Page 275 - ACCCN's Critical Care Nursing

252 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

right atrium, spontaneously generates an activation dispersion). Slow conduction through a region of the
current that conducts across preferential right and left heart may allow enough time for other tissues which have
atrial pathways (producing a P wave on the surface ECG) already been depolarised to recover, and then to be
and then to the atrioventricular node at the lower inter- re-excited by the arrival of the slowly-conducting wave-
atrial septum. After a brief physiological slowing of the front. Once this pattern of out-of-phase conduction and
current (to allow the ventricles to be optimally ‘pre- repolarisation is established, a current may continue to
loaded’), the impulse travels to the Bundle of His in the circulate back and forth between adjacent areas, or around
upper interventricular septum before spreading down a re-entry circuit. Each ‘lap’ of the circuit gives rise to
4,6
through the ventricles via the right and left bundle another depolarisation (P wave or QRS complex). The
branches. These terminate distally as branching Purkinje ultimate rate of the tachycardia depends on the size of
fibres which penetrate and activate the ventricles. This the circuit (micro versus macro reentry) and the conduc-
ventricular activation (or depolarisation) sequence pro- tion velocity around the circuit.
duces a QRS complex on the surface ECG and subsequent
repolarisation gives rise to an electrocardiographic T ARRHYTHMIAS AND ARRHYTHMIA
wave. Pathophysiological processes may disrupt this MANAGEMENT
sequence, giving rise to arrhythmia production. 1,2
Arrhythmias may arise from myocardial or conduction
ARRHYTHMOGENIC MECHANISMS system tissue, and may represent inappropriate excitation
Arrhythmias result from three primary electrophysiologi- or depression of automaticity, altered refractoriness
cal mechanisms; abnormal automaticity, triggered activ- resulting in micro-reentry arrhythmias, or may involve
ity and reentry, each of which is described below. reentry on a larger scale, as between the atria, AV node
and/or ventricles. 3
Abnormal Automaticity The clinical impact of tachyarrhythmias is highly variable
and is influenced by the rate and duration of the
The action potential of sinus and atrioventricular con-
ducting tissue differs from that of the myocardium in that arrhythmia, the site of origin (ventricular vs supraven-
phase 4 of their action potentials are less stable and tricular), and the presence or absence of underlying
possess the property of spontaneous automaticity and cardiac disease. As a result, arrhythmias may require no
consequent depolarisation. This is an important property treatment, at least in the short term, or at worst may
that allows these tissues to assume the role of electro- present as cardiac arrest and require treatment according
physiological pacemaker dominance. However, in some to advanced life support algorithms (as described in
circumstances, such as myocardial ischaemia or cardio- Chapter 24).
stimulatory influences, regional levels of spontaneous Bradyarrhythmias may be due to failure of sinus node
automaticity can be abnormally accelerated, stimulating discharge (sinus bradycardia, pause, arrest, or exit block)
subsidiary pacing cells (such as those within the AV or to failure of AV conduction (second- or third-degree
junction and ventricular Purkinje fibres) to override the AV block). In any of these contexts, junctional or ventricu-
normal sinus rate. 3,4 lar escape rhythms may make their appearance. Failure
of escape foci may result in asystole or ventricular
Triggered Activity standstill.
Arrhythmias may occur through the occurrence of abnor-
mal oscillations within the early and late repolarisation ARRHYTHMIAS OF THE SINOATRIAL
stages of the cardiac action potential that lead to the NODE AND ATRIA
propagation of aberrant ‘triggered’ arrhythmic events. In health, the sinus node controls the heart rate according
Such oscillations are classified as either ‘early after depo- to metabolic demand, responding to autonomic, adrenal
larisations’ that occur during phases 2 and 3 of the action and other inputs, which vary according to exertion or
potential or late after depolarisations, which occur during other stressors. In response to needs, the sinus node
phase 4. Digitalis toxicity, ischaemia, hypokalaemia, discharge rate typically varies from as low as 50 beats/min
hypomagnesaemia and elevated catecholamine levels are to as high as 160 beats/min. In the conditioned heart
5
the more common causes of triggered activity. Excessive (e.g. in athletes), this range extends perhaps down to as
prolongation of the action potential duration enhances low as 40 beats/min, and to as high as 180 beats/min.
the risk of such triggered activity and as such these mech- Peak activity in the elite athlete may even achieve sinus
anisms are implicated in the development of certain rates of 200/min, though this represents the extreme end
subtypes of ventricular tachyarrhythmias, in particular of the sinus rate. Sinus rhythm is illustrated in Figure 11.1.
torsade de pointes (refer to description later in this
chapter). Sinus Tachycardia
In adults, a sinus rate of greater than 100/min is termed
Reentry sinus tachycardia and may occur with normal exertion
7,8
The most common cause of tachyarrhythmias is reentry, (see Figure 11.2). When sinus tachycardia occurs in the
in which current can continue to circulate through patient at rest, reasons other than exertion must be sought
the heart because of different rates of conduction and and include compensatory responses to stress, hypoten-
repolarisation in different areas of the heart (temporal sion, hypoxaemia, hypoglycaemia or pain, in which there