Student-ER.net
Accident and Emergency Medicine, Ninewells Hospital, Dundee
Student-ER.netAccident and Emergency Medicine, Ninewells Hospital, Dundee
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Rhythms and Arrhythmias Charge Nurse Jenny Fitzpatrick, Accident and Emergency Department
Normal Sinus Rhythm This
is the normal rhythm of the
heart. The impulse is initiated at the
sinus node in a regular rhythm at a rate of 60 – 100 bpm. A
P wave appears before each QRS complex The
PR interval is within normal limits. [0.12 – 0.20 seconds] and the QRS is
narrow [< 0.12 seconds]. Sinus tachycardiaIn sinus tachycardia, the sinus node accelerates and initiates an impulse at a rate of 100bpm. The upper limits extend to 160 – 180 bpm. All other ECG characteristics except for heart rate are the same as in normal sinus rhythm. Sinus tachycardia is usually caused by factors relating to an increase in sympathetic tone. Stress, exercise and stimulants such as caffeine and nicotine can produce sinus tachycardia. It is also associated with problems such as fever, anaemia, hyperthyroidism, hypoxia, congestive cardiac failure and shock. Drugs such as atropine, isoprenaline, adrenaline and dopamine can also produce this rhythm. Treatment is usually directed towards eliminating the underlying cause. Sinus
Bradycardia
is defined as a rhythm with impulses originating at the sinus node at a rate of
less than 60bpm. The rhythm may become less regular as a slower heart rate
prevails, otherwise, all other parameters are normal.
Sinus bradycardia is common among all age groups and is present in both normal and diseased hearts. It may occur during sleep, and in highly trained athletes, as well as with severe pain, inferior myocardial infarction, acute spinal cord injury and with certain drugs [e.g. digitalis, beta blockers, verapamil and diltiazem]. Slow
rates are well tolerated in people with healthy hearts. With severe heart
disease, however, the heart may not be able to compensate for a slow rate by
increasing the volume of blood ejected per beat. In this situation, sinus
bradycardia will lead to low cardiac output. No treatment is indicated unless symptoms are present. If the pulse is very slow [< 40 bpm = extreme bradycardia] and symptoms are present, appropriate measures include atropine, or cardiac pacing. Sinus Arrhythmia is a disorder of rhythm. It is said to be present if the R-R intervals on the ECG strip vary by more than 0.12 seconds, from the shortest R-R interval to the longest. This dysrhythmia is due to an irregularity in sinus node discharge, often in association with phases of the respiratory cycle. The sinus node gradually speeds up with inspiration and slows with expiration. There is also a non-respiratory form of this dysrhythmia. Sinus arrhythmia is a normal phenomenon, seen especially in young people in the setting of lower heart rates. It also occurs after enhancement of vagal tone [e.g. digitalis, morphine]. Sinus arrhythmia is a normal finding and therefore does not imply the presence of underlying disease. Symptoms are uncommon unless there are excessively long pauses. Usually, no treatment is required. Sinus arrest and Sinoatrial block Sinus arrest is a disorder of impulse formation. The sinus node fails to discharge one or more impulse, producing pauses of varying lengths due to the absence of atrial depolarisation. The P wave is absent and the resulting P-P interval is not a multiple of the basic P-P interval. The pause ends either when an escape pacemaker from the junction or ventricles takes over, or sinus node function returns. Sinoatrial block often is difficult to differentiate from sinus arrest on a surface ECG tracing. In SA block, the sinus node fires, but the impulse is delayed or blocked from exiting the sinus node. If the block is complete, the duration of the pause is a multiple of the basic P-P interval. Both dysrythmias may be due to involvement of the sinus node by infarction, degenerative fibrotic changes, drug effects [digitalis, beta blockers, calcium channel blockers] or excessive vagal stimulation. These rhythms are usually transient and not significant unless a lower pacemaker fails to take over to pace the ventricles. Treatment is indicated if the patient is symptomatic. The goal is to increase the ventricular rate, which may require the use of atropine or, in the presence of serious haemodynamic compromise, the use of a pacemaker. Premature
Atrial Contraction [Atrial
Ectopics]. A
premature atrial contraction occurs when an atrial impulse discharges
prematurely and, in most cases is conducted in a normal fashion through the AV
conducting system to the ventricles. On
the ECG tracing, the P wave is premature and may even be buried in the preceding
T wave. It may differ in configuration from the sinus P wave, but the QRS
complex usually is of normal configuration and there will be a short pause
present before the next sinus beat. Atrial
ectopics are very common and are seen in all groups of patients, especially
those with rheumatic heart disease, ischaemic heart disease or hyperthyroidism.
It is often seen in those suffering from congestive heart failure. Premature
atrial contractions may be a precursor to an atrial tachycardia, indicating
atrial irritability. Patients
may have a sensation of a ‘pause’ or ‘skip’ in rhythm when atrial
ectopics are present. In
most cases no treatment is necessary. Atrial
Fibrillation
is defined as a rapid atrial ectopic rhythm occurring with atrial rates of 400
– 650 bpm. It is characterised by chaotic atrial activity with the absence of
definable P waves. The ventricular rate and rhythm depend on the ability of the
AV junction to respond to the rapid stimuli from the atria. Initially,
the ventricular response may be 140 – 170 bpm, but with treatment, or disease
of the AV conduction system, the ventricular response may be slower. The
ventricular rhythm is characteristically irregularly irregular. Although
atrial fibrillation may occur as a transient dysrhythmia in healthy, young
people, the presence of permanent atrial fibrillation is almost always
associated with underlying heart disease. This
rhythm commonly occurs in the setting of congestive cardiac failure, ischaemic
or rheumatic heart disease, pulmonary disease and after open-heart surgery. It
is also seen in congenital heart disease. Atrial
fibrillation causes the cardiac output to fall because of 1.
A rapid rate that allows less time for the ventricles to fill. 2.
Loss of effective atrial contractions. Patients
with borderline cardiac function may experience signs and symptoms of
haemodynamic compromise while in this rhythm. A pulse deficit will often be seen
in this setting. The radial pulse is slower than the apical pulse because some
systolic contractions are weak and not palpable in the peripheral arteries. Patients
with chronic atrial fibrillation are at high risk from an embolic event,
including stroke. Because of the passive dilated state of the atria, thromboli
can form on the atrial wall and dislodge, producing embolisation. Atrial
Flutter
is a rapid atrial ectopic rhythm occurring at atrial rates of 250 – 300 bpm.
Unless an abnormal AV conduction path is present, the ventricles can only
respond at half the atrial rate, initially producing a 2:1 flutter. With
treatment, the degree of AV block increases and the ventricular rate slows [3:1
flutter, 4:1 flutter or atrial flutter with a varying ventricular response]. The
rapid and regular atrial rate produces a ‘saw-tooth’ appearance on the ECG.
It is usual for a flutter wave to be partially concealed within the QRS complex
or T wave. The QRS complex is of normal configuration unless there is a
conduction problem. When
the ventricular rate is rapid, the diagnosis of atrial flutter may be difficult.
Vagal manoevers such as carotid sinus massage will often increase the degree of
block and allow recognition of flutter waves. Atrial
flutter is often seen in the patient who has an underlying cardiac problem. If
atrial flutter occurs with a rapid ventricular response, the ventricular
chambers cannot fill adequately, resulting in various degrees of haemodynamic
compromise. No
immediate treatment is necessary if flutter is associated with a high degree of
AV block, so that the ventricular rate remains within normal limits. When the
ventricular rate is rapid, prompt treatment to control the rate or revert the
rhythm to a sinus mechanism is indicated. Paroxysmal
Supraventricular Tachycardia [S.V.T.]
is described as a rapid atrial rhythm occurring at a rate of 150 – 250 bpm.
The tachycardia begins abruptly, in most cases with a premature atrial
contraction, and it ends abruptly. P waves may be seen preceeding the QRS, but
at faster rates may be hidden in the QRS complex or the T wave. The
QRS is usually normal unless there is an underlying conduction problem. The
rhythm is always regular and the paroxysms may last for a few seconds to several
hours or even days. S.V.T.
often occurs in adults with normal hearts and for the same reasons as premature
atrial contractions. When heart disease is present, such abnormalities as
rheumatic heart disease, acute myocardial infarction and digoxin toxicity may be
the cause of the dysrhythmia. Often
the patient has no underlying heart disease and may experience only palpitations
and some light-headedness, depending on the rate and duration of the dysrythmia. With
underlying heart disease, dyspnoea, angina and congestive heart failure may
occur, as ventricular filling time and thus cardiac output, is decreased. Vagal
stimulation will often terminate S.V.T., either carotid sinus massage or the
valsalva manoever. If this is unsuccessful, intravenous drug therapy would be
indicated. Adenosine would be the drug of choice unless contra-indicated. Cardioversion
may be required, if drug therapy is unsuccessful or if the patient is
compromised by the dysrhythmia.
Ventricular
Premature Beat [VPB]
A
ventricular premature beat is an ectopic beat originating prematurely at the
level of the ventricles. This impulse may also be referred to as a PVC
[Premature Ventricular Contraction]. Because
the beat is ventricular in origin, it will not travel through the normal
conduction system. The QRS will not only be premature, but will be wide and
bizarre. A compensating pause often follows the VPB as the heart awaits the next
stimulus from the sinus node. VPB’s
can be described by both their frequency and pattern - they can be rare,
occasional or frequent. If the VPB’s occur after each sinus beat, this is
known as ventricular bigeminy. Ventricular trigeminy is when a VPB occurs after
two consecutive sinus beats. When
VPB’s appear in only one form, they are referred to as unifocal as opposed to
multifocal, when there are two or more forms of the QRS complex. Ventricular
premature beats are the most common of all ectopic beats and can occur in any
age group, with or without heart disease. They are especially common in a person
with myocardial disease [ischaemia or infarction], or with myocardial
irritability, e.g. hypokalaemia, increased levels of catecholamines or
mechanical irritations with a wire or catheter. The
presence of VPB’s is a sign of ventricular myocardial irritability and in some
patients may lead to ventricular tachycardia [VT] or ventricular fibrillation
[VF]. The nature of the patient’s underlying heart disease rather than the
presence of VPB’s will determines the prognosis. The presence of numerous and
multifocal VPB’s in the patient with serious heart disease worsens the
prognosis. Ventricular
premature beats approaching the apex of the T wave are known as R on T
VPB’s and may lead to VF. Ventricular
Tachycardia [VT]
In
theory, two or more consecutive ventricular ectopic beats at a rate equivalent
to more than 100 bpm constitute a run of ventricular tachycardia. In practice,
many more are required and at a much faster rate, before this abnormal rhythm
assumes clinical significance. VT
is recognised by wide, bizarre QRS complexes occurring in a fairly regular
rhythm at a rate greater than 100 bpm. P waves are not usually seen, and if
seen, are not related to the QRS. VT
can present as a short, non-sustained rhythm or be longer and sustained. VT
is rare in adults with normal hearts, but is common as a complication of
myocardial infarction. Other causes are the same as described for VPB’s. Ventricular
tachycardia is a precursor of VF; signs and symptoms of haemodynamic compromise
[ischaemic chest pain, hypotension, pulmonary oedema and unconsciousness] may be
seen if the rate is fast and the tachycardia is sustained. Serious dysrhythmia
progression depends on the underlying heart disease. If
the patient is haemodynamically stable with the dysrhythmia, amiodarone or
lignocaine is the treatment of choice. If the patient becomes unstable,
synchronised cardioversion [or in emergency situations, unsynchronised] is
indicated. Long-term treatment for this dysrhythmia may involve the use of an
AICD [Automatic Implantable Cardioverter defibrillator]. Ventricular
Fibrillation [VF]
Ventricular
fibrillation is defined as rapid, irregular and ineffectual depolarisation of
the ventricle. No distinct complexes are seen, only irregular oscillations of
the baseline are apparent; these may be coarse or fine in appearance. VF
may occur in the following circumstances; myocardial infarction and ischaemia,
catheter manipulation in the ventricles, electrocution, prolonged QT intervals,
or as a terminal rhythm in patients with circulatory failure. Loss
of consciousness occurs within seconds when VF occurs. The patient is pulseless
and there is no cardiac output. Ventricular
fibrillation is the most common cause of sudden cardiac death, and is fatal if
resuscitation is not instituted immediately. If
VF occurs, rapid defibrillation is the management of choice. If the arrest is
witnessed, a precordial thump is indicated before the patient is defibrillated.
The patient should be supported with cardiopulmonary resuscitation and drugs if
there is no response to defibrillation. An
AICD may be indicated for long-term management of this problem. First
Degree AV Block
In
first-degree block, AV conduction is prolonged, but all impulses are eventually
conducted to the ventricles. P waves are present and precede each QRS complex in
a 1:1 relationship. The PR interval is constant, but exceeds the upper limit of
0.20 seconds in duration. This
type of block occurs in all ages and in both normal and diseased hearts. PR
prolongation may be caused by drugs such as digitalis, beta – blockers or
calcium channel blockers, as well as coronary artery disease, a variety of
infectious diseases and congenital lesions. First-degree
block is of no haemodynamic consequence to the patient, but should be seen as an
indicator of a potential AV conduction system disturbance. It may progress to
second or third degree AV block. No
treatment is indicated for first-degree block, but the PR interval should be
monitored closely, watching for further block. The possibility of drug effect
should be evaluated. Second
degree AV Block – Mobitz Type 1
Traditionally,
second degree AV block has been categorised as one of two types. Type 1, also
called the Wenckebach phenomenon and Mobitz type 1. In
this type of second-degree block, AV conduction is delayed progressively with
each sinus impulse, until eventually the impulse is completely blocked from
reacting to the ventricles. The cycle then repeats itself. On
the ECG tracing, P waves are present and related to the QRS complex in a cyclic
pattern. The PR interval progressively lengthens with each beat until a QRS
complex is not conducted. The interval between successive QRS complexes shortens
until a dropped beat occurs. A
Wenckebach or Mobitz type 1 block is usually associated with block above the
bundle of His, therefore any drug or disease process which affects the AV node;
e.g. digitalis or an inferior infarction, may produce this type of second degree
block. The
patient is rarely symptomatic with this type of second-degree block because the
ventricular rate is usually adequate. It is often temporary in nature and may
occasionally lead to third degree or complete block. Second
Degree AV Block- Mobitz type 11
The
second type of second-degree block is called type 11 or Mobitz type 11. This is
less common than type 1, but generally more serious. Mobitz
type 11 is characterised by a constant PR interval preceeding a blocked P wave.
Conducted P waves may display a normal QRS complex if the site of the block is
within the bundle of His A
hallmark of this type of second degree AV block is that the PR interval does not
lengthen before a dropped beat. More than one dropped beat may occur in
succession. This type of block is usually associated with an organic lesion in
the conduction pathway, and unlike type 1 it is rarely the result of increased
parasympathetic tone or drug effect. It is thus associated with a poorer
prognosis, and complete heart block may develop. If
the patient is haemodynamically compromised, a temporary pacemaker may be
required. Third
Degree AV block. [Complete Heart Block]
In
this condition, the block in the AV junctional tissues is complete. No
conduction between the atria and ventricles is possible and they function
independently of one another under the control of separate pacemakers. The
atria usually remain in normal sinus rhythm, although any of the atrial
dysrhythmias may be present, or there may be little or no sign of atrial
activity. The
ventricles usually maintain a slow idioventricular rhythm with broad QRS
complexes but if the site of the block is above the bifurcation of the His
bundles, the QRS complexes have a more normal appearance and may occur at a
faster rate. On the ECG there is no normal relationship between the P and QRS
waves. Complete
heart block is most often caused in adults by heart disease or as a side effect
of drug toxicity. Heart block can also be present at – or even before –
birth. [This is called congenital heart block and is fairly rare.] It
also may result from an injury to the electrical conduction system during heart
surgery. Complete
heart block may be a medical emergency with potentially severe symptoms and a
serious risk of cardiac arrest. A temporary pacemaker can be used to keep the
heart pumping until recovery. Rhythm
strip examples will be added in the near future. |
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