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CHAPTER 18 Acute Heart Failure and Pulmonary Edema 189
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aortic and mitral regurgitation and aortic stenosis may suggest
a cardiogenic cause of pulmonary edema.
ST segment changes on ECG consistent with MI or myocardial
ischemia would suggest an acute cardiac event as the cause of
the pulmonary edema. Also, ECG evidence of LV strain, left
bundle branch block, or other abnormalities of the QRS complex
might indicate an underlying cardiac pathology. Unless there
are major metabolic disturbances, the ECG is usually normal in
patients with pure NCPE.
In NCPE and CPE, arterial hypoxemia is due to changes in
the ventilation-perfusion ratio and intrapulmonary shunting.
Patients with NCPE usually have a more pronounced defect in
oxygenation than is seen in patients with CPE. This is largely
due to the greater shunt fractions found in these patients. In the
clinical setting, higher concentrations of inspired oxygen concentrations (FIO2) and larger positive end-expiratory pressures
are required to achieve acceptable oxygenation in NCPE compared
with CPE.
Similar to other tests, the chest radiograph may be helpful
in differentiating NCPE from CPE. With NCPE, the alveolar and
interstitial disease might show a predominant peripheral distribution; in CPE, a perihilar distribution is more evident, often
associated with Kerley lines or pleural effusions, or both. Heart
size is more commonly increased in CPE than NCPE, but the
lack of cardiomegaly does not exclude CPE. In most patients,
the chest radiograph proves to be of little help. This is due partially
to the fact that patients are often too ill to be examined by
anything other than a portable unit and such films are usually
of suboptimal interpretive quality. An example of acute CPE
and less severe pulmonary congestion is shown in Fig. 18.6.
When the cause of pulmonary edema is clearly evident from
the clinical data (i.e., MI), no further diagnostic tests are needed.
If uncertainty remains regarding the etiology of the pulmonary
edema, further diagnostic tests are appropriate. A BNP level of
less than 100 pg/mL or NT-proBNP level of less than 300 pg/mL
effectively rules out a cardiac cause for respiratory failure. Elevated
BNP levels are found in patients with pulmonary hypertension,
cor pulmonale, pulmonary emboli, and compensated heart failure.
BNP levels are also higher in women, older patients, and patients
with renal failure.39 BNP and NT-proBNP values are also similarly
elevated in patients with severe sepsis or septic shock and AHF
independently of whether they present with or without shock.
Clinical judgment is still required to differentiate CPE from
NCPE. An echocardiogram should be obtained in all patients
with pulmonary edema in whom the cause of pulmonary edema
is unclear. Normal Doppler echocardiography assessments of
systolic and diastolic function strongly point to a noncardiogenic
cause of respiratory failure. If uncertainty persists, it is reasonable
to obtain hemodynamic information via a pulmonary artery
catheter to differentiate CPE from NCPE. With the availability
of BNP levels and two-dimensional Doppler echocardiography,
however, there seems to be less need to proceed with invasive
monitoring.
40
Evaluation and Triage of Patients With Acute
Heart Failure
After the diagnosis of AHF has been established, the initial focus
is to ensure optimal oxygenation and hemodynamic stability.
Several steps are necessary to comprehensively evaluate a patient
with AHF.
Step 1: Define Clinical Severity of Acute Heart Failure. Several
grading classifications of the severity of AHF have been in place
for many years in coronary care units and ICUs. The Killip
classification, based on clinical signs and chest radiography
findings,41 and the Forrester classification, based on clinical signs
and hemodynamic characteristics,42 are discussed elsewhere.
These classifications have been validated in AHF after acute MI
and are most applicable for patients with new-onset AHF. Other
authors have proposed a straightforward clinical tool for classifying the severity of chronic decompensated heart failure. This
classification is based on an assessment of adequacy of perfusion
(warm perfused, cold hypoperfused) and of fluid overload/
congestion or filling pressures (wet congested, dry euvolemic).
A B
Fig. 18.6 Chest radiographs of two patients. (A) The classic features of acute cardiogenic pulmonary
edema. Note the perihilar alveolar infiltrates. (B) Marked interstitial changes in the lung bases.
Note the Kerley B lines (arrows).
190 PART IV Noncoronary Diseases: Diagnosis and Management
CONGESTION (–) CONGESTION (+)
ension
HYPOPERFUSION (–)
HYPOPERFUSION (+)
C
Oligur
Mental confusion
Dizziness
Diminished pulse pressure
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old sweaty extremities
ia
Fig. 18.7 Clinical phenotype based on the presence of congestion
and/or hypoperfusion in acute heart failure.
Patients can be classified as warm and dry, warm and wet, cold
and dry, and cold and wet (Fig. 18.7).
permits attention to specific therapies and can provide prognostic
information.
A pragmatic approach is simply to define the severity of AHF
based on oxygen requirements and blood pressure. The most
critical patient is the patient with the lowest blood pressure and
highest oxygen requirement. A subset of patients with decompensated end-stage heart failure present to the emergency
department in occult shock and are clinically indistinguishable
from patients with mildly decompensated chronic heart failure
and stable heart failure.43 The only parameter differentiating
occult shock patients from nonshock patients is a significantly
elevated lactic acid level.
43
In patients hospitalized with AHF, the risk of in-hospital
mortality can be derived from admission clinical and laboratory
variables. A blood urea nitrogen (BUN) level of 43 mg/dL or
greater, serum creatinine level of 2.75 mg/dL or greater, and
systolic blood pressure of less than 115 mm Hg are independent
predictors of in-hospital mortality.
AHF, the finding of a troponin I level of 1.0 µg/L or greater or
troponin T of 0.1 µg/L or greater is associated with higher inhospital mortality independent of other predictors.45 Several
other variables—such as age, heart rate, sodium, chronic obstructive pulmonary disease, and nonblack race—are also predictive
of in-hospital mortality.
46
Step 2: Establish Etiology of Acute Heart Failure. The most
common causes of AHF are listed in Box 18.1. Echocardiography
is an essential tool for the evaluation of the functional and
structural cardiac changes underlying or associated with AHF.
Step 3: Identify Precipitating Causes of Acute Heart Failure.
Precipitating causes are defined as factors that may precipitate
acute decompensation in patients with underlying cardiac disease
but are unlikely to cause cardiac decompensation in a patient
with a normal heart. Patients with chronic heart failure are prone
to infections. The most common are respiratory or urinary tract
infections, septicemia, or nosocomial infections. Infections often
manifest atypically in patients with AHF. Many patients are sick
Pulmonary edema
Peripheral edema
Jugular venous dist
Hepatomegaly
Ascites
Warm-Dry
Cold-Dry Cold-Wet
Warm-Wet
4,35
Such categorization
14,44
In addition, patients with
BOX 18.2 Precipitants of Heart Failure
Dietary indiscretion
Vigorous fluid administration
Noncompliance to medical regimen
Worsening renal failure
Uncontrolled hypertension
Anemia
Systemic infection
Pulmonary embolism
Myocardial ischemia
Tachyarrhythmias and bradyarrhythmias
Electrolyte disturbances
Severe emotional or physical stress
Hyperthyroidism and hypothyroidism
Cardiodepressant and other drugs
•
Antiinflammatory drugs
• Antiarrhythmic drugs
• Calcium channel blockers
• β-Adrenergic blocking agents
without a fever. Identifying the precipitating causes of acute
hemodynamic decompensation has obvious therapeutic implications. Box 18.2 lists common precipitating causes.
Step 4: Decide on Disposition of Patient. Patients with severe
respiratory failure and patients in shock or preshock should be
admitted to the cardiac intensive care unit (CICU). Although
no validated algorithms exist at this time to guide the clinician
for triaging patients with decompensated chronic heart failure
to regular floor beds or to the CICU, the European Society of
Cardiology proposed the following criteria for admission to the
CICU35:
• Needforintubation(oralreadyintubated)
• Signsandsymptomsofhypoperfusion
• Oxygensaturation(SpO2 ≤90%) despite supplemental oxygen
• Useofaccessory muscles and respiratoryrate≥25 breaths/
hour
• Heartratelessthan40ormorethan130beats/min,systolic
blood pressure less than 90 mm Hg
In North America, 10% to 12% of patients with AHF are
managed in ICUs.
47
Ongoing Evaluation of the Patient
Monitoring of a patient with AHF should be initiated as soon
as possible after admission to the emergency department. The
type and level of monitoring required for any individual patient
vary widely depending on the severity of the cardiac decompensation and the response to initial therapy. Generally, the following
parameters should be measured in all critically ill patients: mental
status, blood pressure, temperature, respiratory rate, heart rate,
and urine output. Some laboratory tests should be done repeatedly
(i.e., electrolytes, creatinine, and glucose, or markers for infection
or other metabolic disorders). Liver function tests and lactate
levels should be measured when there is evidence of hypoperfusion.
Routine arterial blood gas analysis is generally not needed. After
admission to the ICU or step-down unit, patients with AHF
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 191
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TABLE 18.3 Monitoring Patients With
Acute Heart Failure
Goals Parameters
Arterial oxygen saturation
>95%
Blood pressure Automated blood pressure recordings
Normal sinus rhythm Continuous ECG monitoring
Adequate diuretic response Hourly urine production, daily weight
Adequate organ perfusion Reversal of metabolic acidosis, lactic acid
Improved hemodynamics Mean BP >
Maintain calorie and
nitrogen balance
Control hyperglycemia Glucose concentrations
BP, Blood pressure; JVP, jugular venous pressure.
Pulse oximetry, arterial blood gas
Consider placement of an indwelling radial
artery catheter
Frequent assessments (every 5–10 min)
early on to assess BP response to
treatment
BP via indwelling radial artery catheter
levels
Liver function tests
Adequate urine output
Mean BP >
Central venous O2 saturation >65%
Assessment of JVP
Central venous pressure line O
Pulmonary artery catheter
Blood albumin concentrations
Nitrogen balance
65 mm Hg
65 mm Hg
saturation
2
should be carefully monitored to ensure that the treatment goals
are met and continued progress is made toward a stable state.
These goals are summarized in Table 18.3.
Pulmonary Artery Catheter. Controversy exists about the use
of the pulmonary artery catheter in critically ill patients. The
concern about pulmonary artery catheter use arose following
prior studies that showed higher mortality for patients thought
to require a pulmonary artery catheter during hospitalization.
More recent data suggest that the routine use of pulmonary
artery catheters in patients with AHF is unnecessary and unlikely
to lead to a better outcome, although the use of inotropic or
vasoactive support was discouraged in the clinical trial.
48
A
pulmonary artery catheter may be of utility in select patients
such as those with cardiogenic shock, rapidly decompensating
heart failure, patients who are being considered for heart transplantation with significant pulmonary hypertension, obese
patients who may be very difficult to assess and monitor clinically,
and patients with severe LV and RV dysfunction for whom the
response to vasodilator and other therapies may be difficult to
predict.
TREATMENT OF ACUTE HEART FAILURE
The management of patients with AHF is primarily aimed at
restoring perfusion of vital organs and relieving pulmonary and
systemic congestion. In hemodynamic terms, the intention is to
increase cardiac output and to decrease LV filling pressure while
preserving adequate coronary perfusion.
General Measures
Several general measures are advisable for treating most patients
with AHF. Bed rest should be enforced. Patients feel most comfortable in the semi-upright position, with legs dependent.
Oxygenation. Special attention should be paid to maintaining
adequate oxygenation. When there is hypoxia (PaO2 <60 mm Hg
or SpO2 <90%) without hypercapnia, oxygen-enriched inspired
gas may suffice. This can be given through nasal prongs, Venturi
masks, or reservoir bag masks, depending on the severity of gas
exchange abnormality. Noninvasive ventilation by either continuous positive airway pressure breathing or bilevel positive airway
pressure may become necessary when oxygenation cannot be
maintained or there is evidence of progressive hypercapnia despite
aggressive treatment. The use of noninvasive ventilation is
associated with a significant reduction in the need for tracheal
intubation and mechanical ventilation. Failing these interventions,
intubation and mechanical ventilation may be needed to improve
oxygenation and reverse hypercapnia. Intubation is generally
recommended if respiratory failure cannot be managed noninvasively and blood gas demonstrates persistent hypoxemia (PaO2
<60 mm Hg), hypercapnia (PaCO2 >50 mm Hg), and respiratory
acidosis (pH <7.35).
Deep Venous Thrombosis Prophylaxis. Patients with heart
failure who are bedridden or with limited physical mobility are
at high risk for developing deep venous thrombosis. Routine
prophylactic treatment should be given unless there are contraindications to such therapy.
Diabetes. Hyperglycemia occurs commonly in patients with
AHF owing to impaired metabolic control. Routine hypoglycemic
drugs should be discontinued, and glycemic control should be
obtained by using short-acting insulin titrated according to
repeated blood glucose measurements. Intensive insulin therapy
(blood glucose 81 to 108 mg/dL) in critically ill patients has
been shown to increase 90-day mortality and should be avoided.
49,50
Medications
The use of opiates in AHF should largely be avoided.
morphine is used, the patient should be monitored for respiratory
depression, which can be reversed by the narcotic antagonist
naloxone. Morphine should be avoided if the pulmonary edema
is associated with hypotension, intracranial bleeding, disturbed
consciousness, bronchial asthma, chronic pulmonary disease, or
reduced ventilation, specifically in patients with an increased
arterial PCO
.
2
34,35
If
Treatment of Triggers of Decompensation
Acute Coronary Syndrome. The coexistence of an acute coronary
syndrome and AHF identifies a very-high-risk group in which
early revascularization is recommended.
Rapid Arrhythmias and Severe Bradycardia. Unstable tachy-
cardic and or bradycardic rhythm disturbances should be treated
promptly with either cardioversion or temporary pacing.
192 PART IV Noncoronary Diseases: Diagnosis and Management
Ventricular pressure
AB
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Acute Mechanical Instability. Patients usually require circula-
tory support with surgical or percutaneous interventions when
the structural integrity of the heart is compromised by acute
and sudden valvular regurgitation, free wall or septal wall rupture
following ischemic injury, or severely compromised myocardial
function secondary to fulminant myocarditis.
Hemodynamic Goals of Treatment
Reduction of LV preload is highly desirable in patients with AHF
and CPE. It is primarily intended to shift central blood volume
to the periphery, reducing LV diastolic volume and pressure.
When AHF is associated with an expanded circulating volume,
as with acute decompensation of chronic heart failure, substantial
preload reduction can be achieved without a significant decline
in arterial pressure. In the setting of hypertension and normovolemia, aggressive reduction in preload may lead to a substantial
decrease in blood pressure. It is important to decide in advance
whether a patient who presents with AHF is likely to be at
increased risk of developing hypotension with reductions in LV
preload.
Ventricular afterload is increased in most patients with heart
failure; the detrimental effects of afterload excess are proportional
to the degree of LV systolic dysfunction. Afterload reduction
with vasodilator therapy is directed at reducing excessive LV wall
stress, with a resultant increase in stroke volume and a decrease
in end-diastolic pressure. A reduction in afterload provides the
greatest hemodynamic benefit for patients with the most advanced
heart failure; a far greater increase in stroke volume and decrease
in end-diastolic pressure are achieved with similar reductions
in wall stress in patients with severe LV systolic dysfunction
compared with patients with milder forms of heart failure (Fig.
18.8). Although there are no robust randomized data to support
the use of vasodilators and diuretics in AHF, the consensus among
experts is that these agents are first-line therapy in most patients
with AHF. A simple treatment algorithm for the management
of AHF according to the different hemodynamic phenotypes is
outlined in Fig. 18.9.
Specific Interventions
Vasodilators. The endpoints of vasodilator therapy can vary
from patient to patient, but reasonable hemodynamic endpoints
include a reduction in LV filling pressure to 15 mm Hg or less
and an increase in cardiac output that would ensure adequate
tissue oxygen delivery (usually a cardiac index >2.5 L/min/m2)
while maintaining a systemic blood pressure of 90 mm Hg or
greater.
Nitroglycerin
Actions. Nitroglycerin causes vasodilation by stimulating
guanylate cyclase within the vascular smooth muscle of arterial
resistance and venous capacitance vessels.51 The predominant
site of action depends on the dose being administered. At lower
doses, nitroglycerin acts principally on the peripheral veins and
reduces RV and LV filling pressures. At higher doses, nitroglycerin
causes modest arterial vasodilation; consequently, it may improve
cardiac output. Nitroglycerin can reduce the degree of mitral
regurgitation
stiffness by redistributing blood from the central blood pool
(heart and lungs) to the periphery (mesenteric bed),
LV volumes, which decreases the pericardial constraint.
Nitrates reduce subendocardial ischemia by coronary
vasodilation and by reducing myocardial oxygen requirements
through unloading effects. One disadvantage of nitrates is the
rapid development of tolerance, especially when given intravenously in high doses, limiting their effectiveness to 16 to 24
hours only. Nitrates should be given at doses aimed at achieving
52,53
and decreases the preload-dependent chamber
54,55
decreasing
56
Ventricular pressure
Ventricular volume
Fig. 18.8 Schematic diagram of the left ventricular wall stress–volume relationship. The loop has
the same configuration as the pressure-volume relationship. (A) With mild heart failure, a decrease
in wall stress (arrows) results in an increase in stroke volume. (B) With more advanced heart
failure, a similar decrease in wall stress is accompanied by a marked increase in stroke volume.
Vasodilator therapy (i.e., afterload reduction) produces a larger increase in stroke volume in
advanced heart failure than in mild heart failure.
Ventricular volume
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 193
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Hemodynamic
phenotype
“Wet” and “Warm”
Hypertensive AHF
(Mild congestion)
-Vasodilator
-Short term diuretics
(modest doses)
Fig. 18.9 Management of acute heart failure based on the clinical phenotype. (Modified from
Ponikowski P, Voors AA, Anker SD, et al. 2016 ESC Guidelines for the diagnosis and treatment
of acute and chronic heart failure: The Task Force for the diagnosis and treatment of acute and
chronic heart failure of the European Society of Cardiology (ESC). Developed with the special
contribution of the Heart Failure Association (HFA) of the ESC. Eur J Heart Fail. 2016;18:891–975.)
Normotensive AHF
(Severe congestion)
-Long term diuretics
(higher doses)
-Vasodilator
SBP>90 mmHg
-Vasodilator
-Diuretics
-Inotrope when
hypoperfusion
persists
“Wet” and “Cold”
optimal vasodilation, leading to an increase in cardiac index and
decrease in pulmonary wedge pressure.
Use in acute heart failure. Randomized trials in AHF have
established the efficacy of intravenous nitrates in combination
with furosemide and have shown that titration to the highest
hemodynamically tolerable dose of nitrates with low-dose
furosemide is superior to high-dose diuretic treatment alone.57
Nitroglycerin is effective in relieving the symptoms of acute
pulmonary edema and is often the vasodilatory agent of choice
in patients with underlying ischemic heart disease.58 Nitroglycerin
should be administered in a manner to ensure the fastest onset
of action. The intravenous route generally is preferred. The initial
infusion rate is 5 µg/min, and the rate may be increased to 200 µg/
min to achieve desired effects. The dose of nitroglycerin should
not be increased when the systolic arterial pressure is less than
90 mm Hg. From a practical perspective, a reduction of 10 mm Hg
in mean arterial pressure should be achieved.
Nitroglycerin can be administered orally or by inhalation
(glyceryl trinitrate spray, 400 µg [2 puffs] every 5 to 10 minutes),
or buccally (isosorbide dinitrate, 1 or 3 mg), while monitoring
blood pressure. Buccal absorption may be erratic. One should
be particularly cautious when administering nitrates to a patient
with aortic stenosis or hypertrophic obstructive cardiomyopathy.
Nitroprusside
Actions. Nitroprusside infusion improves ventricular per-
formance by decreasing all the major components of LV afterload:
systemic vascular resistance, arterial stiffness, arterial wave
reflectance, and LV size.59 Proper dose selection achieves a
SBP<90 mmHg
-Inotrope
-Vasopressor if shock
persists
-Diuretic when perfusion
is adequate
-Mechanical support
for refractory shock
“Dry” and “Cold”
-Fluid challenge
-Inotrope if
hypoperfusion
persists
“Dry” and “Warm”
No intervention
reduction in afterload and preload with little change in systemic
blood pressure. An often overlooked aspect of afterload reduction
is the reduction of RV load. Vasodilators that are associated with
a decrease in LV filling pressures invariably unload the right
heart.60 Within the confined space of the pericardium, interventions that reduce the excessive volume of the RV have a favorable
hemodynamic effect on the septal interaction between the right
and left ventricles, which consequently may improve LV filling
and diastolic pressures. Nitroprusside is likely to achieve some
of its favorable effects through this mechanism of ventricular
interaction.
The incidence of side effects and toxicity is directly related
to the dose and duration of administration. Cyanide may
accumulate with prolonged high doses of nitroprusside and
contribute to lactic acidosis. Toxicity can be avoided by monitoring
blood lactate and thiocyanate levels.
Use in acute heart failure. Intravenous nitroglycerin is usually
the vasodilator of choice for most patients with AHF, especially
if a patient has underlying ischemic heart disease, but nitroprusside is the vasodilator of choice when a substantial reduction
in LV afterload is required. Although both vasodilators affect
vascular smooth muscle, nitroprusside and nitroglycerin differ in
important ways. Because the magnitude of arterial vasodilation
achieved with nitroprusside is greater than that with nitroglycerin,
nitroprusside has the greater potential to produce hypotension.
Such hypotensive action may lead to more neurohormonal activation, which may be the reason why rebound hemodynamic effects
after abrupt withdrawal of the drug occur more frequently with
nitroprusside than with nitroglycerin.
61
194 PART IV Noncoronary Diseases: Diagnosis and Management
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Nitroprusside is reserved for clinical situations requiring
acute, short-term afterload reduction. Nitroprusside is most
beneficial for hypertensive patients or patients with an elevated
LV filling pressure (≥20 mm Hg) and a systemic arterial pressure
of 100 mm Hg or greater. This clinical picture is commonly
encountered in patients with a large MI, with decompensated
chronic heart failure, with acute valvular regurgitation, or after
cardiopulmonary bypass. The use of nitroprusside in those with
low-output, advanced heart failure (classified in the cold and wet
profile) has been demonstrated to be safe when titrated for a mean
arterial pressure of 65 to 70 mm Hg and appears to benefit both
hemodynamic measurements and, possibly, all-cause mortality.62
Nitroprusside usually represents a stabilizing pharmacologic
bridge to more definitive interventions (e.g., valve replacement
or coronary revascularization). The optimally effective and safe
administration of nitroprusside often requires hemodynamic
monitoring by means of intraarterial catheters. The initial dose
of 5 to 10 µg/min is gradually increased as needed (up to 300 µg/
min) to attain the desired clinical and hemodynamic effects.
Nesiritide
Actions. Nesiritide is a recombinant human BNP that is
identical to the endogenous hormone. Nesiritide has venous,
arterial, and coronary vasodilatory properties that reduce preload
and afterload, and increase cardiac output without direct inotropic
63
effects.
Use in acute heart failure. Nesiritide was compared with
intravenous nitroglycerin and resulted in improvement in
hemodynamics more effectively and with fewer adverse effects,
although this did not translate into improvement in clinical
outcome.64 In a randomized clinical trial, nesiritide had no
significant impact on co-primary endpoints of dyspnea and the
composite endpoint of rehospitalization for heart failure or death
within 30 days in patients with AHF, although it did not worsen
renal failure.65 Nesiritide may cause hypotension, and some
patients are nonresponders. The role of this agent is uncertain
in the context of AHF. In most hospitals, nesiritide is not given
as a first-line agent, but this medication may be considered when
a patient does not respond rapidly to conventional treatment.
The recommended dose of nesiritide is an intravenous bolus of
2 µg/kg followed by a continuous infusion of 0.01 µg/kg/min.
Other Vasodilators. The intravenous use of direct-acting
vasodilators such as hydralazine has a very limited or no role in
the management of AHF and CPE. Other vasodilators, such as
calcium antagonists or α-adrenergic blockers, cannot be recommended as first-line therapy for patients with AHF. Angiotensinconverting enzyme inhibitors are not indicated in the early
stabilization of patients with AHF. Novel agents such as serelaxin
(a recombinant form of relaxin-2) appear to significantly improve
dyspnea, although their impact on mortality requires further
investigation.
66
Decongestive Therapy
Interventions that target congestion or fluid overload are the
principal focus in the management of AHF in the vast majority
of patients. Despite our best efforts, persistent congestion remains
at discharge in more than a quarter of patients.
67,68
Recognition
and avoidance of incomplete decongestion is important since
residual congestion at discharge is associated with increased risks
of rehospitalization and mortality.
69
Diuretics
Actions. Loop diuretics block the Na+/2Cl−/K+ transporter,
resulting in increased urine volume by enhancing the excretion
of water, sodium chloride, and other ions.70 This, in turn, leads
to a decrease in plasma and extracellular fluid volume, total
body water, and sodium. These effects result in a reduction in
RV and LV filling pressures and a decrease in peripheral and
pulmonary congestion. In patients with decompensated chronic
heart failure, the diuretic dose-response curve shifts downward
and to the right to the extent that higher doses are required to
achieve a therapeutic effect.
71,72
Intravenous administration of
loop diuretics also exerts a vasodilating effect, manifested by an
early (5 to 30 minutes) decrease in right atrial and pulmonary
wedge pressure and pulmonary resistances. These hemodynamic
effects result from the direct peripheral arterial and venodilating
actions. It is thought that vasodilation rather than diuresis is
the principal early mechanism by which diuretics alleviate
symptoms of pulmonary edema.73 High bolus doses (>1 mg/kg)
of diuretics may lead to reflex vasoconstriction. As opposed to
long-term use of diuretics, in severe decompensated heart failure,
the use of diuretics improves loading conditions and may reduce
neurohormonal activation in the short term.
74
Use in acute heart failure. Intravenous loop diuretics (furo-
semide, bumetanide) are the most widely used diuretics in the
treatment of AHF and CPE; they should be initiated in the
emergency department without delay. The dose should be titrated
according to the diuretic response and relief of congestive
symptoms. Administration of a loading dose followed by continued infusion of furosemide has been thought to be more
effective than bolus alone.
75,76
However, data from the recent
Diuretic Optimization Strategies Evaluation (DOSE) trial suggest
that there is no significant advantage to continuous furosemide
over the diuretic given as intermittent boluses.77 Thiazides and
spironolactone can be used in association with loop diuretics;
the combination in low doses is more effective and has fewer
secondary effects than the use of higher doses of a single drug.
Combination of loop diuretics with inotropes or nitrates is
another therapeutic approach that is more effective and produces
fewer secondary effects than increasing the dose of the diuretic.
The diuretic doses for patients with mild congestion and newonset AHF are generally much lower than doses for patients
with advanced fluid overload or patients with renal dysfunction.
The doses of diuretics as they relate to severity of AHF are
summarized in Table 18.4.
Diuretic resistance. This is defined as the clinical state in
which diuretic response is diminished or lost before the goal of
treatment has been achieved. Such resistance is associated with
a poor prognosis.78 Mechanisms underlying diuretic resistance
include the “braking phenomenon,” “rebound” effect, and
hyperaldosteronism.79 The braking phenomenon occurs when
long-term diuretic use results in a reduced natriuretic response
due, in part, to nephron adaptations that leads to avid sodium
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 195
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TABLE 18.4 Diuretic Dosing
Clinical Scenario Diuretic Dose
Moderate fluid overload Furosemide
Bumetanide 0.5–1 mg IV q12h
Severe fluid overload Furosemide 40–80 mg IV q12h
Bumetanide 1–2 mg IV q12hb or bolus
Severe fluid overload
and renal dysfunction
(GFR <
30 mL/min)
Diuretic resistance Add hydrothiazide
The IV loop diuretic dose should be equal to or double the outpatient
oral dose for patients with decompensated chronic HF.
a
Double dose if goal not attained.
b
If goal not attained, add a thiazide (see diuretic resistance).
c
Lower dose if systolic blood pressure <100 mm Hg.
GFR, Glomerular filtration rate; HF, heart failure; IV, intravenous.
From Ponikowski P, et al. 2016 guidelines for the diagnosis and
treatment of acute and chronic heart failure: the Task Force for the
Diagnosis and Treatment of Acute and Chronic Heart Failure of the
European Society of Cardiology (ESC) developed with the special
contribution of the Heart Failure Association (HFA) of the ESC. Eur
Heart J. 2016;37(27):2129–2200.
Furosemide 80–200 mg IV q12h or
or metolazone
20–40 mg IV q12h
Bolus of 60 mg IV +
continuous infusion at
10–20 mg/h
of 2 mg IV + continuous
infusion at 0.25–
0.5 mg/h
bolus + continuous
infusion at 20–40 mg/h
25 mg or 50 mg
5 mg or 10 mg 30 min
prior to loop diuretic
a
a
b,c
or
reabsorption at more distal sites.80 This phenomenon argues for
the use of sequential nephron blockade with combinations of
loop and thiazide diuretics in patients who do not have adequate
responses to optimal doses of a loop diuretic. However, their
use has been associated with increased arrhythmia risk due to
hypokalemia. The rebound effect involves postdiuretic sodium
retention, typically in the setting of inadequate dosing frequency
and insufficient sodium restriction.
81
To overcome inadequate response to diuretics, it is important
to adhere to the following principles (also see Table 18.4):
1. Diuretics should be used in moderation; excessive bolus doses
of any single drug should be avoided.
2. A loop diuretic is the diuretic of choice in patients with renal
insufficiency and in patients with more than mild fluid
retention.
3. The diuretic response of loop diuretics is not increased by
giving larger bolus doses, but it may be enhanced by giving
moderate doses more frequently or using continuous infusion
at higher doses (≥20 mg/h).
4. Sodium restriction (<1.5 to 2 g/day) and fluid restriction (1.5
to 2 L/day) may be helpful.
5. The clinician can make use of synergism by adding a thiazide
when there is apparent tolerance to loop diuretics. This diuretic
regimen can be used to achieve euvolemia. Hydrochlorothiazide
combined with spironolactone should be considered to prevent
excessive potassium wasting. Metolazone, a potent thiazide,
could be added to a loop diuretic when hydrochlorothiazide
seems to be ineffective in promoting sodium excretion. This
combination often causes severe electrolyte disturbances.
6. In patients who have poor responses to intermittent doses of
a loop diuretic, a continuous intravenous infusion could be
entertained. A continuous infusion allows for the administration of higher diuretic doses with less risk of ototoxicity. It
may also be reasonable to consider inotropes if diuretic
resistance is thought to be related to low cardiac output.
Worsening renal failure (WRF). Decongestive therapy with
diuretics is complicated by WRF (defined as an increase in serum
creatinine of ≥0.3 mg/dL during hospitalization) in one-third
of heart failure admissions and is associated with increased
length of stay, increased readmission rate, and decreased
short- and long-term survival.
82–84
However, recent data have
suggested that transient WRF during AHF therapy may not affect
postdischarge outcomes.85 It seems reasonable to conclude that
transient WRF may be a reasonable trade-off for decongestion
given that persistent congestion is associated with WRF and
adverse events. Progressive WRF can be avoided in patients with
persistent congestion by decreasing the rate of volume removal
with diureses.86 In some patients, as stated earlier, inotropic
support may be warranted if WRF is deemed to be a manifestation of end-organ hypoperfusion. The differential diagnosis of
WRF should include the possibility of inadequate decongestion
and progressive cardiorenal syndrome. These two ends of the
volume spectrum should be easily distinguishable by history and
physical examination. The overdiuresed patient with WRF will
frequently complain of orthostatic symptoms, have low jugular
venous pressure (JVP) and no or minimal peripheral edema.
The underdiuresed patient with WRF will not be orthostatic,
will have persistent elevations in JVP, and persistent peripheral
edema.
Vasopressin Antagonists. Elevations of arginine vasopressin
(AVP) in HF promote water retention, with resultant congestive
symptoms and hyponatremia.87 AVP antagonists have been
developed to block the action of AVP at the V2 receptor in renal
tubules to promote aquaresis. Currently, two vasopressin antagonists are available for clinical use: conivaptan and tolvaptan. It
may be reasonable to consider a vasopressin antagonist to treat
symptomatic hypervolemic or normovolemic hyponatremia in
34
patients with HF.
Vasopressin antagonists such as tolvaptan
enhance fluid loss, appear safe, and provide moderate benefits
with dyspnea relief in randomized trials, but do not appear to
impact mortality or hospitalization for heart failure.
88–90
Ultrafiltration. Conventional ultrafiltration requires central
venous access and the typical volume of water removed per
ultrafiltration session is 3000 to 4000 mL. In general, the hemodynamic changes produced by ultrafiltration are modest. The
reduction in water with ultrafiltration is accompanied by decreases
in right atrial and pulmonary venous pressures. Cardiac output
and stroke volume are unchanged or increase slightly. In the
Ultrafiltration versus Intravenous Diuretics for Patients Hospitalized for Acute Decompensated Congestive Heart Failure
(UNLOAD) trial, the weight loss was more sustained when
contrasted with the weight loss achieved with furosemide
196 PART IV Noncoronary Diseases: Diagnosis and Management
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treatment.91 However, the enthusiasm for this strategy as a routine
intervention has waned after the results of the Cardiorenal Rescue
Study in Acute Decompensated Heart Failure (CARRESS-HF)
trial.92 This randomized trial, involving patients hospitalized for
acute decompensated heart failure, worsened renal function, and
persistent congestion, showed that the use of a stepped pharmacologic therapy algorithm was superior to a strategy of
ultrafiltration for the preservation of renal function at 96 hours,
with a similar amount of weight loss with the two approaches.
Ultrafiltration was associated with a higher rate of adverse events.
Recent guidelines indicate that in patients for whom diuretic
strategies have been unsuccessful or with severe renal dysfunction
and/or refractory fluid retention, continuous ultrafiltration may
become necessary.
34,35
Circulatory Support
Inotropic Agents. These agents are indicated in the presence
of hypotension and end-organ hypoperfusion (decreased renal
function) with or without congestion or pulmonary edema refractory to diuretics and vasodilators at optimal doses. Anecdotal
experience suggests that positive inotropic agents may be especially
useful in these patients when LV and RV systolic function are
markedly depressed. Their use is potentially harmful because they
increase oxygen demand and calcium loading; thus they should
be used with caution.93 More recent data do not support the
routine intravenous use of these agents as an adjunct to standard
therapy in the treatment of patients hospitalized for decompensated chronic heart failure.94 The choice of agent depends on
the predominant hemodynamic abnormality. Inotropes are not
indicated in patients with preserved systolic function.
Dopamine
Actions. Physiologically, dopamine is the precursor of
norepinephrine and releases norepinephrine from the stores of
the nerve endings in the heart. Dopamine has the valuable
property in severe heart failure of specifically increasing renal
blood flow by activating postjunctional dopaminergic receptors.95
This vasodilatory effect is observed at doses of 1 to 2 µg/kg per
minute and peaks at a dose of 7.5 µg/min: the vasoconstrictive
effect begins at a dose of 10 µg/kg per minute. Because the
inotropic effects of dopamine result primarily from its indirect
effects, its use in advanced heart failure is limited by the
neurotransmitter depletion present in the failing heart.96 In milder
forms of heart failure, dopamine may have similar effects to
dobutamine except for the greater tendency to increase heart
rate and a tendency to increase systemic vascular resistance and
ventricular filling pressures at medium and higher doses.
Use in AHF. Dopamine should be infused through a long,
indwelling catheter because of the risk of extravasation, which
may cause necrosis and sloughing of the surrounding tissue
because of the vasoconstrictive effects of the agent. Infusion with
dopamine should be started at doses of 2 to 5 µg/kg per min and
should not be increased beyond 5 µg/kg per minute in patients
with blood pressures of 100 mm Hg or greater. This agent may be
deleterious in patients with AHF because it may augment the LV
afterload, pulmonary artery pressure, and pulmonary resistance.
It has been proposed that dopamine may improve renal function
in patients with severe heart failure by increasing renal blood
flow and possibly by reducing renal venous pressure, but data
supporting such a potential benefit are limited. Specifically, the
addition of low-dose dopamine to diuretic therapy was not found
to enhance decongestion or improve renal function.97 In markedly
hypotensive patients with peripheral hypoperfusion, large doses
of dopamine can be used to support systemic blood pressure.
Recent data, however, showed that there was no significant difference in the rate of death between patients with shock who
were treated with dopamine as the first-line vasopressor agent
and those who were treated with norepinephrine, but the use
of dopamine was associated with a greater number of adverse
98
events.
Dobutamine
Actions. Dobutamine is a β-adrenergic agonist that stimulates
β1-adrenergic, β2-adrenergic, and α1-adrenergic receptors.99
Cardiac contractility is increased by virtue of its β1 and α1 effects,
but because the α1-adrenergic effects are generally counterbalanced by the β2 actions, there is generally little change in blood
pressure. Dobutamine markedly increases cardiac output but
produces only modest changes in LV filling pressures and virtually
no increase in blood pressure.
100
Heart rate generally increases
only when doses greater than 10 µg/kg per minute are used.
Compared with dobutamine, dopamine is a better vasoconstric-
100
tor
and milrinone is a better vasodilator.
101
The elimination
of the drug is rapid after cessation of infusion, making it a
convenient inotropic agent.
Use in AHF. The usual dose of dobutamine is 2.5 to 20 µg/
kg per minute. Short-term infusions are often extremely effective in the treatment of unstable AHF, especially when systolic
pressures are preserved. Long-term infusion should be avoided
because of the development of hemodynamic tolerance.
102
Dobutamine is likely to increase myocardial oxygen consumption and can cause serious arrhythmias. There are no controlled
trials on dobutamine in AHF patients, and some trials show
unfavorable effects with increased untoward cardiovascular
events.
Milrinone
Actions. Milrinone is a type III phosphodiesterase inhibitor
that produces dose-dependent increases in cardiac output and
decreases in LV filling pressures as a result of the interaction of
its positive inotropic, positive lusitropic, and peripheral vasodilator
actions.
103,104
The net result is a hemodynamic profile similar to
that of the combination of nitroprusside and dobutamine. Because
of its vasodilating effects, milrinone is less likely than dobutamine
to increase heart rate and myocardial oxygen consumption.
Despite these theoretical advantages, myocardial ischemia has
been provoked by these agents, and marked hypotensive episodes
have been observed.
Use in AHF. Milrinone requires a loading dose of 25 to 75 µg/
kg over 10 minutes followed by a maintenance infusion of 0.375
to 0.75 µg/kg per minute. The dose should be adjusted in patients
with decreased renal clearance. This agent may be preferred to
dobutamine in patients receiving concomitant β-blocker therapy,
or with an inadequate response to dobutamine, or both. The
CHAPTER 18 Acute Heart Failure and Pulmonary Edema 197
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data regarding the effects of milrinone administration on the
outcome of patients with AHF are insufficient but raise concerns
about safety.
105
The routine administration of milrinone in AHF
is to be discouraged due to adverse effects on heart failure,
arrhythmias, and blood pressure.
106
Digitalis. Digitalis generally has no role in the treatment of
AHF unless the patient has been taking digitalis for chronic
heart failure or if digitalis is given to control a rapid ventricular
response in atrial fibrillation.
Vasopressors. Vasopressors are largely used to treat cardiogenic
shock and are discussed in Chapter 37. Norepinephrine is an
endogenous α1-adrenergic vasoconstrictor and a β1-adrenergic
agonist that is stored in the sympathetic nerve terminal. This
agonist is now more commonly used as the preferred vasopressor over dopamine to support AHF patients with refractory
hypotension.
98
Mechanical Support
When cardiogenic shock persists despite optimization of the
patient’s volume status and treatment with inotropic drugs and
vasopressors, and if it is considered to be potentially reversible,
a reasonable treatment option is mechanical circulatory support.
The only mechanical modality evaluated by a randomized trial
is the use of an intraaortic balloon pump (IABP) to treat cardiogenic shock due to MI. However, the IABP-Shock-II trial
showed that this intervention did not reduce mortality among
patients with an acute MI who were destined for percutaneous
coronary intervention.
LV and right ventricular assist devices are now available at many
hospitals to stabilize patients as either a bridge to recovery or
bridge to decision. These advanced interventions are discussed
in detail in Chapters 47 and 48.
107
Several other percutaneous and surgical
CONTINUED THERAPY FOR CHRONIC
HEART FAILURE
Patients who are admitted with normotensive AHF should be
maintained on oral disease-modifying heart failure therapy.
Outpatient doses of β-blockers can be safely continued in the
absence of cardiogenic shock.
AHF secondary to a reduced LV ejection fraction should be
started on guideline-directed medical therapy before leaving the
hospital.
34,35
Choice of Therapeutic Regimen
In choosing the appropriate medical regimen, it is helpful to
revisit the different AHF syndromes. These are outlined in Table
18.5. Two special scenarios warrant mention.
Hypertensive Acute Heart Failure. LV systolic function is
normal in patients hospitalized with pulmonary edema and
hypertension. Vasodilator therapy should aim for an initial rapid
(several minutes) reduction of systolic blood pressure of
30 mm Hg, followed by a more measured decrease of blood
pressure to the values obtained during stable periods. No attempt
should be made to restore normal values of blood pressure because
this may cause deterioration in renal function. The initial blood
pressure reduction may be achieved by intravenous loop diuretics,
particularly if the patient is clearly fluid overloaded with a long
history of chronic heart failure, combined with intravenous
nitroglycerin or nitroprusside.
Acute Heart Failure With Preserved Ejection Fraction. The
most effective treatment of patients with AHF with preserved
ejection fraction is to address the underlying cause. The treatment
is similar to hypertensive AHF. In this regard, blood pressure
control and the treatment of underlying ischemia are important
34,35
Patients with newly diagnosed
TABLE 18.5 Treatment for Acute Heart Failure Syndromes
Acute Heart
Failure Syndrome
Hypertensive >
Normotensive
Preshock
Cardiogenic shock <
CPAP, Continuous positive airway pressure; IABP, intraaortic balloon pump; IV, intravenous; LVAD, left ventricular assist device.
Modified from Nieminen MS, Bohm M, Cowie MR, et al. Executive summary of the guidelines on the diagnosis and treatment of acute heart
failure: Task Force on Acute Heart Failure of the European Society of Cardiology. Eur Heart J. 2005;26:384–416.
Systolic Blood
Pressure First-Line Treatment Second-Line Treatment Third-Line Treatment
140 mm Hg Oxygen
CPAP if needed
IV loop diuretic
IV nitroglycerin
100–140 mm Hg Oxygen
CPAP if needed
Loop diuretic
Vasodilators
85–100 mm Hg Oxygen
CPAP
Vasodilator and diuretics
85 mm Hg Oxygen
CPAP
Volume-loading
Norepinephrine
Increase doses of nitroglycerin
or diuretic or both
Increase doses of nitroglycerin
or diuretic or both
Add thiazide diuretic
Dobutamine or milrinone Add norepinephrine
Norepinephrine
Vasopressin
Intravenous nitroprusside
Milrinone when there is evidence
of prerenal azotemia
Mechanical support
IABP
Consider LVAD
198 PART IV Noncoronary Diseases: Diagnosis and Management
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goals. A major goal of therapy is to reduce the left atrial and
pulmonary venous pressures. Diuretics, vasodilators, and other
preload-reducing agents are used as discussed previously. The
steep or stiff diastolic pressure volume curve (see Fig. 18.4) can
be responsible for a substantial decrease in filling pressure with
little change in volume; as a result, hypotension often occurs
with the usual doses of diuretics. Cautious administration of
lower than usual doses of diuretics is advisable.
The full reference list for this chapter is available at
ExpertConsult.com.
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