Judith Ann Hirsch

Residual Pressor Effects of Chronic Alcohol in Detoxified Alcoholics

Although research in population studies has indicated that recent alcohol intake is positively correlated with blood pressure, there is a need to study the relationship of blood pressure to measures of lifetime alcohol intake in alcoholics. To this end, we assessed systolic and diastolic pressures and lifetime alcohol intake through structured interviews with 253 normotensive recovering alcoholics. Blood pressures were first corrected with multiple linear regression for the influence of confounding or modifying variables and then were regressed against alcohol consumption measures. Systolic pressure was significantly correlated (positively) with only a few measures of recent alcohol intake, and the correlations were not high (r2 = .05 to .11, P < .05). Diastolic pressure was found to be highly and positively correlated with the duration of the drinking career, but more so in blacks than in whites. The total lifetime dose of alcohol was found to be positively correlated with diastolic but not systolic pressure, but only in black male alcoholics. The steeper slope of the regression of blood pressure versus lifetime total alcohol or duration of the drinking career in black alcoholics suggests greater cardiovascular susceptibility to alcohol toxicity as lifetime doses increase and as the drinking career lengthens.

Application of Bioelectric Impedance Methodology and Prediction Equations to Determine the Volume of Distribution for Ethanol

In large-scale epidemiologic studies of drinking behavior there is a need for simple and reliable estimates of the body water compartment of subjects. This, in turn, provides an estimate of the volume of distribution of ingested ethanol and a better estimate of tissue exposure levels than the use of total body weight as the volume of distribution for alcohol. The volume of distribution for ethanol (total body water, TBW) was estimated in a racially mixed group of 276 alcoholics and 166 nonalcoholics (aged 20-59 years) by means of bioelectric impedance methodology (BIA) and by means of prediction equations based upon age, body weight, and height. Estimations of mean TBW from BIA were found to be only slightly higher (1-4%) than those provided by the prediction equations. TBW values generated from both prediction equations were also highly correlated with TBW values obtained by impedance methodology, with the highest correlations observed in females (particularly black) and in alcoholics (particularly female).

Role of parasympathetic (vagal) cardiac control in elevated heart rates of smokers

Smokers may develop chronic increases in cardiac rate and alterations in cardiovascular control. If the increased mean heart rate (HR) in cigarette smokers is due in part to a deficit in vagal cardiac rate control, this should be reflected in a decreased amplitude of respiratory sinus arrhythmia (RSA). To test this hypothesis we studied 36 smokers and 36 non‐smokers, matched for age, race, gender and blood pressure. All subjects were studied in the supine and seated positions. Mean heart rate was determined from the ECG during 30 s of quiet breathing; RSA was determined for 10 consecutive deep (>50% vital capacity) slow (5‐7/min) breaths. Mean HRs in smokers were significantly higher than in non‐smokers, but the increases in mean HRs evoked by a shift from the supine to seated position were lower in smokers than in non‐smokers, suggesting that chronic tobacco use may alter the relative contributions of sympathetic and parasympathetic control of cardiac rate. Because neither the RSAs nor the position‐dependent increase in RSA were different between smokers and non‐smokers, we conclude that the elevated mean HRs in smokers were not the result of decreased respiratory or vasomotor modulation of vagal cardiac control, but instead were the result primarily of sympathetic stimulation.

RESPIRATORY SINUS ARRHYTHMIA (RSA) IN MAN: ALTERED INSPIRED O2 AND CO2

Publisher Summary At rest, the heart rate increases on inspiration and decreases on expiration. This oscillation in heart rate is called the respiratory sinus arrhythmia (RSA). A similar oscillation in heart rate is seen at the beginning of an inspiratory breathhold. This first oscillation during breath hold is defined as the zero frequency respiratory sinus arrhythmia. If breathing frequency is increased, the amplitude of this heart rate oscillation decreases, showing that the respiratory sinus arrhythmia is a frequency dependent phenomenon. Static lung volume and tidal volume also influence the amplitude of the heart rate oscillation. Increased lung volumes increase RSA. Although the influences of breathing frequency and tidal volume on RSA have been investigated independently, few attempts have been made to measure RSA while controlling tidal volume during different breathing frequencies. This chapter discusses the relationship of the tidal volume and breathing frequency to RSA in adult humans.