Heart Failure (Fundamental and Clinical Cardiology)

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Another major limitation of inotropic therapy is the complexity of adjusting oral regimens as infusions are weaned. Prolonged physiologic effects of these infusions prior to discharge may mask inadequacy of the diuretic regimen and intolerance to vasodilator doses, setting the stage for readmission. This may be more likely with milrinone due to its long half-life, further prolonged in the presence of renal dysfunction.

For this reason, it is recommended that patients receiving inotropic infusions remain hospitalized for at least 48 hours after inotropic discontinuation. When hypotension prevents weaning of inotropic agents, ACE inhibitors may need to be stopped. In some patients, hydralazine, particularly in combination with nitrates, may facilitate inotropic weaning. Inotropic infusions are frequently used during hospitalization, in part because of initial convenience. Although the benefits of routine inotropic infusions often may not justify the risks, they can be life-saving while definitive procedures are being arranged for patients with rapidly progressive hemodynamic collapse.

When hemodynamic status is initially unclear in patients with severe symptoms, intravenous inotropic infusion may provide temporary stability until a more definitive profile can be defined. For chronic decompensation, brief inotropic therapy may be appropriate in those patients with high baseline blood urea nitrogen levels who have not demonstrated effective diuresis in response to repeated high dose intravenous loop diuretics with combined thiazides.

In general, use of current inotropic agents in heart failure may be considered as "until" therapy: until diuresis, until resolution of transient conditions such as pneumonia, until transplantation, or until death, as discussed below. Patients with profile L, those with low cardiac output without clinical evidence of elevated filling pressure, may be surprisingly stable clinically and often do not present with urgent symptoms.

Those admitted as cold and dry often have unappreciated congestion. Unless they have subnormal filling pressures or excessive vasodilation, they often do not improve acutely with adjustments of oral therapy. Inotropic infusions may lead to inotropic dependence and tachyphylaxis. The clinical assessment used to define profiles Figure 1 is frequently a sufficient guide for initial therapy although bedside skill in estimating hemodynamics has been challenged.

Invasive hemodynamic monitoring is often used when more precise measures of filling pressures, perfusion, and systemic vascular resistance are desired. Urgent hemodynamic monitoring guides initial intervention in critical situations during which therapies must be provided rapidly to avoid circulatory collapse. Hemodynamic monitoring may be particularly helpful when another condition complicates management such as pulmonary disease , the initial profile is not clear from clinical assessment and response, multiple therapies need to be adjusted simultaneously, therapy guided by empiric assessment is ineffective to maintain symptom relief, or intravenous inotropic agents cannot be weaned.

Pulmonary artery catheterization is routinely performed to evaluate pulmonary vascular resistance in potential transplantation candidates. Leaving the catheter in while redesigning therapy over a to hour period has often been followed by prolonged stabilization without transplantation. When therapy is tailored using a strategy of hemodynamic monitoring with clinical assessments, the goals are to approach pulmonary wedge pressure of 16 mm Hg or less and right atrial pressure of 8 mm Hg or less, first with intravenous vasodilators, then with oral therapies.

Although not a primary target of therapy, systemic vascular resistance measurement may guide titration of vasodilators vs diuretics to reduce filling pressures. Invasive hemodynamic measurement may allow rapid achievement of lower filling pressures, but it is not known whether this leads to better long-term outcomes. The availability of newer techniques to estimate hemodynamics may enhance individualization of therapy. The noninvasive bioimpedance device to assess filling pressures and cardiac output and the implanted hemodynamic monitor for home transmission of filling pressures are undergoing evaluation.

Brain natriuretic peptide BNP levels, which are increased by left-ventricular distention, provide an index of volume status 38 somewhat as hemoglobin A 1C provides an index of blood glucose control. Titration of therapy to BNP levels has been proposed 49 but not tested in a large advanced heart failure population.

It remains to be determined as to what extent these monitoring technologies will influence interventions and alter outcomes. Among patients experiencing the late stages of advanced heart failure, the most common reason that symptoms cannot be relieved, despite aggressive management, is the recently recognized cardiorenal syndrome. Some patients, often those with baseline renal impairment, demonstrate progressive decrements in renal function even as diuresis relieves symptoms.

Heart failure

This may be most common with long-standing volume overload, right ventricular dysfunction, and high baseline diuretic requirements. The term prerenal does not clarify either the mechanism or the solution of the cardiorenal syndrome. It was at one time assumed to reflect low cardiac output from excessively reduced filling pressures during diuresis. When measured, filling pressures usually still exceed the optimal levels needed to maintain cardiac output.

Higher creatinine and blood urea nitrogen levels are associated with a lower likelihood of maintaining freedom from congestion 52 and a greater likelihood of rehospitalization and death. Optimal clinical status may be maintained for many patients at a creatinine and blood urea nitrogen level higher than levels during volume overload. In some patients, renal function slowly improves during chronic maintenance of a lower volume state.

The cardiorenal syndrome is 1 of the major factors leading to frequent inotropic infusions, which can relieve congestion temporarily, but the impasse usually reappears once inotropic therapy is weaned. Under these conditions, angiotensin receptor antagonists cannot substitute for ACE inhibitors due to similar renal effects.

Heart Failure - Cardiac Pathology

In rare cases with otherwise good hemodynamic stability, chronic peritoneal or hemodialysis may be considered. The solution to the cardiorenal syndrome awaits better understanding of the mechanisms. Identification and aggressive treatment of elevated filling pressures in advanced heart failure is the major difference between heart failure regimens before and after referral to tertiary care centers.

The average patient referred with severe congestive symptoms undergoes approximately 4 L of net diuresis. When weight gain suggests volume retention, the usual dose is supplemented with transient dose doubling or intermittent addition of a thiazide, in a flexible patient-guided program. The usual patient with advanced heart failure has labile renal function predisposing to hyperkalemia and the risk of hyperkalemia is further increased by diabetes, high ACE inhibitor doses, or combination therapy with angiotensin receptor—blocking agents.

General use should be limited to patients requiring loop diuretics who have serum creatinine levels that are stable and lower than 2. The vasodilator regimen merits reevaluation after the establishment of optimal volume status, when patients often become more sensitive to the hypotensive effects of vasodilators. For ACE inhibitors, the complex actions include both vasodilation, which can be acutely beneficial, and neurohormonal antagonism, which improves long-term prognosis but may decrease cardiac output and blood pressure when circulatory compensation stimulates the renin-angiotensin system.

Captopril, a shorter acting ACE inhibitor given 3 to 4 times daily, may be easier to initiate when difficulty is anticipated due to hypotension. ACE inhibitor doses may occasionally need to be decreased or stopped to allow weaning of intravenous inotropic agents. Once a patient is stabilized and has been released from the hospital, ACE inhibitor doses can be increased as tolerated. Titration to the target doses used in clinical trials mg captopril, 20 mg enalapril maleate, and mg lisinopril 3 , 57 , 58 is recommended when tolerated. Although every attempt should be made to advance beyond the starting doses, there is decreasing emphasis on arbitrary target doses.

Hydralazine has been used effectively to wean some patients apparently dependent on intravenous inotropic infusions. Although hydralazine and nitrates are commonly combined, either can be used alone or in combination with ACE inhibitors. Nitrates were the first vasodilators shown to improve outcome in chronic heart failure.

Although unsupported by commercial interest, the generic nitrate compounds are prescribed by many heart failure consultants to improve symptoms, with minimal adverse effects except headaches. A small controlled trial confirmed improved exercise capacity when nitrates are added to ACE inhibitors in advanced heart failure and suggested decrease in left ventricular dimensions.

In the Digitalis Investigation Group trial, heart failure hospitalizations were decreased, most notably in patients at highest risk. Although inotropic state can be increased acutely with high doses, the major benefit of digoxin is now attributed to autonomic effects seen at low doses. For patients who can be stabilized without evidence of congestion, the focus of further therapy is improvement of long-term outcome by decreasing disease progression and death.

ACE inhibitors are recommended for all stages of heart failure. Improvement correlates in part with reductions in elevated baseline heart rates. Patients must receive detailed instructions regarding early signs of volume retention and the distinction between mild lassitude and circulatory collapse.

Occasionally, severe depression can develop. Although there is strong pressure to discharge patients quickly, the last hospital day consumes fewer resources than the first day of rehospitalization. Criteria for discharge include at least 24 hours of stable fluid status, blood pressure, and renal function on the oral regimen planned for home BOX. Patients who have received intravenous inotropic agents should be observed for at least 48 hours after weaning to avoid masking inadequacy or intolerability of the discharge regimen.

Clinical Status Goals Achievement of dry weight Definition of optimal blood pressure range Walking without dyspnea or dizziness. Stability Goals Twenty-four hours without changes in oral heart failure regimen At least 48 hours off intravenous inotropic agents, if used Fluid balance even on oral diuretics Renal function stable or improving.

Home Maintenance Plan Patient and family education about Sodium restriction Fluid limitation Medication schedule Medication effects Exercise prescription Flexible diuretic plan Scheduled call to patient within 3 days Indications for when to call nurse, physician, or Clinic appointment within 5 to 10 days. First appreciated in transplantation programs and clinical trials, multiple variations exist on the theme of intensive follow-up by specialized heart failure nurses who provide education and preemptive telephone contact to identify problems and allow patients the opportunity to ask questions.

Benefit was not shown for regular follow-up care with a primary physician and nurse team, in which patient satisfaction improved but hospitalization rate increased. Patient education includes frequent review of a flexible diuretic plan adjusted according to daily weights and specific information on sodium restriction. Although low serum sodium does not necessarily indicate excess water intake or respond to free water restriction in this population, it reflects intense neurohormonal activation such that patients may need to restrict fluid intake to maintain fluid balance as diuretics become less effective.

Vaccination for influenza and pneumonia are recommended. For patients without resting symptoms, regular exercise is strongly advised, such as a walking program outside or in enclosed shopping areas or stationary bicycle and treadmill exercise. The randomized controlled trials of exercise training in patients with heart failure have demonstrated remarkable improvements in function and reduced hospitalization rates, with indication that autonomic balance is improved. The scope of this review does not include detailed discussion of therapies not yet incorporated into guidelines.

There is some consensus that evaluation and therapy for nocturnal respiratory disturbances should be pursued. Ongoing trials will help determine the role that this therapy will ultimately play in advanced heart failure. Insertion of implantable cardioverter defibrillators is recommended for patients who have had sustained ventricular arrhythmias or cardiac arrest, or inducible ventricular tachycardia 75 if the prognosis for extended good quality of life remains otherwise good. Risk stratification remains difficult in other patients.

Compromised nutrition represents complex interplays between gastrointestinal tract symptoms that decrease food intake and absorption, transition to a protein-wasting state associated with chronic inflammatory activation similar to many chronic diseases, and, less commonly, increased metabolic rate. Supplementation with micronutrients is under investigation. Stress reduction techniques should be considered for patients with intrinsic and situational anxiety. Depression is increasingly recognized to decrease quality of life, functional capacity, and perhaps survival with heart failure, 80 but pharmacotherapy has not been studied in the population carrying both diagnoses.

Clinical class, although imprecise, consistently provides a general estimate of prognosis. Prognosis at every stage is worsened by even modest degrees of renal insufficiency. The bedside assay for brain natriuretic peptide correlates with clinical severity of heart failure and with prognosis. For patients with known heart failure, it is not known how much prognostic information will be provided beyond that from routine clinical assessment. Although often considered as one of the neurohormonal markers, BNP is released predominantly from the left ventricle under stress and closely reflects left ventricular filling pressures.

Filling pressures have been shown to predict outcome, particularly when measured after adjustment of therapy. Measurements of functional capacity such as peak oxygen consumption from formal exercise testing are useful when following up with individual patients for more aggressive intervention such as cardiac transplantation, 87 for adjusting exercise prescriptions, and for gauging ability to perform physical work. The 6-minute walk distance correlates generally with outcome and is easier to perform, 88 but it is not precise enough for the preceding indications.

Most of the predictive power of exercise tests comes from the highest and lowest ranges, which are frequently evident from a careful history and observation of the patient. All parameters may be more predictive when reassessed after rigorous optimization of therapies within a disease management program. Clinical status remains a useful, perhaps sufficient, predictor for most advanced heart failure. Patients presenting with class IV symptoms who can be stabilized without evidence of congestion can be upgraded to a prognosis similar to that of class III patients. Accurate prediction of survival is meaningful only for large populations.

Numerical estimates of survival on medical therapy are most relevant to those few eligible for high-risk intervention such as cardiac transplantation or trials of new assist devices. Once that is understood, those individuals who still demand specific numbers for life expectancy should receive generous estimates and encouragement to plan ahead for activities and events that provide meaning to their lives. For many patients with advanced heart failure, quality of life is as important as anticipated survival. Some of the frustration with multiple assessment tools results from the limited impact of our current drug therapies on quality of life.

Diuretic therapy, for which there is little trial data but universal acceptance of efficacy, may yield the most immediate and dramatic symptomatic improvement. Although ACE inhibitors have not consistently improved quality of life, they allow better maintenance of current quality of life, seldom perceived by patients as improvement. Patients with heart failure can express preferences for perceived health vs length of survival.

Preferences for quality over length of life correlated with jugular venous pressure elevation, dyspnea, and peak oxygen consumption. The responses suggest that an understanding of patient preferences should help guide selection of therapy for an individual and set parameters by which new therapies for advanced heart failure are evaluated. Functional capacity, quality of life, or both improved early during therapy with some agents subsequently found to increase mortality, such as flosequinan, a vasodilator with some inotropic action, and the inotropic agents pimobendan and vesnarinone.

Although there are currently no known agents for heart failure that produce sustained improvement in quality of life with a small increased risk of death, such an agent, if developed, might be a valuable option for the small population of patients with otherwise refractory heart failure symptoms. Despite the multiple interventions shown to improve survival, heart failure remains a progressive disease. Implantable mechanical cardiac support devices have reversed life-threatening hypoperfusion when used as a bridge for patients awaiting transplantation.

The recently released results of the Randomized Evaluation of Mechanical Assist Treatment for Congestive Heart failure REMATCH trial 4 show that these devices improve survival as destination therapy for patients requiring intravenous inotropic infusions, but serious mechanical, physiologic, and financial limitations remain. A unique aspect of end-stage heart disease as opposed to other chronic conditions is the availability of implantable cardioverter defibrillators.

Although these devices decrease recurrence of life-threatening arrhythmias, 75 the appearance of tachyarrhythmias for some patients heralds a steepening decline of cardiac and clinical function. Increasing hospitalizations for decompensation increase the likelihood of observing nonsustained ventricular tachycardias. Successful defibrillation can prolong the end of life whose quality has diminished to intolerable levels.

In the past and in countries where defibrillators are not often implanted, fewer patients survive to suffer from refractory circulatory failure. Before implanting a device that provides a detour at the end of the road, careful reconnaissance should be made of the outlook for the journey. Patients should understand the option to deactivate the defibrillation mode. The appropriate role of inotropic infusions remains unclear. They are often initiated with the expectation that brief support during decompensation will enhance diuresis and accelerate discharge although this assumption has been challenged.

Patients are occasionally discharged on these infusions awaiting transplantation. Reluctance to confront the impending end of life may lead to the complex prescription of home inotropic infusions, requiring indwelling central catheters with high infection risks, and precious community nursing resources. For most patients truly refractory to other therapies, this approach complicates the end of life while prolonging it by only days or weeks. Although it is anticipated that programs specializing in advanced heart failure will occasionally maintain outpatients who are receiving continuous inotropic infusions as palliative end-stage care, 6 there is more concern about intermittent inotropic infusions administered 1 to 3 times weekly in outpatient infusion clinics.

Improvements described on this therapy have generally been ascribed to the increased frequency of clinical contact. There are currently no accepted indications for this practice. Some lessons learned from the care of terminal malignancy can be translated into end-stage heart failure management. As we recognize the elements of discomfort, often perceived as actual pain, and fearfulness during terminal circulatory failure, 98 we are learning to prescribe anxiolytics and narcotics as well as diuretics. When there is alignment of patient and family wishes and community resources, hospice is increasingly used for patients with end-stage heart failure after implantable defibrillators are deactivated.

The landscape of end-stage heart failure treatment is changing very rapidly, as though viewed from a train. Bases of controlled clinical trial evidence fall far behind the clinical decisions required. Current management as heart failure advances is based more on consensus than on randomized trials.

Current mechanical support devices offer a limited future but increase expectations of immortality. Even as the end approaches, heart failure is characterized by wide excursion between good and bad days, often preserving hope for another good day until the last. Uncertainty regarding time and mode of death exceeds that for other terminal illnesses. Each patient travels a unique journey, on which many share remarkable determination to prevail.

As we embolden our patients to understand and influence their course, as we appreciate their individual preferences for quality and length of life, we will guide each other through the changing management of advanced heart failure. All Rights Reserved. Figure 1. Most patients can be classified in a 2-minute bedside assessment according to the signs and symptoms shown although in practice some patients may be on the border between the warm-and-wet and cold-and-wet profiles.

This classification helps guide initial therapy and prognosis for patients presenting with advanced heart failure. Although most patients presenting with hypoperfusion also have elevated filling pressures cold and wet profile , many patients present with elevated filling pressures without major reduction in perfusion warm and wet profile. Patients presenting with symptoms of heart failure at rest or minimal exertion without clinical evidence of elevated filling pressures or hypoperfusion warm and dry profile should be carefully evaluated to determine whether their symptoms result from heart failure.

Reprinted with permission from Dr Stevenson. Figure 2. The step diagram demonstrates addition of therapies in relation to the clinical severity of heart failure with reduced left ventricular ejection fraction. Angiotensin receptor—blocking agents ARBs are a reasonable alternative for patients who cannot tolerate ACE inhibitors due to angioedema or severe cough but they are not appropriate for patients intolerant to ACE inhibitors due to symptomatic hypotension, renal failure, or hyperkalemia.

Diuretics are prescribed to maintain fluid balance, with spironolactone added in patients with severely symptomatic disease when renal function and potassium handling are preserved. Fluid retention persisting despite high-dose loop diuretic therapy may be better managed with torsemide, a loop diuretic with better absorption. Metolazone effectively potentiates loop diuretic effects, but regular use should be avoided due to severe electrolyte depletion. When severe symptoms persist, patients should be reevaluated to diagnose and treat persistent congestion.


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Some patients may benefit from addition of nitrates with or without hydralazine. Transplantation and mechanical assist devices are relevant to only a very small population with advanced heart failure. Restriction of sodium and fluid intake is increasingly required as heart failure becomes more severe. Exercise is recommended for all patients except those with severe resting dyspnea. Heart failure management programs are most cost-effective in patients at high risk for repeated heart failure hospitalizations, but they may be useful at every stage of disease. Table 1.

Table 2. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. N Engl J Med. Google Scholar. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. Long-term use of a left ventricular assist device for end-stage heart failure. Clinical definition and epidemiology of advanced heart failure. Am Heart J. J Am Coll Cardiol.

Approach to the patient with severe heart failure. In: Rose EA, ed. Management of End-Stage Cardiac Disease. Philadelphia, Pa: Lippincott-Raven, Optimizing therapy for complex or refractory heart failure: a management algorithm. Consensus recommendations for the management of chronic heart failure: on behalf of the membership of the advisory council to improve outcomes nationwide in heart failure. Am J Cardiol. Improving survival for patients with advanced heart failure: a study of consecutive patients.

Low-dose amiodarone for atrial fibrillation. Comparison of the effects of AV nodal ablation versus AV nodal modification in patients with congestive heart failure and uncontrolled atrial fibrillation. Pacing Clin Electrophysiol. Atrial fibrillation is associated with a lower exercise capacity in male chronic heart failure patients.

Moderate alcohol consumption and risk of heart failure among older persons. Results of coronary artery surgery in patients with poor left ventricular function CASS. CABG in advanced left ventricular dysfunction. Cardiol Clin. Ischemic cardiomyopathy: criteria for coronary revascularization and cardiac transplantation. Left ventricular reduction surgery with mitral valve repair.

J Heart Lung Transplant.

The beating open heart for rebuilding ventricular geometry during surgical anterior restoration. Semin Thorac Cardiovasc Surg.

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