Directed management

1. Adequate monitoring (e.g. pulmonary artery catheterisation) and investigation (echocardiography).

2. If evidence exists for hypovolaemia, give 100-200ml colloid fluid challenges to achieve optimal stroke volume.

3. If vasoconstriction persists (SVR >1400dyn/s/cm5), titrate nitrate infusion further to optimise stroke volume and, ideally, reduce SVR <1300dyn/s/cm5. If hypovolaemia is suspected (i.e. stroke volume falls), fluid challenges should be given to re-optimise the stroke volume. Within 24h of nitrate infusion, commence ACE inhibition, initially at low dose but rapidly increased to appropriate long-term doses.

4. Inotropes are indicated if evidence of tissue hypoperfusion, hypotension or vasoconstriction persists despite optimal fluid loading and nitrate dosing. Consider epinephrine, dobutamine or milrinone; while epinephrine may sometimes cause excessive constriction, dobutamine and milrinone may excessively vasodilate. Levosimendan increases cardiac output though not at the expense of increased cardiac work.

5. Intra-aortic balloon counterpulsation augments cardiac output, reduces cardiac work and improves coronary artery perfusion.

6. Angioplasty or surgical revascularization are beneficial if performed early after myocardial infarct. Surgery may also be necessary for mechanical defects, e.g. acute mitral regurgitation.

1. BP and cardiac output adequate to maintain organ perfusion (e.g. no oliguria, confusion, dyspnoea nor metabolic acidosis). A mean BP of 60mmHg is usually sufficient but may need to be higher, especially if premorbid blood pressures are high.

2. A mixed venous oxygen saturation >60%. Excessive inotropes should be avoided as myocardial oxygen demand is increased.

3. Symptomatic relief.

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