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Heart Fail Rev (2007) 12:113–117 DOI 10.1007/s10741-007-9013-6 Algorithm for therapeutic management of acute heart failure syndromes Ramzi Chatti Æ Nabil Ben Fradj Æ Wissem Trabelsi Æ Hakim Kechiche Æ Miguel Tavares Æ Alexandre Mebazaa Published online: 18 April 2007 Ó Springer Science+Business Media, LLC 2007 Abstract As for other critically ill diseases, two key factors may markedly improved morbidity and mortality of acute heart failure syndromes (AHFS): early initiation of treatment and tailored therapy. Early initiation aims to stop the negative cascade of heart dysfunction. Tailored therapy should be based on the level of systolic blood pressure at admission and fluid retention. Indeed, EFICA and OPTIMIZE-HF showed that patients with high systolic blood pressure have a left ventricular systolic function that is likely preserved and those with low systolic blood pressure have a lower left ventricular ejection fraction and frequent signs of organ’s hypoperfusion. Among the proposed treatments, non-invasive ventilation is the only treatment that was consistently proven to be beneficial on morbidity and mortality in almost all types of AHFS. Concerning pharmacological agents, actions should be taken to increase the use of vasodilators and reduce the use of diuretics. Keywords Acute heart failure Non-invasive ventilation Levosimendan Nitrates Diuretics Acute heart failure syndromes: definitions In most textbooks of cardiology or intensive care, in the last 40 years, acute heart failure is considered as a mixture including an acute pulmonary edema following an increased arterial blood pressure and a cardiogenic shock related to acute myocardial infarction. The word ‘‘heart’’ in ‘‘acute heart failure’’ is indeed confusing. Many young physicians still believe that during an acute heart failure episode, the heart, and specially its systolic function is impaired; as described in this review, we know today that this is not true [1, 2]. In addition, as pulmonary edema was described in the 50’s in patients with long history of heart failure, named ‘‘congestive heart failure’’ for years, physicians had the impression that pulmonary edema is always associated with increased volemia and that pulmonary edema should be always treated with diuretics. However, we know today that most episodes of acute pulmonary edema appear in patients with long history of hypertension and are rather euvolemic [2]. Definitions based on physiopathology R. Chatti N. B. Fradj W. Trabelsi H. Kechiche M. Tavares A. Mebazaa (&) Department of Anesthesiology and Critical Care Medicine, Lariboisière Hospital, University Paris 7 Denis Diderot, 2 Rue Ambroise Paré, Paris 75010, France e-mail: [email protected] M. Tavares Department of Anesthesiology and Critical Care, Hospital Geral de Santo António, Porto, Portugal In order to classify patients admitted with acute heart failure syndromes (AHFS), Heart Failure Society of America and the European Society of Cardiology recently defined categories based on physiopathological concepts. Heart Failure Society of America distinguished patients in three categories [3]: (1) the majority of patients hospitalized with acute heart failure have evidence of systemic hypertension on admission and commonly have preserved left ventricular ejection fraction (LVEF); (2) most hospitalized patients have volume overload and congestive symptoms; (3) a distinct minority with severely impaired systolic function, reduced blood pressure and symptoms 123 114 from poor end-organ perfusion. The European Society of Cardiology and the European Society of Intensive Care Medicine further classified acute heart failure patients in six categories [4]: (1) Hypertensive acute HF: signs and symptoms of HF are accompanied by high blood pressure and relatively preserved left ventricular function with a chest radiograph compatible with acute pulmonary edema; (2) Pulmonary edema accompanied by severe respiratory distress, with crackles over lung orthopnea, with O2 saturation usually <90% on room air before treatment; (3) Acute decomposed HF (de novo or as decomposition of chronic HF): signs and symptoms of acute HF that are mild and do not fulfill the criteria for cardiogenic shock, pulmonary edema, or hypertensive crisis; (4) Cardiogenic shock: cardiogenic shock is defined as evidence of tissue hypoperfusion induced by HF after correction of preload. There is no clear definition for hemodynamic parameters, but cardiogenic shock is usually characterized by reduced blood pressure (systolic blood pressure <90 mmHg or a drop of mean arterial pressure >30 mmHg) and/or low urine output (<0.5 ml /kg per hr), with a pulse rate >60 beats per min with or without evidence of organ congestion. There is continuum from low cardiac output syndrome to cardiogenic shock; (5) High output failure is characterized by high cardiac output usually with high heart rate (caused by arrhythmias, thyrotoxicosis, anemia, Paget’s disease, or iatrogenic or other mechanisms), with warm peripheries, pulmonary congestion, and sometimes low blood pressure, as in septic shock; (6) Right HF is characterized by low output syndrome with increased jugular venous pressure, increased liver size, and hypotension. This is the basis of the ‘‘new’’ concept of ‘‘Acute Heart Failure Syndromes’’. These categories have been shown to also represent different outcomes: hypertensive acute pulmonary edema has a lower mortality rate compared to decompensated heart failure or cardiogenic shock [2]. In addition, outcome is likely different when AHFS appears de novo or in a context of decompensated heart failure [5]. Definitions based on blood pressure at admission Although, the classifications proposed by HFSA and ESC were an important first step to categorize AHFS patients, it rapidly appeared that one should use a classification that can be used by any physician, including junior physicians, in charge of AHFS in several settings such as emergency room. Systolic blood pressure (SBP) is shown increasingly as the main predictor of both morbidity and mortality. The French study EFICA studied 581 patients admitted with AHFS in CCU/ICU. In the group of patients without cardiogenic shock (n = 415), patients with SBP > 160 mmHg on admission (n = 90) had a lower four-week mortality rate 123 Heart Fail Rev (2007) 12:113–117 than patients with SBP < 160 mmHg (n = 325) (7% versus 17% respectively, P = 0.03) [2]. Similar difference in mortality was observed between the two subgroups at 1 year. Of note, patients with high SBP are similar to those described in other surveys: old with a history of hypertension, ECG and echocardiographic signs of LV hypertrophy and preserved LVEF. Recently, a study (OPTIMIZE-HF) enrolled 48,612 patients between March 2003 and December 2004 from 259 hospitals across the United States [1]. The major determinant of long-term mortality was systolic blood pressure. Patients were categorized into quartiles based on their admission SBP values: SBP < 120 mmHg; SBP in the range of 120–139 mmHg; SBP in the range of 140– 161 mmHg; SBP > 161 mmHg. More patients in the higher SBP quartiles (140–161 mmHg and >161 mmHg) had preserved systolic function and were black. The inhospital mortality rate was 3.8% in the entire cohort and the mean length of stay was 6.4 days. Higher SBP at admission was associated with substantially lower in-hospital mortality: 7.2% (<120 mmHg), 3.6% (120– 139 mmHg), 2.5% (140–161 mmHg), and 1.7% (>161 mmHg) (P < .001 for overall difference) and 60– 90 day mortality. Treatment of acute heart failure syndromes tailored therapy Based on the both surveys, EFICA and OPTIMIZE-HF, we suggest that the treatment algorithm of AHFS patients should be based on the level of SBP at admission (Fig. 1). Two SBP cut-offs are proposed in this algorithm: 100 and 140 mmHg. Indeed, as described above, at SBP of >140 mmHg, left ventricular systolic function is likely preserved, at SBP of 100–140 mmHg left ventricular systolic function is limited, and many patients with impaired left ventricular systolic function exhibit SBP < 100 mmHg. Patients with high systolic blood pressure are usually treated with diuretics and vasodilators such as nitroglycerin, nitroprusside, nesiritide; while patients with AHFS and low systolic blood pressure have a lower left ventricular ejection fraction, frequent signs of organ’s hypoperfusion and are more likely to receive inotropes. Above all, the only treatment was consistently proven to be beneficial on morbidity and mortality in almost all types of AHFS is non-invasive ventilation. Non-invasive ventilation (NIV) Non-invasive respiratory support (=non-invasive ventilation, NIV) can be instituted early in AHFS, and it can be Heart Fail Rev (2007) 12:113–117 Fig. 1 Algorithm for therapeutic management of acute heart failure syndromes. This algorithm should be apply within minutes of admission. PAC: pulmonary artery catheter 115 Assessments •Non-invasive monitoring (SpO2, BP) •O2 •Non-invasive ventilation (NIV) as indicated •Lab tests •BNP or NT-pro BNP, when diagnosis is uncertain •ECG •CXR •Temperature If SBP > 140 mmHg If SBP 100-140 mmHg If SBP < 100 mmHg NIV + Nitrates NIV + Nitrates + diuretics Fluid challenge + inotropes + vasopressors avoid diuretics unless obvious volume overload provided by either CPAP (continuous positive airway pressure) or bi-level ventilation (both inspiratory and expiratory support, BiPAP). NIV augments cardiac output, decreases left ventricular after load, increases functional residual capacity and respiratory mechanics and reduces the work of breathing. A total of 23 clinical trials and three meta-analyses have assessed the comparison among CPAP, BiPAP and standard therapy, or CPAP and BiPAP [6–8]. Nearly all revealed that both CPAP and BiPAP reduce the need of intubations and reduces mortality in patients with acute cardiogenic pulmonary edema. Some risk factors for intubation have been described in patients treated with conventional therapy: severe acidosis (pH < 7.25), hypercapnia, acute myocardial infarction, low blood pressure, and severely depressed ventricular function. Based on these data, early use of NIV should be considered for the early management of all AHFS patients when dyspnea, respiratory distress, and/or pulmonary edema are present to prevent the need for intubation, its subsequent complications, and potentially, to reduce the risk of mortality. NIV requires minimal nursing resources; however, patient cooperation is necessary. A positive pressure of 5–7.5 cm H2O titrated to clinical response is the most appropriate initial therapy when CPAP is used. Any hospital receiving AHFS patients should have an adequate number of CPAP devices available. Vasodilators Based on registry data, the large majority of AHFS patients present with signs of increased left ventricular filling pressure, high or normal blood pressure and preserved left ventricular systolic function; only a minority present with low blood pressure or cardiogenic shock. Patients with high SBP are ideal candidates for early initiation of vasodilator therapy. Acute therapy with vasodilators can improve both hemodynamics and symptoms. Currently available volume overload is possible PAC if no improvement vasodilators include nitrates, nitroprusside, and nesiritide. In AHFS, intravenous nitroglycerin is preferred [4]. The initial recommended dose is 10–20 lg/min, and it is increased in increments of 5 lg/min forevery 3–5 min as needed. Tachyphylaxis is common, necessitating incremental dosing. The major adverse effects of nitrates are hypotension (mean blood pressure should remain >70 mmHg) and headache. Nesiritide, a recombinant form of human B-type natriuretic peptide, is a venous and arterial vasodilator that may also potentiate the effect of diuretics. It is given intravenously as a 2 lg/kg bolus followed by a 0.01 lg/kg/min infusion. In the VMAC trial, nesiritide lowered PCWP significantly more than either intravenous nitroglycerin or placebo at the 3-h time-point, and it improved dyspnea compared to placebo but not compared to nitroglycerin [9]. Diuretics Surveys indicate that loop diuretics are the first line agent around the world for the treatment of patients with AHFS. This is a paradox. Indeed, the most frequent AHFS clinical scenario includes patients with high systolic blood pressure. Although edema is present in the lungs, those patients are often normo- or even hypovolemic. As increasingly described, AHFS associated to high blood pressure is mostly seen in female old patients with history of systemic hypertension. Those patients are often treated with oral diuretics and are very likely normo- or hypovolemic at the time they are admitted for AHFS. The latter is related to a sudden increase in systolic blood pressure that induces pulmonary edema because of a hypertrophied stiff left ventricle. High dose diuretics in these patients may be detrimental. Of note, only a few studies have evaluated short and long-term clinical outcomes. Appropriate early diuretic use might however be considered in patients with worsening chronic fluid overload. This profile can be suspected based on the patient’s history, 123 116 clinical examination (signs of congestion), signs of right ventricular congestion, symptom severity (moderate decompensation, pulmonary edema, or cardiogenic shock), and blood pressure. Thus, recognizing the appropriate patient profile is important, and it will help to guide the physician’s early management strategy. Parameters for adjusting diuretic therapy have not been established. In general, the lowest dose should be used that produces the desired clinical effect. In chronic heart failure, diuretic therapy is titrated according to fluid balance and the resolution of signs and symptoms. The onset of diuresis may not occur until 30–120 min after administration; thus, urine output alone is not an ideal therapeutic target. Dyspnea, global patient status, respiratory rate, oxygen saturation, or needs for intubation are better targets, especially in critically ill patients. In summary, aggressive diuretic monotherapy is not necessary in the majority of patients. Diuretics should be left only when there is evidence of systemic volume overload. Effects of diuretics must be reassessed after 30– 60 min. Cardiac enhancers and vasoconstrictors Inotropes are a traditional component of the AHFS treatment strategy. The most common inotropes in clinical practice include dobutamine and milrinone, but dopamine is also available. Traditional inotropes are no longer recognized as first line, acute therapy for the majority of AHFS patients, and data from ADHERE, OPTIMIZE, and Euro Heart Failure Survey II indicate that traditional inotropes are used in approximately 10% of AHFS admissions [1, 5, 10, 11]. The OPTIME-CHF study found no benefit for milrinone in 949 patients hospitalized for worsening heart failure [1, 2]. A higher risk of arrhythmias was observed, and patients with ischemic etiology who were randomized to milrinone had worse outcomes. However, early use of inotropic therapy may be appropriate in patients presenting in cardiogenic shock or with evidence of low output who are not responding to other therapies. These patients may include those with SBP < 85–90 mmHg or evidence of organ hypoperfusion including patients who are cold, clammy, or vasoconstricted. Renal impairment, liver dysfunction, or impaired mentation are also possible signs of hypoperfusion. As discussed, these patients account for the minority of AHFS hospitalizations. Inotropes may stabilize patients at risk of progressive hemodynamic collapse or serve as a life-sustaining bridge to more definitive therapy such as mechanical circulatory support, ventricular assist devices, or cardiac transplant. Norepinephrine is recommended alone or in combination with an inotrope or cardiac enhancer in 123 Heart Fail Rev (2007) 12:113–117 order to increase SBP in the situation of persistent organ hypoperfusion (e.g., low urine output clearly related to low blood pressure). Epinephrine is however not recommended as first line therapy; it is rather used as rescue therapy in cardiac arrest. There is no evidence of a renal benefit with low-dose dopamine. Levosimendan is a novel calcium-sensitizer that improves cardiac contractility by binding to troponin-C in cardiomyocytes. The significant vasodilatory properties of levosimendan are mediated through ATP-sensitive potassium channels, causing peripheral arterial and venous dilatation, and increasing coronary flow reserve [12]. Levosimendan has beneficial hemodynamic and clinical effects in patients with AHFS, and it is safe in acute coronary syndrome. In the REVIVE trial, levosemindan significantly improved a composite of clinical signs and symptoms of AHFS as compared to placebo over five days as assessed by patients and their physicians [13]. In the SURVIVE study comparing levosimendan and dobutamine, a statistically significant improvement in survival for levosimendan treated patients was seen early, especially in patients chronically treated with a beta blocker and in patients with prior heart failure, but it was not evident in 180day survival [14]. Why should we promote an early treatment of AHFS? ADHERE registry data indicate that AHFS treatments are often instituted more than 8 h after presentation. The mean time to IV diuretics was 8 hours and the mean time to IV vasoactive therapy was roughly 24 h [11, 15]. Starting earlier the appropriate therapy may be a method to counteract negative effects (1) of AHFS, including hypoxemia, hypotension and (2) of the drugs given to the patients, before irreversible damage has occurred. Nguyen et al. prospectively studied the impact of emergency department (ED) intervention on physiologic scores in 81 patients who presented to the ED with illnesses severe enough to warrant ICU admission [16]. The data from this study indicated that ED intervention might have influenced the progression of critical illnesses. A similar study in patients with severe sepsis or septic shock also demonstrated improved clinical outcomes with early goaldirected therapy [17]. These data suggest that early initiation of treatments for AHFS may be a key factor in improving outcomes among critically ill patients [17–19]. We are proposing here that treatment algorithm should be based on systolic blood pressure at admission. Among the proposed treatments, non-invasive ventilation is the only treatment that was consistently proven to be beneficial on morbidity and mortality in almost all types of AHFS. 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