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The relationship between pulse‐arrival times and diastolic blood pressure was measured in 10 anesthetized dogs. The pulse‐arrival time was measured using the R‐wave of the electrocardiogram (ECG) as a time reference. Pulse‐transit time was also measured between the carotid and femoral pulses. Blood pressure was raised with epinephrine injected intravenously and lowered with vagal stimulation. In all cases, pulse arrival and transit times decreased with an increase in diastolic pressure for diastolic pressures ranging from 15 to 250 mmHg. The correlation between pulse‐arrival time and pressure was poorest when the ECG was used as a timing reference. The best correlation was found with true pulse‐transit time and diastolic pressure. When pulse‐transit time was used to compute pulse‐wave velocity, it was found to increase nearly linearly with blood pressure. From 90–100 mmHg, the pulse‐wave velocity increased typically by slightly less than six percent.

We have developed an ultrasonic technique for determining the dynamic Young's modulus of elasticity (E) of the canine aorta in vivo. Young's modulus was measured in the descending thoracic aorta (DTA) and the abdominal aorta (AA) of 12 dogs over a range of mean blood pressures from 40-200 mmHg. The vessels were excised and dynamic moduli were determined in vitro postmortem from pressure-volume curves. The data so obtained were compared to the in vivo values. In vivo and in vitro moduli increased exponentially with mean distending pressure (P). The equation of best fit for these data was of the form E= E0 exp(aP). Constants E0 and a depended on the site of measurement (AA or DTA) and upon the particular animal. In vivo and in vitro moduli were not significantly different in the AA (AA: in vivo E0 = 667 ± 382 mmHg, a = 0.017 ± 0.004 mmHg -1 ; in vitro E0 = 888 ± 367, a= 0.016 ± 0.002). However, in vivo moduli exceeded in vitro moduli in the DTA. (DTA: in vivo E0 = 687 ± 241, a = 0.016 ± 0.004; in vitro E0 = 349 ± 64, a= 0.018 ± 0.003). The increased stiffness of the DTA compared to the AA in vivo may be due to the in situ tethering of the aorta to the spine by the parietal pleura.

Although prospective studies of defibrillator shock overdose cannot be performed in man, the therapeutic indices of various defibrillating current waveforms can be measured in animals. We determined the ratios TD 50 /ED 50 and LD 50 / ED 50 (where TD 50 = median "toxic" or damageinducing dose, ED 50 = median effective or defibrillating dose, and LD 50 = median lethal dose) as measures of the therapeutic index for damped sine wave defibrillator shocks in dogs. Death of an animal and/or any degree of cardiac damage found by gross or microscopic examination were defined as harmful effects of shock, analogous to drug toxicity. In terms of peak current, the ED 50 , TD 50 , and LD 50 were 1.1, 5.8, and 24 amperes/ kg; the therapeutic indices were TD 50 /ED 50 = 5 for morphologic damage and LD 50 /ED 50 = 22 for death. In terms of delivered energy the ED 50 , TD 50 , and LD50 were 1.5, 30, and 470 joules/kg; the therapeutic indices were TD50/ED50 = 20 for damage and LD 50 /ED 50 = 320 for death. These data indicate a reasonable margin of safety for damped sine wave defibrillator shocks in dogs, and are consistent with reported incidences of suspected shock-induced damage in humans.

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