In congestive heart failure secondary to systolic dysfunction, a depressed, flattened Frank-Starling curve allows diuretic therapy to safely reduce preload by decreasing intravascular volume, as this reduction does not affect an already decreased stroke volume. This is dissimilar to the non-failing heart where a similar reduction would cause a profound stroke volume reduction, however if too much diuresis ensues, or if the patient is already hypovolaemic, diuretic therapy may seriously impair ventricular filling and cardiac output causing a vicious circle of increasing pulmonary congestion. In diastolic dysfunction ventricular filling requires elevated filling pressures because of reduced ventricular compliance, and these patients are even more sensitive to hypovolaemia.
More than 85% of patients presenting with acute pulmonary congestion are markedly hypertensive (systolic arterial pressure >160 mmHg), and Little et al found that LV ejection fraction was similar during an acute episode of hypertensive pulmonary oedema and subsequently, after treatment and control of the blood pressure, suggesting that it is likely that the pulmonary congestion was due to isolated diastolic dysfunction. If this is so, knee-jerk diuretic therapy, based on the widely accepted “fact” that pulmonary oedema is due to “fluid overload” may be positively harmful.
There have been no randomised, controlled trials or meta-analyses to support the use of diuretics in acute rather than chronic heart failure, and it is important to recognise that even patients who present with acutely decompensated heart failure are not always volume overloaded, and may show no other signs of fluid retention. Patients with acute diastolic dysfunction may benefit more from redistribution of circulating volume by using vasodilators. The indiscriminate use of diuretics not only carries the risk of over-diuresis referred to above, but is also related to detrimental effects on renal function, particularly among elderly patients. Even without over-diuresis, high doses of diuretics with concomitant worsening renal function has been tied to both longer hospital length of stay and increased mortality after discharge.
Given the above, should there not be some well-designed research into the true volume status of acute heart failure patients, with the results used to guide a rational and balanced approach to emergently and critically ill patients, rather than a slavish “four legs good, two legs bad” fluid overload approach which is taught as an article of blind faith to our junior doctors?
My dated clinical understanding was that furosamide and morphine were good for acute LV failure because they cause arterial vasodilatation in the short term so quickly off-loading the ventricle
Very interesting question and insightful points.
The flip side is that few medications have been used as often as diuretics over several generations of doctors and overall they do actually work well in acute heart failure. One could argue their value has been proven by their indiscrimiate use.
Diuretics are a godsend for the CHF pt. But that is not saying that using them in the treatment of the acutely decompensated dyspneic heart failure pt. is a good idea. As stated above, many of these pts. present with extreme afterload and may even be euvolemic or hypovolemic. Our old theories that furosemide and morphine are acutely helpful are not born out by physiology: morphine may be downright harmful.
But let me present the flip side. Our cardiologists believe that most of our CHF pts. walk around volume overloaded, and that a sudden onset of severe dyspnea is quite unlikely to happen in a euvolemic pt., regardless of trigger or afterload status. So they feel that these pts. need diuresis: our argument stems from when they need it. In my opinion there is no reason to give these folks furosemide as a first or second intervention when nitrates and non-invasive ventilation virtually cure their complaints within the first hour or two.
There is not allways "fluid overload". Is necessary the correct diagnosis to start the therapy. Use of diuretics is common and frequently correct, but not allways.
It is not always true.First we have to evaluate the cardiac function & electrolytes.Then we have to manage accordingly.Frusemide is only be helpfull in case of flid overload with good cardia function .But in case of bad cardiac function we have to treat it simultaneosly along with frusemide.
Yes good question and insightful discussion. Approximately 40% - 50% of heart failure pts have diastolic dysfunction. As mentioned above administering diuretic routinely assuming fluid overload and systolic dysfunction could be harmful. Pts presenting with "acute decompensation" need rapid assessment evaluating cardiac function to determine if they have primary systolic or diastolic dysfunction (both are "left-sided") so the correct intervention(s) can be administered.
The issue if diuretics (i.v furosemide) should be routinely used in patients with acute left sided heart failure (i.e. acute pulmonary edema) on the universally accepted basis that these patients are always "fluid overloaded” has been appropriately introduced by Paul MacConachie Middleton.
My contribution to the discussion is based on the experience on 4 patients - 3 men and 1 woman in their eighties - urgently admitted to our Cardiology ward because of acute pulmonary edema unresponsive to, and even worsening after, usual drug treatment, in whom dehydration was identified as the probable initial mechanism responsible of a downstream sequence of events leading to pulmonary congestion despite hypovolemia. The main clinical characteristics of these patients were: 1) a high heart rate (130 to 165 beats/min due to sinus tachycardia or atrial fibrillation), 2) absence of jugular veins distention despite remarkable respiratory distress, 3) a hyperkinetic, hypertrophic, and small left ventricle, with normal-reduced right chambers size at echocardiographic examination, 4) unresponsiveness to usual drug treatment by morphine-nitrates-furosemide administration which on the contrary produced further symptoms and hemodynamic worsening, with severe arterial hypotension and impending shock. After echocardiographic demonstration of a normal, small, and well contracting left ventricle the diagnosis of acute diastolic CHF was made and all patients progressively recovered from pulmonary edema after heart rate reduction below 100 beats/min by intravenous metoprolol administration, immediately followed by tailored (usually rapid at the beginning) intravenous saline solution administration to avoid impending shock due to hypovolemia, hypotension and reduced stroke volume aggravated by usual treatment. Normal or reduced right chambers size was present and none of the patients exhibited a systolic anterior motion of the mitral valve (as expression of LV outflow tract obstruction) at the emergency echocardiogram. Although limited, this experience suggests that the marked reduction of filling time associated with persistent supraventricular tachycardia or tachyarrhythmia may cause pulmonary congestion and pulmonary edema even in presence of hypovolemia in the elderly hypertensive. The hypovolemia-induced tachycardia appears to be the initiating factor in this events cascade. In one patient a previously undetected hyperthyroidism was also found. Controlling the increased heart rate is the first therapeutic approach resulting in prompt relief of pulmonary edema and dyspnea; the hypovolemic state and impending shock must then be treated accordingly by tailored, usually rapid, intravenous saline infusion. From this experience it also follows that progressive clinical and hemodynamic deterioration by usual treatment of acute pulmonary edema in the elderly should prompt immediate echocardiographic examination. Proper identification of this previously unrecognized syndrome was life-saving in four of our five patients.
Diuretics are used widely by junior doctors despite the fact that the drug of choice are nitrates. So no I don't use them routinely. In many countries the doctor who first attends to the patient is often relatively inexperienced. This is the case in UK and Ireland, 2 countries that I am familiar with. It is they who commence the treatment and it is my experience that they routinely use diuretics. This is an ongoing battle to get them to move away from diuretics to nitrates which sadly I have not made any progress.Therefore I will persist, who knows someday I might get through to them.
Morphine, IV nitrate, and definitely treatment of the underlying cause are of prime importance in management of acute left heart failure. But administration of these drugs needs monitoring, and preferably ICU/CCU care, which is not readily available in most of the areas in developing countries. On the other hand, IV diuretics, though not ideal, is cheap, easily available and needs less monitoring. This agent is still being popularly used, and has probably saved many lives!
A fast bedside USG to check IVC collapsibility index is a good marker to follow the response of the pt to the tx.
If there is really fluid overload the use of diuretc is correct. But the correct cause of left ventricular failure can be stablished.
The diuretics are the main stay of drug ( Class 1 ) in the management of acute LVF because the Loop diuretics at a dose of 40 - 60 mg is a pre load as well after load reducer. So even in a pulmonary oedema patient with preserved systolic heart function the after load reduction helps in diastolic heart failure pulmonary oedema patients.
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