead space; risk pulmonary oedema; pulmonary hypertension may worsen RV function
  • Optimisation: recruitment manoeuvres, appropriate PEEP, avoid hyperoxia/hypocapnia extremes, ensure adequate LV function and diuresis/ultrafiltration if overloaded, consider inhaled pulmonary vasodilators if PHT
You are asked to help separate from CPB but the patient is profoundly hypotensive with good ventricular function on TEE. What is your differential and management?

This is a common FRCA-style weaning scenario: think vasoplegia, hypovolaemia, anaphylaxis/protamine, tamponade, outflow obstruction, and measurement error.

  • Differential: vasoplegia (low SVR), relative hypovolaemia, residual anaesthetic/vasodilators, protamine reaction/anaphylaxis, sepsis/SIRS, measurement error, occult bleeding; exclude tamponade even if function appears good
  • Immediate actions: confirm arterial trace/zeroing, check rhythm, ABG (lactate, Hb, iCa), temperature; communicate with perfusionist and surgeon
  • Treatment: increase CPB flow temporarily if needed; vasopressors (noradrenaline) ± vasopressin; optimise calcium; cautious volume; consider methylene blue/hydroxocobalamin per protocol if refractory

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