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

Arrhythmias Flashcards by maia ferg

Presentation of arrhythmia

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

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Investigations for arrhythmia

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

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Therapeutic approaches for arrhythmia

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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Supraventricular Tachycardia

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

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

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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Treatment for atrial flutter

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

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atrial flutter

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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Prognosis for ventricular fibrillation

cardiac arrest

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Ventricular Tachycardia (symptoms, causes, tests)

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

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

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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Long QT syndrome

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

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Indications for implantable cardioverter defibrillator (ICD)

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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Sick sinus syndrome post MI

asymptomatic SA node suppression

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Indications for pacing temporarily

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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Indications for pacing permanently

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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What is an arrhythmia?

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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IA Vaughan-Williams classification antiarrhythmics

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

Quinidine. Procainamide, dispyramide

IB Vaughan-Williams classification antiarrhythmics

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

Lidocaine, mexiletine, tocainide

IC Vaughan-Williams classification antiarrhythmics

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

Flecainide, propafenone

II Vaughan-Williams classification antiarrhythmics

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)

III Vaughan-Williams classification antiarrhythmics

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

IV Vaughan-Williams classification antiarrhythmics

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

V Vaughan-Williams classification antiarrhythmics

Others

Digoxin

Class 1 Vaughan-Williams classification antiarrhythmics

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

Amiodarone

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

Digoxin

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

Indications for Digoxin

``` atrial dysrhythmias AF Atrial Flutter (SVT) heart failure ``` Commonly used in the elderly Elderly people often have renal impairment (reduced glomerular filtration rate (GFR)

Digoxin toxicity

Monitor potassium levels, [Digoxin]plasma, and for toxicity. ``` Nausea and vomiting Xanthopsia (yellow vision) Bradycardia Tachycardia Arrhythmias: VT and VF ```

Signs of digoxin toxicity

‘Reverse tick’ appearance of ST segment in lateral leads

Digoxin toxicity: treatment

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

Adenosine

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

Indications for anticoagulation

Atrial fibrillation Risk of stroke, peripheral emboli ``` Metallic Heart Valves DVT/PE Treatment Prophylaxis Surgery High risk medical patients Immobilisation ```

Ideal Anticoagulant

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

Oral Anticoagulants

Warfarin- Vitamin K antagonist Dabigatran- Direct Thrombin Inhibitor Rivaroxaban, Apixaban, Edoxaban- Direct Xa inhibitors

How does warfarin work

inhibits Vitamin K epoxide reductase, vitamin K epoxide reduces vitamin K Reduces vitamin K which reduces formation of complete clotting factors from precursors

Monitoring warfarin therapy

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

Adverse effects of warfarin

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

Drug interaction with Warfarin - drugs that increase warfarin activity

Aspirin, Sulfonamides - Decrease binding to Albumin Cimetidine, erythromycin - Inhibit Degradation Antibiotics (oral) - Decrease synthesis of Clotting Factors

Drug interaction with Warfarin - Drugs that promote bleeding

Inhibition of platelets - Aspirin Inhibition of clotting Factors - Heparin antimetabolites

Drug interaction with Warfarin - Drugs that decrease | Warfarin activity

Barbiiturtes, phenytoin - Induction of metabolizing Enzymes (cytochrome P450) Vitamin K - Promote clotting factor synthesis cholestyramine - Reduced absorption

CYTOCHROME p450 inhibitors

``` Omeprazole Disulfiram Erythromycin Valproate Isoniazid Ciprofloxacin and Cimetidine Ethanol (acutely) Sulphonamides ```

CYTOCHROME p450 inducers

``` Alcohol (chronic use) Barbiturates Carbamazepine Phenytoin Rifampicin Sulphonylureas ```