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Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema

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Slide 1 :

Chapter 53 Congestive 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-aldosterone 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 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

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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

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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 < 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

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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 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

Slide 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)

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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)

Slide 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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