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PHA 222 > cardiac arrthymias 1+2 > Flashcards

cardiac arrthymias 1+2 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
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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

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3
Q

what is the Vaughan Williams Classification?

A

classifies antiarrhythmic drugs 1-4 based on what they block

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4
Q

what does class 1 of the vaughan williams classification block?

A

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

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5
Q

what does class 2 block?

A

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

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6
Q

what does class 3 block?

A

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

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7
Q

what does class 4 block?

A

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

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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

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9
Q

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

A

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

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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

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11
Q

what is the mechanism for class 1A drugs effect?

A

block na+ and K+ channels which decreases excitability+conduction and increases AP duration and ERP

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12
Q

what is class 1A drugs used for?

A

suppression of most forms of supraventricular & ventricular arrhythmias

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13
Q

what is the mechanism for class 1B drugs?

A

potently block voltage-gated Na+channels in depolarised, arrhythmogenic tissue and shorten AP duration

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14
Q

what is class 1B drugs used for?

A

most effective against arrhythmias in depolarised tissues

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15
Q

what is the mechanism for class 1C drugs?

A

potently block fastNa+channels & prolong ERP

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16
Q

what is class 1C drugs used for?

A

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

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17
Q

what is class 1C drugs reserved for?

A

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

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18
Q

what do class 2 drugs do?

A

1) block sympathetic stimulation of b1-receptors in SA & AV nodes which decreases the rate of phase 4 depolarisation (dec SA and AV automaticity) and prolonged repolarisation (inc AV nodal ERP and conduction delay)
2) Block sympathetic stimulation of B1-receptors in cardiac muscle cells causing suppression of triggered activity (DADs)
3) Block Na channels in higher doses and in depolarised tissue

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19
Q

what are examples of class 2 drugs?

A

Atenolol, Metoprolol, Propranolol, Sotalol

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20
Q

Graph of how Class 2 drugs work

A
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21
Q

what class has drugs that exert multiple antiarrhythmic actions?

A

class 3

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22
Q

what do class 3 drugs do?

A

block k+ channels which prolongs ERP and APD

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23
Q

Clinical Use of Class 3 Drugs

A
  • emergency cardioversion during VT & VF (amiodarone)
    -refractory ventricular tachyarrhythmias, SVTs (amiodarone)
  • ventricular premature beats & tachycardia, SVTs (d-sotalol)
    -cardioversion during atrial flutter & atrial fibrillation, and maintenance of sinus rhythm in paroxysmal/persistent AF (amiodarone; dronedarone)
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24
Q

Diagram of Class 3 Antiarrhythmic Agents

A
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25
Q

What do class 4 drugs do?-MOA

A

1) block L-type calcium channels –> dec pacemaker activity and inv AV nodal ERP and AV nodal conduction delay
2) Supress triggered activity (DADs)

26
Q

what is class 4 drugs clinical use?

A

effective against paroxysmal SVTs

reduce the ventricular response rate in atrial flutter & AF

27
Q

Examples of Class 4 Antiarrhythmic drugs

A

Verapamil and Diltiazem (RLCCB’s)

28
Q

what are the two miscellaneous agents?

A

Adenosine and digoxin

29
Q

how does Adenosine work?

A

naturally occurring purine nucleoside
activates A1-receptors –> opening of K+channels inhibition of Ca++channels –> dec pacemaker activity, inc AV nodal ERP and AV nodal conduction delay

30
Q

What is the drug choice for termination of paroxysal SVT

A

Adenosine

31
Q

how does digoxin work?

A

-Inc PNS tone –> dec SA+AV nodal pacermaker activity, inc AV nodal ERP and AV nodal conduction delay
-Used to slow or control the ventricular response rate in AF

32
Q

What are the 3 non-surgical procedures to clinically manage arrhythmias

A
  • Vagal Manoeuvres
  • DC Cardioversion/ Electrical Defibrillation
  • Percutaneous RF Cathetar Ablation
33
Q

What are Vagal manoevres and what are they effective against

A
34
Q

what is synchronized and unsync DC cardioversion called?

A

synchronized(cardioversion)& non-synchronized(defibrillation)

35
Q

What happens when DC electric shock is applied to the heart

A
  • transiently depolarises critical mass of heart cells simultaneously
  • interrupts disorganised / self-perpetuating ectopic impulses
  • allows the SA node to regain control as the dominant pacemaker
36
Q

what is DC cardioversion effective against?

A

effective against tachyarrhythmias due to reentry:
- SVTs, Atrial flutter, AF, VT (cardioversion)
- VF, pulseless VT, VF- induced Cariac Arrest (defib)

37
Q

What is Percutaneous RF Cathetar Ablation

A

-a minimally invasive procedure
-electrophysiological mapping is used to locate the ectopic foci
-catheter inserted via femoral vein & threaded into the heart
-ablation catheter is placed in contact with arrhythmogenic tissue
-RF energy used to ablate arrhythmogenic tissue
-effective against a host of tachyarrhythmias including AVRT (WPW), AVNRT, atrial flutter, AF, VT

38
Q

How do pacemakers work

A
  • battery powered electronic devices
  • monitor heart rate & send electrical impulses to stimulate heartbeat
  • usually inserted between skin & chest wall – just under the shoulder
  • attached electrode leads threaded via a vein into atrial or ventricular chamber(s)
  • rate-responsive – can vary pacing rate, based on patient’s need / state
  • 3 types used: single / dual chamber / biventricular
  • effective against bradyarrhythmias inclunding sick sinus syndrome, AV block
39
Q

What is an implantable cardioverter defibrillator

A

-similar to pacemakers but incorporate a DC cardioverter
-have rate-sensing, pacing & defibrillation capabilities
-detect arrhythmia & attempt suppression via pacing
-deliver DC electric shock to defibrillate, if pacing is unsuccessful
-usually used in combination with antiarrhythmic agents
-indicated for primary and sec prevention of VT, VF & SCD

40
Q

what is an articular fibuluration ?

A

-An atrial or supraventricular tachyarrythmia
-Characterized by rapid, chaotic, uncoordinated(asynchronous) & ineffective atrial activation ->consequent deterioration of atrial mechanical function & irregular ventricular rates

41
Q

What is the COX-Maze Procedure

A

-performed during open heart surgery
-multiple incisions are strategically placed in both atria
-incisions are sutured to form a ‘maze’ of scar tissue
-blocks stray electrical impulses from travelling through atrium
-a single pathway is left intact for normal travel of impulses between atria & ventricles
-new ablation methods with RF, microwave, cryotherapy, laser & high-intensity focused ultrasound

42
Q

Diagram for the Cox Maze Procedure

A
43
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

44
Q

What is the most common form of chronic sustained caardiac arrhythmia

A

atrial fibrillation

45
Q

Atrial Fibrillation is common in….

A

rheumatic heart disease, cardiomyopathies, mitral
valve disease, hyperthyroidism, CHF, CHD, etc

46
Q

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

A

-irregular pulse
-characteristic ECG changes (irregularly irregular RR intervals, high HR, loss of P waves, irregulat arterial activations causing chaotic isoelectric line)
-Symptoms depend mainly on the rate & irregularity (of the arrhythmia) and underlying structural heart disease –> palpitations, dyspnoea, fatigue, low exercise tolerance, chest pain, dizzy,syncope, disordered sleep

47
Q

what is the clinical classification of AF based on?

A

Based on duration or temporal pattern of occurrence

48
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
49
Q

Give a brief description for each type of AF

A

1) First detected or diagnosed AF – first clinical presentation, where the patient is still in atrial fibrillation, independent of its duration & the
presence or absence of any symptoms
2) Paroxysmal AF – recurrent (≥2 episodes) and self-terminating episodes lasting less than 7 days (usually less than 24-48 hours)
3) Persistent AF – episodes lasting for more than 7 days, or requiring termination by either pharmacological or electrical cardioversion
4) Long-standing persistent AF – episodes lasting for more than 1 year when decision is made for rhythm control strategy (catheter ablation)
5) Permanent AF – episodes lasting for more than a year, with decision made by both patient & physician not to pursue restoration of sinus rhythm by any means, including catheter or surgical ablation

50
Q

What is the most common form of heart rhythm disorder

A

atrial fibrillation

51
Q

Why is the number of people with AF expected to double by 2050/2060

A

ageing population worldwide
rising prevalence of chronic heart disease
rising prevalence of AF risk factors – e.g. diabetes, obesity, etc

52
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

53
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

54
Q

AF increases the risk of….

A

associated with high morbidity, mortality & healthcare cost due to complications – e.g. ischaemic stroke, systemic thromboembolism &
heart failure
*AF confers a 5-fold increased risk of stroke
~20-30% of strokes are related to AF: up to 3 million people worldwide have AF-related stroke every year – i.e. one person every 12 seconds!
patients with AF have increased risk of heart failure (RR ~ 3.4)

55
Q

The pathophysiology of AF

A

-enhanced automaticity
-multiple re-entrant circuits
-atrial remodelling (electrical remodelling, cellular (or ionic) remodelling – Ca++ handling abnormalities,
structural remodelling, neurohormonal (or autonomic) remodelling)
- lead to initiation, progression & maintenance of AF

56
Q

What is the most common site of clot formation during AF

A

Left atrial appendage

57
Q

Pathogenesis of AF related stroke

A

1 - Blood pools in Atria
2 - Blood clot forms
3 - Whole or part of blood clot breaks off
4 - Blood Clot travels to brain and blocks a cerebral artery causing a stroke

58
Q

what are the treatment goals and approaches for AF?

A

Treatment Goals
Relieve patient’s symptoms
Prevent complications of thromboembolism (stroke) & tachycardia-induced heart failure

Treatment Approach
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

59
Q
A
60
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)

61
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

62
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 (41 decks)

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