Cover Article

CE Article

Evidence-Based Practice for Acute Decompensated Heart Failure

Nancy M. Albert, RN, MSN, CCNS, CCRN, CNA

Cathy A. Eastwood, RN, 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.

Luke’s Episcopal Hospital, Houston, Tex. Currently, she is a lecturer at Memorial University of

Newfoundland, School of Nursing, in St. John’s, 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. Luke’s 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 ventricle’s 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 this table:

In this window

In a new window

 

Table 1 Characteristics of patients, clinical signs and symptoms, and hospital placement: data

from the Acute Decompensated Heart Failure National Registry3

View this table:

In this window

In a 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 Organizations9

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 patient’s treatment plan at discharge after an admission for

decompensated heart failure stemming from volume overload.10,11

View this table:

In this window

In a new window

 

Table 3 The 4 core measures of the Joint Commission on Accreditation of Healthcare

Organizations

View this table:

In this window

In a new 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.11–14 See Figure 1 and Table 5 for definition and description of

consequences of ventricular remodeling.

View larger version (49K):

In this window

In a new window

 

Figure 1 Ventricular remodeling. Cross-sectional view of left and right ventricles: a, normal; b,

concentric hypertrophy; and c, eccentric hypertrophy.

View this table:

In this window

In a new 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 patient’s placement (telemetry or nonmonitored bed), a nurse’s background

(cardiac, heart failure, or generalist), or a hospital’s 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 cardioverter-

defibrillator to prevent sudden cardiac death, so that appropriate consultations and therapies are

discussed and initiated before patients are discharged from the hospital.

View this table:

In this window

In a new 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 patient’s cardiac performance and help

shape the treatment plan. Nurse caregivers must frequently reassess the patient’s 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 patient’s 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 4–12 mm Hg; in heart failure

treatment, the goal is 8–15 mm Hg) and the mean systemic vascular resistance was 1640

dynes•sec•cm–5 (normal is 800–1200 dynes•sec•cm–5),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,19–23 but

BNP level can also be used to assess clinical status and the effectiveness of therapies during an

admission for acute decompensation.24

View larger version (49K):

In this window

In a 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. Non–potassium-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.26–31 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.35–39

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.40–42 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 this table:

In this window

In a 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 dynes•sec•cm–5 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 reninangiotensin-

aldosterone 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 dose-

dependent, 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 ß-Blocker Therapy

ß-Blocker therapy also affects mechanisms in the kidneys and the renin-angiotensin system. ß-

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 ß-blocker/α-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 ß-blockers. In actuality, maintenance of ß-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, ß-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 short-

term 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 ß-blocker (ß-antagonist) and intravenous dobutamine (ß-agonist)

therapies is controversial. The pharmacological response of dobutamine is inhibited in patients

receiving high doses of ß-blockers because both drugs compete for the same ß-adrenergic

receptors.48 This conflict is especially apparent with carvedilol because it blocks both ß1 and ß2

receptors.48,50

Myth 4: ACE Inhibitors and ß-Blocker Therapies Should Be Temporarily Decreased or

Discontinued During Decompensation

Another belief is that ACE inhibitors and ß-blocker therapies must be decreased or discontinued

or should not be initiated when the patient’s 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 angiotensin-

receptor blocker) and ß-blocker therapies are initiated and maintained in patients with a low

baseline blood pressure (85–90 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 ß-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 ß-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 patient’s 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 ß-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 patient’s 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 ß-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, ß-blockers, or diuretics because of a patient’s 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 patient’s clinical status.

Critical evaluation of each patient’s 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 1995:1–63.

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;7:221–228.[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;7:168–174.

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;161:2337–2342.[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;38:2101–2113.[Free   Full   Text]

11. Jessup M, Brozena S. Heart failure. N Engl J Med. 2003;348:2007–2018.[Medline]

12. Cohn JN, Ferrari R, Sharpe N. Cardiac remodeling: concepts and clinical implications—a

consensus paper from an international forum on cardiac remodeling. J Am Coll Cardiol.

2000;35:569–582.[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):I14–I19.[Medline]

14. Sutton MG, Sharpe N. Left ventricular remodeling after myocardial infarction:

pathophysiology and therapy. Circulation. 2000;101:2981–2988.[Free   Full   Text]

15. Stevenson LW. Tailored therapy to hemodynamic goals for advanced heart failure. Eur J

Heart Fail. 1999;1:251–257.[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;7:105–113.[Medline]

18. Baughman, KL. B-type natriuretic peptide: a window to the heart. N Engl J Med.

2002;347:158–159.[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;37:379–385.[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;111:274–279.[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;144:834–839.[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;37:386–391.[Abstract/Free   Full   Text]

25. Slike B. Diuretic induced changes in symptoms and quality of life. Br Heart J.

1994;72(suppl):S57–S62.[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):S54–S56.[Free   Full   Text]

28. Anand IS, Florea VG. Diuretics in chronic heart failure: benefits and hazards. Eur Heart

J. 2001;3(suppl G):G8–G18.

29. Weinfeld MS, Chertow GM, Stevenson LW. Aggravated renal dysfunction during

intensive therapy for advanced heart failure. Am Heart J. 1999;138:285–290.[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):S44–S47.

32. van ZwietenPA. Neuroendocrine effects of diuretics in heart failure. Br Heart J. 1994;

72(suppl):S51–S53.[Free   Full   Text]

33. Hampton JR. Results of clinical trials with diuretics in heart failure. Br Heart J. 1994;

72(suppl):S68–S72.[Free   Full   Text]

34. Hess B. Chronic heart failure: pathophysiology and therapeutic approaches—why is the

kidney so important? Eur Heart J. 2001; 3(suppl G):G3–G7.

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;291:587–592.

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;81:723–729.[Abstract]

37. Franciosa JA, Silverstein SR. Hemodynamic effects of nitroprusside and furosemide in

left ventricular failure. Clin Pharmacol Ther. 1982;32:62–69.[Medline]

38. Pepine CJ, Nichols WW, Curry RC Jr, Conti CR. Aortic input impedance during

nitroprus-side infusion. J Clin Invest. 1979;64:643–654.

39. Brodie BR, Grossman W, Mann T, McLaurin LP. Effects of sodium nitroprusside on left

ventricular diastolic pressure-volume relations. J Clin Invest. 1977;59:59–68.

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: 1115–1123.[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;85:467–470.

43. Greenberg BH, Hermann DD. Contemporary Diagnosis and Management of Heart

Failure. Newtown, Pa: Handbooks in Health Care Co; 2002:214–217.

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;39:1623–1629.[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;287:1531–1540.[Abstract/Free   Full   Text]

48. Bristow MR, Shakar SF, Linseman JV, Lowes BD. Inotropes and ß-blockers: is there a

need for new guidelines? J Card Fail. 2001; 7(2suppl 1):8–12.[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, O’Connor CM. Inotropic therapy for heart failure: an evidence-based

approach. Am Heart J. 2001;142:393–401.[Medline]

51. Albert N. Heart failure: the pathophysiologic basis for current therapeutic concepts. Crit

Care Nurse. June 1999;18(suppl):2–13.

52. Albert NM. Advanced systolic heart failure: emerging pathophysiology and current

management. Prog Cardiovasc Nurs. Summer 1998;13:14–30.[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; 1999:136–294.

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;7:21–29.[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;19:126–135.[Medline]

58. Miranda MB, Gorski LA, LeFevre JG, Levac KA, Niederstadt JA, Toy AL. An evidence-

based approach to improving care of patients with heart failure across the continuum. J

Nurs Care Qual. 2002;17:1–14.[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 Pasal

CE Pasal

Bukti Berbasis Praktik untuk Gagal Jantung Akut dekompensasi

Nancy M. Albert, RN, MSN, CCNS, CCRN, CNA

Cathy A. Eastwood, RN, MN

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

________________________________________

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 artikel ini, yang tes pengetahuan Anda tentang tujuan-tujuan berikut:

1. Mengidentifikasi inti untuk terapi obat gagal jantung dekompensasi

2. Jelaskan peran tipe B natriuretic peptide pada gagal jantung dekompensasi

3. Jelaskan manajemen farmakologis gagal jantung dekompensasi

________________________________________

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 rata-

rata tinggal adalah 4,4 days.3

Lihat tabel ini:

Dalam jendela ini

Di jendela baru

  

Tabel 1 Karakteristik pasien, tanda dan gejala klinis, dan penempatan rumah sakit: data dari

dekompensasi Gagal Jantung Akut Nasional Registry3

Lihat tabel ini:

Dalam jendela ini

Di jendela 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 bahwa perilaku mereka didasarkan pada bukti saat ini.

Harapan tinggi untuk Bukti 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 tabel ini:

Dalam jendela ini

Di jendela baru

  

Tabel 3 Langkah-langkah inti 4 Komisi Bersama Akreditasi Organisasi Kesehatan

Lihat tabel ini:

Dalam jendela ini

Di jendela baru

  

Tabel pedoman Praktek 4 yang berlaku untuk tahap C * 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 versi yang lebih besar (49K):

Dalam jendela ini

Di jendela baru

  

Gambar 1 renovasi ventrikel. Cross-sectional pandangan ventrikel kiri dan kanan: normal, b,

hipertrofi konsentris, dan c, hipertrofi eksentrik.

Lihat tabel ini:

Dalam jendela ini

Di jendela baru

  

Tabel 5 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), atau sumber daya sebuah rumah sakit.

Penilaian 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 dilakukan sebelum pasien keluar dari rumah sakit.

Lihat tabel ini:

Dalam jendela ini

Di jendela 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 tanda-

tanda distensi vena leher, tekanan tinggi pada vena jugularis yang tepat internal, positif perut-

refleks 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 800-

1200 dyne • sec • cm-5), 15 mencerminkan negara vasoconstricted dan kebutuhan untuk terapi

vasodilator di samping diuresis dan natriuresis (ekskresi natrium).

Tes 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 versi yang lebih besar (49K):

Dalam jendela ini

Di jendela 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 hasil dan meningkatkan kenyamanan.

Mitos dan Realitas 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 yang berkontribusi untuk hasil terbaik.

Mitos 1: Tujuan Pengobatan untuk Gagal Jantung Akut dan Kronis 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 dan mempromosikan pembalikan remodeling ventrikel.

Mitos 2: Mengelola Kelebihan Cairan Setara Penggunaan 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 tabel ini:

Dalam jendela ini

Di jendela 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 telemetri.

Diuretik dan ß-Blocker Terapi

ß-Blocker terapi juga mempengaruhi mekanisme di dalam ginjal dan sistem renin-angiotensin. ß-

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 ß-blocker/α-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 ß-blocker.

Pada kenyataannya, pemeliharaan ß-blocker (dan meningkatkan akhirnya untuk menargetkan

dosis sekali hipervolemia dikendalikan, berdasarkan AHA / pedoman praktek ACC) 10 benar-

benar 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, ß-

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 ß-blocker (ß-antagonis) dan dobutamin intravena (ß-agonis)

terapi adalah kontroversial. Respon farmakologi dari dobutamin dihambat pada pasien yang

menerima dosis tinggi dari ß-blocker karena kedua obat bersaing untuk ß-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 ß-Blocker Terapi Harus Dihentikan Sementara Penurunan atau

dekompensasi Selama

Perawatan Pertimbangan

Lihat tabel ini:

Dalam jendela ini

Di jendela baru