Effects of Procainamide and Lidocaine on Defibrillation Energy Requirements in Patients Receiving Implantable Cardioverter Defibrillator Devices

Effects of Procainamide and Lidocaine on Defibrillation. intntduction: In acute canine studies, lidocaine. but not prucainamidc, increases defibrillation energy requirements. We evaluated the effects of lidocaine or procainamide on defihrillation energy requirements in 27 patients undergoing intraoperative testing fur implantable cardioverter dcfibrillator device placement.
Methods and Results: Patients were tested off antiarrhythmic drugs and again following either lidocaine (200 to 250 mg loading and 3 mg/min maintenance infusions) or procainamide (1 gm loading and 3 to 4 mg/min maintenance infusions). The defibrillation testing protocol consisted of initial testing at 15 J, followed by higher or lower energies to determine the lowest energy producing three consecutive successful defibrillations. Overall, the mean defibrillation energy increased from 14 ± 5 J to 18 ± 7 J during lidocaine (plasma concentration 5.1 ± 1.6 μ/mL; P < 0.02) but were similar at baseline (12 ± 5 J) and during procainamide infusion (13 ± 6 J) (plasma concentration: procainamide 10.7 ± 7.2 μ/rnl.; N-acetyl procainamide 1.0 ± 0.4 μ/niL). A positive linear correlation was found between lidocaine plasma concentration and percent change in defibrillation energy (lidocaine: r = 0.61; P = 0.01). Procainamide raised the defibrillation energy in three patients, two with supra therapeutic plasma concentrations. The increase in defibrillation energy equaled or exceeded 25 J in four patients after lidocaine and in one patient after procainamide.
Conclusion: The data suggest that at high plasma concentrations, lidocaine and procainamide adversely affect defibrillation energy requirements consistent with an adverse, concentration-dependent effect of sodium channel blockade on defibrillation energy requirements in patients.     

Mechanisms of protective immunity against 5. mansoni infection in mice vaccinated with irradiated cercariae. VI. Influence of the major histocompatibility complex

Summary Inbred mouse strains develop different levels of resistance to challenge infection with Schistosoma mansoni in response to vaccination with irradiated cercariae. The role of the major histocompatibility complex (MHC) in determining this genetic polymorphism in acquired resistance was investigated. Previous studies suggested that inbred mice bearing either the b or d MHC haplotypes develop a higher level of vaccine induced resistance than do mice with other MHC haplotypes. An analysis of an Fi cross between an H-2^b strain (C57BL/6) and an H-2^k strain (C3H/HeJ) indicated that the ability to develop high levels of immunity is inherited in a dominant fashion. In order to confirm that the development of high resistance is an MHC associated trait, B10, C3H, BALB and B6 congenic mice bearing different H-2 haplotypes were compared. On either the BIO, B6, or BALB background, substitution of b or d with k or a MHC alleles resulted in a decreased level of vaccine induced immunity. The observed decreases were more pronounced in BALB and B6 than in B10 congenics suggesting an influence of background (non-MHC linked) genes on protective immunity. Similarly, C3H. SW (H-2^b) mice developed a significantly higher level of acquired resistance than C3H/HeSn (H-2^k) mice. Cross and backcross experiments between H-2^b and H-2^k B6 congenic mice confirmed the dominant inheritance of high resistance as well as the MHC linkage of the trait. These data indicate that the MHC locus exerts a quantitative influence on vaccine induced resistance in certain inbred mouse strains and provide further support for the concept that the protection elicited by irradiated cercariae is the manifestation of a specific host immune response.     

Vitamin E Deficiency in the Monkey. IV. Further Studies of the Anemia with Emphasis on Bone Marrow Morphology

Nuclear abnormalities were observed in all the erythroid precursors in thebone marrow of vitamin E-deficient monkeys. Many of these cells were multinucleated. The remainder of the marrow elements appeared normal. Reasonsfor considering the anemia to be primarily due to inadequate erythropoiesisare given.

Serum iron, glutathione stability of the erythrocytes, hemoglobin electrophoresis, osmotic fragilities and platelet counts were all found to be normalin the vitamin E-deficient monkey.

Submitted on March 23, 1962 Accepted on May 12, 1962     

VITAMIN D NUTRITION AND VITAMIN D METABOLISM IN THE PREMATURE HUMAN NEONATE

The effect of supplementation with daily doses of vitamin D2 (1000 IU or 3000 IU, 25-75 micrograms, 63-189 nmol) has been studied in 39 premature neonates, initial gestational age 25-32 weeks. The initial mean plasma 25-hydroxyvitamin D was 25.8 nmol/l (10.3 ng/ml) but in 12 infants, most of whom were born in the winter months, the level was less than 15 nmol/l (6 ng/ml), and in seven babies plasma 1,25-dihydroxyvitamin D was less than 48 pmol/l (20 pg/ml). These findings suggest a considerable degree of maternal vitamin D-deficiency. Maximum attained concentrations of 25-hydroxyvitamin D on treatment were 77.3 nmol/l (30.9 ng/ml), high dose and 86.8 nmol/l (34.7 ng/ml), low dose, the mean rate of increase was greatest during the first two weeks (2.2 nmol/l/d; 0.88 ng/ml/d) and declined over the next 4 weeks. Mean maximum concentrations of 1,25-dihydroxyvitamin D2 were 283 pmol/l, (121 pg/ml), high dose and 309 pmol/l (129 pg/ml), low dose. Apart from a minor contribution to the initial plasma 1,25-dihydroxyvitamin D concentration, no effect of gestational age could be discerned in any of the measured variables. The endogenous pool of 1,25-dihydroxyvitamin D3 decayed with a T 1/2 of 22.5 d, indicating that vitamin D supplementation of these infants was necessary to avoid vitamin D-deficiency.     

Fine Structural Alterations Induced in Platelets by Adenosine Diphosphate

Blood platelets exposed to the nucleotide adenosine diphosphate (ADP)lose their discoid appearance and adhere to one another. The basis for theADP induced shape change has remained obscure. In the present study thestructural transformations of platelets under the influence of ADP have beenexamined in the electron microscope. Loss of lentiform appearance is closelyrelated to a marked reorganization of the platelet hyaloplasm. The marginalbundle of microtubules decreases in circumference and is moved into theinterior of the platelet. Granules and other organelles are transported to thecell center where they are enveloped within a web of microtubules and microfilaments. These changes are completely reversed after the influence of ADPdisappears. The movement of the circumferential bundle of microtubulesfrom its position under the cell wall appears to be the principle cause forthe loss of discoid shape. Constriction of hyaloplasmic elements followed bycomplete recovery of unaltered appearance are indicative of a reversible waveof contraction occurring in the platelet hyaloplasm. Thus the change in plateletsurface contour after exposure to ADP is not due to a direct modification ofthe cell wall by ADP, but to a contractile wave which ADP indirectly triggers in the substance of the cells.

Submitted on March 28, 1967 Accepted on November 1, 1967     

A Case Series: Herpes Simplex Virus as an Occupational Hazard

ABSTRACT

Statement of the Problem: Herpes labialis infections are common and present a serious risk to the dental team. Purpose of the Study: The purpose is to make dentists aware of the risks involved with treatment of patients with active herpes labialis. In addition, evidence‐based risk‐management strategies are presented. Methods and Materials: The incidence and natural history of herpes simplex virus type 1 (HSV‐1) are reviewed. Four previously unreported case histories are presented to illustrate the impact common sequelae of HSV‐1 can have on the dental team. The differences between HSV‐1 and the blood‐borne diseases which are the focus of universal precautions are discussed. In particular, the highly contagious, highly transmissible nature of HSV‐1 and its transmission through aerosols are highlighted. Finally, the need to include protection against aerosols in the profession's understanding of universal precautions is noted. Results: The authors suggest limiting the treatment of patients with active lesions to urgent care only, and treating active HSV‐1 lesions to reduce time of healing. For four common clinical situations involving HSV‐1 infections, evidence‐based methods for protecting the dental team and the patient from cross‐contamination are also presented. Conclusion: While it is clear that the treatment of patients with active herpes labialis lesions increases risk of cross‐infection, there are good protocols for controlling this risk.

CLINICAL SIGNIFICANCE

By bringing common vectors of cross‐infection to light and providing evidence‐based protocols for preventing them, this article provides practitioners with positive steps that can be taken for controlling the risk of spreading herpes infections to the dental team. (J Esthet Restor Dent 24:61–67, 2012)