Heart Failure

Definition

• structural or functional CD• impairs the blood filling/ejecting ability

of ventricles• inability to maintain the metabolic needs

of the body

CausesHeart performance (CO) depends on:• Contractility• Preload• Afterload• Heart Rate

Causes:• Abnormal loading conditions• Abnormal muscle function• Conditions that limit

ventricular filling

Congenital defects Valvular heart diseases Septal defects Hypertension Myocardial infarction Myocarditis Cardiomyopathy Alcoholism Mitral or tricuspid stenosis Pericarditis Ischaemic heart disease Drugs Thyrotoxicosis

CO = SV x HR

Classifications

Backward Failure Forward Failure

High Output

Low Output

RSHF LSHF

Acute vs. ChronicAcute

• Develops rapidly • Can be immediately life

threatening• Dramatic drop in cardiac

output• May be new (e.g. acute MI,

sepsis) or an exacerbation of chronic disease

Chronic

• Long term• More insidious• Associated with the heart

undergoing adaptive responses (e.g. dilation, hypetrophy) to a precipitating cause

Symptoms

• Fatigue• Activity decrease• Cough (especially supine)• Edema• Shortness of breath

SymptomsRVF– Fatigue– Weakness– Lethargy– Weight gain– Anorexia – RUQ pain– Hepatomegaly– Neck vein pulsations– Jugular veinous

distension– Pitting edema

LVF– Fatigue – Anxiety– Insomnia– Tachycardia– Gallop heart sounds (S3,

S4)– Pulmonary crackles,

rales– Orthopnea PND– Cheyne Stokes– Cough

Pathophysiology

Compensatory mechanism:1. Hemodynamic alterations2. Neurohormonal responses (SNS, RAAS, Vasopressin) 3. Ventricular dilation 4. Ventricular hypertrophy

Response Short-Term Effects

Long-Term Effects

Salt and Water Retention Augments preload Pulmonary Congestion, Anasarca

Vasoconstriction Maintains BP for perfusion of vital organs

Exacerbates pump dysfunction (excessive afterload), increases cardiac energy expenditure

Simpathetic stimulation Increases HR and ejection Increases energy expenditure

Frank-Starling Mechanism

• The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

• In heart failure, there is a compensatory increase in venous return which is augmented by neurohormonal mechanisms.

• Due to increase in venous return, there is a temporary increase in stroke volume.

Diagnostic Studies

• X-ray (Kerley B lines)• ECG• Echocardiography (EF)• Laboratory data (cardiac enzymes, BNP, serum

chemistries ,liver function studies ,thyroid function studies and complete blood count)

• Stress testing (exercise or medicine)• Cardiac catheterization- determine heart

pressures ( inc.PAW )

ECG

ECG findings are not diagnostic, but:• Old MI or recent MI• Arrhythmia• Some forms of tachycardia related

cardiomyopathies• LBBB

Approach to the Patient with HF

• Diagnose– Etiology– Severity (LV dysfunction)

• Initiate– Diuretic/ACE inhibitor– -blocker– Spirololactone– Digoxin

• Educate– Diet– Exercise– Lifestyle– CV Risk

• Titrate– Optimize ACE inhibitor– Optimize -blocker