Clinical Disorders

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Author(s) I.A.C. van der Bilt, MD
Moderator T.T. Keller
Supervisor
some notes about authorship

Medication

Digoxin

Typical for digoxin intoxication is the oddly shaped ST-depression

ECG changes typical for digoxin use (digoxin = Lanoxin) are:

  • Oddly shaped ST-depression with 'scooped out' appearance of the ST segment (see figure)
  • Flat, negative or biphasic T wave
  • Short QT interval
  • Increased u-wave amplitude
  • Prolonged PR-interval
  • Sinus bradycardia

ECG changes typical for digoxin intoxication are:

  • Bradyarrhythmias:
    • AV block. Including complete AV block and Wenkebach.
  • Tachyarrhythmias:
    • Junctional tachycardia
    • Atrial tachycardia
    • Ventricular ectopia, bigemini, monomorphic ventricular tachycardia, bidirectional ventricular tachycardia

Intoxication can lead to an SA-block or AV-block, sometimes in combination with tachycardia. NB these effects are increased by hypokalemia. In extreme high concentrations rhythm disturbances (ventricular tachycardia, ventricular fibrillation, atrial fibrillation) may develop.

Antiarrhythmics

  • Anti-arrhythmics: These may lead to several ECG-changes;
    • Broad and irregular P-wave
    • Broad QRS complex
    • Prolonged QT interval (brady-, tachycardia, AV-block, ventricular tachycardia)
    • Prominent U-wave
    • In case of intoxication, the above mentioned characteristics are more prominent

Additionally, several arrhthytmias can be seen.

Beta blockers

ECG of a patient with atenolol intoxication

Beta blocker intoxication can result in bradycardia, hypotension, QRS widening and seizures. In a series of 260 patients with beta blocker intoxication, 41 (15%) developed cardiovascular morbidity and 4 (1.4%) died. Cardioactive coingestant (e.g. calcium channel blockers) was the only factor significantly associated with the development of cardiovascular morbidity. [1]


Nortriptyline Intoxication

An example of severe nortriptyline intoxication. The inhibitory effect on the sodium channel manifests as a broadened QRS complex and a prolonged QT interval.
Another example of severe nortriptyline intoxication.


Amitriptyline Intoxication

An example of a severe amitriptyline intoxication. The inhibitory effect on the sodium channel manifests as a broadened QRS complex.
An ECG of the same patient before the intoxication.


Pericarditis

Pericarditis

Myocarditis

A patient with myocarditis and pericarditis showing diffuse ST elevation

Myocarditis is an inflammation of the myocardium and the interstitium. The symptoms are faint chest pain, abnormal heart rate and progressive heart failure. It can be caused by several factors: viruses, bacteria, fungi, parasites, spirochetes, auto-immune reactions, borreliosis (Lyme's disease) and HIV/AIDS.

Acute peri/myocarditis causes nonspecific ST segment changes. These can be accompanied by supraventricular and ventricular rhythm disturbances and T-wave abnormalities.

Pulmonary Embolism

See the chapter Pulmonary Embolism

Chronic Pulmonary Disease Pattern

An example of right ventricular hypertrophy (and right atrial enlargement) in a patient with chronic pulmonary hypertension due to peripheral embolisation.

The ECG shows low voltage QRS complexes in leads I, II, and III and a right axis deviation. This is caused by the increased pressure on the right chamber. This leads to right ventricular hypertrophy.


Pacemaker

See the chapter Pacemaker

Tamponade

Electrical alternans on the ECG

In case of tamponade, fluid collects in the pericardium. Because the pericardium is stiff, the heart is compressed, resulting in filling difficulties. This is a potentially life-threatening situation and should be treated with pericardiocentesis, drainage of the fluid. Tamponade can be the result of pericarditis or myocarditis. After a myocardial infarction a tamponade can also develop; this is called Dresslers' Syndrome. In case of cancer,increased pericardial fluid may develop. This is usually caused by pericarditis carcinomatosis, meaning that the cancer has spread to the pericardium

The ECG shows:

  • Sinus tachycardia
  • Low-voltage QRS complexes microvoltages
  • Alternation of the QRS complexes, usually in a 2:1 ratio. Electrical alternans can also be seen in myocardial ischemia, acute pulmonary embolism, and tachyarrhythmias
  • PR segment depression (this can also be observed in an atrial infarction)


Ventricular Aneurysm

The ECG pattern suggests an acute MI. All classical signs of MI may occur:; Q waves, ST segment elevations (>1mm, >4 weeks present)and T wave inversions are present. To exclude an acute MI, comparison with old ECG's is compulsory (MI has occurred years before).

Dilated Cardiomyopathy

Often, a LBBB or broadened QRS-complex can be seen. Additionally, nonspecific ST segment changes are present with signs of left atrial enlargement.

Hypertrophic Obstructive Cardiomyopathy

A HOCM is a hereditary illness. On the ECG there are signs of left ventricular hypertrophy and left atrial enlargement.

Electrolyte Disturbances

See chapter: electrolyte disturbances

Hypothermia

An Osborne J wave
  • A 12 lead ECG of a patient with a body temperature of 32 degrees Celsius. Note the sinus bradycardia, the prolonged QT interval (QTc is not prolonged) and the Osborne J wave, most prominently in leads V2-V5

    A 12 lead ECG of a patient with a body temperature of 32 degrees Celsius. Note the sinus bradycardia, the prolonged QT interval (QTc is not prolonged) and the Osborne J wave, most prominently in leads V2-V5

  • An ECG of a patient with a body temperature of 28 degrees Celsius.

    An ECG of a patient with a body temperature of 28 degrees Celsius.

In hypothermia a number of specific changes can be seen;[2]

  • Sinus bradycardia
  • Prolonged QTc-interval
  • ST segment elevation (inferior and left precordial leads)
  • Osborne-waves (slow deflections at the end of the QRS-complex)


ECG Changes after Neurologic Events

ECG of a 74 year old patient with a subarachnoid hemorrhage. Note the negative T-waves and the prolonged QT interval.

In 1938, Aschenbrenner [3] noted that repolarization abnormalities may occur after increased intracranial pressure. Since then, many publications have described ECG changes after acute neurological events.

ECG changes that may occur are:

  • Q waves
  • ST segment elevations,
  • ST segment depressions,
  • T wave changes. Large negative T waves over the precordial leads are observed frequently.
  • Prolonged QT-interval.
  • Prominent u-waves.

These abnormalities are frequently seen after subarachnoid_hemorrhage (SAH) (if measured serially, almost every SAH patients has at least one abnormal ECG.), but also in subdural hematoma, ischemic CVA's, brain Tumors, Guillain Barré, epilepsy and migraine. The ECG changes are generally reversible and have limited prognostic value. However, the ECG changes can be accompanied with myocardial damage and echocardiographic changes. The cause of the ECG changes is not yet clear. The most common hypothesis is that of a neurotramitter "catecholamine storm" caused by sympathetic stimulation.

Cardiac Contusion

Cardiac contusion (in latin: contusio cordis or commotio cordis) is caused by a blunt trauma to the chest, often caused by a car or motorbike accident or in martial arts[4]. Rhythm disturbances and even heart failure can occur. Diagnosis is made using echocardiography and laboratory testing for cardiac enzymes. Possible ECG changes are:[5]

Nonspecific changes

  • Pericarditis-like ST elevation or PTa depression
  • Prolonged QT interval

Myocardial damage

  • New Q waves
  • ST-T segment elevation or depression

Conduction delay

  • Right bundle branch block
  • Fascicular blok
  • AV delay(1st, 2nd, and 3rd degree AV blok)

Arrhythmias

  • Sinus tachycardia
  • Atrial and ventricular extrasystoles
  • Atrial fibrillation
  • Ventricular tachycardia
  • Ventricular fibrillation
  • Sinus bradycardia
  • Atrial tachycardia

Lown Ganong Levine Syndrome

The Lown Ganong Levine Syndrome is a pre-excitation syndrome in which the atria are connected to the lower part of the AV node or bundle of His. On the ECG:

  • Short PR interval, < 120 ms
  • Normal QRS complex
  • No delta wave

Ebstein

ECG from a patient with Ebstein's anomaly showing huge P waves and low amplitude QRS waves. RBBB and T wave inversion are not present on this ECG.

In Ebstein anomaly the tricuspid valve is inserted more apically than normal. This yields a very large right atrium. About 50% of individuals with Ebstein's anomaly have evidence of Wolff-Parkinson-White syndrome, secondary to the atrialized right ventricular tissue.

Other abnormalities that can be seen on the ECG include

  1. signs of right atrial enlargement or tall and broad 'Himalayan' P waves,
  2. first degree atrioventricular block manifesting as a prolonged PR-interval
  3. low amplitude QRS complexes in the right precordial leads
  4. atypical right bundle branch block
  5. T wave inversion in V1-V4 and Q waves in V1-V4 and II, III and aVF.
  6. Q waves in II, III, AVF. These Q waves are thought to reflect fibrotic thinning of the right ventricular free wall and/or septal fibrosis with coexisting left posterior hemiblock[6]


Left and right bundle branch block

See: Conduction delay


Cocaine Intoxication

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Sarcoidosis

In patients with proven pulmonary sarcoidosis ECG changes can be used as a marker of cardiac involvement. Presence of a fractionated QRS or a Bundle Branch Block increases the likelihood of cardiac involvement.[7]


References

  1. Love JN, Howell JM, Litovitz TL, and Klein-Schwartz W. Acute beta blocker overdose: factors associated with the development of cardiovascular morbidity. J Toxicol Clin Toxicol. 2000;38(3):275-81. DOI:10.1081/clt-100100932 | PubMed ID:10866327 | HubMed [bb]
  2. Solomon A, Barish RA, Browne B, and Tso E. The electrocardiographic features of hypothermia. J Emerg Med. 1989 Mar-Apr;7(2):169-73. DOI:10.1016/0736-4679(89)90265-5 | PubMed ID:2738372 | HubMed [hypoth]

  3. Aschenbrenner R, Bodechtel G, Über Ekg.-Veränderungen bei Hirntumorkranken. Journal of Molecular Medicine, 17, 9, 2/1/1938, Pages 298-302, http://dx.doi.org/10.1007/BF01778563

    [Aschenbrenner]
  4. Ashrafian H. Sudden death in young athletes. N Engl J Med. 2003 Dec 18;349(25):2464-5; author reply 2464-5. DOI:10.1056/NEJM200312183492518 | PubMed ID:14681516 | HubMed [Maron]
  5. Sybrandy KC, Cramer MJ, and Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003 May;89(5):485-9. DOI:10.1136/heart.89.5.485 | PubMed ID:12695446 | HubMed [Sybrandy]
  6. Khairy P and Marelli AJ. Clinical use of electrocardiography in adults with congenital heart disease. Circulation. 2007 Dec 4;116(23):2734-46. DOI:10.1161/CIRCULATIONAHA.107.691568 | PubMed ID:18056539 | HubMed [khairy]
  7. Schuller JL, Olson MD, Zipse MM, Schneider PM, Aleong RG, Wienberger HD, Varosy PD, and Sauer WH. Electrocardiographic characteristics in patients with pulmonary sarcoidosis indicating cardiac involvement. J Cardiovasc Electrophysiol. 2011 Nov;22(11):1243-8. DOI:10.1111/j.1540-8167.2011.02099.x | PubMed ID:21615816 | HubMed [schuller]
  8. Rodger M, Makropoulos D, Turek M, Quevillon J, Raymond F, Rasuli P, and Wells PS. Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol. 2000 Oct 1;86(7):807-9, A10. DOI:10.1016/s0002-9149(00)01090-0 | PubMed ID:11018210 | HubMed [Rodger]
  9. Ferrari E, Imbert A, Chevalier T, Mihoubi A, Morand P, and Baudouy M. The ECG in pulmonary embolism. Predictive value of negative T waves in precordial leads--80 case reports. Chest. 1997 Mar;111(3):537-43. DOI:10.1378/chest.111.3.537 | PubMed ID:9118684 | HubMed [Ferrari]
All Medline abstracts: PubMed | HubMed
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