cardiac arrhythmia Flashcards
what are the two different types of cardiac myocytes
non-specialised and specialised conducting myocytes
what is the difference between non-specialised and specialised myocytes
the difference is electrophysiological ie the difference in the character of the action potentials (which are distinct bc of different types and populations of cardiac ion channels)
QRS
the summation of all action potentials in the ventricles
P wave duration (atrial conduction), PR interval (ANV conduction) and the QRS (ventricular depolarisation)
reflects the speed and sequence of depolarisation and cardiac conduction
describe the anatomy of cardiac conduction
the SA node is located near the RA next to the atrial appendage, and this is where the rhythm of the heart originates, the SA node conducts through intranodal tracks to the atrioventricular node, this passes through ht fibrous layer dividing the atria from the ventricles and it connects to the ventricles through the Bundle of His, the Bundle of His then progresses into the ventricles and the conducting fibres divide into two main sections - the left and R bundle - the left bundle consists of two fascicles (the left posterior fascicle and the left anterior fascicle) and these primarily supply the left ventricle
the fascicles then further divide into the purkinje fibres that supply the rest of the myocardium
ectopy
when arrhythmia occurs as single beats
arrhythmia can occur continuously
as persistent/sustained or paroxysmal/non-sustained
SVT
supraventricular arrhythmias
ie happens anywhere above the AV node
> the ECG shows a narrow QRS
» include SVT tachycardia ie AF, atrial flutter, ectopic atrial tachycardia
»bradycardia ie sinus bradycardia and sinus pauses
ventricular arrhythmias
include ventricular ectopics or premature ventricular completes (PVC)
>ventricular tachycardia VT
>ventricular fibrillation VT
>asystole (ie no contraction at all)
AV node arrhythmias
> AVn re-entry tachycardia (AVNRT)
AV reciprocating or AV re-entrant tachycardia (AVRT)
AV block (from 1-3 degrees)
clinical causes of arrhythmias (6)
> abnormal anatomy that allows re-entrant circuits
-accessory pathways
-congenital HD
autonomic nervous system (ANS)
-sympathetic stimulation ie stress, exercise, hyperthyroidism, increased vagal tone causing bradycardia
metabolic
-hypoxia ie PE or chronic pulmonary disease
-ischaemic myocardium ie acute MI / angina
-electrolyte imbalance
inflammation : viral myocarditis - causing scarring on tissue
drugs
genetics
-mutations of genes encoding cardiac ion channels ie the congenital long QT syndrome
electrophysiological mechanisms of arrhythmia (1)
ectopic beats (focal activity)
- beats or rhythm that originate in places other than the SA node
- altered automaticity ie ischaemia /catecholamines (adrenaline)
- triggered activity ie digoxin / long QT syndrome
electrophysiological mechanisms of arrhythmia (2)
re entry : require more than one conduction pathway with different speed of conduction (depolarisation) and recovery of excitability (refractoriness)
-accessory pathway tachycardia, previous MI, congenital heart disease
how abnormal physiology and pathology causes arrhythmia - ones that increase phase 4
the following are ectopics .. hyperthermia, hypoxia, hypercapnia, myocardial stretch, SNS all increase the phase 4 slope causing an increase in HR
how abnormal physiology and pathology causes arrhythmia - ones that decrease phase 4 slope
hypothermia, hyperkalaemia, RNS
these decrease the phase 4 slope causing slowed conduction ie bradycardia and heart block
triggered activity
they are caused when there are premature depolarisations, that occur in the terminal phases of the AP during phase 2/3 (early after depolarisation EAD) or after the AP in phase 4 (delayed after depolarisation DAD)
> if there is sufficient magnitude and reach the depolarisation threshold there is a sustained train of depolarisations and this is termed triggered activity
» this is what underpins the ventricular arrhythmia in digoxin toxicity, long QT syndrome etc
re - entry
occurs when an action potential fails to extinguish itself and reactivates a region that has recovered from refractoriness
- can occur in the presence of an obstacle around which an action potential can travel and result in a self-perpetuating circuit
but !! need more than one conducting pathway and the pathways mist have different speeds of conduction, central blocking by a core of tissue that is completely blocked allows re circulation of the excitation
2 types of re-entry
> bidirectional conduction = conduction is the same so the wavelets confront each other and cancel each other out essentially
unidirectional block = one pathway is slower and so allows the other pathway to recover from refractoriness which can therefore be re-excited and create a circuit
presentation of arrhythmia
palpitations 'pounding heart' 'skipped beat" dysopnea faintness 'presyncope' syncope shock sudden cardiac death angina HF anxiety
investigation for arrhythmia
> 12 lead ECG - important to do in sinus rhythm
bloods (fbc, biochemical, thyroid function)
CXR
echocardiogram
stress ECG
24 hour ECG
event recorder
electrophysiological study (deliberate onset of arrhythmia)
function of the ECG
assesses heart rhythm
but can also reveal if there has been a previous MI and if there has been pre-excitation
function of exercise ECG
reveals if there is ischaemia / exercise induced arrhythmia
*exercise release the catecholamines and some arrhythmias are triggered by the releases of these
function of the echocardiogram
assesses for structural heart disease ie enlarged atria in AF
sinus bradycardia
<60 beats per min
- commonly seen in athletes, if on beta blockers, or if there is ischaemia
- the treatment = atropine (acute) , or pacing (chronic) if haemodynamic compromise ie hypotension
sinus tachycardia
> 100 bpm
can be physiological ie anxiety/fever or drugs
- the treatment is to treat the underlying cause and also Bblockers can be prescribed as well
