Brainscape's Knowledge GenomeTM

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


See full index

PHA 222 > cardiac arrthymias 2&3 > Flashcards

cardiac arrthymias 2&3 Flashcards

1
Q

what are the treatment options for cardiac arrhythmias?

A 
class 1-4 antihypertensive drugs
non pharmacological:
RF catheter ablation
DC cardioversion / defibrillation
pacemaker/ ICDs
maze procedure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the 3 mechanisms for arrhythmias suppression?

A

inhibition of inward/depolarising currents-na and ca
prolongation of the effective refractory period-k+
inhibition of sympathetic autonomic nervous effects on the heart- b-adrenoceptor

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

what is the Vaughan Williams Classification?

A

classifies antiarrhythmic drugs 1-4 based on what they block

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

what does class 1 of the vaughan williams classification block?

A

inhibit / block fast voltage-gated sodium channels (Na+channel blockers)

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

what does class 2 block?

A

inhibit / block adrenergic activity in the heart (b-adrenoceptor blockers)

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

what does class 3 block?

A

delay AP repolarisation & increase ERP(K+channel blockers)

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

what does class 4 block?

A

inhibit / block slow voltage-gated Ca channels (Ca++channel blockers)

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

who sub-classified class 1 drugs? and how

A

Harrison-Campbell
1A- mild inhibition of Na channel
1B- moderate inhibition
1C- marked inhibition

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

what are examples of all the subclassification of class 1 drugs?

A

1A=Quinidine
1B=Lidocaine
1C=Flecainide

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

what does blocking na channels allow for?

A

selectively terminate tachyarrhythmias in depolarised cardiac tissue
suppress ectopic pacemaker activity
prolong the refractory period of cardiac cells
convert areas of unidirectional conduction block to bidirectional conduction block

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

what is the mechanism for class 1A drugs effect?

A

block na+ and K+ channels which increases AP and ERP

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

what is class 1A drugs used for?

A

suppression of most forms of supraventricular & ventricular arrhythmias

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

what is the mechanism for class 1B drugs?

A

potently block Na+channels in depolarised, arrhythmogenic tissue

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

what is class 1B drugs used for?

A

most effective against arrhythmias in depolarised tissues

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

what is the mechanism for class 1C drugs?

A

potently block fastNa+channels & prolong ERP

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

what is class 1C drugs used for?

A

very effective against ventricular extrasystoles & tachyarrhythmias may exacerbate arrhythmias in susceptible patients

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

what is class 1C drugs reserved for?

A

Life-threatening or refractory ventricular tachyarrhythmias
Wolff-Parkinson-White (WPW) tachycardias
Paroxysmal AF

18
Q

what do class 2 drugs do?

A

block sympathetic stimulation of b1-receptors in SA & AV nodes
which decreases the rate of depolarisation and prolonged repolarisation

19
Q

what happens when class 2 drugs are in higher doses?

A

block na + channels and depolarise channels

20
Q

what is class 2 drugs used for?

A

effective against arrhythmias dependent on sympathetic activation
moderately effective against chronic ventricular arrhythmias
reduce incidence of VF & SCD after AMI
reduce the ventricular response rate in atrial flutter & AF

21
Q

what class exerts multiple antiarrhythmic actions?

A

class 3

22
Q

what do class 3 drugs do?

A

block k+ channels which prolongs ERP and APD

23
Q

What do class 4 drugs do?-MOA

A

block L-type calcium channels

24
Q

what is class 4 drugs clinical effect?

A

effective against paroxysmal SVTs

reduce the ventricular response rate in atrial flutter & AF

25
Q

what are the two miscellaneous agents?

A

Adenosine and digoxin

26
Q

how does Adenosine work?

A

naturally occurring purine nucleoside

activates A1-receptors -opening of K+channels inhibition of Ca++channels

27
Q

how does digoxin work?

A

used to slow or control the ventricular response rate in AF

28
Q

what is synchronized and unsync DC called?

A

synchronized(cardioversion)& non-synchronized(defibrillation)

29
Q

what is DC cardioversion effective against?

A

effective against tachyarrhythmias due to reentry

30
Q

what is an articular fibuluration ?

A

characterized by rapid, chaotic, uncoordinated(asynchronous) & ineffective atrial activation ->consequent deterioration of atrial mechanical function & irregular ventricular rates

31
Q

what is the rates for AF?

A

disorganised & very rapid atrial rate ~400-600 beats/min

irregular & rapid ventricular response ~80-180 beats/min

32
Q

what are the 3 clinical presentations/ diagnosis criteria for AF?

A

irregular pulse
characteristic ECG changes
Symptoms depend mainly on the rate & irregularity (of the arrhythmia) and underlying structural heart disease

33
Q

what is the clinical classification of AF based on?

A

Based on duration or temporal pattern of occurrence

34
Q

what are the 5 classifications of AF?

A 
1-First detected or diagnosed AF 
2-Paroxysmal AF
3-Persistent AF 
4-Long-standing persistent AF 
5-Permanent AF
35
Q

what are the established risk factors for AF?

A

Advancing age▪Male sex▪Hypertension▪Valvular heart disease▪Heart failure▪Coronary artery disease▪Cardiac surgery▪Diabetes mellitus▪Hyperthyroidism

36
Q

What are the emerging, but not yet established risk ractors for AF?

A

Obesity▪Chronic kidney disease▪Sleep apnoea▪Biomarkers▪Physical activity▪Excess alcohol consumption

37
Q

what do you want treatment to do for AF?

A

Control of the ventricular rate (rate control)Restoration of sinus rhythm (rhythm control)Prevention of recurrent episodes or reduction of their frequency or duration Prevention of thromboembolic complications

38
Q

what is Thromboprophylaxis and how is it done?

A

prevention of thromboembolic consequences of AF (stroke)
Assess patient’s thromboembolic (stroke) risk using the CHA2DS2-VASc scoring system
Assess patient’s bleeding riskusing the HAS-BLED assessment tool
Initiate oral anticoagulant therapy, as indicated
Vitamin K antagonist OACs –warfarinNovel, Newor Non-vitamin K antagonist OACs (NOACs)

39
Q

what is the MOA of warfrin?

A

inhibits vitamin K epoxide reductase
inhibition of post-translational carboxylation of clotting factors II, VII, IX & X
reduced synthesis of functional coagulation factors inhibition of coagulation cascade

40
Q

what is the MOA of NOCAs?

A

1-Direct Factor Xa Inhibitors-prevent conversion of prothrombin (factor II) to thrombin
2-direct Thrombin (Factor IIa) Inhibitor (dabigatran)-nhibits conversion of fibrinogen to fibrin

PHA 222 (40 decks)

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