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Cardiac Arrhythmias
Mx of patient experiencing an arrhythmia:
 Obtain Rhythm strip
 Assess:
Conscious state
Vital signs
Chest pain/other syx
Reassure Pt
Apply O2
 If no cardiac output/pt unconscious – start CPR
 If witnessed, monitored collapse, & Pt in VT or VF – praecordial thump
 If not hypotensive/dyspnoeic – sitting position
 ECG
 Take bloods for FBE, U&E Ca/Mg/PO4, Cardiac enzymes – Urgent K+
 Check medication – most anti-arrhythmics are pro-arrhythmic and negatively
inotropic
 NB Digoxin may be toxic at therapeutic levels with LOW K+
Ventricular Tachycardia – VT
 Irritable ectopic focus in ventricles, may have re-entry circuit
 Rate: 100-250 bpm
 No P waves
 In about 50% AV dissociation present – map P-P intervals, look for hidden P
waves
 In other 50% - P waves discernible – due to retrograde conduction – hard to
see at higher rates
 “Sustained” = longer than 30 secs
 “Non-Sustained” = less than 30 secs
 4 ventricular ectopics in a row = VT
ECG Characteristics:
 Rate atrial: variable, may be independent of ventricles, or retrograde
ventricular: 100-250bpm
 Regularity:
Ventric response regular, or very slightly irregular
 P-R Interval: indeterminable
 QRS duration: wide >0.12 secs
 Morphology: P waves – variable if present
QRS – wide complex, bizarre looking, may have narrower
fusion beats (superimposed SA node & ventric beats)
ST – often obscured
T – opposite polarity to QRS
Causes
 IHD/AMI
 Hypoxia
  K/Mg/pH (acidosis)
 Digoxin toxicity
 Indwelling cardiac lines/pacemaker
 Reperfusion arrhythmias post thrombolysis
Treatment
Determined by haemodynamic/conscious state of patient
Conscious Patient:
Symptoms include: Asymptomatic
Palpitations
Dizziness/Syncope
Angina
In this setting VT is dangerous as may cardiac output may deteriorate and rhythm can
deteriorate into VF.
Mx: Apply O2, Check obs
12-lead ECG – may help differentiate VT from SVT with aberrancy
Check reversible causes & treat
Lignocaine bolus 1mg/kg
If it corrects – infusion of lignocaine
VT versus SVT with aberrancy
VT
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QRS often > 0.14s
Extreme axis deviation (-90 to –180 degrees)
Fusion/capture beats (narrow complexes amongst wide ones)
Concordance (all +ve or all –ve in V1-V6)
Deflection:
If +ve in V1 and monophasic r wave
 OR biphasic & left > right peak of R wave
If –ve in V1, r wave >0.03s in V1/V2
 slurred S in V1/V2
 any Q in V6
 r to low point of s >0.06s
Unconscious Patient/No pulse:
CPR/BLS
Defibrillate ASAP
Witnessed Monitored Collapse
Pt witnessed to go unconscious & into VT (on monitor) – PRAECORDIAL THUMP
Only other type of unmonitored collapse that should be thumped is
ELECTROCUTION
Ventricular Fibrillation: VF
Classic ‘cardiac arrest’
Multiple ectopic foci discharging simultaneously in ventricles
Disordered chaotic rhythm
Cardiac output = zero! Always unconscious, will die without correction!
ECG Features:
 Rate: atrial/ventricular = indeterminable
 Regularity: irregular
 P-R interval: indeterminable
 QRS duration: indeterminable
 Morphology: Pwaves – absent
QRS – chaotic, no uniformity
ST – indeterminable
Twaves – indeterminable
Causes
 IHD/AMI
 Electrocution
 Drug intoxication
 Trauma
 Hypothermia <30oC
 Other – as per VT
Treatment
CPR/BLS
Defibrillate ASAP
Early difibrillation provides the best chance of survival:
Time in VF pre-defibrillation
% Discharged from hospital
< 1 min
99%
2 mins
50%
> 5 mins
35%
Asystole
No contraction – “flatline” (misnomer as line is not perfectly flat!)
As per VF: Cardiac output = zero! Always unconscious, will die without correction!
ECG Features
 Rate: none or extremely slow
 QRS – none or wide, bizarre looking
Causes
 End stage of advanced cardiac disease
 Severe myocardial depression due to hypoxia/drug overdose
Management
VERIFY ASYSTOLE – to ensure it’s not Isoelectric or “Fine” VF
 On monitor – cycle through leads I, II & III
 If monitoring through paddles – swap paddles to 90o
 Check all connections
 Check that monitoring through correct input (paddles/monitor) on defibrillator
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Then:
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Increase the gain/amplitude on monitor
Check for CPR artefact
If “flat” or straight line consider Monitor not connected
Lead not selected
Malfunction
CPR
Ventilation – ETT 100% O2
Adrenaline 1mg IV, 20ml flush
Continue CPR for 3 minutes
If still in asystole – Atropine 1mg IV
Can repeat Adr/Atropine
Consider temporary pacing (early in asystole, especially if there’s a remnant of
electrical activity)
EMD / PEA
Coordinated electrical activity with no cardiac output
Causes
 AMI/IHD
 Acidosis
 4 H’s & 4 T’s
4 H’s
Hypoxia
Hypovolaemia
Hypothermia
Hypo/Hyperkalaemia
& other metabolic disorders
4 T’s
Tamponade
Tension Pneumothorax
Toxins, poisons, drugs
Thromboembolism
(massive PE, vena caval obstruction)
Non-reversible causes include
 Massive PE
 Ruptured Mitral Valve
 Ruptured ventricle
Management
 CPR/BLS
 Identify & treat reversible causes
 ETT, 100% O2
 Adrenaline 1mg IV
 CPR for 3 minutes
 Atropine 1mg IV
 Continue CPR & Adrenaline every 3 minutes
Idioventricular Rhythm
Automaticity of ventricles, “escape rhythm”
Rate of about 30-40/min (40-100bpm = “accelerated idioventrcular rhythm”)
Each beat has appearance of a ventricular contraction
May degenerate to Asystole
ECG Features
Rate: atrial: nil
ventricular: 30-40
Regularity: Regular
QRS Duration: widened
Morphology: Pwaves – absent
QRS Complexes: wide, bizarre looking
ST: often obscured
T waves: opposite in polarity to QRS
Causes
Indicates severe disruption to conduction system
May be first stable rhythm post conversion of VT/VF/Asystole
 AMI/IHD
 Digoxin toxicity
 Reperfusion (post thrombolysis)
Treatment
Isoprenaline infusion
Temporary pacemaker
Ventricular Ectopics
Commonest ventricular arrhythmia, many names, can occur in any rhythm
Ectopic focus in Purkinje fibres or ventric muscle
Wider complex, larger voltage contraction, as usual conduction paths not followed
NOT a stronger contraction! Actually  CO
T wave in opposite direction to QRS
Features:
Earlier than next expected beat
No P wave
Wide bizarre QRS (often > 0.14sec)
ST segment often obscured
T wave – opposite polarity to QRS
Next beat:
OR
When expected
After compensatory pause
If all ectopics have same morphology – “unifocal”
If they have different morphology – “multi-focal”
May occur in bigeminal, trigeminal or quadrigeminal arrangements
Or in couplets or pairs, or runs of 3 (“Salvos”)
4 or more in a row = VT
Causes
 Most cases = incidental finding
 IHD/AMI
  K/pH
 Digoxin toxicity
 Indwelling cardiac lines
 Bradycardia may allow an ectopic focus to emit an ectopic beat
Treatment
Controversial:
Rough Guide: Only treat if VE’s are ing in number or patient compromised
Some suggest treatment if combination of:
 patient compromised
 more than 5/minute
 multifocal
 runs or Salvos
 R on T phenomenon
 Any of these in the first 24hrs post MI
Remember to exclude/treat causes
In early AMI, Lignocaine is drug of choice
BUT: AT  HR, treatment is to  HR first with Atropine
Lignocaine may  rate/put them into asystole