Approach to Palpitations Flashcards
(37 cards)
How would you classify the nature of palpitations?
Rapid palpitations
- regular: sinus tachycardia atrial flutter, atrial tachycardia, supraventricular re-entry tachycardia
- irregular: atrial fibrillation, multiple atrial or ventricular ectopic beats
Slow palpitations (Described as missed beats or forceful beats): sinus sick syndrome, AV block, occasional ectopics with compensatory pauses, antiarrhythmics
Increased stroke volume (forceful beats)
- Valvular lesions: mitral regurgitation, aortic regurgitation
- High output states: Pregnancy, thyrotoxicosis, pheochromocytoma, fever, anemia
What are the endocrine causes of palpitations?
- Thyrotoxicosis
- Phaeochromocytoma
- Hypoglycemia
- Addison’s (Adrenal Insufficiency)
What are the medications that cause palpitations?
- Sympathomimetic
- Anticholinergic
- Cocaine, caffeine, nicotine
- Amphetamine
- Beta blocker withdrawal
What are the psychiatric causes of palpitations?
- Psychiatric
- Panic attack
- Generalized anxiety disorder
- Somatization
- Depression
What are the supraphysiological causes of palpitations?
High output state
- Pregnancy
- Fever
- Anaemia
What are the clues in hx pointing towards cardiac etiology?
- Male
- Irregular rhythm
- Known history of underlying heart disease
- > 5 min
- Associated with other symptoms e.g syncope, chest pain
What are the clues in hx pointing towards thyroid disease?
- Tremor, Weight Loss, Increased Appetite
- Anxiety, Diarrhoea, Amenorrhea, Heat Intolerance & excessive sweating
- Possible Visual Disturbances
What are the clues in hx pointing towards valvular disease?
Rheumatic fever
What are the clues in hx pointing towards anemia?
Recent operation, Menorrhagia, UBGIT, LBGIT, Haematuria
What are the clues in hx pointing towards toxins/ drugs?
Alcohol, caffeine, amphetamine, antiarrhythmic agents
What are the investigations that are required?
• FBC • Renal panel • Potassium /Calcium/Magnesium /Phosphate • Thyroid function test • CRP/Procalcitonin • CXR • Cardiac enzymes • ECG - Assess rhythm: SVT, AF, VT - Short PR, delta wave - LVH - Q waves - Ectopy - Prolonged QT
What are the clues in hx pointing towards phaeochromocytoma?
Triad of: Headache, Sweating, Tachycardia +/- diarrhoea, abdominal pain, N&V
Usually seconds – minutes, multiple times a day
Screen for MEN Syndrome!
What is the relevant history to characterise the palpitations?
Age of onset
- Younger: AVNRT, AVRT, idiopathic VT, inherited channelopathies
- Older: AT, AF, VT with structural heart disease
Onset and offset
- Instantaneous: Supraventricular or ventricular ectopy, SVT, VT
- Gradual: Sinus tachycardia, AF
- Response to carotid sinus massage, vagal maneuver,
valsalva maneuver
Rate & rhythm
- Fast vs slow
- Regular vs irregular
Character
- Rapid fluttering: sustained ventricular or supraventricular arrhythmia
- Flip flopping: supraventricular or ventricular ectopy
- Pounding: AV dissociation > cannon A wave
Associated symptoms
- Giddiness, syncope: haemodynamically significant
Family hx of SCD
- Young SCD
- Cardiomyopathy
What is the relevant drug hx to ask for palpitations?
- Antidepressants
- Anti-arrhythmics
- Arrhythmogenic drugs (calcium channel blockers, beta 2 agonists, nitrates)
- Sedatives (e.g. Withdrawal of benzodiazepines)
What is the relevant fam hx to ask for palpitations?
- Heart disease
- Sudden cardiac death; Arrhythmias
What is the relevant social hx to ask for palpitations?
- Alcohol
- Smoking
- Recreational drugs (Caffeine, amphetamines, cocaine)
What is the PE to do for palpitations?
General
- Is patient well? Anxious?
- Cyanosis, dypsnoea – suggestive of cardiac failure or lung disease
- Pallor – suggestive of anaemia
- Signs of hyperthyroidism : Exophthalmos, Warm and sweaty hands, Fine tremor
- Raised JVP – congestive cardiac failure
Vital Signs
- Pulse: Regular? Rate?
- Blood pressure: High BP may lead to forceful heart beat that may be felt
- Respiratory rate: Hyperventilation may indicate anxiety
Chest
- Displaced apex beat
- Parasternal heave
- Confirm heart rate and rhythm by auscultation
- Murmurs: Mid-systolic click (Mitral valve prolapse), Harsh holosystolic murmur (Hypertrophic Cardiomyopathy)
- Lung bases for signs of heart failure
Limbs
- Edema
- Signs of thyroid disease: Tremor, Brisk reflexes
Class Ia anti arrhythmics
- mechanism of action
- examples
- indications
Decreases re-entry
- Moderate blockade of fast sodium channels, thus slowing the rate of Phase 0 depolarization and reducing tissue velocities.
- Also prolong the cell’s action potential and refractory period (via blockade of potassium channels responsible for repolarization)
Quinidine, procainamide, disopyramide
Indicated for Ventricular arrhythmias and atrial fibrillation
Class Ib anti arrhythmics
- mechanism of action
- examples
- indications
Decreases re-entry, decrease automacity
- Inhibit the fast sodium channel but shorten the action potential duration and refractory period
- Due to blockade of small sodium currents that normally continue through Phase 2 of the action potential
Lignocaine, mexiletine, tocainide, phenytoin
Indicated for ventricular tachycardia and digitalis induced arrhythmias
Via continuous intravenous infusion due to rapid
distribution and hepatic metabolism
Class Ic anti arrhythmics
- mechanism of action
- examples
- indications
Decreases re-entry, decrease automacity
- Most potent sodium channel blockers, no effect on duration potential
- Markedly decrease the upstroke of the action potential and conduction velocity in atrial, ventricular and Purkinje fibers
Significantly prolong the refractory period within the
AV node and accessory bypass tracts
Flecainide, encainide, propafenone, moricizine
Indicated for SVT in structurally normal hearts
To be AVOIDED in patients with left ventricular dysfunction, CAD (structurally abnormal hearts) –> can precipitate heart failure
Class II anti arrhythmics
- mechanism of action
- examples
Mechanism of Action
- b- adrenoceptor antagonists
- Inhibition of cardiac sympathetic activity
- Reducing automaticity
- Prevent triggered arrhythmias caused by catecholamines with
afterdepolarisations
- Also increase the refractory period of AV node
- Lastly decrease myocardial oxygen demand
- Can cause prolonged PR interval on ECG (1 st deg HB)
Beta blockers
- B1 selective: Acebutolol, Atenolol, Bisoprolol, Esmolol, Metoprolol
- Non B1 selective: Nadolol, proranolol
- Non B selective and a receptor blockers: carvedilol (use in heart failure management), labetalol (IV form is used in acute hypertensive crisis)
Indicated in catecholamine driven tachyarrhythmias , AF, Aflutter, Reentrant SVT, PVCs, ventricular arrhythmias due to prolonged QT (as BB does not prolong QT like class IA drugs)
Class III anti arrhythmics
- mechanism of action
- examples
- indications
Block potassium channels responsible for repolarization, thereby prolonging the action potential with little effect on the rise of Phase 0 depolarisation
Include Amiodarone , Dronedarone , Sotalol , Dofetilide , Ibutilide
Indicated in wide spectrum of VT and SVT, A fib, ventricular arrhythmias
Class IV anti arrhythmics
- mechanism of action
- examples
- indications
- side effects
MOA
- Selective blockade of the L type calcium channel
- Most potent in SA and AV node (AP depends most on calcium currents)
- Decreases the rate of rise of Phase 0 depolarisation and conduction velocity
- Lengthens the refractory period of the AV node
- Raise the threshold potential at the SA node
Verapamil, diltiazem
Indicated in reentrant SVT
Side effects
- Side effects include hypotension
- Use with caution with betablockers due to
combined negative inotropic and chronotropic effects may precipitate heart failure and bradycardia
Class V anti arrhythmics
- mechanism of action
- examples
- Work by other or unknown mechanisms (direct nodal inhibition)
- adenosine, digoxin, magnesium sulfate
Digoxin
- Inhibits Na +/K ATPase pump: increased intracellular Na+ & Ca2+
- Results in: Increased contractility (inotropy), Anti arrhythmic effects (Vagomimetic effects on AV node, prolongation of phase 4 and phase 0)
Adenosine:
- binds Gi protein type 1 receptors to allow rapid potassium efflux and hyperpolarisation, and blocks calcium influx
- Most effective drug for rapid termination of
reentrant SVT
- Very transient side effects of headache, chest pain,
flushing, bronchoconstriction
