Mixed Shock

Mixed shock is circulatory failure from two or more concurrent mechanisms: hypovolaemic, cardiogenic, obstructive and distributive. Examples are septic shock with septic cardiomyopathy, haemorrhage with tension pneumothorax, myocardial infarction with sepsis, and pulmonary embolism with hypovolaemia.

Epidemiology. Many patients in intensive care have more than one shock mechanism. Mortality is higher than for single mechanism shock and treatment of one cause may worsen another.

Common combinations.

• Septic and cardiogenic (septic cardiomyopathy, stress cardiomyopathy).
• Hypovolaemic and cardiogenic (haemorrhage in coronary disease).
• Hypovolaemic and obstructive (trauma with tamponade or tension pneumothorax).
• Distributive and hypovolaemic (pancreatitis, burns, anaphylaxis).
• Cardiogenic and obstructive (pulmonary embolism with right ventricular failure).

Pathophysiology. Combined loss of preload, contractility, afterload or flow. Therapy for one component (large fluid volume, vasopressor, inotrope) can harm another, for example fluid in a failing ventricle, or vasoconstriction in low output.

Presentation is hypotension with mixed signs: warm and cold peripheries together, raised or low jugular venous pressure, pulmonary oedema with poor perfusion, or rising lactate despite treatment. Failure to respond to treatment for the apparent cause is a clue.

Red flags.

• Shock persisting after correction of the obvious cause.
• Rising lactate with high filling pressures, or hypotension with pulmonary oedema.
• Cardiac arrest risk with arrhythmia.

Bedside echocardiography and focused ultrasound (heart, inferior vena cava, lungs, abdomen, pleura, veins) at once and repeatedly. Measure lactate, central venous oxygen saturation, troponin, natriuretic peptide, haemoglobin, cultures, ECG and chest radiograph. Add cardiac output monitoring in complex cases. CT or angiography once stable.

Differential diagnosis. Each single shock type, with each tested for by ultrasound, plus adrenal crisis and drug effects.

Principle. Treat every component at once, order by threat to life, and reassess after each step.

Obstructive causes first. Needle or finger decompression and chest drain for tension pneumothorax, pericardiocentesis for tamponade, and reperfusion for massive pulmonary embolism (alteplase 100 mg IV over 2 hours, or 50 mg bolus in arrest, with unfractionated heparin).

Bleeding. Control the source, give balanced blood products (1 red cell unit to 1 plasma to 1 platelet pool), tranexamic acid 1 g IV over 10 minutes then 1 g over 8 hours in trauma or surgical bleeding.

Sepsis. Antibiotics within 1 hour and source control, with 500 mL fluid boluses directed by response.

Vasopressor and inotrope choice.

• Noradrenaline 0.05 to 1 microgram/kg/min for hypotension.
• Dobutamine 2.5 to 20 microgram/kg/min when cardiac output is low and pressure adequate.
• Adrenaline 0.05 to 0.5 microgram/kg/min when both vasopressor and inotrope are needed.
• Vasopressin 0.03 units/min to spare catecholamine dose.
• Milrinone 0.25 to 0.75 microgram/kg/min (reduce in renal impairment) in right ventricular failure with high pulmonary resistance.

Mechanical support. Intra-aortic balloon pump, microaxial pump or venoarterial ECMO for cardiogenic or mixed shock with persistent hypoperfusion despite maximal support.

Fluid. Give small boluses (250 to 500 mL), checking response with passive leg raising or pulse pressure variation (in the ventilated), and stop when there is no response or pulmonary oedema.

Monitoring. Continuous arterial pressure, ECG, lactate every 1 to 2 hours, cardiac output, urine output and serial ultrasound.

Referral and escalation. Intensive care, cardiology, surgery and extracorporeal support teams.

Special groups. In pregnancy, left lateral tilt and obstetric input. In older adults, expect limited reserve to fluid or vasopressors.