Search

A 62-year-old white patient presents with markedly ischemic electrocardiogram, notable for Tombstone sign.

A 64-year-old man with known coronary disease presented to the hospital with sinus bradycardia, chest pain, and normal cardiac enzymes. During an exercise stress test he developed ventricular fibrillation that spontaneously resolved.

A 27-year-old man presents with successfully resuscitated ventricular fibrillation. Structural and electrical causes of ventricular fibrillation in the young are presented along with a diagnostic strategy. Electrocardiographic features of malignant early repolarization are discussed.

In a 75-year-old woman with left-sided chest pain and an abnormal electrocardiogram the etiology is not cardiac.

A 58-year-old man with his first episode of chest pain had an acute anterior myocardial infarct. After balloon angioplasty and stenting of a completely occluded left anterior descending coronary artery, the anterolateral ST-T changes had largely resolved.

A 66-year-old man presented with a moderate-sized ventricular septal defect and severe pulmonary hypertension that was responsive to vasodilator therapy. His electrocardiogram demonstrated biatrial enlargement and biventricular hypertrophy. Presentation at this age is unusual for this type of shunt.

Several findings on an exercise electrocardiogram predicted left main and/or 3-vessel coronary arterial disease, which was confirmed by coronary arteriography, and the 56-year-old man underwent a multivessel coronary arterial bypass operation the following day.

In a man with a wide-QRS complex tachycardia, a history of an inferior left ventricular scar, atrioventricular dissociation during the tachycardia, and a QRS morphology inconsistent with right or left bundle branch block exclude a diagnosis of supraventricular tachycardia with aberrant ventricular conduction due to bundle branch block or ventricular preexcitation and establish a diagnosis of ventricular tachycardia.

A 37-year-old man came to the emergency department because of several days of intermittent chest pain. An electrocardiogram (ECG) showed sinus rhythm, left atrial and left ventricular enlargement, and an early repolarization pattern. A second ECG recorded 10 minutes later was strikingly different, with ST-segment elevation and large upright T waves in the anterior precordial leads, interpreted as evidence of an ST-segment elevation myocardial infarction, and the cardiac catheterization team was activated. Closer inspection of the ECG, however, disclosed that the changes were because of intermittent ventricular pre-excitation of the Wolff-Parkinson-White type, and no electrocardiographic, echocardiographic, or serum markers of myocardial infarction were found.

A 57-year-old man with diabetes mellitus, systemic arterial hypertension, and end-stage kidney disease came to the hospital because his arteriovenous fistula used for hemodialysis had clotted. His blood hemoglobin level was 12.8 g/dL (reference, 13.5-17.5); and serum chemistry levels were creatinine 6.7 mg/dL (0.7-1.3), sodium 132 mEq/L (136-146), potassium 4.0 mEq/L (3.5-5.1), chloride 94 mEq/L (98-106), carbon dioxide 24 mEQ/L (23-29), calcium 9.1 mg/dL (8.4-10.2), and phosphorus 9.1 mg/dL (2.7-4.5). An electrocardiogram was recorded (Figure 1).

A 27-year-old man was admitted to the coronary care unit because of chest pain and an electrocardiogram (ECG) read by the computer as an inferior infarct and left ventricular hypertrophy (Figure).

Most patients with double-chambered right ventricles are diagnosed in childhood, but some escape definitive diagnosis until adulthood, as was the case in the patient described here.

A family brought their 61-year-old mother to the emergency department because for 4 days she had been confused, incoherent, and somnolent. She also had dysphagia, dysarthria, diplopia, and had fallen out of bed. She had been in the hospital 3 weeks earlier for atrial fibrillation and an exacerbation of congestive heart failure. She also carried a diagnosis of chronic obstructive pulmonary disease and used an albuterol inhaler. She was obese (BMI of 45); and had adult-onset diabetes mellitus. She had a 43 pack-year history of cigarette smoking but had recently quit. Soon after arriving in the emergency department, she had an ECG (Figure);.

Police found a confused 93-year-old woman wandering the streets and brought her to the hospital where an electrocardiogram (ECG) was recorded.

A 61-year-old man came from out of state to attend a football game. He felt well during the game, but when he stood up to leave, he became dizzy and dyspneic. The symptoms lasted 15 to 20 minutes, and when the paramedics arrived, they diagnosed an idioventricular rhythm and brought the patient to the emergency department where a 12-lead electrocardiogram (ECG) was recorded (Figure 1).

In a woman with chest pain

A 49-year-old man visiting New Orleans from Chile comes to the hospital complaining of exertional dyspnea for 2 months with the more recent onset of ankle edema. He is a slender man with a blood pressure of 91/60 mmHg, crackles at both lung bases, and markedly distended neck veins. His cardiac rhythm is irregular. A soft murmur of mitral regurgitation and a soft S-3 are heard at the left ventricular apex. All four pedal pulses are easily palpable. Epigastric tenderness is noted on palpation; although the patient has a history of peptic ulcer disease, the tenderness is probably due to an enlarged left lobe of his liver, the result of hepatic congestion from his heart failure. A chest radiograph shows generalized cardiomegaly with an especially large left ventricle. Pulmonary congestion and small bilateral pleural effusions also are noted. The Figure shows the electrocardiogram recorded on admission.

A 31-year-old man had an hour of pain across the upper portion of his chest anteriorly, and it radiated down the inner aspects of both arms. The pain came while he was walking and gradually disappeared as he sat quietly. Six Rolaid tablets did not seem to alter the pain. The pain was unaccompanied by dyspnea, sweating, nausea or vomiting. The night before the patient had had similar pain relieved by Rolaids and belching. After the second episode of pain, he went to the emergency department of a local hospital where an ECG was recorded.

Severe hypokalemia in the absence of other electrolyte abnormalities, the result of diarrhea, caused striking electrocardiographic changes, generalized weakness, flaccid paralysis of the lower extremities, and biochemical evidence of mild skeletal and cardiac rhabdomyolysis in a 33-year-old man. Repletion of potassium reversed all abnormalities in 24 hours.

A furuncle on the leg of a 23-year-old woman led to methicillin-resistant staphylococcus aureus sepsis and adult respiratory distress syndrome (ARDS) requiring tracheal intubation in the intensive care unit (ICU). Initially her electrocardiograms (ECGs) showed sinus tachycardia, but otherwise were unchanged from prior ECGs. A week into her ICU stay a different rhythm occurred.

Apparently depression ran in this man's family, and when he took an overdose of his tricyclic antidepressant, he also took the tricyclics of his mother and his sister. Most patients who die of an overdose of a tricyclic antidepressant are pronounced dead without reaching a hospital, and those who die after arriving in the emergency room do so within a few hours.2 Central nervous system toxicity of tricyclic antidepressants may manifest as confusion, agitation, hallucinations, coma, myoclonus, or seizures. Generalized seizures often presage cardiopulmonary arrest,2 and within 20 seconds of the ECG with evidence of generalized seizure activity shown here, the QRS duration increased from 188 ms to 212 ms, and the patient died soon thereafter.

An obese 49-year-old man with a history of systemic arterial hypertension, diabetes mellitus, dyslipidemia, three myocardial infarcts, an ischemic cardiomyopathy, a four-vessel coronary artery bypass operation 7 years earlier, and implantation of a cardioverter-defibrillator 2 years earlier comes to the hospital with palpitations and dyspnea. An ECG is recorded.

Sinus rhythm; an atrial premature complex; sagging ST-segments, low T-waves, and prominent U-waves suggesting hypokalemia. The ST-T and U-wave changes described above are characteristic of hypokalemia. When the serum potassium level is between 3.0 and 3.5 mEq/L, one or more of the findings may be present. All three are common when the serum potassium level is below 2.5 mEq/L. At the lowest serum potassium levels the T-wave becomes a notch on the upstroke of a giant U-wave, as occurs here in the ECG of this woman with a serum potassium of 1.7 mEq/L.1,2 This configuration is occasionally mistaken for the ST-segment depression and long QT interval of myocardial ischemia.3 Atrial premature complexes are common with hypokalemia, and atrial fibrillation may occur. This patient's potassium was repleted, and the following day her ECG was essentially normal (Figure 2) and virtually unchanged from an ECG recorded two years earlier.

There is a sinus P wave in front of each QRS, and the rate is 122 beats/min. The QRS voltage is large and meets many criteria for left ventricular hypertrophy: RI13 mm (1.3 mV); RaVF19 mm; SaVR14 mm; SV124 mm; SV230 mm; RV626 mm; RV6RV5; SV1 + RV5 or RV635 mm; SV2 + RV5 or RV645 mm; RaVL + SV320 mm in a woman.1 In addition, there are two non-voltage criteria for LVH: QRS duration = 0.11 s and typical repolarization changes: J-point depression with a downsloping ST segment into an inverted T wave and a more rapid upslope back to the baseline. The prolonged QRS duration and repolarization changes are also typical of incomplete left bundle branch block (ILBBB). LVH is present in most patients with complete LBBB,2,3 and probably in most with ILBBB. The patient underwent aortic valvotomy at age 5 to relieve congenital stenosis. Although different valvular morphologies can result in aortic stenosis, when hemodynamically significant stenosis is present in infancy or early childhood the valve is usually unicuspid/unicommissural. Aortic valvotomy can greatly reduce the left ventricular outflow obstruction in such patients, but the majority eventually need reoperation. This usually means aortic valve replacement. This woman now has severe aortic stenosis and regurgitation with not only left but also right ventricular failure, which is a late development with pure aortic valve disease. She needs aortic valve replacement. Unfortunately having one severe disease does not preclude another, and her operative course will be complicated by multiple sclerosis which she developed some 12 years ago.

Multifocal atrial tachycardia; right bundle branch block. The rhythm is totally irregular at a rate of 103 beats/min and originally was read as atrial fibrillation. Close examination, however, reveals a P wave before each QRS and ≥ 3 different P- wave morphologies with no dominant morphology. These are the criteria for multifocal atrial tachycardia MAT, also known as chaotic atrial rhythm,1 chaotic atrial tachycardia,2 and chaotic atrial mechanism.3 The wide QRS complexes ≥ 0.12 s with broad S waves in leads I, aVL, and the lateral precordial leads and broad R or R´ waves in leads aVR and V1 indicate right bundle branch block. MAT is frequently seen in patients with acute pulmonary or other non-cardiac disease and tends to resolve when the underlying disease is brought under control. Patients with MAT also tend to have bouts of other arrhythmias,2 and 3 months earlier this.

Physical examination, electrocardiograms, and an echo-Doppler study document multiple consequences of a right coronary arterial occlusion.

Sinus bradycardia (48 beats/min), long P-R interval (0.29 s), long QT interval (0.53 s with QTc of 0.47 s), and prominent J waves suggest hypothermia; non-specific ST abnormality.

A 50-year-old man with a murmur since birth developed systemic arterial hypertension as an adult. He came to the hospital because of dyspnea. He had a pulmonic valve ejection click and a murmur of pulmonic stenosis. His echocardiogram showed biventricular hypertrophy, a flat ventricular septum, a D-shaped left ventricle, systolic doming of the pulmonic valve, and Doppler evidence of a 70 mm Hg peak systolic pressure gradient across the pulmonic valve and a peak right ventricular systolic pressure of 100 mm Hg. His electrocardiograms showed no evidence of the right ventricular and right atrial enlargement so evident on echocardiogram, presumably because it was obscured by the marked changes of left ventricular hypertrophy. Three years later, when he was admitted for sepsis and worsening heart failure with anasarca, the voltage changes of left ventricular hypertrophy had virtually disappeared, likely due to the large amount of fluid between the heart and the electrodes.

A 55-year-old man with syncopal episodes was found to have sinus bradycardia at a rate of 37 beats/min, an episode of nonsustained ventricular tachycardia, and left ventricular noncompaction cardiomyopathy. After placement of a dual-chamber cardioverter defibrillator 4 years ago, he has had no further syncopal episodes, and there have been no defibrillator shocks.

An 18-year-old man came to the hospital because of 1 day of chest pain typical of pericarditis. He had had an upper respiratory infection 10 days earlier. His electrocardiograms indicated evolving pericarditis. His echocardiogram showed mild, diffuse left ventricular hypokinesia, and his troponin I level peaked at 47.5 ng/ml. Thus, he had myopericarditis.

A woman with systemic lupus erythematosus and a regular supraventricular tachycardia continues to have electrocardiographic abnormalities after the spontaneous return of normal sinus rhythm.

A 20-year-old Hispanic woman presented to the emergency department complaining of six months of progressive dyspnea on exertion associated with intermittent palpitations. Her only past medical history was a stillbirth at 32 weeks gestation about two years ago. Her vital signs in the emergency department were a heart rate of 120 beats/minute, a blood pressure of 145/86 mmHg, and an arterial oxygen saturation of 98 percent with her breathing air. Significant laboratory values included a blood hemoglobin of 14.5 gm/dL, a hematocrit of 49 percent, a brain naturetic peptide (BNP) level of 177 pg/mL, a D-dimer level of 330 ng/ml, a prothrombin time of 12.85 s with an INR of 1.2, and a partial thromboplastin time of 45.7s. Urine pregnancy test was positive, and serum beta-human chorionic gonadotropin level was 81 MIU/mL consistent with a fetus of 3-4 weeks gestational age. An electrocardiogram was recorded.

In patients with acute chest pain and left bundle branch block, repolarization changes often are helpful in confirming acute myocardial infarction. 1e6 Diagnosing old myocardial infarction in the presence of left bundle branch block is a tougher assignment. In this regard, the presence of Q waves in leads usually devoid of them in patients with left bundle branch block has received considerable attention. For example, in the presence of left bundle branch block, pathologic Q waves in the left lateral leads (I, aVL, V5, and V6) or a Q in lead V6 with a prominent R wave in lead V1 are insensitive but specific markers of an infarct, not in the lateral portion of the left ventricle but in its ante

The clinical and electrocardiographic features of anomalous left coronary artery from the pulmonary trunk, ALCAPA, a frequently fatal congenital cardiac malformation, are described in an 8 1/2-month-old female.

The most striking feature of this electrocardiogram (ECG) is a markedly wide QRS complex with an S wave that merges with a peaked T wave without an isoelectric ST segment (Figure 1). This is best seen in leads I and V4 to V6. No definite P waves are seen, although a long PR interval and fusion of Ps with the preceding T waves cannot be excluded in leads II and V2. This is the ECG of severe hyperkalemia; it belongs to a 35-year-old man with renal failure and a serum potassium level of 8.7 mEq/L. As the serum potassium level rises above the upper limit of normal (5.0 mEq/L), the first electrocardiographic change noted usually is a peaked symmetrical T wave with a narrow base. With ever higher levels of serum potassium, conduction slows resulting in a wide, low Pwave, a long PR interval, and a wide QRS complex with slurring of the S wave into a rapidly ascending limb of the T wave. Eventually P waves disappear, and the QRS comes to resemble a sine wave. Death may result from asystole or ventricular fibrillation. Although the ECG of hyperkalemia may resemble right or left bundle branch block or myocardial infarction, it is usually the absence of typical features of those conditions in someone with the electrocardiographic features described previously and a reason for hyperkalemia that alert the physician to the correct diagnosis. The commonest cause of hyperkalemia is renal failure, and the patient’s ECGmay also reflect hypocalcemia or left ventricular hypertrophy before the ECG is severely distorted as in this case.

Glenn P. Kelley, M.D.,∗ Ghassan A. Dalati, M.D.,∗ Frederick R. Helmcke, M.D.,∗ Neeraj Jain, M.D.,∗ Mohammed Al-Bataineh, M.D.,∗ D. Luke Glancy, M.D.,∗ and Edmund Kenneth Kerut, M.D.∗,†,‡ ∗Section of Cardiology, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans, Louisiana †Heart Clinic of Louisiana, Marrero, Louisiana ‡Departments of Physiology and Pharmacology, Louisiana State University Health Sciences Center, New Orleans, Louisiana

Wolff-Parkinson-White-type ventricular preexcitation was recognized for the first time in a 67-year-old man four days after aortic valve replacement. The preexcitation was intermittent.

A muscular-appearing 50-year-old man was found down in his home by family members. Paramedics documented pulseless electrical activity and began cardiopulmonary resuscitation that included placement of an endotracheal tube. The resuscitation was continued in the hospital emergency department (ED), and after 20 minutes, an arterial pulse returned. An electrocardiogram (ECG) was obtained (Figure 1). Meanwhile, a past history established that the patient was a personal trainer who seemed fit and healthy until 10 days earlier, when he came to the ED because he had begun to lose his balance and fall frequently. Computed tomography (CT) at that time revealed lytic lesions in the fifth lumbar vertebra and extensive retroperitoneal lymphadenopathy involving the aortic, iliac, and obturator chains and the perirectal region. Arrangements had then been made for outpatient workup of a presumed malignancy.

A 90-year-old man with a history of high blood pressure, a cerebrovascular accident without focal residua, dementia, and stage 3 chronic kidney disease went to the emergency department because of dizziness and near syncope. His medications were aspirin 81 mg qd, clopidogrel 75 mg qod, escitalopram oxalate 10 mg qd, quetiapine fumarate 25 mg qd, and memantine hydrochloride 10 mg qd. He had orthrostatic hypotension with supine blood pressure of 173/77 mmHg falling to 116/68 on standing, while pulse increased from 66 to 84 beats/min. He received IV fluid and returned home. Two days later, he saw his primary care physician because of episodes of dizziness and confusion. The Figure shows an electrocardiogram recorded during that visit.

Hypoxia and hypoxia/reoxygenation are known to affect vascular smooth muscle cell physiology. In this study, we first investigated proteoglycan synthesis by human aortic smooth muscle cells exposed to normoxia, hypoxia, or hypoxia/reoxygenation. We then compared the newly synthesized proteoglycans from normoxic and hypoxic-reoxygenation cultures for their ability to bind low density lipoprotein (LDL). Confluent smooth muscle cells under normoxia, hypoxia, or hypoxia/reoxygenation were pulsed with [35S]sulfate, and secreted and cell-associated proteoglycans were analyzed. Secreted proteoglycans in cultures exposed to hypoxia (4 h)/reoxygenation (19 h) increased 28% over those of cells continuously exposed to normoxia. Cell-associated proteoglycans did not differ significantly between the two groups. In contrast, hypoxia (4 h) followed by a 30-min reoxygenation produced a 37% decrease in newly synthesized proteoglycans. Hypoxia alone also resulted in a 24% decrease in secreted proteoglycans and a 20% decrease in cell-associated proteoglycans. Proteoglycans newly synthesized by smooth muscle cells exposed to normoxia and hypoxia/reoxygenation did not differ in their charge densities and molecular size but did differ in glycosaminoglycan composition. Exposure of smooth muscle cells to hypoxia/reoxygenation produced a 60% increase in a proteoglycan subfraction that bound LDL with very high affinity. The incorporation of [3H]leucine into total cellular protein decreased significantly following exposure of smooth muscle cells to hypoxia as well as hypoxia/reoxygenation. These results indicate that hypoxia and hypoxia/reoxygenation cause major alterations in proteoglycan metabolism by vascular smooth muscle cells.