Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema

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Chapter 53Congestive Heart Failure and Acute
Pulmonary Edema

• September 22, 2005

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Epidemiology

• Leading cause of hospitalization among those 65
• Up to 60 rehospitalized within 6 months due to
  recurrent decompensation
• Prevelance doubles each decade
• Cost of HF roughly double that of any cancer
  diagnosis

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Prognosis

• Once symptomatic, 2 year mortality 35, 6 year
  mortality 80 men, 65 women
• 50 survive 1 year after pulmonary edema
• If cardiogenic shock, up to 85 die after 1 week

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Classification System

• NYHA classification system (Table 53-1) is used a
  prognostic scale
• AMA classification system (Table 53-1) uses risk
  factors to determine interventions
• AMA system recognizes early intervention as
  greatest potential for reducing morbidity and
  mortality

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Pathophysiology

• Acute pulmonary edema is a downward spiral of
  decreasing CO and rising SVR in the face of
  underlying cardiac dysfunction
• Small elevations of BP can result in decreased CO
• Decreasing CO triggers increased SVR, which
  further worsens CO
• Threats to CO trigger neurohormonally mediated
  cascade that activates renin-angiotensin-aldostero
  ne system and the SNS

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Pathophysiology

• Levels of NE, vasopressin, TNF and endothelin
  (potent vasoconstrictor) are increased, correlate
  with mortality
• Natriuretic peptides (NPs) are the endogenous
  counterregulatory arm of the neurohormonal
  activation
• Three types are recognized atrial NP, B-type NP
  (BNP) from ventricles and CNP, localized in
  endothelium
• NPs result in vasodilation, natriuresis,
  decreased levels of endothelin and inhibition of
  RAAS and SNS
• BNP is the only NP for which an assay exists

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Classification

• Systolic or diastolic dysfunction, classified by
  EF
• Systolic HF defined by EFischemic heart disease
• Diastolic HF, contractile function preserved,
  impaired relaxation, chronic HTN and LVH are
  often responsible

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Systolic vs Diastolic HF

• In systolic HF, impaired contractility leads to
  increased cardiac volumes and pressure, and
  afterload sensitivity
• With stress, failure to improve cardiac
  contractility, despite increasing venous return
  results in increased cardiac pressures, pulmonary
  congestion and edema
• In diastolic HF, decreased LV compliance and
  higher atrial pressures results in preload
  sensitivity
• Decreased LV compliance necessitates higher
  atrial pressures to ensure adequate diastolic LV
  filling

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Left vs Right-side HF

• Left-sided is associated with dyspnea, fatigue,
  weakness, cough, PND, orthopnea and JVD
• Right-sided is associated with peripheral edema,
  JVD, RUQ pain, hepatojugular reflex
• Most common cause of right-sided HF is left-sided
  HF
• Volume overload is treated uniformly, unless
  there is a suspicion of valvular disease or right
  ventricular infarct

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Diagnosis History and PE

• ED diagnostic error rate is reported as 12,
  equal divided as under- and over-diagnosis
• Dyspnea 50 sensitivity and specificity
• Orthopnea 88 specificity, but no better
  sensitivity
• Rales predictive accuracy of 70
• Edema even worse as a HF indicator
• JVD specificity of 94, sensitivity 39
• Best physical finding is S3 is suggestive of
  elevated PCWP, specificity 99 but sensitivity 20

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Diagnosis Chest Radiography

• Blunt tool, eliminates other diagnosis
• Dilated upper lobe vessels, cardiomegaly,
  interstitial edema, enlarged pulmonary artery,
  pleural effusions, alveolar edema, prominent SVC,
  Kerley B lines in left HF
• Because acute abnormalities lag the clinical
  appearance by up to 6 hours, therapy is not
  withheld pending CXR
• Chronic HF congestive signs have unreliable
  sensitivity, specificity and predictive value
  with high PCWP

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Diagnosis BNP

• Correlate with elevated PCWP
• By NYHA class, BNP levels vary directly with
  severity
• Dyspnea due to COPD, BNP levels 1,000
• BNP 89-96
• BNP 480, 40 death rate or readmission within 6
  mo
• Increased in elderly, women, cirrhosis, renal
  failure, hormone replacement
• Levels below 100 effectively excludes HF with
  good reliability and marked elevation is strong
  evidence of HF

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Treatment

• 100 O2 by face mask to obtain saturation 95
• Maintain airway control and adequate ventilation
• Intubation for unconscious, unstable or tiring
  patients
• Consider CPAP or BiPAP

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Treatment

• Standard care includes cardiac monitoring, pulse
  ox, EKG, IV, frequent vitals
• CBC, electrolytes, cardiac enzymes, CXR, BNP
• Liver enzymes if HSM
• In the presence of widened AG, elevated lactate
  may confirm cardiogenic shock
• Levels, ie digoxin, ETOH, tox
• Foley placed to monitor output

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Treatment

• NTG SL, if no response or ECG shows ischemia NTG
  drip 10 to 30 ug/min and titrate
• Diuretics lasix 40-80 mg IV or bumentanide 0.5 -
  1 mg IV
• Ethacynic acid is used if there is a serious
  sulfa allergy
• If urine output is inadequate in 20 30 min,
  diuretic dose is increased and repeated

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Contraindications to Vasodilation

• Preload dependent states right ventricular
  infart, AS, or volume depletion
• HCM
• If coexisting shock, phenylephrine preferred
  pressor

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Treatment

• Resistant HTN, not responding to NTG,
  nitroprusside
• Nesiritide as alternative to NTG for acute
  decompensated HF without cardiogenic shock
• If hypotensive or need for iontropic support,
  dopamine 5-10 ug/kg/min and titrate for SBP
  90-100
• Consider thrombolytic agents if caused by MI
• Treat coexisiting arrhythmia or electrolyte
  disturbance
• Morphine use PRN, use controversial
• Digoxin acts too slowly for acute setting

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Treatment

• Anuric (dialysis) patients, treatment of choice
  is dialysis
• Long term CHF dietary salt restriction, preload
  reduction via diuretics, afterload reduction via
  Bblockers, ACE inhibitors and digoxin
• Most require inpatient management

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Disposition for Acute Pulmonary Edema

• Patients with acute pulmonary edema require ICU
• If clinical scenario suggests ACS, ICU admission
• If HTN controlled, dyspnea resolved, non-ICU
  monitored
• Receiving titrating NTG, ICU
• Receiving nesiritide, tele

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Disposition for Decompensated HF

• Require hospital admissions, IV diuresis,
  vasodialator therapy, oral medication dose
  titration to targeted levels and correction of
  reversible causes
• Patients with new onset, poor social support,
  hypoxemia, hypercarbia, concurrent infection,
  respiratory distress, syncope or symptomatic
  hypotension should be admitted
• Admission requirements may correlate with BNP,
  further studies needed

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Review of Clinical Trials of Nesirtide

• In acute benefit, 6 hour infusion of nesiritide
  decreased PCWP and improved clinical status
  (Colucci et al, 2000)
• Compared to treatment with single vasoactive
  agent, nesiritide produced a similar significant
  improvement in clinical reduction in dyspnea and
  fatigue, hypotension most common SE, increased
  with concurrent vasodilators such as ACEs
  (Colucci et al, 2000)
• In randomized controlled trial assigned to
  nesiritide, IV nitro or placebo, nesirtide
  decreased PCWP more than IV nitro at 3 and 24
  hours, clinical status vs nitro no difference
  (JAMA 2002)
• Based upon above trials, nesiritide approved for
  acute management of dyspnea, elevated PCWP with
  cardiogenic pulmonary edema

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Review of Clinical Trials of Nesiritide

• Subsequent independent analysis submitted to FDA
  has raised questions about nesiritide on renal
  function and survival. The manufacturer has
  expanded adverse effects, including a possible
  deleterious effect of mortality (FDC Report,
  2005)
• Retrospective review, comparing nesiritide with
  vasodilator or inotropes, suggest greater degree
  of progressive renal insufficiency among
  nesiritide patients (Sackner-Bernstein et al
  2005)
• Retrospective analysis of the pooled results has
  raised concern about nesiritide therapy on 30-day
  mortality, when compared to noninotropic
  vasodilators (Sackner-Bernstein et al, 2005)

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Review of Clinical Trials of Nesiritide

• Pooled analysis from randomized control trials,
  increased 30-day mortality with nesiritide.
  These findings are subject to ongoing debate
• In contrast, nesiritide appears to be less likely
  than dobutamine to provoke ventricular
  arrhythmias among patient with decompensated HF.
  In addition, it has been associated with a trend
  toward a lower readmission rate for any cause or
  for HF (Silver et al, 2002)

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Questions

• True or False
• 1. Levels of BNP value 89-96
• Systolic HF defined as EF under 40 most
  typically from ischemic heart disease
• Contraindications to vasodilation right
  ventricular infarct, aortic stenosis, volume
  depletion, HCM
• Left-sided HF dyspnea, cough, orthopnea,
  peripheral edema
• BNP decreased in elderly, women, cirrhosis, renal
  failure
• 1-3 T, 4 and 5 F (not peripheral edema, increased)