Arrhythmias Flashcards
Arrhythmias are…
disturbances of heart rate (frequency) rhythm (regularity of beats)
Alterations in impulse formation involve….
changes in automaticity (loss of overdrive suppression) or triggered activity
Abnormalities in impulse conduction arise from…
re-entry, conduction block and accessory tracts
The SA node is the _______1______ of the heart, but all components of the cardiac conduction system demonstrate a (slower) spontaneous phase 4 depolarization and thus possess _____2_____
usual physiological pacemaker
automaticity
The SA node possesses overdrive suppression, what does this mean? How does it maintain this?
It has the highest frequency so it supresses the other latent pacemakers. In order for the SA node to exert its normal control of rate and rhythm it must discharge action potentials at a higher, regular, frequency than any other structure in the heart.
What order do latent pacemakers take over and what is the rate of firing?
- If SA node was damaged then first latent pacemaker to take control is AV node 50-60bpm
- Next to take control is Purkinje fibres at 30-40bpm
- Even if all these are broken ventricles can do it on its own but this would be very low
Explain 3 ways loss of overdrive suppression can occur?
1) May occur if the SA node firing frequency is pathologically low, or if conduction of the impulse from the SA node is impaired. A latent pacemaker may initiate an impulse that generates an escape beat (additional cardiac contraction). A run of such impulses may give rise to an escape rhythm, a series of escape beats
2) May occur if a latent pacemaker fires at an intrinsic rate faster than the SA node rate (even if the SA node is functioning normally). Latent pacemaker initiates an ecoptic beat, or a series of such beats generating an ectopic rhythm (i.e. one not generated by the SA node – ectopic meaning in an abnormal place, or position). Ectopic rhythms can result from ischaemia, hypokalaemia, increased sympathetic activity, fibre stretch and other causes
3) Can occur in response to tissue damage (e.g. post myocardial infarction). Even non-pacemaker cells (i.e. myocytes), when partially depolarized, may assume spontaneous activity
Triggered activity occurs when….
- A normal action potential triggers abnormal oscillations in membrane potential termed afterdepolarizations (ADs) that occur during, or after, repolarization
- Can be early depolarisation (EADs) or delayed afterdepolarisations (DADs)
- Repeated after depolarisation of either types may cause sustained depolarisation
- Triggered initially by a normal action potential but do not arrive from activity in the SA node.
Difference between EADs and DADs
EADs= Occur during the inciting action potential within phase 2 mediated by opening of voltage activated calcium channels . Most likely to occur in slow heart rate
DADs= Occurs after complete repolarisation. Most likely to occur in fast heart rate.
Conduction blocks?
1) Partial block- tissue conducts all impulses but more slowly than usual, this is benign and known as First degree AV block, shown as long PR interval
2) Intermittent block- tissue conducts some impulses, but not others- second degree AV block occurring as two types
- Mobitz type I – PR interval gradually increases from cycle to cycle until AV node fails completely and a ventricular beat is missed.
- Mobitz type II –PR interval is constant but every nth. ventricular depolarization is missing.
3) Complete block no impulses are conducted through the affected area- third degree Av block. No relationship between atria and ventricular beats. ventricular pacemaker is now the Purkinje fibres – fire relatively slowly and unreliably – manifest as bradycardia and low cardiac output. Can’t treat with drugs need an intraventricular pace maker
Accessory tract pathways happen when …
individuals possess electrical pathways in parallel to the AV node. A common pathway is the bundle of Kent. The impulse through bundle of Kent is conducted more quickly than that through the AV node. Ventricles receive impulses from both the normal and accessory pathways – can set up the condition for a re-entrant loop predisposing to tachyarrhythmias.
Target for class 1 anti-arrhythmic drugs is?
Voltage-activated Na+ channel and the upstroke of depolarisation
Target for class 2 anti-arrhythmic drugs?
B-adrenoceptor (as antagonists) to decrease rate of depolarization in SA and AV nodes
Target for class 3 anti-arrhythmic drugs?
Voltage-activated K+ channels (plus others) to prolong AP duration increasing refractory period.
Target for class 4 anti-arrhythmic drugs?
Voltage-activated Ca2+ channels to slow conduction in SA and AV nodes. Decrease force of cardiac contraction.
Name seven supra ventricular arrhythmias
Normal sinus arrhythmia Sinus bradycardia Sinus tachycardia Atrioventricular nodal re-entrant tachycardia Atrioventricular re-entrant tachycardia Atrial fibrillation Atrial flutter
Normal sinus arrhythmia is slight variations in heart rate due to _______
reflex changes in vagal tone during the respiratory cycle
Sinus bradycardia can ___1__ or it can be caused by __2___ or ___3____
If it is acute it can be treated with __4_____
If it is chronic and causing haemodynamic compromise then ___5_____
1 physiological 2 drugs 3 ischaemia 4 atropine 5 pacing is required
Sinus tachycardia could be due to __________
You should try and treat the underlying cause but if it is persistent then _______
anxiety, fever, anaemia, hypotension or drugs
beta blockers
ATNRT happens when there are two pathways: __1__and__2__ in AV node
1 fast
2 slow
ATNRT and ATRT present similarly and can both be treated by….
Valsalva manoeuvre (pop ears), right carotid massage, immersion in cold water
If harm-dynamically unstable may require emergency cardioversion
AVRT is due to ___1_____ between the atria and ventricles and results in a macro re-entry circuit where the _2___ are activated after the ___3___
ON ECG P waves are seen ___4____
Accessory pathways that conduct from ventricles to atria are ___5___ on ECG in sinus rhythm.
Those that conduct from atria to ventricles result in _____6______ of the ventricles known as _____7_____
On ECG this is characterised by ___8___
This can be caused by ___9____
1 accessory pathways 2 atria 3 ventricles 4 between QRS and T wave 5 concealed 6 partial depolarisation 7 pre-excitation 8 short PR interval wide QRS and QRS begins with a slurred part known as a delta wave 9 Wolff-Parkinson White syndrome
Is atrial fibrillation common or uncommon?
Common
Causes of atrial fibrillation
rheumatic heart disease, alcohol intoxication, thyrotoxicosis, hyperthyroidism, hypertension and after cardiac surgery. In some patients cause not identified (lone AF)
AF happens with continuous rapid activation of the atria by ____1____ The atria response electrically at this rate but there is no ____2_____ Only a proportion of the impulses are ___3___
1 re entry wavelets
2 co-ordinated mechanical action
3 conducted to the ventricles
Symptoms of AF
Variable but can be asymptomatic or emergency admission with rapid palpitations, dyspnoea and or chest pain after onset.
3 types of AF
Paroxysmal
Persistent
Permanent
In AF the pulse and ECG is
irregularly irregular
In AF
On ECG there are no ___1____ and there is the presence of ___2___ which are __3____
1 p waves
2 f waves
3 oscillations of the base line
2 methods of AF treatment?
Ventricular rate control by drugs
digoxin, beta blockers, verapamil/ dilitiazem
Cardioversion
convert to normal rhythm electrically or with drugs
In AF anticoagulation should always be done if risk of thrombosis-emoblism high as in AF there is a high risk of
stroke
Atrial flutter is similar to AF but
the heart is still beating regularly
Ventricular ectopics cause an __1___ pulse due to __2___ the patient complains of ___3__
1 irregular
2 premature beats
3 extra, missed or heavy beats
Sustained ventricular tachycardia often results in ______1_______
This is a ___2____ rhythm
1 pre-syncope, syncope, hypotension and cardiac arrest
2 shockable
Ventricular tachycardia until proven otherwise if
A wide QRS complex with history of CAD/HF
Ventricular fibrillation results in __1___ It is rapid and ___2__ ventricular activation with ___3___
Treatment is ___4____
1 cardiac arrest
2 irregular
3 no mechanical effect
4 early defibrillation and CPR
ECG on
1) First degree block
2) Mobitz type 1
3) Mobitz type 2
1) prolonged PR interval (more than 0.2 secs)
2) Gradually lengthening Pr interval and then a P waved with missed QRS
3) P wave that doesn’t conduct every nth beat with no changes in other pr intervals
How does adenosine help differentiate between arrhythmias?
Adenosine prolongs AV nodal delay so it slows down the heart rate in SVT but will have no effect in VT
What is Brugada syndrome
genetic abnormality that accounts for VF in patients with no evidence of causative structural cardiac disease.
ECG of brugada syndrome?
domed ST elevation and RBBB in V1-3
In brugada syndrome VF is triggered by…
Sleep, fever, excessive alcohol and large meals.
Management of brugada syndrome?
Avoid certain anti-arrhythmic drugs and triggers
There is lots of variation in QT length but as a general rule it is long if it is more than ….
440ms in males or 450ms in females
In congenital long QT syndrome the hallmark arrhythmia is
Polymorphic VT (Torsades de Pointes VT)
In AF in young person with no other reasons think…
Long QT syndrome
Primary presenting complaint of long QT syndrome?
Dizziness and blackouts
Triggers of long QT syndrome
exercise, sudden auditory stimuli, sleep, qt prolonging states such as medication or hypokalaemia
Management of long QT syndrome?
Avoid QT prolonging drugs, avoid triggers, correct any electrolyte abnormalities and beta blockers
In AF the heart rate is usually more than
300 bpm
AF is due to
Ectopic foci in muscle sleeves in the ostia of the pulmonary veins
In complete heart block the heart rate is
regular
Adenosine will slow down
supra ventricular tachycardias as it works on the AV node
Vagal manouvres work on AV node so will therefore not work in
ventricular tachycardias
Is the patient always haemodynamically unstable in VT?
No
What is torsades de pointes?
A specific type of VT that occurs in people with long QT syndrome
What medications can cause syncope/ bradycardias?
Antihypertensives, tricyclic antidepressants and neuroleptics
