current updates on heart failure

1.  A clinical syndrome in which heart disease
reduces cardiac output, increases venous
pressures, and is accompanied by molecular
abnormalities that cause progressive
deterioration of the failing heart and premature
myocardial cell death.

2.  Impaired myocardial contractility
 Increased ventricular stiffness or impaired
myocardial relaxation
 Others:
• valve disease
• Intra cardiac shunting
• Disorders of heart rate or rhythm
• Increased peripheral blood flow or metabolic
requirements

3. • Infection
• Anemia
• Hypertension
• Myocardial infarction
• Thyrotoxicosis
• Pulmonary infarction
• Pregnancy
• Arrhythmia
• Myocarditis
• Endocarditis

4. Adaptive mechanisms
1. Frank-Starling mechanism
2. Activation of neurohormonal systems
3. Augmented mass of contractile tissue
(remodeling)
 The first 2 occur over minutes to hours, remodeling
develops slowly (weeks to months)

5. ↓ Ventricular
ejection
►↑ residual
volume
►↑tension in non
injured part
►augmented
contraction

6. 1. Sympathetic NS.
• Generally adrenergic activation & parasympathetic
withdrawal i.e. ↑ nor epinephrine (NE)
Adaptive role of nor epinephrine
↑ heart rate, contractility, renin release &
vasoconstriction
• Depleted cardiac NE stores & beta-adrenergic
density

7.  NE loss of adrenergic support
 contractility
 chronotropic response
Arrhythmia
energy demand
remodeling
cardiac dysfunction

9. 2. Rennin angiotensin aldosterone system
Mechanisms of activation
 renal hypoperfusion
 β - adrenergic stimulation
 hyponatremia.
3. Atrial & brain natriuretic peptide
4. Peptides e.g. endothelin
5. Cytokines

10.  vasoconstriction depresses LV function
 Sodium retention worsens the already elevated
ventricular filling pressure
 Direct effects of norepinephrine, angiotensin II,
aldosterone & others on the myocardium →
remodeling

11. The ventricle is altered in structure and shape
so that its mass is increased, and its chamber
volume is increased or both.
Causes
• ↑ wall stress
• direct toxic effect of hormones on myocytes

12. inability of the
ventricle to contract
 cardiac
output
 filling pressure
exercise
intolerance dyspnea
Manifestations of heart failure

13.  Dyspnea
 Orthopnea
 Paroxysmal Nocturnal Dyspnea
 Fatigue and weakness
Cheyne-Stokes respiration
Physical Findings
 ↑ JVP or positive hepato jugular reflux
 S3 gallop
 pulmonary rales
 Edema

14. I No limitation of physical activity
II Slight limitation of physical activity
- ordinary physical activity results in symptoms
IIIMarked limitation of physical activity
- comfortable at rest
- less than ordinary physical activity results in symptoms
IVInability to carryout any physical activity without
discomfort
- symptoms may be present even at rest

15.  Stage A
 At high risk for heart failure but without structural heart disease
or symptoms of HF
 Stage B
 Structural heart disease but without signs or symptoms of HF
 Stage C
 Structural heart disease with prior or current symptoms of HF
 Stage D
 Refractory HF requiring specialized interventions

16.  Chest X-ray
 Electrocardiography
 Echocardiography

17. Principle
• Removal of the precipitating cause
• Control of the heart failure state
• Correction of the cause
• Improve survival

18. Goals of treatment :
Decompensated HF
• to stabilize the patient
• to restore organ perfusion
• to return filling pressure to normal level
Chronic stable HF
• to minimize symptoms
• to enhance survival

19. General measures
 Moderate restriction of salt
 Fluid restriction
 Only in state of hyponatremia
 Exercise
 Should be encouraged
 Heavy labor should be prohibited
 Bed rest during acute decompensation

20. Specific interventions
I. Diuretics
1. Thiazides
 Inhibit selective reabsorbtion of NaCl in the distal cortical
diluting segment
 Decreased potency in patients with impaired renal function
Side effects
- Hypokalemia
- Metabolic alkalosis
- Hyperurecemia
- Hyperglycemia

21. 2. Loop diuretics
Furosemide
 Inhibits reabsorbtion of sodium chloride &
potassium in the thick ascending limb of loop of
Henle
 induces diuresis as high as ¼ of the GFR
3. Potassium sparing diuretics
 Shouldn’t be used in state of
 Hyperkalemia
 Renal failure
Spironolactone
Triametrine & amiloride

22. II. Digoxin
 Positive inotropic
 ↑ automaticity & ectopic activity
 ↑ effective refractory period at AV node
 Slow sinus rate

23. Drugs to antagonize neurohormones
(increase survival)
 Inhibit cardiotoxic effects of neurohormones
 Relieve symptoms by antagonizing vasoconstriction

24. ACE inhibitors
 angiotensin II formation
 ↑kinin
 Helpful in all patients with systolic dysfunction
Aldosterone inhibitors
Angiotensin I receptor blockers

25. Β – adrenergic receptor blockers
 Carvedilol, Metoprolol and Bisoprolol are proven
to increase survival

26. Standard pharmacologic therapy of heart
failure:
Diuretics
ACE inhibitors
Beta blockers
Combination of isosorbide dinitrate and hydralazine
Digoxin
 Aldosterone inhibitors