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Section Three
Non Ischemic Cardiac Disease
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Chapter 12
Acute heart failure
Kevin Reed1 & Amal Mattu2
1 Assistant Professor of Clinical Emergency Medicine, Georgetown University School of Medicine, Department of Emergency Medicine, Washington, USA
2 Professor and Residency Director, Department of Emergency Medicine, University of Maryland School of Medicine, Baltimore, Maryland, USA
Section I: Case presentation
Section II: Case discussion
Dr Peter Rosen: There was a study that suggested a diurnal variation to episodes of acute pulmonary edema. Patients who arrive in the daytime are more likely to have a heart attack as the underlying cause of their congestive failure than patients who arrive in the middle of the night. Have you noticed a similar diurnal variation, and what do you believe is the most common trigger in decompensated congestive heart failure?
Dr Edward Ullman: This is somewhat dependent on your patient population and practice environment. When I was in residency training, most of the cases of congestive heart failure (CHF) I encountered were related to medicinal noncompliance and dietary indiscretion. Now I tend to see more ischemia as a trigger. This may reflect a more savvy patient population who tend not to cheat on their diets as much, and are more compliant with their medications. However, I have not noticed a diurnal variation in either of these populations.
PR: When you see a patient like this who is not yet in fulminant pulmonary edema, but who seems well on the way, what makes you decide whether he is sliding in to hypervolemic high resistance failure as opposed to pump failure? I think this is the first distinction we need to make in congestive failure, since the management is very different. Are there any clues, either from the initial appearance or during the evaluation?
Dr William Brady: Patients who have true pump failure most often are having a large myocardial infarction (MI), and usually appear sicker. They often are in shock. They have an ashen appearance. They have cold extremities. They are not perfusing in any shape, manner, or form. When you look at these patients' EKGs and serum cardiac markers, they will be very abnormal with the waveforms of an acute or subacute MI. Sometimes the EKG may show an old infarction, reflecting acute pump failure related to prior cardiac disease. The blood work will show hypoperfusion demonstrated by a low serum bicarbonate level or a significantly elevated lactate level. Nevertheless, patients in volume overload can also be very ill with acute respiratory failure, and also develop shock and all the sequalae of the pump failure. In general, not only are they are less ill, in some ways they are easier to treat. I believe that looking at the patient's history of present illness, their medical history, and your analysis of what is likely going on can point you in the right direction diagnostically and ultimately therapeutically.
PR: One of the early clues is in the blood pressure, as patients who are volume overloaded tend to have high resistance failure and present, as this man did, with hypertension; in patients with pump failure, the initial blood pressures are often normal to low since when these patients are well, their blood pressures are usually elevated. Another clue that the patient's CHF is related to high resistance failure is respiratory distress. When you see a patient with acute onset of respiratory distress, someone who is in the classic bubbling pulmonary edema, do you think that there are any clues as to what's going on in the heart that causes this, or do you think that there is always just volume overload and high resistance?
Dr Amal Mattu: I look at CHF as having two distinct major causes. One of them is fluid overload or volume dysfunction, and the other is vascular dysfunction, or in other words, very high resistance. When people come in with acute onset CHF, it tends to be associated with more of a vascular problem, oftentimes with acute afterload dysfunction. They present with very high blood pressures. Patients who are fluid overloaded tend to present with a more gradual onset of symptoms. When people come in with a more abrupt onset of symptoms, and appear to be doing pretty well but over the course of an hour they go from looking well to looking very sick, then I steer away from diuretics. In this case, I'm not worried about fluid overload. The most important therapy for these patients is to improve their resistance with quick afterload and preload reduction rather than focusing on diuretics and their volume.
PR: There is one finding on physical examination that can really help you in the face of acute rapid decompensation. When you hear a loud murmur in a patient who suddenly presents with acutely decompensated CHF, you must suspect the patient has a rupture of a papillary muscle. It's helpful to pick up this murmur as these patients need acute cardiac surgery more than they need medical manipulation. What would be your initial approach to management of the patient in this case? Which patients need emergent airway management?
SG: Any patient who presents with airway compromise will need some sort of airway management. Generally, we reserve intubation for those patients who cannot tolerate a noninvasive type of ventilation. A patient who is somnolent or unconscious is not going to be able to tolerate bilevel positive airway pressure (BiPAP) or continuous positive airway pressure (CPAP); these patients will certainly need intubation. If a patient comes in markedly hypotensive or in shock, it is necessary to actively manage the airway. As in all of emergency medicine, first take care of the airway, and then care for breathing and circulation.
PR: I think that's a useful first distinction. In the patient who presents with pump failure, one of the critical first steps in management is to perform intubation to reduce the work of respiration. These patients will not respond to CPAP and to volume manipulation; they're going to need pump assistance.
WB: I would focus on three things: first, make sure the patient is not in extremis. Then, supply some form of high flow oxygen, at least initially a non-rebreather facemask. Lastly, start high dose nitrates, either sublingual, topical, intravenous, or some combination thereof.
SG: I would avoid topical nitrates in this patient as their effect on blood pressure is inconsistent, and their absorption is erratic due to both patient diaphoresis and the nature of a transdermal absorption.
WB: After nitrates, I use noninvasive positive pressure ventilation aggressively. Lastly, I've added ACE inhibitors to my armamentarium, either enalaprilat or sublingual captopril. I have begun to stay away from furosemide, and I try not to use morphine if at all possible. I've recently developed several prehospital protocols for EMS agencies that removed furosemide as a first line drug, and made its use dependent upon a base station medical command. For EMS, we have also significantly deemphasized morphine, and added sublingual captopril.
AM: Maryland has developed similar EMS protocols. Formerly, the paramedics would automatically give morphine and furosemide, but now morphine has been completely excluded from the protocol, and furosemide can only be given upon medical command. Similarly, the state protocols have also incorporated sublingual captopril into prehospital CHF protocols.1
PR: Could you explain why this is the case? Most of us grew up in the period where we were told you had to unload the heart, and you had to produce venous dilatation, as furosemide does, long before it produces diuresis. Morphine also was thought to be a good way to lower peripheral resistance, as well as to interfere with the vicious cycle of hypoxia and adrenalin production by the patient. For years this seemed to work pretty well, so why do we think it's no longer useful?
AM: There are some studies indicating that when you give morphine and furosemide, you get peripheral vasodilatation in the wrist and forearm.2,3 Based on those studies, people extrapolated and assumed that if you had vasodilatation in the wrist and forearm, then you must also be getting a decrease in right heart filling pressures, but this was only an extrapolation. When they actually studied this using pulmonary artery (PA) cathete...
