Post-bypass vasoplegia

Surgical approach (context: cardiac surgery with CPB)

• Median sternotomy (or minimally invasive approach), systemic heparinisation, aortic + venous cannulation, initiation of CPB
  • Myocardial protection with cardioplegia; temperature management (mild hypothermia common)
  • Surgical correction (e.g. CABG, valve surgery, aortic surgery) then rewarming and separation from CPB
• Protamine reversal of heparin; haemostasis; pacing wires and drains; chest closure
  • Surgeon will exclude surgical bleeding/tamponade if hypotension persists post-bypass

Anaesthetic management (context: cardiac surgery with CPB; vasoplegia occurs peri-separation/post-CPB)

• Type of anaesthesia: General anaesthesia with invasive monitoring
  • Airway: ETT (almost always); lung isolation only if specific indication
  • Duration: typically 3–6+ hours depending on procedure complexity
  • Pain: moderate–severe (sternotomy); multimodal analgesia + regional options (e.g. parasternal blocks) as per local practice
• Key monitoring: arterial line, central access, temperature, urine output; TOE commonly used; consider pulmonary artery catheter in high-risk cases
  • Haemodynamic targets post-CPB: adequate MAP for coronary/cerebral perfusion; individualise (often MAP ≥ 65–75 mmHg; higher if chronic HTN/carotid disease)
• Vasoplegia management is primarily haemodynamic + pharmacological; exclude bleeding/tamponade/ventricular dysfunction first (TOE + surgical field)
  • Early vasopressors (noradrenaline first-line) and vasopressin; consider methylene blue/hydroxocobalamin/angiotensin II in refractory cases

Definition and diagnostic features

• Post-bypass vasoplegia (vasoplegic syndrome): distributive shock occurring during/after separation from CPB characterised by low SVR with normal/high cardiac output and hypotension requiring vasopressors
• Typical haemodynamics (guide): MAP < 65 mmHg despite adequate preload; SVR low (e.g. < 800 dyn·s·cm−5); CI normal/high (e.g. > 2.2–2.5 L·min−1·m−2); low filling pressures may or may not be present
• Clinical clues: warm peripheries, wide pulse pressure, low diastolic pressure, high vasopressor requirement, rising lactate if prolonged
• Timing: commonly immediately post-CPB or early ICU period; can be precipitated/worsened by protamine reaction or systemic inflammatory response

Epidemiology and risk factors

• Incidence varies (commonly quoted ~5–25% depending on definition and population); associated with increased ICU stay, AKI, and mortality when severe/refractory
• Patient factors: pre-op ACE inhibitor/ARB use, beta-blockers (less consistent), chronic heart failure/low EF, vasodilatory states, liver disease, chronic renal impairment, diabetes, obesity
• Surgical/CPB factors: prolonged CPB time, complex procedures, re-do surgery, aortic surgery, deep hypothermia, large transfusion/inflammation
• Drug/biochemical factors: heparin–protamine effects, relative vasopressin deficiency post-CPB, catecholamine receptor desensitisation

Pathophysiology (high-yield mechanisms)

• Systemic inflammatory response to CPB: cytokines/complement activation → endothelial dysfunction, vasodilatation, capillary leak
• Excess nitric oxide (NO) production (iNOS upregulation) → increased cGMP → vascular smooth muscle relaxation and catecholamine hyporesponsiveness
• Relative vasopressin deficiency after CPB (depleted stores) → reduced V1-mediated vasoconstriction; contributes to noradrenaline-refractory hypotension
• KATP channel activation and acidosis/hypothermia → reduced vascular tone and reduced response to catecholamines
• Microcirculatory dysfunction and capillary leak → intravascular hypovolaemia despite total body fluid excess

Differential diagnosis of hypotension post-CPB (must-exclude list)

• Bleeding/hypovolaemia (surgical field, drains, Hb, coagulation; TOE: small ventricles)
• Cardiogenic causes: LV/RV dysfunction, ischaemia, graft/valve problem, air embolism; TOE essential
• Mechanical: tamponade (clotted drains), tension pneumothorax, dynamic LVOT obstruction (esp. post-mitral repair), aortic dissection
• Arrhythmia/pacing issues: AF, junctional rhythm, heart block, loss of AV synchrony; check pacing wires and electrolytes
• Protamine reaction: hypotension, pulmonary hypertension, RV failure, anaphylactoid features; timing around protamine administration
• Sepsis (less immediate), adrenal insufficiency (rare but consider in refractory shock), anaphylaxis to drugs/latex

Immediate assessment and investigations (peri-separation/post-CPB)

• Structured approach: confirm MAP/arterial trace; check for artefact; ensure adequate oxygenation/ventilation, anaesthetic depth, temperature, acid–base, ionised calcium
• TOE: assess ventricular function, volume status, valvular/graft issues, tamponade, RV strain, LVOT obstruction, intracardiac air
• Haemodynamic monitoring: CI/SVR if available (PAC or calibrated pulse contour); trend lactate, ScvO2/SvO2, urine output
• Labs: ABG (lactate, Hb), electrolytes incl. Ca2+/K+/Mg2+, coagulation/TEG/ROTEM, glucose

Management principles (stepwise, exam-structured)

• 1) Optimise basics: oxygenation/ventilation, correct acidosis, rewarm, correct hypocalcaemia, treat arrhythmias, ensure adequate anaesthesia/analgesia
• 2) Ensure adequate preload but avoid indiscriminate fluid: small boluses guided by TOE/dynamic indices; consider capillary leak—albumin/crystalloid per local practice; early blood if bleeding
• 3) First-line vasopressor: noradrenaline titrated to MAP target; consider adrenaline if mixed vasoplegia + low output
  • Aim: restore coronary perfusion pressure (diastolic pressure important) and maintain organ perfusion
• 4) Add vasopressin early if high NA requirement or suspected vasopressin deficiency (common post-CPB)
  • Typical infusion: 0.01–0.04 units/min (institution dependent); avoid higher doses due to ischaemia risk
• 5) Refractory vasoplegia (despite NA + vasopressin and optimisation): consider methylene blue, hydroxocobalamin, angiotensin II; consider corticosteroids if adrenal insufficiency suspected
  • Methylene blue: inhibits NO–cGMP pathway (guanylate cyclase inhibition); typical dose 1–2 mg/kg IV over 10–20 min (may follow with infusion per protocol)
  • Hydroxocobalamin: NO scavenger; typical dose 5 g IV over 10–15 min (may repeat); causes red discolouration of skin/urine and interferes with some lab assays
  • Angiotensin II: potent vasoconstrictor; consider in catecholamine-resistant shock with specialist input; monitor for thrombosis/ischaemia
  • Steroids: e.g. hydrocortisone 50 mg IV q6h (or 100 mg bolus then infusion per local policy) if refractory shock/relative adrenal insufficiency considered
• 6) If haemodynamics unstable: return to CPB may be required while diagnosing/treating (e.g. tamponade, severe ventricular dysfunction, protamine reaction)
• 7) ICU management: ongoing vasopressor titration, fluid balance, lactate clearance, renal protection, early source identification if infection suspected, avoid excessive haemodilution

Drug notes and cautions (high-yield)

• Noradrenaline: first-line; improves MAP primarily via α1; may increase afterload—ensure LV function adequate
• Vasopressin: V1-mediated vasoconstriction; catecholamine-sparing; may reduce pulmonary vascular effects compared with high-dose catecholamines; risks: digital/mesenteric ischaemia, hyponatraemia (less relevant acutely)
• Methylene blue cautions: contraindicated in G6PD deficiency (haemolysis risk); risk of serotonin syndrome with SSRIs/SNRIs/MAOIs; may cause pulmonary vasoconstriction; interferes with pulse oximetry readings
• Hydroxocobalamin cautions: can cause hypertension; chromaturia and discoloration; may trigger false alarms in dialysis machines and affect co-oximetry/lab assays
• Angiotensin II cautions: thromboembolic risk; ensure VTE prophylaxis and monitor limb/mesenteric perfusion; specialist/ICU-led use

Outcomes and prevention (what to mention in viva)

• Consequences: prolonged vasopressor use, AKI, gut ischaemia, delirium, increased ICU/hospital length of stay; mortality increases with severity and refractory shock
• Prevention/mitigation: identify high-risk patients (ACEi/ARB, long CPB); consider withholding ACEi/ARB pre-op per local policy; minimise CPB time/inflammation; maintain temperature and acid–base; early vasopressin in high NA requirement
• Communication: early discussion with surgeon/perfusionist/ICU; agree MAP target (e.g. carotid disease, chronic HTN); document vasoplegia and therapies used