Miscellaneous  

In this chapter we will discuss ECG abnormalities due to electrolyte disturbances, other clinical disorders and

 pacemaker effects.

            Subjects covered

               • Electrolyte disorders • Embolism • Pericarditis • Chronic pulmonary disease pattern• Suggests CNS disease• Medication• Pacemaker• Electrical alternans

Electrolyte disorders

1.Hyperkalemia2.Hypokalemia3.Hypercalcemia4.Hypocalcemia

Hyperkalemia

ECG characteristics of hyperkalemia: • Tall peaked T waves.• Flattened P-waves (In extreme

hyperkalemia p-waves can disappear).

• Prolonged depolarization leading to QRS widening (nonspecific intraventricular conduction defect) sometimes > 0.20 seconds.

• During sudden onset of high concentrations (around 7-8 mmol/L) atrial and ventricular fibrillation can occur.

Consecutive ECGs of a patient with hyperkalemia. After correction of potassium levels.

Consecutive ECGs of a patient with hyperkalemia.

Hypokalemia

Hypokalemia results in:• ST depression and flattened 

T waves • QT prolongation• Negative T waves • A U wave may be visible

If extrasystoles occur in the T wave (example) the risk of Torsade de Pointes is high and rhythm monitoring is mandatory

patient A

patient A

Another example of hypokalemia

Patient B                       Patient C (potassium level of 1.5)

Hypercalcemia

 Characteristics of hypercalcemia:• Mild: broad-based tall peaked T waves, shortened QT• Severe: extremely wide QRS, low R wave, disappearance of P

waves, tall peaked T waves

Hypocalcemia

 Characteristics of hypocalcemia:• Narrowing of the QRS complex • Reduced PR interval • T wave flattening and inversion • Prolongation of the QT interval • Prominent U wave • Prolonged ST and ST depression

Pericarditis

Pericarditis is an inflammation of the pericardium. This can lead to ST elevation in all leads. Therefore, it is important to distinguish pericarditis from a mycardial infarction, in which ST elevations are limited to the infarct area. A more definite seperation between the two diagnoses can be made with blood tests and echocardiography.

A 12 lead example, shows PTa depression, but no ST elevation

Pericarditis

Acute pericarditis with clear diffuse ST elevation and some PTa depression

Pericarditis stages

In pericarditis four stages can be distinguished on the ECG: • Stage I: ST elevation in all leads,

PTa depression (depression between the end of the P-wave and the beginning of the QRS-complex).

• Stage II: pseudonormalisation (transition).

• Stage III: inverted T-waves.• Stage IV: normalisation

Keep into account that in stage I pericarditis, ST elevation is present in all leads except in aVR, V1 and III. 

Pulmonary embolism

In case of an embolism several clinical features may be present: • Sinus tachycardia • Stress on the right ventricle:

o Right atrial dilatation o Heartaxis is to the right o Right bundle branch block

• Deep S in lead I • Q and negative T in lead III • T wave inversion anterior

Pulmonary embolism cannot be diagnosed using  only an ECG, but it can be helpful.

ECG of a patient with pulmonary embolism

Acute pulmonary embolism

    Chronic pulmonary disease pattern

Chronic pulmonary disease results in increased pulmonary resistance and chronic hypoxia. The increased pulmonary resistance can be registered on the ECG:

• right atrial and ventricular enlargement• right heart axis• clockwise rotation (due to right ventricular enlargement)

These findings are not specific of 1 type of pulmonary disease (e.g. COPD vs chronic pulmonary embolism).

Chronic pulmonary embolism: no sinus tachycardia, right heart axis, right atrial and ventricular enlargement, clockwise rotation, negative T waves V3-V5.

Chronic obstructive pulmonary disease: sinus tachycardia, right (and in this case left) atrial enlargement, right heart axis, clockwise rotation.

Suggests CNS disease

Pathology of the central nervous system, especially in the acute phase, can result in sometimes bizarre, temporary ECG changes. Repolarization abnormalities are frequently observed: negative precordial T waves.One should be very careful with sending patients with such an ECG to the cathlab for coronary intervention, because in the case of cerebral hemorrhage this can result in devastating extra bleeding after administration of anticoagulants in the cathlab.

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ECG in a patient with acute subarachnoid hemorrhage

Medication

• Digoxin• Anti-arrhythmics

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DigoxinECG changes typical for digoxin intoxication are:

Normal:• Oddly-shaped ST depression• T wave flat, negative or biphasic • Short QT interval • Increased U-wave amplitude • Prolonged PR-interval • Bradyarrhythmias:

o Sinus bradycardiaHigh blood levels:

• AV block. Including complete AV block and Wenkebach

• Tachyarrhythmias: o Junctional tachycardia o Atrial tachycardia o Ventricular ectopia, bigemini,

monomorphic ventricular tachycardia, bidirectional ventricular tachycardia

Pro-arrhythmic effects of digoxin intoxication can be worsened by hypokalemia. 

Digoxin related ST depression is often present in patients who take digoxin, also without digoxin intoxication. 

Antiarrhythmics

These may lead to several ECG changes:• Broad and irregular P wave• Broad QRS complex • Prolonged QT interval (bradycardia, tachycardia, AV-block,

ventricular tachycardia)• Prominent U wave

In case of intoxication, the above mentioned characteristics are more prominent.

Electrical alternans

In electrical alternans there is a beat-to-beat variation in QRS amplitude or axis. This can be the result of physical movement of the heart, as is seen in a swinging-heart cardiac tamponade. But it is sometimes also seen as a result of arrhythmias, such as bundle branch re-entry tachycardia or supraventricular arrhythmias with beat-to-beat variations in block of the conduction system (bundle branch or Purkinje).

Cardiac tamponade with a "swinging heart", one of the causes of electrical alternans.

Electrical alternans: watch V2 and notice the beat-to-beat change in axis in this patient with tamponade

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Pacemaker

A (used) DDDr pacemaker

Chest x-ray of a patient with a pacemaker

Indication

A pacemaker is indicated when electrical impulse conduction or formation is dangerously disturbed. The pacemaker rhythm can easily be recognized on the ECG. It shows pacemaker spikes, vertical signals that represent the electrical activity of the pacemaker. Usually those spikes are more visible in unipolar than in bipolar pacing.

Capture and inhibition

A pacemaker should be able to cause a depolarization of the atria or ventricles when needed but should be silent when pacing is not needed. These two functions are called capture and inhibition.

Capture: a pacemaker pulse is followed by depolarization of the chamber in which the pulse is delivered. Inhibition: when the pacemaker senses an intrinsic depolarization of a chamber (either atria or ventricle), that chamber should not be paced.Malfunction can lead to non-capture (a pulse is given, but there is no depolarization) or failure of inhibiton (a pulse is given inappropiately).Modern pacemakers have many monitoring functions that make pacemaker malfunction a rare phenomenon. Also, modern pacemakers can have very complicated algorithms that can cause apparent irregular rhythms and spikes without anything being wrong. Always check with a pacemaker technician before concluding that a pacemaker is malfunctioning.

Coding

Pacemakers can be categorized according to the NASPE coding system, which usually consists of 3-5 letters

I II III IV V

Chamber(s) paced

Chamber(s) sensed

Response to sensing

Rate modulation

Multisite pacing

O = None O = None O = None O = None O = None

A = Atrium A = Atrium T = Triggered R = Rate modulation

A = Atrium

V = Ventricle V = Ventricle I = Inhibited V = Ventricle

D = Dual (A+V) D = Dual (A+V) D = Dual (T+I) D = Dual (A+V)

The revised NASPE/BPEG generic code for antibradycardia pacing

Examples of atrial and ventricular paced rhythms

In the first example, the atria are being paced, but not the ventricles, resulting in an atrial paced rhythm. Accordingly the ventricular complex is delayed until the atrial signal has passed through the AV node. 

In the second image the ventricles are paced directly, resulting in a ventricular paced rhythm. As ventricular pacing occurs exclusively in the right ventricle the ECG shows a left bundle branch block pattern. An exception to this rule is left ventricular pacing in patients with congenital anomalies and patients with surgically placed epicardial pacemakers. Another exception is septal or RVOT placement of the pacing lead, which results in a less widened to normal QRS complex.

Ventricular paced rhythm shows ventricular pacemaker spikes

Atrial paced rhythm

Atrial sensed ventricular paced rhythm and AV dual paced rhythm

Atrial sensed ventricular                 DDD paced rhythm     paced rhythm

Atrial paced rhythm

AV sequential paced rhythm

Failure of atrial capture in a patient with atrial standstill (notice the absence of a p-wave after the atrial pacemaker spike).

Failure of ventricular capture--ventricular pacemaker spikes, but no QRS complexes.

Failure of atrial inhibition (atrial missensing)--atrial spikes are present right after atrial activity.

Failure of appropiate ventricular inhibition (and failure of ventricular capture)--QRS complexes are not sensed by the

pacemaker, resulting in inappropirate spikes.

Inappropriate ventricular inhibition due to oversensing. The pacemaker should have paced at

the red arrow, but did not, probably as a result of oversensing of atrial activity.

Pacemaker mediated tachycardia; this can occur if T waves (or other signals) are interpreted as P waves

(atrial oversensing).