Chapter 53 Congestive Heart Failure and Acute Pulmonary Edema
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Transcript 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
• Cost of HF roughly double that of any cancer diagnosis
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
• 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
• 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
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
• 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
• 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-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
• 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
• 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
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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
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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
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
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
• Preload dependent states: right ventricular infart, AS, or
volume depletion
• HCM
• If coexisting shock, phenylephrine preferred pressor
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 510 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
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
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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
• 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
• 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
• 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 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
True or False
1.
Levels of BNP <100 yield negative predictive value 89-96%
2.
Systolic HF defined as EF under 40% most typically from ischemic heart
disease
3.
Contraindications to vasodilation: right ventricular infarct, aortic stenosis,
volume depletion, HCM
4.
Left-sided HF: dyspnea, cough, orthopnea, peripheral edema
5.
BNP decreased in elderly, women, cirrhosis, renal failure
1-3 T, 4 and 5 F (not peripheral edema, increased)