Copyright to Australian Family Physician. Reproduced with permission. Permission to reproduce must be sought from the publisher, The Royal Australian College of General Practitioners.BACKGROUND Anything other than normal sinus rhythm can be classified as an arrhythmia. However not all arrhythmias need acute intervention. OBJECTIVE This article reviews which arrhythmias need intervention in an acute setting, and the various options available for intervention. DISCUSSION The impact of an arrhythmia upon perfusion determines what intervention should be considered. Conscious level, cardiac ischaemia secondary to poor perfusion of the coronary arteries and blood pressure need to be assessed. Patients with bradycardias with adequate perfusion are treated initially with oxygen and observation. Sinus bradycardia not responding to increased oxygenation is treated with atropine. For other bradycardias the two alternatives are to drive the inherent rate with a sympathomimetic drug or to pace the patient with an external or internal pacer. Usually supraventricular tachycardias are not life threatening. Unconscious patients with wide complex tachycardia should be treated in a standard cardiac arrest approach. Conscious patients in ventricular fibrillation however, can be treated either chemically or with synchronised cardioversion. If a patient is in cardiac arrest the approach is to establish effective resuscitation and early defibrillation as per Australian Resuscitation Council guidelines.Hugh JM Grantha

Grantham, H.

Adelaide Research &amp; Scholarship

THEME Arrhythmias492  Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007Hugh JM Grantham MBBS, FRACGP, is Medical Director, SA Ambulance Service, Adelaide, South Australia. grantham.hugh@saambulance.com.auBACKGROUNDAnything other than normal sinus rhythm can be classified as an arrhythmia. However not all arrhythmias need  acute intervention. OBJECTIVEThis article reviews which arrhythmias need intervention in an acute setting, and the various options available  for intervention. DISCUSSION The impact of an arrhythmia upon perfusion determines what intervention should be considered. Conscious level,  cardiac ischaemia secondary to poor perfusion of the coronary arteries and blood pressure need to be assessed.  Patients with bradycardias with adequate perfusion are treated initially with oxygen and observation. Sinus bradycardia not responding to increased oxygenation is treated with atropine. For other bradycardias the two alternatives are to drive the inherent rate with a sympathomimetic drug or to pace the patient with an external or internal pacer. Usually supraventricular tachycardias are not life threatening. Unconscious patients with wide complex tachycardia should be treated in a standard cardiac arrest approach. Conscious patients in ventricular fibrillation however, can be treated either chemically or with synchronised cardioversion. If a patient is in cardiac arrest the approach is to establish effective resuscitation and early defibrillation as per Australian Resuscitation Council guidelines. Not all arrhythmias need acute intervention. Some are relatively benign and as such are best not addressed in the acute setting. For instance, atrial fibrillation (AF) should not be addressed in the acute setting unless of very recent origin. Other arrhythmias – while looking dramatic – are still managing to perfuse the brain and are better than the alternatives that might result from an attempt to correct them. An approach to arrhythmias that are still perfusing is to provide support with oxygen and ventilation while observing the patient. The alternative approach of more active management sometimes runs the risk of creating a situation that is worse than the current one.	The 	 c r i te r i a 	 fo r 	 dec id ing 	 that 	 an 	 a r rhythmia	needs 	 i n te r ven t i on 	 va r y 	 w i th 	 t he 	 s i tua t i on	and	 the	 support 	 ava i lab le. 	 Conscious	 level 	 is	probably	 the	 best	 marker	 of	 perfusion	 in	 this	s i tuat ion. 	 Although	 blood	 pressure	 has	 a lways	been	 considered	 as	 a	 key	marker	 it	 is	 probably	 less	 a	useful	 than	 conscious	 level,	 as	 a	marker	 of	 adequate	perfusion.	Mean	 arterial	 pressure	 is	 the	 key	measure	of	 perfusion	 but	 unfortunately	 is	 not	 well	 related	 to	measured	blood	pressure	particularly	at	 the	extremes	of	heart	 rate.	The	 hardest	 decisions	 regarding	 intervention	are	 for	 patients	 who,	 while	 conscious,	 are	 obviously	not	 perfusing	 well	 and	 for	 whom	 the	 consequences	of	 intervention	 may	 include	 an	 even	 worse	 rhythm.	For	 example,	 a	 complete	 heart	 block	with	 a	 junctional	escape	 rhythm	may	 generate	 perfusion	 that,	 although	not	 optimum,	 is	 adequate.	 If	 in	 doubt,	 an	 approach	of	 maximising	 oxygenation,	 optimising	 preload	 and	adopting	 an	 attitude	 of	 optimistic	 expectancy	 is	 the	safest	strategy.	Emergency management of acute cardiac arrhythmiasReprinted from Australian Family Physician Vol. 36, No. 7, July 2007  493Too slowBradycardia	 can	 be	 a	 sinus	 bradycardia	 often	 associated	with	 increased	 vagal	 tone	 (Figure 1)	 or	 secondary	 to	a	 failure	 of	 the	 sinoatrial	 (SA)	 node	 or	 atrioventricular	(AV)	 block.	 Atrioventricular	 block	 is	 a	 problem	 of	 the	conduction	system	with	a	block	at	the	AV	node.	Complete	AV	 block	 results	 in	 the	 failure	 to	 transmit	 any	 impulses	from	 atria	 to	 ventricle	 (Figure 2)	 while	 the	 partial	 AV	block	will	 result	 in	 either	 a	 slower	 transmission	 or	 an	intermittent	transmission.		 The	 degree	 of	 bradycardia	 and	 the	 impact	 upon	perfusion	determine	whether	or	not	intervention	should	be	considered.	Conscious	 level	 is	a	good	guide	of	perfusion,	as	 is	evidence	of	 ischaemic	chest	pain	secondary	 to	poor	perfusion	 of	 the	 coronary	 arteries.	 Blood	 pressure	 and	other	indirect	measures	of	perfusion	(the	ability	to	provide	a	 pulse	wave	 detected	 by	 a	 pulse	 oximeter)	 are	 useful	adjuncts	when	assessing	perfusion	status.	 Evidence	 of	 ischaemia	 in	 the	 right	 coronary	 artery	territory	 (inferior	 leads)	 in	 a	 patient	 who	 is	 not	 yet	bradycardic	raises	the	possibility	of	bradycardia	secondary	to	 failure	 of	 the	 SA	 node	 or	 AV	 node.	 A	 patient	 with	evidence	 of	 ischaemia	 in	 this	 area	 should	 have	 an	intravenous	 (IV)	 inserted	 and	 preparations	 available	 for	pacing	or	drug	intervention.	 The	 initial	 approach	 to	 sinus	 bradycardia	 should	 be	 to	increase	 oxygenation	 and	 ensuring	 an	 adequate	 preload	(Figure 3).	 Simply	 lying	 the	 patient	 down	 and	 raising	the	 legs	will	 improve	 venous	 return	 and	 improve	 the	preload.	 If	 the	 jugular	venous	pulse	 (JVP)	or	pressure	can	be	 assessed	 and	 is	 found	 to	 be	 low,	 a	 little	 additional	 IV	fluid	 judiciously	 given	 is	 appropriate.	 If	 however	 the	 JVP	is	 already	 elevated,	 then	 increasing	 the	 preload	 further	would	be	harmful	as	it	is	likely	to	lead	to	acute	pulmonary	oedema.	Sinus	bradycardia	will	 often	 respond	 to	 atropine	as	atropine	effectively	removes	the	parasympathetic	brake	on	the	SA,	and	to	a	much	lesser	extent	the	AV	node.	The	dose	of	 atropine	should	be	at	 least	1	mg	as	small	 doses	have	 been	 known	 to	 paradoxically	 reduce	 the	 heart	 rate	by	 interfering	with	 the	sympathetic	system.	 In	 reality	 this	means	two	ampoules	of	600	µg	of	atropine	for	an	adult.	 Bradycardia	 that	 is	 not	 sinus	 rhythm	 is	 running	 on	either	 a	 junctional	 or	 a	 ventricular	 pace	maker	 (Figure 4).	Although	 atropine	 tends	 to	 be	 given	 as	 an	 automatic	response	 it	 is	not	 logical	 to	expect	 it	 to	be	very	effective	as	 there	 is	 only	 a	 slight	 parasympathetic	 innovation	 of	the	AV	 node.	 If	 the	 patient	 is	 symptomatic	 and	 oxygen	and	optimising	the	preload	with	posture	has	already	been	tried,	 the	 two	 alternatives	 are	 to	 drive	 the	 inherent	 rate	with	a	sympathomimetic	drug	or	 to	pace	the	patient	with	an	 external	 or	 internal	 pacer	 arrangement.	Adrenaline	 is	 Figure 4. Bradycardia Figure 2. Bradycardia (complete block) Figure 3. Bradycardia improving with oxygen Figure 1. Sinus bradycardiaEmergency management of acute cardiac arrhythmiasTHEME494  Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007an	 excellent	 choice	 of	 sympathomimetic	 drug,	 although	isoprenaline	 is	 often	 the	 drug	 of	 choice.	Whichever	 drug	is	 used	 the	 route	 should	be	 IV	 and	 ideally	 by	 a	 low	dose	infusion	gradually	increasing	the	infusion	rate	until	a	desired	response	is	achieved.	The	issue	here	is	balancing	improved	oxygenation	of	the	coronary	muscle	with	increased	oxygen	demand.	 Although	 improving	 the	 heart	 rate	 improves	coronary	 artery	 perfusion	pressure	 and	 thus	oxygenation,	oxygen	demand	rises	as	heart	rate	and	force	of	contraction	increase.	Usually	the	predominant	effect	 is	beneficial	from	the	increase	in	coronary	artery	perfusion	pressure.	 External ly	 appl ied	 pacemakers	 are	 becoming	commonplace	 and	 can	 be	 easily	 used	 as	 an	 alternative.	The	 self	 adhesive	 pads	 should	 be	 placed	on	 the	 anterior	chest	wall	and	between	the	shoulder	blades	for	optimum	current	 transmission.	The	 patient	 should	 be	warned	 that	this	will	be	uncomfortable.	The	pacing	function	is	selected	at	 an	 initial	 rate	 of	 about	 60	 bpm.	 It	 is	 not	 a	 good	 idea	to	 select	 too	 high	 a	 rate	 initially	 as	 an	 increase	 in	 heart	rate	 increases	 the	oxygen	demand.	The	 current	 delivered	should	 be	 quickly	 increased	 to	 a	 point	where	 capture	occurs.	 Capture	will	 be	 confirmed	 by	 the	 presence	 of	a	 complex	 after	 each	 pacing	 spike	 and	 hopefully	 by	 the	presence	of	a	palpable	pulse.	At	 this	point,	 the	 increased	perfusion	will	be	improving	the	patient’s	conscious	state	to	the	point	where	they	will	be	aware	of	the	distress	caused	by	the	repeated	muscle	contractions.	Once	perfusion	has	been	 achieved	 it	 is	 appropriate	 to	 give	midazolam	 (and	possibly	an	opiate	 in	a	small	dose)	to	relieve	the	patient’s	discomfort	 and	 reduce	 their	memory	 of	 the	 event.	 In	 a	more	intensive	setting,	formal	pacing	with	an	internal	wire	can	be	considered.Too fastTachycardias	can	also	reduce	cardiac	output	as	ventricular	filling	 becomes	 ineffective;	 they	 also	 increase	myocardial	oxygen	demand	making	ischaemia	worse.	 A	 supraventricular	 tachycardia	 (SVT)	 arises	 above	the	 ventricles	 (Figure 5)	 and,	with	 the	 exception	 of	 atrial	fibrillation/flutter,	 has	 an	 atrial	 contraction	 preceding	each	ventricular	 contraction.	This	means	 that	 the	SVT	 is	 likely	to	 have	better	 ventricular	 filling	 and	hence	better	 cardiac	output.	Usually	SVTs	are	not	life	threatening	and	the	patient	remains	 conscious,	 although	 distressed,	 by	 palpitations.	Initial	management	 is	 to	 increase	 the	 vagal	 stimulus	 to	the	AV	 node	 by	 performing	 a	Valsalva	manoeuvre.	To	 do	this	 properly	 the	 patient	 should	 be	 supine	 and	 a	 forced	expiration	against	a	blocked	airway	needs	to	be	maintained	for	 at	 least	 15	 seconds.	The	 vagal	 stimulus	 occurs	 after	letting	 go.	 Rubbing	 the	 carotid	 sinus	will	 also	 produce	vagal	 stimulation,	 however	 this	 is	 considered	 dangerous	Figure 5. Supraventricular tachycardia Figure 6. Ventricular tachycardia Figure 7. Basic life support flowchartReproduced with permission: Australian Resuscitation Council THEMEReprinted from Australian Family Physician Vol. 36, No. 7, July 2007  495in	 anyone	 over	 50	 years	 of	 age	 because	 of	 the	 risk	 of	disturbing	 atherosclerotic	 plaque.	 If	 a	Valsalva	manoeuvre	has	failed,	the	usual	drug	treatment	 is	adenosine	given	 in	increasing	doses	of	6,	12,	and	 if	still	not	effective,	18	mg	as	sharp	IV	pushes	into	a	running	line	(at	 least	18	gauge).	This	 gives	 a	 'chemical	 defibrillation'	 giving	 the	 heart	 an	opportunity	 to	 restart	 in	 sinus	 rhythm.	 Some	 patients	find	 this	 sensation	 distressing	 and	 so	 should	 be	warned	beforehand.	 Rapid	AF	 is	 a	 common	 supraventricular	 arrhythmia	characterised	by	a	rapid	irregular	QRS,	which	is	often	best	heard	by	listening	to	the	rhythm	of	the	beat	via	the	audible	alarm.	Long	 term	AF	should	not	be	 reverted	 in	 the	acute	setting	without	 first	 excluding	 the	 possibility	 of	mural	thrombosis	 in	 the	 atria	which	might	 then	 become	 the	source	of	an	embolus.	Management	of	AF	is	discussed	in	a	separate	article	in	this	issue.		 Ventricular	 tachycardia	 (VT)	 arises	 below	 the	 atria	 and	is	characterised	by	a	broad	complex	tachycardia	that	often	has	 an	 unusual	 axis	 (Figure 6).	The	 unconscious	 patient	should	 be	 treated	 as	 if	 in	 ventricular	 fibrillation	 (VF)	with	a	 standard	 cardiac	 arrest	 approach.	 Conscious	 patients	can	 be	 treated	 either	 chemically	 or	with	 synchronised	cardioversion.	The	advantage	of	cardioversion	is	that	there	is	 no	 after	 effect	 persisting	 after	 treatment	 and	 lowering	of	 cardiac	 output.	Any	 antiarrhythmic	 drug	 used	will	 also	reduce	myocardial	 contractility.	 For	 this	 reason,	 drug	treatment	 of	VT	 should	 be	 reserved	 for	 patients	with	 a	reasonable	initial	cardiac	output	despite	the	VT.	In	the	past,	lignocaine	 (1.5	mg/kg=100	mg	 for	 adults)	was	 commonly	used	 but	 is	 now	 being	 displaced	 by	 amiodarone	 (150	mg	 slowly	 in	 an	 IV	 infusion	 over	 30	minutes	 and	 share	the	 call	with	 a	 cardiologist)	 as	 a	 drug	 of	 choice;	 sotalol	and	magnesium	have	 also	 been	 used	 in	 this	 role.	 If	 the	patient	 is	 not	well	 perfused,	 cardioversion	 is	 preferable	to	 drug	 therapy.	 For	 this	 procedure	 the	patient	 is	 given	 a	small	dose	of	midazolam	to	ensure	that	they	have	little	or	no	memory	of	 the	event,	 but	 not	 enough	 to	 significantly	sedate	them	(up	to	3	mg	 in	an	adult).	Once	the	drug	has	circulated,	which	will	take	time	in	a	compromised	patient,	a	synchronised	DC	shock	is	given	via	the	defibrillator	pads	or	 paddles.	Most	 patients	will	 revert	 at	 50	 J	 but	 starting	at	 100	 J	 gives	 a	 high	 probability	 of	 first	 shock	 success.	The	 shock	 is	 delivered	 ‘synchronised’	 –	 this	means	 you	avoid	defibrillating	in	the	middle	of	the	T	wave	which	might	provoke	VF.	 Supraventricular	 tachycardias	 in	 patients	with	 a	wide	electrocardiogram	(ECG)	complex	can	be	confused	with	VT.	If	 the	patient	 is	poorly	perfused	or	unconscious	 it	 is	safer	to	treat	them	as	a	VT.	The	criteria	that	help	to	differentiate	between	a	broad	complex	ST	and	a	VT	are:	•	the	 presence	 of	 P	waves	 independently	 timed	 to	the	 ventricular	 complexes	 in	VT.	These	 are	 seen	 as	irregularities	behind	 the	QRS	complexes	 that	appear	on	a	regular	basis	but	are	not	there	on	all	beats	•	the	 presence	 of	 fusion	 beats	where	 a	 P	wave	 has	transmitted	 through	 the	 AV	 node	 and	 then	 the	ventricular	depolarisation	has	been	subsumed	by	the	VT	wave	in	VT	•	an	abnormal	axis	 (often	seen	as	 failure	of	 the	chest,	leads	 to	 progress	 from	 negative	 to	 positive;	 often	seen	in	VT)	•	the	 patient’s	 age	 and	 perfusion	 status	 are	 a	 guide,	with	elderly	patients	with	poor	perfusion	status	being	more	likely	to	be	VT.Ventricular ectopicsThe	 presence	 of	more	 than	 the	 odd	 ventricular	 ectopic	used	 to	 be	 a	 trigger	 to	 reach	 for	 an	 antiarrhythmic	 drug	because	of	a	fear	of	the	‘R	on	T	phenomenon’.	This	brought	with	 it	 the	 consequences	 of	 decreased	 contractility	 and	Emergency management of acute cardiac arrhythmiasFigure 8. Adult cardiorespiratory arrestReproduced with permission: Australian Resuscitation Council Emergency management of acute cardiac arrhythmiasTHEME496  Reprinted from Australian Family Physician Vol. 36, No. 7, July 2007sometimes	 a	 proarrhythmic	 effect	 of	 the	 drug.	 Ectopics	are	 better	 treated	 with	 attention	 to	 oxygenation	 and	perfusion	and	preparation	to	defibrillate	should	any	VF	that	occur.	Oxygen	is	a	wonderful	antiarrhythmic	that	does	not	decrease	myocardial	contractility.Cardiac arrestPatients	presenting	in	cardiac	arrest	will	have	an	underlying	rhythm	of:	•	VF/VT	which	is	treatable	with	defibrillation	•	pulseless	 electrical	 activity	 (PEA)	which	 cannot	 be	treated	with	 defibrillation	 and	where	 an	 underlying	cause	should	be	sought,	or•	asystole	which	will	 not	 respond	 to	 defibrillation	 but	can	occasionally	be	encouraged	into	a	more	favourable	rhythm	with	oxygen	and	CPR	with	adrenaline.If	a	patient	is	in	cardiac	arrest,	the	approach	is	to	establish	effective	 resuscitation	 and	 early	 defibrillation.	 The	Australian	Resuscitation	Council	Basic and advanced life support guidelines	 (www.resus.org.au)	 are	 described	 in	Figures 7–9.	The	key	 issues	are	a	 focus	on	minimal	gaps	in	the	chest	compression	rhythm	and	a	steadily	escalating	level	of	adjuncts.	Basic life supportOnce	 cardiac	 arrest	 has	 been	 observed	 and	 the	 airway	confirmed	 as	 clear	with	 no	 respiratory	 effort,	 two	gentle	breaths	 are	 administered.	Try	 not	 to	 overinflate	 the	stomach	 as	 this	may	 cause	 reflux	 and	 airway	 soiling.	The	 pulse	 check	 is	 only	 one	 of	 the	 signs	 of	 life,	 and	 in	a	 patient	 who	 has	 allowed	 two	 ventilations	 without	objection,	 is	probably	not	 indicated.	Compressions	should	be	 commenced	 as	 soon	 as	possible	 at	 a	 rate	 of	 100	per	minute	(ie.	almost	two	per	second)	and	at	a	depth	of	one-third	of	the	chest	anterior	posterior	measurement.	A	ratio	of	30	compressions	to	two	ventilations	is	appropriate	for	all	adults	and	children	regardless	of	the	number	of	operators.	In	a	specialist	advanced	life	support	setting,	children	can	be	managed	with	a	15:2	 ratio	and	neonates	with	a	3:1	 ratio.	However,	a	ratio	of	30:2	will	suffice	in	most	circumstances	encountered	outside	a	specialist	unit.	Defibrillation and drugsDefibrillation	 should	 occur	 as	 early	 as	 possible	 and	confined	 to	 a	 single	 shock	 at	 a	 high	 energy	 setting.	This	means	 360	 J	 in	 an	 older	monophasic	 defibrillator,	 and	200	J	in	a	modern	biphasic	defibrillator.	Children	receive	2	J/kg	followed	by	4	J/kg	rounded	to	the	next	higher	setting,	regardless	of	the	defibrillator	type.		 Once	 the	 shock	 has	 been	delivered	 it	 is	 important	 to	go	 straight	 back	 to	 compressions	 and	 not	waste	 time	watching	 the	 rhythm	 develop.	After	 2	minutes	 of	 CPR	(which	will	 be	 5	 cycles	 of	 30:2)	 it	 is	 time	 to	 see	what	rhythm	 the	defibrillation	produced.	No	harm	will	 be	done	to	 the	 heart	 if	 compressions	 are	 delivered	 on	 top	 of	 a	developing	rhythm.	1	mg	of	IV	adrenaline	is	given	every	3	minutes	to	maintain	peripheral	vascular	tone.		 Advanced	 airway	 techniques	 are	 used	 as	 soon	 as	possible,	however	if	intubation	is	used	there	should	not	be	an	interruption	to	compressions	of	more	than	20	seconds	and	 a	maximum	 of	 two	 attempts	 is	 reasonable.	 Failing	this,	a	laryngeal	mask	airway	provides	an	airway	that	is	far	superior	to	an	ordinary	oropharyngeal	airway.		 If	 the	 patient	 still	 remains	 in	VF	 despite	 repeated	cycles	 of	 CPR,	 defibrillation,	 adrenaline	 and	 improved	oxygenation/ventilation	 then	 an	 anti-arrhythmic	 drug	is	 appropriate	 and	 the	 preferred	 choice	 is	 amiodarone	300	mg	 IV.	 If	 amiodarone	 is	 not	 available,	 lignocaine	100	mg	 IV	 is	 an	 acceptable	 alternative.	 Persistent	VF	 in	this	 situation	 can	 only	 be	 treated	with	more	 CPR	 and	oxygen	 once	 an	 adequate	 dose	 of	 antiarrhythmic	 has	been	given.	Figure 9. Child cardiorespiratory arrest Reproduced with permission: Australian Resuscitation CouncilTHEMEReprinted from Australian Family Physician Vol. 36, No. 7, July 2007  497PEA and asystoleThe	 presence	 of	 PEA	 should	 prompt	 a	 review	 of	 the	reversible	causes	–	the	‘Hs	and	Ts’	(Figure 8):	•	hypoxia	•	hypovolaemia	•	hypo-/hyper-thermia	•	hypo-/hyper-kalemia	and	other	metabolic	disorders•	tamponade	•	tension	pneumothorax	•	toxins,	and	•	thrombosis	(pulmonary	or	coronary).	Asystole	can	be	treated	with	oxygen	CPR	and	adrenaline.	It	 is	 acceptable	 to	 give	 at	 least	 1	mg	of	 atropine	 in	 this	situation	as	vagal	tone	can	produce	asystole.	PostresuscitationPostresuscitation	 care	 focuses	 on	maintaining	 a	 safe	airway,	 adequate	 ventilation	 and	 oxygenation,	 supporting	perfusion,	and	facilitating	transport	to	hospital.ConclusionThe	management	 of	 arrhythmias	 is	 not	 as	 daunting	as	 initially	 seems.	For	 rhythms	 that	 are	 still	 perfusing,	administration	 of	 high	 concentrations	 of	 oxygen,	attention	 to	 optimising	preload	 (JVP)	 and	patience	 are	good	first	responses	which	then	allow	plenty	of	time	to	share	the	problem	with	a	cardiologist	before	embarking	on	 drug	 therapy.	 For	 rhythms	 not	 perfusing,	 the	response	 is	 as	 per	 a	 standard	 cardiac	 arrest	 following	the	ARC	directions	included	in	this	article.Conflict	of	interest:	none	declared.CORRESPONDENCE email: afp@racgp.org.auEmergency management of acute cardiac arrhythmias

Emergency management of acute cardiac arrhythmias

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Emergency management of acute cardiac arrhythmias

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Emergency management of acute cardiac arrhythmias

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