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flerwiJtfirç mtlifcQfca&^Sitt^to&Ciirt ¡Bijdfli itrtttil of an)- evfcrce il pîtssirç «te™ (Sfefl tf> ES Table 2 Therapeutic endpoints

Pharmacological support

The choice of therapeutic agent is dictated by therapeutic benefit, familiarity, and desired pharmacological action. If a drug proves unpredictably detrimental, it should either be substituted by another agent that achieves the required effect or any hitherto unrecognized problem should be dealt with appropriately. Dobutamine may be used as an illustrative agent for both circumstances: in some patients it may induce excessive vasodilatation and hypotension and require substitution with epinephrine, whereas generation of tachycardia or tachyarrhythmias implies possible concurrent hypovolemia requiring volume administration. Familiarity with the drugs being used and awareness of both their actions and potential side-effects are crucial.

1. Oxygen should be administered to ensure (near) complete arterial oxygenation.

2. Pain secondary to ongoing myocardial ischemia is best treated by nitrates, although opiates are useful for their additional anxiolytic and vasodilating properties.

3. Vasodilator agents such as glyceryl trinitrate, hydralazine, and sodium nitroprusside all have effects on both preload and afterload. Significant falls in blood pressure with small doses of the above imply either hypovolemia or flow obstruction. Nitrate tolerance develops after 24 h, with increasing doses required to maintain effect. Cyanide accumulation may develop after 24 h with sodium nitroprusside usage. It is this author's preference to commence angiotensin-converting enzyme inhibitors such as captopril at this time, provided that blood pressure and lack of contraindications permit, in rapidly escalating dosage while slowly weaning the original vasodilator.

4. Judicious fluid challenges are often appropriate as the heart failure patient often arrives in the intensive care unit in a hypovolemic state. The endpoint is no rise in stroke volume to a 100- to 200-ml fluid challenge. In the absence of flow monitoring, a rise in central venous or wedge pressure of 3 mmHg or more following a fluid challenge is suggestive of an adequately filled intravascular compartment.

5. Loop diuretics are often inappropriate and detrimental in the first instance for the reasons described earlier. However, they may be indicated in fluid-overload situations, when the patient is on chronic diuretic therapy, and when symptoms or oliguria persist after adequate loading with fluid and angiotensin-converting enzyme inhibitors.

6. Inotropes are indicated where low pressure and/or low output result in inadequate organ function. Epinephrine usually produces consistent rises in both. Inotropes with associated vasodilator activity, including dobutamine, dopexamine, enoximone, and milrinone, may all usefully improve output although they can occasionally produce excessive falls in blood pressure.

7. Pressors are rarely indicated, although norepinephrine (noradrenaline) is occasionally needed to generate a blood pressure sufficient to perfuse the organs, in particular the heart, to generate an adequate output. These agents should never be used without flow monitoring as they will more frequently compromise flow in the heart failure patient.

Mechanical support

For the reasons described above, positive-pressure ventilation with or without positive end-expiratory pressure (PEEP), CPAP, intra-aortic balloon counterpulsation, and venticular assist devices may be useful adjuncts to treatment. In particular, mechanical ventilation is a much underestimated support mode.

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