The document discusses acute decompensated heart failure (ADHF). It defines ADHF and describes the underlying pathophysiology as complex, involving substrates, triggers, and amplifying mechanisms. Common symptoms include dyspnea and signs of congestion. The physical exam focuses on assessing perfusion and congestion. Classification systems distinguish new onset HF from exacerbation of chronic HF, with the latter being most common.

1. “ACUTE DECOMPENSATED
HEART FAILURE”(ADHF).
BY DR R.D KAMAT
SR CARDIOLOGY IGIMS PATNA

2. Nomenclature and Definition
A variety of overlapping terms have been used to characterize
AHF in the literature, including
“acute heart failure syndrome” (AHFS),
“acute decompensated heart failure”(ADHF),
“acute decompensation of chronic heart failure”(ADCHF),
and “hospitalization for heart failure” (HHF).
Although none of these is universally accepted.

4. AHF can be defined as the new onset or
recurrence of signs and symptoms of HF
requiring urgent or emergent therapy and
resulting in unscheduled care or
hospitalization.
“acute” in the nomenclature suggests a sudden
onset of symptoms.

5. Preserved Versus Reduced Ejection Fraction
On the basis of available registry data, 40% to 50% of patients
hospitalized have HFpEF. The in-hospital mortality of patients
with HFpEF appears to be lower compared with that of patients
with HFrEF.
BUT
Postdischarge rehospitalization rates are similarly high for both
groups.
Patients with AHF and HFpEF are more likely to be
rehospitalized for and to die from noncardiovascular causes than
patients with AHF and reduced EF, reflecting their more advanced
age and greater burden of comorbidity.

6. Age, Race, and Gender
There are significant differences in the epidemiology of
AHF based on age, race, and gender. AHF
disproportionally affects elderly people, with a mean age
of 75 years in large registries. AHF affects men and
women almost equally.

7. Comorbidities
Concomitant diseases are common in patients admitted with AHF,
reflecting the elderly population. These comorbidities not only
represent diseases that are risk factors for the development of HF,
but also can complicate diagnosis and management. Hypertension
is the most prevalent of the concurrent conditions, present in
approximately two thirds of AHF patients , whereas coronary
artery disease (CAD) is present in about half and dyslipidemia in
more than one third.

9. PATHOPHYSIOLOGY
AHF is not a single disease but a heterogeneous clinical
syndrome. As such, pathophysiology of AHF is
complex and highly variable, with many overlapping
pathogenic mechanisms .

12. AHF occur as the result of the interaction of
underlying substrate, initiating mechanisms or
triggers, and amplifying mechanisms.
Substrate refers to underlying cardiac structure and
function. The underlying substrate may be one of
normal ventricular function, for example, patients
without a prior history of HF who develop AHF
because of sudden changes in ventricular function
from an acute insult such as MI or acute myocarditis
.

13. Some patients may have no prior history
of HF but abnormal substrate (e.g., stage B
patients with asymptomatic LV
dysfunction) with a first presentation of
HF (de novo heart failure). Also, most
patients with AHF have a substrate of
chronic compensated HF, who then
decompensate and present with AHF.

14. Initiating mechanisms vary according to, and interact with, the
underlying substrate and may be cardiac or extracardiac.
For patients with normal substrate (normal myocardium), a
substantial insult to cardiac performance (e.g., acute myocarditis)
is required to lead to the clinical presentation of AHF.
For patients with abnormal substrate at baseline (asymptomatic
LV dysfunction), smaller perturbations (e.g., poorly controlled
hypertension, AF, or ischemia) may precipitate an AHF episode.
For patients with a substrate of compensated or stable chronic
HF, medical or dietary nonadherence, agents such as nonsteroidal
anti-inflammatory drugs (NSAIDs) or thiazolidinediones, and
infectious processes are all common triggers for decompensation.

15. Regardless of the substrate or initiating factors, a
variety of “amplifying mechanisms” perpetuate
and contribute to the episode of decompensation.
These include,
* Neurohormonal and inflammatory activation,
* Myocardial injury with progressive myocardial
dysfunction,
* Worsening renal function.

16. CONGESTION
Systemic or pulmonary congestion, often caused by a
high ventricular diastolic pressure, dominates the
clinical presentation of most patients hospitalized for
AHF. In this sense, congestion can be seen as a final
common pathway producing clinical symptoms
leading to hospitalization.
A general view of AHF pathophysiology is that
gradual increases in intravascular volume lead to
symptoms of congestion and clinical presentation,
and normalization of volume status with diuretic
therapy results in restoration of homeostasis.

17. One potentially important concept is the distinction
between “clinical congestion” and “hemodynamic
congestion.” Although patients present with signs and
symptoms of systemic congestion such as dyspnea,
rales, elevated jugular venous pressure, and edema, this
state is often preceded by hemodynamic congestion,
defined as high ventricular diastolic pressures without
overt clinical signs.
Clinical congestion may resolve with treatment but
hemodynamic congestion may persist, leading to a high
risk of rehospitalization.

18. Hemodynamic congestion may contribute to the
progression of HF because it may result in increased wall
stress as well as in renin-angiotensin-aldosterone system
(RAAS) and sympathetic nervous system (SNS)
activation.
Elevated diastolic filling pressures may decrease coronary
perfusion pressure, resulting in subendocardial ischemia
that may further exacerbate cardiac dysfunction. Increased
LV filling pressures can also lead to acute changes in
ventricular architecture (more spherical shape),
contributing to worsening mitral regurgitation.

19. Myocardial Function
Changes in systolic function and decreased arterial filling can initiate
a cascade of effects that are adaptive in the short term but
maladaptive when elevated chronically, including stimulation of the
SNS and RAAS.
Activation of these neurohormonal axes leads to vasoconstriction,
sodium and water retention, volume redistribution from other
vascular beds, increases in diastolic filling pressures, and clinical
symptoms.
In patients with underlying ischemic heart disease, initial defects in
systolic function may initiate a vicious cycle of decreasing coronary
perfusion, increased myocardial wall stress, and progressively
worsening cardiac performance. Increased LV filling pressures and
changes in LV geometry can worsen functional mitral regurgitation,
further decreasing cardiac output.

20. Diastolic dysfunction alone may be insufficient to lead to AHF, but
it serves as the substrate on which other precipitating factors (e.g.,
AF, CAD, hypertension) lead to decompensation.
One underappreciated aspect of myocardial function in AHF relates
to the interdependence of the left and right ventricles. Because of
the constraints of the pericardial space, distention of either ventricle
from increased filling pressures can result in direct impingement of
diastolic filling of the other ventricle. This may be particularly
operative in clinical scenarios leading to abrupt failure of the right
ventricle (e.g., pulmonary embolism or right ventricular infarction),
resulting in diminished filling of the left ventricle and arterial
hypotension.

21. The availability of increasingly sensitive assays for
circulating cardiac troponins has substantially advanced
our understanding of the role of myocardial injury in the
pathophysiology of HF. Data from both registries and
clinical trial populations indicate that circulating cardiac
troponins are elevated in a large proportion of patients
with AHF, even in the absence of clinically overt
myocardial ischemia. In a representative analysis of data
from the RELAX-AHF study using a highly sensitive
assay, 90% of patients enrolled had a troponin T level
above the 99th percentile upper reference limit (URL) at
baseline,

22. RENAL MECHANISMS
The kidney plays two fundamental roles relative to the
pathophysiology of HF: it modulates loading conditions
of the heart by controlling intravascular volume and is
responsible for neurohormonal outputs(i.e., the RAAS
system).
Abnormalities of renal function are extremely common
in patients with AHF and may be underestimated by
creatinine alone—64% of patients in the ADHERE
Registry had a glomerular filtration rate (GFR) less than
60 mL/ min/1.73 m2. Baseline measures of renal
function are well-established risk factors for poor
outcomes in AHF .

23. Cardiorenal syndrome describes the clinical situation
of worsening measures of renal function in the setting of
persistent congestion.
Worsening renal function (WRF) in HF patients relates
to elevated central venous pressure, which is reflected
back to the renal veins and leads directly to changes in
GFR.

24. VASCULAR MECHANISMS
Abnormalities of endothelial function related to nitric oxide (NO)–
dependent regulation of vascular tone are well described in HF.
Peripheral vasoconstriction in AHF redistributes blood centrally,
increasing pulmonary venous congestion and edema. Elevated
central venous pressure reduces renal function, resulting in greater
fluid retention that further elevates venous pressures.
Peripheral arterial vasoconstriction increases afterload, LV filling
pressures, and postcapillary pulmonary venous pressures, resulting
in worsening of pulmonary edema and dyspnea. This increased
afterload causes greater ventricular wall stress and increased
myocardial ischemia and cardiac arrhythmia.

25. NEUROHORMONAL AND INFLAMMATORY
MECHANISMS
Increased plasma concentrations of
norepinephrine, plasma renin , aldosterone, and
endothelin (ET)-1 have all been reported in
patients with AHF—all these axes are associated
with vasoconstriction and volume retention,
which could contribute to myocardial ischemia
and congestion, thus exacerbating cardiac
decompensation.

26. Proinflammatory cytokines such as tumor necrosis factor-
alpha (TNF-α) and interleukin (IL)-6 are elevated in
patients with AHF and have direct negative inotropic
effects on the myocardium as well as increasing capillary
permeability and inducing endothelial dysfunction. In
addition to direct effects, this activation stimulates the
release of other factors, such as the potent procoagulant
tissue factor and ET-1, which can lead to further
myocardial suppression, disruption of the pulmonary
alveolar-capillary barrier, and increased platelet
aggregation and coagulation (potentially worsening
ischemia).

27. EVALUATION OF THE PATIENT WITH ACUTE HEART
FAILURE
The initial evaluation of the patient with acute HF focuses on the
following critical aspects:
(1) Establishing a definitive diagnosis of AHF as rapidly and
efficiently as possible;
(2) Emergent treatment for potentially life-threatening conditions
(e.g., shock, respiratory failure);
(3) Identifying and addressing any relevant clinical triggers or other
conditions requiring specific treatment (e.g., ACS, acute pulmonary
embolism);
(4) Risk stratification in order to triage patient to appropriate
level of care (e.g., intensive care unit, telemetry unit, observation unit);
and
(5) Defining the clinical profile of the patient (based on blood
pressure, volume status, and renal function) in order to rapidly
implement the most appropriate therapy. Fig. 24.4

29. CLASSIFICATION
No single classification system has universal acceptance.
One potentially useful distinction is based on the
presence or absence of a prior history of HF. New-onset
or de novo HF makes up about 20% of hospitalizations
for AHF. These patients may have no prior history of
cardiovascular (CV) disease or risk factors (e.g., acute
myocarditis), but more frequently, they have a
background of risk factors for HF (stage A heart failure
according to the ACC/AHA guidelines) or preexisting
structural heart disease (stage B heart failure according to
the ACC/AHA guidelines )

30. The vast majority of AHF patients, however, have
a history of preexisting chronic HF. These patients
usually have a less dramatic clinical presentation,
since the chronic nature of the disorder has
allowed for recruitment of compensatory
mechanisms and remodeling (e.g., increased
pulmonary lymphatic capacity). Additionally,
these patients are typically already being treated
with neurohormonal antagonists and loop
diuretics, such that neurohormonal activation may
be less profound but diuretic resistance more
common.

31. A simplified classification scheme defines three general
groups of AHF patients (Table 24.2):

32. DECOMPENSATED HEART FAILURE.
This group is composed of patients with worsening signs
and symptoms of congestion on a background of chronic
HF. The time course of worsening may be acute,
subacute, or indolent, with gradually worsening
symptoms over days to weeks. They may have either
preserved or reduced EF, overall, this group represents
the largest portion of patients hospitalized for AHF.

33. ACUTE HYPERTENSIVE HEART FAILURE.
Hypertension is recognized as a common feature of the AHF
presentation, with 50% of patients presenting with systolic
blood pressure (SBP) greater than 140 mm Hg and 25% with
greater than 160 mm Hg.
Hypertension may be triggered by a high sympathetic tone
related to dyspnea and accompanying anxiety (reactive
hypertension), or acute hypertension with accompanying
changes in afterload may be a trigger for decompensation.
Both these mechanisms may be operative in a given patient,
and cause-and-effect relationships may be difficult to
discern.

34. acute hypertensive HF are more likely to have
preserved systolic function, more likely to be
women, and more likely to have sudden onset of
symptoms. Frank pulmonary edema with
evident rales and florid congestion on chest x-
ray film is much more common in this group of
patients than in those with more gradual onset of
symptoms, likely related to difference in LV
compliance, acuity of pressure changes, and
pulmonary lymphatic capacity. This group tends
to respond well to therapy and have lower in-
hospital mortality.

35. CARDIOGENIC SHOCK.
This group presents with signs and symptoms of
organ hypoperfusion despite adequate preload.
SBP is often (although not always) decreased,
and evidence of frank or impending end-organ
dysfunction (renal, hepatic, CNS) is common.
This type of AHF is relatively uncommon (4% of
AHFS presentations in EHFS II) in broad
community registries but more common in
tertiary care settings.

36. While this classification
system does not fully capture
some less common clinical
scenarios (e.g., isolated right
HF or high output HF), it
usefully encompasses the
vast majority of AHF patients
likely to be seen in routine
clinical practice.

37. SYMPTOMS
Dyspnea is the most common symptom and is present in more
than 90% of patients. Dyspnea is typically present at rest or with
minimal exertion by the time the patient presents with AHF.
Patients may also present with symptoms related to systemic
venous congestion, including
 peripheral edema,
 weight gain,
 early satiety, and
 increasing abdominal girth.
Importantly, atypical symptoms can predominate, especially in
elderly patients, where fatigue, depression, altered mental status,
and sleep disruptions may be the primary complaints.

40. PHYSICAL EXAMINATION
“Despite advances in diagnostics
technology, biomarkers, and
imaging, heart failure remains a
clinical diagnosis and the physical
examination continues to play a
fundamental role”

41. A useful framework in the bedside evaluation of patients with
AHF is developed by Stevenson and colleagues, which focuses
on the adequacy of perfusion (“cold” versus “warm”) and
congestion at rest (“wet” versus “dry”; see Fig. 21.3)

42. The jugular venous pressure (JVP) is a barometer of
systemic venous hypertension and is the single most
useful physical examination finding in the assessment
of patients with AHF. The JVP reflects the right atrial
pressure, which typically (although not always) is an
indirect measure of LV filling pressures. JVP may not
reflect LV filling pressures in isolated right ventricular
(RV) failure (e.g., from pulmonary hypertension or RV
infarct), and significant tricuspid regurgitation can
complicate the assessment of the JVP since the large
“CV wave” of tricuspid regurgitation can lead to its
overestimation.

43. Rales or inspiratory crackles are the
most common physical examination
finding and have been noted in 66% to
87% of patients admitted for AHF.
However, rales are often not heard in
patients with a background of chronic
HF and pulmonary venous
hypertension, because of increased
lymphatic drainage, reinforcing the
important clinical pearl that the absence
of rales does not necessarily imply
normal LV filling pressures.

44. Peripheral edema is present in up to 65% of patients
admitted with AHF and is less common in patients
presenting with predominantly low-output HF or
cardiogenic shock. As with rales, the presence of
edema has a reasonable positive predictive value
(PPV) for AHF but a low sensitivity, so its absence
does not exclude that diagnosis. Edema caused by
AHF is usually dependent, symmetric, and pitting. It
is estimated that a minimum of 4 liters of
extracellular fluid is accumulated to produce
clinically detectable edema.

45. OTHER DIAGNOSTIC TESTING
Biomarkers
The natriuretic peptides are a family of important
counterregulatory hormones in HF with vasodilatory and
other effects. Both brain (B-type) natriuretic peptide
(BNP) and N-terminal pro-BNP (NT-proBNP) have been
shown to play an important role in the differential
diagnosis of patients presenting in the emergency
department (ED) with dyspnea and are now strongly
recommended by clinical practice guidelines. For (NP)
testing in the setting of AHF, a critical point is that
negative predictive value (NPV; i.e., the ability to rule
out HF a as a cause of dyspnea) is generally greater than
the PPV (i.e, the ability to definitively identify a
diagnosis of HF as the cause of dyspnea).

46. As with all biomarker testing, false positives
(e.g., due to MI or pulmonary embolism) and
false negatives (primarily due to obesity, which
results in lower NP levels for a given degree of
HF) may occur. Although NP levels tend to be
lower in patients with HFpEF than those with
reduced systolic function,

47. OTHER LABORATORY TESTING
Estimated glomerular filtration rate (eGFR) should be
calculated because serum creatinine may underestimate
the degree of renal dysfunction, especially in elderly
patients. Blood urea nitrogen (BUN) is more directly
related to the severity of AHF than creatinine . In addition
to reflecting intrinsic renal function, serum BUN is
approximately proportional to neurohormonal activation
in AHF.

48. A wide variety of other biomarkers, including
ST2, galectin 3, and GDF15, have been evaluated
in patients with AHF, but none is currently
recommended for routine use in patients with
AHF. In patients in whom the diagnosis of AHF is
uncertain, testing to establish alternative causes
(e.g., D-dimer to evaluate for pulmonary
embolism or procalcitonin to evaluate for
evidence of infection) may be very useful.

49. Chest radiography there was evidence of congestion
in more than 80% of these patients. In patients with a
background of chronic HF and/or slow onset of symptoms,
evidence of congestion on chest x-ray film may be subtle,
and frank pulmonary edema is often absent despite
substantially elevated filling pressures.

50. ECG changes suggestive of ischemia is important, since
troponin elevation is common in AHF regardless of
etiology, and thus many not be a reliable marker of ACS.
Arrhythmias are also a common trigger for AHF, and AF
is present in 20% to 30%.

51. Echocardiography can assess global systolic and
diastolic function, regional wall motion
abnormalities, valvular function, hemodynamics
including estimates of filling pressures and cardiac
output, and pericardial disease. The tissue Doppler
ratio of peak early diastolic transmitral blood flow
velocity (E) to the peak early-diastolic mitral
annular tissue velocity (Ea) (E:Ea ratio) has been
shown to be additive to BNP measures in
diagnosing AHF patients presenting with dyspnea.
An E:Ea ratio greater than 15 predicts a pulmonary
capillary wedge pressure (PCWP) greater than 15
mm Hg.

52. MANAGEMENT OF THE PATIENT WITH
ACUTE HEART FAILURE
( Phases of Management)

54. MANAGEMENT OF THE PATIENT WITH ACUTE HEART FAILURE
( Phases of Management)
Phase I: Urgent/Emergent Care
Dyspnea is the most common complaint in AHF patients, the
initial management of uncomplicated AHF usually targets this
symptom. In patients with severe hypoxemia (oxygen saturation
[SaO2] <90%), O2 administration is recommended.
Although SaO2 on presentation is inversely related to short-term
mortality, inhaled oxygen (FiO2 ≥0.4) may cause adverse
hemodynamic effects (e.g., hyperoxia-induced vasoconstriction) in
patients with systolic dysfunction and therefore is not routinely
recommended for patients without hypoxemia. In patients with
COPD, high FiO2 concentrations should not be used, to avoid the
risk of respiratory depression and worsening hypercarbia.

55. Early clinical studies and meta-analyses suggest that in
patients with cardiogenic pulmonary edema, treatment
with continuous positive airway pressure (CPAP) or
noninvasive intermittent positive-pressure ventilation
(NIPPV) improves symptoms and physiologic variables
and reduces the need for invasive ventilation and
mortality.
Morphine may be useful in patients with severe anxiety or
distress but should be used cautiously or avoided,
especially in the presence of hypotension, bradycardia,
advanced atrioventricular (AV) block, or carbon dioxide
(CO2) retention.

56. Intravenous (IV) loop diuretics are the most
frequently administered therapy for AHF; Although
some patients with volume redistribution rather than
hypervolemia may derive benefit from vasodilators
alone, symptomatic patients with evidence of
congestion consistent with pulmonary or systemic
venous hypertension or edema should generally
receive urgent diuretic therapy for relief of symptoms
related to congestion. Initial therapy is typically a
bolus injection with a dose between 1 and 2.5 times
the patient’s oral loop diuretic dose for those
receiving chronic diuretic therapy .

57. In the absence of hypotension, vasodilators play
an important role in the initial therapy of patients
with pulmonary edema and poor oxygenation. A
treatment strategy of early initiation of IV nitrate
therapy in patients with severe cardiogenic
pulmonary edema has been shown to reduce the
need for mechanical ventilation and the frequency
of MI.

58. Hospitalization should be considered in
patients with worsened congestion, even in
the absence of dyspnea and often reflected
by significant weight gain (≥5 kg), other
signs or symptoms of pulmonary or
systemic congestion, newly diagnosed HF,
complications of HF therapy (e.g.,
electrolyte disturbances, frequent ICD
firings), or other comorbidities.

59. SPECIFIC CLINICAL PRESENTATIONS
Atrial Fibrillation with Rapid Ventricular
Response.
AF with rapid ventricular response is the most
common tachyarrhythmia requiring treatment in
patients with AHF. It may be difficult to determine
with certainty whether the AF was a trigger for
AHF or whether progressive HF decompensation
led to AF.

60. Although the ventricular response frequently
decreases in parallel with the relief of dyspnea, and
consequent decreased sympathetic drive, additional
therapy may be required. Immediate cardioversion
is generally not indicated, except in the unstable
patient, because while the patient remains
significantly decompensated, cardioversion is
associated with a high rate of recurrent AF.

61. In patients with systolic dysfunction, IV
digoxin (in the absence of an accessory
pathway), cautious use of beta-adrenergic
blocker therapy or amiodarone may be
used. Diltiazem and other agents that
suppress ventricular function should be
avoided in patients with significant systolic
dysfunction but may be effective in patients
with preserved function.

62. RIGHT VENTRICULAR HEART FAILURE.
The most common cause of RV HF in AHF is left-sided
failure. Isolated RV HF is relatively rare and is generally
caused by acute RV infarction, acute pulmonary
embolism, or severe pulmonary hypertension. Isolated
RV HF caused by an acute RV infarction is best treated
with early reperfusion, whereas hemodynamically
significant pulmonary embolism may be treated with
thrombolytics. Hemodynamic stabilization by
optimizing central venous pressure (CVP) with carefully
monitored fluid loading (target CVP, approximately 10
to 12 mm Hg), and increasing RV systolic function with
IV inotropic support under invasive hemodynamic
guidance.

63. Selective pulmonary artery vasodilation by
inhaled (NO, prostacyclin analogues) or IV
(prostacyclin analogues, sildenafil) agents may
improve RV function through decreased afterload.
If the patient is mechanically ventilated,
normoxia and hypocarbia should be goals using
moderate tidal volumes (approximately 8 mL/kg)
and as low a PEEP as possible (<12 cm H2O) to
maintain moderate plateau pressures

64. ACUTE CORONARY SYNDROMES
ACS may be the underlying trigger in patients
presenting with AHF, but as previously noted, the
diagnosis is confounded by the high prevalence of
elevated troponins in AHF itself. These patients may
present with chest discomfort, electrocardiographic
changes consistent with ischemia, and elevated serum
troponin. Aggressive therapy for ACS should be rapidly
instituted. In the absence of cardiogenic shock,
inodilators should be avoided in patients with ACS and
with significant asymptomatic CAD because
experimental data have shown that inodilators can cause
necrosis of ischemic and hibernating myocardium.

65. CARDIOGENIC SHOCK
Cardiogenic shock is characterized by marked hypotension (SBP
<80 mm Hg) lasting more than 30 minutes, associated with severe
reduction of cardiac index (usually <1.8 L/min/m2) despite
adequate LV filling pressure (PCWP >18 mm Hg), resulting in
organ hypoperfusion. Cardiogenic shock is an unusual
presentation of AHF, occurring in less than 4% of the patients in
EHFS II, most of whom had MI. Mechanical complications of
AMI such a mitral regurgitation, cardiac rupture with ventricular
septal defect or tamponade, and isolated RV infarct may also be
causes in this setting. IV inotropes or even vasoconstrictors may
be required in these patients, with mechanical circulatory support,
such as intra-aortic balloon pump
(IABP) or left ventricular assist device (LVAD), for critical
refractory cases, as a bridge to heart transplant or other mechanical
intervention.

66. Phase II: Hospital Care
The goals for the management of a patient with AHF during
the hospitalization phase are :
To complete the diagnostic and acute therapeutic processes
that were initiated at the initial presentation;
To optimize the patient’s hemodynamic profile, volume
status, and clinical symptoms; and
To initiate or optimize chronic HF therapy.
Ideally, these goals would be met in a manner to minimize
intensive care and total hospital length of stay (LOS).
Monitoring of daily weights, fluid intake and output, and
vital signs, including orthostatic blood pressure, as well as a
daily assessment of symptoms and signs are crucial.

67. Laboratory monitoring should include daily analysis of
electrolytes and renal function. Diagnostic evaluations
should include an echocardiogram, if not recently
performed. Evaluation for myocardial ischemia may be
needed if there is suspicion of ischemia as a trigger of
decompensation.
Dietary sodium restriction (2 g daily) and fluid restriction
(2 L daily) may be useful to help treat congestion.
The increased risk of venous thromboembolism in HF is
exacerbated by the decreased mobility of hospitalized
patients with AHF, and venous thromboembolism
prophylaxis is indicated in all patients unless there is a
clear contraindication.

68. Most outpatient medications should generally be
continued during inpatient therapy at existing doses,
and it should be recognized that AHF hospitalization
represents an opportunity to review and optimize
chronic HF therapy. Although changes in renal function
may necessitate dose adjustment or temporary
discontinuation of RAAS inhibitors, including
angiotensin-converting enzyme (ACE-I) inhibitors,
angiotensin receptor blockers (ARBs), angiotensin
receptor neprilysin inhibitors (ARNIs), and/or
mineralocorticoid receptor antagonists, in general this
should be avoided where possible.

69. Patients admitted receiving beta blockers have a
lower occurrence of ventricular arrhythmias, a
shorter LOS, and reduced 6-month mortality than
those not receiving them. Patients who had beta
blockers withdrawn had significantly lower
outpatient use of beta blockers and higher in-
hospital mortality, short-term mortality, and
combined short-term rehospitalization and
mortality, even after adjustments for potential
confounders.Therefore, patients should continue
beta-blocker therapy during the admission for
AHF, unless significant hypotension or
cardiogenic shock are present.

70. The Cardiorenal Syndrome in Hospitalized
Patients
There is no consensus definition to date, in the
context of AHF, cardiorenal syndrome is often
described as the clinical state where the volume
overload of HF is resistant or refractory to
treatment due to progressive renal insufficiency.
A commonly used practical definition is an
increase in serum creatinine of more than 0.3
mg/dL (or 25% decreases in GFR) despite
evidence of persistent clinical or hemodynamic
congestion.

71. Using this definition, the cardiorenal
syndrome occurs in approximately 25% to
35% of the patients admitted with AHF,
associated with longer LOS and higher
postdischarge mortality. This definition of the
cardiorenal syndrome emphasizes the
importance of persistent congestion, because
multiple studies have suggested that changes
in renal function during successful
decongestion therapy are usually transient and
may not be associated with adverse outcomes.

72. Since absolute serum creatinine concentrations
can be misleading, eGFR should be calculated in
patients with AHF.
As noted, arterial underfilling from overdiuresis
or low cardiac output does not appear to be the
most frequent primary cause of WRF, although
hypotension can be an important factor.

73. Progressive deterioration of renal function (BUN
>80 mg/dL and creatinine >3.0 mg/dL) or
hyperkalemia may necessitate discontinuation of
RAAS inhibitors, although use of other
vasodilators should be considered, either IV
(nitroglycerin or nitroprusside) or oral (isosorbide
dinitrate and hydralazine).
Increasing doses of diuretics are typically required,
although diuretic resistance may be profound.
Overall, the appropriate management of patients
with cardiorenal syndrome remains a major unmet
clinical challenge in AHF.

74. Phase III: Predischarge Planning
The predischarge phase focuses on the goals of
evaluating readiness for discharge, optimizing
chronic oral therapy, minimizing the side effects
of treatments, and ultimately preventing early
readmission and improving symptoms and
survival.

75. Although careful optimization of medical
regimen before discharge may reduce the
risk of subsequent readmissions and improve
long-term outcomes. Despite that most
patients present with congestion, many are
discharged without significant weight loss,
and available data demonstrate that
persistent clinical congestion at discharge is
associated with a high risk for
rehospitalization.

76. Similarly, elevations of discharge BNP level
have been associated with risk for
rehospitalization after discharge.
Evaluation of functional capacity with simple
maneuvers such as climbing one flight of stairs
or walking down the corridor may be a simple
and valuable tool to use before discharge

77. Pharmacologic therapies known to improve long-term
outcomes in chronic HF, such as beta blockers, ACE
inhibitors or ARBs, and mineralocorticoid receptor
antagonists, should be initiated as soon as reasonable
during the hospitalization and before discharge in
hemodynamically-stable, appropriate patients.
The recent approval of two new therapies for chronic HF
with reduced EF (sacubitril/ valsartan and ivabradine) has
created uncertainty about how to deal with these agents
in the setting of AHF.

78. In patients already treated chronically with
these agents before this episode of AHF, they
should generally be continued during
hospitalization (similar to beta blockers and
other RAAS inhibitors). To date, there are no
data to support the new initiation of either of
these agents in hospitalized AHF patients,
although several studies are ongoing.
Predischarge initiation of a beta blocker
increases the proportion of patients receiving
appropriate therapy at 60 days and may also
reduce 60- to 90-day mortality.

79. Phase IV: Postdischarge Management
Early recurrence of signs and symptoms of HF
suggestive of worsening volume overload and/or
neurohormonal activation are likely to contribute to
the high rates of readmission that are observed in
AHF. Prompt interventions may therefore allow
intervention to prevent the progression of volume
overload and new admissions.
Follow-up appointment is optimally scheduled within
7 to 10 days after discharge, but closer follow-up (<1
week) should be considered or patients with high-risk
features.

80. TREATMENT STRATEGIES
Targeting Congestion
The current general approach focuses on the
successful treatment of clinical and hemodynamic
congestion, while limiting untoward effects on
myocardial or end-organ function, identifying
addressable triggers, and optimizing proven long-
term therapies. This approach incorporates
information from three main aspects of the patient’s
clinical presentation: blood pressure, volume status,
and renal function.

81. Blood Pressure
Most patients present with elevated BP and
consequently will benefit from and safely tolerate
vasodilator therapy. Vasodilators may decrease preload
by reversing venous vasoconstriction and the related
central volume redistribution from the peripheral and
splanchnic venous systems, and reduce afterload by
decreasing arterial vasoconstriction with a resultant
improvement in cardiac and renal function.
Vasodilators are the primary therapy for AHF with
pulmonary edema, and for nonhypotensive patients
with low cardiac output (poor peripheral or central
perfusion with SBP >85 to 100 mm Hg).

82. A systematic review of clinical studies supported the
ability of vasodilators to improve short-term
symptoms and appear safe to administer, but revealed
no data suggesting an impact on mortality. However,
in an international registry of 4953 patients admitted
for AHF (ALARM-HF; 75% admitted to ICU/CCU
care settings), analysis of a propensity-based matched
cohort of 1007 matched pairs demonstrated improved
in-hospital survival in patients treated with
vasodilators and diuretics compared to patients
treated only with diuretics of 7.8% compared to
11.0% in-hospital mortality, respectively (P = 0.016).
Interestingly, this difference in survival was
particularly evident in patients with SBP less than
120 mm Hg (Fig. 24.8).

84. Hypotension (SBP <85 to 90 mm Hg) or signs of
peripheral hypoperfusionare poor prognostic signs in
patients with AHF. Treating the potentially reversible,
underlying etiologies, such as ACS, pulmonary
embolus, and (rarely) hypovolemia, is essential.
Asymptomatic hypotension, as an isolated finding in
the absence of congestion and poor peripheral or
central perfusion, does not require emergent treatment.

85. Inotropic therapy may be indicated for persistent
symptomatic hypotension or evidence of
hypoperfusion in the setting of advanced systolic
dysfunction. An analysis of 954 propensity-
matched pairs of patients from the ALARM-HF
Registry suggested that IV catecholamine use was
associated with 1.5-fold increase in in-hospital
mortality for dopamine or dobutamine use and a
more than 2.5-fold increase for norepinephrine
(NE) or epinephrine use.

86. In most patients, invasive pulmonary artery
catheter monitoring is not necessary, since the
measures of urine output, BP, and end-organ
function may be clinically evaluated. The use of
vasoconstrictors, such as high-dose dopamine,
phenylephrine, epinephrine, or NE, should
generally be avoided unless absolutely necessary
for refractory symptomatic hypotension or
hypoperfusion.

87. Patients with clinically evident congestion typically
have 4 to 5 liters of excess volume and amounts
greater than 10 liters are not uncommon. The choice
of diuretic regimen is influenced by the amount and
rapidity of the desired fluid removal and the renal
function . However, IV vasodilator therapy may
provide more rapid relief in highly symptomatic
patients with evidence of pulmonary congestion. In
fact, many patients with hypertensive AHF may
require minimal diuretics.

88. Thus, careful attention to volume status is
critical because patients’ symptoms of
congestion may resolve despite persistent
hemodynamic congestion (i.e., elevated filling
pressures). Hospital discharge before
hemodynamic congestion is fully treated
appears to be a common cause of
rehospitalization.

89. Renal Function
Renal function is the third main aspect of a
contemporary approach to treatment of the
patient with AHF . Treatment of AHF in the
presence of normal renal function is generally
uncomplicated. Diuretics may be given in
standard doses, although renal function,
electrolytes, and volume status must be carefully
monitored.

90. However, approximately two thirds of patients
present with at least moderate renal insufficiency.
This may be from preexisting kidney disease or
may be a manifestation of worsening HF. Abnormal
renal function is typically associated with some
degree of diuretic resistance, and higher doses of
diuretics or other strategies may be needed .

91. Invasive Hemodynamic Strategy
Invasive hemodynamic management with
pulmonary artery catheterization (PAC) may be a
useful strategy in the management of some
patients with AHF. PAC is an invasive procedure
that provides detailed hemodynamic data,
including direct assessment of filling pressures
and cardiac output, and calculation of pulmonary
and systemic vascular resistance. Potential risks
of PAC include bleeding, infection, arrhythmias,
and rare catastrophic events, such as pulmonary
artery (PA) rupture or infarction.

92. The use of PAC in the routine management of AHF
has been a subject of controversy. Invasive
hemodynamic assessment with PAC may still play
an important role in select patients, especially
those with shock or other severe hemodynamic
compromise, with oliguria or anuria, or with
unclear hemodynamics and poor response to
therapy.