Cardiac Arrhythmias in The Critically Ill

CARDIAC ANAESTHESIA
Cardiac arrhythmias in Learning objectives

the critically ill After reading this article, you should be able to:
C recognize the clinical features of cardiac arrhythmias in the
Matthew Kerton critically ill patient that demand immediate and swift action
Jessica Wiggins C understand the various causes and mechanisms of arrhythmias
in the critically ill
Michael Purkiss
C have a systematic approach in the assessment and manage-
ment of arrhythmias in critically ill patients
C appreciate the changes in the updated 2015 European Resus-
Abstract
citation Council guidelines
Arrhythmias are a common problem in the critically ill and they can
have significant effects on patient outcome. They often require imme-
diate and swift action and it is, therefore, essential that clinicians have
a structured approach to the recognition and management of arrhyth- often revealed through a thorough history, examination and
mias. Here, we provide a framework for the appropriate management relevant investigations. Figure 1 summarizes the various mech-
of the more frequently encountered cardiac arrhythmias in critical care. anism of arrhythmias in the critically ill.
We include the algorithms from the 2015 Resuscitation Council Guide-
lines for reference. Assessing the patient with cardiac arrhythmia
Keywords Arrhythmias; atrial fibrillation; bradycardia; congenital The evaluation and treatment of critically ill patients with ar-
heart disease; ion channelopathies; prolonged QT supraventricular rhythmias has to include supportive, diagnostic, therapeutic and,
tachycardia; temporary cardiac pacing; therapeutic hypothermia; possibly, resuscitative measures encompassing not just the cause of
ventricular tachycardia the arrhythmia but also systemic effects, including impaired end-
organ perfusion and function. Establishing the presence of struc-
Royal College of Anaesthetists CPD Matrix: 3G00
tural heart disease and/or the history of arrhythmias is essential
prior to assessing the arrhythmia. The increasing incidence of adult
congenital heart disease adds complexity to arrhythmia manage-
ment and we emphasize the need for early involvement of specialist
Arrhythmias are common in critically ill patients (Table 1) and cardiologists in the management of these patients.
their clinical manifestation may range from patients being In this article we present a rational, step-wise sequence of
completely asymptomatic to cardiorespiratory arrest. The un- questions to guide management.
derlying causes are often multifactorial, hence the management
and resuscitation of patients must be performed in a systematic
and methodical manner. The aim of this article is to provide a Question 1: Is the patient compromised by the arrhythmia?
framework for the appropriate management of the more The answer to this question determines the speed of treatment:
frequently encountered cardiac arrhythmias in the critically ill. the greater the compromise, the swifter the response needs to be.
Irrespective of the instantaneous degree of compromise, the ever
Causes of arrhythmias (Table 2) present risk of further cardiovascular deterioration or the
development of life-threatening arrhythmias mandates:
Arrhythmias can result from primary pathology in the cardiac
enrichment of the oxygen supply in hypoxaemic patients
conductive pathways or abnormalities in other organ systems. In
rapid ABCDE assessment
the critically ill patient, arrhythmias can be caused or potentiated
establishment of secure venous access
by increased catecholamine levels (endogenous or exogenous),
application of monitors
hypoxia, hypercarbia, severe acidosis, gross electrolyte distur-
peripheral oxygen saturation (SpO2)
bance, and pain or anxiety. The end result is a combination of
ECG
decreased cardiac output and/or increased myocardial oxygen
non-invasive blood pressure (NIBP)
demand. Treatment should be targeted at the underlying cause,
application of stick-on defibrillation pads
right infraclavicular and left anterior axillary line over
the 5th/6th intercostal spaces attached to a compatible
defibrillator to also allow for external cardiac pacing if
Matthew Kerton MB ChB FRCA is an ST6 Anaesthetist at University the patient is bradycardic. With a history of heart failure
Hospital Southampton, UK. Conflicts of interest: none declared. or if the heart is suspected to be dilated a more lateral
Jessica Wiggins BM MSc MRCS FRCA is an ST6 Anaesthetist at position of the left defibrillator pad will allow a greater
University Hospital Southampton, UK. Conflicts of interest: none chance of successful defibrillation
declared. recording a 12-lead ECG as soon as the clinical situation
Michael Purkiss BM BSc MRCP DiMM ACC is a Cardiologist working in allows.
the Cardiac intensive care unit at University Hospital Southampton, And if the clinical condition warrants it:
UK. Conflicts of interest: none declared. removal or withdrawal of precipitants
ANAESTHESIA AND INTENSIVE CARE MEDICINE 19:6 298 Ó 2018 Elsevier Ltd. All rights reserved.
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For personal use only. No other uses without permission. Copyright ©2019. Elsevier Inc. All rights reserved.
CARDIAC ANAESTHESIA
Incidence and impact of arrhythmias in patients in the intensive care unit

Sustained supraventricular Sustained ventricular Conduction No arrhythmias
arrhythmias % arrhythmias % abnormalities % %
Incidence 8 2 2 88
Unadjusted in-hospital death rate 29 73 60 17
Neurological sequelae among 15 38 17 6
survivors
After adjustment for prognostic factors and propensity scores, only ventricular arrhythmias increased mortality (odds ratio 3.53, 95% confidence interval 1.19e10.42).
Table 1
Question 3: Is the heart rate slow or fast?

Some causes of arrhythmias in the critically unwell
The normal heart rate (HR) is between 60 and 100 beats per minute
Arrhythmias arising from Arrhythmias arising secondary (bpm). A HR below 60 is termed a bradycardia, and above 100 a
primary cardiac disease to systemic disease process tachycardia; however, this needs to be taken in context.
Bradycardias C Hypothermia
Question 4: What is the relationship of the P wave to the
C Second-degree and C Hyperkalaemia
QRS complex?
complete heart block C Head injury and raised
C Following inferior MI intracranial pressure Although this is easier to answer if the HR is slow, all 12 leads
C Excessive vagal tone C Drugs, e.g. B-blockade, need to be scrutinized as the P wave might be evident in some
C Chronotropic incompetence calcium channel antagonists leads but not in others. The relationship might be regular,
C Congenital heart disease C Organophosphorus poisoning irregular or there might be no P waves visible.
Tachycardias C Excessive endogenous
C Myopathies catecholamines (pain) Bradycardia
Atrial fibrillation with C Excessive exogenous
rapid ventricular response
Table 3 describes common bradycardias and classifies them ac-
catecholamines
Cardiomyopathies
cording to their relationship to the P wave. The appropriate
C Pyrexia
C Conducting system
treatment decision has to be made in the clinical setting.
C Sepsis
Nodal re-entrant
Asymptomatic second-degree heart block in a non-compromised
C Thyrotoxicosis
AV nodal re-entrant
patient, for example, is going to warrant invasive intervention
C Hypercarbia
Channelopathies
but this may not be immediately required; however, in the
C Hypoxia
C Pacemaker generated
compromised patient, atropine 500 mg (repeated up to 3 mg),
C Hypovolaemia
C Congenital heart disease
isoprenaline or adrenaline as bolus or infusion will temporise the
C Tension pneumothorax
circulation before single- or dual-chamber pacing. The in-
C Pulmonary embolism
dications for pacing are shown in Box 2 and the Resuscitation
C Drug or alcohol withdrawal
Council’s 2015 algorithm for bradycardias is shown in Figure 2.
C Vagolytic drugs
Table 2 Tachycardia
Tachycardias can be difficult to interpret because the P wave may
be absorbed into the QRS complex. Furthermore, retrograde P
measurement of ‘plasma’ Kþ, Mg2þ and Ca2þ.
waves could be present which represent retrograde conduction of
The relevant clinical signs of compromise are described in Box 1.
a ventricular tachycardia (VT) via the atrioventricular (AV) node.
Table 4 describes the possible relationships of the P wave to the
Question 2: Is this a primary arrhythmia or secondary to
QRS complex.
another disease process?
A broad complex tachycardia is either VT or a supraventric-
Is the cardiac rhythm a normal and appropriate response to al- ular tachycardia (SVT) with aberrant conduction (left bundle
terations of physiology or is it pathological? The answer to this branch block or right bundle branch block). It can be compli-
question might be swiftly obtained by means of the history, ex- cated to distinguish between these. The majority of broad com-
amination and appropriate investigations; for example, the pro- plex tachycardias will be VT, and in patients with known
found bradycardia associated with hypothermia. At other times, structural or ischaemic heart disease these are almost always
determining the cause of the arrhythmia might require electro- VTs. Distinguishing between VT and aberrant SVT is important
physiological studies (EPS). in terms of their subsequent management; however, if there is
CARDIAC ANAESTHESIA
Mechanism of arrhythmias
Structural influences Transient influences
1 Myocardial infarction Abnormal automacity 1 Transient ischaemia/

• Acute Slowed impulse conduction reperfusion
• Healed
• Aneurysm 2 Systemic factors
Premature atrial and • Hypoxia
2 Hypertrophy ventricular contractions • Acidosis
• Electrolyte
3 Myopathic ventricle abnormalities
• Dilation
Arrhythmia
• Fibrosis 3 Neurophysiological
factors
• Autonomic tone
• Endogenous
catecholamines
4 Toxicity
• Proarrythymic drugs
• Exogenous
catecholamines
Figure 1
any doubt, treat the arrhythmia as VT because this has the pro- Antiarrhythmic drugs can be classified according to their mech-
pensity to progress to ventricular fibrillation. Clinically, a anism of action on the cardiac action potential or by the source of
changeable pulse pressure, irregular cannon waves in the jugular the arrhythmia they treat. This can be useful in choosing an
waveform and a variable first heart sound are features common appropriate treatment (see also Drugs acting on the heart: anti-
to VT. A useful scheme based on the morphology of the QRS arrhythmics, Anaesthesia & Intensive Care Medicine 2018;
complex is shown in Figure 3. 19(7).) The 2015 revision of the Resuscitation Council (UK)
Additional electrocardiographic features suggestive of a VT guidelines for the treatment of tachyarrhythmias are shown in
are as follows: Figure 4.
Fusion beats: a sinus beat conducts via the AV node to the Management of atrial fibrillation (AF)
ventricles but fuses with a beat arising in the ventricle; the
Atrial fibrillation is extremely common in both critical care and
complex is intermediate between a normal beat and a tachy-
in the perioperative period for both cardiac and non-cardiac
cardia beat.
surgery. New-onset AF in medical intensive care patients has
been shown to be an independent predictor of mortality with a
Capture beats: when an atrial impulse ‘captures’ the normal
twofold increase of in-hospital mortality and death at 60 days.
conduction system and an early, narrow complex is seen.
Initial management of new-onset AF in critical care should
begin as for any arrhythmia. If there are signs of significant
QRS duration: >140 ms.
compromise then immediate DC cardioversion may be indicated
as per the Resuscitation Council adult tachycardia algorithm (see
Axis: extreme left axis.
Figure 4). This will require adequate sedation or general
anaesthesia.
Concordance: all QRS complexes in the chest leads are either
In the absence of adverse signs mandating immediate car-
positive or negative.
dioversion, the patient should be assessed for reversible causes.
Common precipitants include sepsis, hypoxia, fluid shifts and
AV dissociation: present in 20e50% of VTs and almost never in
electrolyte disorders, particularly hypokalaemia and hypo-
an SVT.
magnesaemia. Intrathoracic pathology such as pneumonia and
pulmonary embolism are potent causes of AF.
Atrial tachycardia
Treatment of AF includes addressing any underlying cause, as
The electrocardiographic characteristics of common atrial well as control of the ventricular rate or treatment to restore
tachycardias are presented in Box 3. sinus rhythm, and also consideration of anticoagulation. The
Treatment of tachycardias can be pharmacological or non- National Institute of Health and Care Excellence (NICE) issued
pharmacological using vagal manoeuvres or DC cardioversion. updated guidelines for the management of atrial fibrillation in
CARDIAC ANAESTHESIA
Signs of compromise Indications for temporary cardiac pacing
Shock C Symptomatic bradycardia unresponsive to atropine

C Hypotension C Acute conduction disturbances following MI
C Signs of low cardiac output Anterior MI associated with complete AV block, Mobitz type I
C Reduced level of consciousness or type II AV block, non-adjacent bifascicular or trifascicular
block requires prophylactic pacing
Syncope C Temporary or rarely permanent pacing might be required in infe-
rior MI with complete AV block
Myocardial ischaemia C Complete AV block with rate <50
C Ischaemia on the ECG C Asystole with P wave activity
C Chest pain C Suppression of drug-resistant tachyarrhythmias - ‘overdrive
pacing’
C During or after cardiac surgery (especially in aortic surgery,
Heart failure
tricuspid surgery, ventricular septal defect closure and ostium
C Pulmonary oedema
primum repair)
C Raised jugular venous pressure
C Preoperatively in patients with
Box 1 Second-degree or complete AV block
Intermittent AV block
Trifascicular block
2014. NICE recommend that a rate or rhythm control strategy can First-degree AV block and LBBB
be used in patients in AF for less than 48 hours in the un-
anticoagulated patient. If the duration of AF is thought to be AV, atrioventricular; LBBB, left bundle branch block; MI, myocardial
longer than 48 hours at time of diagnosis, or there is uncertainty, infarction.
then a rate control strategy should be used. After AF has been Box 2
present for more than 48 hours the risk of left atrial thrombus
formation is increased, this is also true for atrial Flutter. AF
occurring post-surgery should be managed with an initial rhythm
control strategy unless contraindicated.
deficiency is common and in this population there is evidence
Recommended first-line drugs for rate control are beta
supporting a better cardioversion rate with magnesium
blockers (other than sotalol) and rate-limiting calcium channel
compared to amiodarone or digoxin alone.
blockers such as diltiazem. NICE do not consider digoxin to be a
In the absence of life-threatening haemodynamic instability,
first-line agent for rate control, although it may be useful in the
where AF has persisted for 48 hours or more patients should not
critical care setting to slow the ventricular rate without conse-
be cardioverted until they have been anticoagulated for at least 3
quent negative inotropy. Beta blockers and calcium channel
weeks.
blockers are contraindicated if decompensated heart failure is
present.
Special circumstances
Recommended rhythm control drugs include amiodarone and
flecainide (although flecainide is contraindicated in the presence Arrhythmias in patients with congenital heart disease
of structural or ischaemic heart disease). Interestingly, NICE do (CHD)
not recommend the use of magnesium for pharmacological car- The majority of patients with congenital heart disease now sur-
dioversion. However, in the critically unwell, magnesium vive to adulthood and by this time many have developed rhythm
disturbance. The disturbances are caused by the initial condition
itself, by scarring in combination with the condition, cyanosis (if
present), surgical scar and by prolonged abnormal pressure and
Common bradycardias classified according to their volume loading of cardiac chambers.
relationship to the P wave To cover the entire range of conditions is beyond this article
and is the reason why expert help should be sought when dealing
Regular relationship Irregular relationship No P waves visible
with CHD. However, gaining an understanding should help
Sinus bradycardia Complete HB Atrial fibrillation remove some of the fear associated with rhythm disturbance in
First-degree HB Mobitz type 2 with slow ventricular these conditions. Many patients will have knowledge of the type
Mobitz type second-degree HB response of rhythm disturbance they are prone to and will already have
1 second degree HB Atrial flutter with slow had investigations and various treatments including medication,
ventricular response ablation and defibrillator implantation.
Conditions can be simply classified into mild forms of CHD
HB, heart block.
(45%) such as ASD and pulmonary valve stenosis, moderate
forms (roughly 40%) such as tetralogy of Fallot and Ebstein’s
Table 3
CARDIAC ANAESTHESIA
Resuscitation Council (UK) 2015 Guidelines. Reproduced with kind permission. AV, atrioventricular;
BP, blood pressure; ECG, electrocardiography; IV, intravenous.
Figure 2
anomaly with the last 15% being severe, consisting of conditions The arrhythmias in adults with CHD are:
such as single ventricular pathology. The incidence of Directly associated with the condition due to a developmental
arrhythmia is more common in the moderate and severe groups. impact on the conducting system: e.g. An accessory pathway
As surgical techniques have improved we hope to see a causing Wolff-Parkinson-White syndrome which effects 20% of
reduction in the arrhythmia burden that develops in these patients with Ebstein’s anomaly. As the right atrium dilates, so
patients. does the chance of developing atrial flutter or fibrillation. This
CARDIAC ANAESTHESIA
Common tachycardias classified according to their The electrocardiographic characteristics of atrial

relationship to the P wave tachycardias
Single P wave per No apparent relationship
Sinus tachycardia
QRS complex between P wave and QRS complex
C P waves have normal morphology
Sinus tachycardia QRS <120 ms QRS >120 ms
C Atrial rate 100e200 beats per minute (bpm)
Sinus node Regular RR SVT with aberrant
C Regular ventricular rhythm
re-entry (HR 130) SVT conduction
C Ventricular rate 100e200 bpm
Intra-atrial re-entry AV re-entrant VT
C One P wave precedes every QRS complex
(HR 140e240) AV nodal re-entrant Fascicular tachycardia
Ectopic atrial Irregular RR interval Atrial tachycardia
tachycardia Atrial fibrillation C Abnormal P wave morphology
AV, atrioventricular; HR, Heart rate; RR, RR interval ¼ distance from the onset
C Atrial rate 100e250 bpm
of the next; SVT, supraventricular tachycardia; VT, ventricular tachycardia. C Ventricular rhythm usually regular
C Variable ventricular rate
Table 4
Atrial flutter
C Undulating saw-toothed baseline F (flutter) waves
C Atrial rate 250e350 bpm
C Regular ventricular rhythm
C Ventricular rate typically 150 bpm (with 2:1, 3:1 or 4:1 atrioven-
Distinguishing features of supraventricular
tricular conduction)
tachycardia with aberrant conduction from
C 1:1 conduction is uncommon
ventricular tachycardia based on the morphology of
the QRS complex
Atrial fibrillation
LBBB C P waves absent; oscillating baseline f (fibrillation) waves
SVT VT C Atrial rate 350e600 bpm
C Irregular ventricular rhythm
Broad R C Ventricular rate 100e180 bpm
Small R Slow descent
Reproduced with permission from Goodacre and Irons.

V1
Box 3
Fast descent 60 ms
can transmit down the accessory pathway causing an extremely
Q high narrow complex ventricular heart rate or occasionally
V6
ventricular fibrillation. Accessory pathways also effect congeni-
tally corrected transposition of the great arteries.
Acquired abnormalities of the conducting system can be
RBBB
associated with damage to the system itself or as a result of ‘short
SVT VT
circuits’ that develop due to scarring, stretching, fibrosis and
suture lines:
rSR pattern Monophasic R qR (or RS)
Sick sinus syndrome: due to direct damage of the SA node after
V1 surgery can cause bradycardia requiring a pacemaker. This was
typically seen after repair of transposition of the great arteries
using the Mustard or Senning repair. Other operations that can
R/S › 1 R/S ‹ 1 or QS pattern
damage the sinus node are Glenn and Fontan procedures.
V6
Sinus node dysfunction: can often be associated with parox-
ysmal atrial tachycardias. The less robust the sinus node function
the higher the chance of an ectopic or aberrant pathway suc-
cessfully hijacking the conducting system.
LBBB, left bundle branch block; RBBB, right bundle branch block;
SVT, supraventricular tachycardia; VT, ventricular tachycardia.
Reproduced with permission from Eckardt et al.2 Macro-re-entry tachycardia: this is the most common mecha-
nism for symptomatic tachycardia in the adult CHD population.
Figure 3 The re-entrant pathway is within the atrial muscle (typically RA)
CARDIAC ANAESTHESIA
Resuscitation Council (UK) 2015 Guidelines. Reproduced with kind permission. AF, atrial fibrillation; BP, blood pressure; DC, direct current;
ECG, electrocardiography; IV, intravenous; SVT, supraventricular tachycardia; VT, ventricular tachycardia.
Figure 4
and can be associated with a site of incision. It is usually slower Ventricular tachycardia
than ‘typical flutter’ with atrial rates of 150e250 cycles per This is rare during the first two decades of life but, as patients
minute and a healthy AV node will be able to conduct 1:1. become older, the risk increases, specifically in certain condi-
Typical symptoms will be hypotension and syncope. If AV con- tions. The haemodynamic consequences of VT also increase
duction is slower (2:1 or 3:1), symptoms can still be present but depending on the condition and age of the patient.
presentation may be delayed, adding to the risk of developing an The highest risk patients are those who have undergone sur-
atrial thrombosis. Re-entry tachycardia can usually be diagnosed gery on the ventricular muscle or patching of certain types of
on a 12-lead ECG sometimes with the help of vagal manoeuvres VSDs. Tetralogy of Fallot repair has a 2% per decade incidence of
or adenosine to unmask the rhythm. Treatment is with D/C sudden cardiac death, largely due to VT. Other conditions prone
cardioversion, overdrive pacing or administration of Class I or III to VT are: TGA, where the RV is the systemic ventricle (Senning
anti-arrhythmic drugs. or Mustard repair); single ventricle conditions (Fontan proced-
If you are unsure if it is a macro-re-entry tachycardia, atrial ure); Eisenmenger’s syndrome and unrepaired tetralogy of Fallot.
fibrillation, flutter or an SVT it is nearly always worth trying
adenosine to help cardiovert or unmask the underlying rhythm. Heart block: this is associated with surgery to the ventricular
septum. Many patients will present initially with a bundle branch
Atrial fibrillation: macro-re-entry tachycardia is more common block, usually RBBB. Development of complete AV block is also
in the ACHD population but atrial fibrillation can develop espe- seen in congenitally corrected transposition of the great arteries.
cially as patients get older. 20% of these patients will have a pacemaker by age 20.
CARDIAC ANAESTHESIA
Resuscitation Council (UK) 2015 Guidelines. Reproduced with kind permission. CPR, cardiopulmonary resuscitation;
ECG, electrocardiography; PEA, pulseless electrical activity; VF, ventricular fibrillation; VT, ventricular tachycardia.
Figure 5
CARDIAC ANAESTHESIA
Prolongation of the QT interval recently been shown to be useful in the management of LQT3
The QT interval represents the depolarization and repolarization and Brugada but many will have ICDs.
phases of the action potential. This is controlled by the interplay
of several ion channels. Increasing the depolarizing, inward so- Management of cardiac arrest
dium or calcium currents or decreasing the repolarizing, outward In 2015, the International Liaison Committee of Resuscitation
potassium current can cause prolongation of the QT interval. updated the guidelines for the management of cardiac arrest
The list of drugs that can prolong the QT interval is formi- based on the latest evidence and expert opinion (Figure 5). In
dable. The effect is most striking when drugs are combined with summary, there is a further emphasis on early, good quality,
a genetic predisposition to prolonged QT, in which case, the QT uninterrupted chest compressions. Atropine is no longer recom-
will greatly increase. When the QTc goes beyond 500ms, the mended for routine use in the treatment of asystolic or pulseless
chance of developing VT (specifically torsade de pointes) in- electrical activity (PEA). In the treatment of VF and pulseless VT,
creases. This can deteriorate into VF and sudden death. adrenaline is given after the 3rd shock at the same time as
Other acquired causes of prolonged QT interval are hypo- 300 mg of amiodarone. The use of three successive shocks in VF
kalaemia, hypomagnesaemia and hypocalcaemia. and pulseless VT is only recommended if used during cardiac
The normal QT interval is measured from the onset of the catheterization in the laboratory or in the period immediately
QRS complex to the end of the T-wave and is normally 0.35e0.45 following cardiac surgery.
seconds (QTc 0.38e0.42). Survivors of cardiac arrest due to primary ventricular
A standard calculation of the QT corrected for heart rate (QTc) arrhythmia, or patients who experience haemodynamically
is as follows: compromising VT, should be referred to a cardiologist to assess
for implantation of a cardioverter defibrillator (ICD). Interna-
Bazett’s formula QTc ¼ QT interval/(ORR interval) tional guidance from both the European Society of Cardiology
RR interval ¼ the onset of one QRS complex to the onset of the (ESC) and the American College of Cardiology (ACC)/American
next. Heart Association (AHA) recommends implantation after evalu-
ation to define the cause of the event and to exclude any
The newer, 12-lead ECG machines often calculate the QTc completely reversible causes, based on survival data from
using a combination of equations giving a more sophisticated several large scale trials of ICD therapy. Implantation should not
estimate. Bazett’s formula tends to over correct at high heart be performed where the primary cause of the arrhythmia is
rates and under correct at low heart rates. ongoing ischaemia. In these circumstances revascularization is
the priority.
Ion channelopathies e the genetic cause of prolonged
QT Post-resuscitation care, targeted temperature
Long QT-1 (LQT1), long QT-2 (LQT2) and long QT-3 (LQT3) management and arrhythmias
make up 90% of all genotype positive cases and warrant further The 2015 resuscitation council guidelines recommend targeted
discussion. temperature management (TTM) for all patients who remain
unresponsive after successful resuscitation following cardiac ar-
LQT1: KCNQ1 gene codes for the a-subunit of the outward (slow) rest, whether from a shockable or an un-shockable rhythm.
rectifier Kþ channel (IKs). This channel is essential for QT The intention of mild therapeutic hypothermia (TH) post-
shortening when heart rate increases and is stimulated by sym- resuscitation is to provide protection for the brain, spinal cord
pathetic activation. When present QT fails to shorten during and perhaps other organs, such as the heart, against ischaemic
tachycardia and arrhythmogenic potential increases. Triggers for
rhythm disturbances are linked to adrenergic activation and
cardiac events tend to be precipitated by exercise or swimming.
Cardiovascular effects of hypothermia (adapted from
LQT2: KCNH2 gene codes for the a-subunit of the outward Polderman, 2004)
(rapid) rectifier Kþ (IKr) channel. Triggers for rhythm disturbance
Temperature Effect
in this group also tend to be linked to increased adrenergic tone
but cardiac events are mainly seen with emotional stress and
35e36 C Tachycardia
auditory stimuli. Both LQT1 and LQT2 are successfully treated
<35 C Bradycardia
with Beta-blockers.
Increased CVP
Decreased CO
LQT3: SCN5A gene codes for the a-subunit of the cardiac sodium
Increased or unchanged mixed venous
channel which conducts the depolarizing sodium current in-
saturation
wards. Dysfunction in this channel prolongs the inward sodium
<34 C Slight increase in BP
current so prolonging the action potential duration.
<33 C ECG changes: Increased PR interval, widening
This usually manifests in teenage years and cardiac events
of QRS complex, increased QT interval
frequently occur at rest or with inactivity and are less likely to be
<28e30 C Tachyarrhythmias, beginning with AF
triggered by adrenergic stress or emotions.
<28 C VF/VT
Brugada syndrome is another sodium channelopathy effecting
the inward depolarizing sodium current. Beta-blockers have Table 5
CARDIAC ANAESTHESIA
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reduced reperfusion injury and cell apoptosis tachycardias in patients without structural heart disease. Heart
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Med 2004; 30: 757e69.
Annane D, Sebille V, Duboc D, et al. Incidence and prognosis of
Baysa SJ. Arrhythmias following the mustard and senning operations
sustained arrhythmias in critically ill patients. Am J Respir Crit Care
for Dextro-transposition of the great arteries clinical aspects and
Med 2008; 178: 20e5.
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Arizona CERT. QT drugs list. Also available at: http://www.azcert.org/
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medical-pros/drug-lists/drug-lists.cfm (accessed 27 Jan 2009).
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therapeutic hypothermia to improve the neurologic outcome after
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Cardiac Arrhythmias in The Critically Ill

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Cardiac Arrhythmias in The Critically Ill

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CARDIAC ANAESTHESIA

Cardiac arrhythmias in Learning objectives

Incidence and impact of arrhythmias in patients in the intensive care unit

Question 3: Is the heart rate slow or fast?

Structural influences Transient influences

1 Myocardial infarction Abnormal automacity 1 Transient ischaemia/

Signs of compromise Indications for temporary cardiac pacing

Shock C Symptomatic bradycardia unresponsive to atropine

Common tachycardias classified according to their The electrocardiographic characteristics of atrial

Reproduced with permission from Goodacre and Irons.

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