Clinical Presentation and Management of Arrhythmias

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  • Created by: LBCW0502
  • Created on: 22-01-19 18:11
What tests are carried out on a patient who has tachycardia?
ECG (check heart rhythm). FBC (full blood count to check for infection/anaemia). U&E (urine and electrolytes). TFT (thyroid function test). Other (JACCO)
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What does JACCO stand for?
Jaundice. Anaemia. Clubbing. Cyanosis. Oedema
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Why is thyroid function tested for a patient who is presenting tachycardia?
Overstimulation of thyroxine can lead to tachycardia (possible cause)
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What are the two types of cardiomyocytes?
Nodal (pace maker, doesn't wait for firing of impulse, spontaneous contraction). Non-nodal (striated muscle, waits for impulse to fire and contraction to take place)
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What are the two types of innervation in cardiomyocytes?
Sympathetic and parasympathetic innervation
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Which type of neurotransmitter and receptor are involved in parasympathetic innervation?
ACh acts on mAChRs (inhibits cAMP, Ca influx, contraction)
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Which type of neurotransmitter and receptor are involved in sympathetic innervation?
Noradrenaline acts on B receptor (activates cAMP, no Ca influx, relaxation)
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Which channels are present on a cardiomyocyte?
Sodium and calcium channels (fast/slow). Potassium channels. Movement of Na, Cl, K ions. Na-K pump to maintain electrical potential
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Which channels are opened when an impulse is received?
Sodium channels open. Sodium influx. Change in electrical potential. Generation of AP
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What is the refractory period?
When the cell cannot contract again (need to move ions in/out cell). Abnormal case – two quick repolarisation steps
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What is the effect of sympathetic stimulation on myocyte and Purkinje cell APs?
Sympathetic innervation – shortens refractory period – heart beats harder/faster
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What is the effect of parasympathetic stimulation on myocyte and Purkinje cell APs?
Parasympathetic/vagal innervation – e.g. hiccups/hold breath, more ACh – decreases force of contraction – slows down refractory period (takes longer for heart to repolarise)
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Describe the effect of noradrenaline and acetylcholine on SA nodal cell
No resting potential, automatic (doesn’t wait for impulse fire)
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Describe features of class I (membrane stabilisers) (1)
Anti-arrhythmia drugs slow the rate of raise of phase 0 of AP by inhibiting fast sodium channels. Indications - SV and ventricular arrhythmias. Side effects - brady/tachycardia, prolong AT interval, predisposes to development of a polymorphic VT
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Describe features of class I (membrane stabilisers) (2)
(Torsades de pointes). Can increase/decrease or have no effect on duration of AP
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Give examples of class I drugs which increase the duration of AP
Disopyramide. Procainamide. Ajmaline and quinidine
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Give examples of class I drugs which decrease the duration of the AP
Lidocaine, mexiletine and phenytoin
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Give examples of class I drugs which have no effect on the duration of the AP
Propafenone, flecainide
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Describe features of class II (beta blockers) (1)
Reduce rate of spontaneous depolarisation of sinus and AV nodal tissue by indirect blockade of calcium channels
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Describe features of class II (beta blockers) (2)
Indirect block of Ca channels, block beta receptors, reduce amount of Ca released from SR, decreases influx of Ca into cell, slows down HR
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Give examples of beta blockers
Bisoprolol, atenolol, esmolol
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Describe features of class III (K+ channel blockers) (1)
Prolong duration of AP and increase the absolute refractory period by reduced influx of K+. Indications - SV and ventricular arrhythmias
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Describe features of class III (K+ channel blockers) (2)
May not affect peak/don’t makes heart beat less strong but beats slower
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Give examples of class III (K+ channel blockers)
Amiodarone, dronedarone, sotalol (high doses, beta blocker at low doses)
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Describe features of class IV (Ca 2+ channel blockers)
Prolong duration of AP and increase absolute refractory period, reduced influx of Ca 2+. Indications - SV and ventricular arrhythmias. Increase repolarisation time, ionotropic
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Describe the proarrhythmic effect of AAD (1)
All AAD have potential to precipitate serious arrhythmias (ventricular tachycardia or fibrillation)
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Describe the proarrhythmic effect of AAD (2)
Need to assess risk-benefit relationship (pro-arrhythmic actions should also be considered)
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What are the risk factors for arrhythmias?
Myocardial hypoxia, stress, smoking, electrolyte disturbances (reduces these risk factors reduce the risk of arrhythmias)
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Outline the pro-arrhythmic rank
Flecainide > propafenone > quinidine > ajmalin > disopyamide > procainamide > mexiletine > lidocaine > sotalol > amiodarone. Class I/C > I/A > I/B > III
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Which class prolongs the QT interval?
Mainly class IA prolongs the QT interval which predisposes to the development of a polymorphic ventricular tachycardia known as 'torsades de pointes'
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Outline the options for pharmacological intervention (1)
Class I agents (e.g. lidocaine) act on sodium channels (prevent Na influx). Class II agents (e.g. atenolol) act on beta receptors. Class III agents (e.g. amiodarone) block K channels. Class IV agents (e.g. verapamil) block calcium channels
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Outline the options for pharmacological intervention (2)
I f channel blockers (e.g. ivabradine) involved in regulation. Atropine – inhibits effect of parasympathetic NS, increase cAMP, heart beats faster
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What is an ECG?
Electrocardiogram - used to view electrical activity in the heart
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What does the P-wave indicate?
SAN depolarisation, amount of electricity released across atria for contraction, SAN firing, atria contracting
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What does the PQ interval indicate?
SAN has fired, atria contracted, blood forced into ventricles, no ventricular contraction yet, delay at AVN
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What does the QRS complex indicate?
AVN fires impulse - travels towards apex of the heart to cause ventricular contraction
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What does the ST interval indicate?
Period of rest
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What does the T-wave indicate?
Period of repolarisation (relaxation, cycle repeats after T-wave)
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What is Starling's Law? (1)
Stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant
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What is Starling's Law? (2)
As a larger volume of blood flows into the ventricle, the blood stretches the cardiac muscle fibres, leading to an increase in the force of contraction (force blood into ventricles, dilation, elastic effect)
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Describe features of sinus tachycardia
Caused by stress, fright and exercises. Illness - thyrotoxicosis, sepsis, volume depletion (dehydration). Medications - beta agonists, vasodilators, nicotine, caffeine, cocaine (possible to treat non-pharmacologically or pharmacologically)
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Describe features of atrial fibrillation (1)
A supraventricular tachyarrhythmia characterised by uncoordinated atrial activation with consequent deterioration of atrial mechanical function (no P-wave, R waves not equal distance)
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Describe features of atrial fibrillation (2)
Suppressed SAN (not fired in systematic way), atrial and ventricular contractions not coordinated, insufficient pumping, ventricles not filled properly
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What are the causes of atrial fibrillation?
Slowed conduction - electrolyte abnormalities, ischaemia, increased vagal tone, reduced sympathetic tone, anti-arrhythmias. Illnesses - thyrotoxicosis. Mechanical factors - hypertension, valvular heart disease, cardiomyopathy
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What is the impact of atrial fibrillation on a patient?
Affects quantity and quality of life. Events associated with AF include - death, stroke, hospitalisation, left ventricular dysfunction and heart failure, cognitive decline and vascular dementia
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What are the extracardiac factors?
Hypertension, obesity, sleep apnea, hyperthyroidism, alcohol, drugs
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What are the atrial structural abnormalities?
Fibrosis, dilation, ischaemia, infiltration, hypertrophy
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Outline the treatment plan for arrhythmias (1)
Acute rate and rhythm control (e.g. beta blockers, cardioversion) - leads to haemodynamic stability
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Outline the treatment plan for arrhythmias (2)
Manage precipitating factors (lifestyle changes, treatment of underlying CV conditions) - CV risk reduction
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Outline the treatment plan for arrhythmias (3)
Assess stroke risk (oral anti-coagulation in patients at risk for stroke) - stroke prevention
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Outline the treatment plan for arrhythmias (4)
Assess HR (rate control therapy) - symptom improvement preservation of LV function
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Outline the treatment plan for arrhythmias (5)
Assess symptoms (AAD, cardioversion, catheter ablation, AF surgery) - symptom improvement. All steps improve life expectance and improve quality of life, autonomy, social functioning
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Describe features of rhythm control
Used for reversible cause, new-onset AF, atrial flutter suitable for CV, continued symptoms after HR has been controlled
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What is cardioversion? (1)
Returning heart back into sinus rhythm either electrically (synchronised DC shock) or pharmacologically (class 1c flecainide in absence of structural heart disease or amiodarone. Anti-coagulation
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What is cardioversion? (2)
Decreased % of going back into sinus rhythm for each electrical cardioversion (maximum of 3 times)
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Describe features of prevention of abnormal rhythm
Patient target groups provided with medicines. Taken when heart has a faster/slower rhythm. Avoid 1c drugs (flecainide or propafenone) to people ischaemic or structural heart disease. Amiodarone for people with heart failure.
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Outline features of rhythm control strategy
Method of treatment determined by flow charts for acute management to restore sinus rhythm and management to maintain sinus rhythm (possible to use catheter to burn electrical pathway causing abnormal rhythm)
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Atrial fibrillation increases the risk of what?
Stroke (risk increases with age)
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Describe how the risk of stroke is assessed (1)
CHA2DS2VASC - gives stroke rate per year (people may die from stroke or survive and are disabled). Score gives % risk of stroke
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Describe how the risk of stroke is assessed (2)
Determines type of treatment e.g. anti-coagulants
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Describe features of left atrial appendage and thrombus formation in AF
Appendage on the left atrium doesn't do harm. But if clot is pumped into systemic circulation, there is an increase risk of stroke (shape/size of clot may indicate cause of stroke)
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Describe features of rate control strategy in AF
Control left ventricular rate (look at left ventricular ejection fraction to determine type of pharmacological treatment)
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Describe features of AF treatment options - rate control
Rate control (if LVEF < 40% use beta blocker and digoxin or amiodarone, if LVEF > 40% use beta blocker and/or diltiazem and/or verapmail and/or digoxin)
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Describe features of AF treatment options - digoxin
Digoxin. Action - blocks Na-K ATPase pump. Effect - reduces HR without reducing force of contraction. Side effects - bradycardia, nausea, vision disorders (requires TDM)
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Describe features of AF treatment options - stroke prevention
Vitamin K antagonist e.g. warfarin, phenindione. Action - blocks synthesis of vitamin K dependent clotting factors. Effect - reduce clotting time (measured by INR). Side effects - haemorrhage, alopecia, skin necrosis, CNS haemorrhage
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Describe features of AF treatment options - oral anti-coagulants (1)
Directly acting eg. dabigatran, apixaban, rivaroxaban, edoxaban factor Xa inhibitor
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Describe features of AF treatment options - oral anti-coagulants (2)
Action - blocks synthesis of vitamin K dependent clotting factors. Effect - reduces clotting time (measured by INR). Side effects - haemorrhage, alopecia, skin necrosis
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How is AF treatment monitored?
CHADSVASC, bleeding risk, adherence, INR if on VKA
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Describe features of ventricular tachycardia
Most common cause of sudden death. Can occur in people with no history of VAs. Genetic links (e.g. long QT syndrome, Brugada) - benefit from ICD or medication
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What are the causes fo ventricular tachycardia?
Familial long QT syndrome, AAD, electrolyte disturbances, hypomagnesaemia, hypokalaemia, hypocalcaemia, hypoxia, acidosis
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What are the symptoms of ventricular fibrillation?
Sudden collapse or become unconscious. Symptoms may occur within minutes to 1 hr before collapse - chest pain, dizziness, nausea, rapid heart beat, SOB (ECG - no defined R waves)
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Describe features of Torsade de Pointes
Electricity moving through the heart quickly, no effective contraction. Treatment - immediate ALS (CPR/defibrillator), ICD/implantable cardioveter-defibrillator, lidocaine IV (mexelitine po), procainamide - class 1b, sotalol or amiodarone
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Which type of training is provided for all HCPs?
First Aid Training. Cardiac arrest is an electrical problem (person will be unconscious), CPR. A heart attack is a circulation problem (person will be conscious)
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Describe features of implantable cardiac defibrillators
Generator embedded in chest, wires in heart. Administer small amounts of electricity to the heart when rhythm becomes faster (feels like a shock)
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Describe the treatment options to prevent VT - amiodarone (1)
Action - mixed action (K+ channel blockade). Effect - reduce HR (without reducing force of contraction). Side effects - arrhythmias, hepatic disorders, hyperthyroidism, nausea, respiratory disorders, skin reactions, constipation, corneal deposits
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Describe the treatment options to prevent VT - amiodarone (2)
Hypothyroidism, movement disorders, photosensitivity reaction, sleep disorders, taste altered, vomiting, hypotension (IV only). Interactions - warfarin (increases INR), other AAD
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Describe the treatment options to prevent VT - mexiletine (1)
Action - Na channel blocker (1b) decreases duration of refractory period. Effect - reduces spontaneous depolarisation. Side effects - tiredness, poor coordination, dry mouth, numbness, tingling, tremor, tinnitus
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Describe the treatment options to prevent VT - mexiletine (2)
Interactions - CYP450 inducers or inhibhitors cimetidine, fluvoxamine, propafenone, rifampin, phenytoin, other AADs
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What is asystole?
No further shocking of the heart will get it back into sinus rhythm. Cardiac arrest (flatline). Heart not functioning
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