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"Permissive Hypotension" in Hibernated Patients with Severe Chronic Heart Failure
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Mohamad Abdelsalam Abdelkader, King Fahd Hofuf Hospital ICU Department
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mohamadabdelsalam{at}hotmail.com Mohamad Abdelsalam Abdelkader
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Heart failure is a complex clinical syndrome that can result from any structural or functional cardiac abnormality that impairs the ability of the left ventricle to fill with or pump blood. The cardinal manifestations of heart failure are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary congestion and peripheral oedema. Heart failure is characterized by inadequate tissue perfusion to meet the metabolic demands of the body. In systolic heart failure, there is reduced myocardial contractility, whereas in diastolic heart failure, there is impaired relaxation and abnormal filling of the left ventricle. Heart failure is primarily a disease of the elderly, with approximately 6 – 10 % of people older than 65 years have heart failure. Although more patients survive acute myocardial infarctions because of the widespread availability of coronary reperfusion therapy, most have at least some residual left ventricular systolic dysfunction which may progress to heart failure [1]. The American College of Cardiology and American Heart Association published a new staging classification of heart failure. Stage A includes patients at risk of developing heart failure but have no structural heart disease. These include patients with hypertension, diabetes and coronary artery disease. Stage B includes asymptomatic patients with structural heart disease (LV dysfunction, previous MI, or valvular heart disease). Stage C includes patients with structural heart disease and symptomatic heart failure. Stage D includes patients with severe refractory heart failure who are markedly symptomatic despite maximal medical therapy and who require specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions or cardiac transplantation. According to this staging classification, patients with heart failure would only be expected to advance from one stage to the next, unless progression of the disease was slowed or stopped by treatment [2]. The New York Heart Association Heart Failure Classification is a functional – not a staging – classification that is used to assess the severity of functional limitation of patients with heart failure. Although imperfect, NYHA functional classification has long been used to categorize patients with heart failure and this classification correlates fairly well with the prognosis of the disease. Modern therapy of heart failure is based on inhibition of the neurohormonal systems that may be initially beneficial but eventually become deleterious. The sympathetic nervous system increases heart rate, myocardial contractility and cardiac output but also causes arteriolar vasoconstriction and increased afterload. Increased circulating catecholamines aggravate myocardial ischemia, potentiate arrhythmias, cause cardiac remodeling, and are directly toxic to the myocytes [2]. Stimulation of the renin-angiotensin- aldosteron system as a result of sympathetic stimulation and decreased renal perfusion results in further arteriolar vasoconstriction and increased aldosterone production. Increased aldosterone levels lead to sodium and water retention, vascular endothelial dysfunction and myocardial fibrosis [3]. Neurohormonal antagonists (including ACE inhibitors, B-blockers and aldosterone antagonists) have been shown in several randomized controlled studies to reduce mortality, alleviate symptoms and improve the functional class of heart failure. On the long term, ACE inhibitors and B-blockers also improve left ventricular performance and ejection fraction [3-4-5]. Despite recent advances in the management of heart failure, mortality remains high, with an estimated 5- year mortality rate of 50%. The mortality is higher among patients with severe heart failure (NYHA class 4) who have a 20% annual mortality rate. Patients with severely depressed myocardial contractility may not tolerate ACE inhibitors because of hypotension or renal impairment. This is due to peripheral vasodilatation and decreased systemic vascular resistance without a compensatory increase in cardiac output, especially when large doses of diuretics are being used. In addition, severely distressed patients have abnormally increased cost of breathing with up to 40 – 50 % of cardiac output being shifted to the overacting respiratory muscles that further compromise systemic perfusion. As a result of low cardiac output and systemic hypoperfusion, the body activates several neurohormonal pathways, leading to cardiac remodelling with left ventricular dilatation and hypertrophy as well as apoptosis, or programmed cell death, leading to worsening of myocardial contractility. Furthermore, left ventricular dilatation causes increased wall tension and may provoke myocardial ischemia in patients with coronary artery disease. If we consider heart failure as a state of imbalance between systemic perfusion and metabolic demands of the body as a result of impaired myocardial contractility, I may postulate that improving systemic perfusion and /or reducing metabolic demands can suppress the detrimental neurohormonal systems. Intubation, mechanical ventilation and sedation (with or without muscle paralysis) can minimize the whole-body oxygen consumption and reduce the burden on the failing heart by being not obliged to pump too much blood to meet the increased metabolic demands. Consequently, I may speculate that neurohormonal systems may be more suppressed in ventilated, sedated and paralysed patients with heart failure. It may be appropriate to measure B-type natriuretic peptide, endothelin 1 and other parameters of neurohormonal activation before and after assisted ventilation. In patients with severe dyspnea, positive- pressure ventilation can significantly reduce the work of breathing and allow the distribution of cardiac output away from the overacting muscles of respiration into more vital organs such as the heart, brain, and kidneys. This may lead to improved coronary perfusion, myocardial oxygen supply and enhanced contractility in patients with ischemic cardiomyopathy. Preload reduction - as a result of reduced venous return - will decrease left ventricular end-diastolic diameter, wall tension, myocardial oxygen demand and ischemia. In addition to improving arterial oxygenation, assisted ventilation can also increase myocardial oxygen supply, reduce demand, improve myocardial ischemia and enhance contractility of the failing heart. In ventilated patients with severe heart failure, the dose of diuretics can be decreased or temporarily discontinued to reduce the risk of hypotension or renal impairment as a result of ACE inhibitor therapy. It is to be remembered that ventilator – induced hypotension is a potential complication in volume – depleted patients and is not considered a significant risk in heart failure patients who are often fluid overloaded. As a result, ventilated patients with severe heart failure may be more tolerant to initially low, gradually increasing doses of ACE inhibitors and B-blockers, particularly when using lower levels of PEEP and tidal volume. Invasive hemodynamic monitoring with Swan-Ganz catheter may be important in selected patients to optimize cardiac filling pressures (central venous pressure and pulmonary capillary wedge pressure) and to monitor cardiac output in order to avoid significant hypotension or renal dysfunction, as a result of ACE inhibitor or B-blocker therapy. ACE inhibitors may be initiated under an umbrella of inotropic support with dobutamine or milrinone in order to increase cardiac output and compensate for decreased systemic vascular resistance as a result of ACE inhibitor – induced systemic vasodilatation. For patients with borderline blood pressure, continuous inotrope infusion can be maintained for few weeks - until ACE inhibitor therapy has been maximized – then can be gradually weaned off. It may be wise to accept some degree of hypotension (without necessarily discontinuing ACE inhibitors) as long as adequate systemic perfusion and tissue oxygenation are maintained, keeping in mind that oxygen consumption is significantly reduced because of ventilation, sedation and muscle paralysis. It must be emphasized that hypotension is not synonymous with shock. Patients with low blood pressure may have normal tissue perfusion if systemic vascular resistance is also decreased. On the other hand, tissue perfusion may be impaired despite normal blood pressure in the presence of low cardiac output and severe systemic vasoconstriction. Provided that coronary, cerebral and renal perfusions are maintained, cardiac output may be allowed to increase progressively, during the period of so-called "permissive hypotension" as a result of afterload reduction and gradually improving left ventricular function. Ultimately, blood pressure can be maintained mainly by cardiac output rather than by intense peripheral vasoconstriction that often occurs at the expense of left ventricular performance and systemic perfusion. Tissue oxygenation can be monitored directly by measuring whole-body oxygen uptake - using calorimetry- or indirectly by calculating oxygen extraction ratio (O2 ER = SaO2 – SvO2 / SaO2) where SaO2 is arterial O2 saturation and SvO2 is mixed venous O2 saturation (of blood taken from pulmonary artery with right-sided cardiac catheter). Other parameters of tissue oxygenation include arterial blood lactate and gastric mucosal pH. In selected patients with relatively low blood pressure, cerebral perfusion can be evaluated by calculating cerebral O2 extraction ratio (cerebral O2 ER = SaO2 – SvjO2 / SaO2) where SvjO2 is O2 saturation of blood taken from internal jugular vein. Similarly, myocardial oxygenation can be directly evaluated by measuring myocardial blood lactate, oxygen extraction ratio, regional pH and base deficit during transvenous catheterization of the coronary sinus (that drains most of the cardiac veins and opens into the right atrium). Non-invasive assessment of myocardial ischemia can be performed with serial ECGs to detect ST segment – T wave changes and repeated echocardiography to evaluate LV function and regional wall motion. Renal function should be closely monitored with urine output, BUN and creatinine. In conclusion, patients with NYHA class 4 heart failure, who are poorly tolerant to ACE inhibitors or B-blockers can be electively intubated, ventilated and sedated in order to minimize oxygen consumption and metabolic demands of the body and to improve arterial oxygenation, myocardial contractility and systemic perfusion. ACE inhibitor therapy can then be gradually introduced (with or without inotropic support) and continued in spite of relatively low blood pressure as long as systemic perfusion and tissue oxygenation are maintained. When ACE inhibitor and B- blocker therapy are maximized and patients are still hemodynamically stable, they can be awaken from "hibernation" and gradually weaned off mechanical ventilator. References 1- American Heart Association. 2001 Heart and Stroke Update. American Heart Association. 2- ACC/AHA Guidelines for the Evaluation and Management of Chronic Heart Failure in the Adult. 2001 by the American College of Cardiology and the American Heart Association. 3- Pitt B, Zannad F, Remme WJ, et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl J Med 1999; 341: 709-717 4- Pitt B, Cohn JN et al. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure (SOLVD) N Engl J Med. 1991;325:293-302. 5- packer M, Coats AJ, Fowler MB et al. Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med.2001; 344:1651-1658 |
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