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ECG Lecture Scott Ewing, D.O. March 23, 2006
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Question #1 The patient is an elderly man who presented to the emergency ward with dizziness and new renal failure
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Hyperkalemia Hyperkalemia (7.6 mEq/L) secondary to renal failure
Findings consistent with severe hyperkalemia Widening of the QRS complex Peaking of the T waves Prolongation of the PR interval and flattening of the P waves If left untreated, the ECG will progress to a sinusoidal pattern and eventually asystole with subsequent hemodynamic collapse and death
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Question #2 A 65-year-old man
What should you do before calling cardiology fellow for a "hyperacute myocardial infarction" here?
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Hyperkalemia Classic hyperkalemia with tall peaked T waves, along with PR prolongation and underlying left ventricular hypertrophy (LVH) (patient has renal disease with hypertension) Note QRS prolongation also seen with moderate-severe hyperkalemia Potassium here was 9.6mEq/L Not all tall positive T waves are "hyperacute“ The latter term should be reserved for increased T wave positivity secondary to transmural ischemia Major clues include narrowness (tenting) of T waves along with other findings noted above
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Question #3 This ECG is most consistent with which diagnosis?
Acute anterior myocardial infarction Accelerated idioventricular rhythm Marked hyperkalemia Marked hypercalcemia Systemic hypothermia
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Hyperkalemia The K+ was 10.5 mEq/L in a patient with renal failure
Note the wide QRS complexes with no evident P waves CK was normal and ST elevations were likely due to hyperkalemia. (Note: The apparent spike after the second QRS complex is an artifact.)
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Question #4 A 38-yr-old woman
What does the ECG show and what is the differential diagnosis?
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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 This pattern is of great importance because it identifies patients at high risk of torsade de pointes type of polymorphic ventricular tachycardia
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Question #5 30-yr-old man with diarrhea, not on medication
What waveform is prominent? What is the diagnosis?
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Hypokalemia There are very (!) prominent U waves with Q-T(U) prolongation He had severe hypokalemia (1.5 mEq/L) due to diarrhea Calcium was normal, as was magnesium (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 which he fortunately did not have before coming to hospital
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Hyperkalemia ECG changes have a sequential progression of effects, which roughly correlate with the potassium level ECG findings may be observed as follows: Early changes include peaked T waves, shortened QT interval, and ST segment depression Followed by bundle branch blocks causing a widening of the QRS complex, increases in the PR interval, and decreased amplitude of the P wave These changes reverse with appropriate treatment Without treatment, the P wave eventually disappears and the QRS morphology widens to resemble a sine wave. Ventricular fibrillation or asystole follows. ECG findings generally correlate with the potassium level, but potentially life-threatening arrhythmias can occur without warning at almost any level of hyperkalemia.
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Hypokalemia ECG 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).
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