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CRP 2 KCP 1 & 2 > Drugs for CHF > Flashcards

Drugs for CHF Flashcards

1
Q

What are the drug classes suitable to treat heart failure?

A
  1. Neurohumoral modulation
    ACEI enalapril
    ARB losartan
    Aldosterone antagonists/K sparing diuretics spironolactone
    Beta-adrenergic receptor blockers metoprolol
  2. Preload reduction
    Diuretics ( loop diuretics furosemide, thiazide diuretics hydrochlorothiazide, aldosterone antagonist, natriuretic peptide recombinant BNP called nesiritide)
  3. Afterload reduction
    Direct Vasodilators hydralazine
    Nitrates isosorbide dinitrate, GTN aka nitroglycerin/glyceryl trinitrate
  4. Inotropic agents
    cAMP-dependent inotropes/bipyridines milrinone
    Myofilament Ca2+ sensitizers levosimendan
    Cardiac Glycosides digoxin/digitalis
    Sympathomimetics/beta agonists dobutamine/dopamine
  5. Heart rate reduction
    Direct bradycardiac agent/ Selective sinus node inhibitor/ funny channel inhibitor ivabradine
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2
Q

Types of heart failure

A
  1. acute/decompensated vs chronic
  2. R vs L
  3. Systolic (HFrEF) vs diastolic (HFpEF)
  4. High output vs low output
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3
Q

Selective inhibitor of cardiac pacemaker channels/If current : Ivabradine>bradycardiac agent

A

treatment for HF and stable angina pectoris in pt who cannot tolerate beta blockers/beta blockers did not sufficiently lower HR

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4
Q

Pharmacokinetics of digoxin

A

Distribution
Large Vd due to tissue protein binding, need loading dose
Metabolism & Excretion
Not extensively metabolised
Need dosage adjustment for renal impaired pt

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5
Q

MOA, therapeutic use & side effect of dobutamine

A

MOA
selective beta 1 agonist at heart
Therapeutic use
beta adrenergic agonist for pt with acute CHF with systolic dysfunction
Side effects
Tachycardia
Increase myocardium oxygen consumption

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6
Q

MOA, pharmacological effects, therapeutic uses & adverse effects of aldosterone antagonist: Spironolactone

A

MOA
block aldosterone in collecting tube
Pharmacological effects
decrease Na retention and decrease K excretion
reduce HF mortality
Therapeutic uses
avoid K+ loss
enhance natriuretic effects of diuretics
delay cardiac remodelling
AE
Hyperkalemia
gynaecomastia

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7
Q

MOA, pharmacological effects, therapeutic effects & adverse effects of thaizide diuretics: hydrochlorothiazide

A

MOA
inhibits Na-Cl symporter in DCT
water and sodium loss
vasodilatation
Pharmacological effects
diuresis (salt & water loss)
decrease in BV, preload and venous return
Therapeutic uses
mild HF to reduce fluid overload and relieve edema
AE
hypokalemia
+digitalis=digitalis toxicity
Mg depletion
impair glucose tolerance
increase serum lipid
increase uric acid=gout

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8
Q

MOA, pharmacological effects, therapeutic effects & adverse effects of loop diuretics: Furosemide/frusemide (IV route) MOST POTENT DRUG OF ITS CLASS

A

MOA
block Na/K/2Cl transporter in renal loop of Henle
pharmacological effects
reduce BV, greater efficacy in pulling water out of body
therapeutic effects
-mod to severe HF: reduce severe congestion, breathlessness and peripheral edema
-acute pulmonary edema (LVHF) :venodilatation
AE
electrolyte imbalance
dehydration
hypokalaemia

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9
Q

MOA, pharmacological effects, therapeutic & adverse effects of natriuretic peptide: Nesiritide

A

recombinant brain natriuretic peptide
MOA & pharmacological effects
increase cGMP in smooth muscle cells
vasodilatation/reduce venous and arteriolar tone
diuresis
Therapeutic effects
acute HF

**short half-life

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10
Q

MOA, pharmacological effects, therapeutic & adverse effects of cardiac glycosides: digoxin/digitalis

A

MOA of inotropic action
inhibit cardiac Na/K ATPase pump
increase intracellular Na and Ca
reduce Na/Ca exchange
increase Ca release from sarcoplasmic reticulum
increase FOC & CO
Pharmacological effects
Cardiac effects:
-mechanical: increase CO
-electrical: low conc will reduce HR, high conc will increase excitability and cause arrhythymia (AE)
Extra cardiac effects:
-GIT m/c site for digitalis toxicity (anorexia, nausea, vomiting and diarrhea)
-CNS effects: visual disturbances & vomiting
-Gynaecomastia
Interactions with electrolytes:
-hypokalemia, hypercalemia, hypomagnesaemia (worsen CG toxicity)
Therapeutic uses
-Cardiac failure: improve exercise tolerance
-Atrial arrhythmias eg Afib and AFL(SVT): delay AV conduction, control ventricular rate
AE
-cardiac: extreme bradycardia, Afib, AV block in healthy person. CG toxicity like ventricular extrasystoles, ventricular tachycardia and fib in pt with structural heart disease
CI: Vtach

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11
Q

MOA, pharmacological effects and adverse effects of ACEI: Enalapril

A

MOA
Inhibits ACE which converts Angiotensin I to Angiotensin II
Decrease Angiotensin II
Decrease vasoconstriction
Decrease aldosterone
Pharmacological effects
Decrease preload & afterload
Decrease TPR
Decrease cardiac workload
Decrease salt and H2O retention
AE
First dose hypotension
Hyperkalemia
Angioedema
Dry cough

**prevent cardiac remodelling process, especially after MI
**delay diabetic nephropathy

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12
Q

MOA, pharmacological effects & adverse effects of beta adrenergic antagonists: Metoprolol

A

can only be used in chronic stable HF, not in acute HF
MOA
reduce harmful compensatory mechanisms of high background sympathetic tone in CHF
prevent NE excess

pharm effect and AE not stated

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13
Q

MOA, pharmacological effects & adverse effects of ARB: Losartan

A

MOA
Block angiotensin receptors
vasodilation
decrease aldosterone
Pharmacological effects
decrease afterload & preload
decrease TPR
decrease salt & H2O retention
decrease cardiac workload
AE
First dose HoTN
Hyperkalemia
Angioedema

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14
Q

MOA of Dopamine

A

-Low dose infusion: direct stimulation of D2 receptors to increase renal BF & maintain adequate GFR, causing diuresis
-Intermediate dose: stimulate cardiac beta1 receptors, enhancing myocardial contractility
-High dose: alpha receptor stimulation, causing peripheral arterial & venous constriction

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15
Q

MOA of calcium sensitizer: levosimendan

A

cardiac inotropic: sensitizes troponin C to Ca, inhibit PDE
vasodilator: opens ATP-sensitive K channels on vascular smooth muscle, vasodilating coronary & systemic vessels

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16
Q

MOA of bipyridines: Milrinone

A

inhibits phosphodiesterase isozyme 3 (PDE-3)
decrease cAMP degradation
increase cAMP
positive inotropic & chronotropic effects in heart increase contractility
decrease preload & afterload vasodilatation

17
Q

MOA & adverse effects of nitrates: glyceryl trinitrate, isosorbide dinitrate

A

MOA
venous pooling
reduce diastolic filling pressure/preload
AE
HoTN
dizziness
headache
DLE

18
Q

MOA & adverse effects of direct vasodilators: hydralazine

A

MOA
direct arteriolar dilator
**prevent nitrate tolerance
**low cost and availability
AE
HoTN
dizziness
headache
DLE

19
Q

Management of digoxin toxicity
1. bradycardia
2. Vtach arrhythmias & low K

A

-STOP Dose reduction/cessation of med [Early signs of toxicity]
-CHANGE Atropine/temp pacemaker [ for extreme sinus bradycardia, sinoatrial block]
-ADD K+ infusion, digibind [for tachycardic ventricular arrthymias & hypokalemia]

GIT most common toxicvity
**electrolyte interactions and caution with diuretics(K+ loss)

*low con: low HR
high con: arrhythmia

20
Q

Management of acute HF/ acute pulmonary edema

A

sit pt up to reduce preload
give high-flow O2 to correct hypoxia
ensure continuous positive airway pressure (CPAP) of 5-10mmHg by tight-fitting mask to reduce preload & pulmonary capillary hydraulic gradient
administer nitrates: IV/ buccal GTN to reduce preload & afterload
administer loop diuretic: furosemide to combat fluid overload

side note: hypercapnic cannot give 100% O2

21
Q

Drugs involved in preload reduction (Treatment principle II) for HF

A
  1. Loop diuretics: Frusemide/furosemide
  2. Thiazide diuretics: Hydrochlorothiazide
  3. K+ sparing diuretics/mineralcorticoid receptor antagonist/aldosterone blocker: Spironolactone
  4. Natriuretic peptide: Nesiritide
22
Q

Drugs involved in neurohumoral modulation (treatment principle I) for HF

A
  1. ACEI: Enalapril
  2. ARB: Losartan
  3. Beta adrenergic receptor antagonist: Metoprolol
  4. Mineralcorticoid receptor antagonist/aldosterone blocker: Spironolactone
23
Q

Drugs involved in increasing cardiac contractility/inotropic agents (treatment principle IV) for HF

A
  1. cAMP-dependent inotropes/dipyridines: Milrinone
  2. Myofilament Ca2+ Sensitizers: Levosimendan
  3. Cardiac glycosides: Digoxin/Digitalis
  4. Sympathomimetics/beta agonist: Dopamine/dobutamine

**Dobutamine is a synthetic catecholamine, which means it is chemically similar to naturally occurring neurotransmitters like epinephrine (adrenaline) and norepinephrine (noradrenaline). Dopamine is a naturally occurring neurotransmitter in the body that plays various roles in the brain and the cardiovascular system.

24
Q

Drugs involved in heart rate reduction (treatment principle V) for HF

A
  1. Direct bradycardia agent/ selective sinus node inhibitor/ funny channel inhibitor: Ivabradine
25
Q

Drugs involved in afterload reduction (treatment principle III) for HF

A
  1. Direct vasodilators: Hydralazine
  2. Nitrates: Glyceryl trinitrate, isosorbide dinitrate
26
Q

Benefits of digoxin in HF

A

Positive Inotropic Effect
Increase CO: peripheral vascular resistance drop
Decrease preload & afterload
Reduce chamber dilation & wall stress
Increase Renal Perfusion
Decrease renin production
Increase diuresis
Decrease preload

CRP 2 KCP 1 & 2 (8 decks)

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