JOURNALOF
Vol. 39, No.
APPLIRD PHYSIOLOGY 3, September 1975.
Printed in U.S.A.
Ventricular carbon
function
monoxide
following
acute
exposure
STEPHAN H. CRAMLET, HOWARD H. ERICKSON, AND HARRY A. GORMAN USAF School of Aerospace Medicine, Aerospace Medical Division, Brooks Air Force Base, Texas 7823.5; and Surgery Laboratory, Colorado State University, Fort Collins, Colorado 80521
(15) flow transducers aorta. A solid-state
were placed around the ascending pressure transducer (model P- 17, Konigsberg Instruments, Pasadena, Calif.) was implanted on the endocardial surface in the apex of the left ventricle to measure left ventricular pressure (LVP), the peak rate of rise in that pressure (dP/dt), and dP/dt maximum divided by instantaneous left ventricular pressure (dP/dt)/IP. Flow transducers (23) and solid-state pressure transducers were calibrated before surgical implantation. A 12-gauge polyvinyl chloride catheter was placed within the left atrium to measure pressure. Lead wires of the pressure transducer, aortic flow probe, and the left atria1 catheter were passed subcutaneously to the left dorsal neck region and exteriorized. Ten days after the thoracotomy a polyvinyl catheter was placed in the left jugular vein and positioned in the right atrium. A minimum of 2 wk after thoractomy was allowed before ventricular function was evaluated. Left atria1 pressure was measured with a pressure transducer (model P23BB, Statham Instruments, Hato Ray, Puerto Rico); the sternal midline (with the dog lying on its right side) was the zero reference. Before each experiment the left ventricular diastolic pressure was zeroed to left atria1 pressure. Subcutaneous needle electrodes placed over the sternum were used to record electrocardiograms and heart rates. A 1,500 ppm carbon monoxide air mixture was inspired through a demand-type regulator (Scott Air-Pak, Scott Aviation, Lancaster, N.Y.) and low resistance valve (Hans Rudolph, Kansas City, MO.) to an endotracheal tube inserted in the tracheostomy. Blood HbCO increased at approximately 1 70 HbCO/min. HbCO was continuously measured by spectrophotometry until a desired level was reached. Ventricular function responses were elicited by infusing lactated Ringer solution, warmed to 38°C from an elevated reservoir, through the catheter in the right atrium. The average infusion was 560 ml in 78 s which was suflicient to allow a slow increase in left atria1 pressure and cardiac output until a steady state was achieved. The electrocardiogram, heart rate, left atria1 pressure, aortic blood flow, and left ventricular pressure were displayed on an oscillographic recorder (Offner type R, Spinco Div., Beckman Instruments, Palo Alto, Calif.) and recorded on magnetic tape (Ampex Corp., Redwood City, Calif.). Preinfusion, infusion, and postinfusion data were recorded both in the absence and in the presence of inspired carbon monoxide. The sequence of 10 %, 20 %, and 30 %
CRAMLET, STEPHAN H., HOWARD H. ERICKSON, AND HARRY A. GORMAN. Ventricular function follozoing acute carbon monoxide exposure. J. Appl. Physiol. 39(3) : 482-486. 1975.-Cardiac output function curves were used to investigate the effects of carbon monoxide on the heart in the conscious dog. Each dog was briefly exposed to 1,500 pprn carbon monoxide through a permanent tracheostomy. Immediately upon attaining either lo%, 20y0, or 30y0 HbCO a rapid infusion of Ringer’s lactate was given to test cardiac capabilities. The combined effects of carbon monoxide and infusion produced significant increases in cardiac output, heart rate, mean left ventricular pressure, dP/dt and (dP/dt)/IP. Cardiac output was sufficient to prevent peripheral hypoxia at all HbCO levels; however, there was evidence of impending cardiac depression beginning at 20% HbCO. ventricular function rate; left ventricular
curves; pressure;
cardiac output; left ventricular
stroke dP/dt
volume;
heart
CARBON MONOXIDE HYPOXIA is believed to harm those organs with high oxygen needs such as the heart. Carboxyhemoglobin (HbCO) 1evels are, however, seldom reported (2, 19) in those who have electrocardiographic irregularities even after carbon monoxide exposure. It is claimed that gross electrocardiogram chances are rarely seen until a 40 % HbCO has bien attained (2, 13), and no intimate correlation has been found between the degree of such change and the HbCO level (12, 22). Since 1967 ventricular output curves of conscious dogs have been thoroughly examined and used to assess the ability of the myocardium to pump blood under a wide variety of conditions (6). In our study, ventricular output curves were obtained to study the heart’s ability to respond when stressed with carbon monoxide at levels of 10 70, 20%, and 30 % HbCO. All experiments were conducted in the conscious dog chronically instrumented to measure aortic flow, left atria1 pressure, and left ventricular pressure. MATERIALS
AND
METHODS
Dogs, 13-20 kg, were premeditated with atropine 0.04 mg/kg and anesthetized intravenously with thiopental sodium 2.5 70. A permanent tracheostomy was then made. After 3 wk, anesthesia was again induced and a thoracotomy was made through the left fourth intercostal space. Electromagnetic (square-wave flow probe and flowmeter, Zepeda Instruments, Seattle, Wash.) or Doppler ultrasonic 482
Downloaded from www.physiology.org/journal/jappl at Midwestern Univ Lib (132.174.254.157) on February 13, 2019.
VENTRICULAR
FUNCTION
FOLLOWING
CO
483
EXPOSURE
HbCO exposures was varied. A minimum of 48 h elapsed between HbCO and control observations. Samples, taken from both the left and right atrium, were collected at indicated times (Tables 1 and 3). Hemoglobin, oxygen saturation, and HbCO saturation of arterial and venous blood were ascertained with a spectrophotometer (model 182 CO-oximeter, Instrumentation Laboratories, Lexington, Mass.). Arterial POT , PcoB , and pH were ascertained by a blood gas analyzer (model 3 13, Instrumentation Laboratories) and corrected to rectal temperature. Arterial samples were also collected for carbon monoxide determination by a HbCO extraction technique (1). Pyruvate and lactate were done with a rapid enzymatic method (Sigma Chemical Co., St. Louis, MO.). Analog and digital computer methods were used to process and analyze the data (14). During infusion the data for three cardiac cycles were averaged every 7.5 s. Ten cardiac cycles were averaged for the pre- and postcarbon monoxide (preinfusion and postinfusion) data. Two-way analysis of variance procedures were used to make all statistical comparisons to determine if significant changes resulted from carbon monoxide exposure and infusion. An average of the replicate runs was computed for each dog. Each standard error was computed as the variability of these averages. Standard errors are presented for descriptive purposes and were not used in statistical evaluations. Comparisons were made between preinfusion and postinfusion values in the absence of inspired carbon monoxide. For each of the 1070, 2070, and 30% HbCO experiments, comparisons were made between pre-HbCO and post-HbCO values and preinfusion versus postinfusion. TABLE 1. Efects of carbon monoxide on respiratory parameters in blood Venous HbCO, %
N
Preco
N
postco
P
N
Preco
10
mmHg 20 30 10
PCo2,
mmHg 20 30 Oxygen sat, %
10 20 30
Lactate PYruvate ratio
:
10 20 30
NS
8 89.7 slt4.2 8 93.5 zt2.7 5 92.5 It2.4 8 27.5 ztl.8 8 29.4 ztl .l 5 29.8 ztl.6 8 93.3 ho.6 8 93.5 Ito. 5 94.6 zto.5 3 15.5 zk5.7 4 12.8 It6.8 4 10.8 It7.0
Values are means = not significant.
N
postco
P
-
--Po2,
k
7 84.8 h5.2 7 79.8 zk4.5 4 84.5 zt4.2 7 27.3 ztl.8 7 27.4 zk1.8 4 24.4 AA.7 7 80.6 Ikl.2 7 69.3 AA.4 4 61.2 &2.5 4 7.9 zk1.3 4 11.3 rt4.3 4 12.7 zt2.2 SE;
NS
Vol. 39, No.
APPLIRD PHYSIOLOGY 3, September 1975.
Printed in U.S.A.
Ventricular carbon
function
monoxide
following
acute
exposure
STEPHAN H. CRAMLET, HOWARD H. ERICKSON, AND HARRY A. GORMAN USAF School of Aerospace Medicine, Aerospace Medical Division, Brooks Air Force Base, Texas 7823.5; and Surgery Laboratory, Colorado State University, Fort Collins, Colorado 80521
(15) flow transducers aorta. A solid-state
were placed around the ascending pressure transducer (model P- 17, Konigsberg Instruments, Pasadena, Calif.) was implanted on the endocardial surface in the apex of the left ventricle to measure left ventricular pressure (LVP), the peak rate of rise in that pressure (dP/dt), and dP/dt maximum divided by instantaneous left ventricular pressure (dP/dt)/IP. Flow transducers (23) and solid-state pressure transducers were calibrated before surgical implantation. A 12-gauge polyvinyl chloride catheter was placed within the left atrium to measure pressure. Lead wires of the pressure transducer, aortic flow probe, and the left atria1 catheter were passed subcutaneously to the left dorsal neck region and exteriorized. Ten days after the thoracotomy a polyvinyl catheter was placed in the left jugular vein and positioned in the right atrium. A minimum of 2 wk after thoractomy was allowed before ventricular function was evaluated. Left atria1 pressure was measured with a pressure transducer (model P23BB, Statham Instruments, Hato Ray, Puerto Rico); the sternal midline (with the dog lying on its right side) was the zero reference. Before each experiment the left ventricular diastolic pressure was zeroed to left atria1 pressure. Subcutaneous needle electrodes placed over the sternum were used to record electrocardiograms and heart rates. A 1,500 ppm carbon monoxide air mixture was inspired through a demand-type regulator (Scott Air-Pak, Scott Aviation, Lancaster, N.Y.) and low resistance valve (Hans Rudolph, Kansas City, MO.) to an endotracheal tube inserted in the tracheostomy. Blood HbCO increased at approximately 1 70 HbCO/min. HbCO was continuously measured by spectrophotometry until a desired level was reached. Ventricular function responses were elicited by infusing lactated Ringer solution, warmed to 38°C from an elevated reservoir, through the catheter in the right atrium. The average infusion was 560 ml in 78 s which was suflicient to allow a slow increase in left atria1 pressure and cardiac output until a steady state was achieved. The electrocardiogram, heart rate, left atria1 pressure, aortic blood flow, and left ventricular pressure were displayed on an oscillographic recorder (Offner type R, Spinco Div., Beckman Instruments, Palo Alto, Calif.) and recorded on magnetic tape (Ampex Corp., Redwood City, Calif.). Preinfusion, infusion, and postinfusion data were recorded both in the absence and in the presence of inspired carbon monoxide. The sequence of 10 %, 20 %, and 30 %
CRAMLET, STEPHAN H., HOWARD H. ERICKSON, AND HARRY A. GORMAN. Ventricular function follozoing acute carbon monoxide exposure. J. Appl. Physiol. 39(3) : 482-486. 1975.-Cardiac output function curves were used to investigate the effects of carbon monoxide on the heart in the conscious dog. Each dog was briefly exposed to 1,500 pprn carbon monoxide through a permanent tracheostomy. Immediately upon attaining either lo%, 20y0, or 30y0 HbCO a rapid infusion of Ringer’s lactate was given to test cardiac capabilities. The combined effects of carbon monoxide and infusion produced significant increases in cardiac output, heart rate, mean left ventricular pressure, dP/dt and (dP/dt)/IP. Cardiac output was sufficient to prevent peripheral hypoxia at all HbCO levels; however, there was evidence of impending cardiac depression beginning at 20% HbCO. ventricular function rate; left ventricular
curves; pressure;
cardiac output; left ventricular
stroke dP/dt
volume;
heart
CARBON MONOXIDE HYPOXIA is believed to harm those organs with high oxygen needs such as the heart. Carboxyhemoglobin (HbCO) 1evels are, however, seldom reported (2, 19) in those who have electrocardiographic irregularities even after carbon monoxide exposure. It is claimed that gross electrocardiogram chances are rarely seen until a 40 % HbCO has bien attained (2, 13), and no intimate correlation has been found between the degree of such change and the HbCO level (12, 22). Since 1967 ventricular output curves of conscious dogs have been thoroughly examined and used to assess the ability of the myocardium to pump blood under a wide variety of conditions (6). In our study, ventricular output curves were obtained to study the heart’s ability to respond when stressed with carbon monoxide at levels of 10 70, 20%, and 30 % HbCO. All experiments were conducted in the conscious dog chronically instrumented to measure aortic flow, left atria1 pressure, and left ventricular pressure. MATERIALS
AND
METHODS
Dogs, 13-20 kg, were premeditated with atropine 0.04 mg/kg and anesthetized intravenously with thiopental sodium 2.5 70. A permanent tracheostomy was then made. After 3 wk, anesthesia was again induced and a thoracotomy was made through the left fourth intercostal space. Electromagnetic (square-wave flow probe and flowmeter, Zepeda Instruments, Seattle, Wash.) or Doppler ultrasonic 482
Downloaded from www.physiology.org/journal/jappl at Midwestern Univ Lib (132.174.254.157) on February 13, 2019.
VENTRICULAR
FUNCTION
FOLLOWING
CO
483
EXPOSURE
HbCO exposures was varied. A minimum of 48 h elapsed between HbCO and control observations. Samples, taken from both the left and right atrium, were collected at indicated times (Tables 1 and 3). Hemoglobin, oxygen saturation, and HbCO saturation of arterial and venous blood were ascertained with a spectrophotometer (model 182 CO-oximeter, Instrumentation Laboratories, Lexington, Mass.). Arterial POT , PcoB , and pH were ascertained by a blood gas analyzer (model 3 13, Instrumentation Laboratories) and corrected to rectal temperature. Arterial samples were also collected for carbon monoxide determination by a HbCO extraction technique (1). Pyruvate and lactate were done with a rapid enzymatic method (Sigma Chemical Co., St. Louis, MO.). Analog and digital computer methods were used to process and analyze the data (14). During infusion the data for three cardiac cycles were averaged every 7.5 s. Ten cardiac cycles were averaged for the pre- and postcarbon monoxide (preinfusion and postinfusion) data. Two-way analysis of variance procedures were used to make all statistical comparisons to determine if significant changes resulted from carbon monoxide exposure and infusion. An average of the replicate runs was computed for each dog. Each standard error was computed as the variability of these averages. Standard errors are presented for descriptive purposes and were not used in statistical evaluations. Comparisons were made between preinfusion and postinfusion values in the absence of inspired carbon monoxide. For each of the 1070, 2070, and 30% HbCO experiments, comparisons were made between pre-HbCO and post-HbCO values and preinfusion versus postinfusion. TABLE 1. Efects of carbon monoxide on respiratory parameters in blood Venous HbCO, %
N
Preco
N
postco
P
N
Preco
10
mmHg 20 30 10
PCo2,
mmHg 20 30 Oxygen sat, %
10 20 30
Lactate PYruvate ratio
:
10 20 30
NS
8 89.7 slt4.2 8 93.5 zt2.7 5 92.5 It2.4 8 27.5 ztl.8 8 29.4 ztl .l 5 29.8 ztl.6 8 93.3 ho.6 8 93.5 Ito. 5 94.6 zto.5 3 15.5 zk5.7 4 12.8 It6.8 4 10.8 It7.0
Values are means = not significant.
N
postco
P
-
--Po2,
k
7 84.8 h5.2 7 79.8 zk4.5 4 84.5 zt4.2 7 27.3 ztl.8 7 27.4 zk1.8 4 24.4 AA.7 7 80.6 Ikl.2 7 69.3 AA.4 4 61.2 &2.5 4 7.9 zk1.3 4 11.3 rt4.3 4 12.7 zt2.2 SE;
NS
