Arrhythmias Flashcards
what are the 2 types of shockable rhythm in a pulseless patient
ventricular tachycardia
ventricular fibrillation
what are the 2 types of non-shockable rhythm in a pulseless patient
- Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole (no significant electrical activity)
how can bradycardia be defined
HR < 60bpm
- absolute: HR <40 bpm
- relative: HR inappropriately slow for the haemodynamic state of the pt. signs which may indicate dynamic instability include SBP<90mmHg, HR < 40bpm, poor perfusion, poor urine output
how can bradycardias be classified
according to the pacemarker which is at fault:
- sinus node
- AV node
what can sinus node dysfunction be due to
- sinus bradycardia
- sick sinus syndrome (tachy-brady)
- sinus arrest alone
- part of vasovagal syncope
not all patients are symptomatic but in those that are, a pacemaker is indicated
what are less common causes of sinus bradycardia
- rheumatic fever
- viral myocarditis
- amyloidosis
- HH
- pericarditis
what is narrow complex tachycardia
fast HR with QRS complex duration <0.12s (3 small squares)
what are the 4 main differentials of a narrow complex tachycardia
- Sinus tachycardia (treatment focuses on the underlying cause)
- Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
- Atrial fibrillation (treated with rate control or rhythm control)
- Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)
describe the ECG features of sinus tachycardia
normal P wave, QRS complex, T wave
- not an arrhythmia but usually a response to an underlying cause e.g. sepsis or pain
describe the ECG features of SVT
looks like a narrow QRS complex followed immediately by a T wave then a QRS complex, etc
- there are P waves but buried in T waves so difficult to see
- distinguish from AF by its regular rhythm and absence of saw-tooth pattern
how can you distinguish SVT from sinus tachycardia
- SVT has an abrupt onset and regualr pattern without variability
- sinus tachy has a more gradual onset and more variability
- sinus tachy also normally has an explanation e.g. pain or fever whereas SVT can appear at rest w no apparent cause
how can SVT further be classified
- AVNRT (AV nodal re-entry tachycardia ~ 60%)
- AVRT (AV re-rentry tachycardia ~ 30%)
what is the 1st line treatment for haemodynamically stable patient with SVT
vagal manouevres
- breath holding/valsalva to slow conduction in AV node and disrupt re-entrant circuit
- carotid massage: carotid sinus for several seconds on the non-dominant cerebral hemisphere side (auscultate for bruit first and do not perform simultaneously)
what is the next option if SVT is not terminated by vagal manouevres
IV adenosine or CCB
how is adenosine best administered for SVT
3 way stopcock - short acting drug that blocks AV node conduction
- given as rapid IV bolus followed by 0.9% NaCl saline flush
- 6mg stat, 12mg if unsuccessful, then further 12mg if still unsuccessful
- antecubital fossa
very short half life
what should the patient be warned about before administering adenosine
chest discomfort, transient hypotension, flushing
what patients should adenosine be avoided in
patients with significant reversible airways disease
what does it suggest if the tachycardia continues despite successful induction of at least some degree of AV blockade
that the rhythm is certainly atrial tachy or AF
- AVRT is excluded and AVNRT is very unlikely
when can synchronised cardioversion be used in SVT
following sedation starting at 150J can be used immediately in pt who are hypotensive, have pulmonary oedema, chest pain with ischaemia or are otherwise stable
what can be used as an alternative to adenosine
- verapamil 5-10mg slowly IV: dangerous and contraindicated in pt already on B-blockers/ with significant LV dysfunction
- flecainide IV: avoid in pt w past or present MI
if both adenosine and verapamil are ineffective or contraindicated in SVT, what should be done
electrical cardioversion under GA or sedation
give examples of second line drugs used to prevent SVT
flecainide
sotalol
amiodarone
what are the ECG features of AF
absent P waves, irregularly irregular ventricular rhythm
how is AF diagnosed
- manual pulse checks: for irregularity in the presence of symptoms for AF e.g. dyspnoea, palpitations, syncope/dizziness, chest discomfort
- ECG: to confirm if irregular pulse is due to AF
what is the next step if paroxysmal AF is suspected
further cardiac monitoring - 24hr cardiac monitor is the 1st line investigation
what are 3 indications for echocardiography
- perform if suspected structural heart disease (either based on symptoms or finding of murmur/signs of heart failure)
- where cardioversion is being considered
- baseline required to inform long term management
what should not be delayed whilst waiting for an echo in AF
anticoagulation if appropriate
what are the 3 broad management principles of AF
- anticoagulation to prevent stroke
- rate control
- rhythm control
what is the CHA2DS2VaSc score
recommended once AF has been documented to quantify the risk of stroke of systemic embolism
how can the CHA2DS2VaSc score be interpreted
- A score of 2 or more is associated with significant risk, where risk of embolic stroke is considered high enough to offer anticoagulation
- A score of 1 in men is considered intermediate risk, where anticoagulation should be considered, and a careful decision has to be made keeping in mind the bleeding risk
- A score of 0 indicates a truly low risk of stroke and anticoagulation is not offered
- A score of 1 in women (due to gender) and a score of 0 are considered low risk, with anticoagulation not advised
what scoring system is used to quantify risk of major bleeding
HAS-BLED
- estimates rate of major bleds per 100 patient years which can be compared to the CHAD2DS2VaSc score
what is the purpose of the HAS-BLED score
inform discussions and enable identification and optimisation of reversible risk factors for bleeding including:
- uncontrolled HTN SBP>160mmHg
- poor INR control
- concurrent meds e.g. aspirin, NSAIDs
- excess alcohol consumption
what are the advantages of DOACs over warfarin for anticoagulation
- DOACs do not require regular testing of levels compared to INR monitoring of warfarin (but excreted by kidneys so monitor renal function yearly)
- no restrictions on food or alcohol
- lower bleeding rates
- better reduction in stroke
what are ECG features of atrial flutter
sawtooth appearance, repeated P waves ~300/min, narrow complex tachycardia
The signal does not usually enter the ventricles on every lap due to the long refractory period of the atrioventricular node. This often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute
what are life threatening features of atrial flutter and what is the treatment for this
LOC, heart muscle ischaemia (chest pain), shock, severe heart failure
- synchronised DC cardioversion under sedation or general anaesthesia
Intravenous amiodarone is added if initial DC shocks are unsuccessful
how is a broad complex tachycardia defined and how is it broken down
QRS complex > 0.12s
* Ventricular tachycardia or unclear cause (treated with IV amiodarone)
* Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
* Atrial fibrillation with bundle branch block (treated as AF)
* Supraventricular tachycardia with bundle branch block (treated as SVT)
how is the QT interval measured and what is the QTc
start of QRS complex to the end of the T wave
- QTc is the corrected QT interval which estimates the QT interval if the HR were 60bpm
how is a prolonged QT interval defined
- More than 440 milliseconds in men
- More than 460 milliseconds in women
what does a prolonged QT interval represent
prolonged repolarisation of the myocytes after a contraction
- this can result in spontaneous depolarisation (afterdepolarisation)
- these can spread through the ventricles causing a contraction before proper repolarisation
When this leads to recurrent contractions without normal repolarisation, it is called torsades de pointes
what are the 2 outcomes of torsades de pointes
- terminate spontaneously and revert to sinus rhythm
- progress to v.tach which can lead to cardiac arrest
what are causes of prolonged QT interval
- Long QT syndrome (an inherited condition)
- Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
- Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
what does management of prolonged QT interval involve
- Stopping and avoiding medications that prolong the QT interval
- Correcting electrolyte disturbances
- Beta blockers (not sotalol)
- Pacemakers or implantable cardioverter defibrillators
what is the acute management of torsades de pointes
- Correcting the underlying cause (e.g., electrolyte disturbances or medications)
- Magnesium infusion (even if they have normal serum magnesium)
- Defibrillation if ventricular tachycardia occurs
magnesium sulfate IV!
what are ventricular ectopics and how do they appear on an ECG
premature ventricular beats caused by random electrical discharges outside the atria
- relatively common in all ages and healthy patients but more common in those with pre-existing cardiac conditions e.g. ischaemic heart disease or HF
what is bigeminy
refers to when every other beat is a ventricular ectopic
what is 1st degree heart block and how does it appear on an ECG
delayed conduction through the atrioventricular node
- despite this, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex
- on an ECG, first-degree heart block presents as a PR interval greater than 0.2 seconds (5 small or 1 big square)
what is 2nd degree heart block and what are the 2 types
some atrial impulses are not conducted via the AV node to the ventricles so there are instances where P waves are not followed by QRS complexes
- mobitz type I (Wenkebach)
- mobitx type II
describe the ECG features of Mobitz Type I heart block
conduction through the atrioventricular node takes progressively longer until it finally fails, after which it resets, and the cycle restarts.
- On an ECG, there is an increasing PR interval until a P wave is not followed by a QRS complex which is dropped. The PR interval then returns to normal, and the cycle repeats itself
can occur in young fit patients with high vagal tone so can be seen during the night if monitored
describe the ECG features of Mobitz Type II heart block
intermittent failure of conduction through the atrioventricular node, with an absence of QRS complexes following P waves - the PR interval remains normal
- usually a set ratio of P waves to QRS complexes
In the absence of a recent acute coronary event, permanent pacing should be arranged (if drugs have been excluded)
what is there a risk of with Mobitz type II
asystole
what are the ECG features of 3rd degree heart block or complete heart block
This is characterised by no conduction from the atria to the ventricles and therefore AV dissociation - there is no relationship between the P waves and QRS complexes
- block can occur above the AV node at the His region (narrow complex escape and usually well tolerated such as congenital complete heart block) or beneath the AV node with broad complex escape (not well tolerated)
- can also be intermittent therefore look for ECGs with trifascicular or bifascicular block (RBBB, left axis deviation with or without prolonged PR interval) and alternating LBBB and RBBB
significant risk of asystole
what are causes of complete heart block
- various anti-arrhythmic drugs - notably digoxin toxicity
- can occur following inferior STEMI(< 10% of cases) and in this context can resolve in hours to days
- more ominous finding following anterior MI (infranodal)
- severe hyperkalaemia (can be treated with IV calcium chloride - 10 ml of 10% solution over 3-5 minutes)
- In the haemodynamically unstable patient, atropine can be administered (600 μg to a maximum of 3 mg)
- Isoprenaline administered at a rate of 5 μg/min can be tried
what treatment is indicated in complete heart block
urgent permanent pacing within 24hrs
what is sick sinus syndrome
encompasses many conditions that cause dysfunction in the sinoatrial node
- often caused by idiopathic degenerative fibrosis of the sinoatrial node
- can result in sinus bradycardia, sinus arrhythmias and prolonged pauses
what does management of unstable patients and those at risk of asystole involve
- Intravenous atropine (first line)
- Inotropes (e.g., isoprenaline or adrenaline)
- Temporary cardiac pacing
- Permanent implantable pacemaker, when available
what are options for temporary cardiac pacing
- Transcutaneous pacing, using pads on the patient’s chest
- Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly
how does atropine work and what are its side effects
antimuscarinic medication and works by inhibiting the parasympathetic nervous system
- side effects: pupil dilation, dry mouth, urinary retention and constipation.
what are the ECG changes seen in hyopthermia
- bradycardia
- ‘J’ wave (Osborne waves) - small hump at the end of the QRS complex
- first degree heart block
- long QT interval
- atrial and ventricular arrhythmias
what are causes of left axis deviation
- left anterior hemiblock
- left bundle branch block
- inferior myocardial infarction
- Wolff-Parkinson-White syndrome - right-sided accessory pathway
- hyperkalaemia
- congenital: ostium primum ASD, tricuspid atresia
- minor LAD in obese people
what are causes of right axis deviation
- right ventricular hypertrophy
- left posterior hemiblock
- lateral myocardial infarction
- chronic lung disease → cor pulmonale
- pulmonary embolism
- ostium secundum ASD
- Wolff-Parkinson-White syndrome - left-sided accessory pathway
- normal in infant < 1 years old
- minor RAD in tall people
what is WPW syndrome
caused by an extra electrical pathway connecting the atria and ventricles which is somtimes called the Bundle of Kent
- additional pathway allows electrical activity to pass between the atria and ventricles, bypassing the atrioventricular node
what are the ECG changes of WPW syndrome
- Short PR interval, less than 0.12 seconds
- Wide QRS complex, greater than 0.12 seconds
- Delta wave
The delta wave appears as a slurred upstroke in the QRS complex. It is caused by the electricity prematurely entering the ventricles through the accessory pathway
what is the definitive treatment of WPW syndrome
radiofrequency ablation of the accessory pathway
what is there a risk of in a patient with combined AF/atrial flutter and WPW syndrome
there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles, causing a polymorphic wide complex tachycardia = life-threatening medical emergency
what medications are contraindicated in WPW syndrome and why
most anti-arrhythmic medications e.g., beta blockers, calcium channel blockers, digoxin and adenosine
- increase this risk by reducing conduction through the AV node and promoting conduction through the accessory pathway
what are indications for synchronised DC cardioversion
- shock: hypotension if systolic BP <90mmHg, pallow, confusion
- syncope
- myocardial ischaemia
- HF
in what patients should GTN be used with caution
hypotensive patients!
how is symptomatic bradycardia treated
IV atropine
when haemodyamically unstable e.g. confusion, clamminess, hypotension
what are indications for cardio version for patients with AF
- symptoms present for < 48 hours
- be anticoagulated
if a pt w AF has a stroke or TIA what is the anti-coagulation of choice
- warfarin
- direct thrombin or factor Xa inhibitor
which clinical sign can be used to differentiate between cardiac tamponade and constrictive pericarditis
positive Kussmaul’s sign - raised JVP that doesn’t fall with inspiration (CP)
what is the 1st line treatment for regular broad complex tachycardia with no adverse features
IV amiodarone
