KIN 540




This is the pathophysiologic tale of two young domestic pigs, both barrows, which served as experimental subjects in a study of hemorrhagic hypotension.  One week prior to the study a chronic carotid catheter was surgically implanted in each animal and exited from the dorsal surface of the neck.  On the day of study each animal was brought into the laboratory in a small, 2 foot by 4 foot, mobile cage and was provided with bedding material.  After 15 minutes or so of chewing, rooting, grunting and bedding rearrangement they voluntarily assumed a recumbent position at which point the carotid catheter was connected to a 3-way stopcock and appropriate pressure tubing, transducers, etc., for the removal of blood and the measurement of functional variables.  After 30 additional minutes of unrestrained, recumbent rest two sets of baseline measurements were made at 15 minute intervals.  Then 60 percent of the estimated blood volume was removed over a one-hour period; blood loss was based, arbitrarily, on an exponential scale such that 10 percent increments of the total blood volume were removed uniformly over successive intervals of about 7, 7.5, 8.5, 10, 12, and 15 minutes.  The various functional measurements were repeated immediately after hemorrhage, at 15 minute intervals during the first two hours of spontaneous recovery and both pigs became nauseous and vomited during the course of hemorrhage.  In both instances these effects were observed when slightly over 40 percent of the estimated blood volume had been removed.  For the most part, both pigs displayed similar physiological and biochemical characteristics immediately after hemorrhage.  Subsequently, however, the functional changes associated with spontaneous recovery differed markedly in the two animals.  One pig, number 54, survived and appeared reasonable healthy 24 hours after hemorrhage.  The other, number 35, showed early signs of recovery but ultimately deteriorated and died at two hours and 50 minutes into the recovery period. 

The data collected from these animals are depicted in Figures 1 through 23.  Some of the pathophysiologic questions raised by these data are listed immediately thereafter. 

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  1. One usually associates tachycardia with hemorrhagic hypotension, yet neither pig showed such an effect immediately after hemorrhage.  How can this be explained?
  2. During recovery from hemorrhage, pig 53 showed, before death, higher heart rates and mean arterial pressures than pig 54 (Figures 1 and 2).  On the basis of the data presented in the other figures what could account for this difference?  In pig 53 what could account for the terminal fall in arterial pressure during the last 15 minutes of study even though tachycardia was maintained?
  3. In pig 53 was death attributable to myocardial or to pulmonary dysfunction.
  4. Pig 54 displayed higher respiratory rates than pig 53 during early recovery (Figure 3) and this was associated with an increase in arterial Po2 (Figure 4.).  What can be inferred from this relationship?  Why would arterial Po2 decrease (dotted line) immediately before death in pig 53?
  5. Immediately after hemorrhage pig 53 had a higher arterial Pco2 than pig 54 but thereafter the values in pig 54 exceeded those in pig 53 (Figure 5).  What could account for these results?  Why did arterial Pco2 increase (dotted line) immediately before death in pig 53?  What would account for the gradual rise in Pco2 during recovery of pig 54?
  6. What could account for the slightly elevated arterial pH values observed in pig 54 (Figure 6) during the early stages of recovery?  What could account for the decreased values observed in pig 53?  What factor might have attenuated the effect seen in pig 54?  What factor might have enhanced the effect seen in pig 53?
  7. During recovery, why did arterial bicarbonate values (Figure 7) continue to decrease in pig 53 but revert toward normal values in pig 54?  Why would the values increase in pig 53 immediately before death (dotted line)?
  8. During the control period body pigs displayed positive base excess values (Figure 8).  How can this be explained?  What is responsible for the decrements in base excess during early recovery ob both pigs?  Why did the values continue to decrease in pig 53 but revert toward normal in pig 54?
  9. What is the probably mechanism responsible for the elevated arterial lactate concentrations (Figure 9) of both pigs during the recovery period?  What could have enhanced the elevation seen in pig 54?  What is the most likely tissue source for the lactate elevations?
  10. Immediately after hemorrhage and for the first hour of recovery progressively reduced hematocrit values were observed in both pigs (Figure10).  Thereafter, the trend continued in pig 54 but values reverting toward normal were observed in pig 53.  What could count for the comparable results observed during the first hour of recovery and the disparate results observed during the second hour?
  11. What is the most likely tissue source for the elevated glucose values seen (Figure 11) in the recovery period?  What is the probable mechanism responsible for this hyperglycemia?  Would the glucose changes have any effect of body water metabolism?  What cold account for the subnormal values recorded just before death in pig 53 and the similar tendency during mid-recovery in pig 54?  What is the likely source and responsible mechanism underlying the gradual rise in plasma glucose in pig 54 during the last 2 hours of recovery?
  12. What could account for the progressive rise in plasma urea concentration seen in both pigs during the recovery period?  What are the physiologic/clinical implications of the continued urea elevation recorded in pig 54?
  13. What is the most likely cellular source of the plasma creatine increase seen in both pigs during the recovery period?  What metabolic mechanism probably underlies these increments?  What are the long term implications of the sustained elevation seen at the end of the recovery measurements in pig 54?
  14. During the recovery period, pig 53 showed progressively increased values for the concentrations of sodium, potassium and magnesium in arterial plasma (Figures 14, 15, and 16).  What cellular mechanisms are probably responsible for these changes?  Why would sodium be expected to decrease and potassium values continue to increase (dotted lines) as this animal neared death?  Pig 54 showed no change in plasma sodium concentration, a slight decrease in potassium concentration and a moderate increase in magnesium concentration during recovery.  What cellular or other factors could account for these changes?
  15. What could account for the increased values for phosphate and total cation concentration in arterial plasma (Figures 17 and 18) taken from pig 53 during the recovery period?
  16. Pig 53 showed increased arterial plasma concentrations for all of the serum enzymes that were measured (Figures 19, 20, 21, 22, and 23).  What are the most likely tissue sources of these enzymes?  What could account for the slight concentration decrements recorded for some of the enzymes during early recovery?  What other plasma enzyme measurements would be needed to more precisely localize areas of tissue or organ damage?
  17. What other interesting questions do these data suggest?

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