Killer ECGs

Severe hyperkalaemia

Hyperkalaemia has numerous effects on the ECG, including:

Symmetrically peaked T waves

Flattening, broadening and disappearance of P waves

Broad QRS complexes, often with bizarre morphology

Any kind of bradyarrhythmia – including sinus bradycardia, junctional or ventricular rhythms, slow AF, second- and third-degree AV block

Sine wave appearance – this is a pre-terminal rhythm

The presence of any of these ECG abnormalities should prompt rapid testing of serum K+ (e.g. by bedside VBG). Consideration should be given to empirical treatment with intravenous calcium whilst awaiting blood results (e.g. in a dialysis patient with profound bradycardia).

Handy Tip – Always consider the diagnosis of hyperkalaemia in patients presenting with bradycardia or complete heart block, particularly if they have a history of dialysis, renal failure or treatment with potassium-elevating agents (ACE inhibitors, ARBs, K-sparing diuretics or K supplements).

Unfortunately, the ECG is not sensitive enough to rule out significant hyperkalaemia — patients with relatively normal ECGs may still experience sudden hyperkalaemic arrest!

Peaked T waves

Broad QRS

Sine wave

Complete AV block

Toxicity

The combination of tachycardia, broad QRS complexes and a positive R’ wave in aVR is strongly suggestive of poisoning with a tricyclic antidepressant (or other sodium-channel blocking agent). Sodium channel blocking agents include:

Tricyclic antidepressants (= most common)

Local anaesthetics, including cocaine

Type Ia + Ic antiarrhythmics (quinidine, procainamide, flecainide)

Quinine-based antimalarials

Dextropropoxyphene

Propranolol

These agents cause seizures and cardiotoxicity (hypotension, broad-complex tachycardia) in overdose.

TCAs also cause tachycardia due to their anticholinergic effects.

ECG Features of Sodium Channel Blockade

QRS prolongation (> 100ms or 2.5 small squares), typically measured in lead II

A terminal or secondary R wave (R’ wave) in aVR > 3 mm

An R’/S ratio in aVR > 0.7

In patients with TCA overdose, the degree of QRS prolongation correlates with the degree of clinical toxicity:

QRS width > 100 ms is predictive of seizures

QRS width > 160 ms is predictive of cardiotoxicity (e.g. broad-complex dysrhythmias, hypotension)

Digoxin Toxicty

ECG Features of Digoxin Toxicity

Digoxin toxicity produces a wide variety of dysrhythmias, due to:

Increased automaticity of atrial and ventricular tissues — via actions at the Na/K and Na/Ca exchangers causing increased intracellular calcium and therefore increased spontaneous depolarisation of cardiac pacemaker cells.

Decreased AV conduction — via increased vagal tone at the AV node.

Digoxin toxicity therefore usually produces some combination of:

Increased atrial automaticity — especially atrial tachycardia, but also atrial ectopics, AF, flutter.

Increased ventricular automaticity — frequent VEBs and bigeminy, polymorphic VT.

AV blocks — including 1st, 2nd and 3rd degree AV block.

Characteristic ECG patterns include:

Atrial tachycardia with high-grade AV block (= the classic dig-toxic rhythm).

“Regularised AF” = AF with complete heart block + accelerated junctional escape rhythm, producing a paradoxically regular rhythm.

Bidirectional VT = polymorphic VT with QRS complexes that alternate between left- and right-axis-deviation, or between LBBB and RBBB morphology.

NB. Digoxin toxicity should not be confused with digoxin effect (= “sagging” ST depression and T-wave inversion in patients on therapeutic doses of digoxin; not predictive of toxicity).

Ventricular bigeminy

Regularised AF

Pericardial effusion

he combination of low QRS voltages and electrical alternans is highly suggestive of massive pericardial effusion. The addition of sinus tachycardia is concerning for pericardial tamponade.

Low voltage generally refers to QRS complex amplitude:

< 5 mm (0.5 mV) in the limb leads

< 10 mm (1 mV) in the precordial leads

Electrical alternans refers to a beat-to-beat variation in the QRS complex height, with alternating taller and shorter QRS complexes. It is thought to be due to the heart swinging backwards and forwards within a fluid-filled pericardial sac.

Sinus tachycardia occurs as a compensatory phenomenon in cardiac tamponade, i.e. to maintain cardiac output in the face of diminishing stroke volume. It is of course non-specific, and may also be due to pain, anxiety, shortness of breath, etc.

Raised ICP

his ECG pattern is characteristic of raised intracranial pressure and is classically seen in the context of massive intracranial haemorrhage, particularly:

Spontaneous subarachnoid haemorrhage

Haemorrhagic stroke / intraparenchymal haemorrhage

Similar ECG patterns have also been reported in patients with raised ICP due to:

Large-territory ischaemic stroke causing cerebral oedema (e.g. MCA occlusion)

Traumatic brain injury

The differential diagnosis for widespread T-wave inversions and QT prolongation includes myocardial ischaemia (e.g. Wellen’s syndrome) and electrolyte abnormalities. However, neither condition would cause the gigantic “cerebral T waves” seen here.

Brugada

n a patient presenting with syncope, this ECG pattern is diagnostic of Brugada syndrome.

Brugada syndrome is:

An inherited arrhythmogenic condition.

Due to mutation of various genes coding for cardiac sodium and calcium channels (“channelopathy”).

Inherited as an autosomal dominant trait.

Most commonly seen in individuals from South East Asia (12/10,000 of the population), particularly males (80% of recorded cases are male), with onset of symptoms typically occurring at age 40.

Associated with increased risk of paroxysmal ventricular arrhythmias (polymorphic VT, VF) and sudden cardiac death.

Patients present with:

Sudden cardiac death.

Symptomatic ventricular arrhythmias (paroxysmal syncope, seizure-like events, nocturnal agonal respirations).

Asymptomatic – after family screening or incidental finding on ECG recording.

The only effective treatment is insertion of an implantable cardioverter-defibrillator (ICD).

ECG Features of Brugada Syndrome

There are three ECG patterns associated with Brugada syndrome, of which only the type 1 ECG is diagnostic. Changes need to occur in at least 2 of the right precordial leads (V1-3). The ECG pattern may vary over time: Patients with symptomatic Brugada syndrome may have a non-diagnostic ECG at the time of assessment (e.g. Type 2 or 3 pattern; even a normal ECG). A diagnostic ECG may be produced in these patients by administration of a sodium-channel blocking agent, typically a class I antiarrhythmic such as flecainide or procainamide. Interestingly, fever has also been shown to unmask the type 1 ECG pattern and may precipitate ventricular arrhythmias.

Brugada ECG Patterns

Type 1 = “Coved” ST elevation > 2mm at the J-point, followed by an inverted T wave

Type 2 = “Saddleback” ST segments with > 2mm J-point elevation, > 1mm ST elevation and a positive or biphasic T wave

Type 3 = Coved or saddleback ST elevation < 1mm

Tip – the sensitivity of the ECG for detecting Brugada syndrome may be increased by placing leads V1 and V2 in the second (rather than the fourth) intercostal space.

Making the Diagnosis of Brugada Syndrome

Diagnosis of Brugada syndrome requires both:

A diagnostic (Type 1) ECG pattern – either spontaneously, or during pharmacological challenge with class I antiarrhythmics

At least one clinical criterion

Clinical Criteria

Positive family history: Sudden cardiac death in family member aged < 45; type 1 ECG pattern in family member.

Arrhythmia-related symptoms: Cardiac syncope; seizure-like events; nocturnal agonal respirations.

Documented ventricular arrhythmias: Polymorphic ventricular tachycardia (PVT); ventricular fibrillation (VF).

Diagnostic difficulties arise when faced with patients that do not meet these criteria, e.g.

Idiopathic type 1 ECG

Type 2 or 3 ECG pattern

How Do I Manage My Patient With A Brugada ECG Pattern?

Symptomatic patients with a type 1 ECG pattern

These patients are admitted for cardiac monitoring and ICD insertion.

Idiopathic type 1 ECG

This refers to patients with a type 1 ECG pattern but no positive clinical criteria. It is unclear whether these patients are at increased risk of sudden cardiac death. Further risk stratification with electrophysiological study (EPS) is recommended. Patients who develop PVT/VF during EPS are classified as higher risk and referred for ICD insertion. Patients with a negative EPS are followed up closely by an electrophysiologist, but do not receive an ICD unless they subsequently develop symptoms.

Type 2 and 3 ECG patterns

As these ECG patterns are non-specific, the extent to which these patients are worked up depends on the individual merits of the case and the degree of clinical suspicion for Brugada syndrome. Patients with a compelling story for Brugada syndrome (e.g. recurrent cardiovascular syncope, resuscitated cardiac arrest) should be admitted for monitoring and further diagnostic workup — e.g. with flecainide challenge. Patients with asymptomatic type 2 and 3 patterns may require further investigation if there is a family history of Brugada syndrome.

Arrhythmogenic Right Ventricular Cardiomyopathy

An inherited myocardial disease (usually autosomal dominant) associated with paroxysmal ventricular arrhythmias and sudden cardiac death.

Characterised by fibro-fatty dysplasia of the right ventricular myocardium.

The second most common cause of sudden cardiac death in young people (after HOCM), causingup to 20% of SCDs in patients < 35 yrs of age.

More common in men than women (3:1) and in people of Italian or Greek descent.

Estimated to affect approximately 1 in 5,000 people overall.

Clinical Features

ARVD causes palpitations or syncope due to Right Ventricular VT.

Symptoms are often precipitated by exercise.

The first presenting symptom may be sudden cardiac death.

Over time, surviving patients also develop features of right ventricular failure, which may progress to dilated cardiomyopathy.

There is usually a family history of sudden cardiac death.

Right Ventricular VT

Hyperkalaemia Overview

Potassium is vital for regulating the normal electrical activity of the heart. Increased extracellular potassium reduces myocardial excitability, with depression of both pacemaking and conducting tissues.

Progressively worsening hyperkalaemia leads to suppression of impulse generation by the SA node and reduced conduction by the AV node and His-Purkinje system, resulting in bradycardia and conduction blocks and ultimately cardiac arrest.

Hyperkalaemia is defined as a potassium level > 5.5 mEq/L

Moderate hyperkalaemia is a serum potassium > 6.0 mEq/L

Severe hyperkalaemia is a serum potassium > 7.0 mE/L

Effects of hyperkalaemia on the ECG

Serum potassium > 5.5 mEq/L is associated with repolarization abnormalities:

Peaked T waves (usually the earliest sign of hyperkalaemia)

Serum potassium > 6.5 mEq/L is associated with progressive paralysis of the atria:

P wave widens and flattens

PR segment lengthens

P waves eventually disappear

Serum potassium > 7.0 mEq/L is associated with conduction abnormalities and bradycardia:

Prolonged QRS interval with bizarre QRS morphology

High-grade AV block with slow junctional and ventricular escape rhythms

Any kind of conduction block (bundle branch blocks, fascicular blocks)

Sinus bradycardia or slow AF

Development of a sine wave appearance (a pre-terminal rhythm)

Serum potassium level of > 9.0 mEq/L causes cardiac arrest due to:

Asystole

Ventricular fibrillation

PEA with bizarre, wide complex rhythm

(Warning! In individual patients, the serum potassium level may not correlate closely with the ECG changes. Patients with relatively normal ECGs may still experience sudden hyperkalaemic cardiac arrest.)

ECG manifestations in hyperkalaemia

Peaked T waves

Prolonged PR segment

Loss of P waves

Bizarre QRS complexes

Sine wave

Handy Tips

Suspect hyperkalaemia in any patient with a new bradyarrhythmia or AV block, especially patients with renal failure, on haemodialysis or taking any combination of ACE inhibitors, potassium-sparing diuretics and potassium supplements.

For an excellent review of the management of hyperkalaemia, check out this podcast by Scott Weingart.

ECG Examples

Example 1

This ECG displays many of the features of hyperkalaemia:

Prolonged PR interval.

Broad, bizarre QRS complexes — these merge with both the preceding P wave and subsequent T wave.

Peaked T waves.

This patient had a serum K+ of 9.3

Example 2

Hyperkalaemia

Tall, symmetrically peaked T waves.

This patient had a serum K+ of 7.0.

Example 3

Hyperkalaemia

Long PR segment.

Wide, bizarre QRS.

Example 4

Hyperkalaemia:

Slow junctional rhythm.

Intraventricular conduction delay.

Peaked T waves.

Example 5

Hyperkalaemia:

Broad complex rhythm with atypical LBBB morphology.

Left axis deviation.

Absent P waves.

Example 6

Hyperkalaemia:

Sine wave appearance with severe hyperkalaemia (K+ 9.9 mEq/L).

Example 7

Hyperkalaemia:

Huge peaked T waves.

Sine wave appearance.

This patient had severe hyperkalaemia (K+ 9.0 mEq/L) secondary to rhabdomyolysis.

Hypokalaemia Overview

Potassium is vital for regulating the normal electrical activity of the heart. Decreased extracellular potassium causes myocardial hyperexcitability with the potential to develop re-entrant arrhythmias

Hypokalaemia is defined as a potassium level < 3.5 mmol/L

Moderate hypokalaemia is a serum level of < 3.0 mmol/L

Severe hypokalaemia is defined as a level < 2.5 mmol/L

Effects of hypokalaemia on the ECG

ECG changes when K+ < 2.7 mmol/l

Increased amplitude and width of the P wave

Prolongation of the PR interval

T wave flattening and inversion

ST depression

Prominent U waves (best seen in the precordial leads)

Apparent long QT interval due to fusion of the T and U waves (= long QU interval)

With worsening hypokalaemia…

Frequent supraventricular and ventricular ectopics

Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia

Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes

T wave inversion and prominent U waves in hypokalaemia

Long QU interval in hypokalaemia

Handy tips

Hypokalaemia is often associated with hypomagnesaemia, which increases the risk of malignant ventricular arrhythmias

Check potassium and magnesium in any patient with an arrhythmia

Top up the potassium to 4.0-4.5 mmol/l and the magnesium to > 1.0 mmol/l to stabilise the myocardium and protect against arrhythmias – this is standard practice in most CCUs and ICUs