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Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema

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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Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema

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  1. Chapter 53Congestive Heart Failure and Acute Pulmonary Edema September 22, 2005

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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%

  11. 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

  12. 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

  13. 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

  14. 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

  15. 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

  16. Contraindications to Vasodilation • Preload dependent states: right ventricular infart, AS, or volume depletion • HCM • If coexisting shock, phenylephrine preferred pressor

  17. 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

  18. 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

  19. 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

  20. 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

  21. 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

  22. 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)

  23. 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)

  24. 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)

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