Cover CE Article Evidence-Based Practice for Acute Decompensated Heart Failure Nancy Cathy M. Albert, A.

RN, MSN, Eastwood, CCNS, RN, CCRN,

Article

CNA MN

Michelle L. Edwards, RN, MSN, FNP, ACNP

Nancy M. Albert is certified as a clinical nurse specialist and has a dual role of director of nursing research in the division of nursing and clinical nurse specialist at the George M. and Linda H. Kaufman Center for Heart Failure of the Cleveland Clinic Foundation, Cleveland, Ohio. She codeveloped heart failure programs along the continuum of care, including emergency care, critical care, and acute care, at the Cleveland Clinic Foundation. Cathy A. Eastwood graduated with a master of nursing degree from the University of Calgary, Canada, after specializing in the care of patients with heart failure. She developed and managed the outpatient heart failure center and oversaw the flow of inpatients with heart failure at St. Lukes Episcopal Hospital, Houston, Tex. Currently, she is a lecturer at Memorial University of Newfoundland, School of Nursing, in St. Johns, Newfoundland, Canada. Michelle L. Edwards earned a master of science degree in nursing from the University of Alabama at Birmingham and is a board-certified family and acute care nurse practitioner. She practiced several years in critical care, specializing in the care of cardiovascular patients. She currently is a cardiology nurse practitioner/outcomes manager at St. Lukes Episcopal Hospital. To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints@aacn.org. This article has been designated for CE credit. A closed-book, multiple-choice examination follows this article, which tests your knowledge of the following objectives:

1. Identify the core drug therapies for decompensated heart failure 2. Describe the role of B-type natriuretic peptide in decompensated heart failure 3. Explain the pharmacological management of decompensated heart failure

Each year, chronic left ventricular systolic and diastolic dysfunction, or heart failure, causes 1 million hospitalizations in the United States.1 Heart failure is the most common Medicare diagnosis related group at discharge1,2 and is associated with poor survival and quality of life. In addition, cost of care is high; in 1998, Medicare paid out $3.6 billion for care related to heart failure.1 The Acute Decompensated Heart Failure National Registry (ADHERE)3 recently reported data on 14716 patients hospitalized for heart failure in the United States (Tables 1 and 2). Generally, patients admitted to the hospital for heart failure were elderly, were female, had a history of heart failure, and were unable to carry out activities of daily living without exercise intolerance. The most common symptom was dyspnea, which was most often associated with other signs and symptoms of fluid retention. Comorbid conditions were common, and patients were equally likely to be admitted with systolic dysfunction (reduced ventricular contractility; ejection fraction 0.40) or diastolic dysfunction (impaired ventricular relaxation or ventricular stiffness that decreases the ventricles ability to fill). One quarter of patients were rehospitalized within 6 months of a previous hospitalization, and Medicare was the primary hospital payor. Most patients spent time in the emergency department before admission as an inpatient, and the most common level of initial care was telemetry. Median length of stay was 4.4 days.3 View In In a this this new table: window window

Table 1 Characteristics of patients, clinical signs and symptoms, and hospital placement: data from the Acute Decompensated Heart Failure National Registry3 View In this this table: window

In

new

window

Table 2 Outpatient medications before hospitalization and medications at discharge: data from the Acute Decompensated Heart Failure National Registry3 The ADHERE data are similar to data from other studies4,5 in which investigators found an equal split of patients with impaired and preserved left ventricular systolic function, signifying hospitalization of patients with systolic dysfunction and patients with diastolic dysfunction. The primary mechanism of diastolic dysfunction that led to signs and symptoms was impaired ventricular relaxation, which was associated with increased age, obesity, hypertension, and cardiovascular disease.4 In addition, ADHERE data were comparable to data from other reports6
8

in that retention of fluid and sodium, as evidenced by admitting signs and symptoms, was a

primary factor in hospitalization. This knowledge provides an opportunity for care improvement that can be championed by nurses, because hospitalization for fluid and sodium retention in patients with systolic or diastolic dysfunction may be avoidable, especially when such retention is due to patients failure to adhere to medication regimens or self-care instructions. In this article, we discuss evidence-based practices for managing patients with acutely decompensated heart failure because in-hospital actions may facilitate an improved experience for patients after hospitalization. The intent is to provide management goals and actions associated with the most common clinical manifestation, fluid retention, and not to focus on management of cardiogenic shock, profound hypoperfusion, or complex decompensation (severe hyper-volemia, hypoperfusion, and acidosis or other conditions such as pneumonia). Assessment of patients, management strategies, and education of patients are highlighted. Myths associated with acute care management are discussed so that nurses will be more aware of appropriate interventions that are safe and effective. Heart failure management has progressed rapidly in recent years. Ultimately, nurses must be proactive in ensuring that their behaviors are based on current evidence. Heightened Expectations for Evidence-Based Care

Nurses are challenged to plan and provide care that promotes the best possible clinical and health-related outcomes. The Joint Commission on Accreditation of Healthcare Organizations 9 recently established 4 core measures in the acute management of patients with heart failure to promote adherence to basic standards of evidence-based care (Table 3). Because of the large number of patients and the high cost of care associated with hospital readmissions, acute and critical care nurses must develop and implement strategies that are associated with improved outcomes for patients and hospitals. In addition, in 2001, the American College of Cardiology (ACC) and the American Heart Association (AHA) published practice guidelines10 for adults with chronic heart failure. These guidelines provide caregivers with recommendations for nonacute care and include the rationale and level of evidence for support of each management strategy. Table 4 provides a list of management strategies, including core drug therapies, that should be a part of each patients treatment plan at discharge after an admission for decompensated heart failure stemming from volume overload.10,11 View In In a this this new table: window window

Table 3 The 4 core measures of the Joint Commission on Accreditation of Healthcare Organizations View In In a this this new table: window window

Table 4 Practice guidelines that apply to stage C* patients If the medication expectations listed in Table 4 are compared with the actual medication

therapies before hospitalization and at discharge indicated in the ADHERE data (Table 2 ), a need for change is evident. New efforts must be undertaken to promote use of consensus guidelines and therapies to meet the overall goal of managing heart failure: promoting regression and preventing progression of left ventricular enlargement (remodeling) to decrease disease

progression and improve survival.1114 See Figure 1 and Table 5 for definition and description of consequences of ventricular remodeling.

View In In

larger this a

version

(49K): window

new

window

Figure 1 Ventricular remodeling. Cross-sectional view of left and right ventricles: a, normal; b, concentric hypertrophy; and c, eccentric hypertrophy. View In In a this this new table: window window

Table 5 Ventricular remodeling: definition and consequences No standardized evidence-based guidelines are available to direct acute care; however, randomized, placebo-controlled research studies provide strong support for actions that are effective and safe. In addition, many actions promoted in the current guidelines for long-term outpatient management of heart failure can be translated to the acute setting and provide a uniform plan of care based on large, multicenter, randomized research studies that focus on the primary management goal of preventing progression of heart failure.10 Nurses can facilitate some practical assessment and management strategies that apply to patients admitted to the hospital with a primary diagnosis of heart failure who are not in cardiogenic shock or do not have profound hypoperfusion or complex decompensation. Implementation of the following strategies might require a change in the philosophy of care, further education, and continuous quality monitoring to ensure that evidence-based strategies are used regardless of the

type of physician, a patients placement (telemetry or nonmonitored bed), a nurses background (cardiac, heart failure, or generalist), or a hospitals resources. Assessment of Patients Before planning interventions for a patient hospitalized with heart failure, the healthcare team must conduct a systematic assessment that includes identification of the cause of the heart failure, aggravating factors, potential risk factors that may influence survival and quality of life, and current clinical status. Patients comorbid conditions, especially active chronic conditions, may act as exacerbating factors (Table 6), affecting the planning of patients care and influencing the timing and intensity of therapies. The treatment plan must include modification of correctable causes of decompensation. Examples include education for sodium indiscretion, alcohol abstinence programs for overconsumption of alcohol, or revascularization strategies for hibernating myocardium (ie, viable but under-perfused myocardial tissue with decreased contractility). In addition, risks related to heart failure must be considered, such as the need for anticoagulation to prevent embolic events or the need for an implantable cardioverterdefibrillator to prevent sudden cardiac death, so that appropriate consultations and therapies are discussed and initiated before patients are discharged from the hospital. View In In a this this new table: window window

Table 6 Exacerbating factors in chronic heart failure that lead to decompensation Hemodynamic Status: Volume and Perfusion

Volume and perfusion status provide useful clues to a patients cardiac performance and help shape the treatment plan. Nurse caregivers must frequently reassess the patients hemodynamic status to determine volume and perfusion status. Volume status is determined by assessing if the patient is wet, dry, or has a balanced fluid level (ie, has hypervolemia, hypovolemia, or euvolemia, respectively), and perfusion is assessed by determining if the patient is cold, cool/lukewarm, or warm (ie, has perfusion that is very low, slightly low, or normal,

respectively). Evidence of congestion includes the signs of neck vein distension, elevated pressure in the right internal jugular vein, positive abdominal-jugular neck vein reflex, edema, ascites, and crackles (rarely) and the symptoms of dyspnea, orthopnea, and paroxysmal nocturnal dyspnea.15 Nurses must be careful not to count on the presence of crackles as an indicator of congestion because chronic movement of fluid into the interstitium (common in patients with a history of chronic heart failure) is associated with increased lymphatic drainage so that crackles are absent and the alveoli remain relatively dry.16 Evidence of very low perfusion includes symptomatic hypotension, especially in patients receiving angiotensin-converting enzyme (ACE) inhibitors, cool extremities (arms and legs, not just hands and feet), mental obtundation or constant sleepiness, worsening renal function (elevation in serum levels of creatinine and urea nitrogen), hyponatremia, narrow pulse pressure, and, most important, a proportional pulse pressure of 25% or less.15,16 Acute care nurses should be educated in calculating proportional pulse pressure. The calculation is simple to do and can provide valuable information about cardiac contractility and perfusion, especially when trends over time are assessed. The formula to determine proportional pulse pressure is (systolic blood pressure - diastolic blood pressure)/systolic blood pressure, resulting in a proportion or percentage.16 An example of a calculation of proportional pulse pressure is (108 66)/108 = 42/108 = 0.389 or 39%. In a hemodynamic study16 of 50 patients with a history of heart failure, 91% of patients with a proportional pulse pressure of 25% or lower had a cardiac index (calculated as cardiac output in liters per minute divided by body surface area in square meters) of less than 2.2; however, systolic and mean arterial blood pressure were poorly correlated with cardiac index or stroke volume index. In a study17 of hemodynamic profiles (wet, dry, cold, and warm) and clinical characteristics of advanced heart failure, a low proportional pulse pressure was the only predictor of wet patients, and among wet patients, proportional pulse pressure was the only predictor of patients in the cold category. A patients hemodynamic profile should influence initiation of pharmacological and other treatment strategies and also guide the adjustment of therapies during the hospitalization.

Of note, patients who are admitted in a congestive or wet state with a high preload (passive stretch of myocardial fibers; reflects left ventricular end-diastolic pressure and volume) often have a high afterload (pressure the heart must pump against; reflects systemic vascular resistance, systolic stress, and systolic impedance) that impairs stroke volume and is reflected as a cool or lukewarm perfusion state. When hemodynamic measurements were recorded in 750 patients with heart failure before tailored therapy at a large university teaching hospital, the mean pulmonary artery occlusive pressure was 26 mm Hg (normal is 412 mm Hg; in heart failure treatment, the goal is 815 mm Hg) and the mean systemic vascular resistance was 1640 dynesseccm5 (normal is 8001200 dynesseccm5),15 reflecting a vasoconstricted state and the need for vasodilator therapy in addition to diuresis and natriuresis (sodium excretion). Diagnostic Tests

In addition to results of tests done at the time of admission (chest radiographs, arterial blood gas levels, liver function tests, hematologic tests, electrocardiograms, basic metabolic profile) and findings on physical examination, the results of point-of-care assays of serum levels of natriuretic peptides can be used to guide treatment in patients with acute decompensated heart failure (Figure 2). B-type natriuretic peptide (BNP) is secreted mainly from the ventricular myocardium in response to elevations in end-diastolic pressure and ventricular volume expansion.18 Not only can rapid measurement of BNP aid in diagnosis of heart failure,1923 but BNP level can also be used to assess clinical status and the effectiveness of therapies during an admission for acute decompensation.24

View In In

larger this a

version

(49K): window

new

window

Figure 2 Acute decompensated systolic heart failure (SHF) or diastolic heart failure (DHF) in patients with chronic heart failure: initial treatment of Abbreviations: BNP, B-type natriuretic peptide; EKG, electrocardiographic; INR, international normalized ratio; IV, intravenous; PT, prothrombin time. *Treatment decisions based on serum BNP results in acute decompensated heart failure DO NOT apply to patients with chronic, stable heart failure who are not acutely dyspneic. Profiles: patient is wet, dry, or has a balanced fluid level (ie, has hypervolemia, hypovolemia, or euvolemia, respectively), and is cold, cool/lukewarm, or warm (ie, has perfusion that is very low, slightly low, or normal, respectively). Point-of-care BNP testing can be a useful adjunct in determining which patients are receiving effective care, which patients are not progressing on the current treatment plan, and which patients might be candidates for end-of-life care. Nurses should consider all components of assessment of patients (etiology, aggravating factors, risks, and clinical status) when communicating and collaborating with members of the healthcare team so that patients have the best opportunity for care strategies that optimize outcomes and promote comfort. Myths and Realities of Management An algorithm provides a systematic approach to decision making as patients with chronic heart failure are assessed and managed during an acute exacerbation (Figure 2 ). The myths associated with management of acute heart failure are replaced with evidence-based actions that contribute to the best possible outcomes. Myth 1: The Goals of Treatment for Acute and Chronic Heart Failure Are Different One of the hurdles in management of heart failure is to overcome the myth that the goals of managing acute decompensated and stable heart failure are different. Today, it is important to gear therapies toward reversal of ventricular remodeling. Reversing ventricular remodeling is important regardless of whether patients are in stable condition or in a decompen-sated state. Historically, the primary goal of treatment of acute decompensated heart failure was to quickly reduce the circulating fluid volume to relieve patients of the pulmonary and peripheral edema. Diuretics dyspnea in the emergency department. have long been the standard type of drug used for decreasing volume and improving hemodynamic status and signs and symptoms.25 Through

research studies, however, it was learned that acute intravenous diuretic therapy was associated with many hazards, including increased mortality. Nonpotassium-sparing diuretic therapy was associated with an increased risk of arrhythmic (sudden) death, increased cardiac mortality, aggravated renal dysfunction, further activation of the reninangiotensin and sympathetic nervous systems with a concomitant increase in systemic vascular resistance that was compounded by a decrease in cardiac output from a reduction in preload, and electrolyte imbalances that caused muscle weakness, depression, reduced contractility (from reduced conductivity), and peripheral vasoconstriction.2631 In patients with acute decompensation, preventing or limiting further activation of neuroendocrine systems by using strategies that target excess intravascular and extravascular volume and vascular resistance will help meet the overall goals of preventing progression of and promoting reversal of ventricular remodeling. Myth 2: Managing Fluid Overload Equals Use of Diuretics

Administration of intravenous and oral loop diuretic agents is an important therapy aimed at decreasing preload (through initial venodilatation and then through diuresis and natriuresis) and ultimately relieving signs and symptoms, but these agents should not be used alone to improve overall morbidity and survival in patients with heart failure. In order to address increased afterload associated with both exacerbation of heart failure and intravenous loop diuretic therapy, pharmacological therapies must include agents that reduce neuroendocrine activation and vasoconstriction because these mechanisms can worsen the heart failure syndrome by worsening ventricular remodeling. Diuretics and ACE Inhibitor Therapy

Although only limited data are available, when an ACE inhibitor was combined with loop diuretics, the combination therapy reduced the pressor (vasoconstriction) response of diuretics. 32 ACE inhibitors reduced the increase in plasma angiotensin II, thus decreasing the sympathetic activation (and associated deterioration in left ventricular pump function) that preceded the diuretic action of diuretics.32 ACE inhibitors ultimately decreased reabsorption of sodium in the distal tubule and decreased aldosterone stimulation in the adrenal glands.33,34 Many randomized, controlled research studies were conducted from the early 1980s through the mid-1990s that added an ACE inhibitor to

diuretic therapy in patients with mild to severe heart failure, as summarized in the consensus guidelines.10 Researchers reported improvements in exercise tolerance, ejection fraction, and survival along with decreased rehospitalization rates.10 Therefore, diuretics are necessary to relieve signs and symptoms but should be used with ACE inhibitor therapy for survival benefit and to counterbalance the alterations in renal and adrenal mechanisms responsible for sodium and water retention. Nurses must proactively recommend increases in dosage of ACE inhibitors based on the ACC/AHA practice guidelines10 during the acute hospitalization period so that patients dosing regimens are on target before the patients are discharged from the hospital. Diuretics and Intravenous Vasodilator Therapy

When patients are admitted with a wet and lukewarm/cool or cold profile without indications of profound hypoperfusion, a combination of intravenous diuretics and vasodilator therapy leads to improved acute outcomes, without the need for inotropic agents (Figure 2 ). Many studies were conducted in the late 1970s and early 1980s in patients with New York Heart Association functional class IV decompensated heart failure to study the effectiveness of intravenous diuretic and vasodilator (nitroprusside and nitroglycerin) therapy in reducing filling pressures (preload) and systemic vascular resistance (afterload) and improving cardiac output. The results indicated that nitroprusside was a clinically effective and powerful agent for reducing afterload that also decreased ventricular systolic and diastolic volumes and improved ventricular diastolic properties. It provided rapid symptomatic relief for patients and improved, stabilized, and optimized hemodynamic parameters.3539 Intravenous nitroglycerin is known predominantly as an agent for reducing preload. However, at high doses, intravenous nitroglycerin reduces systemic and pulmonary vascular resistance. In patients with decompensated chronic heart failure, nitroglycerin was less powerful than nitroprusside in reducing afterload but was effective in reducing preload, increasing cardiac output, and controlling signs and symptoms and hemodynamic derangements.4042 Table 7 is a summary of the dose ranges, actions, and indications of vasoactive medications used in the management of patients with acute decompensated heart failure.43 View In this this table: window

In

new

window

Table 7 Intravenous vasoactive medications indicated in acute decompensated heart failure43 As the overall goal of managing patients with heart failure has shifted from improving hemodynamic status to improving neuroendocrine abnormalities in the hope that ventricular remodeling will be favorably affected, researchers have studied the effectiveness of intravenous vasodilator therapy in modulating the neuroendocrine axis. In a recent study44 of 34 patients with decompensated heart failure who received intravenous diuretics and vasodilator therapies (nitroprusside and ACE inhibitors) to reduce preload and afterload, neurohormonal activation (endothelin, norepine phrine, and BNP levels) decreased rapidly and was associated with improved hemodynamic status. Similar to results of studies conducted in previous decades, in this study,44 the mean cardiac index increased from 1.70 before treatment to 2.58 after treatment. Pulmonary artery occlusive pressure decreased from a mean of 31 to 18 mm Hg, and systemic vascular resistance decreased from a mean of 1780 to 1109 dynesseccm5 from before to after treatment. This research provided further evidence that hemodynamic parameters in patients at rest were significantly modulated by improving preload and afterload, rather than by using agents that increased contractility and cardiac workload. In addition, decreased activation of neuroendocrine hormones might improve short- and long-term outcomes. A newer vasodilator, nesiritide, is indicated for reducing dyspnea and improving hemodynamic status in patients with acute decompensated heart failure. Nesiritide, a recombinant form of human BNP, has actions identical to those of the endogenous BNP molecule.45 Nesiritide produced balanced arterial and venous vasodilatation that resulted in rapid reduction in ventricular filling pressures. This reduction was manifested clinically as a dose-dependent decrease in pulmonary artery occlusive pressure, pulmonary artery pressures, and systemic blood pressure.46 Nesiritide caused diuresis and natriuresis by suppressing the reninangiotensinaldosterone system.47 When intravenous nesiritide was compared with intravenous nitroglycerin during the first 72 hours of signs and symptoms in patients hospitalized with acute heart failure,47 the results favored nesiritide. Nesiritide produced a significantly quicker and greater reduction in pulmonary

artery occlusive pressure than did nitroglycerin. Patients reported and caregivers measured a greater reduction in dyspnea when the patients received nesiritide rather than nitro-glycerin. The combined actions of vasodilatation, diuresis, and natriuresis led to preload and afterload reduction to achieve the goal of enhanced cardiac output and reduced pulmonary and systemic congestion. The investigators47 concluded that nesiritide should be the drug of choice in patients admitted with a wet and cool to cold hemodynamic profile because it was less potent and less toxic than intravenous nitroprusside and more easily administered than intravenous nitroglycerin. During the first 24 hours of infusion, neither symptomatic nor asymptomatic hypotension differed significantly between patients receiving intravenous nitroglycerin, patients receiving nesiritide, and control subjects.47 During the research trial, hypotension, which was dosedependent, was easily assessed with regular monitoring of blood pressure (ie, noninvasively every 15 minutes for an hour, then every 4 hours). Thus, infusion of nesiritide does not require placement of an arterial catheter for blood pressure monitoring and admission to a critical care unit (as nitroprusside infusion does) or telemetry monitoring. Diuretics and -Blocker Therapy

-Blocker therapy also affects mechanisms in the kidneys and the renin-angiotensin system. Blockers are the only oral medications in the core pharmacological therapy for heart failure that decrease renin release, thereby indirectly decreasing proximal reabsorption of sodium (by decreasing angiotensin II levels).34 When a nonselective -blocker/-blocker such as carvedilol is used, renal blood flow may improve from a reduction in renal vascular resistance.34 Nurses should not assume that an acute exacerbation of heart failure requires termination of treatment with or decrease in dosage of -blockers. In actuality, maintenance of -blockers (and eventual increase to target dosage once hypervolemia is controlled, based on AHA/ACC practice guidelines)10 may actually improve signs and symptoms and quality of life by antagonizing mechanisms that cause excessive sodium and water retention. Myth 3: Low Systolic Blood Pressure Requires Treatment With Intravenous Inotropic Agents Some myths are associated with interventions when patients with heart failure have low systolic blood pressure. One belief is that a systolic blood pressure of less than 90 mm Hg requires intravenous infusion of inotropic agents. Unless the hypotension is severe (systolic blood

pressure <80 mm Hg), it is important to assess for indications of hypoperfusion and not to rely just on systolic blood pressure readings when determining whether intravenous inotropic agents are needed. Is the patient mentally obtunded or oliguric? Does the patient have cold arms or legs or long-lasting orthostasis (ie, dizziness and lightheadedness that lasts longer than 15 minutes after a change in body position from lying to sitting or standing)? Is the proportional pulse pressure less than 25%? In combination, these signs are more reflective of profound hypoperfusion and low cardiac output than is systolic blood pressure.16 Patients who do not have these signs generally tolerate ACE inhibitor, -blocker, and diuretic therapies, especially when the dosing scheme is staggered so that therapies do not reach peak effectiveness at the same time. It is important to consider that a lower systolic blood pressure reflects lower myocardial wall tension (stress) and afterload. Afterload reduction decreases activation of the neuroendocrine axis to promote regression of cardiac remodeling and improve clinical outcomes. Nurses must educate patients about the benefits of maintaining a low systolic blood pressure and adhering to core pharmacological therapies that decrease neuroendocrine activation and decrease blood pressure. Additionally, use of intravenous inotropic agents is not supported in patients in an acute setting except as temporary treatment of diuretic-refractory complex decompensation.48 Intravenous inotropic therapies (continuous or intermittent infusion of milrinone or dobutamine) have been associated with increased mortality when used in patients requiring inotropic support, even though these agents improve hemodynamic status10 (Table 7 ). In an effort to learn if a shortterm infusion (48 hours) might lead to short- or intermediate-term improvements in patients hospitalized for exacerbation of heart failure who had a wet and cool to cold profile but in whom intravenous inotropic support was not essential, the study called Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-HF) was conducted.49 Investigators randomized patients to receive short-term intravenous milrinone or placebo. The 2 groups did not differ significantly in hospital and 60-day posthospitalization mortality or in the median number of days patients were hospitalized for cardiovascular causes in the first 60 days after discharge. In addition, sustained hypotension or new atrial arrhythmias were significantly more likely to develop in the patients receiving milrinone than in the patients receiving placebo. The results of this research, that receiving an inotropic agent without clear

evidence of significant hemodynamic compromise does not enhance clinical or economic outcomes, led to a tempering of the use of intravenous inotropic agents unless absolutely warranted. Further, concomitant use of -blocker (-antagonist) and intravenous dobutamine (-agonist) therapies is controversial. The pharmacological response of dobutamine is inhibited in patients receiving high doses of -blockers because both drugs compete for the same -adrenergic receptors.48 This conflict is especially apparent with carvedilol because it blocks both 1 and 2 receptors.48,50 Myth 4: ACE Inhibitors and -Blocker Therapies Should Be Temporarily Decreased or Discontinued During Decompensation

Another belief is that ACE inhibitors and -blocker therapies must be decreased or discontinued or should not be initiated when the patients blood pressure is low. These agents help suppress maladaptive neuroendocrine responses that lead to increased wall stress, ventricular hypertrophy, and worsening cardiac remodeling and cardiac output.51 Unless symptomatic low blood pressure occurs or intravenous vasodilator agents are used, core oral therapies used to manage patients with chronic heart failure should be maintained whenever possible. Blood pressure may not decrease or the reduction may be self-limiting when vasodilator (ACE inhibitor or angiotensinreceptor blocker) and -blocker therapies are initiated and maintained in patients with a low baseline blood pressure (8590 mm Hg). If blood pressure decreases but indications of hypoperfusion are absent, nurses should assess patients for hypovolemia (from overdiuresis). In addition, nurses must communicate expected effects of core agents for treating heart failure to patients so that patients are prepared for potential dizziness or other symptoms associated with drug actions and interactions and understand the self-limiting nature of these changes.52 Myth 5: Once Core Therapies Are Unsuccessful, They Should Not Be Tried Again Some may believe that once ACE inhibitor or -blocker therapy is unsuccessful in a patient because of low blood pressure, these therapies should not be tried again. Assessment and correction of mechanisms that cause low blood pressure (such as initiating ACE inhibition when the serum level of sodium is less than 130 mmol/L) may make the preceding statement a false claim. Core pharmacological therapies known to improve health-related outcomes can be

successfully implemented without episodes of low blood pressure in most patients, as evidenced by low dropout rates in randomized controlled studies. The acute care episode is a perfect setting for trying ACE inhibitors or -blockers again, when appropriate, because patients can be carefully monitored and resources are readily available. Low-dose, shorter-acting agents in each drug class (such as captopril and carvedilol) are the drugs of choice in patients with a history of low blood pressure. Nursing Considerations

In addition to assessment of patients, nursing actions that are central to patients outcomes are administration of medications, evaluation of treatment effectiveness, and education and ongoing communication with patients, patients families, and the healthcare team. If a patients dyspnea improves but weight loss, urination, intake and output, or proportional pulse pressure do not improve, nurses must be assertive in providing timely communication of these findings to peers and the physician team because delays can diminish high-quality care, hinder achievement of clinical goals, and harm the hospital financially. Table 8 outlines nursing actions and goals that reflect critical thinking and foster communication when managing patients with heart failure. View this table: In this window In a new window

Table 8 Nursing considerations: critical thinking and communication Nurses often take an active role in prompting initiation and adjustment of medication therapies. Nurses must know the actions, dosing, and effects of heart failure medications and must promote decisions that will affect the overall goal of management of heart failure (reversal of cardiac remodeling). This goal can be achieved during the acute hospitalization by adding, maintaining, and increasing dosages of vasodilators (ACE inhibitors) and maintaining -blocker therapy per consensus recommendations. Nurses must not focus on pharmacological therapies that simply improve symptoms (eg, diuretics), because these therapies also increase cardiac workload, activate adverse neuroendocrine systems, and increase mortality. When in doubt about therapeutic priorities, it is always helpful to reassess the patients clinical status. When patients

have congestion and inadequate organ or peripheral perfusion (cool/lukewarm to touch), intravenous diuretic and vasodilator therapy (along with maintenance of prehospital -blocker therapy) may decrease afterload and preload to improve perfusion and cardiac index. When profound hypoperfusion compromises organ function, an intravenous inotropic agent may be the preferred agent of choice (Figure 2 ). It is especially important for nurses not to withhold doses of vasodilators, -blockers, or diuretics because of a patients low blood pressure unless the patient has orthostatic hypotension or other signs and symptoms reflecting hypoperfusion or hypovolemia. Nurses must use multiple clinical parameters, not just blood pressure values, to determine that withholding drugs will benefit a patients clinical status. Critical evaluation of each patients progress involves ongoing assessment of electrolyte and fluid status. Such assessment is especially important in managing patients with heart failure because activation of neuroendocrine systems, renal dysfunction, and current drug therapies may disrupt the fine balance of electrolytes and cause shifts in sodium, potassium, calcium, and magnesium.53 It is important for nurses to develop and use advanced measurement and cardiac auscultation skills to monitor fluid status (eg, assessment of jugular venous pressure and the presence or worsening of systolic murmurs and S3 or S4 heart sounds) because patients may still have intravascular volume overload after obvious interstitial fluid retention (crackles, edema) dissipates. Freedom from congestion in the early weeks after hospital discharge was an independent predictor of survival in patients hospitalized with New York Heart Association functional class IV symptoms.54 In order to prevent readmission and maintain clinical stability, patients who have evidence of clinical and subclinical congestion before discharge should be considered for aggressive follow-up (cardiologist specializing in heart failure) and interventions aimed at promoting euvolemia (eg, increased restriction in sodium diet or fluid intake, diuretic self-management program, heart failure nurse clinic). Serum BNP values provide another mechanism for monitoring fluid status in the early hours after hospitalization and for assessing patients outcomes. In patients with symptomatic, functional class III or IV heart failure who were undergoing tailored therapy for their congested state, hourly changes in BNP levels were significantly correlated with hourly changes in pulmonary artery occlusive pressure.55 When BNP levels at initial hospital assessment and within 24 hours of discharge or death were compared as an outcome variable,24 successfully

treated patients (as compared with patients who died during the index hospitalization or were readmitted within 30 days of discharge) had a mean decrease in BNP level of 216 pg/mL. Patients who were readmitted or died had levels that increased during the course of hospitalization. Last, communication between healthcare providers and patients and patients families about the patients clinical status and management plan is essential. Proactively assessing the knowledge base of patients and their families to promote understanding of the current plan of care and asking if there are questions can aid communication and information sharing. Information sharing and ongoing communication with patients and their families enhances perceived control, potentially decreasing stress.56 This communication is especially important because loss of functional mobility and role changes that occur with the progression of heart failure lead to a perceived loss of control57 that can ultimately affect coping, lifestyle modifications, and behaviors. Examples of important factors to address in patients education are found in the first item in Table 3 and in Table 4 . It is well recognized that improving patients knowledge of heart failure and providing support, encouragement, and positive reinforcement of self-care behaviors improves outcomes in patients with heart failure.58 References 1. American Heart Association. 2003 Heart and Stroke Statistical Update. Dallas, Tex: American Heart Association; 2002. 2. Scios Inc. ADHERE Acute Decompensated Heart Failure National Registry: 2nd Quarter 2002 Benchmark Report. San Diego, Calif: Scios Inc; 2002. 3. Graves EJ. National Hospital Discharge Survey: annual summary, 1993. Vital Health Stat 13. August 1995:163. 4. Dauterman KW, Go AS, Rowell R, Gebret-sadik T, Gettner S, Massie BM. Congestive heart failure with preserved systolic function in a statewide sample of community hospitals. J Card Fail. 2001;7:221228.[Medline]

5. Redfield MM, Jacobsen SJ, Burnett JC Jr, Mahoney DW, Bailey KR, Rodeheffer RJ. Burden of systolic and diastolic ventricular dysfunction in the community: appreciating the scope of the heart failure epidemic. JAMA. 2003;289:194

202.[Abstract/Free Full Text] 6. Bennett SJ, Huster GA, Baker SL, et al. Characterization of the precipitants of hospitalization for heart failure decompensation. Am J Crit Care. 1998;7:168174. 7. Joshi PP, Mohanan CJ, Sengupta SP, Salkar RG. Factors precipitating congestive heart failure: role of patient non-compliance. J Assoc Physicians India. 1999;47:294 295.[Medline] 8. Tsuyuki, RT, McCelvie RS, Arnold MO, et al. Acute precipitants of congestive heart failure exacerbations. Arch Intern Med. 2001;161:23372342.[Abstract/Free Full Text] 9. Joint Commission on Accreditation of Healthcare Organizations. Specification Manual for National Implementation of Hospital Core Measures Version 2.0: implementation to begin with July 2004.discharges (last updated 4/26/04). Available at:

http://www.jcaho.org/pms/core+measures/information+on+final+specifications.htm. Accessed September 21, 2004. 10. Hunt SA, Baker DW, Chin MH, et al. ACC/AHA guidelines for the evaluation and management of chronic heart failure in the adult: executive summary. A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to revise the 1995 Guidelines for the Evaluation and Management of Heart Failure). J Am Coll Cardiol. 2001;38:21012113.[Free Full Text] 11. Jessup M, Brozena S. Heart failure. N Engl J Med. 2003;348:20072018.[Medline] 12. Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling: concepts and clinical implicationsa consensus paper from an international forum on cardiac remodeling. J Am Coll Cardiol. 2000;35:569582.[Abstract/Free Full Text]

13. Kurrelmeyer K, Kalra D, Bozkurt B, et al. Cardiac remodeling as a consequence and cause of progressive heart failure. Clin Cardiol. 1998;21(12 suppl I):I14I19.[Medline] 14. Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction: pathophysiology and therapy. Circulation. 2000;101:29812988.[Free Full Text] 15. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J Heart Fail. 1999;1:251257.[Medline] 16. Stevenson LW, Perloff JK. The limited reliability of physical signs for estimating hemodynamics in chronic heart failure. JAMA. 1989;261:884

888.[Abstract/Free Full Text] 17. Shah MR, Hasselblad V, Stinnett SS, et al. Hemodynamic profiles of advanced heart failure: association with clinical characteristics and long-term outcomes. J Card Fail. 2001;7:105113.[Medline] 18. Baughman, KL. B-type natriuretic peptide: a window to the heart. N Engl J Med. 2002;347:158159.[Medline] 19. Dao Q, Krishnaswamy P, Kazanegra R, et al. Utility of B-type natriuretic peptide in the diagnosis of congestive heart failure in an urgent-care setting. J Am Coll Cardiol. 2001;37:379385.[Abstract/Free Full Text] 20. Krishnaswamy P, Lubien E, Clopton P, et al. Utility of B-type natriuretic peptide levels in identifying patients with left ventricular systolic or diastolic dysfunction. Am J Med. 2001;111:274279.[Medline] 21. Maisel AS, Krishnaswamy P, Nowak RN, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure. N Engl J Med. 2002;347:161 167.[Medline]

22. McCullough PA, Nowak RM, McCord J, et al. B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure. Circulation. 2002;106:416 422.[Abstract/Free Full Text] 23. Wieczorek SJ, Wu, AH, Christensen R, et al. A rapid B-type natriuretic peptide assay accurately diagnoses left ventricular dysfunction and heart failure: a multicenter evaluation. Am Heart J. 2002;144:834839.[Medline] 24. Cheng V, Kazanagra R, Garcia A, et al. A rapid bedside test for B-type peptide predicts treatment outcomes in patients admitted for decompensated heart failure: a pilot study. J Am Coll Cardiol. 2001;37:386391.[Abstract/Free Full Text] 25. Slike B. Diuretic induced changes in symptoms and quality of life. Br Heart J. 1994;72(suppl):S57S62.[Free Full Text] 26. Cooper HA, Dries DL, Davis CE, Shen YL, Domanski, MJ. Diuretics and risk of arrhythmic death with left ventricular dysfunction. Circulation. 1999;100:1311 1315.[Abstract/Free Full Text] 27. Satorstein L. Electrophysiological impact of diuretics in heart failure. Br Heart J. 1994; 72(suppl):S54S56.[Free Full Text] 28. Anand IS, Florea VG. Diuretics in chronic heart failure: benefits and hazards. Eur Heart J. 2001;3(suppl G):G8G18. 29. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal dysfunction during intensive therapy for advanced heart failure. Am Heart J. 1999;138:285290.[Medline] 30. Kelly DT. Vascular effects of diuretics in heart failure. Br Heart J. 1994;72(suppl): S48 S50.[Free Full Text] 31. Raftery EB. Haemodynamic effects of diuretics in heart failure. Br Heart J. 1994; 72(suppl):S44S47.

32. van ZwietenPA. Neuroendocrine effects of diuretics in heart failure. Br Heart J. 1994; 72(suppl):S51S53.[Free Full Text] 33. Hampton JR. Results of clinical trials with diuretics in heart failure. Br Heart J. 1994; 72(suppl):S68S72.[Free Full Text] 34. Hess B. Chronic heart failure: pathophysiology and therapeutic approacheswhy is the kidney so important? Eur Heart J. 2001; 3(suppl G):G3G7. 35. Guiha NH, Cohn JN, Mikulik E, Franciosa JA, Limas CJ. Treatment of refractory heart failure with infusion of nitroprusside. N Engl J Med. 1974;291:587592. 36. Leier CV, Magorien RD, Boudoulas H, Lewis RP, Bambach D, Unverferth DV. The effect of vasodilator therapy on systolic and diastolic time intervals in congestive heart failure. Chest. 1982;81:723729.[Abstract] 37. Franciosa JA, Silverstein SR. Hemodynamic effects of nitroprusside and furosemide in left ventricular failure. Clin Pharmacol Ther. 1982;32:6269.[Medline] 38. Pepine CJ, Nichols WW, Curry RC Jr, Conti CR. Aortic input impedance during nitroprus-side infusion. J Clin Invest. 1979;64:643654. 39. Brodie BR, Grossman W, Mann T, McLaurin LP. Effects of sodium nitroprusside on left ventricular diastolic pressure-volume relations. J Clin Invest. 1977;59:5968. 40. Leier CV, Bambach D, Thompson MJ, Catteneo SM, Goldberg RJ, Unverferth DV. Central and regional hemodynamics effects of intravenous isosorbide dinitrate, nitroglycerin, and nitroprusside in patients with congestive heart failure. Am J Cardiol. 1981;48: 11151123.[Medline] 41. Armstrong PW, Armstrong JA, Marks GS. Pharmacokinetic-hemodynamic studies of intravenous nitroglycerin in congestive heart failure. Circulation. 1980;62:160 166.[Free Full Text]

42. Chatterjee K, Drew J, Parmley WW, Klausner SC, Polansky J, Zacherle B. Combination vasodilator therapy for severe chronic congestive heart failure. Ann Intern Med. 1976;85:467470. 43. Greenberg BH, Hermann DD. Contemporary Diagnosis and Management of Heart Failure. Newtown, Pa: Handbooks in Health Care Co; 2002:214217. 44. Johnson W, Omland T, Hall C, et al. Neuro-hormonal activation rapidly decreases after intravenous therapy with diuretics and vasodilators for class IV heart failure. J Am Coll Cardiol. 2002;39:16231629.[Abstract/Free Full Text] 45. Hobbs RE, Mills RM. Therapeutic potential of nesiritide (recombinant B-type natriuretic peptide) in the treatment of heart failure. Expert Opin Investig Drugs. 1999;8: 1063 1072. 46. Marcus LS, Hart D, Packer M, et al. Hemo-dynamic and renal excretory effects of human brain natriuretic peptide infusion in patients with congestive heart failure: a double-blind, placebo-controlled, randomized crossover trial. Circulation. 1996;94: 3184

3189.[Abstract/Free Full Text] 47. Publication Committee for the VMAC Investigators (Vasodilatation in the Management of Acute CHF). Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: a randomized controlled trial [published correction appears in JAMA. 2002;288:577]. JAMA. 2002;287:15311540.[Abstract/Free Full Text] 48. Bristow MR, Shakar SF, Linseman JV, Lowes BD. Inotropes and -blockers: is there a need for new guidelines? J Card Fail. 2001; 7(2suppl 1):812.[Medline] 49. Cuffe MS, Califf RM, Adams Jr KF, et al. Short-term intravenous milrinone for acute exacerbation of chronic heart failure. JAMA. 2002;287:1541

1547.[Abstract/Free Full Text] 50. Felker GM, OConnor CM. Inotropic therapy for heart failure: an evidence-based approach. Am Heart J. 2001;142:393401.[Medline]

51. Albert N. Heart failure: the pathophysiologic basis for current therapeutic concepts. Crit Care Nurse. June 1999;18(suppl):213. 52. Albert NM. Advanced systolic heart failure: emerging pathophysiology and current management. Prog Cardiovasc Nurs. Summer 1998;13:1430.[Medline] 53. Gawlinski A, McCloy K, Caswell D, Quinones-Baldrich WJ. Cardiovascular disorders. In: Gawlinski A, Hamwi D, ed. Acute Care Nurse Practitioner: Clinical Curriculum and Certification Review. Philadelphia, Pa: WB Saunders Co; 1999:136294. 54. Lucas C, Johnson W, Hamilton MA, et al. Freedom from congestion predicts good survival despite previous class IV symptoms of heart failure. Am Heart J. 2000;140:840 847.[Medline] 55. Kazanegra R, Cheng V, Garcia A, et al. A rapid test for B-type natriuretic peptide correlates with falling wedge pressures in patients treated for decompensated heart failure: a pilot study. J Card Fail. 2001;7:2129.[Medline] 56. Miller JF. Coping With Chronic Illness: Overcoming Powerlessness. 2nd ed. Philadelphia, Pa: FA Davis Co; 1992. 57. Johnson JL, Morse JM. Regaining control: the process of adjustment after myocardial infarction. Heart Lung. 1990;19:126135.[Medline] 58. Miranda MB, Gorski LA, LeFevre JG, Levac KA, Niederstadt JA, Toy AL. An evidencebased approach to improving care of patients with heart failure across the continuum. J Nurs Care Qual. 2002;17:114.[Medline]

1. +Anda 2. Web 3. Gambar 4. Maps

5. Berita 6. Terjemahan 7. Gmail 8. Lainnya 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 1. Masuk 2. 3. 1. Terjemahan

Penutup CE Bukti Nancy Cathy Michelle L. Berbasis M. Praktik Albert, A. Edwards, untuk RN, Gagal MSN, Eastwood, RN, MSN, Jantung CCNS, RN, FNP, Akut

Pasal Pasal dekompensasi CNA MN ACNP

CCRN,

________________________________________ Nancy M. Albert disertifikasi sebagai spesialis perawat klinis dan memiliki peran ganda direktur riset keperawatan di divisi spesialis perawat keperawatan dan klinis di M. George dan Linda H. Kaufman Pusat Gagal Jantung dari Cleveland Clinic Foundation, Cleveland, Ohio. Dia program gagal jantung codeveloped sepanjang kontinum perawatan, termasuk perawatan darurat, perawatan kritis, dan akut perawatan, di Cleveland Clinic Foundation.

Cathy A. Eastwood lulus dengan gelar master keperawatan dari University of Calgary, Kanada, setelah yang mengkhususkan diri dalam perawatan pasien dengan gagal jantung. Dia dikembangkan dan dikelola pusat rawat jalan gagal jantung dan mengawasi aliran pasien rawat inap dengan gagal jantung di St Luke Episkopal Rumah Sakit, Houston, Texas Saat ini, ia adalah dosen di Memorial University of Newfoundland, Sekolah Keperawatan, di St John, Newfoundland, Kanada.

Michelle L. Edwards mendapatkan gelar master ilmu keperawatan dari Universitas Alabama di Birmingham dan adalah keluarga dewan bersertifikat dan praktisi perawat perawatan akut. Dia berlatih beberapa tahun dalam perawatan kritis, yang mengkhususkan diri dalam perawatan pasien kardiovaskular. Dia saat ini adalah seorang perawat kardiologi praktisi / pengelola hasil di Rumah Sakit St Luke Episkopal.

Untuk membeli cetak ulang, hubungi Grup INNOVISION, 101 Columbia, Aliso Viejo, CA 92656. Telepon, (800) 809-2273 atau (949) 362-2050 (ext 532); faks, (949) 362-2049, e-mail, reprints@aacn.org. Artikel ini telah ditunjuk untuk kredit CE. Sebuah buku tertutup, pilihan ganda pemeriksaan berikut 1. 2. 3. artikel ini, yang inti tipe B tes pengetahuan terapi Anda obat tentang gagal gagal tujuan-tujuan jantung jantung berikut:

Mengidentifikasi Jelaskan peran

untuk

dekompensasi dekompensasi dekompensasi

natriuretic

peptide

pada gagal

Jelaskan

manajemen

farmakologis

jantung

________________________________________ Setiap tahun, kronis sistolik ventrikel kiri dan disfungsi diastolik, atau gagal jantung, menyebabkan 1 juta rawat inap dalam kegagalan States.1 Jantung Serikat adalah Medicare paling umum kelompok diagnosis terkait di discharge1, 2 dan berhubungan dengan kelangsungan hidup miskin dan kualitas hidup. Selain itu, biaya perawatan yang tinggi, pada tahun 1998, Medicare membayar $ 3600000000 untuk perawatan yang berkaitan dengan jantung failure.1

Para dekompensasi Jantung Akut Gagal Registrasi Nasional (mematuhi) 3 data yang baru-baru ini melaporkan pada 14.716 pasien rawat inap untuk gagal jantung di Amerika Serikat (Tabel 1 dan 2). Umumnya, pasien dirawat di rumah sakit untuk gagal jantung lansia, adalah perempuan, memiliki sejarah gagal jantung, dan tidak mampu untuk melaksanakan aktivitas hidup sehari-hari tanpa intoleransi latihan. Gejala yang paling umum adalah dispnea, yang paling sering dikaitkan dengan tanda-tanda lain dan gejala retensi cairan. Kondisi komorbiditas yang umum, dan pasien sama-sama mungkin dirawat dengan disfungsi sistolik (dikurangi kontraktilitas ventrikel; fraksi ejeksi 0,40) atau disfungsi diastolik (relaksasi ventrikel terganggu atau kekakuan ventrikular yang menurunkan kemampuan ventrikel untuk mengisi). Seperempat dari pasien rehospitalized dalam waktu 6 bulan dari rumah sakit sebelumnya, dan Medicare adalah pembayar rumah sakit utama. Kebanyakan pasien menghabiskan waktu di departemen darurat sebelum diterima sebagai pasien rawat inap, dan tingkat yang paling umum dari perawatan awal telemetri. Panjang ratarata Lihat Dalam Di tinggal adalah tabel jendela jendela 4,4 days.3 ini: ini baru

Tabel 1 Karakteristik pasien, tanda dan gejala klinis, dan penempatan rumah sakit: data dari dekompensasi Lihat Dalam Di Gagal Jantung tabel jendela jendela Akut Nasional Registry3 ini: ini baru

Tabel obat rawat jalan rawat inap dan 2 sebelum obat di debit: data dari dekompensasi Gagal Jantung Akut Nasional Registry3

Para mematuhi data mirip dengan data dari studies4 lainnya, 5 di mana peneliti menemukan split sama pasien dengan gangguan fungsi ventrikel kiri sistolik dan diawetkan, yang berarti rawat inap pasien dengan disfungsi sistolik dan pasien dengan disfungsi diastolik. Mekanisme utama dari disfungsi diastolik yang menyebabkan tanda dan gejala gangguan relaksasi ventrikel itu, yang dikaitkan dengan usia meningkat, obesitas, hipertensi, dan kardiovaskular disease.4 Selain itu, mematuhi data sebanding dengan data dari lain reports6-8 dalam retensi yang cairan dan

natrium, sebagaimana dibuktikan dengan mengakui tanda dan gejala, merupakan faktor utama dalam rawat inap. Pengetahuan ini memberikan kesempatan untuk perbaikan perawatan yang dapat diperjuangkan oleh perawat, karena rawat inap untuk cairan dan retensi natrium pada pasien dengan disfungsi sistolik atau diastolik mungkin dihindari, terutama bila retensi tersebut karena kegagalan pasien untuk patuh pada rejimen pengobatan atau diri instruksi perawatan. Pada artikel ini, kita membahas praktek-praktek berbasis bukti untuk mengelola pasien dengan gagal jantung dekompensasi akut di rumah sakit karena tindakan dapat memfasilitasi pengalaman baik untuk pasien setelah rawat inap. Tujuannya adalah untuk menyediakan tujuan manajemen dan tindakan yang terkait dengan manifestasi klinis yang paling umum, retensi cairan, dan tidak fokus pada manajemen syok kardiogenik, hipoperfusi yang mendalam, atau dekompensasi kompleks (berat hiper-volemia, hipoperfusi, dan asidosis atau kondisi lain seperti sebagai pneumonia). Penilaian pasien, strategi manajemen, dan pendidikan pasien yang disorot. Mitos yang terkait dengan manajemen perawatan akut dibahas sehingga perawat akan lebih menyadari intervensi yang tepat yang aman dan efektif. Manajemen jantung kegagalan telah berkembang pesat dalam beberapa tahun terakhir. Akhirnya, perawat harus proaktif dalam memastikan Harapan bahwa tinggi perilaku mereka didasarkan Bukti pada bukti saat ini.

untuk

Berbasis

Perawatan

Perawat ditantang untuk merencanakan dan memberikan perawatan yang mempromosikan hasil klinis dan kesehatan yang berhubungan dengan sebaik mungkin. Komisi Bersama Akreditasi Kesehatan Organizations9 baru ini didirikan 4 langkah inti dalam manajemen akut pasien dengan gagal jantung untuk mempromosikan kepatuhan terhadap standar dasar perawatan berbasis bukti (Tabel 3). Karena sejumlah besar pasien dan tingginya biaya perawatan yang terkait dengan readmissions rumah sakit, perawat perawatan akut dan kritis harus mengembangkan dan menerapkan strategi yang berhubungan dengan hasil yang lebih baik bagi pasien dan rumah sakit. Selain itu, pada tahun 2001, American College of Cardiology (ACC) dan American Heart Association (AHA) menerbitkan guidelines10 praktek untuk orang dewasa dengan gagal jantung kronis. Pedoman ini memberikan pengasuh dengan rekomendasi untuk perawatan nonacute dan termasuk alasan dan tingkat bukti untuk mendukung setiap strategi manajemen. Tabel 4 memberikan sebuah daftar strategi manajemen, termasuk terapi obat inti, yang harus menjadi bagian dari rencana perawatan setiap pasien di debit setelah masuk untuk gagal jantung dekompensasi yang berasal dari volume overload.10, 11

Lihat Dalam Di

tabel jendela jendela

ini: ini baru

Tabel 3 Langkah-langkah inti 4 Komisi Bersama Akreditasi Organisasi Kesehatan Lihat Dalam Di tabel jendela jendela ini: ini baru

Tabel

pedoman

Praktek

yang

berlaku

untuk

tahap

pasien

Jika harapan obat yang tercantum dalam Tabel 4 dibandingkan dengan terapi obat yang sebenarnya sebelum rawat inap dan di discharge ditunjukkan dalam mematuhi data (Tabel 2), kebutuhan untuk perubahan jelas. Upaya baru harus dilakukan untuk mempromosikan penggunaan pedoman konsensus dan terapi untuk memenuhi tujuan keseluruhan pengelolaan gagal jantung: mempromosikan regresi dan mencegah perkembangan pembesaran ventrikel kiri (renovasi) untuk mengurangi perkembangan penyakit dan meningkatkan survival.11-14 Lihat Gambar 1 dan Tabel 5 untuk definisi dan deskripsi konsekuensi dari remodeling ventrikel.

Lihat Dalam Di

versi

yang

lebih jendela jendela

besar

(49K): ini baru

Gambar 1 renovasi ventrikel. Cross-sectional pandangan ventrikel kiri dan kanan: normal, b, hipertrofi Lihat Dalam Di konsentris, dan tabel jendela jendela c, hipertrofi eksentrik. ini: ini baru

Tabel

renovasi

ventrikel:

definisi

dan

konsekuensi

Tidak ada bukti-berbasis standar pedoman yang tersedia untuk mengarahkan perawatan akut, namun, secara acak, placebo-controlled studi penelitian memberikan dukungan yang kuat untuk

tindakan yang efektif dan aman. Selain itu, banyak tindakan dipromosikan dalam pedoman saat ini untuk jangka panjang manajemen rawat jalan gagal jantung dapat diterjemahkan ke pengaturan akut dan memberikan rencana seragam perawatan berdasarkan besar, multicenter, acak penelitian yang berfokus pada tujuan utama dari manajemen mencegah perkembangan hati failure.10 Perawat dapat memfasilitasi beberapa penilaian praktis dan strategi manajemen yang berlaku untuk pasien dirawat di rumah sakit dengan diagnosis utama gagal jantung yang tidak di syok kardiogenik atau tidak memiliki hipoperfusi mendalam atau dekompensasi kompleks. Pelaksanaan strategi berikut mungkin memerlukan perubahan dalam filosofi perawatan, pendidikan lanjutan, dan pemantauan kualitas berkelanjutan untuk memastikan bahwa strategi berbasis bukti yang digunakan terlepas dari tipe dokter, pasien penempatan (telemetri atau tempat tidur nonmonitored), seorang perawat latar belakang (jantung, gagal jantung, atau generalis), Penilaian atau sumber daya sebuah rumah sakit. Pasien

Sebelum merencanakan intervensi untuk pasien rawat inap dengan gagal jantung, tim kesehatan harus melakukan penilaian yang sistematis yang mencakup identifikasi penyebab gagal jantung, memperparah faktor, faktor-faktor risiko potensial yang dapat mempengaruhi kelangsungan hidup dan kualitas hidup, dan status klinis saat ini. Pasien 'kondisi komorbiditas, kondisi kronis terutama aktif, dapat bertindak sebagai memperburuk faktor (Tabel 6), yang mempengaruhi perencanaan pasien perawatan dan mempengaruhi waktu dan intensitas dari terapi. Rencana pengobatan harus mencakup modifikasi dari penyebab diperbaiki dekompensasi. Contohnya termasuk pendidikan untuk perselingkuhan natrium, program pantang alkohol berlebihan alkohol, atau strategi revaskularisasi untuk hibernate miokardium (yaitu, jaringan miokard layak, tetapi di bawah-perfusi dengan penurunan kontraktilitas). Selain itu, risiko yang berkaitan dengan gagal jantung harus dipertimbangkan, seperti kebutuhan untuk antikoagulasi untuk mencegah kejadian emboli atau kebutuhan untuk implan cardioverter-defibrilator untuk mencegah kematian jantung mendadak, sehingga konsultasi yang tepat dan terapi yang dibahas dan Lihat Dalam Di dilakukan sebelum pasien tabel jendela jendela keluar dari rumah sakit. ini: ini baru

Tabel 6 faktor memperparah pada gagal jantung kronis yang menyebabkan dekompensasi Status hemodinamik: Volume dan Perfusi

Volume dan perfusi status yang memberikan petunjuk berguna untuk kinerja jantung pasien dan membantu membentuk rencana pengobatan. Perawat perawat sering harus menilai kembali statusnya hemodinamik pasien untuk menentukan volume dan status perfusi. Status volume ditentukan dengan menilai jika pasien basah, kering, atau memiliki tingkat cairan seimbang (yaitu, telah hipervolemia, hipovolemia, atau euvolemia, masing-masing), dan perfusi dinilai dengan menentukan jika pasien dingin, dingin / hangat, atau hangat (yaitu, telah perfusi yang sangat rendah, sedikit rendah, atau normal, masing-masing). Bukti kemacetan termasuk tandatanda distensi vena leher, tekanan tinggi pada vena jugularis yang tepat internal, positif perutrefleks leher jugularis vena, edema, asites, dan krepitasi (jarang) dan gejala-gejala dispnea, ortopnea, dan dispnea nokturnal paroksismal. 15 Perawat harus berhati-hati untuk tidak mengandalkan kehadiran crackles sebagai indikator kemacetan karena gerakan kronis cairan ke interstitium (umum pada pasien dengan riwayat gagal jantung kronis) berhubungan dengan drainase limfatik meningkat sehingga crackles tidak hadir dan alveoli tetap relatif dry.16 Bukti perfusi yang sangat rendah termasuk gejala hipotensi, terutama pada pasien yang menerima angiotensin-converting enzyme (ACE) inhibitor, ekstremitas dingin (tangan dan kaki, bukan hanya tangan dan kaki), mental obtundation atau konstan kantuk, memburuknya fungsi ginjal (elevasi dalam tingkat serum kreatinin dan nitrogen urea), hiponatremia, tekanan nadi sempit, dan yang paling penting, tekanan nadi proporsional 25% atau less.15, 16 perawat perawatan akut perlu dididik dalam menghitung tekanan nadi proporsional. Perhitungan sederhana untuk dilakukan dan dapat memberikan informasi berharga tentang kontraktilitas jantung dan perfusi, terutama ketika tren dari waktu ke waktu dinilai.

Rumus untuk menentukan tekanan nadi proporsional (tekanan darah sistolik - tekanan darah diastolik) / tekanan darah sistolik, menghasilkan proporsi atau percentage.16 Sebuah contoh perhitungan tekanan nadi proporsional (108 -66) / 108 = 42 / 108 = 0,389 atau 39%. Dalam hemodinamik study16 dari 50 pasien dengan riwayat gagal jantung, 91% dari pasien dengan tekanan nadi proporsional 25% atau lebih rendah memiliki indeks jantung (cardiac output dihitung sebagai dalam liter per menit dibagi dengan luas permukaan tubuh dalam meter persegi) kurang dari 2,2, namun, sistolik dan tekanan darah arteri rata-rata yang buruk berkorelasi dengan

indeks jantung atau stroke volume indeks. Dalam study17 profil hemodinamik (basah, kering, dingin, dan hangat) dan karakteristik klinis gagal jantung stadium lanjut, suatu tekanan nadi rendah proporsional adalah prediktor hanya pasien basah, dan di antara pasien basah, tekanan nadi proporsional adalah prediktor hanya pasien dalam kategori dingin. Profil hemodinamik Seorang pasien harus mempengaruhi inisiasi strategi pengobatan farmakologis dan lainnya dan juga membimbing penyesuaian terapi selama rawat inap tersebut.

Dari catatan, pasien yang dirawat dalam keadaan kongestif atau basah dengan preload tinggi (peregangan pasif serat miokard; mencerminkan ventrikel kiri akhir diastolik tekanan dan volume) sering memiliki afterload tinggi (tekanan jantung harus memompa melawan; mencerminkan vaskular sistemik resistensi, stres sistolik, dan impedansi sistolik) yang merusak stroke volume dan ini tercermin sebagai negara dingin atau suam-suam kuku perfusi. Ketika pengukuran hemodinamik tercatat dalam 750 pasien dengan gagal jantung sebelum terapi disesuaikan di rumah sakit pendidikan universitas besar, tekanan arteri paru rata-rata adalah 26 oklusif mmHg (normal adalah 4-12 mm Hg; dalam pengobatan gagal jantung, tujuannya adalah 8 - 15 mm Hg) dan resistensi vaskular sistemik berarti 1640 dyne sec cm-5 (normal adalah 8001200 dyne sec cm-5), 15 mencerminkan negara vasoconstricted dan kebutuhan untuk terapi vasodilator Tes di samping diuresis dan natriuresis (ekskresi natrium). Diagnostik

Selain hasil tes yang dilakukan pada saat masuk (dada radiografi, tingkat gas darah arteri, tes fungsi hati, tes hematologi, electrocardiograms, profil metabolik dasar) dan temuan pada pemeriksaan fisik, hasil point-of-perawatan tes dari tingkat serum natriuretik peptida dapat digunakan untuk memandu pengobatan pada pasien dengan gagal jantung akut dekompensasi (Gambar 2). B-jenis natriuretic peptide (BNP) disekresi terutama dari miokardium ventrikel dalam menanggapi peningkatan pada akhir diastolik ventrikel tekanan dan volume yang expansion.18 Tidak hanya dapat pengukuran yang cepat bantuan BNP di diagnosis gagal jantung ,19-23 tetapi tingkat BNP juga dapat digunakan untuk menilai status klinis dan efektivitas terapi selama masuk untuk decompensation.24 akut

Lihat Dalam Di

versi

yang

lebih jendela jendela

besar

(49K): ini baru

Gambar sistolik 2 dekompensasi akut gagal jantung (SHF) atau gagal jantung diastolik (DBD) pada pasien dengan gagal jantung kronis: pengobatan awal Singkatan: BNP, tipe B natriuretic peptide, EKG, elektrokardiografi, INR, rasio normalisasi internasional; IV, intravena ; PT, prothrombin time. * Pengobatan keputusan berdasarkan hasil serum BNP di gagal jantung akut dekompensasi TIDAK berlaku untuk pasien dengan kronis, gagal jantung yang stabil yang tidak akut dispnea. Profil: pasien basah, kering, atau memiliki tingkat cairan seimbang (yaitu, telah hipervolemia, hipovolemia, atau euvolemia, masing-masing), dan dingin, dingin / hangat, atau hangat (yaitu, telah perfusi yang sangat rendah, sedikit rendah, atau normal, masing-masing). Point-of-perawatan pengujian BNP dapat menjadi tambahan yang bermanfaat dalam menentukan mana pasien menerima perawatan yang efektif, yang pasien tidak berjalan sesuai rencana pengobatan saat ini, dan yang pasien mungkin menjadi kandidat untuk end-of-kehidupan peduli. Perawat harus mempertimbangkan semua komponen penilaian pasien (etiologi, faktor yang memberatkan, risiko, dan status klinis) ketika berkomunikasi dan berkolaborasi dengan anggota tim kesehatan sehingga pasien memiliki kesempatan terbaik untuk strategi perawatan yang mengoptimalkan Mitos hasil dan dan meningkatkan Realitas kenyamanan. Manajemen

Algoritma memberikan pendekatan sistematis untuk pengambilan keputusan sebagai pasien dengan gagal jantung kronis yang dikaji dan dikelola selama eksaserbasi akut (Gambar 2). Mitos yang terkait dengan manajemen gagal jantung akut adalah diganti dengan tindakan berdasarkan bukti Mitos 1: yang Tujuan berkontribusi Pengobatan untuk Gagal untuk Jantung Akut hasil dan Kronis terbaik. Berbeda

Salah satu rintangan dalam pengelolaan gagal jantung adalah untuk mengatasi mitos bahwa tujuan pengelolaan gagal jantung dekompensasi akut dan stabil yang berbeda. Hari ini, adalah penting untuk terapi gigi ke arah pembalikan remodeling ventrikel. Membalikkan remodeling ventrikel adalah penting terlepas dari apakah pasien dalam kondisi stabil atau dalam keadaan decompen-puas. Secara historis, tujuan utama pengobatan gagal jantung dekompensasi akut adalah untuk cepat mengurangi volume cairan bersirkulasi untuk meringankan pasien edema paru dan perifer. Diuretik dispnea di departemen darurat. telah lama jenis standar obat yang digunakan untuk mengurangi volume dan memperbaiki status hemodinamik dan tanda-tanda dan symptoms.25 Melalui studi penelitian, bagaimanapun, diketahui bahwa terapi diuretik intravena

akut dikaitkan dengan bahaya, termasuk peningkatan mortalitas. Non-hemat kalium terapi diuretik dikaitkan dengan peningkatan risiko arrhythmic (tiba-tiba) kematian, meningkatnya kematian jantung, disfungsi ginjal diperburuk, aktivasi lebih lanjut dari reninangiotensin dan sistem saraf simpatik dengan peningkatan bersamaan dalam resistensi vaskular sistemik yang diperparah oleh penurunan output jantung dari penurunan preload, dan elektrolit

ketidakseimbangan yang menyebabkan kelemahan otot, depresi, kontraktilitas berkurang (dari konduktivitas dikurangi), dan perifer vasoconstriction.26-31 Pada pasien dengan dekompensasi akut, mencegah atau membatasi aktivasi lebih lanjut dari sistem neuroendokrin oleh menggunakan strategi yang menargetkan volume intravaskular dan ekstravaskular kelebihan dan resistensi vaskuler akan membantu memenuhi tujuan keseluruhan untuk mencegah perkembangan Mitos 2: dan Mengelola mempromosikan Kelebihan pembalikan Cairan Setara remodeling Penggunaan ventrikel. Diuretik

Administrasi agen lingkaran diuretik intravena dan oral merupakan terapi yang penting bertujuan untuk mengurangi preload (melalui venodilatation awal dan kemudian melalui diuresis dan natriuresis) dan akhirnya menghilangkan tanda-tanda dan gejala, namun agen ini tidak boleh digunakan sendiri untuk meningkatkan morbiditas dan kelangsungan hidup secara keseluruhan pada pasien dengan gagal jantung. Dalam rangka untuk mengatasi afterload meningkat terkait dengan kedua eksaserbasi gagal jantung dan terapi diuretik intravena lingkaran, terapi farmakologis harus mencakup agen yang mengurangi aktivasi neuroendokrin dan vasokonstriksi karena mekanisme dapat memperburuk sindrom gagal jantung oleh memburuknya remodeling ventrikel. Diuretik dan ACE Inhibitor Terapi

Meskipun hanya data yang terbatas yang tersedia, ketika sebuah penghambat ACE yang dikombinasikan dengan diuretik loop, terapi kombinasi mengurangi pressor (vasokonstriksi) respon diuretics.32 ACE inhibitor mengurangi peningkatan angiotensin II dalam plasma, sehingga mengurangi aktivasi simpatik (dan kerusakan yang terkait dalam fungsi pompa ventrikel kiri) yang mendahului tindakan diuretik diuretics.32

ACE inhibitor akhirnya penurunan reabsorpsi natrium di tubulus distal dan penurunan rangsangan aldosteron di glands.33 adrenal, 34 Banyak acak, studi penelitian terkontrol yang dilakukan dari awal 1980-an sampai pertengahan 1990-an yang ditambahkan inhibitor ACE untuk terapi diuretik pada pasien dengan ringan sampai gagal jantung parah, seperti diringkas

dalam konsensus guidelines.10 Para peneliti melaporkan peningkatan dalam toleransi latihan, fraksi ejeksi, dan kelangsungan hidup bersama dengan rehospitalization menurun rates.10 Oleh karena itu, diuretik diperlukan untuk menghilangkan tanda-tanda dan gejala tetapi harus digunakan dengan ACE inhibitor terapi untuk manfaat kelangsungan hidup dan untuk mengimbangi perubahan dalam mekanisme ginjal dan adrenal bertanggung jawab untuk natrium dan retensi air. Perawat harus secara proaktif merekomendasikan peningkatan dosis inhibitor ACE berdasarkan praktik ACC / AHA guidelines10 selama periode rawat inap akut sehingga rejimen bahwa pasien 'dosis yang pada target sebelum pasien dipulangkan dari rumah sakit. Diuretik dan Terapi vasodilator intravena

Ketika pasien dirawat dengan profil basah dan hangat / dingin atau dingin tanpa indikasi hipoperfusi mendalam, kombinasi dari diuretik intravena dan terapi vasodilator mengarah ke hasil akut membaik, tanpa perlu untuk agen inotropik (Gambar 2). Banyak penelitian dilakukan di akhir 1970-an dan 1980-an awal pada pasien dengan New York Heart Association fungsional kelas IV gagal jantung dekompensasi untuk mempelajari efektivitas diuretik intravena dan vasodilator (nitroprusside dan nitrogliserin) terapi dalam mengurangi tekanan pengisian (preload) dan resistensi vaskular sistemik (afterload) dan meningkatkan output jantung. Hasil penelitian menunjukkan bahwa nitroprusside adalah seorang agen klinis efektif dan ampuh untuk mengurangi afterload yang juga menurun dan volume ventrikel sistolik diastolik ventrikel dan sifat ditingkatkan diastolik. Hal ini memberikan bantuan gejala yang cepat bagi pasien dan membaik, stabil, dan hemodinamik dioptimalkan parameters.35-39

Nitrogliserin intravena dikenal terutama sebagai agen untuk mengurangi preload. Namun, pada dosis tinggi, nitrogliserin intravena mengurangi resistensi pembuluh darah sistemik dan pulmonal. Pada pasien dengan gagal jantung kronis dekompensata, nitrogliserin kurang kuat daripada dalam mengurangi afterload nitroprusside tetapi efektif dalam mengurangi preload, meningkatkan output jantung, dan tanda-tanda dan gejala dan mengontrol hemodinamik derangements.40-42 Tabel 7 adalah ringkasan dari rentang dosis, tindakan, dan indikasi obat vasoaktif yang digunakan dalam pengelolaan pasien dengan hati dekompensasi akut failure.43 Lihat Dalam Di tabel jendela jendela ini: ini baru

Tabel 7 obat vasoaktif Intravena ditunjukkan dalam hati dekompensasi akut failure43 Sebagai tujuan keseluruhan mengelola pasien dengan gagal jantung telah bergeser dari meningkatkan status hemodinamik untuk meningkatkan kelainan neuroendokrin dengan harapan bahwa remodeling ventrikel akan terpengaruh baik, peneliti telah mempelajari efektivitas terapi vasodilator intravena dalam modulasi sumbu neuroendokrin. Dalam study44 terbaru dari 34 pasien dengan gagal jantung dekompensasi yang menerima diuretik intravena dan terapi vasodilator (nitroprusside dan inhibitor ACE) untuk mengurangi preload dan afterload, aktivasi neurohormonal (endotelin, phrine norepine, dan tingkat BNP) menurun dengan cepat dan dikaitkan dengan perbaikan hemodinamik status. Mirip dengan hasil penelitian yang dilakukan pada dekade-dekade sebelumnya, dalam penelitian ini, 44 indeks jantung rata-rata meningkat dari 1,70 sebelum perawatan untuk 2,58 setelah perawatan. Tekanan arteri oklusif paru menurun dari rata-rata 31-18 mm Hg, dan resistensi vaskular sistemik menurun dari rata-rata 1780-1109 dyne sec cm-5 dari sebelum sampai sesudah pengobatan. Penelitian ini memberikan bukti lebih lanjut bahwa parameter hemodinamik pada pasien saat istirahat secara signifikan dipengaruhi oleh meningkatkan preload dan afterload, daripada dengan menggunakan agen yang meningkatkan kontraktilitas dan beban kerja jantung. Selain itu, penurunan aktivasi hormon neuroendokrin dapat meningkatkan hasil jangka pendek dan jangka panjang.

Sebuah vasodilator baru, nesiritide, diindikasikan untuk mengurangi dispnea dan meningkatkan status hemodinamik pada pasien dengan gagal jantung akut dekompensasi. Nesiritide, bentuk rekombinan manusia BNP, telah identik dengan tindakan orang-orang dari Nesiritide molecule.45 BNP endogen diproduksi vasodilatasi arteri dan vena yang seimbang yang mengakibatkan pengurangan cepat dalam tekanan ventrikel mengisi. Penurunan ini secara klinis dimanifestasikan sebagai penurunan dosis-tergantung pada tekanan oklusif arteri pulmonalis, tekanan arteri paru-paru, dan darah sistemik pressure.46 Nesiritide disebabkan diuresis dan natriuresis dengan menekan aldosteron reninangiotensin-system.47

Ketika nesiritide intravena dibandingkan dengan nitrogliserin intravena selama 72 jam pertama tanda dan gejala pada pasien rawat inap dengan gagal jantung akut, 47 hasil disukai nesiritide. Nesiritide menghasilkan penurunan secara signifikan lebih cepat dan lebih besar dalam tekanan arteri pulmonalis oklusif dari nitrogliserin itu. Pasien melaporkan dan pengasuh diukur penurunan lebih besar pada dispnea ketika pasien menerima nesiritide daripada nitro-gliserin. Tindakan gabungan dari vasodilatasi, diuresis, dan natriuresis menyebabkan preload dan

afterload pengurangan untuk mencapai tujuan output jantung ditingkatkan dan mengurangi kongesti paru dan sistemik. Para investigators47 menyimpulkan bahwa nesiritide harus menjadi obat pilihan pada pasien mengaku dengan basah dan keren untuk profil hemodinamik dingin karena kurang manjur dan kurang toksik dibandingkan nitroprusside intravena dan lebih mudah dikelola dibandingkan nitrogliserin intravena. Selama 24 jam pertama infus, hipotensi tidak bergejala atau bergejala berbeda secara signifikan antara pasien yang menerima nitrogliserin intravena, pasien yang menerima nesiritide, dan kontrol subjects.47 Selama uji coba penelitian, hipotensi, yang tergantung dosis, dengan mudah dinilai dengan pemantauan teratur tekanan darah (yaitu, noninvasively setiap 15 menit selama satu jam, maka setiap 4 jam). Dengan demikian, infus nesiritide tidak memerlukan penempatan kateter arteri untuk pemantauan tekanan darah dan masuk ke unit perawatan kritis (seperti infus nitroprusside tidak) atau pemantauan Diuretik dan -Blocker telemetri. Terapi

-Blocker terapi juga mempengaruhi mekanisme di dalam ginjal dan sistem renin-angiotensin. blocker adalah satu-satunya obat oral dalam terapi farmakologis inti untuk gagal jantung yang menurunkan pelepasan renin, sehingga secara tidak langsung menurunkan reabsorpsi natrium proksimal (dengan menurunkan tingkat angiotensin II) .34 Ketika -blocker/-blocker nonselektif seperti carvedilol digunakan, aliran darah ginjal dapat meningkatkan dari pengurangan vaskular ginjal resistance.34 Perawat tidak boleh berasumsi bahwa eksaserbasi akut dari gagal jantung memerlukan penghentian pengobatan dengan atau penurunan dosis -blocker. Pada kenyataannya, pemeliharaan -blocker (dan meningkatkan akhirnya untuk menargetkan dosis sekali hipervolemia dikendalikan, berdasarkan AHA / pedoman praktek ACC) 10 benarbenar dapat meningkatkan tanda-tanda dan gejala dan kualitas hidup dengan mekanisme berlawanan yang menyebabkan natrium berlebihan dan retensi air.

Mitos 3: Sistolik Tekanan Darah Rendah Pengobatan Membutuhkan Agen inotropik intravena Dengan Beberapa mitos yang berhubungan dengan intervensi ketika pasien dengan gagal jantung memiliki tekanan darah sistolik rendah. Satu keyakinan adalah bahwa tekanan darah sistolik kurang dari 90 mm Hg memerlukan infus intravena agen inotropik. Kecuali hipotensi yang parah (tekanan darah sistolik <80 mm Hg), penting untuk menilai indikasi hipoperfusi dan tidak bergantung hanya pada pembacaan tekanan darah sistolik ketika menentukan apakah agen

inotropik intravena diperlukan. Apakah pasien tidak sadar atau oliguria mental? Apakah pasien memiliki lengan dingin atau kaki atau jangka panjang orthostasis (yaitu, pusing dan ringan yang berlangsung lebih dari 15 menit setelah perubahan posisi tubuh dari berbaring ke duduk atau berdiri)? Apakah tekanan nadi proporsional kurang dari 25%? Dalam kombinasi, tanda-tanda ini lebih mencerminkan hipoperfusi mendalam dan curah jantung rendah daripada darah sistolik pressure.16 Pasien yang tidak memiliki tanda-tanda ini umumnya mentolerir ACE inhibitor, blocker, dan terapi diuretik, terutama bila skema dosis yang terhuyung-huyung sehingga bahwa terapi tidak mencapai keefektifan puncaknya pada saat yang sama.

Penting untuk mempertimbangkan bahwa tekanan darah sistolik lebih rendah mencerminkan ketegangan dinding rendah miokard (stres) dan afterload. Menurunkan afterload pengurangan aktivasi dari sumbu neuroendokrin untuk mempromosikan regresi remodeling jantung dan meningkatkan hasil klinis. Perawat harus mendidik pasien tentang manfaat mempertahankan tekanan darah sistolik rendah dan mengikuti terapi farmakologis yang menurunkan inti aktivasi neuroendokrin dan tekanan darah menurun.

Selain itu, penggunaan agen inotropik intravena tidak didukung pada pasien dalam pengaturan akut kecuali sebagai pengobatan sementara diuretik-refrakter terapi inotropik kompleks decompensation.48 intravena (infus kontinu atau intermiten milrinone atau dobutamin) telah dikaitkan dengan peningkatan mortalitas bila digunakan dalam pasien yang memerlukan dukungan inotropik, meskipun agen ini meningkatkan status10 hemodinamik (Tabel 7). Dalam upaya untuk mengetahui apakah infus jangka pendek (48 jam) dapat mengakibatkan perbaikan pendek atau menengah-panjang pada pasien yang dirawat di rumah sakit untuk eksaserbasi gagal jantung yang memiliki dukungan di inotropik yang basah dan dingin ke profil dingin, tapi intravena tidak penting, studi yang disebut Hasil dari Percobaan Calon Milrinone Intravena untuk Eksaserbasi Gagal Jantung Kronis (Optime-HF) adalah conducted.49 Penyidik pasien diacak untuk menerima jangka pendek milrinone intravena atau plasebo. 2 kelompok tidak berbeda secara signifikan di rumah sakit dan 60-hari kematian posthospitalization atau dalam jumlah hari rata-rata pasien dirawat di rumah sakit menyebabkan kardiovaskular dalam 60 hari pertama setelah debit. Selain itu, hipotensi berkelanjutan atau aritmia atrium baru yang secara bermakna lebih mungkin untuk mengembangkan pada pasien yang menerima milrinone dibandingkan pada pasien yang menerima plasebo. Hasil penelitian ini, bahwa menerima agen inotropik tanpa bukti yang jelas dari kompromi hemodinamik tidak signifikan meningkatkan

hasil klinis maupun ekonomi, menyebabkan percampuran dari penggunaan agen inotropik intravena kecuali benar-benar diperlukan.

Selanjutnya, seiring penggunaan -blocker (-antagonis) dan dobutamin intravena (-agonis) terapi adalah kontroversial. Respon farmakologi dari dobutamin dihambat pada pasien yang menerima dosis tinggi dari -blocker karena kedua obat bersaing untuk -adrenergik yang sama receptors.48 Konflik ini terutama jelas dengan carvedilol karena blok SS1 dan SS2 baik receptors.48, 50

Mitos 4: ACE Inhibitor dan -Blocker Terapi Harus Dihentikan Sementara Penurunan atau dekompensasi Selama

Perawatan

Pertimbangan

Lihat Dalam Di

tabel jendela jendela

ini: ini baru