Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology > cardiac arrhythmias > Flashcards

cardiac arrhythmias Flashcards

1
Q

what does supraventrciular mean?

A
  • no specific term

- origin is above the ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the supraventricular arrhythmias?

A
  • supreventrivcular tachycardia eg AF, atrial flutter, ectopic atrial tachycardia
  • bradycardia eg sinus bradycardia and sinus pauses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the ventricular arrhythmias?

A
  • ventricular ectopics or premature ventricular complexes
  • ventricular tachycardia
  • ventricular fibrillation
  • asystole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what abnormal activity can cause arrhythmias?

A
  • LVH
  • accessory pathways
  • congenital HD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

how does the autonomic nervous system cause arrhythmias?

A
  • sympa stimulation : stress, exercise, hyperthyroidism

- increased vagal tone causing bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how can inflammation cause arrhythmias?

A
  • viral myocarditis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how can drugs casue arrhythmia?

A
  • electrophysiologic effects of via ANS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how can genetics cause arrhythmias?

A
  • mutations of genes encoding cardiac ion channels eg the congenital long QT syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the clinincal causes of arrhythmias?

A
  • abnormal anatomy
  • ANS
  • metbaolic
  • inflammation
  • drugs
  • genetic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what ar eelectrophysiological mechanisms?

A
  • ectopic beats

- re-entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what causes an increase in phase 4?

A
  • hyperthermia
  • hypoxia
  • hypercapnia
  • cardiac dilation
  • hypokalaemia, prolongs repolarisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what causes a decrease in phase 4?

A
  • hypothermia

- hyperkalaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

what is the treatment for sinus bradycardia?

A
  • atropine ( if acute eg acute MI)
26
Q

what is sinus tachycardia?

A
  • > 100 bmp
  • physiological (anxiety, fever, hypotension, anaemia)
  • inappropriate drugs
  • treatment = b-adrenergic blockers
27
Q

what is the treatment for sinus tachycardia?

A
  • b-adrenergic blockers
28
Q

what are the symptoms for atrial ectopic beats?

A
  • asymptomatic

- palpitations

29
Q

what is the treatment for atrial ectopic beats?

A
  • no treatment
  • b-adrenergic blockers may help
  • avoid stimulants eg caffeine cigarettes
30
Q

what is regular supra ventricular tachycardia do to?

A
  • AV nodal re-entrant tachycardia
  • AV reciprocating tachycardia
  • ectopic atrial tachycardia
31
Q

how is supraventriuclar tachycardia managed?

A
  • 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
Q

what is raidofrequency catheter albation?

A
  • selective cautery of cardiac tissue to prevent tachycardia targeting either an automatic focus or part of a re-entry circuit
33
Q

what does an electrophysiologic study and RFCA involve?

A
  • 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
Q

what are the casues of AVN conduction disases (heart block)?

A
  • 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
Q

what is first degree heart block?

A
  • 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
Q

what is second degree haert block?

A
  • 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
Q

what is third degree heart block?

A
  • no action potentials from the SA node / arita get through the AV node
38
Q

what are the types of pacemkaers?

A
  • 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
Q

what causes ventriuclar ectopics?

A
  • 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
Q

what is ventriular tachycardia?

A
  • life threatening but may be haemodynamicall stable
  • most patients have significant heart disease = coronary artery disease, a previous MI
  • rare causes = cardiomyopathy, inherited
41
Q

what is ventricular fibrillation?

A
  • chaotic ventricular electrical activity which causes the heart to lose the ability to function as a pump
42
Q

what is the acute treatment of ventricular fibrillation?

A
  • 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
Q

what is the long term treatment for VT?

A
  • correct ischemia if possible
  • optimise CHF therapies
  • VT catheter ablation
44
Q

if someone has a wide QRS tachycardia with history of CAD/HF?

A
  • VT until proven otherwise
45
Q

are anti-arrhythmic drugs effective on survival??

A

no but are ofthen used wih ICDs to reduce symptoms

Cardiology (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions