I have recently heard of some cases of worsening heart failure that have resulted from the underlying disease of heart failure but also due to under treatment with diuretics and over administration of fluid.
For example, a young female admitted to another hospital with acute oliguric renal failure from sepsis was being provided over 2.5 litres per day in IV fluid and she was unable to be extubated due to acute heart failure, bilateral effusions and type 1 respiratory failure.
She required daily haemofiltration to remove the excessive fluid but this was still insufficient to treat the problem. It was clear that fluid balance needed to be controlled. In a usual healthy patient, daily 'insensible losses' e.g. fluid loss from breathing, sweating and loss in faeces is approximately 500ml in a stable condition. This will increase in pathological conditions e.g. fever, hot conditions, diarrhoea etc.
In the absence of urine production such as in acute oliguric renal failure, in order to attain the status quo, fluid input should match fluid output through considering insensible losses once euvolaemic. This may be quite difficult to acieve especially when intravenous drugs need to be given plus nutrition. However, it is of importance to help control acute heart failure and hypertension which are obvious problems.
Furosemide was also given by the attending physician in this setting but proved ineffective in stimulating urine output and this is in keeping with the observations that Furosemide is not associated with any significant clinical benefit in the prevention and treatment of acute renal failure in adults and with high doses being associated with ototoxicity. BMJ 2006;333:420-3.
After taking advice, the attending physician in reducing the fluid input and continuing daily haemofiltration, the acute heart failure with effusions reduced so that the patient could come off the ventilator.
An example at the other end of the spectrum, was in an elderly patient at another hospital with heart failure who had presented with 'asthma'. She had a history of heart failure and had been treated for asthma with steroids for one month but she developed recent worsening respiratory function which suggested that the cause was perhaps 'cardiac asthma' from her underlying heart failure.
She was using BIPAP and the Xray showed a mixture of CHF and infection. MRSA had been identified in 3 out of six blood cultures. One concern was she was also receiving over 1 litre of intravenous fluid per day and daily furosemide dose was just 20mg/day with only an additional furosemide dose if the urine output decreased below 100ml/hour.
This is not standard treatment for heart failure as you either diurese a patient to reduce fluid or if dehydrated, given judicious fluids to maintain kidney function, but not both at the same time otherwise there will never be an accurate and continued fluid loss.
This is a bit like filling a container from the top but opening the tap from below and hoping to keep the fluid level the same. In other words, the heart failure will not be effectively treated.
When a patient is fluid overloaded with a background of cardiac failure, such patients need fluid restriction to approximately 500ml orally (see insensible losses above) per day to ensure that they go into a NEGATIVE fluid balance through diuresis, that we commonly refer to as 'drying out the patient'.
Patients should be weighed daily to ensure sustained weight loss and a general rule is to lose approximately 1kg per day in excess fluid unless renal dysfunction occurs in which case a slower diuresis can be effected.
Patients should also have no added salt in their diet. If IV fluids are to be given, they should not contain sodium, and hence, dextrose should be provided. ACE inhibitor or ARB therapy should started and Spironolactone considered (to treat secondary hyperaldosteronism) if the patient has excess oedema and the CHF does not respond to the ACE-I/ARB alone.
Moreover, it is somewhat dangerous to have ACE-I/ARB plus Spironolactone used together as it may cause worsening renal dysfunction and HYPERKALAEMIA especially in the elderly who tend to suffer with heart failure the most. However, close monitoring of renal function should be instituted. Spironolactone reduces mortality from CHF so its use should be considered.
Patients commonly need intravenous furosemide at much higher doses than 20mg/day, and I am used to giving at least 40 to 160mg of furosemide per day to patients on a case-by-case basis to establish a controlled cardiac state. As oral bioavailability of furosemide is only about 50% and that this may be reduced further from gastric oedema in heart failure, it is always preferable to give intravenous furosemide in advanced heart failure.
A very good question was 'What about the patient having low blood pressure'.
Well, if one considers why the patient has low blood pressure, the answer can be simply made. In heart failure with systolic compromise (rather than the diastolic compromise), the more the ventricle is over stretched, the less the muscle can contract (Starling Effect) and hence blood pressure may decrease despite rises in heart rate and central venous pressure. As there is a high output of aldosterone and catecholamines, a low blood pressure in the absence of another cause, suggests poor cardiac function.
Renal failure in CHF is contributed from the vasoconstrictive effect, and hence by reducing the ventricular filling and improving the ejection fraction in theory, the vasoconstrictive effect should be reduced leading to better renal perfusion and better diuresis.
In advanced heart failure, injection of furosemide causes a greater release of renin and plasma norepinephrine resulting in vasoconstriction but with an acute initial drop in ventricular function and rising filling pressures. However, blood pressure increases. This is an acute effect of furosemide injection seen in the first hour. Ann Intern Med 1985 Jul;103(1):1-6
In such cases of low blood pressure, counter-intuitively, furosemide causing diuresis, can aid in raising the blood pressure. However, furosemide can also cause venodilatation, similar to the venous morphine-effect, and can drop the blood pressure further especially if blood pressure is dependent on heart rate and raised central venous pressure when there is poor ventricular function, and so using it alone may be problematic especially when it is not known which are the greater contributors to maintaining the blood pressure.
It is likely that there is an interplay between venodilatation, vasconstriction (from secondary hyperaldosteronism), diuresis and reduction in circulatory volume thereby reducing pre-load and after-load with the use of furosemide.
However, if patients have severe cardiac failure and low blood pressure (shock) they essentially have cardiogenic shock, and ionotropes can be used to support such patients in the short term such as Noradrenaline, Dobutamine or High Dose Dopamine.
It should be mentioned at this juncture that despite the beneficial blood pressure elevating effects of inotropes, they have not been shown to improve survival.
CPAP is also a good short term measure of aiding heart failure and improving oxygenation, BUT if patients have low blood pressure, such non-invasive ventilation can worsen BP control and hence such therapy may be relatively contra-indicated.
Providing renal dose dopamine to ensure continued renal perfusion is of unproven benefit (Lancet 2000; 356: 2139-43) and the general opinion based on current evidence is not to use renal-dose dopamine in renal failure (UpToDate 15.1: Use of vasopressors and inotropes; Intensive Care Med 1996 Mar;22(3):213-9)
Hence, in this patient, the suggestion was to reduce daily fluid administration and to increase the daily amount of furosemide with the consideration to curtail unproven therapies such as renal-dose dopamine.