Congestive cardiac failure is defined as a chronic condition where the heart is unable to pump enough blood to meet the body's needs. It can be classified as systolic, diastolic, acute or chronic. Common causes include arrhythmias, myocardial infarction, hypertension, and obesity. Symptoms include fatigue, shortness of breath, and edema while signs include tachycardia and edema. Diagnosis involves tests such as ECG, echocardiogram, and blood tests. Management consists of medications like ACE inhibitors, diuretics, beta-blockers and lifestyle modifications like diet, exercise and smoking cessation.

1. CONGESTIVE CARDIAC FAILURE
PRESENTED BY
THUSHARA. C
1st YEAR M.PHARM
GRACE COLLEGE OF PHARM

2. CONTENTS
1. DEFINITION
2.CLASSIFICATION
3. ETIOLOGY
4.CLINICAL MANIFESTATION
5.PATHOPHYSIOLOGY
6.DIAGNOSIS
7.MANAGEMENT

3. DEFINITION
 Heart failure is defined as a chronic and
progressive condition where the heart
muscle is unable to pump enough blood
through the body to meet the body’s need for
blood and oxygen

4. CLASSIFICATION
 Systolic heart failure
 Diastolic heart failure
 Acute heart failure
 Chronic heart failure
 Left side heart failure
 Right side heart failure

5. ETIOLOGY
 Arrythmias
 Myocardial infraction
 Hypertension
 Anemia
 Atherosclerosis
 Infection
Obesity
Alcohol and tobaco use

6. CLINICAL MANIFESTATIONS
SYMPTOMS SIGNS
 Fatigue
 Weakness
 Shortness of Breath on
exertion
 Shortness of Breath at Rest
 Cough and wheezing
 Anorexia / loss of appetite
 Paroxymal nocturnal dyspnea
 Nausea
 Abdominal pain
 Nocturia
 Pulmonary edema
 Pleural effusion
 Tachycardia
 Narrow pulse pressure
 Cardiomegaly
 Peripheral edema
 Jugular vein distension

7. LABORATORY TESTS
 BNP > 100g/ml
 Electrocardiogram may be normal., or it could show
numberous
abnormalities include ST-T wave changes
Serum creatinine increased due to hypoperfusion
Complete blood count is useful to determining heart failure is
due to a reduced oxygen carrying capacity
 Chest x-ray useful for detecting cardiac enlargement,,
pulmonary edema and pleural effusion
 Hyponatremia: Serum sodium <130mEq/L is associated with
reduced survival and indicating worsening volume overload
and/or disease progression

8. PATHOPHYSIOLOGY

9. DIAGNOSIS
 Electrocardiogram (ECG)
 Chest x-ray
 Echocardiography (“Echo”)
 Heart catheterization
 Angiography
 Blood tests

10. MANAGEMENT
NON PHARMACOLOGICAL MANAGEMENT
 Bed rest
 Consuming small but frequent meals
 Moderate sodium restriction (2-4g/day)
 Smoking cessation
 Avoid alcohol intake

11. TREATMENT (MEDICATION)
 ACE Inhibitors
 Diuretics
 Inotropic Agents
 Beta Blockers
 Calcium Channel Blockers
 Vasodilators
 Digitalis glycosides
 Aldosterone antagonist
 Angiotensin receptor blockers
PHARMACOLOGICAL MANAEMEN

12. DIURETICS

13. THIAZIDES
 Hydrochlorothiazide, metolazone, chlorthalidone.
 Block sodium reabsorption in the cortical diluting segment at
the terminal portion of the loop of Henle and in the proximal
portion of the distal convoluted tubule
 Thiazides are ineffective when the GFR falls below 30–40
mL/min.
 Decrease preload and improve ventricular efficiency by
reducing circulating volume
 Remove peripheral edema and pulmonary congestion
 ADR: Hypokalaemia, hearing loss, Hypercalcaemia, Mg
depletion
GIT and CNS disturbances

14. LOOP DIURETICS
 Furosemide, bumetanide and torsemide.
 Rapid onset and a relatively short duration of
action
 Two or more doses are preferable to a single
larger dose.
 Inhibit chloride reabsorption in the ascending
limb of the loop of henle, which results in
natriuresis, and metabolic alkalosis.
 Increases systemic venous capacitance and
produce rapid symptomatic relief
 ADR: Hpokalaemia, alkalosis

15. POTASSIUM SPARING DIURESTICS
 Spironolactone, triamterene, and amiloride
 Spironolactone is a specific inhibitor of
aldosterone.

16. INHIBITORS OF THE
RENIN–ANGIOTENSIN–
ALDOSTERONE
SYSTEM

17. ACE Inhibitors
•Captoprill, enalaprill, isnoprill
• it inhibit angiotensin converting enzyme
•ACE inhibitors causes feed back increase in renin release resulting in ove
production of Ang1, since its conversion to Ang2 is blocked. Ang1 divert to
Produce more Ang(1-7) which produce vasodilation,
• Decrease in Ang2 and aldosterone attenuates many of the deleterious
effects
this neurohormones , including ventricular remodeling, myocardial
fibrosis,
cardiac hypertrophy , norepinephrine release, sodium and water retention
• ADR : Hypotension, renal insufficiency, dizziness, lightheadedness,
blurred vision, syncope, hyponatremia, hypovolemia, dry cough,
Angioedema
• Contraindicated during second and third trimester of pregnancy due to
increased risk of fetal renal failure.

18. ANGIOTENSIN RECEPTOR BLOCKERS
Losartan ,candesartan,valsartan
 Angiotensin 2 ,a vasocontrictor is concerned with ventricular remodelling
and fluid retention.
 These drugs inhibit the binding of angiotensin 2 to its AT₁ receptor.
 Thus they preclude the a bove mentioned effects of angiotensin 2.
 These agents do not exert any action on bradykinin and thus do not
produce cough.
 Has comparable effect to ACE I
 Can be used in certain conditions when ACE I are contraindicated
18
Adverse drug reactions
•Hypotension
•Impariment of renal functioning
Dose
Candesartan
•Initial: 4-8mg
•Targeted dose -32mg
Valsartan
•Initial:40mg
•Targeted dose -160mg

19. INOTROPES
 Increase force of contraction
 All increase intracellular cardiac Ca++ concentration
 Eg:
 Digitalis (cardiac glycoside)
 Dobutamine (β-adrenergic recepter agonist)
 Amrinone (PDE inhibitor)
19

20. DIGOXIN
20
 It inhibits the
 Functions in the exchange of Na⁺ for k⁺ ions.
 Such blockage results in intracellular
accumulation of Na⁺ ions .
 These ions are then exchanged with Ca₂⁺
ions through Na⁺ - Ca₂⁺ exchange carries.
 These ca₂⁺ ions increase the contractility of
the myocardium which is beneficial to the
failing heart.
 Digoxin enhances the cholinergic activity
which reduces the HR and AV conduction .
 Due to this the time required for diastolic
filling gets enhanced while the myocardial o2
consumption is retarted.
 The sympathetic outflow comprising renin,
aldosterone is also decreased by dioxin
inhibit Na +,K + ATPase , pump which

21. DRUG REACTION
 Bradycardia
 Nausea
 Vomiting
 Visual disturbances
 Non paroxysomal
junctional tachycardia
 Supraventricular
tachycardia
 Sexual dysfunction
 Neuralgic pain
USES:
 For tachyarrhythmias
 For ventricular
arrhythmias
21

22.  Dopamine acts at a variety of receptors (dose dependant)
 Rapid elimination- can only be administered as a continuous infusion
22
•Stimulates beta-adrenergic receptors and produces a positive
inotropic response.
•Unlike the vasoconstriction seen with high doses of dopamine,
dobutamine produces a mild vasodilatation
β -Adrenergic Agonists
DOPAMINE
DOBUTAMINE

23. Β ADRENERGIC AGONIST
23

24. Β1 BLOCKERS
MOA
 Heart failure is accompanied by
an increase activation of
sympathetic nervous system.
 This brings about structural &
functional modification in the
myocardium.
 β Blockers inhibit the
sympathetic outflow of
norepinephrine and counteract
the changes produced.
 The ventricular remodelling in
heart failure is also reversed by
β Blockers
 Increases beta receptor
sensitivity.
Adverse drug reaction
 Hypotension
 Bradycardia
 Worsening of CHFsymptoms.
24
bisoprolol, carvedilol , metoprolol

25.  Isosorbide dinitrate, isosorbide mononitrate, and hydralazine also used
specially in patients who cannot tolerate ACE inhibitors.
25
VASODILATO
RS

26. VASODILATOR(HYDRALAZINE)
 It directly relaxes the arterioles & arteries reducing the peripheral
vascular reesistances & preload.
 It also help to reduce after load.
Adverse drug reaction:
 Nausea
 Palpitation
 Tachycardia
 Salt & water retention on prolong therapy.
26

27. BIPYRIDINES
PHOSPHODIESTERASE INHIBITORS
 Targets PDE -3 (found in cardiac and smooth muscle)
 Ex. Inamrinone , milrinone
27
alter the intracellular
movements of calcium by
influencing the sarcoplasmic
reticulum
increasing inward
calcium flux
in the heart during
the
action potential
increase myocardial contractility
Inhibition of
PDE3
Increase in cAMP
the conversion of inactive protein
kinase to active form
Protein kinases are responsible for
phosphorylation of Ca channels
increased Ca entry into the cell
↑ Vascular Permeability leads to
↓ in intravascular fluid Volume
increase in
contractility
vasodilation

28. NITRATES & NITRITES
Nitroglycerin is denitrated by
glutathione S -transferase in smooth muscle
Free nitrite ion is released, which is then converted to
Nitric Oxide
activation of guanylyl cyclase enzyme
increase in cGMP
dephosphorylation of myosin light chain , preventing the
interaction of myosin with actin(Myosin light chain
kinase essential for smooth muscle contraction).
Results in vasodilation
28

29. CALCIUM CHANNEL BLOCKERS
 Verapamil, diltiazam, nefedipine
 It blocks the calcium channel and prevent the entry of calcium in to the
cell
 There by prevent the contraction and arterial dialation occur

30. The beneficial effects of spironolactone derive from the
direct and competitive blockade of specific aldosterone
receptors.
Aldosterone inhibitors therefore have three types of effects: -
 Diuretic effect, which is most noticeable when fluid retention
and
increased levels of aldosterone are present
Antiarrhythmic effect, mediated by the correction of
hypokalemia
and hypomagnesaemia.
Antifibrotic effect. This effect, demonstrated in animal models,
can
contribute to a decrease in the progression of structural changes
in
patients with heart failure.
ALDOSTERONE RECEPTOR ANTAGONIST
• EG: SPIRONOLACTONE

31. Stage A
At high risk of heart failure
but without structural heart disease
or symptoms of heart disease
Stage B
Structural heart disease,
but without sign or
symptoms of heart failure
Stage C
Structural heart disease
with prior or
symptoms of heart failure
Stage D
Refractory heart failure
requiring
specialized interactions
Patient with: HTN,
Atherosclerotic
disease
,DM,Obesity, family
history of
cardiomayopathy
Patients with:
Previous mayocardial
infraction,left ventricl
e remodelling, including
left ventricular
hypertrophy and low
ejection factor,valvular
disease
Patient with:
Known structural
heart disease and
shortness of
breath and
fatigue,
reduced exercise
tolerance
Patients with: patient
who are marked
symptoms at rest
despite
maximal medical
therapy,such as those
who are currently
hospitalised or cannot
be safely discharged
from the hospital
without specialised
intervention
Structura
l HF
Devol
epme
nt of
HF
sympt
oms
Therapy
Goals
•Treat HTN, lipid
disoders,
encourage
smoking
cessation,discour
age alcohol intake
•Drugs: ACE
inhibitor or ARB
in appropriate
patients for
vascular disease
or DM
Therapy
Goals: All measures
under stage A
Drugs: ACE inhibitor
or ARB in appropriate
patients
Βeta blocker in
appropriate patient
Therapy
Goals: All measures
under stage A
, B, dietary salt
restriction, drugs for
routine use,
Diuretics for fluid
retention,
ACE inhibitors, beta
blockers, ARB,
digitalis,hydrallazine or
Therapy
Goals: Appropriate
measures under
stages A,B,C
Descion based on
appropriate level of
care options
Compassionate end
of life care
Extraordinary
measures: heart
transpantation,