cardiogenic shock case study

Case History

Patient

38-year-old female.

Chief Complaint

Severe headache, nausea, vomiting, and palpitations.

History of Present Illness

The patient presented to the emergency department (ED) with headache, nausea, vomiting, palpitations, severe dyspnea, diaphoresis, and nodal tachycardia that was treated with metoprolol.
read more Her electrocardiogram (ECG) showed ST-segment depression in leads II, III, aVF, and V4-V6; ventricular ectopy; and a short episode of AV-junctional escape rhythm (Figure 1). Because of increasing concentrations of cardiac troponin I (cTnI) and creatine kinase (CK) ( Table 1 ), an acute coronary syndrome was presumed. The patient was treated with aspirin, heparin, tirofiban, and intravenous metoprolol and transferred to our university center for invasive diagnostic procedures. During transport, her condition worsened with development of pulmonary edema requiring intubation and mechanical ventilation. Subsequently, however, she became hemodynamically unstable and, on 2 occasions, required inotropic support and a short episode of cardiopulmonary resuscitation.

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Figure 1.Electrocardiogram 1 hour after admission: ST-segment depression in II, III, aVF, and V4-V6 and a short episode of AV-junctional escape rhythm.

Past Medical History

History of migraine headaches since childhood and short episodes of palpitations during the last year not documented by ECG and no cardiovascular risk factors, especially no history of hypertension.

Family History

Noncontributory.

Physical Exam Findings

In the ED, she was afebrile and had a sinus rhythm with a heart rate of 100 beats/min (bpm) and blood pressure of 176/117 mm Hg. The day after admission to our center, she developed a fever (39.5°C), her C-reactive protein (CRP) level was elevated, and she was hypertensive (170/120 mm Hg) with a sinus tachycardia of up to 160 bpm.

Principal Laboratory Findings

Table 1 .
Additional Diagnostic Procedures
Emergency heart catheterization excluded coronary artery disease but showed a severely depressed left ventricular ejection fraction (LVEF) of 20% with only apically preserved wall motion (Figure 2). A cerebral computed tomography (CT) scan showed no evidence of bleeding. A CT scan of the chest and abdomen was negative for infectious foci; however, a left adrenal mass was noted (Figure 3). In addition, toxicology, serologic, and microbiology tests (ie, blood cultures) were all negative. The presence of the adrenal mass prompted collection of a 24-h urine sample for quantification of catecholamines and, based on the results ( Table 1 ) of this testing, an iodine-123 metaiodobenzylguanidine ([123I]MIBG) scan was performed. Myocardial [123I]MIBG uptake is related to myocardial noradrenaline content (ie, cardiac sympathetic activity). Our patient's [123I]MIBG scan demonstrated increased uptake in the left adrenal gland. Initial cardiac magnetic resonance images (MRI) showed no evidence of myocardial fibrosis or scars but did show global hyperintense myocardium indicative of myocardial edema, which disappeared 4 weeks later (Figure 4). The patient's cardiac function improved, and repeat transthoracic echocardiography, performed 2 weeks after admission to our center, revealed normal regional wall motion and left ventricular function. Moreover, she was normotensive but still showed intermittent sinus tachycardia.

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Figure 2.Left ventriculogram in right anterior oblique view in systole and diastole. Note the midventricular akinesis and only apical preserved wall motion. The left ventricular ejection fraction was 20%. Coronary angiography revealed normal epicardial coronary arteries.

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Figure 3.Computed tomography scan showing left adrenal mass (arrow).

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Figure 4.Acute magnetic resonance exam (7 days after presentation). (A) T2-weighted images (triple inversion recovery) showing global hyperintense myocardium when compared with skeletal muscle indicative of myocardial edema. (B) In the T1-weighted images after gadolinium application (inversion recovery technique), no hyperintense signal and no myocardial fibrosis or necrosis can be found. (C and D) Follow up after 10 weeks. (C) T2-weighted image: the former hyperintense signal of the myocardium in T2-weighting is decreased. (D) T1-weighted image after gadolinium application. No myocardial fibrosis or necrosis.
original article
http://www.medscape.com/viewarticle/574937