55-yr-old female with dyspnea

Interpretation: SR with LAA and RVH Sinus rhythm at 70 bpm Vertical axis at 80-90 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)

60-yr-old male with chest pain

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

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

Hyperkalemia

65-yr-old male

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

Obtunded elderly female

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

Elderly male with dizziness and new renal failure

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

Patient with renal failure

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

Elderly female

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

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

Hypokalemia

38-yr-old female

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

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

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

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).

Hypercalcemia

49-year-old male with muscle weakness and constipation

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

35-yr-old male

Hypercalcemia Classic (!) ECG changes Ca++ 13.9 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)

71-yr-old male

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 8.4-10.2) Diagnosis was primary hyperparathyroidism

Hypocalcemia

Hypocalcemia Ca++ 8.2 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.

47-yr-old female with acute pancreatitis

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++ 7.2 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

Hyperthyroidism

Middle-aged woman with recent onset palpitations

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

Digoxin Toxicity

92-yr-old female with slow pulse

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

TCA Overdose

20-year-old woman is found unresponsive

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