1. 55-yr-old female with dyspnea

2. Interpretation: SR with LAA and RVH
Sinus rhythm at 70 bpm
Vertical axis at degrees
Left atrial abnormality
Biphasic P in V1 with broad negative component
Broad P waves elsewhere
Right ventricular hypertrophy
Tall R in V1
R/S ratio in V1 > 1
Rightward axis
Combination of LAA with RVH in dyspneic patient consistent with severe mitral stenosis (likely secondary to rheumatic heart disease)

3. 60-yr-old male with chest pain

4. Interpretation: SR with LBBB and AMI
Sinus rhythm at 70 bpm
Left axis deviation at -40 degrees
LBBB
Prior and possibly evolving myocardial infarction superimposed on LBBB
Prior MI is indicated by Q waves as part of a qR in I and V6
Notching of the ascending limb of the S wave in the mid-left chest leads is also consistent with prior MI (Cabrera's sign)
Biphasic T waves in the mid-left chest leads raise consideration of evolving ischemia/MI
Anterior ST elevations non-diagnostic

5. ECG 101 – ECG Changes in Non-Cardiac Conditions
Scott E. Ewing DO

6. Hyperkalemia

7. 65-yr-old male

8. Hyperkalemia Classic hyperkalemia Potassium here was 9.6mEq/L
Tall peaked / narrow T waves, i.e. “tenting”
PR prolongation
Also, underlying LVH (patient has renal disease with hypertension)
Potassium here was 9.6mEq/L
Not all tall positive T waves are “hyperacute”, term reserved for increased T wave positivity secondary to transmural ischemia
Note: QRS prolongation also seen with moderate-severe hyperkalemia

9. Obtunded elderly female

10. Hyperkalemia
Hyperkalemia (K+ 8.7 mEq/L) secondary to acute renal failure
Symmetric peaked ("tented") T waves associated with potassium levels in excess of 6 mEq/L
Broad and flattened P waves that precede frank sino-ventricular conduction seen with severe hyperkalemia (i.e. conduction from the sinus node to the ventricles through specialized inter-nodal tissue without atrial depolarization)
This conduction pattern may simulate a junctional rhythm
The narrow QRS complex in this tracing is somewhat atypical for severe hyperkalemia

11. Elderly male with dizziness and new renal failure

12. Hyperkalemia Hyperkalemia (7.6 mEq/L) secondary to renal failure
Findings consistent with severe hyperkalemia
QRS widening
Peaked T waves
PR interval prolongation
P wave flattening
LBBB? Not likely with extreme QRS prolongation and other findings
If untreated, will progress to a sinusoidal pattern and eventually asystole

13. Patient with renal failure

14. Hyperkalemia K+ 10.5 mEq/L Wide QRS with no evident P waves
ST elevations were likely due to hyperkalemia (cardiac enzymes were normal)

15. Elderly female

16. Hyperkalemia Extremely wide complex rhythm (QRS 0.28 sec) at 70 bpm
Pattern approaching “sine-wave” morphology indicative of severe hyperkalemia
Atrial activity is not apparent
Serum potassium level ½ hr before 6.8 mEq/L (and likely higher at the time of this ECG)
End-stage renal disease BUN 78 mg/dL and serum creatinine 5.2 mg/dL
Emergency therapy of hyperkalemia is required based on this ECG finding

17. Hyperkalemia - Summary
ECG changes roughly correlate with K+ level
Early changes include peaked T waves, shortened QT interval, and ST changes
Followed by widening of the QRS, increases in PR interval, decreased P wave amplitude
Without treatment, P wave eventually disappears and QRS widens to resemble a sine wave, ventricular fibrillation or asystole follows
Life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia

18. Hypokalemia

19. 38-yr-old female

20. Hypokalemia
Sinus bradycardia with diffuse T wave flattening or inversions and markedly prominent U waves
Best seen in leads V2 and V3
Most common causes
Hypokalemia (K+ here was 2.4 mEq/L)
Drugs such as quinidine, phenothiazines, tricyclics
Patients with hereditary long QT syndromes may show a similar finding
Pattern is of great importance because it identifies patients at high risk of torsade de pointes

21. 30-yr-old man with diarrhea, not on medication

22. Hypokalemia Very (!) prominent U waves with Q-T(U) prolongation
Severe hypokalemia (1.5 mEq/L) due to diarrhea
Calcium was normal (remember pure hypocalemia prolongs ST segment primarily but doesn't give large U waves)
Obviously, this acquired-type long-QT(U) syndrome puts subject at risk for torsade de pointes

23. Hypokalemia - Summary EKG findings may be observed as follows
Flattening of the T wave, which is the earliest change
A "U wave" then develops, associated with ST-T wave flattening and sometimes slight ST depression
ST depression is more  noticeable and the U wave increases in amplitude until ultimately the U wave overtakes the T wave.
At this point distinguishing between the T wave and U wave may be almost impossible ("Q-U" prolongation).

24. Hypercalcemia

25. 49-year-old male with muscle weakness and constipation

26. Hypercalcemia Hypercalcemia
Very short ST segment with a consequently short QT interval
Prominent U waves (esp. in V3)
QTc inversely proportional to the calcium level up to 16 mg/dl
At higher levels, the T wave begins to prolong, essentially making the QT interval normalize, though the ST segment remains short
In addition, prominent U waves are often seen
Chief causes of short QT are hypercalcemia and digoxin therapy (associated with characteristic "scooping" of the ST-T complex)
May cause AV block, sinus arrest, SA block, V Tach. Cardiac arrest reported, usually with rapid IV injections of calcium
This patient's serum calcium was 16 mg/dl secondary to hyperparathyroidism

27. 35-yr-old male

28. Hypercalcemia Classic (!) ECG changes
Ca mg/dl
Very abbreviated ST segment such that the T wave looks like it takes off directly from QRS in some leads
High take-off of ST segment in V2/V3 is also sometimes seen in this context
Hypocalcemia is just the opposite:
Prolonged QT due to long ST segment (corresponding to changes in action potential plateau phase duration)

29. 71-yr-old male

30. Hypercalcemia
Sinus rhythm at 70 bpm (with short sinus pause at the beginning)
Shortened Q-T interval (about 280 msec) and markedly abbreviated ST segment consistent with hypercalcemia
Subtle “doming” of the ST-T complex in leads V1-V3 with slight J point/ST elevations in the right chest leads is also sometimes seen in this setting
Serum calcium very elevated at 14.8 mg/dL (normal range )
Diagnosis was primary hyperparathyroidism

31. Hypocalcemia

33. Hypocalcemia
Ca mg/dl with minimally low albumin in patient post thyroidectomy
QT prolongation because ST segment is stretched out
Secondary to prolongation of the plateau phase of action potential
Ventricular repolarization can also be long because of 1) wide QRS; 2) flat, wide T waves (e.g. quinidine, sotalol, hypokalemia, etc); and/or 3) prominent U waves melding with T wave
The latter two syndromes, representing dispersion of ventricular refractoriness, are most likely to be associated with torsade de pointes.

34. 47-yr-old female with acute pancreatitis

35. Hypocalcemia Acute pancreatitis
Sinus tachycardia
Long QT/QTc (.34 sec/.46)
Low limb lead and lateral QRS voltages
Non-diagnostic slow R wave progression V1-V3
Non-specific ST-T changes
Long QT (ST segment component is stretched out) is due to hypocalcemia (Ca mg/dL with serum albumin of 2.7 g/dL)
Sinus tachycardia is due to neuroautonomic activation in this context and the low voltage is consistent with ascites/anasarca

36. Hyperthyroidism

37. Middle-aged woman with recent onset palpitations

38. Hyperthyroidism Atrial fibrillation with RVR
Left ventricular hypertrophy
Patient was markedly hyperthyroid
5-15% of patients (esp. elderly) with hyperthyroidism will develop atrial fibrillation
Conversely, 5% of patients with recent onset atrial fibrillation (or fluuter) will have hypothyroidism

39. Digoxin Toxicity

40. 92-yr-old female with slow pulse

41. Digoxin Toxicity
Atrial fibrillation with a slow (average rate around 38 bpm) ventricular response
ST-T complexes (“scooping” of the ventricular repolarization waveform) are consistent digoxin effect (not necessarily toxicity)
In concert with the rhythm findings, digitalis excess is strongly suggested
The patient’s digoxin level was in fact in the toxic range at 2.2 nanograms/ml
The ECG also shows left ventricular hypertrophy (LVH) due underlying aortic stenosis
The ST-T abnormalities may in part be due to the LVH or to ischemia
Digitalis toxicity in the presence of atrial fibrillation may cause excessive slowing and/or regularization (due to AV junctional mechanisms)
Digitalis glycoside toxicity causes a variety of bradyarrhythmias by augmenting cardiac vagal tone at the AV node (as in the case here) or SA node
Cardiac glycoside poisoning can also occur from ingestion of various plants (e.g., foxglove) and animal toxins (e.g., venomous bites from the cane toad (Bufo marinus)
Severe digitalis intoxication can also lead to marked hyperkalemia via Na+/K+ pump inhibition
Serum potassium in this case was normal

42. TCA Overdose

43. 20-year-old woman is found unresponsive

44. TCA Overdose Key findings of TCA overdose
Obtunded
Sinus tachycardia
Wide QRS / intraventricular conduction delay
Long QT
IVCD in these cases is often associated with a terminal S wave (rS) in lead I, and a terminal R wave (qR) in aVR
P waves are difficult to see (V1, for example) and in some leads (II, aVF) appear to merge with the end of the T wave