Schematic for assessment of clinical profiles. Congestion was assessed by the presence of orthopnea, jugular venous distention, rales, hepatojugular reflux, ascites, peripheral edema, leftward radiation of the pulmonic heart sound, or a square-wave blood pressure response to the Valsalva maneuver. Compromised perfusion was assessed by the presence of a narrow proportional pulse pressure, pulsus alternans, symptomatic hypotension (without orthostasis), cool extremities, and/or impaired mentation
The Hemodynamic Model for Heart Failure
Until the advent of the neurohumoral hypothesis, heart failure was seen as a hemodynamic disorder that should be corrected by the use of inotropes and diuretics [4]. Perhaps as a holdover from this hemodynamic paradigm, the etiology for worsening renal function in patients with heart failure has generally been assumed to be the result of low cardiac output. There are some data to support this view. Physiologic studies in patients with advanced heart failure have provided evidence that cardiac output could be improved by adding positive inotropic agents or reducing afterload [1, 5, 6]. Patients often improve when inotropes are added with improvements of serum creatinine observed at the same time. Data exist that with very low cardiac index <1.5 L/min/m2, renal blood flow is reduced with a consequent worsening of renal function [7]. Prolonged hypotension, often associated with reduced cardiac output, has long been shown to cause worsening renal function and even acute tubular necrosis [8].
Blood Pressure or Cardiac Output?
As the evidence for the survival benefits of neurohumoral modulators increased, the role of positive inotropic agents have been questioned on several fronts. Use of inotropes, whether used intravenously or oral, is associated with increased mortality [9, 10]. On the other hand, drugs which decrease contractility (e.g. beta blockers) improve survival and ventricular function over the long-term [11–13]. Casting more doubt on the role of low cardiac output as the cause of cardiorenal syndrome, a pivotal study by Mullens et al. in patients with hemodynamic monitoring for advanced heart failure has demonstrated that high central venous pressure rather than low cardiac output is more frequently associated with worsening renal function [14]. This confirms animal data about the detrimental effect of high central venous pressure on renal function [15, 16]. Finally, the beneficial effect of inotropes may be related more to their improvement in blood pressure rather than a rise in cardiac output [9].
Treatment Pearls for the Case Vignette
So how should we evaluate the patient from the case vignette in the light of these data? Clearly the patient displays an advanced stage of heart failure complicated by cardiorenal syndrome. The creatinine has more than doubled and there is even mental impairment suggesting low cerebral perfusion. Mental alteration is common in shock and pre-shock states and patients undergoing cardiac transplantation have reduced cerebral blood flow [17, 18]. Cold extremities are also associated with shock and thought to be due to low cardiac output or reduced blood pressure. Indeed, cardiac index is severely reduced at nearly 1 L/min/m2. Blood pressure, although reduced, is not at a level that is commonly thought of as shock (mean arterial pressure <60 mmHg). Hence systemic vascular resistance is very high, masking severely depressed cardiac function. The latter is amenable to pharmacological treatment (e.g. hydralazine). Filling pressures are elevated, but not to the extent to invoke renal congestion as a cause of cardiorenal syndrome. In this case, the presentation of the patient with kidney dysfunction seems predominantly related to low cardiac output, which was relieved by a combination of drugs to improve contractility and reduce afterload.
In this case, invasive hemodynamics are obtained on admission, which plays a key role in identifying the patient’s severe reduction in cardiac index and markedly elevated systemic vascular resistance. This information leads to the initiation of an inotrope and oral vasodilators. Later, efforts to wean the inotrope were unsuccessful because of a reduction in urine output. The patient is fortunate that renal dysfunction is reversible, but it is imperative in these situations to realize that this is now advanced stage D heart failure and the clinical improvement is temporary [9, 19]. Inotropic therapy has shown to improve cardiac output/index, improve peripheral blood flow, renal function, vasodilate and with dopamine at higher doses improves blood pressure [6, 19–21]. Although, inotropic agents have never been shown to improve mortality, they have had a significant impact on quality of life and reduction in hospitalizations for advanced heart failure patients. These findings have also shown cost reduction when factoring in readmission costs [21]. Unfortunately, yearly mortality approaches 50%, even when inotropes are continued. Left ventricular assist devices or cardiac transplantation offers a much better prognosis in appropriately selected patients [1, 20, 21]. In many cases palliative care may be considered early on.
Treatment Pearls from the Case Vignette
Management of the cold & wet patient
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