Abnormal EKG’s and Corresponding Arterial Waveforms

Tachycardia

The Normal Sinus Rhythm

Normal sinus rhythm refers to the usual case in healthy adults where the SA node is the cardiac pacemaker and the heart rate is 60 - 100 beats per minute (BPM).

With a normal sinus rhythm one would expect the following:

a normal ECG with P, QRS and T waves
a PR interval of 0.12 - 0.20 seconds
a regular interval between each QRS complex (R-R interval) of 0.60 - 1.00 seconds
a distinct a wave in the CVP trace due to atrial contraction
a regular arterial pulse pressure (difference between systolic and diastolic pressures)
there may be minor regular variation in heart rate and pulse pressure associated with respiration (sinus arrhythmia)

However it is often the case in the clinical situation that the patient does not have a normal sinus rhythm and it is important to be able to recognize and identify these abnormal cases. The following pages of this tutorial will describe and illustrate various abnormal situations.

Sinus Bradycardia

Sinus bradycardia refers to a sinus rhythm (ie originating in the SA node) which is slower than 60 BPM. (brady - slow, cardia - heart). Sinus bradycardia may occur with vagal (parasympathetic) stimulation, such as in trained athletes or in patients with the carotid sinus syndrome (in whom baroreceptors are overly sensitive to pressure, resulting in excessive vagal stimulation). Sinus bradycardia may also occur as a result of pharmacological beta-blockade.

The rhythm is similar to normal sinus rhythm, except that the R-R interval is greater than one second. The pulse pressure may be greater due to a greater stroke volume (resulting in greater systolic pressure) and increased time for diastolic run-off (resulting in lower diastolic pressure).

Sinus Tachycardia

Sinus tachycardia refers to a sinus rhythm with a heart rate greater than 100 BPM (tachy - fast). Sinus tachycardia may be due to fever, which results in increased excitability of the SA node. Sympathetic stimulation (from a variety of causes) and cardiac toxicity may also cause sinus tachycardia.

The rhythm is similar to normal sinus rhythm, except that the R-R interval is less than 0.6 seconds. The a wave may tend to merge with the v wave in the CVP trace, and the P wave may be obscured by the T wave in the ECG (not apparent in this trace). The pulse pressure may be lesser due to a lower stroke volume and decreased time for diastolic run-off.

Atrial Fibrillation

In atrial fibrillation small areas of atrial tissue repeatedly depolarize but in a disordered way relative to neighboring areas of atrial tissue. This is believed to involve a microreentry mechanism. There is no concerted depolarization or contraction of the atria. Also, due to the chaotic nature of atrial depolarizations, there is irregular penetration of the AV node, resulting in irregular ventricular contractions.

Atrial fibrillation is most common in individuals with atrial enlargement, often associated with valvular pathologies.

Notice the lack of P waves due to continual, irregular depolarisations of different areas of atrial tissue. The QRS complexes have normal shape, due to normal ventricular conduction, however the R-R intervals vary from beat to beat with no regular pattern.

Notice that the systolic arterial pressure varies from beat to beat as ventricular filling time changes. Also the diastolic pressure changes from beat to beat with changes in diastolic runoff time. So the pulse pressure also may vary significantly from beat to beat.

Key features of atrial fibrillation:

absence of P waves
irregular R-R interval
varying pulse pressure
no a waves in the CVP trace

Ventricular Ectopics

ectopic - 'in abnormal place or position' from the Greek 'ektopos' - out of place.

An ectopic beat occurs from an abnormal site (called an ectopic focus) before the expected time of the next contraction. Ectopic beats (also called extrasystoles or premature contractions) may originate in the atria, the AV junction or the ventricles. There are numerous possible causes of ectopics including local ischaemia, drugs (caffeine is a good example), calcified plaques and physical contact (such as contact of the heart with catheters or surgical instruments).

Take a close look at the following diagram:

This ventricular ectopic - or premature ventricular contraction (PVC) - has had an effect on all three traces in the above diagram:

The ECG

QRS earlier than expected (premature) i.e. shorter RR interval than normal
QRS wider than normal
QRS voltage higher than normal
inverted T wave
obscured P wave
next RR interval longer than normal

The arterial pressure

ejection earlier than expected
low systolic pressure generated

The CVP

large a wave
a wave at expected time (not premature)

These observations can be explained by considering the abnormal pathway of ventricular depolarization:

The depolarization of the ventricles was initiated prematurely at an ectopic focus, not a part of the His-Purkinje network, so the wave of depolarization traveled slower through the myocardium via unconventional pathways, resulting in a wide, unusually-shaped QRS.

The slow conduction resulted in a less concerted contraction of the ventricles. This, as well as less time for ventricular filling and lack of atrial priming of the ventricles (ventricles depolarized before the atria), accounts for the poor ejection and low systolic arterial pressure.

When the ventricles depolarize normally, voltages on one side of the heart tend to be balanced by voltages on the other (due to the heart's symmetry). However with an ectopic depolarization voltages on one side may have no counterpart, due to the slower propagation of the wave of depolarization, resulting in a greater measured voltage in the ECG. That is why a PVC can result in a QRS with a higher voltage than normal.

The slow ventricular depolarization resulted in those areas of myocardium first depolarised being able to repolarize first (in contrast with the case of a normal depolarization). This pattern of repolarization resulted in the inverted T wave.

The SA node fired at the expected time. The atria contracted but, because the ventricles were already contracting, they were unable to eject into the ventricles, resulting in markedly increased pressure in the atria and hence a large CVP a wave (cannon wave). The a wave was larger than normal but occurred at the expected time.

The two waves of depolarization (one from the SA node and the other from the ectopic focus) met in the AV node. The ectopic depolarization did not reset the SA node, so the next SA node firing occurred exactly as if there had been no ectopic depolarization. The next RR interval, by being longer than normal, exactly compensated for the prematurity of the ectopic . This is termed a fully compensatory pause.

Characteristics of (most) PVCs

wide and bizarre QRS, often with a high voltage and inverted T wave
reduced or no left ventricular ejection
large CVP a wave
fully compensatory pause

Supraventricular Paroxysmal Tachycardia

Take a close look at the following diagram:

Note the sudden onset of tachycardia which results in a decreased mean arterial pressure (due to decreased filling time)

Also note that the QRS complexes are not abnormal in shape, indicating a supraventricular irritable focus.

Ventricular Fibrillation

Ventricular fibrillation is analogous to atrial fibrillation and similar phenomena are believed to give rise to it. However ventricular fibrillation is a very serious condition because the uncoordinated contractions of ventricular myocardium result in ineffective pumping. If immediate action is not taken the results are fatal.

These traces were recorded in a patient undergoing cardiopulmonary bypass, so that blood flow was maintained mechanically.

The following features can be seen in the above diagram :

random, unrelated waves in the ECG
lack of significant pulse pressure