Resuscitation
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A 42-year-old man presented with shortness of breath, weakness, and diaphoresis, and developed a new left bundle branch block while under evaluation in the Emergency Department. At emergency cardiac catheterization, he was found to have only insignificant coronary disease, and a hyperdynamic ventricle. ⋯ He gradually improved over several days and made a full recovery, after which he admitted to taking multiple calcium channel blockers (CCBs) in an attempt to self-medicate for symptoms he related to his lifelong paroxysmal supraventricular tachycardia. This is the first report of a CCB overdose mimicking an acute myocardial infarction, and highlights the fact that CCB overdose must be considered in the differential diagnosis of some patients who present with apparent acute myocardial infarction.
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Comparative Study
Tracheal epinephrine or norepinephrine preceded by beta blockade in a dog model. Can beta blockade bestow any benefits?
Tracheal epinephrine (adrenaline) has been associated with two major deletorious side effects: increased heart rate (HR) and an initial decrease of blood pressure (BP). This prospective randomized animal study compared the haemodynamic responses to tracheally administered epinephrine or norepinephrine (nor adrenaline) alone versus each after pretreatment with propranolol for ameliorating those two untoward effects associated with epinephrine administration. Five anaesthetized mongrel dogs underwent 25 experiments of tracheal epinephrine or norepinephrine (0.02 mg/kg diluted with normal saline to 5 ml total volume) with or without an I/V non-selective beta-blocker (propranolol 0.1 mg/kg) pretreatment, and served as their own controls. ⋯ While both epinephrine or norepinephrine after pretreatment with propranolol produced a significant increase in both diastolic (from 106 to 166 mmHg and from 118 to 169 mmHg, respectively) (P<0.01) and mean BP (from 122 to 183 mmHg and from 133 to 188 mmHg, respectively) (P<0.01), only propranolol-pretreated tracheal epinephrine yielded a significant decrease in HR (from 52 to 33/m, P=0.002). Pretreatment with a beta-blocker protected against the deleterious tachycardia associated with epinephrine or norepinephrine and, by doing so, may improve the myocardial oxygen supply-and-demand balance. At the same time, the pretreatment augmented the relatively mild diastolic BP increase associated with the beta-adrenergic effect of epinephrine.
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Acidosis may contribute to brain injury from asphyxia, but its role is unclear. In order to evaluate the association between brain acidosis and cerebral injury, we subjected piglets to hypoxia and hypotension (HYP-HOTN) or hypoxia alone (HYP) to inflict varying amounts of brain damage. We hypothesized that piglets with a more severe brain injury would have a lower brain pH. ⋯ The time needed for brain pH to recover after asphyxia, but not its severity, was associated with the amount of brain injury. Further study is warranted to determine whether immediate restoration of brain pH will reduce brain damage.