Continuous Central Venous Oximetry and Shock Index in the Emergency Department: Use in the Evaluation of Clinical Shock MOHAMED Y. RADY, MB BCHIR, MD(Cantab), EMANUEL P. RIVERS, MD, MPH, GERARD B. MARTIN, MD, HOWARD SMITHLINE, MD, TIMOTHY APPELTON, RICHARD M. NOWAK, MD initial therapy of shock in the emergency department (ED)emphasizes the normalization of physiologic variables such as heart rate (HR), mean arterial pressure (MAP), and central venous pressure (CVP) rather than restoration of adequate tissue oxygenation. After hemodynamic stabiiization of MAP, CVP, and HR, the authors examined tissue oxygenation as indicated by continuous central venous oximetry (Scvo,), lactic acid concentration, and shock index (Si). Sixteen consecutive nonrandomized patients presenting to the ED of a large urban hospital in shock (MAP < 60 mm Hg, HR > 120 beats/min, and altered sensorium) were initially resuscitated with fluid, blood, inotropes, and/or vasoactive drug therapy to normalize MAP, CVP, and HR. In addition, SCVO~,arterial lactate concentration, and SI were measured affer completion of resuscitation in the ED. Eight patients (group no. 1) had inadequate tissue oxygenation reflected by low Scvo, (less than 65%). Four patients in group no. 1 had elevated arterial lactic acid concentration. Ail group no. 1 patients had an elevated SI (>0.7) suggesting persistent impairment of left ventricular stroke work. Eight patients (group no. 2) had normal or elevated Scvo, (>65%). In group no. 2, arterial lactic acid concentration was elevated in six and Si in seven patients. Normalization of hemodynamic variables does not adequately reflect the optimal endpoint of initial therapy in shock in the ED. Most (94%) of these patients continue to have significant global ischemia and cardiac dysfunction as indicated by reduced Scvo, and elevated lactic acid concentration and Si. Systemic tissue oxygenation should be monitored and optimized in the ED in these critically iii patients. Measurement of Scvo,, arterial lactic acid concentration, and Si may provide valuable additional information on the adequacy of systemic oxygenation and cardiac function during initial therapy of shock in the ED. (Am .I Emerg Med 1992;10:536-541. Copyright 0 1992 by W.3. Saunders Company)
The emergency department (ED) 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 showed that normalization of these hemodynamic variables did not improve the morbidity or mortality in shock.‘-4 Early therapy directed to relieve tissue hypoxia and repay systemic oxygen debt incurred due to deficit o2 use has been shown to
From the Department of Emergency Medicine, Henry Ford Hospital, Detroit, Ml. Manuscript received January 7,1992; revision accepted July 8, 1992. Address reprint requests to Dr Rady, Department of Emeraencv Medicine. Hew Ford Hosoital. 2799 W Grand Blvd. De. Goit,‘MI 48202. . Key Words: Shock, hemodynamics, oxygenation, shock index, continuous central venous oximetry. Copyright 0 1992 by W.B. Saunders Company 0735-6757/92/l 006-0006$5.00/0 536
improve clinical outcome in shock irrespective of its etiology.‘-’ Therefore, resuscitation of shock in the ED should be monitored by its impact on tissue oxygen supply to demand. Mixed venous oxygen saturation obtained from pulmonary artery (Svo,) and central venous oxygen saturation (Scvo,) have been shown to reflect the balance of systemic oxygen delivery (supply) to consumption (demand).*-l3 These studies indicated that there was a close correlation between mixed venous Svo, and central Scvo,. A previous study verified the usefulness of continuous monitoring of Scvo, to indicate the return of spontaneous circulation in human cardiopulmonary resuscitation.‘4 Shock index (SI = heart rate/systolic arterial pressure) was shown to be inversely related to left ventricular stroke work (LVSW) in acute circulatory failure. i5,16 Elevation of SI indicated deterioration in LVSW. This study was designed to test the hypothesis that Scvo,. arterial lactic acid concentration, and SI provided additional information to estimate the adequacy of systemic oxygenation and therefore resuscitation in shock in the ED. PATIENTS AND METHODS
This study was approved by the Institutional Review Board for Human Research of Henry Ford Hospital (Detroit, MI). Sixteen consecutive patients arriving to the ED in clinical shock with an initial MAP < 60 mm Hg or systolic pressure ~80 mm Hg (measured noninvasively), HR > 120 beats/ min, altered sensorium, delayed capillary refill, respiratory rate (>40 or 97%, or a rising arterial Pco, greater than 60 mm Hg. Femoral or radial arterial and central venous catheters were inserted for direct pressure measurement during initial resuscitation and catheter position was confirmed radiologically.
RADY ET AL W CENTRAL
TABLE 1.
Resuscitation
VENOUS
Protocol
OXIMETRY
and Endpoints
& SHOCK
INDEX
of Therapy
539
IN SHOCK
in Shock
in the Emergency
Inspired o, to maintain peripheral pulse oximetry > 97% Endotracheal intubation and mechanical ventilation: Protection of the airway Relief of respiratory distress despite supplementary oxygen Necessity of inspired o, concentration > 60% to maintain arterial saturation Rising arterial Pcop > 60 mm Hg Blood volume expansion with crystalloid and red cell concentrate Central venous pressure (CVP lo-15 cm H,O) Hemoglobin concentration (10 to 12 g/dL) lnotropes (dobutamine) and vasoactive drugs (eg, norepinephrine, dopamine, (eg, cardiogenic, septic) To achieve HR (70 mm Hg), CVP (lo-15 cm H,O)
Blood volume expansion with crystalloid was guided by CVP and arterial hemoglobin concentration. Hemoglobin was maintained between 10 to 12 g/dL by transfusion with red cell concentrate. Later, cardioactive (eg, dobutamine) and/or vasoactive drugs (eg, norepinephrine) were used at the clinician’s discretion depending on the etiology of shock to achieve normalization of HR and MAP. Septic shock was diagnosed according to criteria described by Edwards et al.” Following initial resuscitation, a 7F fiberoptic 20-cm triple lumen catheter (Baxter Health Care, Irving, CA) was placed in the right atrium through a Touhey Borst introducer (Cook Critical Care Inc, Bloomgiton, IA) and the position was confirmed radiologically. Each fiber-optic catheter was calibrated in vitro (preinsertion) and in vivo (post-placement). The Scvo, was measured continuously by American Edwards SAT-Corn-2 (Baxter Health Care). Lactic acid was measured by lactic acid oxidase enzymatic assay in duplicate. Invasive systemic arterial pressures and HR were recorded and SI calculated as HR/systolic arterial pressure. Measurements of HR. MAP, CVP, SI, Scvo,, and arterial blood lactic acid concentration were taken after completion of resuscitation. The endpoints of resuscitation in the ED were normalization of HR (70 mm Hg) and CVP (lo-15 cm H,O). These were the variables and endpoints most commonly chosen by the ED physician to indicate the adequacy of resuscitation in shock in the ER. Differences between the two groups were analyzed with unpaired t-test and significance was at P < .05. RESULTS The clinical features of the 16 patients who were treated in the ED for shock are summarized in Table 2. The etiology of shock in this study included: hemorrhagic, cardiogenic, traumatic, and septic shock which are commonly seen in many ED. Nine patients (56%) were in septic shock. Mechanical ventilation was required in 10 patients (63%) for criteria indicated previously. Patients were categorized according to their Scvo, values measured after completion of resuscitation in the ED (Table 3). A normal Scvo, is greater than 65%. Group no. 1 (eight patients) had low Scvo, (less than 65%) and group no. 2 (8 patients) had normal Scvo, (greater than 65%) after normalization of HR, MAP, and CVP. Arterial hemoglobin concentration and oxyhemoglobin saturation were not significantly different between groups no. 1 and 2. The mean SI was abnormally raised (greater than 0.7) in both groups.
Department
> 97%
nitroglycerin):
depend
on etiology
of shock
In group no. 1 four patients had elevated arterial lactic acid concentration (~2 mmol/L) and all had abnormally high SI (>0.7) implying reduced LVSW (Table 4). In group no. 2 six patients had elevated arterial lactic acid concentration and seven had raised SI (Table 4). DISCUSSION Close correlation between pulmonary artery mixed venous Svo, and central venous Scvo, have been shown in shock states.*.‘* Both Svo, and Scvo, may reflect the balance between systemic oxygen delivery (supply) and oxygen consumption (demand).‘“*” The SCVO, usually overestimates Svo, because of the significant desaturation of myocardial venous blood draining into the coronary sinus and directly to the right ventricle in shock.i3 The SI has been shown to correlate with LVSW in acute circulatory failure and its rise implies a deterioration in LVSW.‘5*‘6 Shock index was measured in conjunction with Scvo, to assess indirectly the left ventricular mechanical performance following TABLE 2. Therapy
Patients’
Characteristics,
in the Emergency
Diagnosis,
and
Initial
Department Respiratory Rate
Diagnosis Group no. 1 Pancreatitis Gastrointestinal bleeding Sepsis/COPD Cardiogenic shock Pneumonia Chest contusion Sepsis/ARDS Pancreatitis Group no. 2 Sepsis/ARF SepsislDKA Post-CPR Septicemia SepsislARDS Sepsis/CRF SepsidHF Sepsis/urinary
Age (Y)
(min)
Therapy
65 62
::
F F + blood
66 66
MV MV
MV + F MV + Dob
46 42
40 MV
F + Dop MV + F + Dob
61 66
MV 30
MV + F F + Dop
63 66 26 40 58 60 65 71
MV MV MV MV MV MV 24 20
MV + F MV + F + hemodialysis MV + Epi MV + F + Dop MV + F MV + F + Norepi F + Dop F + Dop
ABBREVIATIONS: F, lactate Ringer fluid; COPD, chronic obstructive pulmonary disease; MV, mechanical ventilation; Dob, dobutamine; Dop, dopamine; ARDS, adult respiratory distress syndrome; ARF, acute renal falure; DKA, diabetic ketoacidosis; Post-CPR. post-cardiopulmonary arrest; Epi. epinephrine; CRF, chronic renal failure; Norepi, norepinephrine; HF. hepatic failure.
AMERICAN
540
TABLE 3. Hemodynamic No. 1 and 2 After initial
and Oxygenation Resuscitation Group
HR (beats/min) MAP (mm Hg) CVP (cm H,O) SI Hg (g/dL) Sao, (%) scvo, (%) Lact (mmol/L)
JOURNAL
Variables
No. 1
OF EMERGENCY
in Groups
Group
No. 2
(n = 8) 110 (15) 87 (15)
(n = 8) 104 (14) 67 (27)
12 (4) 0.9 (0.2)
12 (7) 0.9 (0.2)
11 (2) 99 48 (9)’ 2.2 (0.6)
10 (2) 99
NOTE. Values shown are means (SD). ABBREVIATIONS: Hg, hemoglobin concentration; blood lactic acid concentration. * P < ,001 versus group no. 2.
81 (8) 7.0 (8.0)
Lact,
arterial
hemodynamic stabilization in clinical shock. Patients were separated into two (groups no. 1 and 2) according to Scvo, (measured after treatment) as this reflected different patterns of derrangement in systemic oxygenation. Despite normalization of HR, MAP, and CVP, 50% of patients had low Scvo, suggestive of inadequate o2 supply to meet systemic o, demand and for high tissue oxygen extraction. This also suggested continued anaerobic metabolism and elevated lactic acid concentration and persistent oxygen debt in four patients. Four patients with low Scvo, and normal arterial lactic acid concentration might have alactic oxygen debt. “Alactic” oxygen debt was first described by Cain in an experimental shock model in which systemic O, delivery and Svo, were significantly reduced and lactic acid concentration was normal. ‘8,‘9 Alactic oxygen debt seen in these patients represents the use of intracellular stores of high energy phosphate bonds and oxygen reserve bound to myoglobin. Anaerobic metabolism with normal lactic acid concentration can also be seen in patients with augmented hepatic and renal clearance of lactic acid.*’ Lactic acid concentration was measured after the clinician’s completion of treatment of shock. Although group no. 1 (50% of patients studied) were resuscitated to normalize HR, MAP, and CVP, SCVO, remained 65% SI < 0.7 SI > 0.7 Lactate > 2.0 mmol/L
Group No. 1 (n = 8)
Group No. 2 (n = 8)
8 0 0 8 4
0 8 1 7 6
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crease systemic o, delivery and consumption.4,5 Optimal hemoglobin concentration (lo-12 gm/dL) is required to ensure adequate arterial oxygen content in shock.2’ Further augmentation of o, delivery relies predominantly on increasing cardiac output and stroke volume. Supranormal cardiac output (50% above normal) may be necessary to meet o, demand in clinical shock. Controlled plasma volume expansion and inotropes can significantly increase stroke volume and cardiac output and o2 delivery in certain shock states.2’ In patients with significant cardiac dysfunction or a fixed cardiac output (eg, cardiogenic shock) o, delivery is limited and initial therapy should aim to reduce left ventricular afterload and o2 demand. Reduction in o2 demand can be accomplished by mechanical ventilation, sedation, control of hyperpyrexia, and skeletal muscle paralysis.‘3 Therapeutic reduction in o, demand may restore the balance of oZ delivery to o2 demand and normalize SCVO~. Group no. 2 (50% of patients studied) were resuscitated to normalize their HR, MAP, and CVP; the Scvo, values were normal or raised. However, seven of these patients had raised SI implying reduced LVSW.16 Six patients had elevated lactic acid concentration reflecting persistent global tissue ischemia and unpaid o, debt. Alternatively. these patients may have had a delayed clearance of the extracellular lactate pool. Although it is difficult to extrapolate the clearance rate of blood lactic acid from a single measurement, its persistent elevation indicated inadequate resuscitation. The increase in arterial lactic acid concentration and SI may indicate persistent impairment of tissue oxygenation and cardiac function. In the presence of an adequate o2 delivery to demand, therefore, a normal or raised SCVO,, this o2 demand was inadequate to repay the o2 debt (ie, an o2 use defect). This is observed in patients with trauma, sepsis, multiple organ failure syndrome, postcardiac arrest, and hypothermia.24-28 Therapy with pharmacologic agents in this group of patients should aim to augment o, delivery at microcirculation level and to improve peripheral oxygen use and extraction.27 This study highlights the adjuvant use of the SI to indicate persistent deterioration of left ventricular function during therapy in the ED. Shock index was elevated in 15 out of 16 patients (94%) indicating poor recovery of LVSW following normalization of HR, MAP, and CVP. In group no. 2. (50% of patients) Scvo, was normal or raised and an unreliable indicator of persistent LV dysfunction. This finding was consistent with our previous study in which LVSW was reduced with concomitant elevation in SI; however, Svo, was normal or high in human septic shock.16 This study has limitations: Scvo, and arterial lactic acid concentration were measured to indicate indirectly the adequacy of systemic oxygenation after completion of resuscitation. Although systemic oxygenation should be assessed by direct measurement of systemic oxygen delivery and consumption, normalization of both Scvo, and arterial lactic acid concentration in shock may indicate that systemic oxygenation is adequate. The short-term outcome was not addressed in this particular study because of its design. Prospective randomized controlled study have shown that therapy aimed to augment systemic oxygenation reduced morbidity and mortality rates compared with standard therapy in shock.6 Arterial lactic acid concentration, ScvoZ and
RADY ET AL n CENTRAL
VENOUS
OXIMETRY
& SHOCK INDEX IN SHOCK
SI were measured to indicate that persistent global ischemia and cardiac dysfunction coexisted with normalized HR, MAP, and CVP in patients resuscitated in the ED. These patients would require further invasive monitoring to optimize their therapy and improve outcome. We conclude that common physiologic markers (ie, HR. MAP, and CVP) fail to reflect adequate resuscitation of patients in shock. Other measures of the adequacy of tissue oxygenation are needed to guide ED resuscitation protocols. CONCLUSION Initial therapy in the ED 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 Scvo,, arterial lactic acid concentration, and SI may provide additional information to assess the balance of systemic o, delivery to o, demand and left ventricular dysfunction in the ED. REFERENCES 1. 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 i 975;78:304 2. 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 3. 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 4. Shoemaker WC: Relationship of oxygen transport patterns to the pathophysiology and therapy of shock states. Intensive Care Med 1987;13:230 5. 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 6. Shoemaker WC, Appel PL, Kram HE, et al: Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988;94:1176 7. 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 8. 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 9. Reinhardt K: Principles and practice of Svo, monitoring. Intensive Care World 1988;5:121 10. Kasnitz P, Druger GL, Yorra F, et al: Mixed venous oxygen
541
tension and hyperlactataemia severe cardiopulmonary disease. JAMA 1976;236:570 11. 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: i 289 12. 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 13. Nelson D: Mixed venous oximetery. In Synder JV, Pinskey MR (eds): Oxygen Transport In The Critically Ill. Chicago, IL, Year Book Medical Publishers, 1987. D 235 14. 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) 15. Radv MY, Niahtinaale P. Edwards JD. et al: Shock index: A re-evaluation in’ acute circulatory faiiure. Resuscitation 1992;23:227-234 16. Rady MY, Nightingale P, Edwards JD, et al: Evaluation of shock index in human septic shock. Intensive Care Med (in press) 17. Edwards JD, Brown GC, Nightingale P, et al: Use of cardiorespiratory values as therapeutic goals in septic shock. Crit Care Med 1989;17:1098 18. Cain SM: 0, deficit incurred during hypoxia and its relation to lactate and excess lactate. Am J Physiol 1967;213(1):57-63 19. Cain SM: Relative rates of arterial lactate and oxygen deficit accumulation in hypoxic dogs. Am J Physiol 1973;224:1190 20. Perret C, Enrico J, Poli S: Acid-base disturbances and lactate metabolism in shock. Eur J Clin Invest 1970;1:387 21. Czer LS, Shoemaker WC: Optimal hematocrit value in critically ill postoperative patients. Surg Gynecol Obstet 1978;147: 363 22. Shoemaker WC, Appel PL, Kram HB: Haemodynamic and oxygen transport effects of dobutamine in critically ill general suroical patients. Crit Care Med 1986:14:1032 23. Aubier M, Viires N, Syllie G, et al: Respiratory muscle contribution to lactic acidosis in low cardiac output. Am Rev Respir Dis 1982;126:648 24. Shah DM, Newell JC, Saba TM: Defects in peripheral oxygen utilization following trauma and shock. Arch Surg 1981; 116:1277 25. Wolf YG, Cotev S, Perel A, et al: Dependence of oxygen consumption on cardiac output in sepsis. Crit Care Med 1987; i5:i9a 26. Black PR, Devanter SV, and Cohn LH: Effects of hypothermia on systemic and organ system metabolism and function. J Surg Res 1976;20:49 27. Demling RH: Current concepts on adult respiratory distress syndrome. Circ Shock 1990;30:297 28. Rivers EP, Rady MY, Martin GB, et al: Characterization of a defect in systemic oxygen consumption after human cardiac arrest. Crit Care Med 1992;2O:S73
The emergency department (ED) 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 showed that normalization of these hemodynamic variables did not improve the morbidity or mortality in shock.‘-4 Early therapy directed to relieve tissue hypoxia and repay systemic oxygen debt incurred due to deficit o2 use has been shown to
From the Department of Emergency Medicine, Henry Ford Hospital, Detroit, Ml. Manuscript received January 7,1992; revision accepted July 8, 1992. Address reprint requests to Dr Rady, Department of Emeraencv Medicine. Hew Ford Hosoital. 2799 W Grand Blvd. De. Goit,‘MI 48202. . Key Words: Shock, hemodynamics, oxygenation, shock index, continuous central venous oximetry. Copyright 0 1992 by W.B. Saunders Company 0735-6757/92/l 006-0006$5.00/0 536
improve clinical outcome in shock irrespective of its etiology.‘-’ Therefore, resuscitation of shock in the ED should be monitored by its impact on tissue oxygen supply to demand. Mixed venous oxygen saturation obtained from pulmonary artery (Svo,) and central venous oxygen saturation (Scvo,) have been shown to reflect the balance of systemic oxygen delivery (supply) to consumption (demand).*-l3 These studies indicated that there was a close correlation between mixed venous Svo, and central Scvo,. A previous study verified the usefulness of continuous monitoring of Scvo, to indicate the return of spontaneous circulation in human cardiopulmonary resuscitation.‘4 Shock index (SI = heart rate/systolic arterial pressure) was shown to be inversely related to left ventricular stroke work (LVSW) in acute circulatory failure. i5,16 Elevation of SI indicated deterioration in LVSW. This study was designed to test the hypothesis that Scvo,. arterial lactic acid concentration, and SI provided additional information to estimate the adequacy of systemic oxygenation and therefore resuscitation in shock in the ED. PATIENTS AND METHODS
This study was approved by the Institutional Review Board for Human Research of Henry Ford Hospital (Detroit, MI). Sixteen consecutive patients arriving to the ED in clinical shock with an initial MAP < 60 mm Hg or systolic pressure ~80 mm Hg (measured noninvasively), HR > 120 beats/ min, altered sensorium, delayed capillary refill, respiratory rate (>40 or 97%, or a rising arterial Pco, greater than 60 mm Hg. Femoral or radial arterial and central venous catheters were inserted for direct pressure measurement during initial resuscitation and catheter position was confirmed radiologically.
RADY ET AL W CENTRAL
TABLE 1.
Resuscitation
VENOUS
Protocol
OXIMETRY
and Endpoints
& SHOCK
INDEX
of Therapy
539
IN SHOCK
in Shock
in the Emergency
Inspired o, to maintain peripheral pulse oximetry > 97% Endotracheal intubation and mechanical ventilation: Protection of the airway Relief of respiratory distress despite supplementary oxygen Necessity of inspired o, concentration > 60% to maintain arterial saturation Rising arterial Pcop > 60 mm Hg Blood volume expansion with crystalloid and red cell concentrate Central venous pressure (CVP lo-15 cm H,O) Hemoglobin concentration (10 to 12 g/dL) lnotropes (dobutamine) and vasoactive drugs (eg, norepinephrine, dopamine, (eg, cardiogenic, septic) To achieve HR (70 mm Hg), CVP (lo-15 cm H,O)
Blood volume expansion with crystalloid was guided by CVP and arterial hemoglobin concentration. Hemoglobin was maintained between 10 to 12 g/dL by transfusion with red cell concentrate. Later, cardioactive (eg, dobutamine) and/or vasoactive drugs (eg, norepinephrine) were used at the clinician’s discretion depending on the etiology of shock to achieve normalization of HR and MAP. Septic shock was diagnosed according to criteria described by Edwards et al.” Following initial resuscitation, a 7F fiberoptic 20-cm triple lumen catheter (Baxter Health Care, Irving, CA) was placed in the right atrium through a Touhey Borst introducer (Cook Critical Care Inc, Bloomgiton, IA) and the position was confirmed radiologically. Each fiber-optic catheter was calibrated in vitro (preinsertion) and in vivo (post-placement). The Scvo, was measured continuously by American Edwards SAT-Corn-2 (Baxter Health Care). Lactic acid was measured by lactic acid oxidase enzymatic assay in duplicate. Invasive systemic arterial pressures and HR were recorded and SI calculated as HR/systolic arterial pressure. Measurements of HR. MAP, CVP, SI, Scvo,, and arterial blood lactic acid concentration were taken after completion of resuscitation. The endpoints of resuscitation in the ED were normalization of HR (70 mm Hg) and CVP (lo-15 cm H,O). These were the variables and endpoints most commonly chosen by the ED physician to indicate the adequacy of resuscitation in shock in the ER. Differences between the two groups were analyzed with unpaired t-test and significance was at P < .05. RESULTS The clinical features of the 16 patients who were treated in the ED for shock are summarized in Table 2. The etiology of shock in this study included: hemorrhagic, cardiogenic, traumatic, and septic shock which are commonly seen in many ED. Nine patients (56%) were in septic shock. Mechanical ventilation was required in 10 patients (63%) for criteria indicated previously. Patients were categorized according to their Scvo, values measured after completion of resuscitation in the ED (Table 3). A normal Scvo, is greater than 65%. Group no. 1 (eight patients) had low Scvo, (less than 65%) and group no. 2 (8 patients) had normal Scvo, (greater than 65%) after normalization of HR, MAP, and CVP. Arterial hemoglobin concentration and oxyhemoglobin saturation were not significantly different between groups no. 1 and 2. The mean SI was abnormally raised (greater than 0.7) in both groups.
Department
> 97%
nitroglycerin):
depend
on etiology
of shock
In group no. 1 four patients had elevated arterial lactic acid concentration (~2 mmol/L) and all had abnormally high SI (>0.7) implying reduced LVSW (Table 4). In group no. 2 six patients had elevated arterial lactic acid concentration and seven had raised SI (Table 4). DISCUSSION Close correlation between pulmonary artery mixed venous Svo, and central venous Scvo, have been shown in shock states.*.‘* Both Svo, and Scvo, may reflect the balance between systemic oxygen delivery (supply) and oxygen consumption (demand).‘“*” The SCVO, usually overestimates Svo, because of the significant desaturation of myocardial venous blood draining into the coronary sinus and directly to the right ventricle in shock.i3 The SI has been shown to correlate with LVSW in acute circulatory failure and its rise implies a deterioration in LVSW.‘5*‘6 Shock index was measured in conjunction with Scvo, to assess indirectly the left ventricular mechanical performance following TABLE 2. Therapy
Patients’
Characteristics,
in the Emergency
Diagnosis,
and
Initial
Department Respiratory Rate
Diagnosis Group no. 1 Pancreatitis Gastrointestinal bleeding Sepsis/COPD Cardiogenic shock Pneumonia Chest contusion Sepsis/ARDS Pancreatitis Group no. 2 Sepsis/ARF SepsislDKA Post-CPR Septicemia SepsislARDS Sepsis/CRF SepsidHF Sepsis/urinary
Age (Y)
(min)
Therapy
65 62
::
F F + blood
66 66
MV MV
MV + F MV + Dob
46 42
40 MV
F + Dop MV + F + Dob
61 66
MV 30
MV + F F + Dop
63 66 26 40 58 60 65 71
MV MV MV MV MV MV 24 20
MV + F MV + F + hemodialysis MV + Epi MV + F + Dop MV + F MV + F + Norepi F + Dop F + Dop
ABBREVIATIONS: F, lactate Ringer fluid; COPD, chronic obstructive pulmonary disease; MV, mechanical ventilation; Dob, dobutamine; Dop, dopamine; ARDS, adult respiratory distress syndrome; ARF, acute renal falure; DKA, diabetic ketoacidosis; Post-CPR. post-cardiopulmonary arrest; Epi. epinephrine; CRF, chronic renal failure; Norepi, norepinephrine; HF. hepatic failure.
AMERICAN
540
TABLE 3. Hemodynamic No. 1 and 2 After initial
and Oxygenation Resuscitation Group
HR (beats/min) MAP (mm Hg) CVP (cm H,O) SI Hg (g/dL) Sao, (%) scvo, (%) Lact (mmol/L)
JOURNAL
Variables
No. 1
OF EMERGENCY
in Groups
Group
No. 2
(n = 8) 110 (15) 87 (15)
(n = 8) 104 (14) 67 (27)
12 (4) 0.9 (0.2)
12 (7) 0.9 (0.2)
11 (2) 99 48 (9)’ 2.2 (0.6)
10 (2) 99
NOTE. Values shown are means (SD). ABBREVIATIONS: Hg, hemoglobin concentration; blood lactic acid concentration. * P < ,001 versus group no. 2.
81 (8) 7.0 (8.0)
Lact,
arterial
hemodynamic stabilization in clinical shock. Patients were separated into two (groups no. 1 and 2) according to Scvo, (measured after treatment) as this reflected different patterns of derrangement in systemic oxygenation. Despite normalization of HR, MAP, and CVP, 50% of patients had low Scvo, suggestive of inadequate o2 supply to meet systemic o, demand and for high tissue oxygen extraction. This also suggested continued anaerobic metabolism and elevated lactic acid concentration and persistent oxygen debt in four patients. Four patients with low Scvo, and normal arterial lactic acid concentration might have alactic oxygen debt. “Alactic” oxygen debt was first described by Cain in an experimental shock model in which systemic O, delivery and Svo, were significantly reduced and lactic acid concentration was normal. ‘8,‘9 Alactic oxygen debt seen in these patients represents the use of intracellular stores of high energy phosphate bonds and oxygen reserve bound to myoglobin. Anaerobic metabolism with normal lactic acid concentration can also be seen in patients with augmented hepatic and renal clearance of lactic acid.*’ Lactic acid concentration was measured after the clinician’s completion of treatment of shock. Although group no. 1 (50% of patients studied) were resuscitated to normalize HR, MAP, and CVP, SCVO, remained 65% SI < 0.7 SI > 0.7 Lactate > 2.0 mmol/L
Group No. 1 (n = 8)
Group No. 2 (n = 8)
8 0 0 8 4
0 8 1 7 6
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6 n November
1992
crease systemic o, delivery and consumption.4,5 Optimal hemoglobin concentration (lo-12 gm/dL) is required to ensure adequate arterial oxygen content in shock.2’ Further augmentation of o, delivery relies predominantly on increasing cardiac output and stroke volume. Supranormal cardiac output (50% above normal) may be necessary to meet o, demand in clinical shock. Controlled plasma volume expansion and inotropes can significantly increase stroke volume and cardiac output and o2 delivery in certain shock states.2’ In patients with significant cardiac dysfunction or a fixed cardiac output (eg, cardiogenic shock) o, delivery is limited and initial therapy should aim to reduce left ventricular afterload and o2 demand. Reduction in o2 demand can be accomplished by mechanical ventilation, sedation, control of hyperpyrexia, and skeletal muscle paralysis.‘3 Therapeutic reduction in o, demand may restore the balance of oZ delivery to o2 demand and normalize SCVO~. Group no. 2 (50% of patients studied) were resuscitated to normalize their HR, MAP, and CVP; the Scvo, values were normal or raised. However, seven of these patients had raised SI implying reduced LVSW.16 Six patients had elevated lactic acid concentration reflecting persistent global tissue ischemia and unpaid o, debt. Alternatively. these patients may have had a delayed clearance of the extracellular lactate pool. Although it is difficult to extrapolate the clearance rate of blood lactic acid from a single measurement, its persistent elevation indicated inadequate resuscitation. The increase in arterial lactic acid concentration and SI may indicate persistent impairment of tissue oxygenation and cardiac function. In the presence of an adequate o2 delivery to demand, therefore, a normal or raised SCVO,, this o2 demand was inadequate to repay the o2 debt (ie, an o2 use defect). This is observed in patients with trauma, sepsis, multiple organ failure syndrome, postcardiac arrest, and hypothermia.24-28 Therapy with pharmacologic agents in this group of patients should aim to augment o, delivery at microcirculation level and to improve peripheral oxygen use and extraction.27 This study highlights the adjuvant use of the SI to indicate persistent deterioration of left ventricular function during therapy in the ED. Shock index was elevated in 15 out of 16 patients (94%) indicating poor recovery of LVSW following normalization of HR, MAP, and CVP. In group no. 2. (50% of patients) Scvo, was normal or raised and an unreliable indicator of persistent LV dysfunction. This finding was consistent with our previous study in which LVSW was reduced with concomitant elevation in SI; however, Svo, was normal or high in human septic shock.16 This study has limitations: Scvo, and arterial lactic acid concentration were measured to indicate indirectly the adequacy of systemic oxygenation after completion of resuscitation. Although systemic oxygenation should be assessed by direct measurement of systemic oxygen delivery and consumption, normalization of both Scvo, and arterial lactic acid concentration in shock may indicate that systemic oxygenation is adequate. The short-term outcome was not addressed in this particular study because of its design. Prospective randomized controlled study have shown that therapy aimed to augment systemic oxygenation reduced morbidity and mortality rates compared with standard therapy in shock.6 Arterial lactic acid concentration, ScvoZ and
RADY ET AL n CENTRAL
VENOUS
OXIMETRY
& SHOCK INDEX IN SHOCK
SI were measured to indicate that persistent global ischemia and cardiac dysfunction coexisted with normalized HR, MAP, and CVP in patients resuscitated in the ED. These patients would require further invasive monitoring to optimize their therapy and improve outcome. We conclude that common physiologic markers (ie, HR. MAP, and CVP) fail to reflect adequate resuscitation of patients in shock. Other measures of the adequacy of tissue oxygenation are needed to guide ED resuscitation protocols. CONCLUSION Initial therapy in the ED 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 Scvo,, arterial lactic acid concentration, and SI may provide additional information to assess the balance of systemic o, delivery to o, demand and left ventricular dysfunction in the ED. REFERENCES 1. 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 i 975;78:304 2. 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 3. 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 4. Shoemaker WC: Relationship of oxygen transport patterns to the pathophysiology and therapy of shock states. Intensive Care Med 1987;13:230 5. 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 6. Shoemaker WC, Appel PL, Kram HE, et al: Prospective trial of supranormal values of survivors as therapeutic goals in high risk surgical patients. Chest 1988;94:1176 7. 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 8. 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 9. Reinhardt K: Principles and practice of Svo, monitoring. Intensive Care World 1988;5:121 10. Kasnitz P, Druger GL, Yorra F, et al: Mixed venous oxygen
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tension and hyperlactataemia severe cardiopulmonary disease. JAMA 1976;236:570 11. 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: i 289 12. 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 13. Nelson D: Mixed venous oximetery. In Synder JV, Pinskey MR (eds): Oxygen Transport In The Critically Ill. Chicago, IL, Year Book Medical Publishers, 1987. D 235 14. 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) 15. Radv MY, Niahtinaale P. Edwards JD. et al: Shock index: A re-evaluation in’ acute circulatory faiiure. Resuscitation 1992;23:227-234 16. Rady MY, Nightingale P, Edwards JD, et al: Evaluation of shock index in human septic shock. Intensive Care Med (in press) 17. Edwards JD, Brown GC, Nightingale P, et al: Use of cardiorespiratory values as therapeutic goals in septic shock. Crit Care Med 1989;17:1098 18. Cain SM: 0, deficit incurred during hypoxia and its relation to lactate and excess lactate. Am J Physiol 1967;213(1):57-63 19. Cain SM: Relative rates of arterial lactate and oxygen deficit accumulation in hypoxic dogs. Am J Physiol 1973;224:1190 20. Perret C, Enrico J, Poli S: Acid-base disturbances and lactate metabolism in shock. Eur J Clin Invest 1970;1:387 21. Czer LS, Shoemaker WC: Optimal hematocrit value in critically ill postoperative patients. Surg Gynecol Obstet 1978;147: 363 22. Shoemaker WC, Appel PL, Kram HB: Haemodynamic and oxygen transport effects of dobutamine in critically ill general suroical patients. Crit Care Med 1986:14:1032 23. Aubier M, Viires N, Syllie G, et al: Respiratory muscle contribution to lactic acidosis in low cardiac output. Am Rev Respir Dis 1982;126:648 24. Shah DM, Newell JC, Saba TM: Defects in peripheral oxygen utilization following trauma and shock. Arch Surg 1981; 116:1277 25. Wolf YG, Cotev S, Perel A, et al: Dependence of oxygen consumption on cardiac output in sepsis. Crit Care Med 1987; i5:i9a 26. Black PR, Devanter SV, and Cohn LH: Effects of hypothermia on systemic and organ system metabolism and function. J Surg Res 1976;20:49 27. Demling RH: Current concepts on adult respiratory distress syndrome. Circ Shock 1990;30:297 28. Rivers EP, Rady MY, Martin GB, et al: Characterization of a defect in systemic oxygen consumption after human cardiac arrest. Crit Care Med 1992;2O:S73
