Congestive heart failure is present when a patient is showing clinical signs as a consequence of retention of an excessive volume of fluid secondary to the presence of heart disease. Heart disease leads to an “underfilling” of the arterial circulation, which initiates a cascade of nervous and endocrine compensatory responses. Chronic stimulation of these pathways results in retention of excessive sodium chloride and water, leading to an expansion of the circulating fluid volume. This additional volume is primarily retained in the venous vasculature leading to elevated venous and capillary pressures. Ultimately venous and capillary pressures become so elevated that fluid can no longer be retained within the vasculature. This fluid leaks out into tissues in the form of oedema, or into body cavities in the form of effusions such as a pleural effusion or ascites. When a patient is demonstrating clinical signs as a consequence of this excessive retention of fluid, they can be said to be showing signs of congestive heart failure.

Some patients with congestive heart failure are concurrently showing signs of inadequate cardiac output. These signs will be apparent as signs of poor perfusion such as pallor, cold extremities, weakness and lethargy. These patients may be found to be hypotensive if blood pressure is measured. The presence of concurrent signs of poor output complicates the treatment of congestive heart failure.

When treating patients with signs of heart disease and heart failure, clinicians should ideally practice “evidence-based medicine”. There is good evidence to support the use of some agents in the treatment of patients with chronic congestive heart failure—particularly those with common underlying diseases such as degenerative mitral valve disease (DMVD) and dilated cardiomyopathy (DCM). Few if any clinical trials have evaluated the effectiveness of different agents in the setting of acute heart failure management. The most effective treatment of patients presenting acutely with signs of congestive heart failure therefore depends upon an understanding of what can be achieved with the different agents available.

There are a few key questions that clinicians need to ask themselves when managing these patients, and the management process will be explained by going through these questions and possible responses.

Are the clinical signs definitely a consequence of congestive heart failure?

Typical signs of congestive heart failure are signs of increased respiratory rate and effort. Sometimes other signs may be present, such as abdominal distension. Increased respiratory rate and effort and abdominal distension can also occur secondary to diseases of other body systems. In order for treatment to be effective, it must be targeted at the appropriate underlying cause.

To conclude that a patient definitely has congestive heart failure, one must establish that the patient has heart disease of sufficient severity to be likely to be the cause of the signs and evidence that those signs directly relate to the patient’s heart disease. A diagnosis of heart failure is therefore usually made on the basis of a combination of a history of clinical signs indicative of heart failure, physical examination findings indicative of the presence of heart disease, and the results of ancillary diagnostic tests which help to establish that the observed signs are a consequence of the patient’s heart disease. Some causes of heart failure are best managed in ways other than through the administration of drugs. The best example of this is in patients with right-sided congestive heart failure secondary to a pericardial effusion; patients with this presentation require pericardiocentesis, and drug therapy is not necessary.

If a patient is sufficiently stable to undergo diagnostic testing prior to initiation of treatment, it may be valuable to obtain a thoracic radiograph with or without echocardiography.

Is the patient showing signs of poor perfusion and low cardiac output at the same time as the signs of congestion?

This is important, because drugs that are likely to be used to manage congestive heart failure will at best have a neutral effect on cardiac output and at worst, worsen signs of poor output. Patients with signs of poor output are likely to require additional treatment in an effort to improve perfusion as well as simply treatment aimed at reducing signs of congestion.

Dealing with Signs of Congestion

The most effective agents for the control of signs of congestion are diuretics, with or without concurrent administration of venodilating agents. These agents will hopefully reduce the circulating fluid volume and, through dilatation of the veins, increase the capacity of the venous vessels to hold fluid at lower pressures. Reducing the volume of fluid and increasing the capacity of the veins should reduce pressure sufficiently to eliminate the tendency for fluid to leak out of the capillaries. If hydrostatic pressures fall sufficiently, the oedema that has established in tissues should be reabsorbed back into the intravascular volume. This will lead to resolution of clinical signs caused by oedema.

Where signs of increased respiratory rate and effort are present due to a pleural effusion, rapid improvement will be obtained by thoracocentesis. Medical management should also be introduced to prevent the reformation of the effusion. Sometimes a large volume of ascites may cause respiratory embarrassment by interfering with the movement of the diaphragm. If this is the case, abdominocentesis may also be of benefit. In patients with ascites that is not compromising respiration, medical management alone may be sufficient, as reducing circulating fluid volume and venous pressures should lead to the reabsorption of the abdominal effusion.

The most frequently used diuretic is furosemide. It has a wide dose range and can be administered by a wide variety of routes. In the acute heart failure setting, intravenous administration is preferable, as the onset of action will be rapid. This is usually started as intravenous boluses initially at 1–2 mg/kg every 6–8 hours. In patients with severe signs or in those that have developed signs of congestion despite already being on diuretics, higher doses and shorter intervals between doses may be necessary. Doses of 4 mg/kg can be given as repeated bolus injections with intervals of as little as 1 hour between doses. The drug can also be given by constant-rate infusion. Although daily doses in excess of 12 mg/kg can be administered in the acute setting, if a patient is poorly responsive to repeated boluses of furosemide, then adding other types of drug to the treatment regimen may well be necessary.

Venodilators can be given in addition to diuretics to reduce filling pressures and relieve signs of congestion. Some nitrate vasodilators (e.g., glyceryl trinitrate) are thought to have their effect predominantly through vasodilation. Balanced vasodilators such as nitroprusside also have effects on veins as well as arteries. Evidence for the effectiveness of venodilators is not strong, and nitroprusside can only safely be administered in an ICU setting where patients can be monitored very carefully.

Dealing with Signs of Poor Output

Diuretics and venodilators will, at best, have a neutral effect on cardiac output (i.e., they will not improve signs of poor perfusion), and the best one can hope for is that these signs will not be worsened by aggressive diuresis. Decreasing venous pressures will tend to decrease cardiac filling pressure, which in some situations may lead to a worsening of signs of poor cardiac output.

In patients with signs of poor perfusion due to non-cardiac diseases, as a general rule, cardiac output may be improved by the administration of intravenous fluids. In patients with heart failure, this is not the case. When heart failure is present, hypovolaemia does not underlie the poor perfusion. If the patient is showing signs of congestive failure, there is direct clinical evidence that they have an excessive circulating fluid volume. The problem here is one of distribution of fluid. Intravenous fluid therapy is almost always contraindicated in patients with active signs of congestive heart failure. The only exception is as a means of delivery of drugs when the patient 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 regimen. 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 of 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 treatment. The development of hypotension in a patient undergoing vigorous diuresis will necessitate either a modification of the diuretic regimen 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 of potassium. If urea and creatinine begin to increase significantly, this may be a sign of the patient’s renal perfusion being compromised by the intensity of diuresis. This may require modification of the diuretic regimen or concurrent administration of agents that may improve perfusion, such as inotropic drugs.

Have the Aims of Therapy Been Achieved?

If the aims of treatment have been achieved—well done! You should now be in a position to transfer the patient from their acute treatment protocol onto a more suitable chronic regimen.

If the aims of treatment have not been achieved, then intensification of therapy may be necessary. Re-evaluate the original diagnosis and go back through the various steps above to choose which treatment is most likely to help achieve your aims.

Has treatment been associated with the development of any complications?

If complications have developed, are they sufficiently severe to warrant decreasing the intensity of heart failure therapy? For instance, it may be necessary to reduce diuretic doses in patients that develop azotaemia or hypotension. Other drugs may need to be added to the treatment regimen in an effort to address the complications observed.