Transcript Acute Heart Failure - Advocate Health Care

Acute Heart Failure
Kendra Marsh, MD
Clinical Instructor, Cardiology Fellow
Department of Cardiology
University of Illinois at Chicago
Objectives
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
Acute Heart Failure
• Rapid onset of symptoms and signs
related to abnormal cardiac function
• As a result of Systolic Dysfunction,
Diastolic Dysfunction, Arrhythmias, or
Preload-After load Mismatch
Related Clinical Conditions
• De Novo or Chronic Decompensated
• Hypertensive
• Pulmonary Edema
• Cardiogenic Shock
• High Output Heart Failure: Arrhythmias,
Thyrotoxicosis, Anemia, Paget’s Disease
• Right Heart Failure
Killips Classification
This classification system uses the clinical exam to determine
the degree of cardiomyopathy after an acute MI.
• Stage I: No Heart Failure
• Stage II: Heart Failure
S3 gallop, Pulmonary venous Hypertension, Rales <1/2 of the lung fields
• Stage III: Severe Heart Failure
Frank pulmonary Edema, rales through out the lung field
• Stage IV: Cardiogenic Shock
Systemic hypotension, peripheral vasoconstriction, endorgan failure,
cyanosis, diaphoresis
Clinical Severity Classification
Warm/Dry
Warm/Wet
Cold/Dry
Cold/Wet
• PERFUSION
• CONGESTION
– Auscultation of the lungs
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
Epidemiology
• We have greatly improved our
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management of acute myocardial
infarctions.
Large component of care is
inpatient
Expensive to manage
High mortality in patients status
post MI.
The leading cause of
hospitalization in patients over 65
1 million hospitalizations per year
with HF as primary diagnosis
2.5 million hospitalizations with
heart failure as secondary
diagnosis
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
A Vicious Circle
In an effort to maintain adequate tissue perfusion the body has three defenses:
increase heart rate, vascular tone and circulating volume.
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
• Definitions
• Epidemiology
• Pathophysiology
• Diagnosis
• Management
• Summary of Guidelines
• Recommended Reading
General Therapeutic Approach
Oxygen
• Class I, C
– Improves oxygen delivery and tissue perfusion
– Goal Saturation should be 95-98%, beyond
that there is no indication for increased FIO2
– Always consider CPAP first or Non Invasive
Positive Pressure Ventilation First
– Endotrachial Intubation as a last resort
Pharmacotherapy
• Morphine
• Anticoagulation
• Vasodilators
• Diuretics
• Beta Antagonists
• Inotropic Agents
Morphine
• Class IIb, B
– Great Early in management
– Venodilation
– Mild Arterial Dilation
– Slows Heart rate
Anticoagulation
• No evidence to support anticoagulation for
Acute Heart Failure alone
• Yes in the case of Atrial Fibrillation
• Yes in the case of LV thrombus
• Large Placebo Control Trial with Enoxiparin
at 40mg SC showed no mortality benefit
Vasodilators
• Nitrates: Class I, B
– Improves Cardiac Output
and decreases PCWP
– Best with diuretics
– Low doses, venodilation
– High doses, arterial dilation
– Preload and Afteroad
– Good for 16-24 hours
• Sodium Nitroprusside:
Class I, C
– Severe Heart Failure with
Hypertension
– Primarily arterial dilation
– Need for arterial invasive
monitoring
– Stop if active ischemia due
to coronary steal
phenomenon
Niseritide
• Recombinant B-type Brain Naturetic
Peptide
• Venous, Arterial and coronary affects
• Enhanced sodium excretion
• Suppresses RAAS and sympathetic system
Vasodilators in the Management of
Acute Heart Failure Trial (VAMC)
Design
Enrolled
Agents
Primary End
Point
Randomized
DoubleBlinded
Control
Effects at 3
hours
489
Acute CHF
PCWP>
20mmHg
Niseritide
Change in PCWP
Bolus 2 micr/kg from baseline
Reduced dyspnea
compared to
Nitroglycerine
standard therapy
IV
alone
Outcomes
Significant
reduction in
dyspnea score
and PCWP with
addition of
NIseritide to
standard therapy
• No good data to support adverse affects on renal
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function and niseritide
Retrospective analysis of VMAC showed potential for
increased creatinin with increasing niseritide dose.
Summary of Vasodilators
Diuretics
• Class I, B
Diuretic Resistance can be
associated with increased mortality.
Ultrafiltration
• RAPID-CHF Trial
– 40 patients
– ADHF and Renal
Insufficiency (Cr >1.5)
– Ultrafiltration had
significant increase in fluid
removal after 24 hours
– 4650 L vs 2838L
• UNLOAD Trial
– 200 patients
– Renal insufficiency was not
a criteria for inclusion
– Standard care vs ultra
filtration
– 48 Hours 4.6 L vs 3.3L
– 90 Days fewer
rehospitalizations .22 vs
.46 and fewer unscheduled
clinic visits 21 vs 44
Option in the setting of failed diuretic and
vasodilator therapy
Beta Blockers
• No data to support benefits in AHF
• Traditionally considered a contra indication
• Consider if there is active ischemia and
blood pressure tolerates.
• Ischemia and Tachycardia, Class IIb, C
• Acute MI after stabilization, Class IIa, B
• Chronic CHF after stabilization, Class I, A
Inotropic Agents
• Peripheral Hypoperfusion refractory to
vasodilators and diuretics, Class IIa, C
• Danger: May increase oxygen demand and
calcium loading
Dopamine and Dobutamine
• Dopamine:
– Vasodilator of Renal,
Coronary, splanchnic and
Cerebral Vascular beds
– Hypotensive patients
– Drawbacks: arrhythmia,
increased pulmonary
vascular resistance and
increased afterload
• Dobutamine, Class IIa, C
– Hypotension and low Urine
output
– Beta 1 and 2 agonist
– At high doses increases
SVR
– Additive effect with
Phosphodiesterase
inhibitors
– Draw Backs- arrhythmia,
reflex decrease in
sympathetic tone
Phosphodiesterase Inhibitors
• Milrinone and Enoximone
– Hypoperfusion despite Diuretics
and Vasodilators with good blood
pressure. Class IIb, C
– Lucitropic, Inotropic, vasodilator
– Inhibits degredation of Cyclic AMP
– Increase CO, CI, Stroke Volume,
– Decrease PAP, PVR and PCWP
– Immediate Action
– Effect is Distal to Beta receptors,
can be used in the setting Beta
Blocker therapy. Class IIa, C
Outcomes of a Prospective Trial of Intravenous Milrinone
For Exacerbations of Congestive Heart Failure
OPTIME-CHF
JAMA 2002
Design
Randomized, Control, Double Blinded
Milrinone versus Placebo
Enrolled
Broad Population with systolic dysfunction
Without low output syndrome
949 patients
Primary Endpoints
Repeat hospitalization for cardiovascular causes
Outcomes
No difference in primary end point between
Milrinone and placebo.
Higher instance of atrial arrhythmia and
hypotension with Milrinone.
Milrinone is associated a 30% increase in mortality
Conclusions
Not indicated in routine use with standard medica
therapy.
within 60 days of discharge.
Levosimendan
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Calcium ion sensitization
Also Pimobendon
Increases Contractility
A little PDI activity as well
Severe dysfunction with
preserved blood pressure
• Drawback: very proarrhythmogenic
Clinical Trials
• LIDO Trial
– Levosimendan 24 hr
infiusionvs Dobutamine
– 203 Patients
– Severe Decompensated HF,
AHF, HF after CABG
– Excluded if cardiogenic
shock
– Endpoints, increased CI
(35% vs 25%) and reduced
PCWP (28% vs 15%) in
favor of Levosimendan
• SURVIVE Trial
• Levosimendan vs
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Dobutamine 24 hour
therapy
1327 patients
Endpoints symptomatic
relief and BNP
Levosimendan Greater
reduction in BNP but no
difference in symptomatic
relief
Pressors
• Vasopressin: Cardiogenic shock in
conjunction with inotropic therapy
• Epinephrine B1 and B2,
• Norepinephrine alpha receptors
• Cardiac Glycosides: Inhibit cardiac Na/K
ATPase, increases Ca/Na exchange
mechanism. Tachycardia induced
Cardiomyopathy.
Cardiac and Ventricular Assist
Devices
Temporary Devices
• IABP
• Tandem Heart
• ECMO
• Ventricular Assist Devices
IABP
ECMO
• ECMO removes carbon dioxide
from and adds oxygen to
venous blood via an artificial
membrane lung
Severe respiratory failure
Cardiac Failure with inability to
wean off Bypass
Bridge to Cardiac Transplant
Temporary Devices:
Tandem Heart pVAD
• Continuous-flow centrifugal
assist device placed
extracorporeally
• Cannula in femoral vein
through intraatrial septum into
LA
• Pump withdraws oxygenated
blood from the left atrium,
propels it by a magnetically
driven impeller through the
outflow port
• Blood returns into femoral
artery via arterial cannula
Longer-term implantable devices
• Novacor
• HeartMate XVE
• HeartMate II
• Next Generation Devices
Operative Mortality Prediction Score
• Requirement for ventilator support
— 4 points
• Clinical picture of post-cardiotomy
shock — 2 points
• Use of temporary LVAD prior to
Heart-Mate insertion — 2 points
• Central venous pressure >16
mmHg — 1 point
• Prothrombin time >16 seconds —
1 point
• Scoring
– 0-5: Low risk
• Mortality 8%
– 5-7: Intermediate Risk
• Mortality 32%
– 8-10: High Risk
• Mortality 49%
Novacor- Long-term Device
Cardiac Replacement
Bridge to Transplant
Magnetic Actuator
Blood Propelled via
collapsing bladder and to
prosthetic valves
One Year Survival
No risk factors, 60%
1 Risk factor, 24%
25% risk of
Thromboembolic Event
Heart-mate
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Rehabilitation and hospital discharge
$70,000
LV apex to ascending aorta
Textured surface allows for endotheliazation to reduce need for anticoagulation
Improves perfusion: decrease renal failure and pulmonary HTN
Complications: infection, bleeding, monomorphic VT, RV failure and Aortic Stenosis
HeartMate II
Suggested Reading
• Randomized evaluation of Mechanical Assistance for
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Treatment of Chronic Heart Failure (Rose et al. NEJM
2001)
Evaluation and management of patients with acute
decompensated heart failure. Journal of Cardiac Failure.
Vol.12 No. 1 2006
Medical Management of Advanced Heart Failure. JAMA,
February 6,2002- Vol. 27, No. 5
http://www.med.umich.edu/AnesCriticalCare/Documents
/Rosenberg_Circulatory_Assist_Devices.pdf
http://texasheart.org/Research/Devices/thoratec_heartm
ateii.cfm
Thank you!
• Special Thanks to
– Dr. Chad Feldman, Associate Director of
Medicine Advocate Christ Hospital
– Dr. Ali Zadi, Clinical Instructor, Cardiology
Fellow
– Dr. Saba Khan, Heart Failure Fellow