Cases reported "Heart Arrest"

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1/52. deceleration-dependent shortening of the QT interval: a new electrocardiographic phenomenon?

    In clinical cardiology, deceleration-dependent QT interval shortening is considered to be an extraordinary electrocardiographic phenomenon. We present an early premature born 4-year-old African-American girl with complications related to her premature birth, developmental delay, and several episodes of cardiac arrest. An episode of severe transient bradyarrhythmia was documented on Holter monitoring. The unique feature of the rhythm strips was paradoxical gradual shortening of the QT interval to 216 ms with accompanying transient T-waves abnormalities. The activation of the Ik, ACh due to an unusually high vagal discharge to the heart is proposed as a possible mechanism responsible for both slowing of the heart rate and shortening of the QT interval.
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2/52. Radiofrequency catheter ablation in a haemodynamically compromised premature neonate with hydrops fetalis.

    A preterm infant was born at 35 weeks gestation after failed antenatal antiarrhythmic therapy. The infant had an incessant supraventricular tachycardia, impaired ventricular function and hypotension and failed to respond to adenosine, cardioversion and intravenous amiodarone. After resuscitation from cardiovascular collapse, a successful radiofrequency catheter ablation (RFA) of a left free wall atrioventricular pathway was performed at 24 h of age without extracorporeal support. The infant is normal on follow up at 12 months of age. Whilst most fetal and neonatal supraventricular tachyarrhythmias respond to antiarrhythmic medications and RFA is not required, this is the earliest RFA to be performed on a premature infant when antiarrhythmics have failed.
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3/52. ventricular fibrillation in a patient with prominent J (Osborn) waves and ST segment elevation in the inferior electrocardiographic leads: a brugada syndrome variant?

    Recurrent ventricular fibrillation was observed in a 29-year-old Vietnamese man who did not exhibit structural heart disease. The patient's ECG showed prominent J (Osborn) waves and ST segment elevation in the inferior leads that were not associated with hypothermia, serum electrolyte disturbance, or myocardial ischemia. Rate-dependent change in the amplitude of J waves and ST segment elevation also were observed. An implantable cardioverter defibrillator (ICD) was implanted. Adjunctive treatment with amiodarone reduced J wave amplitude, preventing ventricular fibrillation and ICD shocks. Prominent J waves and ST segment elevation in the inferior leads may serve as an important diagnostic sign to detect high-risk individuals with a history of unexplained syncope. ICD implantation plus amiodarone is the treatment of choice.
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4/52. Preservation of the brainstem auditory evoked potential in non-convulsive status epilepticus.

    Brainstem auditory evoked potentials (BAEPs) were recorded from a patient simultaneously experiencing non-convulsive generalized status epilepticus (NGSE). Waves I, III and V were normal but all subsequent waves were absent. This finding indicates that structures within the brainstem adjacent to the generators for the BAEP are likely not affected by NGSE and also illustrates the resilient nature of the BAEP. This is the first report of the recording of an evoked potential during a naturally occurring generalized seizure.
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5/52. Hemodynamic applications of capnography.

    The measurement of the pressure of exhaled carbon dioxide (PetCO2) via capnography has several useful hemodynamic applications. This article discusses integrating PetCO2 values with hemodynamic assessment. capnography can be applied to hemodynamic assessment in three key ways: (1) identification of end-expiration during pulmonary artery and central venous pressure measurements, (2) assessment of pulmonary perfusion and alveolar deadspace, (3) assessment of cardiopulmonary resuscitative efforts. The article presents research, sample waveforms for end-expiration identification, and case examples.
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6/52. An exceptional case of complete neurologic recovery after more than 5-h cardiac arrest.

    We describe a case of more than 5 h cardiac arrest in a 60-year-old patient who underwent general anesthesia for a urologic operation. Before extubation, the patient suddenly developed ventricular fibrillation, pulseless ventricular tachycardia and asystole which was immediately treated by advanced life support (ALS) measures. Thirty minutes later seizures developed and were controlled by 200 mg of thiopentone and 10 mg of diazepam. A pattern of ventricular tachycardia, coarse ventricular fibrillation and asystole lasted for nearly 120 min. Termination of resuscitation maneuvers was considered, but long-term life support was continued for 5 h. After this time, peripheral pulses, with a supraventricular tachycardia-like rhythm and regular spontaneous breathing reappeared. Seven hours later, the patient had a glasgow coma scale (GCS) of 5, dilated unresponsive, absence of pupils, and a systolic arterial pressure of 100 mmHg. He was then transferred to intensive care unit (ICU). The morning after, the patient was awake, responded to simple orders, breathing spontaneously, and free from sensomotor deficit. He was, therefore, extubated. Subsequently, other episodes of transitory ST-line upper wave followed by ventricular fibrillation appeared, suggesting Prinzmetal angina. This was successfully treated by percutaneous coronary angioplasty. The first electroencephalogram recorded the day after cardiac arrest showed a mild widespread background slowing. An electroencephalogram 6 days later showed a return to alpha rhythm with only mild theta-wave abnormalities. Four weeks after the first cardiac arrest the patient was discharged. This is an exceptional experience compared with the others reported. We believe that all the efforts must not be given up when such an event occurs during anesthesia and there are optimal conditions for resuscitation maneuvers.
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7/52. Bilateral extracorporeal shock wave lithotripsy in a spinal cord injury patient with a cardiac pacemaker.

    OBJECTIVES: To review the precautions to be observed before and during extracorporeal shock wave lithotripsy (ESWL) in spinal cord injury (SCI) patients with a cardiac pacemaker and the safety of bilateral ESWL performed on the same day. DESIGN: A case report of bilateral ESWL in a SCI patient with a permanent cardiac pacemaker. SETTING: The Regional spinal injuries Centre, Southport, the lithotripsy Unit, the Royal Liverpool University hospitals NHS trust, Liverpool, and the Department of cardiology, Manchester Royal Infirmary, Manchester, UK. SUBJECT: A 43-year-old male sustained a T-4 fracture and developed paraplegia with a sensory level at T-2. During the post-injury period, he developed episodes of asystole requiring implantation of a dual chamber (DDD) permanent pacemaker. Twenty-one months later, he developed a right ureteric calculus with hydronephrosis. A radio-opaque shadow was seen in the left kidney with no hydronephrosis. During right ureteric stenting, the ureteric stone was pushed into the renal pelvis. 1,500 shock waves were delivered to this stone on the right side, followed by ESWL to the left intra-renal stone with 1250 shock waves. RESULTS: The patient tolerated ESWL to both kidneys. The pacemaker was reprogrammed to a single chamber ventricular pacing mode at 30 beats per minute with a reduced sensitivity during lithotripsy. There were no untoward cardiac events during or after lithotripsy. The serum creatinine was 45 micromol/l before lithotripsy and 44 micromol/l two weeks after ESWL. CONCLUSION: SCI patients with a cardiac pacemaker may be able to undergo extracorporeal shock wave lithotripsy following temporary reprogramming of the pacemaker. Bilateral, simultaneous ESWL is safe in the vast majority of patients provided that there is no risk of simultaneous ureteric obstruction by stone fragments. However, it should be remembered that a decrease in renal function could occur following bilateral ESWL of renal calculi.
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8/52. Neurocardiogenic syncope in a 10-year-old boy.

    We present a case with a suspected epileptic disorder. This may be a result of a neurocardiogenic syncope leading to seizures. A 10-year-old boy suffered two episodes of sudden loss of consciousness after getting injections. electrocardiography (ECG) and electroencephalography recordings during a venipuncture showed asystole of 6 seconds followed by a generalized seizure with clonic jerks of the right arm and leg while theta waves in the EEG were noted. Tilt-table testing could not provoke a pathological reaction.
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9/52. Aborted sudden death, transient Brugada pattern, and wide QRS dysrrhythmias after massive cocaine ingestion.

    Although cocaine is one of the leading causes of drug-related deaths, there is little clinical information describing the precise sequence of events leading to death in the cocaine intoxication. Usually, cocaine-related sudden deaths are unwitnessed, its electrocardiographic features are not attainable, and the majority of these patients have a rapidly fatal course and die before arriving at the hospital. We report a patient with massive cocaine ingestion who developed psychomotor agitation and generalized seizures followed by asystolic cardiac arrest. ventilation with supplemental oxygen by endotracheal intubation immediately restored spontaneous heart beat. After resuscitation, a severe metabolic acidosis (pH 6.65) and cardiac dysrrhythmias consistent with sodium channel poisoning were detected. The electrocardiogram showed accelerated junctional rhythm at 85 beats/min with right bundle branch block and left anterior hemiblock configuration, prolongation of QRS (0.16 sec) and QTc (0.52 sec) intervals, and terminal J wave associated with coved ST-segment elevation in leads V(1) and V(2) resembling the brugada syndrome. sodium bicarbonate administration was quickly followed by normalization of the cardiac conduction disturbances. This article discusses the clinical and electrophysiologic implications of these findings.
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10/52. life threatening cardiopulmonary failure in an infant following protamine reversal of heparin after cardiopulmonary bypass.

    life threatening cardiopulmonary failure following protamine reversal of heparin after cardiopulmonary bypass (CPB) was reported to occur in adults but rarely in children. Atrial septal defect closure was performed in a 6-week-old infant erroneously suspected to suffer from right atrial thrombosis in addition. Protamine administration after CPB led to critical pulmonary hypertension and severe haemorrhagic pulmonary oedema resulting in severe hypoxia. Inhaled nitric oxide, together with high frequency oscillation ventilation supplemented by intravenous prostacycline, enabled complete recovery of cardiopulmonary and neurological function. life threatening cardiovascular compromise after intravenous protamine can occur even in young infants which then require challenging paediatric critical care.
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