Transcript Update on the Treatment of Acute Decompensated Heart Failure

ACUTE DECOMPENSATED HEART FAILURE
University of Ottawa Medical School
Curriculum
Sharon Chih MBBS, FRACP, PhD
Assistant Professor, University of Ottawa
January 13h, 2016
Learning Objectives
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Define acute heart failure and describe its pathophysiology
with reference to: impaired -contractility or ventricular filling
and increased afterload.
List examples of conditions that cause left and right-sided
heart failure.
Review the clinical manifestation of heart failure.
Review the treatment of heart failure with reference to:
diuretics, vasodilators, inotropic drugs
Distinguish between pulmonary edema of cardiogenic vs
noncardiogenic origin.
Management of Acute HF - Outline
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Review of the clinical presentation of acute HF
 Causes
 Clinical signs and symptoms
 Diagnosis
What are the important management strategies?
 What are the important prognostic markers?
 How do we use diuretics?
 How and when do we use inotropes or vasodilators
Definition: Heart Failure
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Condition where the heart cannot pump an
adequate supply of blood at normal filling
pressures to meet the metabolic needs of the body
Clinically
 Reduced
cardiac output
 Congestion
 Impaired quality of life
 Reduced life expectancy
Distinguish from cardiomyopathy:
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Pathologic abnormality of myocardium resulting in
abnormal myocardial structure - cardiac dilatation
and hypertrophy
All patients with cardiomyopathy do not have HF
Acute vs. Chronic HF?
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Acute HF or Acute heart failure syndrome or ADHF
 First
presentation of new onset HF symptoms
 Acute
worsening of symptoms
 Previously
stable HF that has deteriorated
Acute vs. Chronic HF
Chronic HF
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Management
 Beta
blockers
 ACE inhibitors / ARB
 Spironolactone
 ICD /CRT
Acute HF
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Management
 Symptom
based
 Relieve congestion
 Diuretics
 Improve
perfusion
 Inotropes
 Remove
agent
precipitating
General Causes of HF
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Coronary artery disease
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Myocardial infarction
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Valve disease
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Idiopathic cardiomyopathy
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Hypertension
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Myocarditis / pericarditis
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Arrhythmias
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Thyroid disease
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Pregnancy
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Toxins (alchohol, chemotherapy)
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Inherited cardiomyopathies
Mechanisms and Causes of HF
Impaired Contractility
Myocardial infarction
Transient ischemia
Chronic volume overload
MR/AR
Dilated cardiomyopathy
Increased Afterload
AS
Uncontrolled HTN
Systolic Dysfunction
Left Sided HF
Diastolic Dysfunction
Obstruction of LV filling
MS
Pericardial constriction or
tamponade
Impaired ventricular relaxation
LVH
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Transient ischemia
Mechanisms and Causes of HF
Cardiac Causes
Left sided HF
Pulmonary stenosis
Right ventricular infarction
Right Sided HF
Pulmonary Vascular Disease
Pulmonary embolism
Pulmonary HTN
Right ventricular infarction
Parenchymal pulmonary disease
COPD
Interstitial lung disease
Chronic infections
Adult respiratory distress syndrome
Increased contractility
Normal
A
Heart Failure
Hypotension
Stroke volume (cardiac output)
Heart Failure: Pathophysiology
B
C
Pulmonary congestion
Left ventricular end diastolic pressure (volume)
Heart Failure Neurohumoral Activation
Myocardial insult
LV dysfunction
Neurohormonal
Activation
LV Remodeling
•Sympathetic
•Renin-angiotensin
•ADH
• Initially restores CO and organ perfusion
• Ultimately highly negative impact on ventricular function
Diagnosis of HF
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There is no single diagnostic test that can confirm
the diagnosis of heart failure
Constellation of symptoms and signs
CXR findings
Confirmation of cardiac abnormality
 Invasive
hemodynamic studies
 Echocardiogram
 Serum BNP testing
Symptoms and Signs of HF
Increased filling pressures
Congestion
Poor Cardiac Output
Poor Perfusion
Congestion – left sided
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Left-Sided
 Symptoms
 Dyspnea
 Orthopnea
 Shortness of breath when supine
 Paroxysmal nocturnal dyspnea
 Acute awakening from sudden dyspnea
 Fatigue
 Signs
 S3 gallop
 Displaced apex
 MR
 Pulmonary rales
 Loud P2
Congestion – Right Sided
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Right-Sided
 Symptoms
 Peripheral
edema
 Abdominal bloating
 Nausea
 Anorexia
 Signs
 Elevated
JVP
 Hepatomegaly
 Ascites
 Edema
Evaluating the JVP
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Consensus: <2 cm above the
sternal angle considred
normal and >4cm ASA is
abnormal
http://cal.fmc.flinders.edu.au
/gemp/ClinicalSkills/clinskil/
year1/cardio/cardio04.htm
Assessing Perfusion
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Symptoms
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Fatigue
Confusion
Dyspnea
Sweating
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Signs
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Hypotension
Tachycardia
Cool extremities
Altered mental status
Decreased urine
output/Rising creatinine
Liver enzyme abnormalities
Pulmonary Edema
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General Considerations
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Increase in the fluid in the lung
Generally, divided into cardiogenic and non-cardiogenic categories.
Pathophysiology
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Fluid first accumulates in and around the capillaries in the interlobular
septa (typically at a wedge pressure of about 15 mm Hg)
Further accumulation occurs in the interstitial tissues of the lungs
Finally, with increasing fluid, the alveoli fill with edema fluid (typically
wedge pressure is 25 mm Hg or more)
Cardiogenic vs. Noncardiogenic
pulmonary edema
Cardiogenic pulmonary edema
 Heart failure
 Coronary artery disease with left
ventricular failure.
 Cardiac arrhythmias
 Fluid overload -- for example,
kidney failure.
 Cardiomyopathy
 Obstructing valvular lesions
 Myocarditis and infectious
endocarditis
Non-cardiogenic pulmonary edema
- due to changes in capillary
permeability
 Smoke inhalation.
 Head trauma
 Overwhelming sepsis.
 Hypovolemia shock
 Acute lung re-expansion
 High altitude pulmonary edema
 Disseminated intravascular
coagulopathy (DIC)
 Near-drowning
 Overwhelming aspiration
 Acute Respiratory Distress
Syndrome (ARDS)
CXR Findings of Pulmonary Edema
Cardiogenic pulmonary edema
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Kerley B lines (septal lines)
 Seen at the lung bases, usually no
more than 1 mm thick and 1 cm
long, perpendicular to the pleural
surface
Pleural effusions
 Usually bilateral, frequently the
right side being larger than the
left
 If unilateral, more often on the
right
Fluid in the fissures
 Thickening of the major or minor
fissure
Peribronchial cuffing
 Visualization of small doughnutshaped rings representing fluid in
thickened bronchial walls
Non-cardiogenic pulmonary edema
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Bilateral, peripheral air space
disease with air bronchograms or
central bat-wing pattern
Kerley B lines and pleural
effusions are uncommon
Typically occurs 48 hours or more
after the initial insult
Stabilizes at around five days and
may take weeks to completely
clear
On CT
 Gravity-dependent
consolidation or ground glass
opacification
cuffing
Alveolar
edema
Kerley B
Clinical Presentation of Acute HF
Hypertension
and acute
pulmonary
edema
10-20%
Hypotension
and markedly
low CI
<10%
Gradual
worsening of
symptoms
60-80% -less pulmonary
congestion and
more edema or
weight gain
->70% ADHF is
worsening chronic
HF
-50% of these
patients may have
SBP>140
Presentation – Symptoms and Signs
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Patient profile
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Older - median 75y.o
Female ~50%
HFpEF ~50%
Comorbidities common: AF, DM, CKD
Dyspnoea 70-90%
Other: oedema, fatigue, subtle
 Young: abdo pain, nausea, anorexia
 Old: confusion and lethargy
JVP most sensitive
 Estimate of left sided filling pressures (PCWP)
 R = 0.64 for JVP and PCWP
 Dissociation b/w JVP and PCWP in lung disease, obesity, PE, RV infarct
Poor sensitivity: rales, oedema, S3
Majority hypertensive
 50% SBP >140 mmHg; 45% SBP 90 – 140 mmHg; 5% SBP <90 mmHg
Predictors of Adverse Outcome During Acute HF
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Clinical
 Hypotension (SBP <100)
 Older age
 Ischemic etiology
 Recurrent hospitalisations
 NYHA IV (>90 days)
Laboratory
 Renal dysfunction (Cr >220)
 Anemia (acute or chronic)
 Hyponatremia (Na <132)
 EF<40%
 Elevated troponin or BNP (>500)
ADHF Treatment Goals
1.
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Relieve symptoms: congestion and low out-put
Optimise volume status
Identify aetiology
Identify precipitating factors
Initiate and optimise chronic oral therapy
Minimise side effects
Educate patient/family: medications and self assessment
HFSA guidelines: Journal of Cardiac Failure Vol. 16 No. 6 2010
Precipitants of HF
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Increased metabolic demands
 Fever, anemia, infection, tachycardia, hyperthyroidism,
pregnancy
Increased circulating volume
 Excessive salt or fluid in diet
Progression of
 Renal failure
underlying disease
Increased afterload
 Hypertension
 PE
Impaired contractility
 Negative inotropes
 Ischemia
Failure to take medications
ADHF Evaluation and Treatment
According to clinical haemodynamic profiles
↓BP
↑Cr
P
E
R
F
U
S
I
O
N
Dry & Warm
Wet & Warm
ACEI/BB/Aldost inhib
Diuretics
± IV Vasodilators
Dry & Cold
Wet & Cold
↓Vasodilators
↓Diuretics
Diuretics
Inotropes/Vasodilators
CONGESTION
Stevenson et al. Eur J Heart Failure 1999: 1: 251-257
↑JVP
Crackles
Oedema
Therapy
Diuretics
1.
Reduce fluid overload
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Vasodilators
2.
Decrease preload and/or afterload
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Inotropes
3.
Augment contractility
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4.
Mechanical circulatory support
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Unresponsive to medical therapy
Intravenous Diuretics
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Essential for the
management of
congestion
Restore volume by
increasing excretion
of Na and water
Loop diuretics are
first line
Diuretic resistance
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Dosing
Combination therapy
with thiazide
Neurohormonal
blockade
Lasix Administration and Dosing
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Bioavailability of oral dosing variable (20-80%)
 Gut wall edema, reduced blood flow, protein binding
IV rate preferred in acute HF
Initial dose should be double maintenance or 40-80 mg IV –
titrate to clinical response
Consider continuous infusions if large bolus ineffective
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Dose trial: no difference between bolus vs. infusion
Associated with hypotension, renal dysfunction, electrolyte
disturbance (K, Mg, Ca), RAAS activation
Diuretic Responsiveness
Ellison et al. Cardiology 2001; 96:132-143
Beneficial effects of volume restoration
Negative sodium and water balance
Decreased cardiac filling pressure
Decreased ventricular dilatation
Decreased ventricular wall stress
and endomyocardial ischemia
Improved pulmonary congestion
Decreased functional MR/TR
Improved myocardial function
Improved renal function
Vasodilators
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Reduce filling pressures, afterload: increase CO
Class IIa Recommendation, Level of evidence B
In patients with evidence of severely symptomatic fluid overload in the
absence of systemic hypotension, vasodilators such as intravenous
nitroglycerin, nitroprusside, or nesiritide can be beneficial when added to
diuretics and/or those who do not respond to diuretics alone
Little data for specific choice: Nitroglycerin vs. Nitroprusside vs. Nesiritide
Vasodilator Therapy in Acute HF
Nitroglycerin
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Stimulates guanylate
cyclase
Dose dependent venous
and arteriole dilatation
Decreases filling pressures
without increasing oxygen
demand
Headache
Nitrate tolerance
Nitroprusside
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Equipotent venous and
arteriolar dilation
Useful for HTN, valvular
dysfunction (AR, MR)
Short half life
Methemoglobinaemia
Cyanide toxicity
Who is the Ideal Candidate for IV
vasodilator therapy?
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“wet and warm” profile
Patients with acute pulmonary
edema/dyspnea and preserved BP (SBP
>90)
Acute HF and concurrent cardiac ischemia
Vasodilator Dosing
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Nitroglycerin
 Intravenous
infusions 5-10 ug/min titrated for desired
clinical effect
 Oral: isordil 10-30 mg tid
 Transdermal:0.2-0.8 mg/hr by patch
Inotropic Use in Acute HF
Dobutamine
PDE
Milrinone
Levosimendan
Adapted from Dorn; Circulation 2004
Inotropes and Harm
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Increased mortality through variety mechanisms
 Increase HR
 Arrhythmias
 Increase myocardial oxygen demand
 Direct toxic effect to myocardium: accelerated apoptosis
NOT effective in broad populations of patients with ADHF
 Routine use in “wet and warm” detrimental (OPTIME-HF)
 Majority of ADHF patients are not in low output state
 Increased rates of HF rehospitalisation, mortality with
inotropes (ESCAPE, ADHERE)
Role of Inotropic Therapy
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Reserved for those with low output HF
 “wet
and cold”
 Evidence of poor tissue perfusion
 Symptomatic hypotension despite adequate filling
pressures
 Poor response to diuretics with worsening renal function
 Unresponsive or intolerant to vasodilators
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Short term
Lowest dose
No evidence that one is agent is superior to other
Inotrope Dosing
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Dobutamine
 2-6 ug/kg/min infusions –larger doses needed if profound
shock/hypotension
Milrinone
 0.25-0.75 ug/kg/min infusion
Dopamine
 2-5 ug/kg/min infusions
What about oral HF medications?
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Beta blockers
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ACE Inhibitors
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Usually maintained in mild-moderate acute HF
Dose reduced or held when patients felt to have significant
reduction in perfusion or need for inotropes
Dose escalation not advised in setting of acute HF
Dose usually maintained unless significantly hypotensive or acute
renal failure
Dose escalation ok once acute symptoms improved (if no
worsening renal function)
Digoxin
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Dose maintained unless digoxin toxicity
Acute HF: Summary
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Acute HF results when heart function can no longer meet needs
of body
Can be caused by pump failure, or resistance on either side of
heart
Key strategy in management is to identify underlying cause
Diuretics are essential
Vasodilators reserved for acute HF with HTN, ischemia or
pulmoary edema
Inotropes should only be used in patients with poor perfusion
 Novel inotropes have not proved more safe or effective
than current care