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)

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Pulmonary congestion

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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