cardiac arrhythmias Flashcards
1
Q
what does supraventrciular mean?
A
- no specific term
- origin is above the ventricle
2
Q
what are the supraventricular arrhythmias?
A
- supreventrivcular tachycardia eg AF, atrial flutter, ectopic atrial tachycardia
- bradycardia eg sinus bradycardia and sinus pauses
3
Q
what are the ventricular arrhythmias?
A
- ventricular ectopics or premature ventricular complexes
- ventricular tachycardia
- ventricular fibrillation
- asystole
4
Q
what are the AV node arrhythmias?
A
- AVN re-entry tachycardia
- AV reciprocating or AV reentrant tachycardia
- AV block (1st, 2nd, 3rd degree)
5
Q
what abnormal activity can cause arrhythmias?
A
- LVH
- accessory pathways
- congenital HD
6
Q
how does the autonomic nervous system cause arrhythmias?
A
- sympa stimulation : stress, exercise, hyperthyroidism
- increased vagal tone causing bradycardia
7
Q
how do metabolic causes causes arrhythmias?
A
- hypoxic: chronic pulmonary disease, pulmonary embolus
- ischaemic myocardium: acte MI, angina
- electrolyte imbalances: K+, Ca2+, Mg2+
8
Q
how can inflammation cause arrhythmias?
A
- viral myocarditis
9
Q
how can drugs casue arrhythmia?
A
- electrophysiologic effects of via ANS
10
Q
how can genetics cause arrhythmias?
A
- mutations of genes encoding cardiac ion channels eg the congenital long QT syndrome
11
Q
what are the clinincal causes of arrhythmias?
A
- abnormal anatomy
- ANS
- metbaolic
- inflammation
- drugs
- genetic
12
Q
what ar eelectrophysiological mechanisms?
A
- ectopic beats
- re-entry
13
Q
what are ectopic beats?
A
- they originate in places other than the SA node
- altered automaticity eg ischaemia, catecholamines
- triggered activity eg digoxin, long QT syndrome
14
Q
what is re-entry?
A
- required more than one conduction pathway, with different speed of conduction and recovery of excitability
- accessory pathway tachycardia (WPWS), previous myocardial infarction, congenital heart disease
15
Q
what are the mechanisms of tachycardia?
A
- the ectopic focus may cause single beats or a sustained run of beats that if faster than sinus rhythm, will take over intrinsic rhythm
- re entry: triggered by an ectopic beat, resulting in a self perpetuating current
16
Q
what causes an increase in phase 4?
A
- hyperthermia
- hypoxia
- hypercapnia
- cardiac dilation
- hypokalaemia, prolongs repolarisation
17
Q
what causes a decrease in phase 4?
A
- hypothermia
- hyperkalaemia
18
Q
what is triggered activity?
A
- in the terminal phase of AP (phase 3 ), a small depolarisaiton mat occur (afterdepolarisation), and if of sufficient magnitude may reach depolarisation threshold and lead to a sustained train of depolarisation, termed triggered activity
- the mechanism underlying digoxin toxicity, is the long QT syndrome and hypokalaemia
19
Q
what are the mechanisms of re-entry?
A
- required more than one conduction pathways with different speed of conduction and recover of excitability
- structural abnormalities: accessory pathways, scar from myocardial infarction, congenital heart disease
- functional: conditions that depress conduction velocity or shorten refractory period promote functional blockage eg ischaemeia, drugs
20
Q
what are the symptoms of cardiac arrhythmias?
A
- palpitations”pounding heart”
- SOB
- dizziness
- syncope
- faintness
- sudden cardiac death
- angina, heart failure
21
Q
what investigations would you carry out for cardiac arrhythmias?
A
- 12 lead ECG - asses rhythm, previous MI, WPWS
- CXR
- echocardiogram - assess structural heart eg enlarged
- stress ECG
- 24 hours ECG holter - assess paroxysmal arrhythmia
- event recorder
- electrophysiological study - to trigger clinical arrhythmia and study it’s mechanism/ pathway
22
Q
why would you use en eCG for cardiac arrhythmias?
A
- to assess rhythm
- for signs of previous MI (Q waves), pre-excitaiton (wolf parkinson white syndrome)
23
Q
what is normal sinus arrhythmia?
A
- variation in hear rate due to reflex changes in vagal tone during the resp cycle
- inspiration reduced vagal tone and increases heart rate
- normal
24
Q
what is sinus bradycardia?
A
- <60 bmp
- physiological eg athlete
- drugs (b-blockers) will cause
- ischaemia = common in inferior STEMIs
- treamtent = atropine
25
what is the treatment for sinus bradycardia?
- atropine ( if acute eg acute MI)
26
what is sinus tachycardia?
- >100 bmp
- physiological (anxiety, fever, hypotension, anaemia)
- inappropriate drugs
- treatment = b-adrenergic blockers
27
what is the treatment for sinus tachycardia?
- b-adrenergic blockers
28
what are the symptoms for atrial ectopic beats?
- asymptomatic
| - palpitations
29
what is the treatment for atrial ectopic beats?
- no treatment
- b-adrenergic blockers may help
- avoid stimulants eg caffeine cigarettes
30
what is regular supra ventricular tachycardia do to?
- AV nodal re-entrant tachycardia
- AV reciprocating tachycardia
- ectopic atrial tachycardia
31
how is supraventriuclar tachycardia managed?
- acute managment: increase vagal tone: valsalva, carotid massage
- slow conduction in the AVN , IV adenosine, IV verapamil
chronic managemnt
- avoid stimulants
- electrophysiologic study
- beta blockers
- antiarrhythmic drugs
32
what is raidofrequency catheter albation?
- selective cautery of cardiac tissue to prevent tachycardia targeting either an automatic focus or part of a re-entry circuit
33
what does an electrophysiologic study and RFCA involve?
- ECG catheters placed in heart via femoral vein
- intracardiac ECG recorded during sinus rhythm, tachycardia and during pacing manoeuvres to find the location and mechanism of the tachycardia
- catheter placed over focus / pathway and tip heated to 55-65 C
34
what are the casues of AVN conduction disases (heart block)?
- ageing process
- acute myocridal infarction
- myocarditis
- infiltrative disease
- drugs- b lbockers and calcium channels
- calcific aortic valve dieasse
- post aortic valve surgery
- genertic ; lenergres disease, myotonic dystrophy
35
what is first degree heart block?
- conduction following each P wave but it takes longer
- P-R interval longer than normal >0.2 sec
- no treatment
- rule out other pathology
- long term follow up recommenede as more advanced block may develop over time
36
what is second degree haert block?
- intermittent block at the AVN (dropped beats)
- 2 types:
- mobitz 1 = progresisve lenghtenig of the PR interval, eventuallt resulting in a dropped beat
- usually vagal in origin
- morbitz 2 = pathological, may progress to complete heart block (3rd degree HB)
- usually 2:1 or 3:1 bu may be variable
- permanent pacemake rindicated
37
what is third degree heart block?
- no action potentials from the SA node / arita get through the AV node
38
what are the types of pacemkaers?
- single chambers = paces the right atria or right ventricle only)
- dual chamber = paces RA nad RV
- maintains AV synchrony (reserves atrial kick)
- used for AVN disease
39
what causes ventriuclar ectopics?
- structural causes = :VH, heart fialure, myocarditis
- metabolic = ischaemia heart disease, electrolytes, may be marker for inherited cardiac conditions
- if worse on exercise need to investigate further
- beta blockers, albation of focus
40
what is ventriular tachycardia?
- life threatening but may be haemodynamicall stable
- most patients have significant heart disease = coronary artery disease, a previous MI
- rare causes = cardiomyopathy, inherited
41
what is ventricular fibrillation?
- chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
42
what is the acute treatment of ventricular fibrillation?
- direct current cardio version is unstable
- if stable consider pharmacologic cardioversion with AAD, in the meantime prepare for DCCV
- if unsure if VT, consider adenosine to make a diagnosis
43
what is the long term treatment for VT?
- correct ischemia if possible
- optimise CHF therapies
- VT catheter ablation
44
if someone has a wide QRS tachycardia with history of CAD/HF?
- VT until proven otherwise
45
are anti-arrhythmic drugs effective on survival??
no but are ofthen used wih ICDs to reduce symptoms
