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problem here is one of distribution of fluid. Intravenous fluid therapy is almost always contra-indicated in patients with active signs of congestive heart failure. The only exception is as a means of delivery of drugs when
the patient is requires a constant rate infusion. Giving more fluid will only worsen the signs of congestion and probably not improve the signs of poor perfusion. Other ways of improving perfusion will be necessary.
Signs of poor perfusion may be improved in patients with heart failure by the administration of drugs that increase the force of cardiac contraction (inotropes) such as pimobendan or dobutamine; drugs that decrease vascular resistance (arteriodilators) such as pimobendan, Angiotensin Converting Enzyme (ACE) inhibitors or nitroprusside; and drugs that optimise cardiac rate and rhythm in patients with arrhythmias (anti-arrhythmic drugs). If a patient presents with concurrent signs of congestion and poor perfusion it is likely that at least one of these classes of agent will need to be administered
in addition to treatment aimed directly at relieving congestion.
Pimobendan is widely available as an inotropic and vasodilating agent. There is good evidence for its effectiveness in the treatment of more common causes of congestive heart failure in dogs. It should therefore be given to most dogs with congestive heart failure
as part of their chronic treatment regime. Pimobendan therapy can be initiated in the acute setting and in some countries an intravenous formulation enables effective initiation of therapy by injection. There is also some evidence of the effectiveness of this agent in the treatment of cats with heart failure secondary to myocardial disease.
Dobutamine is a sympathomimetic inotrope that can be given intravenously. It has to be given by constant rate infusion and may be pro-arrhythmic at higher infusion rates. This limits its administration to the hospital setting where the patient can be closely monitored during administration.
Oral or intravenous vasodilating agents can help improve perfusion by decreasing the resistance to ejection
of blood from the left ventricle. Some hypotensive patients may not tolerate vasodilation because they are unable to increase their cardiac output to compensate for the decrease in systemic vascular resistance. This can lead, in some cases to worsening of signs of poor perfusion. Vasodilators should therefore be administered with caution to patients that are already hypotensive
and blood pressure should be monitored during their administration.
What are you trying to achieve with your therapy?
It is implicit in the above discussion that drugs are being administered to patients with specific aims in mind. At the outset of therapy these aims should be defined and then the patient should be monitored to see whether these aims are being achieved. Patients should also be carefully monitored for evidence of an adverse reaction to therapy.
As evidence of a response to therapy some or all the following could be monitored
Respiratory rate – this is one of the most useful parameters to monitor as an indication of a response to therapy. Ideally the respiratory rate of a patient with heart failure should begin to decline within the first few hours of treatment. A failure of the respiratory rate to reduce would be a sign of a poor response to treatment.
Systolic arterial blood pressure – in a patient that was hypotensive on presentation a good response to therapy would be an increase in blood pressure. If a patient is not hypotensive then it may still be worth monitoring blood pressure as this may provide an indication of how well the patient is tolerating their treatment. The development of hypotension in a patient undergoing vigorous diuresis will necessitate either a modification of the diuretic regime or the concurrent administration of other therapy targeted at improving output.
Radiographic evidence of heart failure – if a radiograph was obtained demonstrating the presence of changes consistent with heart failure such as a pleural effusion
or pulmonary congestion and oedema, it is useful to demonstrate that these changes are resolving after successful treatment. If however a patient’s respiratory rate and effort are not improving in response to treatment there may be little point in re-radiographing a patient; unless it is to reconsider the original diagnosis.
Bodyweight – bodyweight should reduce considerably with successful diuresis.
Urination – a desired effect of treatment is to make the patient urinate. If they do not show an increase in urination in response to therapy it may be that they are poorly responsive to diuresis or the treatment may not have been effectively administered.
It is also worthwhile monitoring patients for the development of complications. In addition to the monitoring of systolic arterial blood pressure described above it is also worth monitoring indicators of renal function and electrolytes. These are likely to be
altered by the administration of diuretics and the reduction in circulating fluid volume. The development of hypokalaemia is particularly common following the administration of furosemide. If detected then concurrent administration of an ACE inhibitor or a potassium sparing diuretic is likely to be necessary and supplementation
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