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
atrial ectopic beats
present with palpitations or nothing at all !!
there is not really any treatment
B-adrenergic blockers may help
and also avoiding stimulants such as caffeine
AVNRT vs AVRT // micro circuit vs macro circuit
they are both re-entry tachycardia using the AV node but in the AV node re-entrant tachycardia - the circuit is within the AVn itself whereas AVRT circuit uses AVn and another pathway
SVT arrhythmia management
acute: increase vagal tone - valsalva, carotid massage
slow conduction in the AVN - IV adenosine, IV verapamil
chronic: avoid stimulants, electrophysiologic study and radiofrequency ablation, antiarrythmic drugs, beta blockers
RFCA
radio frequency catheter ablation
it is the selective cautery of cardiac tissue to prevent tachycardia, targeting either an automatic focus or part of a re-entry circuit
causes of AVn conduction disease (heart block)
ageing acute MI myocarditis infiltrative disease ie amyloid/sarcoidosis drugs calcific aortic valve disease post-aortic surgery genetics
1st degree av block
conduction following P wave takes longer
2nd degree av block
intermittent block at the av node (dropped beats)
- mobitz 1 = progressive lengthening of the PR interval eventually resulting in mobitz 1
- mobitz 2 = pathological (ie caused by scarring of the av node) and need a pacemaker
3rd degree av block
= complete heart block ie your life is on the line
no action potentials from the SA node/atria can get though to the AV node»_space; ASYSTOLE AND THEN DEATH
function of the pacemaker
can get single chamber pacemakers ie pacing the RA or RV only
can get dual chamber (paces both)
>maintains AV synchrony >used for AVN disease
causes of ventricular ectopics - VEs
structural causes include LVH, HF, myocarditis
metabolic causes include ischaemic heart disease, electrolytes … may be a marker for in hearted cardia conditions
if worse on exercise, need to investigate further
beta blockers, ablation of focus
causes of ventricular ectopics - VEs
structural causes include LVH, HF, myocarditis
metabolic causes include ischaemic heart disease, electrolytes … may be a marker for in hearted cardia conditions
if worse on exercise, need to investigate further
treatment = beta blockers, ablation of focus
causes of VT
usually have significant heart disease ie coronary artery disease
a previous MI
HF
.. less frequent causes include inherited cardiomyopathy
inherited channelopathy
treatment of VF
defibrillation, cardiopulmonary resuscitation
treatment of VT
acute : direct current cardio version (DCCV)
if stable, consider pharmacological cardio version with AAD
>if unsure of VT administer adenosine to make a diagnosis
treatment of VT
acute : direct current cardio version (DCCV)
if stable, consider pharmacological cardio version with AAD
>if unsure of VT administer adenosine to make a diagnosis
correct triggers - look for the causes ie electrolytes, ischaemia, hypoxia, pro-arrhythmic medications
chronic : revascularisation if possible
optimise CHF therapies
implantable cardioventor defibrillators if life threatening
VT catheter ablation
CIEDs
cardiac implantable electronic devices ie pacemakers and ICDs
VT/VF s need to know !!
> A WIDE QRS TACHYCARDIA WITH HISTORY OF CAD/HF = VT UNTIL PROVEN OTHERWISE
>MOST VENTRICULAR ARRHYTHMIAS OCCUR IN THE SETTING OF STRUCTURAL HEART DISEASE IE CHF,CAD
»ANTIARRHYTHMIC DRUGS ARE INEFFECTIVE ON SURVIVAL, BUT ARE OFTEN USED TOGETHER WITH ICDs TO REDUCE SYMPTOMs
»>OPTIMAL MANAGEMENT OF THE UNDERLYING CONDITION REDUCES RISK OF PATIENT DEVELOPING ARRHYTHMIA
»»PRIMARY ARRHYTHMIC CONDITIONS ie when vt/vf is in a structurally normal heart and so could be genetic and their could be a risk for their relatives and also lots of arrhythmias are drug induced
patterns of AF
> paroxysmal - is paroxysmal and lasts less than 48 hours, is often recurrent
persistent - an episode of AF lasting greater than 48 hours, which can still be cardioverted to NSR, unlikely to spontaneously revert to NSR
permanent - inability of pharmacological or non-pharmacological methods to restore NSR
causes of AF
can be structural, metabolic ... hypertension congestive HF sick sinus syndrome CHD obesity thyroid disease familia cardiac valve disease alcohol abuse congenital heart disease cardiac surgery COPD/pneumonia septicaemia pericarditis / tumours vagal cause ie high endurance athletes
complications of AF
tarsi are no longer meaningfully contracting and contributing to CO, this lost ‘atrial kick’ and decreased filling time from shortened period in cardiac diastole results in reduced CO
»this can result in congestive HF .. reduces pressure in the capillaries in pulmonary vasculature leading to pulmonary oedema
» ventricular rates <60 mom suggest AV conduction disease and so caution with drugs and rate controlling drugs as could lead to complete heart block and … may require permanent pacing
management strategies - rate control
> goal is to maintain SR
-drugs to slow down AVn conduction ie digoxin, betablockers, verapamil, diltiazem (can use these alone or in combination)
management strategies - rhythm control
> goal is to accept AF and control ventricular rates
-restoration of NSR =
cardio version ie antiarrhythmic drugs - amiodarone / DCCV
-maintenance of NSR = anti arrhythmic drugs, catheter ablation of atrial focus/pulmonary veins, surgery (maze procedure)
management strategies - prevention of thromboembolism
oral and long term anti coagulation / antiplatelets
warfarin for mitral valve disease
anti arrhythmic drugs (AADs) - mode of action
are classified according to the ion channels that they block and they work through electrophysiological mechanisms where they block these currents - Vaughan william classifications
AAD - class 1
reducing sodium channel current
>lignocaine quinidine flecainide propafenone
AAD - class 2
b adrenergic antagonists
>propranalol
AAD - class 3
action potential prolongation
>amiodarone, sotalol
>dronedarone !!
AAD class 4
calcium channel antagonists
>verapamil
AAD - class 1
reducing sodium channel current >lignocaine, only IV quinidine flecainide, effective for treating AF but contraindicated with CAD propafenone "
AAD - class 2
b adrenergic antagonists
>propranalol,
AAD - class 3
action potential prolongation
>amiodarone, sotalol
>dronedarone !!
ability to prolong the QT and if it does this excessively its really bad
AAD class 4
calcium channel antagonists
>verapamil
slow HR
AF can cause thrombosis-embolic stroke
more likely to happen if patient has .. thyrotoxicosis hypertrophic cardiomyopathy mitral valve disease non-valvular AF with 2 or more risk factors
risk factors for AF
75years+ hypertension HF precios MI / ischaemia CAD/ DM diabetes
AF can cause thrombosis-embolic stroke
blood clot likely to form in the left atrial appendage due to stasis of blood flow associated with AF
>more likely to happen if patient has ..
thyrotoxicosis
hypertrophic cardiomyopathy
mitral valve disease
non-valvular AF with 2 or more risk factors
risk factors for AF
75years+ hypertension HF precios stroke CAD/ DM diabetes being a woman
atrial flutter
more organised AF >rapid and regular form of AF >paroxysmal or persistent pattern >sustained by a macro-reentrant circuit >confined to RA but can spread to LA >risk of stroke
atrial flutter treatment
>RF ablation >slow the ventricular rate >restore sinus rhythm >maintain sinus rhythm >cardioversion >OACs
