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Cardiovascular System > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

Presentation of arrhythmia

A

Asymptomatic
Palpitations, dyspnoea, chest pain, fatigue
Embolism

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2
Q

Investigations for arrhythmia

A

Document arrhythmia on ECG –12 lead, 24 hour recording, event recorder
Blood tests esp thyroid function
Echocardiogram

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3
Q

Therapeutic approaches for arrhythmia

A

Therapeutic approaches
Rate control versus rhythm control
Digoxin/beta blocker/ca-antagonist plus warfarin (or aspirin if low risk) versus class Ic/III drugs +/-DC cardioversion
Electrical approaches (occasionally)
Pace & ablation of AV node
Substrate modification eg Pulmonary vein ostial ablation, maze procedures
Consider anticoagulation

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4
Q

Supraventricular Tachycardia

A

Supraventricular tachycardia (SVT), also called paroxysmal supraventricular tachycardia, is defined as an abnormally fast heartbeat. It’s a broad term that includes many forms of heart rhythm problems (heart arrhythmias) that originate above the ventricles (supraventricular) in the atria or AV node.

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5
Q

AV-nodal re-entrant tachycardia (type of SVT)

A 
c/o palpitations, dyspnoea, diziness
Good prognosis
No treatment
Drugs (so-so) or RFA (radio frequency ablation)
RFA success rate >95%
5% recurrence
1 in 1500 mortality
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6
Q

AV re-entrant tachycardia (due to accessory pathway –WPW if overt) (type of SVT)

A 
Usually good prognosis
No treatment
Drugs (so-so) or RFA
RFA success rate 85->95%
5% recurrence
1 in 1500 mortality
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7
Q

Treatment for atrial flutter

A

Control ventricular rate & thromboembolic risk
Usually cardiovert
Prevent with AA (adrenergic antagonists) drugs or RFA of cavotricuspid isthmus

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8
Q

atrial flutter

A

starts with high heart rate, a type of abnormal heart rate, or arrhythmia. It occurs when the upper chambers of your heart beat too fast. When the chambers in the top of your heart (atria) beat faster than the bottom ones (ventricles), it causes your heart rhythm to be out of sync. less chaotic than fibrillation

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9
Q

Prognosis for ventricular fibrillation

A

cardiac arrest

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10
Q

Ventricular Tachycardia (symptoms, causes, tests)

A

Palpitations, CP, dyspnoea, dizziness, syncope
Usually structural heart disease
Bloods, echo, angio etc

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11
Q

Torsades de Pointes due to CHB(complete heart block)/AF

A

a specific type of abnormal heart rhythm that can lead to sudden cardiac death. It is a polymorphic ventricular tachycardia that exhibits distinct characteristics on the electrocardiogram (ECG).

Note the ‘short-long-short’ RR intervals & prolonged repolarisation

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12
Q

Long QT syndrome

A
  • congenital or acquired
  • may cause TdP
  • Px drugs, pacing or ICD (implantable cardioverter-defibrillator)
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13
Q

Indications for implantable cardioverter defibrillator (ICD)

A

Secondary prevention
Cardiac arrest due to VF/VT not due to transient or reversible cause eg early phase of acute MI
Sustained VT causing syncope or significant compromise
Sustained VT with poor LV function

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14
Q

Sick sinus syndrome post MI

A

asymptomatic SA node suppression

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15
Q

Indications for pacing temporarily

A

Temporary
intermittent or sustained symptomatic bradycardia, particularly syncope
prophylactic when patient at high risk for development of severe bradycardia eg 2nd or 3rd degree AV block, post anterior MI, even when asymptomatic

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16
Q

Indications for pacing permanently

A

symptomatic or profound 2nd/3rd degree AV block, particularly when cause (?) unlikely to disappear
probably Mobitz type II 2nd/3rd degree AV block even if asymptomatic
AV block associated with neuromuscular diseases
after (or in preparation for) AV-node ablation

alternating RBBB/LBBB (bundle branch blocks)
syncope when bifascicular/trifascicular block and no other explanation
sinus node disease associated with symptoms
carotid sinus hypersensitivity/malignant vasovagal syncope

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17
Q

What is an arrhythmia?

A

A deviation from the “normal” rhythm of the heart

(Sinus arrhythmia- HR increases as breath in)

Tachycardias
Supraventricular arrhythmia
Atrial fibrillation

SVT (junctional)
Ventricular arrhythmia
Ventricular tachycardia
Ventricular fibrillation

(Bradycardias (Heart block))

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18
Q

IA Vaughan-Williams classification antiarrhythmics

A

IA-(Moderate) sodium-channel blockade, thus reducing amplitude of AP and conduction velocity.

Quinidine. Procainamide, dispyramide

19
Q

IB Vaughan-Williams classification antiarrhythmics

A

(Weak) sodium-channel blockade, thus reducing amplitude of AP and conduction velocity

Lidocaine, mexiletine, tocainide

20
Q

IC Vaughan-Williams classification antiarrhythmics

A

Strong sodium-channel blockade, thus reducing amplitude of AP and conduction velocity

Flecainide, propafenone

21
Q

II Vaughan-Williams classification antiarrhythmics

A

B-Adrenergic receptor antagonism

Atenolol, bisoprolol

Acts via β1 receptors to block sympathetic stimulation of the heart,
Prolongs phase 4 depolarization
∴ Slows SA discharge and AV conduction
Reduces excitability in non nodal cardiac tissue
Shortens Phase 2
∴ has a negative effect on contractility
Now first line for atrial fibrillation (Bisoprolol)

22
Q

III Vaughan-Williams classification antiarrhythmics

A

Prolong refractoriness (Slow K flow out of cells)

Amiodarone, bretylium, sotalol

Increase action potential duration
Prolong repolarization in phase 3
Prolongs ERP
Used for dysrhythmias that are difficult to treat
Life-threatening ventricular tachycardia or fibrillation, atrial fibrillation or flutter—resistant to other drugs
Sustained ventricular tachycardia

23
Q

IV Vaughan-Williams classification antiarrhythmics

A

Calcium channel blockade

Diltiazem, verapamil

Calcium channel blockers- bind to Lcard -type voltage gated Ca channels
Depress phase 4 depolarization in SA and AV nodes
Slow the heart rate (decrease automaticity and slows AV conduction
Shorten phase 2 Plateau phase (reduce contractility)
Show use dependence (ie. More effective at higher HR)
Used for paroxysmal supraventricular tachycardia; rate control for atrial fibrillation and flutter

24
Q

V Vaughan-Williams classification antiarrhythmics

A

Others

Digoxin

25
Q

Class 1 Vaughan-Williams classification antiarrhythmics

A

Membrane-stabilizing agents
Decrease the amplitude (size of Action potential)
Reduces velocity of conduction/Excitability
Act on “Fast” sodium channel responsible for Phase 0
Present in “Non- Nodal” cells
Divided into Ia, Ib, and Ic agents, according to effect on AP duration and therefore the effective refractory period (ERP)
Show use dependence (ie. More effective at higher HR)

Flecainide is the agent you are most likely to see used

26
Q

Amiodarone

A

Used for VT and occasionally in supraventricular tachycardia
Many interactions with other drugs: particularly digoxin
Because of tissue effects has striking side effect profile
Thyroid (hypo or hyperthyroidism)
Pulmonary fibrosis
Slate – grey pigmentation
Corneal deposits
LFT abnormalities

27
Q

Digoxin

A

Cardiac glycoside
Inhibits the sodium-potassium ATPase pump
Increases vagal tone through unclear mechanism
Slows SA/AV node conduction
Complex effect on the Cardiac action potential
Reduces the refractory period in myocardium
Increases [Ca2+]intracellular
Positive Inotropic effect

Half life: 36-48 hours, increased in renal impairment
50-70% of digoxin is excreted almost entirely unchanged by the kidneys
Excretion proportional to GFR

28
Q

Indications for Digoxin

A 
atrial dysrhythmias
AF
Atrial Flutter
(SVT)
heart failure

Commonly used in the elderly
Elderly people often have renal impairment (reduced glomerular filtration rate (GFR)

29
Q

Digoxin toxicity

A

Monitor potassium levels, [Digoxin]plasma, and for toxicity.

Nausea and vomiting
Xanthopsia (yellow vision)
Bradycardia
Tachycardia
Arrhythmias: VT and VF
30
Q

Signs of digoxin toxicity

A

‘Reverse tick’ appearance of ST segment in lateral leads

31
Q

Digoxin toxicity: treatment

A

Stop digoxin
If levels very high and risk of significant arrhythmia: Give Digibind
Digibind
Digoxin immune antibody
Binds with digoxin, forming complex molecules
Excreted in urine
Digoxin toxicity is more serious if potassium levels are low

32
Q

Adenosine

A

Slows/ Blocks conduction through the AV node
Used to convert paroxysmal supraventricular tachycardia to sinus rhythm
Very short half-life
Only administered as fast IV push
May cause asystole for a few seconds
Other side effects minimal

33
Q

Indications for anticoagulation

A

Atrial fibrillation
Risk of stroke, peripheral emboli

Metallic Heart Valves
DVT/PE
Treatment
Prophylaxis
Surgery
High risk medical patients
Immobilisation
34
Q

Ideal Anticoagulant

A

Oral
No need for monitoring
No interaction with food or drugs
Given once or twice a day with fixed dose irrespective or weight/age

35
Q

Oral Anticoagulants

A

Warfarin- Vitamin K antagonist

Dabigatran- Direct Thrombin Inhibitor
Rivaroxaban, Apixaban, Edoxaban- Direct Xa inhibitors

36
Q

How does warfarin work

A

inhibits Vitamin K epoxide reductase, vitamin K epoxide reduces vitamin K

Reduces vitamin K

which reduces formation of complete clotting factors from precursors

37
Q

Monitoring warfarin therapy

A

International normalised ratio (INR)

Actual PROTHROMBIN time/Standard PROTHROMBIN time

Normal INR is 1
Therapeutic INR is normally 2.5 – 4.0 depending on the clinical indication

Alcohol intake and patient education

38
Q

Adverse effects of warfarin

A 
Bleeding  (dose related)
Interaction with multiple other drugs
Pregnancy 
Teratogenic (chondrodysplasia)
(Retroplacental bleeding and fetal intracerebral bleeding).
Avoid in first and third trimesters
39
Q

Drug interaction with Warfarin - drugs that increase warfarin activity

A

Aspirin, Sulfonamides
- Decrease binding to
Albumin

Cimetidine, erythromycin - Inhibit Degradation

Antibiotics (oral) - Decrease synthesis of
Clotting Factors

40
Q

Drug interaction with Warfarin - Drugs that promote bleeding

A

Inhibition of platelets - Aspirin

Inhibition of clotting Factors - Heparin antimetabolites

41
Q

Drug interaction with Warfarin - Drugs that decrease

Warfarin activity

A

Barbiiturtes, phenytoin - Induction of metabolizing
Enzymes (cytochrome P450)

Vitamin K - Promote clotting factor synthesis

cholestyramine - Reduced absorption

42
Q

CYTOCHROME p450 inhibitors

A 
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin and Cimetidine
Ethanol (acutely)
Sulphonamides
43
Q

CYTOCHROME p450 inducers

A 
Alcohol (chronic use)
Barbiturates
Carbamazepine
Phenytoin
Rifampicin
Sulphonylureas

Cardiovascular System (33 decks)

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