fellows school: acute heart failure fellows school: acute heart failure brent c. lampert, do aug 4,...
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Fellows School: Acute Heart Failure
Brent C. Lampert, DO
Aug 4, 2014
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Outline
Definitions
Incidence
Diagnosis
Treatment Diuretics, vasodilators, inotropes, UF, advanced
therapies Transition to discharge
RHC interpretation
Terminology
AHF Acute decompensated HF (ADHF) Acute on chronic systolic / diastolic HF Acute biventricular HF Acute HF syndrome Acute decompensation of chronic HF HFpEF HFrEF AHA 2013 HF Guidelines
GDMT
Heart Failure
Affects ~ 6 million people in the U.S.
Expected to increase > 25% by 2030
60,000 deaths per year directly attributed to HF
Half of patients die w/in 5 yrs of diagnosis
Costs $34.4 billion annually in the U.S.
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Go, et al. Circulation 2013.Heidenriech, et al. Circulation 2011
Hospital Discharges for HF by sex
Introduction: AHF
Definition: new, gradual, or rapidly worsening heart failure signs & symptoms requiring urgent therapy
1 million annual admissions in US: HF as primary diagnosis
3 million annual admissions in US: HF as primary or secondary dx
Gheorhiade M, et al. JACC 2009
Heart Failure Rehospitalizations
30 day rehospitalization rate 27% in Medicare patients
40% due to HF (at OSU within 7 days)
Higher early follow-up rate (in 7 days of discharge) associated with reduced 30 day event rates
Median Survival Decreases after HF Hospitalizations
Miller L. JACC. 2013
Etiologies of HF
Ischemia (#1)
Hypertension (#2)
Valvular
Inflammatory Myocarditis, infectious,
autoimmune.
Medications Chemotherapy,
chloroquin
Toxins Ethanol, cocaine
Deposition Amyloid,
hemochromatosis
Rheumatologic
Endocrine disorders
Neuromuscular disease
Miscellaneous Peripartum, tachycardia-
related,familial, sleep apnea, sarcoid.
Idiopathic (#3)
Common Factors Precipitating the HF Hospitalization Noncompliance
Myocardial ischemia / infarction
Hypertension
Atrial fibrillation / arrhythmia
Addition of negative inotropic drugs (verapamil/diltiazem, β-blockers)
Pulmonary embolus
NSAID’s
Excessive ETOH / drugs
Endocrine abnormalities
Concurrent infections (Pneumonia, viral illness)
ADHF Diagnosis - Presentation
No single finding conclusive for diagnosing Most common symptoms: progressive dyspnea,
fatigue, cough, orthopnea, PND, edema, and/or weight gain
PE: Tachypnea Tachycardia Crackles or wheezing (“cardiac asthma”) Extra cardiac sounds (S3 and/or S4) Elevated jugular venous pressure (use central lines
for CVP) Edema Nausea / poor appetite
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AHF: Clinical Parameters
ADHERE(150,000 pts)
OPTIMIZE-HF(48,612 pts)
EURO HF(11,327 pts)
Any Dyspnea 89 90 70
Rest Dyspnea 34 45 40
Fatigue 32 23 35
Rales 68 65 N/A
Pulm. edema 66 65 23
Systolic BP
<90 2 <8 <1
90-140 48 44 70
>140 50 48 29
Fonarow GC. Rev Cardiovasc. Med. 2003Gheorghiade M. JAMA 2008Cleland JGF. Eur Heart J 2003
ADHF Diagnosis - Presentation
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Table 9.2 Modified Framingham Criteria for the Diagnosis of Congestive Heart Failure
Major Criteria Minor Criteria
Paroxysmal nocturnal dyspnea or orthopnea Neck vein distention Crackles / Rales Acute pulmonary edema S3 gallop Central venous pressure >16 cm H2O Weight loss >4.5 kg in 5 days in response to treatment Echocardiographic left ventricular dysfunction
Bilateral ankle edema Pleural effusion Nocturnal cough Dyspnea on exertion Hepatomegaly Tachycardia (heart rate>120 beats/min) Weight loss >4.5 kg in 5 days caused by heart failure where factors other than treatment of CHF could have contributed to weight loss
*For diagnosis of heart failure, 2 major criteria or 1 major criteria and 2 minor criteria are needed. Source: McKee PA, Castelli WP, McNamara PM, Kannel WB. The natural history of congestive heart failure: the Framingham study. N Engl J Med. 1971;285:1441-1446.
ADHF Diagnosis - Testing
EKG to identify underlying causes (LVH, MI, afib)
CXR may reveal pulmonary vascular congestion, but normal chest x-raydoes not exclude ADHF
CBC to identify anemia or infection
Chemistries to evaluate for renal dysfunction
Cardiac biomarkers if ischemia is suspected
BNP useful when the diagnosis is uncertain > 400 pg/mL predictive of heart failure as cause of dyspnea < 100 pg/mL have a very high negative predictive value for
heart failure as a cause of dyspnea
Echocardiography in all patients with new onset heart failure
LHC in patients with suspected ACS
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Hemodynamic Profile Assessment
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ADHF – Initial treatment
Focus on hemodynamic & volume abnormalities and correct precipitating factors (ischemia/arrhythmias)
Diuretics, diuretics, diuretics! Start w/equal or greater dose of loop diuretic (IV) than outpatient
regimen (furosemide - NOT BUMEX) Short half-life; requires multiple doses or continuous infusion IV continuous infusion & bolus dosing have similar efficacy Be cognizant of detrimental effects on renal blood flow, GFR,
electrolytes, neurohormones
Volume status, evidence of congestion, daily I/O, daily wts, potassium and creatinine frequently assessed
Low sodium diet (2 g daily or less) and fluid restriction (at least <2 L daily) should be considered
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Ellison. Cardiology. 2001;96:132-143.
Dose Response Curves for Loop Diuretics in ADHF Are Altered
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18
16
14
12
10
8
6
4
2
0
[Furosemide], µg/mL
0.01 0.1 1 10 100
Normal
CRF
CHFSecretory
Defect
DecreasedMaximalResponse
FE
Na ,%
Fractional Na Excretion
increased NH reduced renal perfusion poor absorption receptor unresponsive
Most Common Intravenous Medications
0
10
20
30
40
50
60
70
80
90
100
Pat
ient
s (%
)
IV Diuretic Dobutamine Dopamine Milrinone Nesiritide Nitroglycerin Nitroprusside
IV Vasoactive Meds
88%
6% 6%10%
3% 1%
10%
ADHERE® Registry. Benchmark Report. 2004.
All Enrolled Discharges (n=105,388) October 2001–January 2004
Acute HF – Options When Initial Diuretics Fail Is there persistent “congestion” ?
Careful exam (JVP), labs, BNP May need invasive hemodynamics
Continuous infusion of furosemide 5-40 mg/hr
Add thiazide (distal tubule diuretic) Ultrafiltration Additional Vasoactive therapy Inotropes Advanced therapies
Thiazide diuretics – “Booster”
• HCTZ
• Metolazone
• Long ½ life
• Does not need to be administered 30 min prior
• Significant electrolyte disturbances
• Chlorothiazide (Diuril)
• IV
• $$$
Ultrafiltration for Acute Heart Failure
Useful in patients w/ ADHF + renal insufficiency or diuretic resistance
Advantages: adjustable fluid removal rates, no effect on electrolytes, decreased neurohormonal activity
CARESS-HF 188 pts w/ ADHF, worsened renal function Stepped pharmacologic care (loop
diuretics, metolazone, selective inotropes or vasodilators) vs. UF
No difference in weight loss UF with increased Cr and more adverse
events
Vasodilators
Rapid resolution of congestive symptoms, angina, HTN
Most patients will have high SVR (MAP/CO)
Improve SV, C.O., right and left sided filling pressures without increase HR
Nitroglycerin, Nesiritide, Nitroprusside
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Vasodilators - Nitroglycerin
Reduces LV filling pressures primarily through venodilation
Variable effect on SVR (depends on degree of elevation)
Improves myocardial blood flow (coronaries, LVEDP, HR)
Start at 5-10 mcg/min and can titrate rapidly to effect (as high as 400 mcg/min)
Attention to intravascular volume (resistance in those with high RAP) and hypotension in those with low IVV, RV dysfunction, diastolic HF
Short half life
Tachyphylaxis can occur within hours
Avoid with PDE inhibitors
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Vasodilators - Nitroprusside
Potent vasodilator with balanced venous & arterial effects Short half-life (effects are gone w/in 10 minutes) Rapidly reduces filling pressures, MVO2, valve
regurgitation Rapidly increases SV Significant increase in HR (or drop in BP) should stop
infusion Typically use with invasive hemodynamics Potential for cyanide toxicity (rare) – limit to 48 hours Dose starts at 0.5 mcg/kg/min and titrate to
hemodynamic effect Q 3-5 minutes.
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Vasodilators - Nesiritide
Recombinant human BNP Venous and arterial dilation. Reduces BP, filling
pressures and mild increase in CO; no increase in HR
Limited evidence for “natriuretic” effect in clinical studies. Does not replace diuretics.
Start at 0.005 – 0.01 mcg/kg/min; +/- bolus. Limited dose titration necessary. Long half-life.
As with all vasoactive therapies, must monitor BP, symptoms, renal function closely (multiple times per day)
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Conclusions:Mild benefit in dyspneaNo effect on outcomesNo adverse effect on renal functionIncreased hypotension
O’Connor et al. NEJM 2011
ADHF Treatment - Inotropes
Milrinone and dobutamine For “cold” patients with evidence of hypoperfusion Short-term therapy to maintain systemic perfusion
and preserve end-organ performance until definitive therapy (revascularization, MCS, Transplant) or palliative therapy
Require continuous rhythm and frequent BP monitoring
Symptomatic hypotension or tachyarrhythmias should prompt consideration of dose reduction or discontinuing
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ADHF Treatment - Milrinone
PDE inhibitor that increases myocardial inotropy by inhibiting degradation of cyclic AMP
Reduces systemic and pulmonary vascular resistance (via inhibition of peripheral phosphodiesterase)
Improves left ventricular diastolic compliance (lusitropy)
Increases cardiac index and decreases left ventricular afterload and filling pressures
Can be given with B-blockers Typical dose: 0.25 – 0.75 mcg/kg/min
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ADHF Treatment - Dobutamine
Acts primarily on beta-1 adrenergic receptors, with minimal effects on beta-2 and alpha-1 receptors
Increases stroke volume and cardiac output Modest decreases in systemic vascular
resistance and pulmonary capillary wedge pressure
Consider decrease / withdrawal B-blockers ? Increased ventricular ectopy Typical dose: 2-20 mcg/kg/min
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ADHF Treatment - Inotropes
Continue until euvolemia is achieved, or definitive therapy delivered
Wean gradually to avoid effects of sudden withdrawal including precipitous decreases in cardiac output
Failure to wean should prompt consideration of additional advanced therapies
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ADHF Treatment – Advanced therapies
IABP is the most commonly used, easily placed, and least expensive support device
ECMO can provide cardiopulmonary support Temporary support for patients failing all other therapies Bypasses the pulmonary circulation and oxygenated blood
returns to the patient via an arterial or venous route Venovenous ECMO: primarily supports patients with
severe respiratory failure Venoarterial ECMO utilizes an extracorporeal pump to help
with hemodynamic support
Short term VADS can be placed percutaneously or surgically
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ADHF – Predictors of outcome
Most important predictor of short term outcomes is adequacy of diuresis prior to discharge
BNP, troponin predict in-hospital mortality
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Peacock F, et al. NEJM 2008
Fonarow et al. JACC 2007;49:1943-50
ADHF – Discharge criteria
Recommended for all Patients Should be considered
Exacerbating factors addressed Near optimal volume status observed Transition from intravenous to oral diuretic successfully completed Patient and family education completed, including clear discharge instructions Left ventricular ejection fraction (LVEF) documented Smoking cessation counseling initiated Near optimal pharmacologic therapy achieved, including ACE inhibitor and beta blocker (for patients with reduced LVEF), or intolerance documented Follow-up clinic visit scheduled, usually for 7 to 10 days
Oral medication regimen stable for 24 hours No intravenous vasodilator or inotropic agent for 24 hours Ambulation before discharge to assess functional capacity after therapy Plans for postdischarge management (scale present in home, visiting nurse or telephone follow up generally no longer than 3 days after discharge) Referral for disease management, if available
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Source: Lindenfeld, J, Albert NM, Boehmer JP, Collins SP, Ezekowitz JA, Givertz MM, Klapholz M, Moser DK, Rogers JG, Starling RC, Stevenson WG, Tang WHW, Teerlink JR, Walsh MN. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail 2010;16:e1-e194.
ADHF - RHC
Value of RHC remains controversial Randomized ESCAPE trial showed no benefit (or
increased risk) of using RHC in mortality or days alive out of the hospital
Did not enroll all consecutive patients b/c many physicians would not enroll and risk a 50% chance of not having PA catheter
Routine RHC in HF not recommended; useful in subset of patients
2013 ACC/AHA heart failure guideline: perform in patients “with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate”
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ADHF - RHC
Filling pressures Cardiac output
TD Fick PA saturation
TPG Mean PAP – PCWP Normal value ≤ 12 mmHg
PVR PVR = Normal value is < 3 Wood units (or 240 dynes-sec-
cm-5)
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Pressure, mmHg
Chamber Average Range
Right atrium 5 ± 2
Right ventricle
25/5 ± 5 / ± 2
Pulmonary artery
25/10 ± 5 / ± 2
Left atrium (PCWP)
10 ± 2
ADHF - RHC PH associated with HF
Heart Failure PAH “In proportion”
“Out of proportion”
RA (mmHg) Normal or ↑ Normal or ↑ Normal or ↑ Normal or ↑
RV (mmHg) Normal or ↑ ↑ ↑ ↑
Mean PA (mmHg)
Normal or ↑ ≥ 25 ≥ 25 ≥ 25
PCWP (mmHg) > 15 ≤ 15 > 15 > 15
CO (L/min) Normal or ↓ Normal or ↓ Normal or ↓ Normal or ↓
TPG (mmHg) Normal > 12 ≤ 12 > 12
PVR (Wood units)
Normal > 3 < 3 > 3
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ADHF - RHC
RA 10, PA 50/24 (33), PCWP 26
CO/CI 4.7/2.4, PA saturation 65%
Diagnosis?
Treatment?
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ADHF - RHC
RA 20, PA 50/24 (33), PCWP 26
CO/CI 4.7/2.4, PA saturation 65%
Diagnosis?
Treatment?
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ADHF - RHC
RA 20, PA 50/24 (33), PCWP 26
CO/CI 3.1/1.5, PA saturation 43%
Diagnosis?
Treatment?
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ADHF - RHC
RA 18, PA 84/25 (45), PCWP 10
CO 5.0/2.6, PA saturation 68%
Diagnosis
Treatment
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ADHF - RHC
RA 18, PA 84/25 (45), PCWP 36
CO 5.0/2.6, PA saturation 68%
Diagnosis
Treatment
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Questions
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