2. • The term heart failure literally means a condition in which the heart
is unable to pump sufficient amount of blood to meet the metabolic
demands of the body and also unable to receive it back because
every time after a systole, some residual blood remains in its
ventricles.
3.
4.
5.
6. Cardiac remodeling
• The most important intrinsic compensatory mechanism is myocardial hypertrophy with
the resultant increase in more spherical shape of the heart referred to as ‘ cardiac
remodelling’ which means type of dilatation other than that due to passage, stretch of
heart muscle
• During remodelling, there is proliferation of the connective tissue cells as well as of
abnormal myocardial cells under the influence of angiotensin II.
• Initially the increase in muscle mass helps to maintain cardiac performance. But after the
initial beneficial effects, hypertrophy can lead to ischaemic changes and alterations in
ventricular geometry
• The ventricular wall tension increases, mechanical performance decreases, blood in both
the ventricles is retained, which ultimately worsens the remodelling process. Over the time
myocyte in the failing heart die through apoptosis.
7. Phenomenon of decompensated heart
failure
• After certain period, the compensatory mechanisms become
exhausted, and increasingly ineffective, entering a vicious circle of
decompensation in which the compensatory mechanisms become
self-defeating.
• As the strain continues, total peripheral resistance and after load
increase, thereby decreasing the ejection fraction per heartbeat.
Preload is also increased in heart failure because of increased blood
volume and Venous tone.
30. Side effects of digoxin
NON CARDIAC SIDE EFFECTS
NAUSEA , VOMITING
ABDOMINAL PAIN
GYNECOMASTIA :BLOCK TESTOSTERONE RECEPTOR
YELLOW VISION (XANTHOPSIA)
HYPERKALEMIA
31. CARDIAC SIDE EFFECTS
● CAUSE VARIETY OF SIDE EFFECTS
● EXTRASYSTOLE (PREMATURE VENTRICULAR BEAT )
● VENTRICULAR FIBRILLATION DOC- LIGNOCAINE
● ATRIAL FIBRILLATION + AV NODE BLOCK
● COUPLED BEATS (BIGEMINY)
32. DIGOXIN TOXICITY
● No role of hemodialysis —--- as high Vd
● Avoid loop and thiazide diuretic as they cause hypokalemia—-- increase
digoxin toxicity
● Antidote of digoxin —- digibind —- 40 mg antibody neutralise 0.6 mg
digoxin
● In case of drug induced arrhythmia – if tachycardia occur –give KCL
If bradycardia occur – give
atropine
If SVT give —------------propranolol
● If arrhythmia is more serious — parenteral K and lidocaine
34. DRUG INTERACTION OF
DIGOXIN
● Loop and thiazide diuretics — cause hypokalemia — increase digoxin
toxicity
● P-gp inhibitors — inc. plasma conc. of digoxin
Quinidine
Verapamil
Amiodarone
Clarithromycin
Ketoconazole
● Clarithromycin and antacid—----- decrease absorption of digoxin from GIT
35. C/ I OF DIGOXIN
Hypokalemia increase digoxin toxicity
● In children below 10 yrs of age and elderly patients
● MI patients
● Hypothyroidism
● Wolff parkinson white syndrome
● High cardiac output heart failure
● Av node block
● Renal failure patients
37. NOR EPINEPHRINE
● Given i/v
● Act on all alpha and beta receptor —-
● DOC —Acute decompensated heart failure + hypotension (SBP<85 mmHg )
● Act on beta 1 receptor —increase HR
● Act on alpha 1 receptor on BV —-vasoconstriction —-inc. BP
39. DOPAMINE
● ACT ON ALPHA , BETA 1 , D1 RECEPTOR DEPENDING ON CONC .
● At dose of – 1-2 ug/kg/min —---- +D1 renal VD
2-10 ug/kg/min—--- +B1 stimulate heart
>10 ug/kg/min —--- +_a2 cause vasoconstriction
● GIVEN IN ACUTE DECOMPENSATED HEART FAILURE WITH OLIGURIA
● ACT ON D1 RECEPTOR —--- VD in kidney —inc. GFR
40. PDE-3 INHIBITOR
● Inhibit degradation of cAMP
● In heart —- inotropic effect
● In BV —-VD
● SO THEY ARE KNOWN AS IONOPHORES
● Eg. milrinone , inamrinone , vesnarinone, enoximone
● Use – DOC in AHF due to beta blocker overdose
41. Levosimendan
● It has 3 actions —---- PDE 3 inhibitor
Calcium sensitizer (inc. binding of ca to troponin c )
K channel opener (cause vasodilation )
43. • DIURETICS:
• Loop diuretics like bumetanides and
furosemide promptly reduce pulmonary
oedema due to rapid diuresis which result in
the ECF , venous return, and subsequently
decrease in the right ventricular output.
44.
45. • Spironolactone ,being aldosterone antagonist, enhances diuresis by
promoting Na+ and water excretion (while retaining k+) and prevents
myocardial as well as vascular fibrosis which is responsible for
pathological remodeling of heart .
• Thiazide diuretics (hydrochlorothiazide and metolazone) are used
less frequently in HF . However, in advanced CHF , after chronic use,
resistance develops to loop diuretics .
46. • ACE inhibitors
• It is considered as first choice in management of HF.
• Action: block conversion of Ang1 to ang2
: prevent breakdown of bradykinin to promote
vasodilation
:decrease aldosterone secretion.
:it prolong the survival by preventing pathological remodeling
of heart and blood vessel.
:reduce death rate due to arrythmias.
47. • Drugs : Ramipril, enalapril,
lisinopril, etc.
• Combination of ACE
inhibitors with
spironolactone provides
more beneficial and reduce
mortality.
48. BETA BLOCKER
• Certain beta blockers like
bisoprolol, carvedilol and
metoprolol, improve
ventricular function and
prolong the survival in
these patients.
49. Other HF drugs and guideline
for management of heart
failure
50. VASODILATORS
• Reduce pulmonary congestion and increase cardiac output by
reducing preload and afterload .
•
• Arterial dilator venodilator dilator
• hydralazine nitroglycerine and
• other
10/9/2021 PRESENTATION TITLE 50
52. • In patient of heart failure with dyspnea, venodilator like
nitroglycerine are preferred.
• But, in patient having low ventricular output arteriolar dilator
such as hydralazine is preferred.
• NESIRITIDE- recombinant form of human B type natriuretic
peptide, has been introduced for acute HF. It increases cGMP in
vascular smooth muscle and therefore reduces venous as well
as arteriolar tone.
• It used in patient of acutely decompensated HF.
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53. • VASOPRESSIN receptor antagonist :
• 1. conivaptan : mixed V1 + V2 antagonists , has been approved
for patients having acute heart failure with hyponatremia.
• 2. tolvaptan: oral V2antagonist.
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54. • VERICIGUAT:
• It stimulates soluble guanylate cyclase , which catalyse
cGMP production.
• USE: for adults with symptomatic, chronic heart failure.
• Adverse effect: nausea, vomiting, hypotension, anemia and
allergic reaction.
10/9/2021 PRESENTATION TITLE 54
55.
56. • Other silent feature or guideline-
• For hypokalemia due to ACEIs , potassium binder like patiromer
and sodium zirconium can be used to improve outcome.
• For patient with symptomatic stable chronic heart failure :
• Ivabradin can be beneficial to reduce HF hospitalization and
CVS death.
10/9/2021 PRESENTATION TITLE 56
