Robert A. Strickland

Calcium attenuates epinephrine's beta-adrenergic effects in postoperative heart surgery patients.

Epinephrine and calcium possess both cardiac inotropic and vasopressor activity. In addition, epinephrines cardiovascular effects are mediated via increases in intracellular calcium. As a result, many clinicians administer the two agents together in an attempt to augment their effects. Although this approach seems rational, it has never been proven effective. We evaluated the cardiovascular and hyperglycemic actions of epinephrine (10 and 30 ng/kg/min), with and without calcium chloride administration (10 mg/kg bolus followed by 2 mg/kg/hr infusion), in a prospective, randomized, blinded, crossover designed study. Twelve adult patients were studied 1 day after aortocoronary bypass surgery. Calcium chloride raised ionized calcium levels from 1.06 +/- 0.03 (mean +/- SEM) to 1.44 +/- 0.05 mM (p less than 0.05). Calcium raised mean arterial pressure from 85 +/- 1 to 94 +/- 2 mm Hg (p less than 0.05) but had no significant effect on cardiac index. Epinephrine alone at 10 and 30 ng/kg/min significantly raised cardiac index from 2.7 +/- 0.2 to 3.0 +/- 0.2 (p less than 0.05) and 3.6 +/- 0.3 (p less than 0.05) l/min/m2. After calcium, epinephrine failed to significantly increase cardiac index. Epinephrine at 30 ng/kg/min significantly increased mean arterial pressure from 87 +/- 1 to 95 +/- 2 mm Hg (p less than 0.05). After calcium, epinephrine had no significant effect on blood pressure. In addition, epinephrines hyperglycemic effect was blunted by calcium. Plasma epinephrine levels were similar during control and calcium infusions. We conclude that calcium blunts epinephrines beta-adrenergic actions in postoperative cardiac surgery patients.

Bedside blood gas and electrolyte monitoring in critically ill patients.

A major advantage of near-patient testing is time savings that facilitate important diagnostic and therapeutic decisions. Recent technologic advances have made available a number of systems that allow for near-patient testing. The reliability of these instruments must be validated in the clinical setting in the hands of their intended users. We evaluated the Gemstat blood gas, electrolyte, and Hct portable analyzer in the critical care setting when used by numerous individuals with no previous laboratory training. Blood gas, Na, K, and Hct results were highly correlated with those from the clinical laboratories (PaO2, r = .96; PaCO2, r = .92, pH, r = .96; Na, r = .93; K, r = .95; Hct, r = .91). The Gemstat represents a new generation of portable, rapid, safe, and accurate instruments that are well suited for ICU settings. The instrument can facilitate clinical management of patients, and may improve patient care.

Calcium does not augment phenylephrine's hypertensive effects.

Ca and phenylephrine, both of which increase mean arterial pressure (MAP), are often administered concurrently during resuscitation of critically ill patients. To determine whether the response to phenylephrine is potentiated by Ca administration, we studied eight adult patients 24 h after aortocoronary bypass surgery. Each patient received three doses of phenylephrine (150, 300, and 450 ng/kg.min), administered both with and without CaCl2 (5 mg/kg bolus followed by a 2-mg/kg.h infusion). Phenylephrine alone at 150, 300, and 450 ng/kg.min increased MAP by 2%, 6%, and 17%, respectively. Ca alone increased serum ionized Ca levels from 1.00 +/- .03 (SEM) to 1.20 +/- .02 mM (p less than .05) and increased MAP from 84 +/- 1 to 90 +/- 2 mm Hg (p less than .05), but had no effect on cardiac index (CI). When administered concurrently with Ca, phenylephrine at 150, 300, and 450 ng/kg.min increased MAP by 6%, 7%, and 13%, respectively. Phenylephrine had no effect on CI, pulmonary capillary wedge pressure, CVP, or heart rate whether or not it was administered with Ca. We conclude that concomitant Ca administration does not augment the hypertensive response to phenylephrine in normotensive patients recovering from open heart surgery.

Bedside analysis of arterial blood gases and electrolytes during and after cardiac surgery

Intraoperative changes in arterial blood gas tensions and serum electrolyte concentrations may contribute to the development of arrhythmias and cardiovascular insufficiency. Rapid intraoperative assessment of these parameters may improve patient care by permitting earlier treatment of abnormalities. We evaluated a portable blood gas and electrolyte analyzer in six patients undergoing coronary artery bypass surgery. Evaluation by anesthesia personnel took place in the operating room. The analyzer produced rapid, accurate, and reliable data that were comparable to clinical laboratory data. Correlation coefficients between the analyzer and laboratory determinations for PaO2, PaCO2, pH, K+, Ca++, and hematocrit were all greater than 0.92. Large changes in circulating ionized calcium (18%) and potassium (38%) concentrations were noted during cardiac surgery. Bedside blood gas and electrolyte analyzers represent a new technology worthy of further evaluation.

Sexual dreaming during anesthesia: early case histories (1849-1888) of the phenomenon.

THE authors have encountered the problem of sexual ideations or dreams in sedated or anesthetized patients in their own anesthesia practices, in reports from colleagues, through expert witness testimony, and in the review of contemporary civil and criminal proceedings. A recent review article examined the roles of the benzodiazepines (especially midazolam), propofol, and nitrous oxide in producing sexually related dreams during dental analgesia and surgical analgesia and anesthesia. Soon after the introduction of midazolam into clinical practice, The Lancet published two medicolegal editorials reviewing its association with sexual ideations. Even allegations of sexual abuse can occur from patients who have been sedated in intensive care units. These allegations are truly believed by the patient to be real; however, in many of these allegations, it would be impossible for a sexual assault to have occurred because of the proximity of other healthcare personnel and family members. As part of our studies, we were led to the historical aspects of this phenomenon, first reported in The Lancet in 1849. We found these historical case histories to be of note because they illustrate that within 3 yr of the public demonstration of ether anesthesia in Boston, practitioners recognized the potential for general anesthetics to produce dreaming and identified the need for a chaperone during anesthesia. In this historical review, we focus on dreams and hallucinations with the earliest anesthetics, ether and chloroform. However, it is well recognized that drugassisted sexual abuse is still today a true entity and a gross violation of ethical principles. The first reported case of alleged sexual abuse during anesthesia occurred in Paris, France, in 1847. This was less than 1 yr after the first public demonstration of ether anesthesia in Boston, Massachusetts, on October 16, 1846. A Parisian dentist was accused of using ether to assist in sexually assaulting two girls on successive days. A physical examination performed by a physician and supporting evidence presented in court indicated that the first girl truly may have been assaulted. Also, she stated that she recalled specific aspects of the alleged assault. The second girl was able to recall details of her assault, but at the time she felt that she was unable to resist because of the effects of the ether, stating that she “felt paralyzed, her limbs were heavy, and she was unable to fight off” the dentist. Quoting records of the proceedings found in the French medical journals Abeille Médicale and Gazette Médicale from 1847, Dr. Edward Hartshorne (Surgeon, Philadelphia, Pennsylvania, and Editor, The Medical Examiner; 1818–1886) stated that the court entertained the possibility that these accusations were an ether-induced dream. So, it is apparent that dreams or hallucinations were already known to occur with ether. Despite the dentist’s claims of innocence, the court determined that sexual assault had occurred, and he was convicted and sentenced to prison on October 30, 1847. Less than 2 yr later, physicians were debating whether sexual dreaming could be a side effect of anesthesia. In January, 1849, a discussion of “Chloroform in Midwifery” occurred during a meeting of the Westminster Medical Society in England. One of the physicians, Dr. G. T. Gream (Obstetrician, Queen Charlotte’s Lying-In Hospital, London, England) enumerated several reasons why he did not think that chloroform was appropriate for obstetric use, and in so doing, he “alluded to several cases in which women had, under the influence of chloroform, made use of obscene and disgusting language. This latter fact alone he considered sufficient to prevent the use of chloroform in English women.” Later in this discussion, “Dr. Tanner mentioned a case of an operation in King’s College Hospital on the vagina of a prostitute in which ether produced lascivious dreams. Dr. Henry Hancock [Surgeon, London, England; 1809–1880] had noticed this effect in some cases he had operated upon.” In a subsequent issue of The Lancet, notes from the Medico-Chirurgical Society of Edinburgh of February 7, 1849, were published. Sir James Young Simpson (Obstetrician, Edinburgh, Scotland, developer of chloroform anesthesia, and President of the Royal College of Physicians in 1849; 1811–1870) stated that after 15 months of use in thousands of cases, “he had never seen, nor had he ever heard of any other person having seen, any manifestation of sexual excitement result from the exhibition of chloroform. . . . The excitement, he was * Associate Professor of Anesthesiology, Department of Anesthesiology, Wake Forest University School of Medicine. † Professor of Anesthesiology, Department of Anesthesia, Indiana University School of Medicine.

Judicial Opinion in North Carolina Regarding Physician Participation in Capital Punishment

For personal use. Mass reproduce only with permission from Mayo Clinic Proceedings. 7. Denno DW. The lethal injection quandary: how medicine has dismantled the death penalty. Fordham Law Review. 2007;76(1):49-128. http://papers .ssrn.com/sol3/papers.cfm?abstract_id=983732. Accessed November 5, 2007. 8. Pucino F, Danielson BD, Carlson JD, et al. Patient tolerance to intravenous potassium chloride with and without lidocaine. Drug Intell Clin Pharm. 1988;22(9):676-679. 9. Goder R, Habler HJ, Janig W, Michaelis M. Receptive properties of afferent nerve fibres associated with rat saphenous vein. Neurosci Lett. 1993; 164(1-2):175-178. 10. Nelson v Campbell, Commissioner, Alabama Department of Corrections, et al. No. 03-6821. US Supreme Court. No. 03-6821: 3. (May 24, 2004) http://supreme.justia.com/us/541/637/case.html. Accessed November 5, 2007. 11. The Florida Governor’s Commission on the Administration of Lethal Injection. The Florida Governor’s Commission on the Administration of Lethal Injection met again February 19, 2007 [transcript]. http://lethal-injection -florida.blogspot.com/2007/02/transcript-florida-governors-commission.html. Accessed November 5, 2007. 12. Davis P. Expert: Lethal injection executions need doctor supervision. Associated Press. Monday, February 12, 2007. http://lethal-injection-florida .blogspot.com/2007/02/expert-lethal-injection-executions-need.html. Accessed November 5, 2007.

Comparison of two formulas to calculate alveolar oxygen tension in canine oleic acid pulmonary edema

Alveolar oxygen tension (PAO2) is calculated by either of two mathematical formulas incorporating various respiratory variables. The first formula, Equation 1, assumes a constant RQ of 0.8; the second formula, Equation 2, uses the mixing equation and requires analysis of inspired, mixed expired, and end-tidal gas samples. We tested the consistency of these formulas before and after asymmetric oleic acid pulmonary edema, then calculated and compared venous admixture values using the PAO2 value derived from each formula. Before oleic acid, Equations 1 and 2 were similar (213 +/- 22 vs. 211 +/- 22 [SD] torr, respectively), as were venous admixture values (8.7 +/- 2.9% vs. 8.5 +/- 2.9%, respectively). After oleic acid injury, Equation 1 was significantly lower than Equation 2, thus slightly but consistently underestimating venous admixture (29.9 +/- 12.2% vs. 30.2 +/- 12.3%; p less than .01). However, the venous admixture values obtained after oleic acid injury calculated from Equations 1 and 2 correlated closely (r2 = .998; p less than .001), and the clinical differences yielded by the two formulas would be minimal. We recommend using the simpler formula (Eq. 1) when calculating PAO2.