Resuscitation, 24 (1992) 55-60 Elsevier Scientific Publishers Ireland Ltd.
55
The role of central venous oximetry, lactic acid concentration and shock index in the evaluation of clinical shock: a review Mohamed Y. Rady Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202 (USA)
(Received June lOth, 1992; Accepted July 3rd, 1992)
Initial therapy of shock in the emergency department emphasizes the normalization of hemodynamic variables e.g. heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP) rather than optimization of systemic and regional oxgenation. Central venous oximetry (S,o& arterial lactic acid concentrations (Lact) and the shock index (SI) were examined during initial hemodynamic stabilization of clinical shock in the emergency room. Although initial therapy normalized MAP, CVP and HR; &,,oz, Lact and SI continued to be abnormal indicating inadequate systemic oxygenation and left ventricular (LV) performance. Measurement of S,q, Lact and SI may provide valuable additonal information on the adequacy of systemic oxygenation and LV function during initial therapy of shock. This may identify patients who require further monitoring and intervention to optimize systemic oxygen transport and cardiac performance and reduce their morbidity and mortality.
Key words: shock; central venous oximetry; lactic acid concentration;
systemic oxygenation; shock index
The emergency department evaluation and therapy of shock is commonly guided by physiologic variables of mean arterial pressure (MAP), central venous pressure (CVP) and heart rate (HR). Several clinical studies have shown that normalization of these hemodynamic variables does not indicate the underlying derangement of systemic and regional oxygenation lw7. Inadequate systemic and regional oxygenation correlate with increased morbidity and mortality in shocklW4. Early therapy directed to relieve tissue hypoxia and to repay systemic oxygen debt incurred due to deficit in O2 utilization has been shown to improve clinical outcome in shock irrespective of its etiology 5-7. Therefore, initial resuscitation of shock in the emergency department should be guided by its impact on systemic or regional oxygen supply in relation to oxygen demand. Systemic and regional tissue oxygenation can be examined directly by measurement of systemic oxygen delivery (DO*) and consumption (Voz) or indirectly by mixed venous oxygen saturation (Z&O,)and lactic acid Correspondence to: Mohamed Y. Rady, Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202, USA.
0300-9572/92/%05.00 0 1992 Elsevier Scientific Publishers Ireland Ltd. Printed and Published in Ireland
56
venous
Mixed
02
4
75%
Stress
*
Pain
.
Hyperthermia
??
b
+
v
f’vo, .
saturation
f’
DO2
+@
DO2
vo2
+
PaC2
* f
Pa02
a
Hypothermia
??
f
Hg cont.
*f
Hg cont.
*
Anaesthesia
??
f
Cardiac output
*f
Cardiac output
Shtverlng
Determinants
of total
body 0,
balance
Fii. 1. Determinants of mixed venous oxygen saturation (S,O~) and systemic oxygen balance; VO,, oxygen consumption, and Doz. oxygen delivery.
concentration (Fig. 1). Although VO, can be measured noninvasively by indirect calorimetry, reliable measurement of Do2 requires the insertion of thermodilution pulmonary artery catheter to measure cardiac output’. S,O, is measured on mixed venous blood which is obtained through a pulmonary artery catheter. Central venous oximetry (Scvo2) utilizes the fiberoptic technology to continuously measure oxygen saturation (oxyhemoglobin fraction of total hemoglobin) in the right atrium9. The oximetric catheter can be inserted through a central vein and correctly positioned with relative ease. This review examines the role of Scvoz, in conjunction with arterial blood lactic acid concentration and shock index (ratio of heart rate to systolic arterial pressure) to guide the adequacy of resuscitation in clinical shock. Reduction in pulmonary arterial mixed venous oxygen saturation (SO,) has been shown to be an indicator of severity of hemorrhagic, traumatic and cardiogenic shock and a predictor of poor outcome 7,10-‘4. Persistent reduction in Svo2 and increased systemic oxygen extraction after initial aggressive treatment was observed Table I. Clinical studies showing reduced mixed venous oxygen saturation (S,OJ and increased oxygen extraction ratio (OER) in nonsurvivors following initial treatment of traumatic shock. These values were obtained within 3 h of trauma. Study
Sturm et al. 1979 Kazarian et al. 1980 Rady et al. 1992
Nonsurvivors
Survivors S”O2
OER
w2
OER
75 46 82
24 52 19
70 36 73
28 60 29
51
in patients who had increased incidence of multiple organ system dysfunction and mortality (Table I) “J’J~ . These abnormalities in S,O, and OER were observed after adequate resuscitation to nomalize HR, MAP, CVP and pulmonary capillary pressure in nonsurvivors. Svoz has been shown to correlate with ScvoZ in experimental and clinical studies’5y’6. Continuous Scvo2 oximetry was of value in monitoring human cardiopulmonary resuscitationg. S,O, of greater than 40% was predictive of a return of spontaneous circulation following cardiac arrest. A prospective study of continuous ScvoZ oximetry showed that 50% of patients treated for shock in the emergency department continued to have low ScvoZ after normalization of HR, MAP and CVP (Table II)17. This was suggestive of increased oxygen extraction because of inadequate DO* to meet systemic Vo2 “J . In clinical shock a significant correlation was observed between Sc,,02 and Svo2 at ScvoZ values greater than 50%16. This correlation, however, was poor when Scvoa was less than 50%. Scvoq consistently underestimated S,O, by up to 20%. This may be due to inadequate mixing of superior and inferior vena cava blood in the right atrium especially at low cardiac output. Furthermore, the mixing of coronary sinus and thebsian venous drainage of the myocardium with systemic venous blood is usually complete in the right ventricle*‘. Therefore, at low Scvo2, true Svo2 value may be significantly lower and can limit the use of Scvo2 in indicating the true balance of systemic VOWin relation to DO*. Scvo2 was normal or raised in 50% of patients treated in the emergency department (Table II). However, these patients had elevated arterial lactic acid concentration. It seemed that Vo2 was inadequate to repay the oxygen debt in this group of patients (i.e. an O2 utilization defect)17. Defect in peripheral O2 utilization and extraction may limit the usefulness of Scvo2 in assessing the adequacy of global and
Table II.
Hemodynamic and oxygenation variables in Group I and II after initial resuscitation of variety of shock states (traumatic, hemorrhagaic, septic and cardiogenic). Values shown are means * SD. Group I includes patients with abnormally low E$.,o~. Group II includes patients with normal Scvol.
Variable N
HR (beats/mm) MAP (mmHg) CVP (cmH,O) SI Hg Wdl) S,oz@) ~,o,W)
Lact (mM/l)
Group I
8 110 87 12 0.9 11 99 48 2.2
f 15 *15 *4 f 0.2 *2 3~9; f 0.8
Group II 8 104 81 12 0.9 10 99 81 1.0
?? 14 f 21 *I * 0.2 *2
zt8 f 8.0
HR, heart rate; MAP, mean arterial pressure; CVP, central venous pressure; SI, shock index (heart rate/systolic arterial pressure); I-Ig, hemoglobin concentration; Sao2, arterial oxygen saturation; Scvo2, central venous oxygen saturation; Lact, arterial blood lactic acid concentration. *P < 0.01 Group I versus Group II (see Ref. 17).
58
regional oxygenation’Y. This was observed in patients with trauma, sepsis, multiple organ dysfunction, post-cardiac arrest cardiogenic shock and hypothermia21-26. Therefore, simultaneous measurement of Vo2 by indirect calorimetry and arterial lactic acid concentration clearance are essential to identify the underlying O2 utilization defect in these states. Arterial lactic acid concentration has been shown to be raised in variety of shock states2’. This usually indicates anaerobic metabolism, tissue ischemia and accumulation of oxygen debt28,29.Previous studies attempted to correlate the mortality rate and lactic acid concentration in different shock states2’. However, it is unreliable to infer the severity of ischemic tissue insult or the magnitude of oxygen debt from blood lactic acid concentration. Aerobic glycolysis and increased production of pyruvate and lactate has been observed in hyperdynamic hypermetabolic states3’. Aerobic production of blood lactic acid may be distinguished from anerobic production by measuring blood lactate to pyruvate concentrations ratio. This ratio is increased during anaerobic metabolism. Furthermore, the relative rate of lactate production by anaerobic metabolism and its elimination rate by the hepatic and renal systems determine blood lactic acid concentration and this may limit its accuracy to quantify oxygen debt in shock 3’,32. Alactic oxygen debt i.e. the presence of significant tissue ischemia with normal blood lactic acid concentration was first described by Cain in experimental shock model in which systemic DO, and $40~ were significantly reduced and lactic acid concentration was normalz9. Similar pattern was observed in 50% of patients presenting in shock and resuscitated in the emergency department (Table II)“. The utilization of oxygen reserve in residual lung volumes and bound to hemoglobin and myoglobin as well as the intracellular store of high energy phosphate bonds may contribute to alactic oxygen debt. Anaerobic metabolism with normal lactic acid concentration can also be seen in patients with augmented hepatic and renal clearance of lactic acid3’. It seems that the rate of clearance of an already elevated lactic acid is more valuable than individual measurements to predict outcome in shock33. This may reflect either an adequate tissue oxygenation to repay the oxygen debt or alternatively an augmented hepatic and renal function to clear the extracellular pool of lactate. The shock index (SI) i.e. the ratio of heart rate to systolic arterial pressure, was found to be elevated in patients with either low Scvo2 and normal lactate or normal/ high S,O, and elevated lactate (Table II). SI was shown to correlate with left ventricular stroke work (LVSW) in hypodynamic and hyperdynamic shock34. Persistent elevation of SI (normal range 0.5-0.7) indicated poor recovery of LVSW after treatment in the emergency department. LVSW is dependent on preload, afterload, diastolic compliance and systolic contractility of left ventricle LVi4 and any of these factors singly or in combination may contribute to the elevation of SI. A previous study showed that the SI was of limited value to assess the adequacy of systemic oxygenation in normodynamic and hyperdynamic shock34). Although Scvo2 and arterial lactic acid concentration may indicate indirectly the adequacy of systemic oxygenation, SI provides an additional information on the performance of LV. Reduced Scvo2, elevated arterial lactic acid concentration and persistent elevation of SI in patients resuscitated in the emergency department indicate global ischemia and LV dysfunction. Such a group of patients require
59
invasive hemodynamic monitoring to optimize LV function, systemic Do2 and VOW and to improve their outcome. CONCLUSION
Initial therapy based on stabilization and normalization of MAP, CVP and HR in clinical shock does not necessarily correct the primary derangement in systemic oxygenation. Monitoring of ScvoZ, arterial lactic acid concentration and SI may provide additional information to assess the adequacy of systemic oxygenation and LV function in the emergency department. REFERENCES
1
2 3 4 5 6 I 8 9 10 11 12 13 14 15 16 17
18 19
Baek SM, Makabali G, Bryan-Brown CW et al, Plasma expansion in surgical patients with high central venous pressure (CVP); the relationship of blood volume to hematocrit, CVP, pulmonary wedge pressure and cardiorespiratory changes. Surgery 1975; 78: 304-315. Shoemaker WC, Appel PL, Bland R et al. Clinical trial of an algorithm for outcome prediction in acute circulatory failure. Crit Care Med 1982; 10: 390-397. Bland R, Shoemaker WC, Abraham E et al. Haemodynamic and oxygen transport patterns in surviving and nonsurviving postoperative patients. Crit Care Med 1985; 13: 85-90. Shoemaker WC. Relationship of oxygen transport patterns to the pathophysiology and therapy of shock states. Int Care Med 1987; 13: 230-243. Shoemaker WC, Appel PL, Waxman K et al. Clinical trial of survivors’ cardiorespiratory patterns as therapeutic goals in critically ill postoperative patients. Crit Care Med 1982; 10: 398-403. Shoemaker WC, Appel PL, Kram HB et al. Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988; 94: 1176-l 186. Shoemaker WC, Appel PL, Kram HB. Tissue oxygen debt as a determinant of lethal and nonlethal postoperative organ failure. Crit Care Med 1988; 16: 1117-I 120. Siegel LC, Pearl RG. Noninvasive cardiac output measurment: troubled technologies and troubled studies. Anesth Analg 1992; 74: 790-792 Rivers EP, Martin GB, Rady MY et al. The clinical implication of continuous central venous oxygen saturation monitoring during human CPR. Ann Emerg Med 1992. In press. Sturm JA, Lewis FR, Trentz 0 et al. Cardiopulmonary parameters and prognosis after severe multiple trauma. J Trauma 1979; 19: 305-318. Kazarian K, Del Guercio LR. The use of mixed venous blood gas determinations in traumatic shock. Ann Emerg Med 1980; 9: 179-182. Kasnitz P, Druger GL, Yorra F et al. Mixed venous oxygen tension and hyperlactataemia severe cardiopulmonary disease. J Am Med Assoc 1976; 236: 570-574. Richard C, Thuillez C, Pezzano M et al. Relationship between mixed venous oxygen saturation and cardiac index in patients with chronic congestive heart failure. Chest 1989; 95: 1289-1294. Rady MY, Edwards JD, Nightingale P. Early cardiorespiratory findings after severe blunt thoracic trauma and their relation to outcome. Br J Surg 1992; 79: 65-68 Scalea TM, Houman M, Fuortes M et al. Central venous blood oxygen saturation: An early accurate measurement of volume during hemorrhage. J Trauma 1988; 28: 725-732. Tahvanainen J, Meretoja 0, Nikki P. Can central venous blood replace mixed venous blood samples? Crit Care Med 1982; 10: 758-761. Rady MY, Rivers EP, Martin GB et al. Continuous central venous oximetry and the shock index in the emeregency department: its use in the evaluation of clinical shock. Am J Emg Med 1992. In press. Reinhardt, K, Rudolph T, Bredle DL et al. Comparison of central-venous to mixed-venous oxygen saturation during changes in oxygen supply/demand. Chest 1989; 95: 1216. Reinhardt K. Principles and practice of SvOl monitoring. Int Care World 1988; 5: 121-124.
60
20 21 22 23 24 25
26 21 28 29 30 31 32 33 34
Nelson D. Mixed venous oximetery. In: Synder JV, Pinskey MR, editors. Oxygen transport in the critically ill. Year Book Medical Publishers Inc, 1987: 235-248. Shah DM, Newell JC, Saba TM. Defects in peripheral oxygen utilization following trauma and shock. Arch Surg, 1981; 116: 1277-1281. Edwards JD, Brown CX, Nightingale P et al. Use of cardiorespiratory values as therapeutic goals in septic shock. Crit Care Med 1989; 17: 1098-1103. Wolf YG, Cotev S, Perel A et al. Dependence of oxygen consumption on cardiac output in sepsis. Crit Care Med 1987; 15: 198-203. Demling RH. Current concepts on adult respiratory distress syndrome. Circ Shock 1990; 30: 297-309. Rivers EP, Rady MY, Martin GB et al. Supranormal mixed venous oxygen saturation after resuscitation from human cardiac arrest: a charaterization of systemic oxygen utilization defect. Chest 1992. In press. Black PR, Devanter SV, Cohn LH. Effects of hypothermia on systemic and organ system metabolism and function. J Surg Res 1976; 20: 49-54. Vitek V, Cowley. Blood lactate in the prognosis of various forms of shock. Ann Surg 1971; 173: 308-313. Cain SM. Oz deficit incurred during hypoxia and its relation to lactate and excess lactate. Am J Physiol 1967; 213 (1): 57-63. Cain SM. Relative rates of arterial lactate and oxygen deficit accumulation in hypoxic dogs. Am J Physiol 1973; 224: 1190-l 194. Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med 1992; 20: 80. Perret C, Enrico J, Poli S. Acid-base disturbances and lactate metabolism in shock. Eur J Clin Invest 1970; 1: 387-390. Wall PJ, Record CO. Lactate elimination in man: Effects of lactate concentration and hepatic dysfunction. Eur J Clin Invest 1979; 9: 397-404. Bakker J, Leon M, Coffemils M et al. Serial blood lactate levels can predict multiple organ failure in septic shock patients. Crit Care Med 1992; 20: S56. Rady MY, Nightingale P, Little RA, Edwards JD. Shock index: a re-evaluation in acute circulatory failure. Resuscitation 1992; 23 (3): 227-234.
55
The role of central venous oximetry, lactic acid concentration and shock index in the evaluation of clinical shock: a review Mohamed Y. Rady Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202 (USA)
(Received June lOth, 1992; Accepted July 3rd, 1992)
Initial therapy of shock in the emergency department emphasizes the normalization of hemodynamic variables e.g. heart rate (HR), mean arterial pressure (MAP), central venous pressure (CVP) rather than optimization of systemic and regional oxgenation. Central venous oximetry (S,o& arterial lactic acid concentrations (Lact) and the shock index (SI) were examined during initial hemodynamic stabilization of clinical shock in the emergency room. Although initial therapy normalized MAP, CVP and HR; &,,oz, Lact and SI continued to be abnormal indicating inadequate systemic oxygenation and left ventricular (LV) performance. Measurement of S,q, Lact and SI may provide valuable additonal information on the adequacy of systemic oxygenation and LV function during initial therapy of shock. This may identify patients who require further monitoring and intervention to optimize systemic oxygen transport and cardiac performance and reduce their morbidity and mortality.
Key words: shock; central venous oximetry; lactic acid concentration;
systemic oxygenation; shock index
The emergency department evaluation and therapy of shock is commonly guided by physiologic variables of mean arterial pressure (MAP), central venous pressure (CVP) and heart rate (HR). Several clinical studies have shown that normalization of these hemodynamic variables does not indicate the underlying derangement of systemic and regional oxygenation lw7. Inadequate systemic and regional oxygenation correlate with increased morbidity and mortality in shocklW4. Early therapy directed to relieve tissue hypoxia and to repay systemic oxygen debt incurred due to deficit in O2 utilization has been shown to improve clinical outcome in shock irrespective of its etiology 5-7. Therefore, initial resuscitation of shock in the emergency department should be guided by its impact on systemic or regional oxygen supply in relation to oxygen demand. Systemic and regional tissue oxygenation can be examined directly by measurement of systemic oxygen delivery (DO*) and consumption (Voz) or indirectly by mixed venous oxygen saturation (Z&O,)and lactic acid Correspondence to: Mohamed Y. Rady, Department of Emergency Medicine, Henry Ford Hospital, 2799 West Grand Boulevard, Detroit, MI 48202, USA.
0300-9572/92/%05.00 0 1992 Elsevier Scientific Publishers Ireland Ltd. Printed and Published in Ireland
56
venous
Mixed
02
4
75%
Stress
*
Pain
.
Hyperthermia
??
b
+
v
f’vo, .
saturation
f’
DO2
+@
DO2
vo2
+
PaC2
* f
Pa02
a
Hypothermia
??
f
Hg cont.
*f
Hg cont.
*
Anaesthesia
??
f
Cardiac output
*f
Cardiac output
Shtverlng
Determinants
of total
body 0,
balance
Fii. 1. Determinants of mixed venous oxygen saturation (S,O~) and systemic oxygen balance; VO,, oxygen consumption, and Doz. oxygen delivery.
concentration (Fig. 1). Although VO, can be measured noninvasively by indirect calorimetry, reliable measurement of Do2 requires the insertion of thermodilution pulmonary artery catheter to measure cardiac output’. S,O, is measured on mixed venous blood which is obtained through a pulmonary artery catheter. Central venous oximetry (Scvo2) utilizes the fiberoptic technology to continuously measure oxygen saturation (oxyhemoglobin fraction of total hemoglobin) in the right atrium9. The oximetric catheter can be inserted through a central vein and correctly positioned with relative ease. This review examines the role of Scvoz, in conjunction with arterial blood lactic acid concentration and shock index (ratio of heart rate to systolic arterial pressure) to guide the adequacy of resuscitation in clinical shock. Reduction in pulmonary arterial mixed venous oxygen saturation (SO,) has been shown to be an indicator of severity of hemorrhagic, traumatic and cardiogenic shock and a predictor of poor outcome 7,10-‘4. Persistent reduction in Svo2 and increased systemic oxygen extraction after initial aggressive treatment was observed Table I. Clinical studies showing reduced mixed venous oxygen saturation (S,OJ and increased oxygen extraction ratio (OER) in nonsurvivors following initial treatment of traumatic shock. These values were obtained within 3 h of trauma. Study
Sturm et al. 1979 Kazarian et al. 1980 Rady et al. 1992
Nonsurvivors
Survivors S”O2
OER
w2
OER
75 46 82
24 52 19
70 36 73
28 60 29
51
in patients who had increased incidence of multiple organ system dysfunction and mortality (Table I) “J’J~ . These abnormalities in S,O, and OER were observed after adequate resuscitation to nomalize HR, MAP, CVP and pulmonary capillary pressure in nonsurvivors. Svoz has been shown to correlate with ScvoZ in experimental and clinical studies’5y’6. Continuous Scvo2 oximetry was of value in monitoring human cardiopulmonary resuscitationg. S,O, of greater than 40% was predictive of a return of spontaneous circulation following cardiac arrest. A prospective study of continuous ScvoZ oximetry showed that 50% of patients treated for shock in the emergency department continued to have low ScvoZ after normalization of HR, MAP and CVP (Table II)17. This was suggestive of increased oxygen extraction because of inadequate DO* to meet systemic Vo2 “J . In clinical shock a significant correlation was observed between Sc,,02 and Svo2 at ScvoZ values greater than 50%16. This correlation, however, was poor when Scvoa was less than 50%. Scvoq consistently underestimated S,O, by up to 20%. This may be due to inadequate mixing of superior and inferior vena cava blood in the right atrium especially at low cardiac output. Furthermore, the mixing of coronary sinus and thebsian venous drainage of the myocardium with systemic venous blood is usually complete in the right ventricle*‘. Therefore, at low Scvo2, true Svo2 value may be significantly lower and can limit the use of Scvo2 in indicating the true balance of systemic VOWin relation to DO*. Scvo2 was normal or raised in 50% of patients treated in the emergency department (Table II). However, these patients had elevated arterial lactic acid concentration. It seemed that Vo2 was inadequate to repay the oxygen debt in this group of patients (i.e. an O2 utilization defect)17. Defect in peripheral O2 utilization and extraction may limit the usefulness of Scvo2 in assessing the adequacy of global and
Table II.
Hemodynamic and oxygenation variables in Group I and II after initial resuscitation of variety of shock states (traumatic, hemorrhagaic, septic and cardiogenic). Values shown are means * SD. Group I includes patients with abnormally low E$.,o~. Group II includes patients with normal Scvol.
Variable N
HR (beats/mm) MAP (mmHg) CVP (cmH,O) SI Hg Wdl) S,oz@) ~,o,W)
Lact (mM/l)
Group I
8 110 87 12 0.9 11 99 48 2.2
f 15 *15 *4 f 0.2 *2 3~9; f 0.8
Group II 8 104 81 12 0.9 10 99 81 1.0
?? 14 f 21 *I * 0.2 *2
zt8 f 8.0
HR, heart rate; MAP, mean arterial pressure; CVP, central venous pressure; SI, shock index (heart rate/systolic arterial pressure); I-Ig, hemoglobin concentration; Sao2, arterial oxygen saturation; Scvo2, central venous oxygen saturation; Lact, arterial blood lactic acid concentration. *P < 0.01 Group I versus Group II (see Ref. 17).
58
regional oxygenation’Y. This was observed in patients with trauma, sepsis, multiple organ dysfunction, post-cardiac arrest cardiogenic shock and hypothermia21-26. Therefore, simultaneous measurement of Vo2 by indirect calorimetry and arterial lactic acid concentration clearance are essential to identify the underlying O2 utilization defect in these states. Arterial lactic acid concentration has been shown to be raised in variety of shock states2’. This usually indicates anaerobic metabolism, tissue ischemia and accumulation of oxygen debt28,29.Previous studies attempted to correlate the mortality rate and lactic acid concentration in different shock states2’. However, it is unreliable to infer the severity of ischemic tissue insult or the magnitude of oxygen debt from blood lactic acid concentration. Aerobic glycolysis and increased production of pyruvate and lactate has been observed in hyperdynamic hypermetabolic states3’. Aerobic production of blood lactic acid may be distinguished from anerobic production by measuring blood lactate to pyruvate concentrations ratio. This ratio is increased during anaerobic metabolism. Furthermore, the relative rate of lactate production by anaerobic metabolism and its elimination rate by the hepatic and renal systems determine blood lactic acid concentration and this may limit its accuracy to quantify oxygen debt in shock 3’,32. Alactic oxygen debt i.e. the presence of significant tissue ischemia with normal blood lactic acid concentration was first described by Cain in experimental shock model in which systemic DO, and $40~ were significantly reduced and lactic acid concentration was normalz9. Similar pattern was observed in 50% of patients presenting in shock and resuscitated in the emergency department (Table II)“. The utilization of oxygen reserve in residual lung volumes and bound to hemoglobin and myoglobin as well as the intracellular store of high energy phosphate bonds may contribute to alactic oxygen debt. Anaerobic metabolism with normal lactic acid concentration can also be seen in patients with augmented hepatic and renal clearance of lactic acid3’. It seems that the rate of clearance of an already elevated lactic acid is more valuable than individual measurements to predict outcome in shock33. This may reflect either an adequate tissue oxygenation to repay the oxygen debt or alternatively an augmented hepatic and renal function to clear the extracellular pool of lactate. The shock index (SI) i.e. the ratio of heart rate to systolic arterial pressure, was found to be elevated in patients with either low Scvo2 and normal lactate or normal/ high S,O, and elevated lactate (Table II). SI was shown to correlate with left ventricular stroke work (LVSW) in hypodynamic and hyperdynamic shock34. Persistent elevation of SI (normal range 0.5-0.7) indicated poor recovery of LVSW after treatment in the emergency department. LVSW is dependent on preload, afterload, diastolic compliance and systolic contractility of left ventricle LVi4 and any of these factors singly or in combination may contribute to the elevation of SI. A previous study showed that the SI was of limited value to assess the adequacy of systemic oxygenation in normodynamic and hyperdynamic shock34). Although Scvo2 and arterial lactic acid concentration may indicate indirectly the adequacy of systemic oxygenation, SI provides an additional information on the performance of LV. Reduced Scvo2, elevated arterial lactic acid concentration and persistent elevation of SI in patients resuscitated in the emergency department indicate global ischemia and LV dysfunction. Such a group of patients require
59
invasive hemodynamic monitoring to optimize LV function, systemic Do2 and VOW and to improve their outcome. CONCLUSION
Initial therapy based on stabilization and normalization of MAP, CVP and HR in clinical shock does not necessarily correct the primary derangement in systemic oxygenation. Monitoring of ScvoZ, arterial lactic acid concentration and SI may provide additional information to assess the adequacy of systemic oxygenation and LV function in the emergency department. REFERENCES
1
2 3 4 5 6 I 8 9 10 11 12 13 14 15 16 17
18 19
Baek SM, Makabali G, Bryan-Brown CW et al, Plasma expansion in surgical patients with high central venous pressure (CVP); the relationship of blood volume to hematocrit, CVP, pulmonary wedge pressure and cardiorespiratory changes. Surgery 1975; 78: 304-315. Shoemaker WC, Appel PL, Bland R et al. Clinical trial of an algorithm for outcome prediction in acute circulatory failure. Crit Care Med 1982; 10: 390-397. Bland R, Shoemaker WC, Abraham E et al. Haemodynamic and oxygen transport patterns in surviving and nonsurviving postoperative patients. Crit Care Med 1985; 13: 85-90. Shoemaker WC. Relationship of oxygen transport patterns to the pathophysiology and therapy of shock states. Int Care Med 1987; 13: 230-243. Shoemaker WC, Appel PL, Waxman K et al. Clinical trial of survivors’ cardiorespiratory patterns as therapeutic goals in critically ill postoperative patients. Crit Care Med 1982; 10: 398-403. Shoemaker WC, Appel PL, Kram HB et al. Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988; 94: 1176-l 186. Shoemaker WC, Appel PL, Kram HB. Tissue oxygen debt as a determinant of lethal and nonlethal postoperative organ failure. Crit Care Med 1988; 16: 1117-I 120. Siegel LC, Pearl RG. Noninvasive cardiac output measurment: troubled technologies and troubled studies. Anesth Analg 1992; 74: 790-792 Rivers EP, Martin GB, Rady MY et al. The clinical implication of continuous central venous oxygen saturation monitoring during human CPR. Ann Emerg Med 1992. In press. Sturm JA, Lewis FR, Trentz 0 et al. Cardiopulmonary parameters and prognosis after severe multiple trauma. J Trauma 1979; 19: 305-318. Kazarian K, Del Guercio LR. The use of mixed venous blood gas determinations in traumatic shock. Ann Emerg Med 1980; 9: 179-182. Kasnitz P, Druger GL, Yorra F et al. Mixed venous oxygen tension and hyperlactataemia severe cardiopulmonary disease. J Am Med Assoc 1976; 236: 570-574. Richard C, Thuillez C, Pezzano M et al. Relationship between mixed venous oxygen saturation and cardiac index in patients with chronic congestive heart failure. Chest 1989; 95: 1289-1294. Rady MY, Edwards JD, Nightingale P. Early cardiorespiratory findings after severe blunt thoracic trauma and their relation to outcome. Br J Surg 1992; 79: 65-68 Scalea TM, Houman M, Fuortes M et al. Central venous blood oxygen saturation: An early accurate measurement of volume during hemorrhage. J Trauma 1988; 28: 725-732. Tahvanainen J, Meretoja 0, Nikki P. Can central venous blood replace mixed venous blood samples? Crit Care Med 1982; 10: 758-761. Rady MY, Rivers EP, Martin GB et al. Continuous central venous oximetry and the shock index in the emeregency department: its use in the evaluation of clinical shock. Am J Emg Med 1992. In press. Reinhardt, K, Rudolph T, Bredle DL et al. Comparison of central-venous to mixed-venous oxygen saturation during changes in oxygen supply/demand. Chest 1989; 95: 1216. Reinhardt K. Principles and practice of SvOl monitoring. Int Care World 1988; 5: 121-124.
60
20 21 22 23 24 25
26 21 28 29 30 31 32 33 34
Nelson D. Mixed venous oximetery. In: Synder JV, Pinskey MR, editors. Oxygen transport in the critically ill. Year Book Medical Publishers Inc, 1987: 235-248. Shah DM, Newell JC, Saba TM. Defects in peripheral oxygen utilization following trauma and shock. Arch Surg, 1981; 116: 1277-1281. Edwards JD, Brown CX, Nightingale P et al. Use of cardiorespiratory values as therapeutic goals in septic shock. Crit Care Med 1989; 17: 1098-1103. Wolf YG, Cotev S, Perel A et al. Dependence of oxygen consumption on cardiac output in sepsis. Crit Care Med 1987; 15: 198-203. Demling RH. Current concepts on adult respiratory distress syndrome. Circ Shock 1990; 30: 297-309. Rivers EP, Rady MY, Martin GB et al. Supranormal mixed venous oxygen saturation after resuscitation from human cardiac arrest: a charaterization of systemic oxygen utilization defect. Chest 1992. In press. Black PR, Devanter SV, Cohn LH. Effects of hypothermia on systemic and organ system metabolism and function. J Surg Res 1976; 20: 49-54. Vitek V, Cowley. Blood lactate in the prognosis of various forms of shock. Ann Surg 1971; 173: 308-313. Cain SM. Oz deficit incurred during hypoxia and its relation to lactate and excess lactate. Am J Physiol 1967; 213 (1): 57-63. Cain SM. Relative rates of arterial lactate and oxygen deficit accumulation in hypoxic dogs. Am J Physiol 1973; 224: 1190-l 194. Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med 1992; 20: 80. Perret C, Enrico J, Poli S. Acid-base disturbances and lactate metabolism in shock. Eur J Clin Invest 1970; 1: 387-390. Wall PJ, Record CO. Lactate elimination in man: Effects of lactate concentration and hepatic dysfunction. Eur J Clin Invest 1979; 9: 397-404. Bakker J, Leon M, Coffemils M et al. Serial blood lactate levels can predict multiple organ failure in septic shock patients. Crit Care Med 1992; 20: S56. Rady MY, Nightingale P, Little RA, Edwards JD. Shock index: a re-evaluation in acute circulatory failure. Resuscitation 1992; 23 (3): 227-234.
