Congestive Heart Failure,

Prepared By Dr.Mustafa Click to edit Master subtitle style Alshehabat

3/20/12

Terminology
Heart Failure: The inability of the
heart to maintain an output adequate to maintain the metabolic demands of the body.

Pulmonary Edema: An abnormal

accumulation of fluid in the lungs.

CHF with Acute Pulmonary

Edema: Pulmonary Edema due to Heart

Failure (Cardiogenic Pulmonary Edema)

What is HF
Complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation.

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Pathophysiology
Main Causes of Heart Failure:

Ischemic Heart Disease (35-40%) Cardiomyopathy(dilated) (30-34%) Hypertension (15-20%) Valvular Heart Disease. Congenital Heart Disease. Alcohol and Drugs. Arrhythmias

Other Causes:

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Pathophysiological Changes in HF
Ventricular Dilatation. Myocyte Hypertrophy. Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction.

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Signs & Symptoms

Symptoms:
Exertional Dyspnoea Orthopnia Paraxysmal Nocturnal Dyspnoea

Signs:
Cardiomegaly Elevated Jugular Venous Pressure Tachycardia
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Classification of heart failure

I.

No limitation. Normal physical exercise doesnt cause fatigue, dyspnea or palpitations.

II. Mild limitation. Comfortable at rest but

normal physical activity produces fatigue, dyspnea or palpitations. gentle physical activity produces marked symptoms of HF. by any physical activity.

III. Marked limitation. Comfortable at rest but

IV. Symptoms of HF occur at rest and are

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Kussmauls Sign
This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also

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PMI
The apex beat, also called the point of

maximum impulse (PMI), is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt. The cardiac impulse is the result of the heart rotating, moving forward and striking against the chest wall during systole.

The normal apex beat can be palpated in the

precordium left 5th intercostal space, at the point of intersection with the left midclavicular 3/20/12 In children the apex beat occurs in the line.

Heart Sounds

S1 The first heart

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sound - S1 - is in time with the pulse in your carotid artery in your neck. The sound of the tricuspid valve

Edema
Bilateral lower extremity edema

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Hypertension
Hypertrophic Cardiomyopathy

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Compensatory Mechanisms
Increased Heart Rate
Sympathetic = Norepinephrine

Dilation
Frank Starling = Contractility

Neurohormonal
Redistribution of Blood to the Brain

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CHF Vicious Cycle

Low Output

Increased Preload

Increased Afterload

Norepinephrine

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Increased Salt Renin Angiotension I Angiotension II Aldosterone Vasoconstriction Renal Blood Flow

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Infiltration of Interstitial Space

l

Normal Microanatomy

Micro-anatomy with fluid movement.

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Acute Pulmonar y Edema

a true lifethreatening emergency
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Treatment

Prevention. Control of risk factors Life style Treat etiologic cause / aggravating factors Drug therapy Personal care. Team work

All

Selected patients

Revascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator) Ventricular resyncronization Ventricular assist devices

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Treatment Objectives Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms
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(Cost)

Treatment Pharmacologic Therapy

Diuretics ACE inhibitors Beta Blockers

Digitalis Spironolactone

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Diuretics Essential to control symptoms secondary to fluid retention

Prevent progression from HT to HF Spironolactone improves survival New research in progress

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Diuretics
Thiazides

Cortex

Inhibit active exchange of ClNa in the cortical diluting segment of the K-sparing ascending loop of Henle Inhibit reabsorption of Na in the distal convoluted and collecting tubule

Loop diuretics

Medull a
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Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle

Loop of Henle

Collecting tubule

Diuretics. Indications
1.

Symptomatic HF, with fluid retention

Edema Dyspnea Lung Rales Jugular distension Hepatomegaly Pulmonary edema (Xray)

AHA / ACC HF guidelines 2001 3/20/12 ESC HF guidelines 2001

Loop Diuretics / Thiazides. Practical Use

Start with variable dose. Titrate to achieve dry weight Monitor serum K+ at frequent intervals
Reduce dose when fluid retention is controlled

Teach the patient when, how to change dose Combine to overcome resistance Do not use alone
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Loop diuretics. Dose (mg)

Initial Bumetanide Furosemide Torsemide Maximum 0.5 to 1.0 / 12-24h 10 / day 20 to 40 / 12-24h 400 / day 10 to 20 / 12-24h 200 / day

3/20/12 AHA / ACC HF guidelines 2001

Thiazides, Loop Diuretics. Adverse Effects K+, Mg+ (15 - 60%) (sudden death ???) Na+

Stimulation of neurohormonal activity Hyperuricemia (15 - 40%)

Hypotension. Ototoxicity. Gastrointestinal.
Sharpe N. Heart failure. Martin Dunitz 2000;43 Kubo SH , et al. Am J Cardiol 1987;60:1322

3/20/12 MRFIT, JAMA 1982;248:1465

Alkalosis. Metabolic

ACE-i. Mechanism of Action VASOCONSTRICTI

ONALDOSTERONE
VASOPRESSIN SYMPATHE
Angiotensinogen TIC RENIN Angiotensin I

VASODILATATIO
PROSTAGLANDINS N Kininogen tPA
Kallikrein

BRADYKININ

A.C.E.
ANGIOTENSIN 3/20/12

Inhibito r

Kininase II Inactive
Fragments

ACE-I. Clinical Effects

Improve symptoms Reduce remodelling / Reduce hospitalization Improve survival

progression

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ACE-i. Indications

Symptomatic heart failure Asymptomatic ventricular - LVEF < 35 - 40 %

dysfunction

AHA / ACC HF guidelines 2001 3/20/12 ESC HF guidelines 2001

Selected high risk subgroups

ACE-I. Adverse Effects

Hypotension (1st dose effect) Worsening renal function Hyperkalemia Cough Angioedema

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ACE-I. Contraindications

Intolerance (angioedema, anuric renal

fail.)

Bilateral renal artery stenosis Pregnancy Renal insufficiency (creatinine > 3 mg/dl)

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-Adrenergic Blockers Mechanism of action

Density of 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic

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-Adrenergic Blockers Clinical Effects

Improve symptoms (only long term) Reduce remodelling / progression Reduce hospitalization Reduce sudden death Improve survival

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-Adrenergic Blockers Indications

Symptomatic heart failure Asymptomatic ventricular - LVEF < 35 - 40 %

dysfunction

AHA / ACC HF guidelines 2001 3/20/12 ESC HF guidelines 2001

After AMI

-Adrenergic Blockers Adverse Effects

Hypotension Fluid retention / worsening heart failure Fatigue Bradycardia / heart block

Review treatment (+/-diuretics, other drugs) Reduce dose Consider cardiac pacing
3/20/12 Discontinue beta blocker only in severe cases

Na-K ATPase
N K a+

Digitalis

Na-Ca Exchange
N Ca a+

++

Myofilaments

N a+

Ca

+
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++
CONTRACTILITY

Digitalis. Mechanism of Action

Blocks Na+ / K+ ATPase => Ca+ +

Inotropic effect Natriuresis Neurohormonal control

Plasma Noradrenaline Peripheral nervous system

activity
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RAAS activity
NEJM

Digitalis. Clinical Effects

Improve symptoms Modest reduction in hospitalization Does not improve survival

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Digitalis. Indications
When no adequate response to
ACE-i + diuretics + beta-blockers
AHA / ACC Guidelines 2001

In combination with ACE-i + diuretics

if persisting symptoms
ESC Guidelines 2001 3/20/12 AF,

to slow AV conduction

Aldosterone Inhibitors

Spironolactone
Competitive antagonist of the aldosterone receptor (myocardium, arterial walls,
kidney)

ALDOSTERON

E
Collagen

Retention Na+

Edema

Retention

deposition

H2O
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Arrhythmia

Fibrosis -

Spironolactone. Practical use

Do not use if hyperkalemia, renal insuf. Monitor serum K+ at frequent intervals Start ACE-i first Start with 25 mg / 24h If K+ >5.5 mmol/L, reduce to 25 mg / 48h If K+ is low or stable consider 50 mg / day
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New studies in progress

Angiotensin II Receptor Blockers (ARB)

Angiotensinoge n Other pathway AT1 s Receptor Blockers RENIN Angiotensin I AC ANGIOTENSIN II E REC AT1
Proliferative Action

EPT ORS

AT2

Vasoconstriction
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Vasodilatation Antiproliferative

NITRATES HEMODYNAMIC 1- VENOUS EFFECTS Pulmonary VASODILATATION Preload

congestion Ventricular size Vent. Wall stress MVO2

Cardiac Blood pressure

2- Coronary vasodilatation output

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Myocardial perfusion

Nitrates. Clinical Use

CHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency)

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Heart Transplant. Indications

Refractory cardiogenic shock Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities

Contraindications: age, severe comorbidity

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Heart Failure and Myocardial Ischemia

Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia

Angina No angina

coronary angio and revascularization

Search for ischemia and viability in all ? Coronary angiography in all ?

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HEART FAILURE MODELS

CONGESTIVE - Digoxin, Diurtics HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors

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THANK YOU

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