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
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
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.
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
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,
Notes de l'éditeur
Treatment of congestive heart failure.
Aldosterone inhibitors: Mechanism of action
Aldosterone acts directly on specific receptors. At the renal level it produces retention of sodium and water, resulting in an increase in preload and afterload, edema formation and the appearance of symptoms of pulmonary and systemic venous congestion. In addition, it increases the elimination of potassium and magnesium, creating an electrolyte imbalance which may be responsible in part for cardiac arrhythmias. At the tissue level, aldosterone stimulates the production of collagen, being in large part responsible for the fibrosis that is found in hypertrophied myocardium and in the arterial walls of patients with heart failure.