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An 84-year-old woman with hypertension and type 2 diabetes mellitus isbrought to the emergency department (ED) after an episode of nearsyncope.When emergency medical service personnel initially assessed her,blood pressure was 96/60 mm Hg and heart rate was “slow”; however, shehad no symptoms.
n 84-year-old woman with hypertension and type 2 diabetes mellitus isbrought to the emergency department (ED) after an episode of near syncope.When emergency medical service personnel initially assessed her,blood pressure was 96/60 mm Hg and heart rate was "slow"; however, shehad no symptoms.In the ED, the patient is awake and comfortable. She has no chestpain, nausea, or diaphoresis. Temperature is 37.2
F); heart rate,78 beats per minute; respiration rate, 24 breaths per minute; blood pressure,100/58 mm Hg; and oxygen saturation, 95% on room air. Slight jugularvenous distention is noted. Rales are audible at both lung bases, andheart rate is regular, without murmurs, gallops, or rubs. The abdomen andlower extremities are normal.The patient's initial ECG is shown here. The computer interprets thetracing as "normal sinus rhythm; low-voltage QRS; septal infarct, ageundetermined."
Which of the following conditions is best supported by theECG findings?
Acute myocardial infarction.
Pericardial effusion with possible tamponade.
THE COMPUTER ISN'T ALWAYS RIGHT
The diagnostic performance of9 computer programs for ECG interpretationwas analyzed, with mixedresults.
Although the median performanceof the programs across anumber of diagnoses was strong (91%correctly classified) and only slightlybelow that of the cardiologists whoserved as the gold standard (96% correctlyclassified), the computer interpretationswere notably unsatisfactoryin cases of MI, especially inferiorMI (median number of cases correctlyclassified, 59%).Another study looked at computerECG interpretation specificallyas it pertained to acute MI. The positivepredictive value of computerinterpretations of the ECG (94%) exceededthat of the physicians tested(86%); however, the negative predictivevalues of both were lower (computerinterpretations, 81%; physicians,85%).
This is a key point,given that the ECG is used primarilyas a screening tool and thus requireshigh sensitivity. ECGs arealso used for point-in-time exclusionof a diagnosis (eg, acute MI, especiallyin patients who need emergentpercutaneous coronary interventionor fibrinolysis)--another setting in which a high negative predictivevalue is desirable.Doubtless most clinicians wouldhave admitted this patient and proceededto "rule out" MI with serialECGs and measurements of cardiacserum markers. Thus, the diagnosisof acute MI would eventually havebeen made. However, the opportunityto reduce morbidity and mortalitythrough early revascularization, oreven aspirin and heparin therapy,might have been missed. Meanwhile,the diagnosis was available all alongon the ECG.It would be unwise to ignore acomputer printout that blares "acuteMI" across the top of the tracing(even though other diagnoses, suchas myopericarditis, ventricular hypertrophywith repolarization abnormality,benign early repolarization,and ventricular aneurysm, shouldalso be seriously considered whenthat computer diagnosis appears).However, it is also unwise to be reassuredby the absence of a computerdiagnosis of MI.
INTERPRETING THE LOW-VOLTAGE ECG
Diminished amplitude of thewaveforms on the ECG, or "lowvoltage," is generally defined as a QRS amplitude of less than 0.5 mV(5 mm) in all limb leads and lessthan 1.0 mV (10 mm) in all precordialleads. Low voltage is a nonspecificfinding: it is associated withvarious causes of fluid retention(myxedema, congestive heart failure,nephrotic syndrome, and anasarca),pericardial effusion, pleuraleffusion, pneumothorax, chronicobstructive pulmonary disease, obesity,and infiltrative cardiomyopathies.
In short, anything thatcomes between the ECG electrodeand the heart--distance, air, fat,fluid, etc--may diminish the amplitudeof the waveforms on the ECG.Thus, a finding of low voltageshould prompt a search to excludethe above-mentioned syndromes. Aprevious ECG is often invaluable inestablishing the newness of the process.Results of thyroid studies werenormal in this woman, which ruledout hypothyroidism (choice B). Nopericardial effusion (choice D) wasseen on an echocardiogram, and achest radiograph showed no evidenceof pneumothorax, pulmonaryedema, or pleural effusion. The findingof low voltage on her ECG waslikely caused by her body habitus.Low voltage also affects thedegree of ST-segment elevation/depression and Q-wave amplitude.Typically, ST-segment elevation isconsidered significant only whenit is greater than 1 mm in the limbleads. In a patient such as this woman,Q-wave duration/amplitudewould be considered significant onlyif it were 0.03 second or greater inlead II or lead aVF or 0.04 second orgreater in lead III (or if the Q-wavedepth were more than 25% of that ofthe corresponding R wave). However,when R-wave amplitude is low,ST-segment elevation is correspondinglylow. Thus, the degree of STsegmentelevation regarded as significantneeds to be modulatedwhen an ECG shows low voltage. Inaddition, wave width is now thoughtto be more important than depth inthe determination of whether Qwaves are pathologic.
Although myopericarditis(choice E) could produce the degreeof ST-segment elevation seenhere, this diagnosis is unlikely forseveral reasons:
CLINICAL DIAGNOSIS AND THE ECG
In a patient who has had anepisode of syncope or near-syncope,give early consideration to cardiaccauses of ischemia and dysrhythmia.(Although it is less likely, alsoconsider outflow obstruction, whichcould result from aortic stenosis,pericardial tamponade, or other conditions.)Consider as well other catastrophiccauses of syncope, suchas pulmonary embolism (choice A)and aortic dissection (which may bepainless, especially in the elderly).
Because of this woman's historyof transient low heart rate andlow blood pressure following hernear-syncopal episode, the diagnosisof acute MI--and in particular, acuteinferior MI--moved up in the listof differential diagnoses. Thus, theECG was examined with special attentionto rhythm disturbances (anydegree of atrioventricular heartblock, sinus or junctional bradycardias) and inferior ischemic changes.Reciprocal ST-segment depression(seen here in lead aVL [see
]) adds specificity to an ECGdiagnosis of acute ST-segment elevationMI. Lead aVL is the key lead toexamine for this finding when acuteinferior infarction is suspected; it liesroughly opposite (150 degrees inthe opposite direction) to lead III interms of the QRS frontal plane axisvector.
Finally, the fact that the ST-segmentelevation was greater in leadIII than in lead II was a clue to theanatomy of the lesion; such a findingindicates that the right coronaryartery is likely the culprit vessel.(ST-segment elevation in lead IIequal to that in lead III, on the otherhand, is a strong predictor of left circumflexcoronary artery occlusion.7An easy way to remember this is torecall that lead III is more rightwardin its vector than lead II, which ismore leftward.)Another reason to consider adiagnosis of MI early on (when warrantedby the clinical picture andECG) is that ECG findings are notonly subtle at times but also canbe transient. Note the changes--orlack thereof--in this patient's secondtracing, obtained just 20 minutesafter the first one
The STsegments are less elevated in the inferiorleads, and the ST-segment depressionin lead aVL is resolving.
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