Dysrythmias Flashcards

1
Q

Discuss bloods supply of the SA node, AV node, bundles of HIS

A

SA -60% RA 40% LAD
AV- 90% RA 10% LAD (left dominant)

RBB and left anterior superior bundle are supplied via the LAD
Left posterior inferior bundle is supplied via the RAC

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2
Q

Discuss mechanims of dysrythmias

A

Enchanced automaticity refers to spontaneous depolarization in non pacemaker cells or depolarization at an abnormally low threshold in pacemaker cells
Classic examples of enhanced automaticity include the idioventricular rhythms of severe hyperkalaemia or myocardial ischemia and the junctional rhythm associated with digitalis toxicity

Triggered acitivty refers to abnormal impulses resulting from afterdepolarizations
Afterdepolarizations are fluctuations in membrane potential that occur as the resting potential is restored. They can occur just prior to resting potentional being reached (early afterdepolarizations) or after full resting potential is reached (delayed afterdepol)
-Typically seen in torsades

Re-entry dysrhtyhtmias arise from repititive conduction of impulses thorugh a slef sustaining circuit, TO maintain a re-entry one conduction pathway must have a londer refractory period than the other so that when an impuls exits one limb of the circuit it may reenter the other in a retrograde fashion

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3
Q

Discuss bradydysrythmias associated with sinus node

A

Sinus Brady

  • P -wave normal morphology with a fixed P-P and R-R interval and a ventricular rate below 60 BPM
  • Found in healthy individuals particulalry well conditioned atheltes - with high resting vagal tone
  • Can be pathalogical randing from autonomic mediated syncope to haemoperitoneum or acute inferior wall myocardial infarction. Hypothermia, hypoxia, drug effects and intrinisc sinus node disease

Sinus dysrhythmia
- manifestation of the natural variation in heart rate that occurs during the respiratory cycle manifested on the surface ECG as normally conducted P wavs with a variable P-P interval

Sinus Arrest and sinoartrial exti block

  • a lack of atrial depolarization can occur becuase of failure of the sinus node to generate an impulse or failure of impulse conduction out of the SA node (exit block)
  • SA exit block is not uncommon to see dropped P wave in regularly occuring patterns 2:1, 3:1 and 4:1
  • May be a manifistation of intrinsic SA nod disease but can also be seen under condition of increased vagal tone whether benign or pathologic.
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4
Q

Discuss sick sinus syndrome

A

Sick sinus syndrome is a group of dysrhtymias caused by disease of the sinus node and its surrounding tissues creating sinus bradyacrdai, sinus arrest or SA exit blocl.

A variant of SSS known as bradycardia-tachycardia syndrome is characterized by one or more of these bradydysrhythmias alternating wit a tachydysrhtyhmia typically AF

SSS is most commonly seen in elderly patient as a result of fibrotic degneration. It is also seen in cardiomyopathies, connective tissue disease and certain drug.

Long term management requires pacemaker placement

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5
Q

Discuss AV block

A

1st degree: is from prolonged conduction at the level of the atria, AV node or His-Purkinje system. On the ECG first degree AV block shows a prlonged PR interval >20 sec, typically with a narrow QRS complex.
-Normal variant in 2% of healthy adults

2nd degree
-one or more (but not all) atrial impulses fail to reach the ventricles. The conduction ratio is the number of P waves to the number of QRS complexes over a period of time
#Type 1 (Wenckebach, Mobitz 1)
-Associated with progressive impairment of conduction within the AV node. THe surface ECG shows a lengthening of the PR interval from beat to beat until a P wave is entirely blocked
-Occur in a variety of conditions, these are associated with increased vagal tone and do not require specific treatment if stable
-IN MI type 1 is generally transiet with a good prognosis
# Type 2 (Mobitz 2)m
-Conduction block just below the level of the AV node
-No realative refractory period – all or non conduction
-On the surface ECG conduction of atrial impulses is sporadic and typically periodic but the PR interval dose not widen from beat to beat.
-Usually narrow but concomitant bundle branch blocks can occur
-Arise as a result of senescent degeneration, drug toxicity, ischaemia or other pathological condition and generally carry worse prognosis than type1
- In MI type 2 is associated with anterior wall injury and is oftern a precursor to complete heart block

3rd degree (complete)

  • Often accompanied by a slow escape rhythm with width depending on the origin of the escape complex
  • pacemaker above the bundle of HIS are generally narrow and at a rate of 45-60BPM
  • Below the bundle 30-45 BPM and wide
  • Hallmark is AV dissociation with an RR interval longer than the PP intraval
  • The presence of AV dissociation with an RR interval shorter than the PP interval does not imply 3rd degree block
  • Classically associated with digitalis, also seen in congenital pathology, acute ischaemia, tox and some infectious disease (CHaga’s disease, Lyme)
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6
Q

Discuss Approach to symptomtaic bradycardia

A

Atropine 600-1000mic Q5minutely
Isoprenaline or adrenaline at 2mic/min up to 10 mic/minute as needed
transcutaneous pacing
transvenous pacing /pacemaker

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7
Q

Describe approach to transcutaneous pacing and define electrical and mechanical capture

A

Indications

  • symptomatic bradycardia unresponsive to drug therapy
  • 3rd degree heart block
  • Mobitz 2 if unstable
  • overdrive pacing

Method

  • Place pads ideally in AP position
  • Connect ECG leads
  • Set pacemaker to demand
  • Turn pacing rate to 30BPM greater than patient intrinsic rate
  • Set mA to 70
  • Start pacing and increase mA until pacing rate capture on monitor
  • If pacing rate not capture at 120-130mA- resit electrodes
  • Once pacing captured set current at 5-10mA above threshold

Electrical capture: each pace marker is followed by a wide QRS and t-wave

Mechanical capture: Electrical capture with output

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8
Q

Describe sinus tachy

A

Narrow complex tachycardia wiht normal p waves preceding each QRS complex on the ECG
IN adult rarely exceeds 170 and in infants rarley 200-225

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9
Q

Describe atrial tachycardia

A

Atrial rhythm with more tahn 100 QRS complexes/min arising from a non-sinus node site within the left or right atrium.

The ECG hallmark of AT is morphologically abnromal P-waves all mostly related to a QRS - depedning on the atrial rate the conduction can be 1:1 or 2:1 or higher.

Multifocal atrial tachycadia is a form of AT wiht three or more distinct P wave morphologies and varying PR and PP intervals from the multiple ectopic atrial foci. MAT is associated with
-pulmonary disease in up to 60% (COPD)
-Can be seen in primary cardiac pathology
HR >100 can be as high as 250 (usually 100-150)

For both MAT and AT – treat underlying causes - as they are aften precipitated by the underlying illnes DC cardioversion often fails

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10
Q

List causes of completely irregular rhythms

A

AF

  • AT or flutter with varying conduction
  • MAT
  • Multiple extrasystoles
  • Wandering pacemaker
  • parasystole
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11
Q

Describe AF

A

Is identified by electrical chaos - it starts from unpatterned depolarisation of atrial tissue caused by multiple re-rentry circuits generating 300-600 impulses/min
-Reduces cardiac output from a loss of co-ordination of atial contraction and from rapid ventricular rate both of which limit diastolic filling.

Patients with atrial fibrillation can develop left atrial thrombi especially in the left atrial appendage and consequent embolic events

Typically the ventricualr rate does not exceed 150-170 BPM and often is slower particularly in the presence of nodal blocking agents.
AF with rates exceeding 200 strongly suggested accessory pathways

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12
Q

Describe Ashman phenomenon

A

Aberrant ventricular conduction of an early arriving atrial impulse following a relatively long R-R interval the result of a partially refractory HIS bunde

Characterised by short salvo of widened QRS following a particularly long RR interval

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13
Q

List causes of AF

A

CVS

  • HTN
  • cardiomyopathy
  • IHD
  • Valvular disease
  • CCF
  • SSS
  • Pericarditis
  • Myocardial contusion
  • Cardiac surgery
  • accessory pathways -WPW

ENdo
-Thyroid

Res
-PE

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14
Q

Discuss management of AF

A

Rate or rhythm control
if unstable DC cardioversion
Rate - metoprolol, magnesium, treat underlying cause

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15
Q

Discuss AFFIRM and RACE trials

A

The AFFIRM and RACE trial demonstarted that embolic events occurred with equal frequency regardless of whether rate or rhythm control was pursued. Further more most embolic events occured after anticoagulation had been stopped and indicates taht patients with rate control should still be anticoagulated as per chadsvasc and has bled

There are at least 3 explanation for the above

1) despite successful cardioversion and antiarryhtmic drug therapy teh recurrence rate of either intermittent or persistent AF is 35-60% at one year with intermittent monitoring and 88% with continuous
- up to 90% of AF recurrence are asymptomatic and episdoes lasting more than 48 hours are not uncommon - enough time for left atrial appendage thrombi to form
2) patients with nonvalvular AF that is not due to reversible disease often ahve other predisposing risks for stroke
3) there may be discordance between the body of the left atrium demonstrating sinus mechanims while the atrial appendage dispalys an AF contraction pattern

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16
Q

Discuss limitations to AFFIRM and RACE trials

A

1) -The mean ages of AFFIRM adn RACE were 70 and 68 years respectively it is therefore uncertain if younger healthy patients may benefit from more aggressive rhythm control
2) Largely gathered before catheter ablation

17
Q

Discuss the EAST-AFNET 4

A

Randomly assigned 2789 patients with early AF to early rhythm control with antiarryhthmic drus or ablation or to usual care

  • The primary composite outcome (CVS death, stroke or serious adverse event related to rhythm control) occured less often with rhythm control
  • Death from CVS causes occured less often in rhythm control 1% vs 1.3%
  • Stroke occured less commonly in the rhythm control group 0.6% vs 0.9%
18
Q

Discuss rate vs rythym control

A

Rate control for
-asymptomatic patients with AF particularly long standing recurrent AF

Rhythm control (with option for catheter ablation)

  • High cardiovascular risk patients
  • failure of rate control
  • Heart failure
  • Young
19
Q

Discuss Hasbled

A

Estimates risk of major bleeding for patients on anticoavulation to assess risk beneift in AF care

HTN
Renal disease (Cr >200, dialysis or tranplant)
LIver disease
Stroke
Prior major bleeding or predisposition to bleeding
Labile INR
Age >65
Medication usage predisposing to bleeding
ETOH >8 drinks a week

Score of 0-1 -anticoagulation should be considered
Scores 1-2 - anticoagulation can be considered
Scores 3 and above alternative to anticoagulation should be considered

20
Q

Discuss Chadvasc2

A
Calculates stroke risk for patients with AF
Age: 
-<65
-65-74 +1
->75+2

Sex

  • female +1
  • male 0
CHF history 
HTN history 
Stroke/TIA/thromboembolism history 
vascular disease history 
diabetes history 

Scores of 0 are low risk and may not require any anticoagulation
Scores of 1 is low -moderate and should considered antiplatelet
Scores 2 and greter are moderate to high and should bd anticoagulated unless contraindication

21
Q

Describe a flutter

A

Characterised by atrial depolarization occuring at a regular rate of 250-350BPM caused by re-entry
Flutter waves are broad sawtooth in appearance
The ventricular rate in a flutter is rapid but in the absence of a bypass tract the conduction ratio is limited by the refractory period of the AV node and a hr of 150 is classical.

Because AV conduction occurs at fixed ratio av nodal blocking agents may cause a abrupt rate change making it more challenging to titrate therapy to a desired rate.

More sensitive to DC cardioversion usually require lower energy 50j

22
Q

Discuss accelerated junctional rythym

A

Occur when the rate of the AV junctional pacemaker exceeds that of the sinus node. THis situation arises when there is increased automatciity in the AV node couple with decreased automaticity in the sinus node

Cause

  • Dig toxicity (Classic cause of AJR)
  • Beta-agonist
  • MI
  • Myocarditis
  • cardiac surgery

ECG:

  • Narrow complex rhythm -QRS duration <120
  • Ventricualr rate usually 60-100 BPM
  • Retrograde p wave may be present and can appear before during or afgter the QRS complex
  • retrograde p waves are usually inverted in the inferior leads and upright in AVR
  • AV dissociation may be present with the ventricular rate usually greater than the atrial rate
  • Cocurrent signs of dig toxicity

Juntcional escape - 40-60 BPM
Accelerated junctional rhytghm 60-100BPM
Junctional tachycarida > 100 BPM

23
Q

Discuss accelerated idioventricular rhythm

A

Occurs when the rate of the ectopic ventricular pacemaker exceeds taht of the sinuns node - often associated with increased vagal tone and decreased sympathetic tone

Causes

  • Reperfusion phase of an AMI
  • Betta sympathomimetics
  • Drug toxicity (especially dig)
  • Electrolyte abnormalities
  • CMX
  • ROSC

ECG:

  • Regular rhythm
  • Rate 55-110BPM
  • Three or more ventricular complexes
  • QRS complexes >120
  • Fusion and capture beats

AIVR is benign rhythm in most setting that does not require treatment
-usually slef limiting and resolves when sinus rate exceeds that of the ventricular foci
administgration of anti-arrythmics may cause precipitous HD deterioation and should be avoided
Treat underlying causes if present

24
Q

Discuss approach to rate and rhythm control for AF as per the 2020 canadian CVS society

A

1) Paraxysmal AF
- low recurrence burden – reasonable to observe
- high recurrence burden –> appropriate AAD + referral for catheter ablation

2) persistant AF - Rhythm controlled goal this is used for patient who
-recently diagnosed with AF (within 1 year)
-highly symptomatic or significant QOL impairment
-multiple recurrences
-difficult to achive rate control
-arrhytmia induced CMX
These patient should be cardioverted and then referred for catheter ablation

3) Perstant AF - with optimised rate control
- symptoms persist cardiovert - if symptoms improve with rhythm control for ablation if not then for continued long term rate control
- symptoms well contolled for long term rate control

25
Q

Discuss timing for acute rhythm control

A

Can be cardioverted if NVAF duration <12 hours without recent stroke or TIA or
NVAF 12-48 and Chads2 score of 0-1

Otherwise will require iniation of OAC and rate control + TOE