B: 14-16 Flashcards

1
Q

Pharmacotheraputic aims of Manangement of HF

A

↓ Preload
↓ Afterload
↓ Cardiac muscle remodeling
↑ Contractility (Ionotropic)

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2
Q

What is Preload?

A

Volume of blood in the ventricles at the end of diastole

Stretch

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3
Q

What is Afterload?

A

Resistance left ventricle must ovrcome to pump blood

Squeeze

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4
Q

Which drugs can help lower preload?

A

Diuretics
ACEI
ARB’s
Venodilators

Less blood in the heart system

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5
Q

Which drugs can help lower afterload?

A

ACEI
ARB’s
Arteriodilators

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6
Q

Which drugs can help increase contractility?

A

Digoxin
B agonists
PDE-III inhibitors

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7
Q

Which drugs can help lower cardiac muscle remodeling?

A

ACEI
ARB’s
Spironolactone
B blockers

Help improve survival!

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8
Q

Digoxin is for Acute/chronic management of HF?

A

Chronic

systolic failure!!

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9
Q

Which diuretics are given in case of HF?

A

Thiazides: Hydrochlorothiazides
Loop diuretics: Furosemide
K+ sparing agents: Spironolactone

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10
Q

ACE inhibitors which are given in case of HF?

A

Captopril
Enalapril
Perindopril
ramipril

אפריל מהאופיס קצת דומה לאייס

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11
Q

ARB’s which are given in case of HF?

A

Losartan
Valsartan
Irbesartan

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12
Q

B blockers which are given in case of HF?

A

Metoprolol (B1 selective antag.)

Carvedilol (B and a)

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13
Q

Positive iontropic agents

A

Cardiac glycosides: Digoxin, Digitoxin
Sympathomimetics: Dobutamine
PDE-inhibitor: Milrinone

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14
Q

Cardiac glycosides MOA

A

Inibition of cadiac Na/K ATPase → Na/Ca exchanger wont work as well → I.C Ca2+ conc. ↑ → increased Ca release from SR → Increased actin-myosin interaction → positive ionotropic (contractility)

Inhibition of neuronal Na/K ATPase → vagal activity ↑ → Negative chronotropic (HR)

AV conduction ↓ → Negative dromotropic (AV conduction)

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15
Q

Digoxin drug properties

A
Oral: bioavailability 75%
Narroe theraputic index
Onset of action 0.5-1 h
Elimination half life 30-40 h: requires loading dose
Renal elimination
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16
Q

Digoxin displacement by which other drugs?

A

Quinidine
Amiodarone
Verapamil

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17
Q

Digoxin indications

A

Chronic HF (positive inotropic) systolic failure

Arrhythmias: SVT, A.Fib, A.Flutter ( decreases AV conduction, increases AV refractory period)

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18
Q

Digoxin adverse effects

A
Hyperkalemia
GI
ECG changes
Conduction blocks
Arrhythmias
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19
Q

Predisposing factors for Digoxin toxicity

A

Renal impairment
Hypokalemia
Hypomangesemia
Hypercalcemia

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20
Q

Treatment for Digoxin toxicity

A

Correcting electrolyte (Mg , K )

Class Ib: Lidocaine, Phenytoin

digoxin Antibodies (Fab fragment)

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21
Q

Digoxin contraindications

A

Hypertrophic cardiomyopathy
AV block
Diastolic HF

WPW syndrome

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22
Q

Digitoxin drug properties

A

Oral: bioavailability 90%
Onset of action 3-6 h
Elimination half life 5-7 h: requires loading dose
Hepatic metabolism

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23
Q

Digitoxin indications

A

CHF

Arrhythmias: SVT, A.Fib, A.Flutter

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24
Q

Dobutamin

Tell me about it

A

B1 selective agonist
Parenteral
Duration is minutes

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25
Q

Dobutamine indications and CI

A

Acute HF: Systolic function ↑

CI : in chronic treatment due to tolerance, low oral bioava, arrythmogenic effect

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26
Q

PDE inhibitor for the management of AHF?

A

Milrinone

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27
Q

Milrinone MOA

A

PDE-inhibitor

↑ cAMP in heart muscle: Positive ionotropic (Contractility)
↑ cAMP in vascular smooth muscle: TPR ↓

28
Q

How to give Milrinone?

A

IV

29
Q

Milrinone indication and contra

A

AHF

Contra. in chronic treatment due to increased morbidity, mortality)

30
Q

Levosimenadan MOA

A

Ca2+ sensitizing agent:

  • Sensitize troponin to Ca –> (Positive ionotropic)
  • Inhibits PDE (Vasodilation)
  • Open ATP-sensitive K ch (Vasodilation)
31
Q

Ca2+ sensitizing agent

A

Levosimenadan

32
Q

Levosimenadan indications

A

Acute decompensated HF`

33
Q

Levosimenadan contra.

A

Hypotension

34
Q

What each class I AA do to the Action potential?

A

Ia (procainamide) : Prolonged AP

Ib (lidocaine, phenytoin) : Shorten AP in some cardiac tissue esp. purkinje

Ic (flecainide) : No effect on AP

35
Q

Class Ia MOA and names

A
  • Blocks open/inactive FAST Na+ ch “state dependent blockade”
  • tissues undergoing Frequent depol are more susceptible to inhibition
  • Blocks K+ ch so prolonged repol.
  • increased AP duration, Effective refractory period

Procainamide
Quinidine
disopyramide

36
Q

Class Ib MOA and names

A
  • Blocks inactivated Na ch.

(minimal effect on normal tissue bcz selectively affect ischemic or depolarized purkinje & ventricle)
little effect on atria

shorten AP & refractory period

Lidocaine
mexiletine
phenytoin

37
Q

Lidocaine indications

A

Ventricular arrhythmias
Post MI
Digoxin toxicity

38
Q

Lidocaine side effects

A

Seizures

Least cardiotoxic!

39
Q

Class Ic MOA and names

A
  • Block fast Na ch.
  • His-Purkinje tissue
  • No ANS effects

Propafenone
flecainide

40
Q

flecainide, Propafenone is given

A

Oral

41
Q

Class II AA

A

Esmolol
(Propranolol)
metoprolol

42
Q

Esmolol AA indications

A

Perioperative

thyrotoxicosis arrhythmias

emergency acute arrythmias

43
Q

Class III AA MOA

A

K+ ch. blockrs (prolongs AP, RP)

Rhythm control

amiodarone
Dronedarone

sotalol (BB + K-blocker)

44
Q

Class III AA drugs

A

Amiodarone

Sotalol

45
Q

Amiodarone drug properties

A

Blocks Na, B-adrenoreceptor, K, Ca, ( has group 1, 2, 4 AA actions)

greatest AP prolonging effect

HR ↓
AV node conduction ↓

Elimination half life 1-10 weeks
Binds to tissues

Inhibits CYP450 (Careful with Warfarin, Statins)

oral, parenteral

46
Q

Amiodarone side effects

A

Thyroid abnormalities
Skin and cornea deposition
Pulmonary fibrosis
optic neuritis

47
Q

Sotalol MOA

A

Blocks K+ ch.

Non selective B blocker

48
Q

Sotalol

How to give? Duration?

A

Oral

7 h

49
Q

Sotalol indications

A

Ventricular arrhythmias
A.Fib

(May cause Dose dependent TdP)

50
Q

Class IV AA MOA

A

Blocks L type Ca2+ ch.

Non-dihydropyridines more selective for myocardium!!

51
Q

Class IV AA drugs

How to give?

A

Verapamil
Oral, parenteral D= 7hrs

Diltiazem oral, parenteral

D= 6hrs

52
Q

Verapamil indications

Diltiazem indic

A

Verapamil : AV nodal arrhythmias esp in prophylaxis

Diltiazem : Rate control in atrial fibrillation

53
Q

Verapamil, diltiazem side effects

A
  • Cardiac depression
  • Constipation
  • Hypotension
54
Q

Class V AA drugs

A

Adenosine
Mg2+
Digoxin

55
Q

Adenosine R and their G protein

A

A1-R-(Gi): K+ current ↑, Ca2+ current ↓, hyperopolariz.

-increase in diastolic K current –> hyperpolar –> conduction block

A2-R-(Gs) : Vasodilation

56
Q

Adenosine

How to give? Duration?

A

IV

10-15 seconds!

57
Q

Adenosine indications

A

-Acute nodal tachycardia (book)

AV arrhythmias
Paroxysmal SVT

58
Q

Adenosine side effects

A
  • bronchospasm
  • chest pain
  • Flushing
  • headache
59
Q

Adenosine can be antagonized with

A

Theophylline

60
Q

Mg++ as an AA

A
  • possibly increase in Na/K ATPase
61
Q

Mg++ is given how

A

IV

62
Q

Mg++ indications

A

TdP
Long QT syndrome

Digitalis induced arrhythmias
arrythmias if serum K is low

63
Q

Digoxin as an AA

A

Inhibition of neuronal Na/K ATPase → Vagal tone ↑ → negative chronotropic

AV conduction ↓ → negative dromotropic

inhibits Na/K ATPase –> interfere with Ca/Na exchanger–> increased IC Ca –> increase inotropy (contractility)

64
Q

Rate control. Which AA will we choose? Indications?

A

Class II (BB) and IV (CCB)

Age > 65
Hypertension
AF

65
Q

Rhytm control. Which AA will we choose? Indications?

A
Class I and III
Age < 65
More symptomatic
No hypertension
New AF