ECG abnormalities in drugs, temperature, electrolyte , metabolic and temperature changes.

ecg changes

1. ECG abnormalities in drugs, electrolytes,metabolic, temperature and CNS disorders. Dr SUMEDH RAMTEKE

2. HYPOTHERMIA AND HYPERTHERMIA

3. Hypothermia is defined as a core body temperature of < 35 degrees centigrade Mild hypothermia is 32-35 degrees Moderate hypothermia is 29-32 degrees Severe hypothermia is < 29 degrees ECG Changes in Hypothermia Bradyarrhythmias (see below) Osborne Waves  (= J waves) Prolonged PR, QRS and QT intervals Shivering artefact Ventricular ectopics Cardiac arrest due to VT, VF or asystole Bradyarrhythmias Sinus bradycardia (may be marked) Atrial fibrillation with slow ventricular response Slow junctional rhythms Varying degrees of AV block (1st-3rd) Hypothermia overview

4. EX.1-Marked sinus bradycardia (30bpm) secondary to hypothermia

5. EX.2- Atrial fibrillation with slow ventricular response due to hypothermia

6. EX.3 -ECG with the classic features of hypothermia: bradycardia, Osborn waves and shivering artefact. The   Osborn wave (J wave)  is a positive deflection at the J point (negative in aVR and V1). It is usually most prominent in the precordial leads. The height of the Osborn wave is roughly proportional to the degree of hypothermia.

7. EX.4- Prolonged QTc (620ms) due to severe hypothermia

8. EX.5- Shivering Artefact Shivering artefact is seen as a “fuzziness” of the ECG baseline. It is not specific to hypothermia and may be seen with other conditions associated with tremor (e.g. Parkinson’s disease). Shivering artefact in a patient with hypothermia (note also the Osborn waves, bradycardia, prolonged QT)

9. The ECG findings in hyperthermia include: Sinus tachycardia Diffuse non specific  ST segment  changes Non specific ischemic changes Prolonged QT interval HYPERTHERMIA Hyperthermia is when core temperature exceeds that normally maintained by homeostatic mechanisms Fever  or pyrexia is an elevation of body temperature above the normal range of 36.5–37.5 °C (97.7–99.5 °F) due to an increase in the temperature regulatory set point Uncontrolled hyperthermia differs from fever in that the body temperature is elevated above the theromoregulatory set point due to excessive heat production and/or insufficient heat dissipation

10. CNS Disorders

11. ECG Abnormalities with Raised Intracranial Pressure Raised ICP is associated with certain characteristic ECG changes: Widespread giant  T-wave inversions  (“cerebral T waves”). QT prolongation . Bradycardia  (the Cushing reflex – indicates imminent brainstem herniation). Other possible ECG changes that may be seen: ST segment elevation / depression —  this may mimic myocardial ischaemia or pericarditis. Increased  U wave  amplitude. Other rhythm disturbances: sinus tachycardia, junctional rhythms, premature ventricular contractions, atrial fibrillation. In some cases, these ECG abnormalities may be associated with echocardiographic evidence of regional ventricular wall motion abnormality (so-called “neurogenic stunned myocardium”) Causes ECG changes due to raised ICP are most commonly seen with massive intracranial haemorrhage: Subarachnoid haemorrhage Intraparenchymal haemorrhage (haemorrhagic stroke) They may also be seen with: Massive ischaemic stroke causing cerebral oedema (e.g. MCA occlusion) Traumatic brain injury Cerebral metastases (rarely)  

12. Widespread, giant T-wave inversions (“cerebral T waves”) secondary to subarachnoid haemorrhage. The QT interval is also grossly prolonged (600 ms). Subarachnoid Haemorrhage

13. Subarachnoid Haemorrhage Widespread T-wave inversions with slight ST depression secondary to subarachnoid haemorrhage. The QT interval is prolonged (greater than half the R-R interval). This ECG pattern could easily be mistaken for myocardial ischaemia as the T-wave morphology is very similar, although obviously the clinical picture would be very different (coma versus chest pain).

14. Traumatic Brain Injury This ECG was taken from a previously healthy 18-year old girl with severe traumatic brain injury and massively raised intracranial pressure (30-40 mmHg). There is widespread ST elevation with a pericarditis-like morphology and no reciprocal change (except in aVR and V1). She had no cardiac injury / abnormality to explain the ST elevation. The ST segments normalised as the intracranial pressure came under control (following treatment with thiopentone and hypertonic saline).

15. METABOLIC DISORDERS

16. The most common ECG changes seen with thyrotoxicosis are: Sinus tachycardia Atrial fibrillation  with rapid ventricular response High left-ventricular voltage Supraventricular arrhythmias  (premature atrial beats, paroxysmal supraventricular tachycardia,  multifocal atrial tachycardia ,  atrial flutter ) Non-specific ST and T wave changes Ventricular extrasystoles

17. Myxoedema coma This is the admission ECG of a 79-year old man who was referred to ICU with coma, hypothermia, severe bradycardia and hypotension refractory to inotropes. TSH was markedly elevated with an undetectable T4. The ECG shows marked bradycardia (30 bpm) with low QRS voltages (esp. in the limb leads) and widespread T-wave inversions, typical of severe myxoedema.

18. DRUG ABNORMALITY AND ECG

19. Sodium Channel Blocking Medications Tricyclic antidepressants (= most common) Type Ia antiarrhythmics (quinidine, procainamide) Type Ic antiarrhythmics (flecainide, encainide) Local anaesthetics (bupivacaine, ropivacaine) Antimalarials (chloroquine, hydroxychloroquine) Dextropropoxyphene Propranolol Carbamazepine Quinine ECG Features of Sodium-Channel Blockade Features consistent with sodium-channel blockade: Interventricular conduction delay  — QRS > 100 ms in lead II Right axis deviation  of the terminal QRS: Terminal R wave  > 3 mm in aVR R/S ratio > 0.7 in aVR Patients with tricyclic overdose will also usually demonstrate  sinus tachycardia secondary to muscarinic (M1) receptor blockade.

20. Typical ECG of TCA toxicity demonstrating: Sinus tachycardia with first-degree AV block (P waves hidden in the T waves, best seen in V1-2). Broad QRS complexes. Positive R’ wave in aVR.

21. There is subtle ECG evidence of fast sodium channel blockade: Note the QRS widening (135 ms), 1st degree heart block (PR 240ms) and small  secondary R wave  in aVR. Carbamazepine Cardiotoxicity

22. Quetiapine Toxicity Brisk  sinus tachycardia  (HR = 120 bpm ) Prolonged QTc interval  (QTc = 560ms; the absolute QT interval is more than half the R-R interval)

23. DIGOXIN The classic digoxin toxic dysrhythmia combines: supraventricular tachycardia  (due to increased automaticity) slow ventricular response  (due to decreased AV conduction)   Other common dysrhythmias associated with digoxin toxicity include: Frequent PVCs  (the most common abnormality), including ventricular bigeminy and trigeminy Sinus bradycardia Slow  Atrial Fibrillation Any type of AV block ( 1st degree ,  2nd degree  &  3rd degree ) Regularised AF  = AF with complete heart block and a junctional or ventricular escape rhythm Ventricular tachycardia , including polymorphic and bidirectional VT  

24. Bigeminy Atrial tachycardia with high-grade AV block and PVCs Coarse atrial fibrillation with 3rd degree AV block and a junctional escape rhythm DIGOXIN TOXICITY

25. “Paroxysmal” atrial tachycardia with block and frequent PVCs Atrial flutter with a slow ventricular rate due to digoxin toxicity. DIGOXIN TOXICITY

26. Sinus bradycardia with 1st-degree AV block: Slow junctional rhythm BETA BLOCKER TOXICITY

27. Complete heart block sotalol overdose: Sinus bradycardia. Very long QT interval (~600ms). BETA BLOCKER TOXICITY

28. Electrolyte imbalance and ECG

29. Hypercalcaemia EX.1 - Osborn waves  in severe hypercalcaemia (4.1 mmol/L) EX.2-Hypercalcaemia causing marked shortening of the QT interval (260ms).

30. HYPOCALCAEMIA Hypocalcaemia causes  QTc prolongation  primarily by prolonging the ST segment. The T wave is typically left unchanged. Dysrhythmias are uncommon, although atrial fibrillation has been reported. Torsades de pointes  may occur

31. Serum potassium > 5.5 mEq/L   - repolarization abnormalities: Peaked T waves (usually the earliest sign of hyperkalaemia) Serum potassium > 6.5 mEq/L   - progressive paralysis of the atria: P wave widens and flattens PR segment lengthens P waves eventually disappear Serum potassium > 7.0 mEq/L   - conduction abnormalities andbradycardia: 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 Hyperkalaemia Overview

32. EX.1 - Prolonged PR interval. Broad, bizarre QRS complexes. Peaked T waves. EX.2 -Long PR segment. Wide, bizarre QRS . HYPERKALAEMIA

33. HYPERKALAEMIA EX.3 -Slow junctional rhythm. Intraventricular conduction delay. Peaked T waves. EX4-Broad complex rhythm with atypical LBBB morphology. Left axis deviation. Absent P waves.

34. 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 Hypokalaemia Overview

35. EX.2 -Hypokalaemia causing  Torsades de Pointes Note the atrial ectopic causing ‘R on T’ (or is it ‘R on U’?) that initiates the paroxysm of TdP EX.1 -ST depression. T wave inversion. Prominent U waves. Long QU interval. HYPOKALAEMIA

36. Hypomagnesaemia Overview Normal serum magnesium = 0.8 – 1.0 mmol/L. Hypomagnesaemia = <0.8 mmol/L ECG changes in Hypomagnesaemia   prolonged QTc . Atrial and ventricular ectopy, atrial tachyarrhythmias and  torsades de pointes  

37. Hypomagnesaemia EX.1- Hypomagnesaemia causing long QTc (510ms)

38. Hypermagnesaemia ECG (as for hyperkalaemia)Increase PR and QTc Prolonged QRS Peaked T waves and flattened p waves Complete AV block and asystole