Abstract and Introduction
Abstract
Heart failure (HF) is a highly prevalent disease in Western society, reaching epidemic proportions in the United States.[1] Although current therapies have improved quality of life and survival for HF patients, mortality and morbidity remain high. Astute management is essential for decreasing mortality. This article discusses the pathophysiology of systolic and diastolic dysfunction, pharmacologic strategies to treat HF, cardiac resynchronization therapy (CRT), implantable hemodynamic monitoring devices, and patient assessment and outcome evaluation. The advanced practice nurse (APN) plays an integral role in the evaluation and treatment of patients with HF.
Introduction
HF is a progressive and debilitating disease. The incidence of HF increases with age, such that 75% of the male HF patients and 85% of the female HF patients are older than age 65 years.[2] There are 4 to 5 million patients with HF in the United States, with approximately 400,000 to 500,000 newly diagnosed cases and 250,000 deaths annually.[3,4] In addition, treatment of patients results in 7 million hospital days annually with 44% incidence of readmission within the next 6 months.[5]
HF can result from systolic dysfunction or diastolic dysfunction. The former is seen in two thirds of patients and is caused primarily by ischemic heart disease; patients with this type of dysfunction demonstrate a left ventricular (LV) ejection fraction (EF) < 30%. Diastolic dysfunction is seen in one third of patients and is commonly caused by hypertension, hypertrophic and restrictive cardiomyopathy, constrictive pericarditis, myocardial infiltration, and possibly diabetes.
Pathophysiology of Systolic and Diastolic Dysfunction
From the traditional view, the hemodynamic point of view, HF is defined as a pathophysiologic condition in which impaired cardiac performance is responsible for the heart's inability, at normal filling pressures, to increase cardiac output in adequate proportion to meet the patient's metabolic demands.[6] In turn, it was thought, the heart responds to the reduced cardiac output by compensatory mechanisms affecting the Frank-Starling curve relationship, the thickness of the ventricular wall, and sympathetic nervous system functionality.
However, a mounting body of evidence supports the hypothesis that activation of the neurohormonal system triggers a cascade of hemodynamic changes and symptoms that adversely affect outcomes. Reflex activation of hormones is not simply a compensatory mechanism, but also leads to apoptosis (myocardial cell death), endothelial dysfunction, decreased vasodilator capacity, abnormal redistribution of blood, and many other problems that are detrimental to the patient. The major neurohormonal systems that are activated in HF are the renin-angiotensin system, the sympathetic nervous system, endothelin pathway, natriuretic peptides, and tissue necrosis factor (Table 1).
Ventricular remodeling and dysfunction ensue. The geometric shape of the ventricle is altered; it becomes more spherical and dilated. Negative consequences of remodeling include increased wall tension, increased oxygen consumption, decreased subendocardial perfusion, and decreased myocyte shortening.
In addition, remodeling is itself a risk factor for ventricular arrhythmias.[8,9] Indeed, geometric alteration affects prognosis both by affecting hemodynamic function and by increasing the risk of arrhythmias, such that sudden cardiac death is seen in 40% to 60% of persons with systolic dysfunction.[10] Abnormal physiologic effects associated with remodeling include neurohormones affecting the structure and metabolism of the heart, increasing hypertrophy and subsequent dilatation via alterations in preload, afterload, stretch, wall stress, interstitial collagen deposits, and direct toxic effects. (See Table 2 for a glossary of terms.)
Symptoms may relate to hemodynamic abnormalities; therapies are instituted to interfere with and to prevent remodeling.
Pharmacologic Strategies
In patients with HF secondary to systolic dysfunction, the goals of therapy depend on the severity of the disease. In mild disease, the primary objectives are to decrease disease progression, improve survival, and decrease symptoms. In severe disease, decreasing symptoms is a more critical objective, with the ultimate goal of improving survival and decreasing disease progression.
Therapy should be targeted to the stage of the disease. The American College of Cardiology (ACC) and the American Heart Association (AHA) have identified 4 classes of disease (Table 3).
Clinical Trials in HF
A number of randomized clinical trials (Table 4) have demonstrated the benefits of pharmacologic treatment strategies for patients with HF.[11-27]
Available Agents
Pharmacologic treatment (Table 5) has been expanded to include the blocking of maladaptive neurohormonal responses. Optimal pharmacologic therapy can result in regression of LV dysfunction and remodeling and improved systolic function. Conventional therapy includes angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) and diuretics. Digoxin is recommended for patients who remain symptomatic on ACE inhibitors and diuretics. ß-blockers should be considered for patients with stable Class II-III HF unless they have a contraindication to its use.
ACE inhibitors are considered the cornerstone of pharmacologic treatment for HF. The benefits of maximizing therapy with these agents include decreased mortality, symptom improvement, and reduction in hospitalization rates. ARBs are recommended if patients are ACE intolerant (Figure 1). Diuretics have become standard therapy for HF patients. They are often needed to treat the volume overload even if patients are on other appropriate therapies. Digoxin is recommended to improve the clinical status of patients with HF; the benefits are related to the effects on the autonomic nervous system rather than to the inotropic effects.
The evidence is overwhelming that ß-blockers provide substantial benefit in patients with mild to moderate HF by improving EF and reducing mortality. Spironolactone (Aldactone) merits consideration in patients with more advanced HF. Hyperkalemia is a concern with use of spironolactone, especially with concomitant administration of an ACE inhibitor.
The hydralazine-nitrate combination should not be used in HF patients who have no prior use of ACE inhibitors. This combination should be considered in patients who are ACE intolerant because of renal insufficiency or hypotension.
Nonpharmacologic Therapy and Tools
CRT
CRT may offer a unique and promising therapeutic approach to patients with an interventricular conduction defect and HF. Several studies have suggested that a wide QRS complex is a marker for decreased cardiac performance and increased mortality in patients with HF.[29-33] This delayed activation may result in ventricular dyssynchrony, septal dyskinesis, presystolic mitral regurgitation, reduced diastolic filling times, and reduced dp/dt (see Table 2).[34,35]
The therapeutic intent of CRT is to maintain atrial synchrony and to allow simultaneous activation of the right and left ventricles. Clinical data from current ongoing or recently closed trials reveal an improvement in hemodynamic performance, with a significant improvement in the patient's quality of life.
Initially, LV pacing was achieved with an epicardial approach requiring an open chest procedure. Currently, a transvenous approach is being used. Standard pacing leads are placed into the right atrium and ventricle, with a pacing lead advanced into the coronary sinus (CS) and advanced to one of the LV epicardial cardiac veins. The preferred position in the CS lead is a lateral or posterolateral cardiac vein.
Implantable Hemodynamic Monitoring Devices
The purpose of implantable hemodynamic monitoring devices is to provide data that will allow titration of HF medications on an outpatient basis and to allow analysis of the patient's response. These stand-alone devices permit early identification of impending hemodynamic deterioration, diagnosis of symptomatic events in the outpatient setting, and use of chronic hemodynamic data to optimize patients' long-term management.
These systems, undergoing clinical investigation in North America, employ an activity sensor and are activated automatically or by patient triggers. An interactive remote monitor permits downloading of device information at home by the patient. The information is networked via the Internet to allow the physician access to the patient data
Assessing Integrated Therapies to Promote Optimal Outcomes
Optimal treatment of patients with HF requires an approach that considers each patient's unique medical, psychosocial, behavioral, and financial circumstances. The diversity and complexity of these issues mandate a multidisciplinary approach and the need for outcome-based knowledge.[36]
Outcome-based patient assessment relies upon a systematic approach to serial assessments as well as responses to changes in the patient's status. These include:
- The cause of LV dysfunction;
- Contributing factors, such as tachycardias, anemia, alcohol consumption, ischemia, uncontrolled hypertension, obesity, recreational drug use, nonsteroidal anti-inflammatory drug use, thyroid disorders, and atrial fibrillation;
- Present circulatory status, such as resting profile, presence of congestion, orthopnea, paroxysmal nocturnal dyspnea, exertional cough, jugular venous distention, crackles, signs of hypoperfusion, hypotension, narrow pulse pressure, cool extremities, altered mentation, hyponatremia, and rising creatinine;
- Activity tolerance and limitations;
- Potential for gains with medication adjustment
- Associated risks, such as arrhythmias, embolic events, recurrent ischemia, and polypharmacy; and
- Psychosocial risk, such as anxiety, depression, social isolation, nonadherence to prescribed regimen, and adequacy of financial resources.[37]
Outcome-based collaborative interventions include achieving clinical stability, maintaining clinical stability, evaluating stability, and preventing disease progression.
Implications for Nursing
APNs, through their education, expertise, and advanced assessment skills, are in a unique position to lessen the progression of HF with early identification and intervention. APNs will continue to become primary providers for this patient population. Alterations in poor lifestyle behaviors and adherence to the prescribed plan of care can lead to improved quality of life and a reduction in mortality. APNs can encourage patients to control hypertension, diabetes, and hyperlipidemia; quit smoking; maintain an ideal body weight; limit alcohol consumption; and restrict dietary sodium. Nursing interventions can have the greatest impact on HF patients in these areas.[40]
The APN can educate patients about new treatment options and identify patients that may benefit from new modalities of therapy such as CRT and implantable hemodynamic monitors. As primary care practitioners, APNs must develop good relationships with cardiologists and electrophysiologists in order to make expedient referrals and effectively comanage the patient with CHF.
