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Pediatric cardiac arrest is a relatively rare but devastating presentation in infants and children. In contrast to adult patients, in whom a primary cardiac dysrhythmia is the most likely cause of cardiac arrest, pediatric patients experience cardiovascular collapse most frequently after an initial respiratory arrest. Aggressive treatment in the precardiac arrest state should be initiated to prevent deterioration and should focus on support of oxygenation, ventilation, and hemodynamics, regardless of the presumed cause. Unfortunately, outcomes for pediatric cardiac arrest, whether in hospital or out of hospital, continue to be poor.

Most pediatric intubations that occur in the emergency department are in patients without identifiable risk factors for difficulty. Infants and children go through a predictable pattern of development that impacts airway management. A careful, stepwise approach to the identification of the truly difficult pediatric airway is critical to avoid morbidity and mortality. Difficulty can be encountered in cases of challenging anatomy such as congenital airway or midface abnormalities or with acquired conditions such as croup or epiglottitis. Physiologically, intrinsic lung disease (ie, asthma) and shock states have unique features that impact airway management.

Background Overdoses of calcium channel blocker agents result in hyperglycemia, primarily due to the blockade of pancreatic L-type calcium channels and insulin resistance on the cellular level. The clinical significance of the hyperglycemia in this setting has not previously been described. Methods This study is a retrospective review of all adult (age, >or=15 yrs) patients with a discharge diagnosis of acute verapamil or diltiazem overdose at five university-affiliated teaching hospitals. The severity of overdose was assessed by determining whether a patient met the composite end points of in-hospital mortality, the necessity for a temporary pacemaker, or the need for vasopressors. We compared the initial and peak serum glucose concentrations with hemodynamic variables between patients who did and did not meet the composite end points. Results A total of 40 patients met inclusion criteria, with verapamil and diltiazem accounting for 27 of 40 (67.5%) and 13 of 40 (32.5%) of the ingestions, respectively. For those patients who did and did not meet the composite end points, the median initial serum glucose concentrations were 188 (interquartile range, 143.5-270.5) mg/dL and 129 (98.5-156.5) mg/dL, respectively (p = .0058). The median peak serum glucose concentrations for these two groups were 364 (267.5-408.5) mg/dL and 145 (107.5-160.5) mg/dL, respectively (p = .0001). The median increase in blood glucose was 71.2% for those who met composite end points vs. 0% for those who did not meet composite end points (p = .0067). Neither the change in the median heart rate nor the change in systolic blood pressure was significantly different in any group. Conclusion Serum glucose concentrations correlate directly with the severity of the calcium channel blocker intoxication. The percentage increase of the peak glucose concentration is a better predictor of severity of illness than hemodynamic derangements. If validated prospectively, serum glucose concentration alone might be an indicator to begin hyperinsulinemia-euglycemia therapy.

Dr. Nathan Mick: Today’s case is that of a 46-year-old man who was struck by a car traveling at approximately 35 mph. According to witnesses, the patient was facing the car when he was hit and thrown 20 feet. When first responders arrived, the patient was found to have a Glascow Coma Scale (GSC) score of 6 and obvious bilateral lower extremity deformities. Pre-hospital personnel at the scene called for helicopter evacuation to a trauma center. The helicopter transport team found the patient supine on a long board with his cervical spine immobilized. The GCS was 6 with sonorous respirations. Vitals signs were as follows: heart rate (HR) 120 beats per minute, systolic blood pressure (BP) 120 mm Hg, and respiratory rate (RR) 10 breaths per minute. Two large bore antecubital intravenous (i.v.) lines were placed. He was pre-oxygenated and then intubated using rapid sequence induction with etomidate 20 mg i.v. and succinylcholine 100 mg i.v. Endotracheal tube placement was confirmed with a colorimetric end-tidal CO2 detector; the patient received midazolam 2 mg i.v. and vecuronium 8 mg i.v. En route to the hospital, the patient received 2000 cc of crystalloid i.v. and was noted to be persistently tachycardic. Dr. Eric Nadel: Are there any questions regarding the pre-hospital course? Dr. Barbara Masser: Why did the on-scene personnel elect to call the helicopter rather than transport the patient via ground ambulance? Dr. Stephen Thomas: Due to the extent of the patient’s injuries and the fact that rush hour traffic would delay transport to the nearest level I trauma center, I think that their choice was a prudent one. The question of when and how to best utilize aeromedical transport vehicles in the urban trauma setting has been long debated. It is generally accepted that the combination of timedistance factors and injury severity reliably predicts who might benefit from air transport to a Level I trauma center (1). Dr. Nathan Mick: The patient arrived in the Emergency Department (ED) at 1900 hours, approximately 45 minutes after being struck. The primary survey revealed that he was sedated, chemically paralyzed, and orally intubated; endotracheal tube placement was confirmed by auscultation of bilateral breath sounds and capnography. Femoral and carotid pulses were 2 and equal. The vital signs were BP 80/56 mm Hg, HR 115 beats/minute, mechanically ventilated RR 12 breaths/minute, oxygen saturation 100%. Secondary survey revealed a GCS of 3. There was a 2-cm laceration over the right eye with pupils that were 3 mm, symmetric and non-reactive. There was soft tissue swelling over the left parietal scalp without palpable deformity. The neck was immobilized; the trachea was midline. Examination of the chest revealed bilateral breath sounds with no crepitance or flail segments. The abdomen was non-distended without palpable masses.

Dr. Nathan Mick: Today’s case is that of a 6-month-old female presenting with decreased responsiveness. The patient was well until that morning when she was difficult to arouse from sleep. The patient’s mother noted that during the past week the child had begun to sleep through the night without waking. At 7:00 that morning when she went in to awaken the child and couldn’t, she assumed the child was “tired” and allowed her to remain sleeping. One hour later, she again had difficulty waking her daughter and called her pediatrician who urged her to have her daughter evaluated in the Emergency Department (ED). The mother reported that her daughter was an only child with no recent sick contacts and that the house contained no prescription medications. The child’s past medical history was notable for a normal term labor and vaginal delivery. There had been no significant illnesses. She was breast fed until 3 months of age and then transitioned to formula. The patient was cared for by her maternal grandmother during the daytime as her parents both worked outside the home. She had met normal developmental milestones to date. She was on no prescription medications, had no allergies, and was up to date on all immunizations including the pneumococcal vaccine. The patient lived with her mother and father, who had been married 5 years. Dr. Eric Nadel: Are there any questions about the initial history? Dr. Jessica Peters: Was there any history of trauma? Dr. Nathan Mick: The mother denied any history of trauma in the preceding week. The child was able to crawl but not walk and there were no stairs or other “high risk” areas in the home. The child’s initial vital signs were: pulse 140 beats/ minute, respiratory rate 30 breaths/minute, oxygen saturation 99%, temperature 37°C, and blood pressure 96/50 mm Hg. The physical examination revealed a well-developed, well-nourished 6-month-old lying quietly on a gurney. The skin examination revealed no petechiae or ecchymoses. The head and neck examinations revealed no signs of otitis media, trauma, nuchal rigidity, or pharyngitis. The pupils were normal, round and reactive. There was no respiratory distress and breath sounds were clear. The heart and abdominal examinations were normal. The child was listless with open eyes and very little movement of the extremities. She did not respond negatively to separation from her mother and did not respond to venipuncture and vascular access. Dr. Eric Nadel: Are there any questions regarding the physical examination? Dr. Todd Thomsen: Perhaps the most ominous finding on examination is the lack of response to “stimulation” via needle stick. Was this child protecting her airway? Dr. Nathan Mick: The child was handling her secretions without difficulty and was ventilating normally with a normal oxygen saturation, so immediate airway

Dr. Martin Lucenti: Today’s case is that of a 46-yearold man with a history of aortic insufficiency, who was in his usual state of health when he developed shortness of breath while playing golf. He had associated mild chest discomfort, which he described as heaviness, and a sensation that his heart was racing. Shortly after the onset of these symptoms he developed a cough with bloody sputum. He became more short of breath and was brought to a community hospital by his friends. Vital signs upon presentation to the outside hospital were: temperature 36.4°C (97.6°F), blood pressure 198/68 mm Hg, heart rate 119 beats per minute, respiratory rate 25 breaths per minute, and oxygen saturation 90% on room air. The patient was described as mildly diaphoretic, sitting upright, and working hard to breath. The lung examination revealed bilateral crackles, and the heart was tachycardic with a question of a heart murmur. The patient was placed on a cardiac monitor, supplemental oxygen was administered, and an intravenous line was placed. Laboratory data showed a white blood cell count of 11.4 k/mm, hematocrit 42%, platelet count 331 k/mm, sodium 140 mmol/L, potassium 4.7 mmol/L, chloride 107 mmol/L, carbon dioxide 22.9 mmol/L, BUN 22 mg/dL, creatinine 1.0 ng/dL, and glucose 120 mg/dL. The electrocardiogram was interpreted as sinus tachycardia with left ventricular hypertrophy. The chest X-ray study showed bilateral infiltrates and cardiomegaly. The patient was given ceftriaxone 1 gram i.v., azithromycin 500 mg orally, and vancomycin 1 gram i.v. due to a concern for possible pneumonia. The patient developed worsened hypoxia at the community hospital and he was transferred to our Emergency Department (ED) for further evaluation. Dr. Eric Nadel: Are there any questions about the prehospital course? Dr. Nathan Mick: Was there consideration of etiologies other than pneumonia, including cardiac etiologies such as myocardial infarction or congestive heart failure (CHF)? Dr. Lucenti: It is unclear whether other etiologies were considered. There was no treatment administered for ischemic heart disease or CHF. Upon arrival in our ED, the patient was diaphoretic and in moderate respiratory distress, sitting upright, and speaking in 2–3 word phrases. He complained of palpitations but denied chest pain, abdominal pain, nausea and vomiting. The patient’s past medical history was significant for severe aortic insufficiency. He had an echocardiogram 1 year prior to presentation that showed a bicuspid aortic valve with moderate aortic insufficiency, normal right-sided heart function, left ventricular hypertrophy, and an ejection fraction of 65%. The patient also had a history of gastroesophageal reflux and hypercholesterolemia. The patient was taking nifedipine, omepra

The effects of arginine vasotocin (AVT) were examined in isolated gar arteries (afferent branchial, ABA; conus arteriosus, CA; ventral aorta, VA) and veins (hepatic, HV; intestinal; ovarian). AVT (10 −11 –10 −7 M ) had no effect in CA, produced contraction in ABA and VA and stimulated relaxation in veins. In precontracted HV, AVT relaxation was dose-dependent, long-lived (>30 min) and reduced total tension by 49.0 ± 10.7%. EC 50 s for AVT, arginine vasopressin, oxytocin, desmopressin, and isotocin in gar HV were 1.4 ± 0.3, 3.6 ± 0.2, 5.3 ± 1.7, 11.0 ± 6.5, and 19.0 ± 0.4 n M, respectively. AVT was more potent compared with isotocin. Strength of relaxation (percentage decrease in total tension) of AVT and structural analogs was similar (range = 32.5 to 55%). Endothelium removal did not alter percentage relaxation or sensitivity to AVT in HV. AVT relaxation was not inhibited by nitric oxide synthase inhibitors or propranolol or reversed by addition of methylene blue but it was significantly enhanced by indomethacin (10 −5 M ). Arginine vasopressin-receptor antagonists (V 1 - or V 2 -type selectivity; 10 −6 M ) were equally effective inhibitors, each blocked 99% of AVT relaxation. Forskolin (10 −6 M ) and papaverine (10 −4 M ) relaxed precontracted gar arteries and veins. The adenylyl cyclase inhibitors SQ 22536 and MDL 12,330A (10 −5 M ) produced transient contraction and stable relaxation, respectively, but did not inhibit AVT-induced relaxation in HV. Atrial natriuretic peptide (3 × 10 −8 M ) and sodium nitroprusside (10 −4 M ) had no effect in precontracted HV. AVT acts directly on gar venous smooth muscle cells via a nonclassical AVP receptor, possibly by increasing [cAMP]. AVT is a potent vasoconstrictor in vertebrate vasculature but produces a novel relaxation in gar veins.