Braunwald Lecture

Series
Chapter 24
Diagnosis and Management of
Acute Heart Failure
Angela McClanahan, DO
Definition and Classification of
Acute Heart Failure
 Rapid or gradual onset of signs and
symptoms of heart failure that result
in urgent unplanned hospitalizations
or office or emergency department
visits.
 3 Crucial Elements
– TIMING- Symptoms must occur rapidly
– SYMPTOMS-Congestion/fluid retention
– SEVERITY- Need for urgent intervention
 Classification Schemes
 Acute de novo heart failure
– No known hx of heart failure or
dysfunction
– Sympathetic activation
– Redistribution of intravascular fluid
– Systemic vasoconstriction
 Acute decompensation of chronic
heart failure
– Known hx of failure
– Less dramatic clinical picture due to
presence of compensatory mechanisms,
remodeling
 Categorization Based on
Clinical Presentation
 Acute Decompensated heart failure
– presents with mild to moderate signs and
symptoms of congestion and does not meet
criteria for other categories.
 Hypertensive AHF
– relatively preserved LV systolic function,
markedly elevated blood pressure, and signs
and symptoms of acute pulmonary edema.
 AHF with pulmonary edema
– severe respiratory distress, orthopnea, signs of
pulmonary edema, and hypoxemia
 Categorization Based on
Clinical Presentation
 Low-output syndrome
– Evidence of tissue hypoperfusion, impending
risk of end organ damage from decreased
cardiac output.
 High output failure
– Warm peripheral extremities, pulmonary
congestion, low BP, high cardiac output, and
increase HR
– Underlying conditions include arrhythmias,
anemia, thyrotoxicosis, and Paget disease.
 Right-sided AHF
– Increased JVP, evidence of right-sided
congestion (hepatomegaly, edema), and
evidence of a low-output syndrome with
 Heart Failure Stats
 In the US, there were 1,093,000 hospital
discharges with a primary diagnosis of HF
in 2003, representing a 174% increase
since 1979.
 Approximately 3 million hospitalizations
each year with HF as one of the discharge
diagnoses
 The magnitude of this problem is even
greater in Europe, where the ESC
estimates that more than 10 million
people within their population of 900
million have heart failure.
 Heart failure consumes 1-2% of total
 Pathophysiology
 Cardiac Dysfunction
– Permanent or transient decreases in
systolic performance
– Decreases in cardiac function can be
caused by
 neurohormonal and inflammatory
stimulation
 myocardial ischemia because of acute
coronary syndromes
 reduced coronary perfusion from
hypotension
 relative ischemia caused by myocardial
distention and increased myocardial oxygen
 Cardiac Dysfunction
 Approximately 1/2 of the patients
who present with AHF have
preserved systolic function ( EF >
40%), these patients usually have
diastolic heart failure
 R sided HF can also be seen in pts
with COPD, atrial fibrillation, valvular
disease
 Vascular Dysfunction
 Pathological vasoconstriction can be
viewed as the central abnormality in most
cases of AHF.
 Redistributes blood centrally
– increasing pulm congestion, edema, and
symptoms of dyspnea and fatigue.
 Increased afterload
– greater ventricular wall stress and increased
myocardial ischemia and cardiac arrhythmias
 Poor organ perfusion
– contributing to renal failure and symptoms of
fatigue, confusion, anorexia, and abdominal
discomfort.
 Usually treated with vasodilators
 Renal Dysfunction
 Kidney is intimately involved in the
pathophysiology of AHF due to its role in
volume homeostasis.
 Neurohormonal stimulation of the kidney
results in activation of the RAS system,
endothelin production which causes
vasoconstriction
 Many of the therapies used to treat heart
failure can have adverse renal effects.
 Cardiorenal syndrome- volume overload of
heart failure is resistant or refractory to
treatment because of progressive renal
dysfunction.
 Pulmonary Edema
 Imbalance in fluid resorption/accumulation in the
pulmonary interstitium and alveolar space by a
sequence of three stages: pulmonary venous
engorgement, interstitial edema, then alveolar
edema.
 Marked dyspnea, tachypnea, anxiety, and
sympathetic stimulation accompany severe
hypoxemia because of profound reductions in gas
exchange
 Increases in plasma concentrations of surfactant
protein-B (SP-B), (small protein normally confined to
the alveolar space with a short half-life) have been
found in pts with HF and the levels remain elevated
for at least 3 days after resolution of the inciting
increase in blood pressure and volume overload,
suggestive of significant alveolar capillary structural
 Myocardial Injury
 Can be an instigating factor for
cardiac decompensation and as an
adverse result of the AHF itself.
 42% of the pts admitted to the ICU
with AHF had at least one elevated
biomarker of myocardial injury
 Elevated biomarkers can be from
ACS or non-ACS related injury
 Precipitants of Acute Heart
Failure
 Poor dietary or medication compliance
 Reduction in cardiac meds by physician
 Taking a med that worsens CHF
– NSAIDS, Ca blockers, BB, anti-TNF
 Poorly controlled HTN
 Anemia
 Excessive ETOH
 MI
 Endocrine abnormalities
 Valvular dysfunction
 Infection
 Clinical Manifestations
 Sx related to Vol Overload
– Dyspnea, PND, cough, wheezing, leg
swelling, abd swelling/discomfort, wt
gain
 Sx related to Hypoperfusion
– Fatigue, AMS, drowsiness, dizziness,
pre-syncope
 Other general sx
– Sleep disturbances, depression,
palpitations
 Physical Exam
(I hope we know this!)
 General- cachexia, obesity, scleral icterus,
conversational dyspnea, pallor, fever
 BP- high vs low, orthostasis, pulsus
paradoxus
 JVP
 Cardiac exam- S3, S4, murmurs
 Lungs- rales, rhonchi, pl effusion
 Abdomen- hepatomegaly, ascites
 Extremities- edema, coolness
 Diagnostic Evaluation
(hope we know this too!)
 Electrolytes  ECG
 Renal Function  ECHO
 LFTs  PA catheter
 CBC – Only used in
extreme shock or
 BNP when diagnosis
 Cardiac Enzymes questionable
 CRP – ESCAPE trial did not
show benefit, and
caused more
adverse events
 Management of Acute Heart
Failure
 STAGE I URGENT/EMERGENT care
– Establish diagnosis (hopefully done by
ER, but not always the case as we
know…)
– Diagnostic tests
– Meds- morphine
– Oxygen of hypoxemic
– BIPAP or intubation if needed
– Tx arrhythmia if present
 Management of Acute Heart
Failure
 STAGE 2: Hospitalization
– Complete the diagnostic and acute
therapeutic processes started in ER
– Monitor the patient
– Optimize the patient's hemodynamic
profile, volume status, and clinical
symptoms
– Initiate or adjust a maintenance
regimen
 Management of Acute Heart
Failure
 STAGE 3: Pre-Discharge
– Optimizing chronic oral therapy
– Minimizing the side effects of treatments
– Ultimately preventing early readmission
and improving symptoms and survival
 Treatment Strategies
 Stevenson and colleagues developed an
approach for the evaluation and treatment
of decompensated advanced chronic
systolic heart failure on a heart
transplant/cardiomyopathy service.
 This approach is predicated on the
assumption that hemodynamic
abnormalities are the immediate cause of
the symptoms and signs of AHF
 Addressing these derangements, patients
will also improve symptomatically
 Treatment Strategies
 Currentgeneral approach
incorporates information from three
main aspects of the patient's clinical
presentation:
– blood pressure- vasodilators vs
inotropes
– volume status –diuretics vs no diuretics
– renal function – diuretics +/- UF based
on vol status in baseline renal
dysfunction or worsening function
 Other treatment strategies
 Invasive hemodynamic monitoring
with PA catheters
 Symptom-guided therapy
 Improvement in biomarkers (BNP)
 Noninvasively measured
hemodynamics
– Changes in bioimpedance which is a
measurement of current across thorax
with BP, HR, etc. (no utility seen yet)
 Doppler Echocardiography
 Pharmacological Tx
 Diuretics
– Continuous infusion should be used for
significant fluid overload
 Vasodilators
– Nitrates- arteriolar vasodilators, reduces
afterload and increases cardiac output
 Tolerance develops in 24 hrs, HA,
Hypotension
– Sodium Nitroprusside
 Works well in elevated afterload from
Mod/Sev MR
 Short-acting, reduces filling pressures,
afterload
 Pharmacological Tx
 Nesiritide (recombinant human BNP)
– Identical to the endogenous peptide and causes
potent vasodilation in the venous and
arterial/coronary vasculature
– Indicated for treatment of patients with acutely
decompensated CHF who have dyspnea at rest or
with minimal activity
– It should not be administered for the indication of
replacing diuretics, enhancing diuresis, protecting
renal function, or improving survival
– High cost, lack of clear clinical benefit beyond
other less expensive and more readily titratable
agents, and potential safety concerns (increased
mortality) have limited its use
 Pharmacological Therapies
 Adrenergic Agonists
– Dobutamine
 Improves cardiac output through direct increases in
inotropy and decreases in afterload, as well as increasing
chronotropy
 Indicated in patients with low output AHF and SBP < 85-
90 mmHg, often in addition to a vasodilator
– Dopamine
 Low dose- selective dilation of renal, splanchnic and
cerebral arteries, potentially increasing renal blood flow
in a selective manner
 Intermediate dose-enhanced norepinephrine release,
stimulating cardiac receptors with an increase in inotropy
and mild stimulation of peripheral vasoconstricting
receptors
 High dose-causes peripheral and pulmonary artery
vasoconstriction, mediated by direct agonist effects on
alpha1 adrenergic receptors
 Pharmacological Tx
 Adrenergic Agonists cont.
– Epinephrine
 Full beta-receptor agonist and potent inotropic agent
w/balanced vasoconstrictor/vasodilator effects
– Norepinephrine
 Potent agonist of beta1 and alpha1 receptors, weak
agonist of beta2 receptors which results in
vasoconstriction
 Calcium Sensitizers
– Levosimendan- increases myocardial contractility
and produces peripheral vasodilation
– REVIVE-II, SURVIVE studies showed some initial
benefits, but also w/many adverse events- afib,
hypotension, ventricular ectopy
 Pharmacological Tx
 Phosphodiesterase Inhibitors (Milrinone)
– Organ-specific improvements in hemodynamics
through increasing myocardial and vascular
smooth muscle cell cAMP
– In OPTIME-CHF, 951 patients admitted with
exacerbation of systolic heart failure not
requiring intravenous inotropic support were
randomized to milrinone or placebo infusion.
– There was no difference in the primary endpoint
of days hospitalized for cardiovascular causes
with 60 days, but significant increases in
sustained hypotension and new atrial
arrhythmias were noted in the milrinone-treated
patients .
 Potential Future Therapies
 Cardiac Myosin Activators
 Isaroxime
 Naturetic Peptides
 Adenosine Antagonists
 Vasopressin Antagonists
 Endothelin Antagonists
Clinical Outcomes/Prognosis in
Acute Heart Failure
 Median length of hospital stay is 4.3-6.4
days, with a median ICU/CCU length of
stay of 2.4 days
 Rehospitalization within 60-90 days occurs
in approximately 30% of patients.
 Patients have an in-hospital mortality of
approximately 4-7%
 Postdischarge mortality at 60-90 days
varies widely depending on the study –
approx 8-10%, and up to 30% at one year.
Clinical Outcomes/Prognosis in
Acute Heart Failure
 Renal dysfunction, lower systolic BP,
greater age, and evidence of myocyte
necrosis are predictors of increased
mortality
 Increased BNP levels have been shown to
predict in-hospital outcomes as well as
readmission and post-discharge mortality
 Minor increases in troponins can predict in-
hospital worsening of heart failure and
post-discharge morbidity and mortality.
 Anemia is another previously
underappreciated predictor of poor
outcomes in patients with AHF, and it is
currently a therapeutic target under
 Thank you!
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Holidays