bradycardia and pacemakers Flashcards
what areas of the heart does the parasympathetic system innervate
only SAN and AVN
what areas of the heart does the sympathetic system innervate
all the areas (SAN, AVN, ventricles, atria, purkinje fibres etc.)
what is the implication of different areas of the heart having different ANS innervation?
drugs that need to affect innervation of areas outside the SAN/AVN but target the sympathetic nervous system to be effective
what cells drive the heart rate
cardiac cells that depolarise the fastest
top 3 pacemaker cells
SAN (upper, 60-100bpm); AV junction (middle, 40-60bpm); purkinje (lower, 20-40bpm)
physiological reasons for bradycardia (2)
sleep (high vagal tone during sleep); high athletic conditioning
what is bradycardia
a heart rate <60bpm
acquired causes of bradycardia (9)
- degenerative - ageing leads to the degeneration of pacing/conductive systems
- ischaemic heart disease - valve replacements, RCA
- drugs - beta blockers
- electolyte/metabolic
- infection - infective endocarditis, MS, AR etc.
- iatrogenic - ablation, cardiac surgery
- infiltrative disease - amyloid, sracosis
- neuromuscular disease - duchenne’s, myotonic dystrophy etc.
- arrhythmias - AF may destroy the ANV -> may result in bradycardia
symptoms of bradycardia (8)
dizziness; fatigue; difficulty concentrating; syncope; breathlessness; exercise intolerance; falls
why is the SAN easily damage in surgery
due to its superficial location - just under the epicardium, at the junction of the Sup. vena cava and RA
why can SAN disfunction occur with aging
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
what are the 2 main categories of SAN failure
failure to generate a current (sinus bradycardia, sinus arrest); failure to conduct an impulse (sinoatrial block)
what is sinus bradycardia
when there are fewer impulses generated than normal; HR is <60bpm (or <40bpm in physiologically fit people)
treatment for sinus bradycardia
atropine in acute situations; otherwise no treatment usually, treat underlying cause
causes for sinus bradycardia
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
what is sick sinus syndrome
SAN dysfunction including that results in long pauses between beats and arrhythmias
what is sinus arrest
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
what is sinoatrial block
when an impulse is generated but doesn’t leave the SAN; insulating fibrous tissue expands stopping the conduction of impulses
sinoatrial block ECG
pauses are seen, they are the exact length of a multiple of an R-R interval
sinus arrest ECG
pauses on ECG, escape rhythms seen; 40-60pbm
what is a junctional escape rhythm
a delayed heart beat that originated from somewhere within the atrioventricular junction, rather than the SAN/atria
junctional escape rhythm ECG
narrow QRS, no relationship between P waves and QRS; 40-60bpm
what is a ventricular escape rhythm
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
ventricular escape rhythm ECG
broad QRS, may have LBBB/RBBB morphology (M); 20-40bpm
what is tachycardia-bradycardia syndrome
a sick sinus syndrome in which there is Alternating bradycardia with paroxysmal tachycardia, often supraventricular in origin
tachycardia-bradycardia syndrome ECG
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
tachycardia-bradycardia syndrome treatment
pacing (pacemaker); B-blockers; anticoagulation
how many classes of AV block are there
3
what is first degree heart block
increase in time for an impulse to be conducted through to the ventricles - the PR interval is longer
first degree heart block ECG
prolonged PR interval; relationship between every P and QRS complex; PR distance >1 big square (>300ms)
causes of first degree heart block (6)
damage to the AVN (fibrosis etc.); parasympathetic activation - increase vagal tone e.g. during sleep; athletic training; inf MI; drugs; electrolyte imbalance
what is second degree heart block (type 1, Wenckebach)
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.)
what is second degree heart block (type II mobitz)
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)
Wenckebach ECG
Progressive prolongation of the PR interval culminating in a non-conducted P wave; PR interval is longest immediately before dropped beat
mobitz II ECG
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
what is a fixed AV block
Second-degree heart block with a fixed ratio of P waves: QRS complexes; arise from a Wenckebach or Mobitz II pattern
fixed AV block ECG
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)
emergency treatment of bradycardia (evidence of life-threatening signs -9)
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
emergency treatment of bradycardia (no evidence of life-threatening signs)
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
atropine MOA
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.
isoprenaline
non-selective β-adrenergic agonist. It has positive inotropic and chronotropic effects, increasing cardiac output by increasing the heart rate and cardiac contractility
types of temporary pacing (2)
transvenous; transcutaneous
when is transcutaneous pacing used (6)
bradycardia unresponsive to drug therapy
3rd degree heart block
Mobitz type II second-degree heart block when haemodynamically unstable
overdrive pacing
asystole
transcutaneous pacing steps (8)
- place pads in AP position (black on anterior chest, red on posterior chest)
- connect ECG leads
- set pacemaker to demand
- turn pacing rate to > 30bpm above patients intrinsic rhythm
- set mA to 70
- start pacing and increase mA until pacing rate captured on monitor
- if pacing rate not captured at a current of 120-130mA -> resite electrodes and repeat the above
- once pacing captured, set current at 5-10mA above threshold
what are the 3 kinds of pacemakers
traditional pacemaker (wried, but can also be wireless); implantable cardioverter defibrillator (ICD); cardiac resynchronisation therapy (CRT)
what device can be used to detect cardiac arrhythmias that a normal ECG may not
implantable loop recorder - can stay in place for up to 3 years
what is a pacemaker?
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
what are the 2 roles of a pacemaker
to sense (detect the patient’s own intrinsic impulses) and capture (depolarise the heart if thee aren’t impulses when there should be)
cons of a traditional pacemaker (wired -2)
leads can become infected, leads can fail over time
what can wireless pacemakers treat and why
they can only treat AF as they can only be inserted into the RV (via femoral vein)
what conditions are pacemakers used to treat
sick sinus syndrome; wenckebach (if it doesnt resolve); mobitz II (all pts); 3rd degree heart block (all pts)
what is an ICD
a specialised pacemaker that treats life-threatening ventricular arrhythmias by defibrillation
when is an ICD indicated
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)
how does an ICD work (rate, rhythm detection etc.)
- looks at rate - if >220 then shock is delivered
- 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
what are the different kinds of shock that an ICD can deliver (4)
ventricle: anti-tachycardia, cardioversion, defibrillation
atrium + ventricle: bradycardia pacing
what is cardioversion
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)
why may a subcut ICD be preferred over venous and why not
easier to remove if it become damaged; cannot treat bradycardia or give anti-tachy pacing
how can an ICD be deactivated?
a pacing physiologist can deactivate it; a strong magnet can be used in emergency situs
what is cardiac resynchronisation therapy?
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
3rd degree heart block ECG
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)
blockages of what artery can result in arrhythmia and why
right circumflex artery - it supplies the SAN and AVN
