Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiovascular Module > Pharmacology arrythmias > Flashcards

Pharmacology arrythmias Flashcards

1
Q

Why is conduction through the AV node slow (0.15s)

A

To allow Atrial contraction to propel blood into ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Arrythmias caractéristics

A

Abnormal site of origin of impulse
Abnormal raté or regularity of impulse
Abnormal conduction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fréquence of electrical pulse at sino atrial node

A

60-100 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Only conduction pathway between the atria and the ventricles

A

The atrioventricular node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

P wave

A

Generated by atrial depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

QRS

A

Ventricular muscle depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T wave

A

Ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

PR interval

A

Conduction time from atrium to ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

QT interval

A

Duration of ventricular action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aim of Therapy of arrhythmias

A

Reduce Ectopic pacemaker activity more than the one of SA node

Modification of conduction and refractories in reentry circuits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pharmacologic mechanisms available

A

Sodium channel block

Sympathetic block in the heart

Prolongation of effective refractory period

Calcium channel block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the consequence of blocking Na or Ca channel of depolarized cells

A

Decrease conduction and excitability

Increase refractory period only in depolarized cells and not in polarized cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

To what type of channels the channel blockers impact ?

A

Activated channel in phase 0

Inactivated channel in phase 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens if a drug binds to a normal cell

A

Will lose the drug rapidly from the receptors during resting portion of the cycle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What happens if a drug binds to cell that is constantly depolarized

A

Gisele will recover slowly from the block or not at all

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In cells with abnormal automaticity how do drugs reduce the phase 4 slope

A

Block ca and Na channel which brings equilibrium close to potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the two targets by drugs on reentry arrhythmias to completely prevent extra systole and reduce late propagation

A

Slow conduction by reducing the number of available unblocked channels

Prolong the recovery time of channels which increases the effective refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is drug-induced arrhythmias possible

A

When dosage increases , normal tissue are also targeted by the drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How can an anti arrhythmic drug become proarrythmic

A

If there’s fast heart rate, acidosis hyperkalemia , ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Classes of drugs

A

Class I sodium channel blockade

Class 2 sympatholytic

Class 3 prolongation of Action potential duration

Class 4 blockade of cardiac calcium current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Which drug share all four classes of action

A

Amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What drug do not fit in any classes

A

Adenosine , magnesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Class 1A drugs

A

Procainamide
Quinidine
Disopyramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Class 1B drugs

A

Lidocaine
Mexiletine
Tocainide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Class IC drugs

A

Flecainide
Encainide
Propafenone
Moricizine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Class I drug with weak anti cholinergic effect

A

Procainamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Class I drug with moderate anti cholinergic effect

A

Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Class I drug with strong anti cholinergic effect

A

Disopyramide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Actions of procainamide

A

Slows upstroke of action potential
slows conduction
prolongs the QRS
prolongs the APD ( class 3 action )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Is procainamide more effective than quinidine at suppressing ectopic pacemaker activity

A

No , less effective

More effective in blocking NA channel tho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Extra cardiac effects of procainamide

A

Ganglion block => Reduced peripheral vascular resistance => hypotension especially when IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Procainamide toxic effects

A

Cardiotoxicity ( excessive AP prolongation leading to torsades de pointes arrythmia and syncope. Too slowed conduction leads to new arrythmias )

lupus erythematous like syndrome when long term therapy ( arthritis, arthralgia)

Serologic abnormalities which shouldn’t make you stop treatment if no symptoms

Pleuritis

Pericarditis

Parenchymal pulmonary disease

Nausea

Diarrhea 
Rash
Fever
Hepatitis 
Agranulocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Route of administration of procainamide

A

Per os
IV
IM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Procainamide elimination

A

Hepatic metabolism to NAPA
NAPA ( has class III activity ) eliminated by kidney
So should pay attention in renal failure

Reduced dosage of low distribution and renal clearance ( risk of heart failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

When should use procainamide

A

Atrial and ventricular arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Would you pick procainamide as first choice in treatment of sustained ventricular arrythmias due to Acute MI

A

No

It’s drug of second or third choice after lidocaine and amiodarone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Cardiac effects of quinidine

A

Slows upstroke of action potential
slows conduction
prolongs the QRS
prolongs the APD ( class 3 action )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Toxic cardiac effects of quinidine

A

Excessive QT interval leads to torsade de pointes

Slowed conduction in heart if toxic concentration.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Extra cardiac effects of quinidine

A

1/3 to 1/2 of patients have GI effect (diarrhea , nausea )

Cinchonism At toxic drug =>headache, dizziness, tinnitus

Immunologic rxns ( thrombocytopenia, hepatitis, angioneurotic edema, fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Elimination of quinidine

A

Hepatic metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

How often is quinidine used

A

Rarely because of adverse effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Disopyramide cardiac effects

A

Slows upstroke of action potential
slows conduction
prolongs the QRS
prolongs the APD ( class 3 action ) => more pronounced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Why should you administer a drug that slows AV with dysopiramide in atrial flutter/ fibrillation or add B blockers/CCB

A

Because disopyramide has high antimuscarinic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Toxic effects of disopyramide

A

Heart failure ( negative inotropic effect)

Atropine like effects ( urinary retention, dry mouth, blurred vision, constipation, glaucoma worsening)

diarrhea , nausea

Cinchonism At toxic drug =>headache, dizziness, tinnitus

Immunologic rxns ( thrombocytopenia, hepatitis, angioneurotic edema, fever)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Is disopyramide a first line antiarrythmic agent ?

A

No

And should avoid it in heart failure patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Route of administration of disopyramide

A

Oral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

In what type of patient should you reduce dose of disopyramide

A

Renal failure patient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

In what type of condition is dysopiramide used as treatment t

A

Ventricular arrythmias

Some supraventricular arrythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Route of administration of lidocaine

A

Only IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Cardiac effects of lidocaine

A

activated and inactivated NA Channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Least cardiotoxic NA channel blocker

A

Lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

When can lidocaine cause hypotension

A

In large doses

If preexisting heart failure patients

53
Q

Most common adverse effects of lidocaine

A 
Paresthesias 
Tremor
Nausea 
Lightheadedness 
Hearing disturbances 
Slurred speech 
Convulsions
54
Q

I’m case of seizures due to lidocaine , what drug can you give IV

A

Diazepam y

55
Q

Why is lidocaine only given IV

A

Extensive first pass metabolism -97%

56
Q

Why can patient with MI tolerate and require higher lidocaine dose

A

Because they have increased a1-acid glycoproteins which normally binds lidocaine
So there would be less drug available for distribution

57
Q

Why should you reduce lidocaine dose in heart failure patient

A

volume of distribution and total body clearance are decreased

58
Q

In liver disease, why should you reduce lidocaine maintenance dose but can keep usual loading dose ?

A

Plasma clearance is reduced but volume of distribution increased

59
Q

Drugs that can reduce lidocaine clearance

A

Propranolol

Cimetidine

60
Q

Therapeutic use of lidocaine

A

Agent of choice for ventricular tachycardia

Prevention of ventricular fibrillation after cardio version ( can increase mortality)

Arrythmias

61
Q

Mexiletine route of administration

A

Oral

62
Q

Therapeutic use of mexiletine

A

Ventricular arrythmias

Pain due to diabetic neuropathy and nerve injury

63
Q

Dose related toxic effects of mexiletine

A

Tremor
blurred vision
Lethargy
Nausea

64
Q

Mexiletine action ressembles action of …

A

Lidocaine

65
Q

Na Channel blocker who has also k channel blocking activity

A

Flecainide

66
Q

Therapeutic use of flecainide

A

Normal hearts with supraventricular arrythmias

Auprès premature ventricular contraction

67
Q

Fleicanide elimination

A

Hepatic metabolism

Kidney

68
Q

Propafenone action is similar to …

A

Quinidine but does not prolong AP

69
Q

Therapeutic use of propafenone

A

Supraventricular arrythmias

70
Q

Propafenone adverse effects

A

Metal taste
Constipation
Arrythmias exacerbation

71
Q

Moricizine therapeutic use

A

Was used for Ventricular arrythmias

72
Q

Class II DRUGS ( beta adrenoreceptor blocking drugs)

A

Propranolol
Esmolol
Sotalol

73
Q

Are class II drugs more effective in in suppression of ventricular ectopic depolarization than class I drug

A

No , less effective

74
Q

Esmolol short acting b blocker therapeutic use

A

Antiarrythmic drug for jntraoperative and acute arrythmias

75
Q

Which b blocker has class 3 action

A

Sotalol (non selective beta blocker )

76
Q

Class III drugs ( prolong effective refractory period by prolonging action potential)

A

Amiodarone

Dronedarone

Celivarone

Vernakalant

Sotalol

Dofetilide

Ibutilide

77
Q

When are class III drugs putting at risk of torsades de pointes

A

When slow heart rate

78
Q

Amiodarone route of administration

A

IV

ORAL

79
Q

Amiodarone therapeutic use

A 
Serious Ventricular arrythmias 
Supraventricular arrythmias ( atrial fibrillation)

Récurent ventricular tachycardia

80
Q

Dronedarone is an analog of

A

Amiodarone

81
Q

Dronedarone therapeutic use

A

Atrial flutter

Atrial fibrillation

82
Q

Celivarone therapeutic use

A

Prevention of ventricular tachycardia recurrence

83
Q

Amiodarone cardiac effects

A

IK blocked

AP prolonged

Block Na channel

Weak class Iv and class II action

84
Q

Amiodarone extra cardiac effects

A

Peripheral vasodilation ( when IV )

85
Q

Amiodarone toxicity

A

Bradycardia and Heart block ( if sinus or AV node disease)

Can accumulate in heart, lung, liver, skin, tears

Dose related pulmonary toxicity

Abnormal liver function
Hypersensitivity hepatitis

Photodermatitis and gray blue skin discoloration

Corneal micro deposits

Optic neuritis which can progress to blindness

High iodine

Hypo or hyperthyroidism

86
Q

How long can effect of amiodarone be present after discontinuation

A

1-3 months

Can still be found in tissues in a 1y

87
Q

If cyp3A4 Is inhibited, amiodarone level …

A

Increases

88
Q

If cyp3A4 is induced, amiodarone level ..

A

Decreases

89
Q

Drugs affected by amiodarone inhibiting CYP450

A

Increased statins, digoxin, warfarin

90
Q

Why was dronedarone manufactured

A

To avoid thyroid issues like in amiodarone

91
Q

Dronedarone block…

A 
IKs
IKr
ICa 
INa
B adrénergic receptor
92
Q

How does food intake impact dronedarone

A

Absorption of dronedarone increased 2-3fold

93
Q

Elimination of dronedarone

A

Non rénal

94
Q

Why can’t you give dronedarone with cyp3A4 inhibitor

A

Because also has inhibitory action even tho it is its substrate

95
Q

Vernakalant therapeutic use

A

Atrial fibrillation

96
Q

Vernakalant cardiac effect

A

Multi ion channel blocker

Slows conduction over AV node

No QT interval change

Increase only atrial effective refractory period

97
Q

Adverse effect of vernakalant

A

Dysgeusia

Sneezing

Paresthésia

Cough

Hypotension

98
Q

Enzyme that metabolize vernakalant

A

CYP2D6

99
Q

Sotalol action

A

Class 2 and class 3 action

100
Q

Excretion of sotalol

A

Kidney in unchanged form

101
Q

Cardiac toxic effect of sotalol

A

Torsade de pointes

Further left ventricle dépression in patients with heart failure

102
Q

Sotalol therapeutic use

A

Ventricular arrythmias
Maintenance of sinus rythm

Used in children for supraventricular and ventricular arrythmias

103
Q

Dofetilide action

A

Class 3 block Ikr

104
Q

Which drug treatment should start in hospital after measuring QT

A

Dofetilide

105
Q

Dofetilide therapeutic use

A

Maintenance of restoratioof normal sinus rhythm in patients with atrial fibrillation

106
Q

Ibutilide action

A

Slow cardiac depolarization by blocking IKr

107
Q

Route of administration of ibutilide

A

IV

108
Q

Clearance of ibutilide

A

Hepatic metabolism

Metabolites cleared by kidneys

109
Q

Ibutilide therapeutic use

A

Conversion of atrial flutter/ fibrillation to normal sinus rythm

110
Q

Adverse effects of ibutilide

A

Excessive QT PROLONGATION

Torsade de pointes

111
Q

Class IV - calcium channel blockers

A

Verapamil

Diltiazem

112
Q

Cardiac effects of verapamil

A

Block activated and inactivated L type ca channel

Av node conduction and refractory period increased

113
Q

Verapamil extra cardiac effects

A

Peripheral vasodilation ( good in hypertension

114
Q

Verapamil toxicity

A

Hypotension and ventricular fibrillation if patient has ventricular tachycardia but was misdiagnosed with supraventricular tachycardia

Large dose can lead to AV block in AV diseases patient ( atropine and B agonist can help)

Comstipation

Nervousness
lassitude

Peripheral edema

115
Q

Bioavailability of verapamil

A

20%

116
Q

Verapamil therapeutic use

A

Supraventricular tachycardia (this and adenosine preferred )

Reduce ventricular rate in atrial fibrillatikn and flutter

Sometimes useful in ventricular arrythmias

117
Q

Diltiazem therapeutic

A

As useful as verapamil in supraventricular arrythmias

118
Q

Diltiazem adverse effects

A

Hypotension

Brady arrythmias

119
Q

Drugs that do not fit any class

A

Digitalis

Adenosine

Magnesium

Potassium

RAAS drugs

Fish oil

Statins

120
Q

Adenosine action

A

Activation inward rectifier K+
Inhibits calcium current

When given as bolus , will inhibit AV node conduction and increase AV refractory period

121
Q

For what condition is adenosine drug of choice

A

Conversion of paroxysmal supraventricular tachycardia tonsinus rythm

122
Q

Adenosine receptor blocker that reduce its activity

A

Theophylline

Caffeine

123
Q

Adenosine reuptake inhibitor that increase its activity

A

Dipyridamole

124
Q

Adenosine toxicity

A

Flushing

Shortness of breath 
Chest burning 
Av block 
Atrial fibrillation 
Headaches 
Hypotension 
nausea 
Paresthesia
125
Q

Magnesium therapeutic use

A

Digitalis induced arrythmias if hypomagnesemia

Torsades de pointes even if mg normal

126
Q

Potassium action

A

Resting potential depolarizing action

Stabilize membrane potential

Hyperkalemia depresses ectopic pacemakers , slows conduction

127
Q

Pretreatment evaluation steps

A

Eliminate cause ( hypoxia, electrolyte abnormalities, drug therapy, cardiac disease etc)

Make diagnosis

Determine baseline condition

Question need for therapy

128
Q

Only drugs associated with reduced mortality in asymptotic patients

A

B blockers

Cardiovascular Module (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions