chapter 53 congestive heart failure and acute pulmonary edema l.
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Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema. September 22, 2005. Epidemiology. Leading cause of hospitalization among those >65 Up to 60% rehospitalized within 6 months due to recurrent decompensation Prevelance doubles each decade

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epidemiology
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
prognosis
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
classification system
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
pathophysiology
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-aldosterone system and the SNS
pathophysiology6
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
  • NP’s result in vasodilation, natriuresis, decreased levels of endothelin and inhibition of RAAS and SNS
  • BNP is the only NP for which an assay exists
classification
Classification
  • Systolic or diastolic dysfunction, classified by EF
  • Systolic HF defined by EF<40%, most commonly from ischemic heart disease
  • Diastolic HF, contractile function preserved, impaired relaxation, chronic HTN and LVH are often responsible
systolic vs diastolic hf
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
left vs right side hf
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
diagnosis history and pe
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%
diagnosis chest radiography
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
diagnosis bnp
Diagnosis: BNP
  • Correlate with elevated PCWP
  • By NYHA class, BNP levels vary directly with severity
  • Dyspnea due to COPD, BNP levels < 100, HF > 1,000
  • BNP <100 yield negative predictive value of 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
treatment
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
treatment14
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
treatment15
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
contraindications to vasodilation
Contraindications to Vasodilation
  • Preload dependent states: right ventricular infart, AS, or volume depletion
  • HCM
  • If coexisting shock, phenylephrine preferred pressor
treatment17
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
treatment18
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
disposition for acute pulmonary edema
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
disposition for decompensated hf
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
review of clinical trials of nesirtide
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 ACE’s (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
review of clinical trials of nesiritide
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)
review of clinical trials of nesiritide23
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)
questions
Questions

True or False

1. Levels of BNP <100 yield negative predictive 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)