Arrhythmias Flashcards
Presentation of arrhythmia
Asymptomatic
Palpitations, dyspnoea, chest pain, fatigue
Embolism
Investigations for arrhythmia
Document arrhythmia on ECG –12 lead, 24 hour recording, event recorder
Blood tests esp thyroid function
Echocardiogram
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
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.
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
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
Treatment for atrial flutter
Control ventricular rate & thromboembolic risk
Usually cardiovert
Prevent with AA (adrenergic antagonists) drugs or RFA of cavotricuspid isthmus
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
Prognosis for ventricular fibrillation
cardiac arrest
Ventricular Tachycardia (symptoms, causes, tests)
Palpitations, CP, dyspnoea, dizziness, syncope
Usually structural heart disease
Bloods, echo, angio etc
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
Long QT syndrome
- congenital or acquired
- may cause TdP
- Px drugs, pacing or ICD (implantable cardioverter-defibrillator)
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
Sick sinus syndrome post MI
asymptomatic SA node suppression
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
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
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))
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
