Vasoplegic Shock

Vasoplegic shock is distributive shock with profound loss of vascular tone: low mean arterial pressure (under 50 to 65 mmHg), low systemic vascular resistance (under 800 dyn.s/cm5), and normal or high cardiac output (cardiac index over 2.2 L/min/m2), refractory to usual doses of catecholamines and fluid.

Epidemiology. Vasoplegia occurs in about 5 to 25% of patients after cardiac surgery with cardiopulmonary bypass, with higher rates after heart transplant, ventricular assist device implantation and in those taking angiotensin converting enzyme inhibitors or receptor blockers.

Causes and associations. Cardiopulmonary bypass, cardiac transplantation, sepsis, anaphylaxis, protamine reaction, severe burns, liver failure, pancreatitis, adrenal insufficiency, prolonged ischaemia and reperfusion, and drug toxicity (calcium channel blockers, nitrates).

Risk factors after cardiac surgery. Preoperative angiotensin converting enzyme inhibitor or receptor blocker use, amiodarone, beta blocker, low ejection fraction, long bypass time, endocarditis and preoperative heart failure.

Pathophysiology. Inflammatory activation, nitric oxide excess, potassium channel activation (ATP-sensitive channels) in smooth muscle, vasopressin deficiency and catecholamine receptor downregulation reduce vascular tone.

Presentation is hypotension with warm peripheries, brisk capillary refill, low diastolic pressure, normal or high cardiac output, rising vasopressor needs and rising lactate in late cases. Fever and leucocytosis may be present.

Red flags.

• Noradrenaline over 0.25 microgram/kg/min, or lactate rising.
• Rapid onset after protamine, blood product or drug.
• Mesenteric, renal or limb ischaemia during treatment.

Haemodynamic profile by arterial line and cardiac output measurement or echocardiography: low systemic vascular resistance with normal or high cardiac output. Exclude hypovolaemia, bleeding, tamponade, tension pneumothorax, anaphylaxis, sepsis (cultures, lactate, procalcitonin), adrenal insufficiency (cortisol) and myocardial dysfunction.

Differential diagnosis. Septic shock, anaphylaxis, adrenal crisis, cardiogenic shock, hypovolaemia and neurogenic shock.

Fluid. Correct hypovolaemia only. Avoid excessive crystalloid.

Vasopressors.

• Noradrenaline 0.05 to 1 microgram/kg/min.
• Vasopressin 0.03 to 0.06 units/min added early, since it is effective in vasopressin deficient states. Doses over 0.06 units/min raise ischaemic risk.
• Phenylephrine 0.5 to 6 microgram/kg/min only for tachyarrhythmia with preserved cardiac output.

Rescue therapy.

• Methylene blue 1.5 to 2 mg/kg IV over 20 to 30 minutes, which can be followed by an infusion of 0.25 to 1 mg/kg/h for a limited time. Avoid in G6PD deficiency, pulmonary hypertension and with serotonergic drugs. Expect transient oximetry error and blue urine.
• Hydroxocobalamin 5 g IV over 15 to 30 minutes, which scavenges nitric oxide and hydrogen sulphide. It interferes with co-oximetry and creatinine assays.
• Angiotensin II 10 to 20 nanogram/kg/min, titrated to a maximum of 80 nanogram/kg/min in the first 3 hours (maintenance up to 40 nanogram/kg/min), where available.

Corticosteroid. Hydrocortisone 50 mg IV every 6 hours, or 200 mg daily by infusion, when refractory.

Correct metabolic factors. Ionised calcium over 1.1 mmol/L (calcium chloride 10% 10 mL IV), pH over 7.2, normothermia.

Reverse the cause. Stop angiotensin converting enzyme inhibitors, treat anaphylaxis, treat sepsis and drain collections.

Monitoring. Arterial pressure, cardiac output, lactate, urine output, mixed venous saturation and limb perfusion.

Referral and escalation. Cardiac intensive care and the surgical team. Consider mechanical support when there is mixed shock with myocardial dysfunction.

Special groups. After heart transplant, check graft function. In renal impairment, avoid nephrotoxic rescue dosing.