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ACUTE DECOMPENSATED HEART FAILURE
University of Ottawa Medical School Curriculum
Lisa M Mielniczuk MD FRCPCAssistant Professor, University of Ottawa January 15h, 2014
Learning Objectives 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
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
Condition where the heart cannot pump an adequate supply of blood at normal filling pressures to meet the metabolic needs of the body
Clinically Ventricular dysfunction Reduced exercise capacity Impaired quality of life Shortened life expectancy
Distinguish from cardiomyopathy: Pathologic abnormality of myocardium
resulting in abnormal myocardial structure - cardiac dilatation and hypertrophy
All patients with cardiomyopathy do not have HF
Heart Failure
Increased contractility
Normal
Heart Failure
Left ventricular end diastolic pressure (volume)
Str
oke
volu
me
(ca
rdia
c o
utpu
t)
A
B C
Pulmonary congestion
Hy
po
ten
sio
n
What is the Difference Between Acute and Chronic HF? Acute HF
First presentation of new onset HF symptoms
Previously stable HF that has deteriorated Acute worsening of symptoms
“Acute heart failure syndrome”
Acute vs. Chronic HF
Management Beta blockers ACE inhibitors /
ARB Spironolactone ICD /CRT
Management Symptom based Relieve congestion
Diuretics Improve perfusion
Inotropes Remove
precipitating agent
Chronic HF Acute HF
General Causes of HF
Coronary artery disease Myocardial infarction Valve disease Idiopathic cardiomyopathy Hypertension Myocarditis / pericarditis Arrhythmias Thyroid disease Pregnancy Toxins (alchohol,
chemotherapy) Inherited cardiomyopathies
The Heart Failure Continuum
Mechanisms and Causes of HF
Left Sided HF
Impaired ContractilityMyocardial infarctionTransient ischemiaChronic volume overload
MR/ARDilated cardiomyopathy
Increased AfterloadASUncontrolled HTN
Systolic Dysfunction
Diastolic Dysfunction
Impaired ventricular relaxationLVHHypertrophic cardiomyopathyRestrictive cardiomyopathyTransient ischemia
Obstruction of LV fillingMSPericardial constriction or tamponade
Mechanisms and Causes of HF
Right Sided HF
Cardiac CausesLeft sided HFPulmonary stenosisRight ventricular infarction
Parenchymal pulmonary diseaseCOPDInterstitial lung diseaseChronic infections Adult respiratory distress syndrome
Pulmonary Vascular DiseasePulmonary emobolismPulmonary HTNRight ventricular infarction
STAGE A•High risk for developing HF (diabetes, CKD, HTN)•No structural disorder of the heart
STAGE B•Structural disorder of the heart (e.g.. Previous MI)•Not yet developed symptoms of HF
STAGE C•Past or current symptoms of HF•Symptoms associated with underlying structural heart disease
STAGE D•End stage disease•Requires specialized treatment strategies
CLASS I•No symptoms and no limitations in physical activity•No shortness of breath when walking, climbing stairs etc.
CLASS II•Mild symptoms and slight limitation during ordinary physical activity
CLASS III•Marked limitation in activity due to symptoms (fatigue, shortness of breath) with less than ordinary activity (e.g.. Short distances or ADL’s)
CLASS IV•Severe limitation, may experience symptoms at rest
NYHA FUNCTIONAL CLASS
ACC/AHA STAGES OF HEART FAILURE
INCREASING SEVERITY OF HEART FAILURE
Functional Classification
Diagnosis of HF
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 Perfusion
Poor Cardiac Output
Heart Failure results in neurohormonal activation leading to sodium and water retention
Heart Failure
Vasopressin ↑Renin ↑Catecholamines ↑
Thirst
aldo ↑
Na reabsoprtion in collecting duct ↑
Na reabsorption proximal tubules↑
Na reabsorption proximal and distal tubules ↑
Excretion of free water in collecting tubule↓
Congestion – left sided
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
Evaluating the JVP
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
Congestion – Right Sided
Right-Sided Symptoms
Peripheral edema Abdominal bloating Nausea Anorexia
Signs Elevated JVP Hepatomegaly Ascites Edema
Assessing Perfusion
Symptoms Fatigue Confusion Dyspnea sweating
Signs Hypotension Tachycardia Cool extremities Altered mental status Rising creatinine Liver enzyme
abnormalities
Pulmonary Edema
General Considerations
Increase in the fluid in the lung Generally, divided into cardiogenic and non-cardiogenic
categories.
Pathophysiology
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 -- for example 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 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 doughnut-shaped rings representing fluid in thickened bronchial walls
Non-cardiogenic pulmonary edema 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
Air bronchograms are common
cuffing
Kerley B
Alveolar edema
Predictors of Adverse Outcome During Acute HF
Clinical Hypotension Older age Ischemic etiology Previous HF admission
Laboratory Renal dysfunction Anemia (acute or chronic) Hyponatremia EF<40% Elevated troponin or BNP
Clinical Presentation of Acute HF
10-20%
<10%
60-80%
Hypertension and acute pulmonary edema
Hypotension and markedly low CI
Gradual worsening of symptoms-less pulmonary congestion and more edema or weight gain->70% ADHF is worsening chronic HF-50% of these patients may have SBP>140
A ‘Clinical Profile’ Approach to acute HF Management
Goals of Therapy
Immediate Treatment Goals Relieve congestion Optimize cardiac function
Further Goals Achieve euvolemic status Identify underlying precipitant
Stabilization Recalibrate overall care, optimization of chronic meds Education Development comprehensive care plan
Precipitants of HF
Increased metabolic demands Fever, anemia, infection, tachycardia,
hyperthyroidism, pregnancy Increased circulating volume
Excessive salt or fluid in diet Renal failure
Increased afterload Hypertension PE
Impaired contractility Negative inotropes Ischemia
Failure to take medications
Progression of Progression of underlying diseaseunderlying disease
Hemodynamic Profile Assessment
Congestion at RestCongestion at Rest
LowPerfusionat Rest
NoNo
NoNo YesYes
YesYes
Warm & DryWarm & Dry Warm & WetWarm & Wet
Cold & WetCold & WetCold & DryCold & Dry
Signs/symptoms of congestion:• Orthopnea/PND
• JVD
• Ascites
• Edema
• Rales (rare in HF))
Possible evidence of low perfusion:• Narrow pulse pressure• Sleepy/obtunded• Low serum sodium
• Cool extremities• Hypotension with ACE inhibitor• Renal dysfunction (one cause)
Stevenson LW. Eur J Heart Fail 1999;1:251
20%
HR mortality 2.10
HR mortality 3.66
50-60%
<2%
Noninvasive Ventilation in Acute Pulmonary Edema
Hemodynamic Benefits-alters cardiac transmural presures
-Decreases venous return (preload)
-decreases afterload
-no change or increase in cardiac index
Respiratory Benefits
-increases tidal volume-unloads respiratory muscles-decreases dead space ventilation
Intravenous Diuretics
Essential for the management of congestion
Restore volume by increasing excretion of Na and water
Loop diuretics are first line
Rapid reduction in fluid overload and relief of symptoms
Doses
Furosemide Bioavailability of oral dosing variable (20-
80%) Gut wall edema, reduced blood flow, protein
binding IV rate preferred in acute HF 40-80 mg IV initially – titrate to clinical
response
Intravenous Diuretics
Initial dose should be double maintenance dose
Continuous infusions may be more effective than large bolus doses
Associated with hypotension, renal dysfunction, hypokalemia and neurohormonal abnormalities
Beneficial effects of volume restoration
Negative sodium and water balance
Decreased cardiac filling pressure
Improved pulmonary congestion
Decreased ventricular wall stress and endomyocardial ischemia
Decreased ventricular dilatation
Decreased functional MR/TR
Improved myocardial function
Improved renal function
Vasodilator Therapy in Acute HF
Stimulates guanylate cyclase
Dose dependent venous and arteriole dilatation
Decreases filling pressures without increasing oxygen demand
Nitrate tolerance
Equipotent venous and arteriolar dilation
Usually increases LV stroke volume and CO
Rapidly decreases neurohormonal activation
Signal of increased risk when used in acute MI setting
Nitroglycerin Nitroprusside
Who is the Ideal Candidate for IV vasodilator therapy?
Patients with acute HF and evidence of pulmonary edema
Acute HF and concurrent cardiac ischemia
Dyspnea and marked limitation Preserved systolic BP (SBP>90) “wet and warm” profile
Vasodilator Dosing
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
Side effects Headache hypotension
Inotropic Use in Acute HF
Adapted from Dorn; Circulation 2004
Dobutamine
Levosimendan
MilrinonePDE
Inotropes and Harm
Increased mortality through variety mechanisms Can exacerbate underlying ischemia or
malignant arrhythmias Increase contractility at the expense of
increased oxygen demand Direct toxic effect to myocardium
Accelerated apoptosis
Role of Inotropic Therapy
Reserved for those with low output HF “wet and cold” Marginal BP: Evidence of poor tissue
perfusion Symptomatic hypotension despite
adequate filling pressures Poor response to diuretics with worsening
renal function Unresponsive or intolerant to vasodilators
Inotrope Dosing
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
Side Effects Arrhythmias Alterations in blood pressure Cardiac ischemia Vein toxicity if high doses infused in peripheral vein
When to Use Intravenous Vasoactive Medications?
Inotropes: “cold and wet” Poor perfusion,
diuretic resistance Short term and
lowest doses No evidence that
one is superior to another
IV vasodilators as BP allows “wet and warm” Best benefit when
acute dyspnea/pulmonary edema, HTN
Invasive monitoring needed if nitroprusside considered
What about oral HF medications? Beta blockers
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 ACE Inhibitors
Dose usually maintained unless significantly hypotensive or acute renal failure
Dose escalation ok once acute symptoms improved (if no worsening renal function)
Digoxin Dose maintained unless digoxin toxicity
Acute HF: Summary
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
Recommended