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ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
ANSWER
The correct interpretation is sinus rhythm with a first-degree atrioventricular (AV) block, right superior axis deviation, and low voltage QRS complexes. The measured PR interval of 360 ms is correct!
The P waves are best seen in precordial leads V1 to V3. Notice that the P waves fall between the QRS complex and the T wave. The P wave is upright and not inverted, so it is not occurring retrograde from the preceding QRS complex. The sinus node depolarizes, and a long delay occurs within the atria and AV node before conducting down the normal conduction system in the ventricles. This conduction delay is so long that the preceding beat (QRS complex) is still repolarizing (T wave) by the time the sinus node depolarizes again. Thus, the P wave is responsible for the next QRS complex after duration of 360 ms.
A right superior axis deviation, also known as an extreme right axis deviation, is evidenced by an R-wave axis of 192°. Low-voltage QRS complexes are due to the patient’s body habitus. Morbid obesity significantly diminishes the electrical vectors measured by the surface ECG electrodes.
Finally, extra credit is due if you recognize the long QTc interval as well. The maximum normal QTc adjusted for a heart rate of 100 beats/min in men is 310 ms. This ECG barely meets that criteria; in this case, the prolonged QTc interval is of no significance.
A 64-year-old man who is morbidly obese is admitted to the medical service with a two-week history of increasing shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea. He states that he has depleted his finances for the month and has resorted to taking his medications every other day in order to make them last until next payday. He denies chest pain but notes that he has had a lot of “heaviness” in his anterior chest for the past week and now has a persistent, nonproductive cough. His medical history is remarkable for a cardiomyopathy due to alcohol abuse, frequent pneumonias, and renal insufficiency. He has a history of sleep apnea and uses continuous positive airway pressure (CPAP) at night in order to sleep. The patient is divorced, unemployed, lives alone in a subsidized apartment, and collects disability. Prior to filing for disability, he worked as a longshoreman. He is a former smoker who quit two years ago after several pulmonary infections. He attributes quitting smoking to his current weight problem. He states he has been an alcoholic for many years, and at one point consumed one bottle of whiskey per day along with one or two six-packs of beer. He has been to two alcohol rehab programs in the past five years and says he recently started drinking again when he learned his disability checks were not going to be increased. Family history is positive for coronary artery disease (mother) and diabetes (father). His parents and both of his siblings are being treated for hypertension. He has no known drug allergies. Current medications include aspirin, extended-release metoprolol, hydralazine, isosorbide mononitrate, torsemide, docusate, and senna. The review of systems is remarkable for chronic low back pain, corrective lenses, and multiple small venous ulcers on both legs that he states will “just not go away.” The physical exam reveals a morbidly obese male in mild distress. His weight is 494 lb and his height, is 70 in. His blood pressure is 120/82 mm Hg; pulse, 90 beats/min and regular; respiratory rate, 18 breaths/min; temperature, 96.8°F; and O2 saturation, 92% on room air. Pertinent physical findings include jugular venous distension to 12 cm, coarse rales in both lower lung fields, distant heart sounds without evidence of a murmur or rub, an obese abdomen without palpable organomegaly or ascites, and 3+ pitting edema in both lower extremities to the level of the knees. There are multiple old and new small, superficial venous ulcers on both lower legs. The skin is warm and pink; however, pulses are not palpable. Upon his admission, a cardiac catheterization is performed, which shows a right dominant system with angiographically normal coronary arteries, a left ventricular ejection fraction of 44%, and no evidence of valvular disease. Right heart pressures include a pulmonary artery pressure of 70/62 mm Hg with a mean of 51 mm Hg. The wedge pressure is 35 mm Hg, the transpulmonary gradient is 10, and the cardiac output is 12.5 L/min with a cardiac index of 4.4 L/min. These data are consistent with moderate-to-severe pulmonary hypertension with severely elevated left-sided filling pressures. A transthoracic echocardiogram is remarkable for elevated left ventricular end diastolic volumes with diffuse hypokinesis and an ejection fraction of 40%. The patient is also found to have a small pericardial effusion and bilateral pleural effusions. An ECG reveals the following: a ventricular rate of 98 beats/min; PR interval, 360 ms; QRS duration, 116 ms; QT/QTc interval, 24/314 ms; P axis, 54°; R axis, 192°; and T axis, 24°. As you review these measurements, you are skeptical of a PR interval of 360 ms and refer to the tracing. What is your interpretation of this ECG, and is the PR interval of 360 ms correct?
