congestive heart failure ppt

1. CONGESTIVE HEART FAILURE
Priyanka priyadarsani nayak
M.PHARM
R.NO:256215887006
ADVANCES IN PHARMACOLOGY

2. NORMAL HEALTHY HEART
♥ Muscle
♥ Four Chambers
♥ Four Valves
♥ Vena Cava – O2 poor
♥ Pulmonary Veins – O2
rich
♥ Aorta

3. ION MOVEMENT IN CARDIAC MUSCLE

4. CONGESTIVE HEART FAILURE
 Congestive heart failure is a
major contributor to morbidity
and mortality worldwide.
 Congestive heart
failure(CHF)is a condition in
which the heart is unable to
pump sufficient blood to meet
the needs of the body.
 CHF can be caused by an
impaired abillity of the cardiac
muscle to contract or by an
increased workload imposed
on the heart.

6. SYMPTOMS

7. SYMPTOMS

8. CONGESTIVE HEART FAILURE
TYPES
1.Left-sided heart failure
 There are two types of left-sided heart failure
 Systolic dysfunction
 Diastolic dysfunction
2.Right-sided heart failure

9. TYPES OF HEART FAILURE
Systolic dysfunction
(contraction) 2/3 of patients
The heart becomes weak and
enlarged.
The weakened muscle can’t contract.
Not enough blood is pumped from the
chambers.
Diastolic
dysfunction(relaxation)
Chambers don’t fill up so less blood
pumped to the lungs and body.
 Stiff heart muscle can’t relax.
Not enough blood fills the chambers.

11. PATHO PHYSIOLOGICAL MECHANISMS OF
HEART

12. DRUG TREATMENT FOR CHF
TREATMENT FOR CONGESTIVE HEART FAILURE

13. DRUGS FOR CHF
1.Inotropic
drugs
Eg:digoxin
dobutamine
Dopamine
Amrinone
milrinone
2.Diuretics
Eg:furosemide,
thiazides. 3.RAS
inhibitors
Eg:ACE
inhibitors,
ARBs
4.Vasodilators
Eg:
hydralazine
Nitrate
Nitroprusside
5.β-blockers
Eg:metoprol
olbisoprolol
carvedilol
6.Aldosteron
e antagonist
Eg:spironola
ctone,eplere
none

14. CARDIAC GLYCOSIDES(DIGITALIS)
 These are glycosidic drugs having
cardiac inotropic property.
 The cardiac glycosides are often called
digitalis or digitalis glycosides because
most of the drugs come 'from the
digitalis (foxglove) plant.
 They are a group of chemically similar
compounds that can increase the
contractility of the heart muscle and are
therefore widely used in treating heart
failure.
• The cardiac glycosides influence the
sodium and calcium ion flows in the
cardiac muscle, there by increasing
contraction of the atrial and ventricular
myocardium (positive inotropic
action).

15. MOA OF CARDIAC GLYCOSIDES

16. EFFECTS OF DIGITALIS ON
HEART

17. PHARMACOKINETIC FEATURES OF
DIGOXIN
1.Oral absorption: 60-80%
2.Plasma protein binding: 25%
3.Time course of action :
-Onset:15-30 min
-Peak :2-5 hr
-Duration :2-6 days
4.Plasma t1/2:40 hr
5.Therapeutic concentration:0.5-1.4 ng/ml
6.Toxic concentration:> 2ng/ml
7.Daily maintenance dose:0.125-0.5 mg
8.Daily elimination:35%
9.Route of elimination:Renal excretion
10.Route of administration:oral,I.V.

18. DIGITALIS TOXICITY EFFECTS
1.Extra cardiac:
 Anorexia ,nausea,vomiting.
 Fatigue,malaise,headache,mental
confusion,restlessness,disorientation,psychosis,andvisual
disturbances.
2.Cardiac :
 Arrythmias,
 Nodal and ventricular extrasystoles
 Ventricular tachycardia
 Severe bradycardia,atrial extra systoles.

19. -ADRENERGIC AGONISTS
1.Dobutamine :
 β-Adrenergic stimulation improves cardiac performance by positive
inotropic effects and vasodilation.
 Dobutamine(2-8 μg/kg/min) is the most commonly used inotropic agent
other than digitalis.
 Dobutamine leads to an increase in intracellular CAMP, which results
in the activation of protein kinase.
 Slow calcium channels are one important site of phosphorylation by protein
kinase. When phosphorylated,the entry of calcium ion into the myocardial
cells increases,thus enhancing contraction.
 Dobutamine must be given by intravenous infusion, and is primarily used in
the treatment of acute heart failure.

20. 2.DOPAMINE
 Dopamine (3-10μg/kg/min by i.v infusion) has been used in
cardiogenic shock due to MI and other causes.
 Dopamine tends to increase after load,at high rates of
infusion(>5μg/kg/min).
 Low rates of dopamine infusion(2μg/kg/min) cause selective renal
vasodilation which improves renal perfusion and g.f.r.

21. -AGONIST MECHANISM OF
ACTION

22. PHOSPHODIESTERASE INHIBITORS
 Amrinone :
 This is a bipyridine derivative and it is a selective
phosphodiesterase-3(PDE3) inhibitor.
 Amrinone increases myocardial CAMP and transmembrane
influx of Calcium.
 The two most important actions of amrinone are positive
inotropy and direct vasodilation has been called an
‘inodilator’.
 T1/2:4-8hr
 Adverse effects:
Thrombocytopenia,nausea,diarrhoea,abdominal pain,liver
damage,fever and arrythmias.
 Milrinone :
 T1/2-40-80 min.

23. A.C.E INHIBITORS
 ACE inhibitors are the agents of choice in CHF and
are superior to other vasodilators.These drugs block
the enzyme that cleaves angiotensin I to form the
potent vasoconstrictor, angiotensin II.
 These agents also diminish the rate of bradykinin
inactivation.
 Eg:captopril(t1/2-2hr),enalapril,lisinopril,benzapril(t1/2-
10-12 hrs).
 By reducing circulating angiotensin II levels, ACE
inhibitors also decrease 'the secretion of aldosterone,
resulting in decreased sodium and water retention.

24. MOA OF A.C.E INHIBITORS

25. ADVERSE EFFECTS OF A.C.E
INHIBITORS
 These include postural hypotension, renal insufficiency,
hyperkalaemia, and a persistent dry cough.
 The potential of symptomatic hypotension with ACE inhibitor
therapy requires careful monitoring.
 ACE inhibitors should not be used in pregnant womens.

26. ANGIOTENSIN RECEPTOR-2
ANTAGONIST
 Losartan (t1/2-2 hr),candesartan(t1/2-8-12 hr),valsartan(t1/2-
6-9 hr).
 It inhibits the central and peripheral sympathetic
stimulation,release of aldosterone,vasoconstriction,salt and
water reabsorption.
 Adverse effects :
 Hypotension
 Hyperkalemia
 Headache
 Dizziness
 Upper G.I side effects .

27. DIURETICS
 Diuretics relieve pulmonary congestion and peripheral edema. These
agents are useful in reducing the symptoms of volume overload,
including orthopnea and paroxysmal nocturnal dyspnea.
 Diuretics decrease plasma volume and subsequently decrease venous
return to the heart (preload). This decreases the cardiac workload
and oxygen demand.
 Diuretics also decrease afterload by reducing plasma volume, thus
decreasing blood pressure.

28. VASODILATORS (DIRECT SMOOTH
MUSCLE RELAXNTS)
 Dilation of venous blood vessels leads to a decrease in cardiac
preload by increasing venous capacitance; arterial dilators
reduce systemic arteriolar resistance and decrease afterload.
 Nitrates are commonly employed venous dilators for patients
with congestive heart failure.
 If the patient is intolerant of ACE inhibitors, the combination
of hydralazine and isosorbide dinitrate is most commonly
used.
 Amlodipine and felodipine have less negative ionotropic
effect than other calcium channel blockers, and seem to
decrease sympathetic nervous activity.

29. ALDOSTERONE ANTAGONISTS
 In cases of severe heart failure low doses of
Spironolactone are added to the therapy while regularly
checking creatinine and electrolyte levels.
 Spironolactone is a weak diuretic. It blocks
aldosterone receptors in the distal renal tubules and
reduces increased aldosterone levels in CHF.
 In low doses (25 mg/24 h) Spironolactone potentiates
the effects of ACE inhibitors.It also saves K+ and Mg2+
and has anti- arrhythmic activity.
 Spironolactone prevents myocardial fibrosis, caused by
aldosterone, and in this way increases myocardial
contractility.
 Similar to spironolactone is another aldosterone
antagonist – Eplerenone.

30. WHAT CAN I DO TO PREVENT PROGRESSION
OF THE DISEASE?
♥ Become Conscious of Lifestyle Choices!
♥ Make Better Choices…
☺ Quit Smoking
☺ Reduce Weight
☺ Avoid Excess Alcohol and Drugs
☺ Exercise
☺ Take Medication

31. REFERENCES
1.Pharmacology 7th edition by RANG AND DALE.
2.The pharmacological basis of therapeutics by GOODMANN AND
GILMAN’S.
3.Modern pharmacology with clinical applications by LIPPINCOTT.
4.Essentials of medical pharmacology by KD TRIPATHI MD.

32. THANK
YOU