Page 170 - WSAVA2018
P. 170

 25-28 September, 2018 | Singapore
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 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 one 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 regime 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

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