Heart Failure

1. Heart Failure

2. Definition
• structural or functional CD
• impairs the blood filling/ejecting ability
of ventricles
• inability to maintain the metabolic needs
of the body

3. Causes
Heart 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

4. Classifications
Backward Failure Forward Failure
High Output
Low Output
RSHF LSHF

5. Acute vs. Chronic
Acute
• 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

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

8. Symptoms
RVF
– 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

9. Pathophysiology
Compensatory mechanism:
1. Hemodynamic alterations
2. Neurohormonal responses (SNS, RAAS,
Vasopressin)
3. Ventricular dilation
4. Ventricular hypertrophy

10. 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

11. 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.

12. 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 )

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

14. 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