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cvs drugs > anti-arrythmics + anti-angina + cardiac glycosides > Flashcards

anti-arrythmics + anti-angina + cardiac glycosides Flashcards

1
Q

what is a non-pacemaker blockade

A

suppress abnormal atrial or ventricular cells to restore normal sinus rhythm (RHYTHM control)
- Na channel blocker and potassium channel blocker

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2
Q

what is an AVN blockade

A

suppress AV node to prevent high atrial rate from causing high ventricular rate (RATE control)
- beta blocker and calcium channel blocker

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3
Q

types of sodium channel blocker

A

increasing degree of blockade of Na channel: B,A,C

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4
Q

MOA of Class 1C Na channel blocker

A

eg flerainide
MOA: slows phase 0 depolarisation

use: refractory ventricular tachycardia

1C=no change

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5
Q

MOA of Class 1A Na channel blocker

A

eg procainamide
MOA: slow phase 0 depolarisation
prolonged effective refractory period (moment cell starts repolarising) and action potential duration becase drug has K channel blockade

1A = after = prolong AP

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6
Q

MOA of CLass 1B Na channel blocker

A

eg lidocaine
MOA : slow phase 0 depolarisation and shorten phase 3 repolarisation

decrease action potential duration but ERP unchanged

1B=before=shorten AP

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7
Q

MOA of K channel blocker

A

eg SAD
Sotalol
Amiodarone
Dofelitide
MOA: slow down phase 3 repolarisation -> increase ERP and APD

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8
Q

use of K channel blocker

A
  • atrial fibrillation
  • prevent reentrant ventricular tachycardia => instead of completing normal circuit, electrical signal has alt loop back upon itself (self perpetuating rapid and abnormal activation)
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9
Q

special quality about K channel blocker

A

Amiodarone is metabolised by liver into active metabolites
this means that effect persist even after discontinuation of the drug (long half life: effect maintained 1-3mths after discontinuation)

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10
Q

MOA of beta blockers

A

block binding of NE to beta receptor so voltage gated Ca channels cannot open and calcium cannot enter

reduced slope of 4 (depolarisation to threshold potential and slope of 0 (when calcium channels supposed to open)

takes longer time before can depoalrise so reduced frequency of action potential moving through AV node -> decrease HR and contractility

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11
Q

uses of beta blockers

A

tachycardia
atrial fibrillation
protective effect after MI

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12
Q

AE of beta blockers

A

bradycardia
hypotension -> decrease contractility if beta blockers block contractile portion of myocardium

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13
Q

MOA of calcium channel blocker

A

non dihydropridine calcium channel blockers: (primarily affect myocardium)(IV)
diltiazem
verapamil

block calcium entry into cell -> decrease slope of 4 and 0 in AV node
block atrial signals from processing through AV node and into ventricles

  • prolonged ERP and APD (prolong both depol and repol)
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14
Q

use of calcium channel blockers

A

supraventricular tachycardia
hypertension
angina

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15
Q

AE of calcium channel blockers

A

hypotention
contraindicated: pre-existing depressed cardiac output -> further inhibit AV nodal conduction

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16
Q

types of anti angina drugs

A
  • vasodilators: nitrates, calcium channel blockers
  • cardiac depressants: calcium channel blockers, beta blockers
  • ivabradine
17
Q

MOA of nitrates

A

form NO which activates guanylyl cyclase which phosphorylates GTP to cGMP

inactivates myosin-LC so relaxation, causing vasodilation

effect of vasodilation on
- veins: decrease venous return, hence preload (at low conc)
- arteries: reduce peripheral resistance, decrease afterload (at high conc)
- coronary arteries: lower pressure in arteries because heart does not stretch as much so improvement in subendocardial blood flow

decreased workload on heart so increase supply of blood and oxygen to coronary arteries

18
Q

types of nitrates

A

glycerol nitrate
PK: injecton-> slow onset but long DOA
sublingual (under tongue) -> quick onset but slow DOA

isosorbide dinitrate
isosorbide mononitrate
PK: oral -> slow onset but long DOA

19
Q

how are nitrates angina pectoris prophylaxis

A

if end diastolic pressure and volume is high, heart would enlarge and press on coronary arteries. This would affect subendocardial blood flow.

nitrates would dilate coronary arteries so it is able to receive greater blood flow

20
Q

AE of nitrates

A

reflex tachycardia (baroreflex)
hypotension
headache -> meningeal artery vasodilation

21
Q

MOA of calcium channel blockers in anti-angina

A

decrease contractility -> decrease O2 requirement -> decrease workload on heart

22
Q

ranking of calcium channel blockers as cardiac depressants

A

verapamil> diltiazem > nifedipine

23
Q

MOA of ivabradine

A

inhibit cardiac pacemaker current that controls spontaneous diastolic depolarization in SA node -> lower HR

results in decreased cardiac workload -> decreased myocardial o2 consumption

Uses: stable angina, chronic HF

24
Q

AE of ivabradine

A

visual problems
bradycardia associated symptoms: hypotension, dizziness, fatigue, malaise

25
Q

what are cardiac glycosides (digitalis)

A

late stage HF drug
- goal: increase HR

PK:
oral
digitoxin
- extensive metabolism in liver and excreted through faeces
- slow onset, long DOA
digoxin
- not metabolised in liver and excreted through urine
- quick onset, short DOA

26
Q

MOA of digitalis

A

inhibit Na/K ATPase. Efflux of Na from cell through the pump maintains the sodium gradient across the cell membrane and Na-Ca exchanger ruses energy from sodium gradient to pump calcium out of cell.

by inhibiting Na/K ATPase, cannot maintain sodium gradient so calcium cannot be pumped out and accumulates in cell. More calcium available for contraction, resulting in stronger contractions

27
Q

effects of digitalis

A

mechanical effect: increase contractility -> increase CO -> decrease sympathetic activity and increase renal blood flow which would release more renin -> decrease preload and afterload

electrical effect: increase contractility -> more parasympathetic activity ->decrease AV conduction -> decrease ventricular rate

28
Q

AE of digitalis

A

dysrhythmia (AV block, A F, VF)
GI effects
CNS effects

29
Q

digitalis toxicity

A

increased intracellular Ca can lead to
- tachycardia, atrial fibrillation, automaticity, extra systole

what to do
- discontinue
- anti-arrthymic drugs (eg lidocaine, propanaol)
- digoxin antibody

30
Q

for angina, which drug is the most appropriate for long term therapy aimed at reducing the incidence and severity of vasospasm

A

Diltiazem

31
Q

anti-arrthymatics drug classes

A

some block potassium channels

class 1- sodium blocker
class 2- beta blockers
class 3- potassium
class 4- Ca2+ channel

cvs drugs (3 decks)

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