Heart failure
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Heart Failure. By:Dawit Ayele ( MD,Internist ). Definition. “ Heart (or cardiac) failure is the pathophysiological state in which the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only

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Heart Failure

By:DawitAyele(MD,Internist)


Definition

  • “Heart (or cardiac) failure is the pathophysiological state in which

  • the heart is unable to pump blood at a rate commensurate with

  • the requirements of the metabolizing tissues or can do so only

  • from an elevated filling pressure.”

  • - Eugene Braunwald

  • “Congestive heart failure (CHF) represents a complex clinical

  • syndrome characterized by abnormalities of left ventricular

  • function and neurohormonal regulation, which are accompanied

  • by effort intolerance, fluid retention, and reduced longevity”

  • - Milton Packer


Heart Failure: Epidemiology

􀁺 Burden of CHF is staggering

􀁺 5 million in US (1.5% of all adults)

􀁺 500,000 cases annually

􀁺 In the elderly

􀁺 6-10% prevalence

􀁺 80% hospitalized with HF

􀁺 250,000 death/year attributable to CHF

􀁺 $38 billion (5.4% of healthcare cost)


Underlying Etiologies

  • Alcohol--

  • Diabetes—

  • Cardiomyopathies

  • Coronary artery disease-

  • HTN--both

  • Valvular heart disease (especially aorta and mitral disease)--chronic

  • Congenital


Precepitating factors

  • Infection

  • Arrhythmia

  • Physical,Fluid,Dietary,Env’tal,Emotional excess

  • MI

  • Anemia

  • Pulmonary embolism

  • Worsening of HTN

  • Thyrotoxicosis

  • Infective endocarditis

  • Rheumatic,viral or other myocarditis..


Forms of Heart Failure

  • SYSTOLIC VERSUS DIASTOLIC FAILURE

  • LOW-OUTPUT VERSUS HIGH-OUTPUT HEART FAILURE

  • ACUTE VERSUS CHRONIC HEART FAILURE

  • RIGHT-SIDED VERSUS LEFT-SIDED HEART FAILURE

  • BACKWARD VERSUS FORWARD HEART FAILURE


Typical presentations of heart failure

  • 1. Syndrome of decrease exercise tolerance

  • 2. Syndrome of fluid retention

  • 3. No symptoms but incidental discovery of LV

  • dysfunction


Heart Failure is a Clinical Diagnosis

  • 􀁺 Minor Criteria

  • 􀁺 Ankle edema

  • 􀁺 Night cough

  • 􀁺 Exertionaldyspnea

  • 􀁺 Hepatomegaly

  • 􀁺 Pleural effusion

  • 􀁺 Tachycardia (>120)

  • 􀁺 Decrease VC

  • 􀁺 Weight loss with CHF tx

  • Framingham Criteria

  • Major Criteria

  • 􀁺 Orthopnea/PND

  • 􀁺 Venous distension

  • 􀁺 Rales

  • 􀁺 Cardiomegaly

  • 􀁺 Acute pulm edema

  • 􀁺 Elevated JVP

  • 􀁺 HJR

  • 􀁺 Circ time >25s


NYHA Class

􀁺

  • Class I: Symptoms with more than ordinary activity

  • Class II: Symptoms with ordinary activity

  • Class III: Symptoms with minimal activity

  • Class IIIa: No dyspnea at rest

  • Class IIIb: Recent dyspnea at rest

  • Class IV: Symptoms at rest


Stages of Heart Failure

At Risk for Heart Failure:

STAGE A High risk for developing HF

  • STAGE B Asymptomatic LV dysfunction

  • Heart Failure:

  • STAGE C Past or current symptoms of HF

  • STAGE D End-stage HF


Stages of Heart Failure

  • Designed to emphasize preventability of HF

  • Designed to recognize the progressive nature of LV dysfunction


Stages of Heart Failure

  • COMPLEMENT, DO NOT REPLACE NYHA CLASSES

  • NYHA Classes - shift back/forth in individual patient (in response to Rx and/or progression of disease)

  • Stages - progress in one direction due to cardiac remodeling


  • Left Ventricular Failure with PE

    • When pressure becomes too high, the fluid portion of the blood is forced into the alveoli.

    • decreased oxygenation capacity of the lungs

    • AMI common with LVF, suspect

    • Occurs when the left ventricle fails as an effective forward pump

    • back pressure of blood into the pulmonary circulation

    •  pulmonary edema

    • Cannot eject all of the blood delivered from the right heart.

    • Left atrial pressure rises  increased pressure in the pulmonary veins and capillaries


    Signs and Symptoms of LVF

    • Diaphoresis—

      • Results from sympathetic stimulation

    • Pulmonary congestion

      • Often present

      • Rales—especially at the bases.

      • Rhonchi—associated with fluid in the larger airways indicative of severe failure

      • Wheezes—response to airway spasm

    • Severe resp. distress–

      • Evidenced by orthopnea, dyspnea

      • Hx of paroxysmal nocturnal dyspnea.

    • Severe apprehension, agitation, confusion—

      • Resulting from hypoxia

      • Feels like he/she is smothering

    • Cyanosis—


    • Jugular Venous Distention—not directly related to LVF.

      • Comes from back pressure building from right heart into venous circulation

    • Vital Signs—

      • Significant increase in sympathetic discharge to compensate.

      • BP—elevated

      • Pulse rate—elevated to compensate for decreased stroke volume.

      • Respirations—rapid and labored


    Compensatory Mechanisms in CHF

    • Neurohormonalsystem

    • Renin-angiotensin-aldosteronesystem

    • Ventricular hypertrophy


    Neurohormonal Activation Contributes to the Progression of CHF

    Myocardial Disease

    Impedance

    LV Dysfunction

    LV RemodelingVascular Remodeling

    Vasoconstriction

    Neurohormonal Activation

    Renal Blood Flow

    Preload

    Na Retention


    Renin-Angiotensin Mechanism

    • Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys

      • Aldosterone is released  increase in Na+ retention  water retention

      • Preload increases

      • Worsening failure


    Ventricular Hypertrophy

    • Long term compensatory mechanism

    • Increases in size due to increase in work load ie skeletal muscle


    Patient approach & Mgt

    • Principles:thoroughHx & P/E

    • Supplemental investigations especially:BNP,ECG,Echocardiography,CXR

    • Management:(1) general measures;

      (2) correction of the underlying cause;

      (3) removal of the precipitating cause;

      (4) prevention of deterioration of cardiac function; and

      (5) control of the congestive HF state


    Heart Failure: Disease Management

    Control Volume Slow Disease Progression

    +

    Diuretic

    RAAS

    Inhibition

    Beta-Blockade

    Treat residual

    symptoms

    DIGOXIN

    SPIRONOLACTONE

    Am J Cardiol 1999;83(suppl 2A):9A-38A


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