Arrhythmias Flashcards
Bradycardia
HR is slow (
Tachycardia
SHR is fast (>100 bpm)
More likely to be symptomatic when arrhythmia is fast and sustained
Subdivided into supra ventricular tachycardias (SVTs) and ventricular tachycardias (VTs)
What is the normal cardiac pacemaker?
the sinus node
What controls the sinus node?
Autonomic nervous system with parasympathetic predominating, resulting in slowing of the spontaneous discharge rate
When is sinus bradycardia normal?
During sleep and in well-trained athletes
Causes of sinus bradycardia that are intrinsic to the heart
Acute ischaemia + infarction of sinus node (from MI)
Chronic degenerative changes e.g. fibrosis from atrium and sinus node (sick sinus syndrome) - elderly
What 2 things can sick sinus syndrome be caused by?
Sinus arrest
SA block
What would an ECG show for sick sinus syndrome?
Intermittent pauses between consecutive P waves (>2s, dropped P waves) and bradycardia
What is the normal PR interval?
0.12 - 0.20 seconds
Aetiology of heart block
Coronary artery disease
Cardiomyopathy
Fibrosis of the conducting tissue (esp. elderly)
What causes an atrioventricular block?
Block in the AV node or His bundle?
What does a block inferior to the AV node/His bundle in the conduction system cause?
Bundle branch blocks (right or left)
What is a 1st degree AV block?
Delayed AV conduction
Prolonged PR interval (>0.22 s) on the ECG
No change in the HR and Tx unnecessary
Whats a 2nd degree AV block?
Some atrial impulses fail to reach ventricles
Intermittent failure of AV impulse
What is Wencheback block phenomenon also called?
Type I block (in second degree AV block)
What happens in type I second degree AV block?
Progressive PR interval prolongation until a P wave fails to conduct (i.e absent QRS after the P wave)
PR wave then returns to normal + cycle repeats itself
What happens in type II 2nd degree AV block?
Dropped QRS complex isn’t proceeded by progressive PR interval prolongation. Usually QRS complex is wide
what type of heart block is this:
When every 2nd or 3rd P wave conducts the ventricles
e.g. 2 P waves to each QRS complex
2:1 or 3:1 (advanced) type of second degree AV block
What heart block is it when P waves and QRS complexes occur independently of teach other on the ECG
Third degree AV block/ complete heart block
All atrial activity fails to reach the ventricles
In complete atrioventricular heart block how are ventricular contractions maintained?
By a spontaneous escape rhythm originating below the site of the block in either the His bundle or the His-Perkinje system
In bundle branch block, what does the shape of the QRS complex depend on?
Whether the right or left bundle is blocked
It will be wide though as its always a complete block
RBBB - what happens and what kind of patients does it occur in?
The 2 ventricles dont contract simultaneously
Sequential spread of an impulse –> secondary R wave
Healthy pts, PE, RV hypertrophy, IHD and congenital
LBBB indicates what?
underlying pathology
IHD, LVH, aortic valve disease + after cardiac surgery
Where do supra ventricular tachycardias arise from?
The atrium or the atrioventricular junction
Conduction is via the His-Purkinje system
Sinus tachycardia cause
Physical response during exercise + excitement
Also occurs with: fever, anaemia, HF, thyrotoxicosis, acute PE, hypovolaemia and drugs
Tx sinus tachycardia
Treat underlying cause
BBs may be used to slow sinus rate
Whats a tachycardia? and the 2 types?
> 100 bpm
SV ones - from the AV node
Ventricular ones - from bundle of His
3 cellular mechanisms for cardiac arrhythmias
- abnormal conduction/re-entry
- abnormal automaticity: depolarisation-induced automaticity
- triggered activity:
- EAD
- DAD
Early (EAD) and delayed (DAD) after depolarizations
How can non-pacemaker sites result in enhanced automaticity and therefore an arrhythmia?
Depolarised tissue e.g. ischamia, scar Metabolic/electrolyte imbalance Relatively 'depolarised' MP Reduced threshold potential Increased Ca2+ current
What are AV junctional tachycardias a result of?
re-entry circuits in which there are 2 separate pathways for impulse conduction
What is AVNRT?
Whats it a result of
Atrioventricular nodal re-entry tachycardia
Most common SVT
Due to a ring of conducting pathway in AV node. ‘Limbs’ have differing conduction times + refractory periods
Re-entry circuit. Impulse –> circus movement tachycardia
What would the ECG of AVNRT show?
discrete P waves not visible
QRS complex usually normal shape as ventricles are activated in the normal way, down BoH
Whats AVRT?
AV reciprocating tachycardia.
NOT NODAL
Due to presence of accessory pathway that connects the atria and the ventricles
What is the delta wave a feature of?
Wolff-PArkinson-White syndrome
- a congenital abnormality
(a type of AVRT)
ECG of Wolff-Parkinson-White syndrome
Path allows some of the atrial depolarisation to pass quickly to the ventricle before it gets through AV node
Early depolarisation of part of the ventricle –> shortened PR interval and a slurred start to the QRS (delta wave) QRS is narrow
What does the magnitude of the delta wave depend on?
how much of myocardium is affected by the accessory pathway
Symptoms of AV junctional tachycardias
rapid regular palpitations usually with abrupt onset and sudden termination
other: dizzy, dyspnoea, central chest pain + syncope
Acute management of AV junctional tachycardia
Aim: to restore + maintain sinus rhythm
- emergency cardioversion
Acute Mx for AV junctional tachycardia if haemodynamically stable?
Increase vagal stimulation of the sinus node by Valsalva mechanism
Adenosine
What is adenosine and what’s its mechanism of action?
short-acting AV nodal-blocking drug that will terminate most junctional tachycardias
Increases AV node refractoriness, breaking the re-entry circuit –> cardioversion
Features of atrial fibrillation?
- irregularly irregular
- varying rate
- absent p waves
Presentation of atrial fibrillation?
usually incidental finding
but we worry about CLOTS (associated with 5 fold increase in stroke)
no clear p waves on ECG
the 3 aspects to atrial fibrillation management
a. rate control
b. rhythm control
c. thromboprophylaxis
How would you control the rate therapeutically for AF?
BB or calcium antagonists
Rhythm control management for AF?
Electrical direct current (DC) cardioversion and then administration of BBs to suppress the arrhythmia
Symptoms of ventricular ectopic premature beats
asymptomatic. or extra beats/ missed beats/ heavy beats
What happens in ventricular ectopics ECG
beat isn’t conducted to ventricles through the normal conducting tissue
QRS complex on ECG is widened with bizarre configuration
Tx for ventricular ectopics
beta blockers if symptomatic e.g. atenolol
ECG for sustained ventricular tachycardia
> 30 seconds. rapid ventricular rhythm with broad abnormal QRS complexes
What is non-sustained ventricular tachycardia?
VT >/= 5 consecutive beats but lasting
How is recurrence of sustained ventricular tachycardia prevented?
beta-blockers or implants bel cardiac defibrilator
What’s long QT syndrome?
ventricular depolarisation is greatly prolonged
Causes of long QT syndrome?
congenital
electrolyte disturbances
variety of drugs
Symptoms of long QT syndrome
palpitations, syncope (from polymorphic VT which normally stops spontaneously but may degenerate into VF)
Tx of long QT syndrome
underlying cause + IV isoprenaline
What natural hormone is isoprenaline similar to?
epinephrine/adrenaline
What would no effective CO cause?
cardiac arrest!!!
Atrial flutter rate?
Atrial rate is typically 300 bpm and AV node usually conducts every second flutter beat, giving ventricular rate of 150 bpm
Atrial flutter ECG
‘sawtooth’ flutter waves (F waves)