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2C week 3 - arrhythmias > bradycardia and pacemakers > Flashcards

bradycardia and pacemakers Flashcards

1
Q

what areas of the heart does the parasympathetic system innervate

A

only SAN and AVN

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2
Q

what areas of the heart does the sympathetic system innervate

A

all the areas (SAN, AVN, ventricles, atria, purkinje fibres etc.)

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3
Q

what is the implication of different areas of the heart having different ANS innervation?

A

drugs that need to affect innervation of areas outside the SAN/AVN but target the sympathetic nervous system to be effective

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4
Q

what cells drive the heart rate

A

cardiac cells that depolarise the fastest

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5
Q

top 3 pacemaker cells

A

SAN (upper, 60-100bpm); AV junction (middle, 40-60bpm); purkinje (lower, 20-40bpm)

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6
Q

physiological reasons for bradycardia (2)

A

sleep (high vagal tone during sleep); high athletic conditioning

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7
Q

what is bradycardia

A

a heart rate <60bpm

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8
Q

acquired causes of bradycardia (9)

A
  1. degenerative - ageing leads to the degeneration of pacing/conductive systems
  2. ischaemic heart disease - valve replacements, RCA
  3. drugs - beta blockers
  4. electolyte/metabolic
  5. infection - infective endocarditis, MS, AR etc.
  6. iatrogenic - ablation, cardiac surgery
  7. infiltrative disease - amyloid, sracosis
  8. neuromuscular disease - duchenne’s, myotonic dystrophy etc.
  9. arrhythmias - AF may destroy the ANV -> may result in bradycardia
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9
Q

symptoms of bradycardia (8)

A

dizziness; fatigue; difficulty concentrating; syncope; breathlessness; exercise intolerance; falls

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10
Q

why is the SAN easily damage in surgery

A

due to its superficial location - just under the epicardium, at the junction of the Sup. vena cava and RA

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11
Q

why can SAN disfunction occur with aging

A

the SAN cells are set in a dense fibrous material which increases with age, the fibrosis of cells can involve the pacemaker cells which leads to sinus node dysfunction

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12
Q

what are the 2 main categories of SAN failure

A

failure to generate a current (sinus bradycardia, sinus arrest); failure to conduct an impulse (sinoatrial block)

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13
Q

what is sinus bradycardia

A

when there are fewer impulses generated than normal; HR is <60bpm (or <40bpm in physiologically fit people)

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14
Q

treatment for sinus bradycardia

A

atropine in acute situations; otherwise no treatment usually, treat underlying cause

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15
Q

causes for sinus bradycardia

A

SAN disease (anything that affects the atrium e.g. ageing);
sick sinus syndrome;
inferior MI (SAN supplied by RCA which can be affected in inferior MI);
drugs (B-blockers, digoxin, opiates);
hypothyroidism, hyperkalemia;
brainstem pathology

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16
Q

what is sick sinus syndrome

A

SAN dysfunction including that results in long pauses between beats and arrhythmias

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17
Q

what is sinus arrest

A

when the SAN fails to make and impulse; escape rhythms are seen because the heart must rely on the ventricular/purkinje cells for automaticity now

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18
Q

what is sinoatrial block

A

when an impulse is generated but doesn’t leave the SAN; insulating fibrous tissue expands stopping the conduction of impulses

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19
Q

sinoatrial block ECG

A

pauses are seen, they are the exact length of a multiple of an R-R interval

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20
Q

sinus arrest ECG

A

pauses on ECG, escape rhythms seen; 40-60pbm

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21
Q

what is a junctional escape rhythm

A

a delayed heart beat that originated from somewhere within the atrioventricular junction, rather than the SAN/atria

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22
Q

junctional escape rhythm ECG

A

narrow QRS, no relationship between P waves and QRS; 40-60bpm

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23
Q

what is a ventricular escape rhythm

A

a heartbeat that originates from within the ventricles from pacemakers cells (e.g. purkinje fibres) because the rate of supraventricular impulses arriving at the AV node or ventricle is less than the intrinsic rate of the ectopic pacemaker

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24
Q

ventricular escape rhythm ECG

A

broad QRS, may have LBBB/RBBB morphology (M); 20-40bpm

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25
Q

what is tachycardia-bradycardia syndrome

A

a sick sinus syndrome in which there is Alternating bradycardia with paroxysmal tachycardia, often supraventricular in origin

26
Q

tachycardia-bradycardia syndrome ECG

A

On cessation of tachyarrhythmia may be a period of delayed sinus recovery e.g. sinus pause or exit block; junctoinal escape rhythm may be seen; flutter waves followed by QRS

27
Q

tachycardia-bradycardia syndrome treatment

A

pacing (pacemaker); B-blockers; anticoagulation

28
Q

how many classes of AV block are there

A

3

29
Q

what is first degree heart block

A

increase in time for an impulse to be conducted through to the ventricles - the PR interval is longer

30
Q

first degree heart block ECG

A

prolonged PR interval; relationship between every P and QRS complex; PR distance >1 big square (>300ms)

31
Q

causes of first degree heart block (6)

A

damage to the AVN (fibrosis etc.); parasympathetic activation - increase vagal tone e.g. during sleep; athletic training; inf MI; drugs; electrolyte imbalance

32
Q

what is second degree heart block (type 1, Wenckebach)

A

Malfunctioning AV nodal cells tend to progressively fatigue until they fail to conduct an impulse; occurs due to increase vagal tone, MI, drugs (BBs, CCBs, digoxin, amiodorone etc.)

33
Q

what is second degree heart block (type II mobitz)

A

failure of conduction at the level of the His-Purkinje system (i.e. below the AV node); more likely to be due to structural damage to the conducting system; due to fibrosis of conduction system, anterio-septal MI (bundle of His lies here)

34
Q

Wenckebach ECG

A

Progressive prolongation of the PR interval culminating in a non-conducted P wave; PR interval is longest immediately before dropped beat

35
Q

mobitz II ECG

A

intermittent non-conducted P waves without progressive prolongation of the PR interval; The P waves ‘march through’ at a constant rate; wide QRS (if distal to bundle of His); RR interval surrounding the dropped beat is an exact multiple of the preceding RR interval

36
Q

what is a fixed AV block

A

Second-degree heart block with a fixed ratio of P waves: QRS complexes; arise from a Wenckebach or Mobitz II pattern

37
Q

fixed AV block ECG

A

2:1 - atrial rate is approximately 75 bpm while ventricular is 38bpm, 2 P waves for every QRS, p waves may look attached to the end of T waves
3:1 - Atrial rate is 90bpm while ventricular is 30bpm, 3 p wave for every QRS complex, P waves almost entirely concealed within T wave (when QRST complex present)

38
Q

emergency treatment of bradycardia (evidence of life-threatening signs -9)

A

ABCDE -> give oxygen/obtain IV access -> monitor ECG, BP etc. -> identify and treat reversible causes e.g. electrolyte abnormalities -> check for life-threatening signs (shock, syncope, ischemia, heart failure) -> give atropine IV 500mcg (if satisfactory then see risk of asystole) -> if unsatisfactory give Atropine IV and repeat to max dose of 3mg, Isoprenaline, adrenaline or transcutaneous pacing -> seek expert help -.> arrange transverse pacing

39
Q

emergency treatment of bradycardia (no evidence of life-threatening signs)

A

ABCDE -> give oxygen/obtain IV access -> monitor ECG, BP etc. -> identify and treat reversible causes e.g. electrolyte abnormalities -> check for life-threatening signs -> check for asystole risk (recent asystole, Mobitz II AV block, complete heart block w broad QRS, ventricular pause >3s) -> observe if no -> if yes then interim measures( atropine, isoprenaline, adrenaline, transcutaneous pacing) -> seek expert advice -> transvenous pacing

40
Q

atropine MOA

A

binds to and inhibits muscarinic acetylcholine receptors, competitively blocking the effects of acetylcholine and other choline esters; blocks vagal stimulation - increases HR in sinus bradycardia and AVN disease.

41
Q

isoprenaline

A

non-selective β-adrenergic agonist. It has positive inotropic and chronotropic effects, increasing cardiac output by increasing the heart rate and cardiac contractility

42
Q

types of temporary pacing (2)

A

transvenous; transcutaneous

43
Q

when is transcutaneous pacing used (6)

A

bradycardia unresponsive to drug therapy
3rd degree heart block
Mobitz type II second-degree heart block when haemodynamically unstable
overdrive pacing
asystole

44
Q

transcutaneous pacing steps (8)

A
  1. place pads in AP position (black on anterior chest, red on posterior chest)
  2. connect ECG leads
  3. set pacemaker to demand
  4. turn pacing rate to > 30bpm above patients intrinsic rhythm
  5. set mA to 70
  6. start pacing and increase mA until pacing rate captured on monitor
  7. if pacing rate not captured at a current of 120-130mA -> resite electrodes and repeat the above
  8. once pacing captured, set current at 5-10mA above threshold
45
Q

what are the 3 kinds of pacemakers

A

traditional pacemaker (wried, but can also be wireless); implantable cardioverter defibrillator (ICD); cardiac resynchronisation therapy (CRT)

46
Q

what device can be used to detect cardiac arrhythmias that a normal ECG may not

A

implantable loop recorder - can stay in place for up to 3 years

47
Q

what is a pacemaker?

A

a device that sends an electrical current through the heart in order to initiate depolarisation at a set rate; contains a generator and pacing leads

48
Q

what are the 2 roles of a pacemaker

A

to sense (detect the patient’s own intrinsic impulses) and capture (depolarise the heart if thee aren’t impulses when there should be)

49
Q

cons of a traditional pacemaker (wired -2)

A

leads can become infected, leads can fail over time

50
Q

what can wireless pacemakers treat and why

A

they can only treat AF as they can only be inserted into the RV (via femoral vein)

51
Q

what conditions are pacemakers used to treat

A

sick sinus syndrome; wenckebach (if it doesnt resolve); mobitz II (all pts); 3rd degree heart block (all pts)

52
Q

what is an ICD

A

a specialised pacemaker that treats life-threatening ventricular arrhythmias by defibrillation

53
Q

when is an ICD indicated

A

primary prevention - someone is at high risk of a ventricular arrhythmia e.g. severe LV impairment, inherited cardiac conditions
secondary preventions - someone who has previously had VF/VT (with no clear cause)

54
Q

how does an ICD work (rate, rhythm detection etc.)

A
  1. looks at rate - if >220 then shock is delivered
  2. rhythm - if >180 it will look at the rhythm and its associated features e.g. how did it start (gradual/sudden), regular vs irregular, narrow or broad QRS
55
Q

what are the different kinds of shock that an ICD can deliver (4)

A

ventricle: anti-tachycardia, cardioversion, defibrillation
atrium + ventricle: bradycardia pacing

56
Q

what is cardioversion

A

Electrical cardioversion involves the delivery of a high voltage DC biphasic shock to completely depolarise the heart, terminating the tachyarrhythmia; the shock is synchronised to the QRS complex (unline in defib where the shock is asynchronous)

57
Q

why may a subcut ICD be preferred over venous and why not

A

easier to remove if it become damaged; cannot treat bradycardia or give anti-tachy pacing

58
Q

how can an ICD be deactivated?

A

a pacing physiologist can deactivate it; a strong magnet can be used in emergency situs

59
Q

what is cardiac resynchronisation therapy?

A

a treatment for ventricles that don’t depolarise at the same time - patients with severe systolic heart failure, broad QRS and still have symptoms despite treatment

60
Q

3rd degree heart block ECG

A

Rate tends to be less than 50 bpm; Constant P–P and R–R intervals but apparent AV dissociation; QRS complexes may be narrow (junctional escape rhythm) or wide (subjunctional escape rhythm)

61
Q

blockages of what artery can result in arrhythmia and why

A

right circumflex artery - it supplies the SAN and AVN

2C week 3 - arrhythmias (6 decks)

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