ORIGINAL CONTRIBUTION bradycardia, relative, trauma; trauma, relative bradycardia

Relative Bradycardia in Patients With Isolated Penetrating Abdominal Trauma and Isolated Extremity Trauma A relative bradycardia is sometimes seen in patients w~th hemorrhagic shock. The phenomenon of relative bradycardia in civilian patients with isolated penetrating abdominal trauma and isolated severe extremity trauma who presented to an urban trauma center was studied retrospectively Relative bradycardia was defined as a pulse rate of less than 100 with a concomitant systolic blood pressure of less than 100 m m Hg. There were 256 patients with isolated penetrating abdominal trauma and 938 patients with isolated severe extremity trauma. The incidence of relative bradycardia was 3.I% (eight of 256) in the group with abdominal trauma and 1.8% (17 of 938) in the group with extremity trauma. A pulse rate less than 100 was documented in 35.2% of all patients presenting with a systolic blood pressure less than 100 m m Hg (25 of 71). A pulse rate of less than i00 was documented in 45.8% of all patients presenting with a systolic blood pressure less than 90 m m Hg (11 of 24). No increased mortality was seen in the patients who evidenced relative bradycardia. The effect of intraperitonea] bleeding on the normal tachycardic response to hemorrhage also was studied. After controlling for volume status using various operational definitions of shock, no statistically significant (P < .01) difference in pulse rates was noted between patients with isolated penetrating abdominal trauma and isolated extremity trauma. This result suggests that the previously theorized vagal-mediated bradycardia unique to intraperitoneal bleeding m a y not exist. [Thompson D, Adams SL, Barrett J: Relative bradycardia it1 patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med March 1990;19:268-275.]

David Thompson, MD* Stephen L Adams, MD, FACP, FACEP* John Barrett, MDt Chicago, Illinois From the Section of Emergency Medicine, Northwestern University Medical School;* and the Trauma Unit, Cook County Hospital,I- Chicago, Illinois. Received for publication April 14, 1989. Revision received September 7, 1989. Accepted for publication October 26, 1989. Address for reprints: Stephen L Adams, MD, FACP, FACER Section of Emergency Medicine, 1204 Olson Pavilion, Northwestern Memorial Hospital, 233 East Superior, Chicago, illinois 60611.

INTRODUCTION T h e f a m i l i a r and t r a d i t i o n a l d e s c r i p t i o n of a p a t i e n t in h e m o r r h a g i c shock includes signs of hypotension, taehycardia, and poor peripheral perfusion. 1-6 The tachycardia appears to be a physiologic response of the heart in an a t t e m p t to m a i n t a i n cardiac o u t p u t in the face of h y p o v o l e m i a and a decreased stroke volume. This is m e d i a t e d by various neuroendocrine controls as a result of s t i m u l a t i o n of baroreceptors w i t h i n the cardiovascular system. 1 The cessation of a tachycardic response has been considered a p r e t e r m i n a l event. 5-7 Recently, several reports have suggested t h e o c c u r r e n c e of a r e l a t i v e bradycardia in the presence of hemorrhagic shock, s-13 This p h e n o m e n o n has i n t e r c h a n g e a b l y been described as relative bradycardia, 8 lo,13 absence of t a c h y c a r d i c response,8,1o,~2,13 and p a r a d o x i c a l bradycardia. 11 T h e absence of an appropriate tachycardic response to h y p o v o l e m i a has now been reported in p a t i e n t s w i t h splenic rupture, 9,1] degenerating fundal fibroid, 8 b l e e d i n g o v a r i a n cyst, lo r u p t u r e d e c t o p i c pregnancy, 8,1o,11 p o s t o p e r a t i v e a b d o m i n a l bleeding, s w a r - r e l a t e d p e n e t r a t i n g a b d o m i n a l t r a u m a , 12 thoracic trauma, 9 and e x t r e m i t y vascular injury.11 Further review of the literature reveals reports of patients who presented w i t h such a relative bradycardia, y e t no m e n t i o n was m a d e of this s e e m i n g l y p a r a d o x i c a l finding. 14-17 It was concluded by the various authors w h o did r e m a r k on the bradycardia that tachycardia is a poor indicator of hypovolemia, that it should be used w i t h caution in diagnosing the presence or absence of h e m o r r h a g i c s h o c k , a n d t h a t it does n o t n e c e s s a r i l y h e r a l d a p r e t e r m i n a l event. 8-13 Some current textbooks on t r a u m a and emergency m e d i c i n e spe-

19:3 March 1990

Annals of Emergency Medicine

268/81

RELATIVE BRADYCARDIA Thompson, Adams & Barrett

cifically refer to this relative bradycardia in their discussion of shock, s,6 whereas others do not. 1-4 As noted above, intraperitoneal bleeding is one setting in which this phenomenon has been described. Authors have theorized that the presence of blood in the abdominal cavity stimulates the peritoneum and t h e r e b y increases v a g a l - p a r a s y m pathetic tone, which results in bradycardia.S, lo,~2,ts, 19 This t h e o r y suggests that there is something unique about hemorrhagic shock from intraperitoneal bleeding and that bradycardia should not be as manifest in other causes of hemorrhagic shock. The main purpose of this study was to determine the incidence of relative bradycardia in civilian patients with isolated penetrating abdominal trauma and isolated severe extremity trauma who presented to an urban trauma center. The s e c o n d a r y purpose of this study was to compare the vital signs of patients with isolated penetrating abdominal trauma with those of patients with isolated severe extremity trauma. Given the theory that there is a vagal response to intraperitoneal hemorrhage and the apparent paucity of case reports documenting relative bradycardia secondary to hemorrhage from extremity injury, our hypothesis was that those patients with penetrating abdominal trauma would have a lessened tachycardic response to hemorrhage than patients with isolated extremity injury.

METHODS Study data were obtained from a retrospective analysis of the computerized trauma registry at the Cook County Hospital Trauma Unit from January 1, 1984, through December 31, 1987. All patients treated at the Cook County Hospital Trauma Unit are entered into this registry. The initial evaluation of the patient takes place in the trauma unit resuscitation area. At the time of disposition of the patient from the resuscitation area to an area for further care (eg, operating room, intensive care unit, observation unit), a secondyear resident on the trauma service is responsible for entering information about each patient and the resuscitation into the computer. Included in the entered data is a code for location and severity of injury. The eight locations include head, face, neck, chest, 82/269

TABLE 1. Descriptive statistics for patients with isolated penetrating abdominal trauma and isolated extremity trauma

Variable

Isolated Penetrating Abominal Trauma

Isolated Extremity Trauma

P

No, of patients

256

938

Sex Male (%) Female (%)

91.5 8.5

82.8 17.2

< .001

Age Mean (yr) Range (yr)

28.6 8 - 62

33.9 2 - 95

< .001

Systolic pressure Mean (mm Hg) Range (mm Hg)

124.9 40 - 240

135.8 60 - 230

< .001

Pulse Mean Range

92.3 56 - 150

88.5 48 - 176

< .001

Respirations Mean (breaths/min) Range (breaths/min)

22.4 12 - 44

20,5 10 - 44

< .001

Hematocrit Mean Range

39.1 14 - 54

12

Crystalloid Mean (L) Range (L)

0.0

TS index Mean Range

2.21 10.0

11.1 1 - 25

a b d o m e n , v e r t e b r a l c o l u m n and pelvis, upper extremities, and lower extremities. The severity codes are zero for no injury, 1 for negligible, 2 for m o d e r a t e , 3 for severe, 4 for might result in death, and 5 for unlikely to survive. To identify a group of patients with isolated penetrating abdominal trauma, all patients whose mechanism of injury was either a stab wound or gunshot wound, who went to laparotomy, and who had a coding of 0 or 1 for injury to other locations of the body excluding the abdomen were included. An assumption was made that if a patient went to laparotomy, the patient had penetration of the abdominal cavity. This assumption seemed reasonable as most gunshot wounds are penetrating and stab wounds with clinical evidence of penetration are managed at Cook County Hospital by ]aparotomy. In general, p a t i e n t s w i t h stab wounds to the abdomen who present Annals of Emergency Medicine

0.0

39.7 56

NS

1.37 15.0

< .001

10.4 9 - 33

< .021

to the Cook County Hospital trauma unit with stable vital signs and no clinical evidence of penetration arc observed. Evidence of penetration includes peritoneal signs, free air on abdominal film, retained stabbing implement, spreading tenderness on sequential examinations, blood in the nasogastric tube, blood on rectal examination, or evisceration. To identify patients with isolated severe extremity injury, all those patients who had a coding of 3 or higher in either the upper or lower extremities and had a coding of 0 or 1 in all other locations of the body were included. Obtained from the computerized trauma registry on all patients included in the study were age, sex, initial vital signs (blood pressure, pulse, respirations), m e c h a n i s m of injury, hematocrit, initial crystalloid resuscitation, surgery performed, Trauma Score (TS) index, indication for laparotomy, and whether the patient ap19:3 March 1990

TABLE 2. Comparison of patients with isolated penetrating abdominal trauma and patients with isolated extremity

trauma for different definitions of shock

Definition of Shock Systolic pressure ~< 100 mm Hg

Systolic pressure ~< 90 mm Hg

peared to be in shock at the t i m e of presentation. T h e TS index is a calc u l a t e d s u m - s q u a r e of t h e s e v e r i t y codes for each p a r t of the body. A higher score indicates a m o r e significant injury. Data analysis was performed using the PRODAS statistical software package. To identify variables associated w i t h pulse rate, univariate tests were u s e d ; c o n t i n u o u s variables bet w e e n groups w e r e c o m p a r e d u s i n g t w o - s a m p l e t t e s t s w h i l e Xz t e s t s were used in the case of discrete or categorical variables. Forward stepwise m u l t i p l e regression t e c h n i q u e s were u s e d to i d e n t i f y the c o m b i n a tion of variables related to pulse rate. P < .05 was considered statistically significant. A f t e r c o m p l e t i o n of the analyses, c h a r t s w e r e r e v i e w e d on t h e subgroups of patients in the a b d o m i n a l group or e x t r e m i t y group t h a t evid e n c e d r e l a t i v e bradycardia. For the p u r p o s e s of t h i s r e v i e w , r e l a t i v e b r a d y c a r d i a was defined as a p u l s e rate of less than 100 w i t h a concomitant s y s t o l i c b l o o d p r e s s u r e of less than 100 m m Hg. 19:3 March 1990

Variable Pulse No. of patients > 100 (%) ~< 100 (%) Mean Hematocrit Mean Crystalloid Mean (L) TS index Mean Pulse No. of patients > 100 (%) 100 (%) Mean Hematocrit Mean Crystalloid Mean (L) TS index Mean

Isolated Penetrating Abdominal Trauma

Isolated Extremity Trauma

41 23 (56.1) 18 (43.9) 104.6

54 23 (42.6) 31 (57.4) 100.9

34.7

33.4

3.32

3.17

16.3

11.5

26 17 (65.4) 9 (34.6) 109.1

25 14 (56.0) 11 (44.0) 110.4

33.7

31.4

3.48 18.2

RESULTS Between 1984 and 1987, there were 269 p a t i e n t s who m e t the i n c l u s i o n c r i t e r i a for i s o l a t e d p e n e t r a t i n g abd o m i n a l trauma. There were 13 cases excluded because of i n c o m p l e t e data, resulting in a total of 256 cases for analysis. Stab w o u n d s were responsible for 53.5% of the penetrating injuries and gunshot w o u n d s for the rem a i n d e r . D e s c r i p t i v e s t a t i s t i c s for this group of patients are given (Table 1). Between 1984 and 1987, there were 993 p a t i e n t s w h o m e t the i n c l u s i o n criteria for isolated severe e x t r e m i t y t r a u m a . T h e r e w e r e 55 c a s e s exc l u d e d b e c a u s e of i n c o m p l e t e data, r e s u l t i n g in a t o t a l of 938 cases of isolated extremity trauma between 1984 and 1987 for analysis. Descriptive s t a t i s t i c s for this group of patients are given (Table 1). T h e r e were s i g n i f i c a n t differences (P < .05) b e t w e e n these two groups in sex, age, s y s t o l i c pressure, m e a n p u l s e rate, r e s p i r a t o r y rate, crystall o i d r e s u s c i t a t i o n , a n d TS i n d e x . T h e r e was no s i g n i f i c a n t difference b e t w e e n t h e t w o g r o u p s in h e m a Annals of Emergency Medicine

4.70 12.6

P

NS NS NS NS < .001

NS NS NS NS < .002

t o c r i t on p r e s e n t a t i o n . The p a t i e n t s w i t h isolated penetrating a b d o m i n a l t r a u m a t e n d e d to be y o u n g e r a n d m a l e and have a l o w e r i n i t i a l pressure, a h i g h e r i n i t i a l pulse, and a h i g h e r i n i t i a l r e s p i r a t o r y rate. T h e y also received greater c r y s t a l l o i d res u s c i t a t i o n and had a higher TS index. In s u m m a r y , t h e s e d e s c r i p t i v e statistics suggest that the patients w i t h isolated p e n e t r a t i n g a b d o m i n a l t r a u m a were m o r e c r i t i c a l l y i n j u r e d and hypovolemic than those with isolated e x t r e m i t y trauma. U s i n g o p e r a t i o n a l d e f i n i t i o n s of shock as a systolic pressure less t h a n or equal to 100 m m Hg or less than or equal to 90 m m Hg, further comp a r i s o n s were m a d e b e t w e e n t h e s e t w o groups (Table 2). For the 100-mm Hg definition of shock, patients w i t h a b d o m i n a l t r a u m a w e r e j u d g e d by the t r a u m a resident to be m o r e critically injured as evidenced by the TS index (P < .001). However, there was no significant difference b e t w e e n the patients with isolated abdominal trauma and isolated extremity t r a u m a in m e a n pulse rate, crystalloid resuscitation, or h e m a t o c r i t . For 270/83

RELATIVE BRADYCARDIA Thompson, Adams & Barrett

the 90-mm Hg definition of shock, patients with abdominal trauma again were judged to be more critically injured as evidenced by the TS index (P < .002). However, again there was no significant difference in mean pulse rate, crystalloid resuscitation, or hematocrit. Additional comparisons between these two groups are made with operational definitions of shock (Table 3). The operational definitions of shock chosen were systolic blood pressure equal to or less than 100, 90, and 80 m m Hg and crystalloid more than 2.0, 3.0, and 4.0 L. There was no statistically significant difference between mean pulse rates for patients in shock from abdominal or from extremity trauma. Regardless of the operational definition of shock used, pulse rate differences between the shock and nonshock groups were always significant (P < .05) for extremity trauma and for all but one operational definition (crystalloid of more than 4.0 L) for abdominal trauma. M u l t i p l e regression t e c h n i q u e s were also used to determine the effect of blood loss from abdominal and extremity trauma on pulse rate. Multiple regression is a method in w h i c h the r e l a t i o n s h i p b e t w e e n pulse rate and other presenting variables is examined. Discrete variables were sex and injury type (abdominal versus extremity). Continuous variables used in this technique were age, respirations, crystalloid volume, hematocrit, and systolic pressure. Correlation coefficients between pulse rate and age, crystalloid volume, respirations, hematocrit, and systolic blood pressure were -.008, +.226, +.377, -.236, and -.147, respectively. Pulse rate was positively related (P < .001) to respiratory rate and crystalloid v o l u m e and negatively related (P < .001) to systolic blood pressure and hematocrit. The value of - . 0 0 8 for age indicates that it is a poor predictor of pulse rate. Using a four-variable model with respiratory rate, hcmatocrit, crystalloid volume, and systolic pressure, less than 20% of the variability in the presenting pulse rate can be explained. Furthermore, it is possible to conclude from this multiple regression analysis that presenting pulse rate is not statistically significantly affected by injury type (abdomen versus extremity) after conditioning on the effects of these four variables. 84/271

TABLE 3. Mean pulse rates in patients with extremity and abdominal

trauma for various operational definitions of shock Abdominal Trauma

Extremity Trauma

89.7 104.6 < .001

87.7 100.9 < .001

> 90 mm Hg ~< 90 m m Hg P

90.1 109.1 < .001

87.9 110.4 < .001

NS

> 80 m m Hg ~< 80 m m Hg P

90.7 112.3 < .002

88.1 112.5 < .004

NS

Crystalloid < 2.0 L ~> 2.0 L P

89.3 94.1 < .019

87.0 91.4 < .001

NS

< 3.0 L /> 3.0 L P

90.2 96.6 < .005

87.7 94.7 < .003

NS

< 4.0 L I> 4.0 L P

91.5 97.2 NS

87.8 101.6 < .003

NS

Definition of Shock Systolic b l o o d pressure > 100 m m Hg ~< 100 m m Hg P

P NS

Pulse rate differences between shock and nonshock groups were always statistically significant (P < .05) except for the abdominal group with shock defined by crystalloid equal to or more than 4.0 L. There was no statistically significant difference in mean pulse rates for patients with shock from abdominal or extremity trauma.

An attempt at chart review was made on all patients in either the abdominal group or extremity group who had relative bradycardia. Individual chart review was consistent with the computerized trauma registry. Eight of 256 patients (3.1%) in the abdominal group manifested relative bradycardia. Seventeen of 938 p a t i e n t s (1.8%) in the e x t r e m i t y group had relative bradycardia. In the abdominal subgroup of patients with a relative bradycardia, five of eight charts were located. All five of these patients survived, and all were normothermic at presentation and had blood in the peritoneal cavity documented at the time of laparotomy. In each of these five patients, relative bradycardia at admission was confirmed in their charts. Subsequent blood pressures during the remainder of the hospitalization were always higher, confirming that they were hypotensive at presentation. ECGs and arterial blood gases showed no consistent or remarkable findings. No patient had a history of cardiac disease or was on medications. Annals of Emergency Medicine

In the extremity subgroup with relative bradycardia, 11 of 17 charts were located. All 11 of these patients survived, and all were normothermic. In all but one patient, relative bradycardia at admission was confirmed in the chart. All but one had subsequently higher blood pressures during the remainder of the hospitalization. This patient had one subsequent systolic blood pressure of 90 m m Hg, which was less than his admission blood pressure of 98 m m Hg. He presented with the history of having gone through his automobile's windshield during an accident without loss of consciousness. He had a radial artery laceration and required 6 L of crystalloid in the resuscitation area; this, combined with a presenting blood pressure of 98 m m Hg, suggests that he was hypotensive and hypovolemic. A diagnosis of myocardial contusion also was considered in this patient because of the mechanism of injury. However, his ECG and technetium 99m scan were normal, and no CPK MB elevation was noted. No patient had a history of cardiac disease or was on medica19:3 March 1990

Relative

FIGURE. S c a t t e r p l o t o f p u l s e and systolic blood pressure data .for all p a t i e n t s w i t h a b d o m i n a l a n d ext r e m i t y trauma. * Irldicates one data point, a n u m b e r indicates the n u m ber of data points, and + indicates ten or more data points.

Bradycardia

Pulse

150

+

*

2

2

*

•

120

+

2

2

3

5*2 2

* 2** •* 2 5 3* 2 33 ** 24 33

5 5 *3 -

90

2

2

+

*

2

9*2+*5

* 5 3

* 2***

*2*4

3 5 *+*+53+2+4*+*9*25 2 25 22+53+ +3*627 3*5 3+*++++8+34+3+*2+ • 3 *82+4*+3+*2+34

* 2

3 2 3

*

*

6 4

7 2

*

*

* *

25 3

* *

228*2+*++2+8+5++4+**5*3 • 60

+

. . . . . .

*

+ . . . . . . . . .

40

** •* •*

7

7282*6

**2*

2*3

+ . . . . . . . . .

80

tions. A scatterplot of pulse rate and systolic blood pressure data for all patients with penetrating abdominal t r a u m a and e x t r e m i t y t r a u m a is shown (Figure). DISCUSSION The main purpose of this study was to document the incidence of relative bradycardia in patients pre ~ senting to an urban trauma center with either isolated penetrating abdominal trauma or isolated extremity trauma. Eight of the 256 patients (3.1%) with isolated penetrating abdominal trauma manifested relative bradycardia. Of the 938 patients with isolated severe extremity trauma, 17 (1.8%) manifested relative bradycardia. Considering only the patients who were in shock as defined by a presenting systolic blood pressure of less than 100 mg Hg, a substantial percentage were found to have inappropriate pulse rates of less than 100. There were 71 patients (29 with abdominal trauma and 42 with extremity trauma) who presented with a systolic blood pressure of less than 100 m m Hg. Of these, 25 patients (eight with abdominal trauma and 17 with extremity trauma) had an initial pulse rate of less than 100. The rate of relative bradycardia in this subgroup was 35.2%. (There was no statistically significant difference in the rates of relative bradycardia in those

2

+ . . . . . . . . .

120 Systolic

19:3 March 1990

+22+*+**+

324*

2*

4

3

*

*

5

2

*

*

+ . . . . . . . . .

160

Blood

*

2

+ . . . . . . . . .

200

+

240

Pressure

with abdominal or extremity injuties: 27.6% and 40.5%, respectively.) Similarly, if only patients who were in shock as defined by a presenting systolic blood pressure of less than 90 m m Hg are considered, a substantial percentage (45.8%) were found to be inappropriately bradycardic. There were 24 patients who had a systolic blood pressure of less than 90 m m Hg; 11 (three with abdominal t r a u m a and eight with e x t r e m i t y trauma) of the 24 had an initial pulse rate of less than 100. This definition of relative bradycardia was chosen to exclude pa h tients who normally might have a systolic blood pressure of, for example, 100 m m Hg and a pulse of 80. Our chart review shows that this defi n i t i o n a d e q u a t e l y excluded norm o v o l e m i c patients. The chart review documented severely injured patients who were resuscitated with an average of 2.8 L crystalloid and in nearly all cases had subsequently higher blood pressures during their hospitalizations. However, this definition does not include all patients who potentially manifested relative bradycardia. For example, a patient who normally has a systolic blood pressure of 180 m m Hg and presented with a systolic blood pressure of 100 m m Hg and a pulse of 96 would have been hypotensive and hypovolemic and would not have been included in this defini h tion. Similarly, a patient who preAnnals of Emergency Medicine

sented with a systolic blood pressure of 82 m m Hg and a pulse of 100 would not have been included in our chosen definition of relative bradycardia. By expanding the definition to a blood pressure less than or equal to 100 m m Hg and a pulse less than or equal to 100, the overall incidence in our penetrating abdominal trauma group becomes 7.0% and the overall incidence in the extremity trauma group becomes 3.3%. Thus, this definition is relatively specific for the phenomenon of relative bradycardia but may not be sufficiently sensitive. The second purpose of this study was to address the q u e s t i o n of w h e t h e r i n t r a p e r i t o n e a l bleeding alone was a risk factor for the development of relative bradycardia. This was evaluated by comparing pulse rates in a group of patients with isolated penetrating abdominal trauma with those of a group of patients with isolated extremity trauma using various operational definitions of shock. If our hypothesis had been correct, the subgroup of patients with penetrating abdominal trauma and in shock by one of the operational definitions chosen should have had a lower mean pulse rate. Instead, there was no statistically significant difference in pulse rates between the pat i e n t s in s h o c k w i t h a b d o m i n a l trauma and those in shock with extremity trauma. A separate analysis using a multiple regression model also failed to show any difference in pulse rate attributable to the type of injury. The results of the present study, therefore, suggest that i n t r a p e r i t o n e a l bleeding alone is not a predisposing risk factor for the development of relative bradycardia. U s i n g a d e f i n i t i o n of r e l a t i v e bradycardia as a systolic blood pressure of less than 100 m m Hg and a concomitant pulse rate of less than 100, the incidence of relative bradycardia was 3.1% in the isolated penetrating abdominal group and 1.8% in the isolated extremity group. This difference in incidence of relative bradycardia in patients with isolated 272/85

RELATIVE BRADYCARDIA Thompson, Adams & Barrett

abdominal trauma and those with isolated extremity trauma is not offered as evidence to support a peritoneal-associated vagal response because of the various statistically significant differences between these two groups in addition to the presence or absence of intra-abdominal bleeding (Table 1). Notable is the fact that the patients with isolated penetrating abdominal trauma had higher mean initial pulse rates and lower mean systolic blood pressures and were given more crystalloid. These differences suggest that the patients with abdominal trauma were more hypovolemic as a group at presentation than the patients with extremity trauma. One limitation of our study is that ideally a direct comparison of pulse rate with blood volume should be made to clearly relate pulse response to blood loss. Instead, operational definitions of shock based on hypotension and fluid resuscitation, indirect measures of blood loss and volume status, were used. Although this is a limitation, it does not appear that this method would have biased the results. To the best of our knowledge, no previous studies have been designed to specifically address the effect of intraperitoneal bleeding on relative bradycardia. Previous references to the phenomenon of relative bradycardia in the setting of intraperitoneal hemorrhage, w h i c h theorized the possibility of a vagal response from blood stimulating the peritoneal lining, were based on a study population of only a few patients.8,12 In 1973, Burri et al performed a prospective analysis of 176 patients w i t h h e m o r r h a g e to i d e n t i f y the usefulness of various hemodynamic parameters (eg, pulse, blood pressure) in e s t i m a t i n g blood loss. 19 T h e y measured blood volume in patients with hemorrhage from extremities, the intestinal tract, chest, and intraperitoneal sites using radioiodinated albumin. They noted a wide scatter of heart rate data in relation to blood loss. Regardless of the source of blood loss, they noted a heart rate increase with increasing blood loss but stated that this rate increase for intra-abdominal bleeding was not statistically significant. They also noted that acute hemorrhage into the abdominal cavity caused less of an increase in heart rate than did losses of 86/273

TABLE 4. Factors affecting the pulse rate in the trauma patient Tachycardia

Bradycardia

Hypovolemia

Relative bradycardia: possible vagal, hypovolemic, humoral, ischemic etiology; possible superimposed vasovagal reaction to pain, fear Vasovagal reaction to pain, fear

Emotional or sympathetic response: anxiety, fear Cardiac or structural: cardiomyopathy, valvular Cardiac: tachydysrhythmias Drugs: stimulants, anticholinergics, vasodilators, etc Hyperthermia Cardiac tamponade Endocrine: hyperthyroidism Age: children Intubation or laryngoscopy or surgical procedures Tension pneumothorax Anemia Sepsis Other

Cardiac: bradydysrhythmias Acidosis Drugs: cholinergics, 13-blockers, calcium channel blockers, etc Hypothermia Physical training Endocrine: hypothyroidism Age: adults Increased ICP: Cushing response Hypoxia Hypoglycemia Spinal cord injury Other

other etiologies. They did not state how many patients in their subgroup had intra-abdominal bleeding. Several experiments performed in human beings have investigated the effects of the introduction of blood into the peritoneal cavity; none have described the p h e n o m e n o n of relative bradycardia. Mengert et al described 16 female patients who preoperatively received an intra-abdominal injection of autologous blood (up to 500 mL). The purpose was to correlate s y m p t o m s with quantity of free blood. Patients were noted to have abdominal pain, fullness, and tenderness. No mention was made of bradycardia or hypotension occurring. 2o Pritchard et al studied the uptake of labeled blood from the peritoneal cavity into the circulation. Labeled blood 1475 to 1,150 mL) was introduced into the abdominal cavity just before the completion of a surgical procedure; there was no mention of bradycardia or hypotension developing in t h e i r p a t i e n t s . 21 S i m i l a r Annals of Emergency Medicine

studies have been performed in dogs, with no relative bradycardia being described.22, z3 Cole and Montgomery reported their experience with intraperitoneal blood transfusion in 1928. They reported 237 transfusions in 117 infants and children, and bradycardia and hypotension were not mentioned as side effects. 24 In the patients in this study, there was a statistically significant negative correlation between pulse rate and blood pressure in patients with isolated abdominal penetrating trauma and in those with isolated extremity trauma. However, the correlation was weak, and in the multiple regression model, less than 20% of the pulse variability could be explained using hematocrit, systolic blood pressure, age, injury type, respiratory rate, and sex as predictors. Vayer et al studied 96 battlefield patients with isolated penetrating abdominal trauma and failed to show a statistically significant correlation between pulse and systolic blood pressure3 ¢ It is possible that the fail19:3 March 1990

ure of Vayer et al's study (in comparison w i t h our study) to achieve statistical significance could be explained by d i f f e r e n c e s b e t w e e n t h e s t u d y populations. A n obvious difference in the s t u d y p o p u l a t i o n s was t h a t Vayer et al's patients were battlefield casualties and our p a t i e n t s had c i v i l i a n t r a u m a with, perhaps, lower muzzlevelocity weapons. However, there was no s t a t i s t i c a l difference in t h e n u m b e r of p a t i e n t s in t h e p r e s e n t study w h o had blood pressures of 100 m m Hg or less (16.3% vs 12.4%). Another difference between the two s t u d y p o p u l a t i o n s was age; none of t h e i r p a t i e n t s were less t h a n 18 years old. After excluding all patients less t h a n 18 years old in our study, there is still a s t a t i s t i c a l l y significant negative correlation between pulse and blood pressure. The m o s t l i k e l y explanation for the fact that the present s t u d y achieved statistical significance and Vayer et al's did not is the larger n u m b e r of patients in the present study. A n o t h e r study, by Snyder and D r e s n i c k , w i t h even fewer patients also failed to achieve statistical significance. 13 Regardless of the difference in results b e t w e e n these two studies and ours, t h e s a m e c o n c l u s i o n can be reached: Pulse rate is a poor predictor of h y p o v o l e m i a i n p a t i e n t s w i t h h e m o r r h a g i c shock.9,12,13 A scatterplot of the pulse rate data from the present study illustrates this (Figure). T h e e t i o l o g y of t h i s a b s e n c e of a p p r o p r i a t e t a c h y c a r d i c response to h y p o v o l e m i a r e m a i n s o b s c u r e , as does the appropriate t r e a t m e n t for it; it is p r o b a b l y m u l t i f a c t o r i a l , a n d t r e a t m e n t w i l l reflect this. Theories that have been p u t forth by various a u t h o r s refer to m y o c a r d i a l i s c h e mia, s-7 a p r e t e r m i n a l event, s-7 intraabdominal hemorrhage,a,10,12,13 vagal effects, lO,19,25,26 and h y p o v o lemia.9, ~1,26 Our study showed no s t a t i s t i c a l l y significant effect of i n t r a - a b d o m i n a l bleeding on pulse rate. In those pat i e n t s in our s t u d y w h o h a d E C G s performed, n o n e d e m o n s t r a t e d myocardial i s c h e m i a . Also n o t a b l e was that in our study, relative bradycardia was not a p r e t e r m i n a l event; each patient who manifested relative b r a d y c a r d i a s u r v i v e d . A r e v i e w on the topic of relative bradycardia also suggests that it does not necessarily indicate irreversible shock. 26 Significant h y p o v o l e m i a alone ret9:3 March 1990

m a i n s a l i k e l y p r i m a r y e t i o l o g y for this relative bradycardia. Bradycardia in the face of h y p o v o l e m i a has been reproduced e x p e r i m e n t a l l y in h u m a n beings.9,2~Y M u r r a y et al used negative lower body pressure to reduce effective blood v o l u m e and, thus, study h e m o d y n a m i c r e s p o n s e to p r o g r e s sive h y p o v o l e m i a . ~7 In their study of seven patients, graded negative press u r e w a s a p p l i e d to t h e l o w e r extremities until syncope occurred. T h e y n o t e d t h a t all seven p a t i e n t s e x p e r i e n c e d n a u s e a just before syncope and then hypotension and b r a d y c a r d i a at t h e t i m e of syncope. They concluded that this method was a reproducible, comfortable, effective, and practical w a y of inducing h y p o v o l e m i a and vasodepressor syncope. Similarly, effective blood volu m e has been r e d u c e d using a tilttable w i t h e q u i v a l e n t results. 9 T h i s l a t t e r s t u d y favored a vagal m e c h a n i s m as an explanation for the relat i v e b r a d y c a r d i a and r e c o m m e n d e d i m m e d i a t e v o l u m e r e p l a c e m e n t as therapy. Bradycardia during hemorrhage also has been reproduced experimentally in animals.28, 29 It has been post u l a t e d that the bradycardia is a prot e c t i v e reflex d e s i g n e d to i n c r e a s e diastolic filling in the presence of severe hypovolemia. 29 One recent study by Barriot et al of t r a u m a patients w i t h relative bradycardia described v o l u m e r e p l a c e m e n t and t h e u s e of m i l i t a r y a n t i s h o c k t r o u s e r s as e f f e c t i v e t r e a t m e n t . H S e c h e r a n d Bie, in t h e i r r e c e n t review, also r e c o m m e n d a t t e n t i o n to increasing effective blood v o l u m e as the m a i n therapy. 26 C o n f o u n d i n g t h e c l a r i f i c a t i o n of the etiology of relative bradycardia is the m y r i a d of other factors that have an effect on h e a r t rate (Table 4) m e d i c a t i o n s , cardiac disease, p h y s i cal conditioning, pain, emotion, temp e r a t u r e , and o t h e r s . T h e effect of t h e s e v a r i a b l e s is r e f l e c t e d in t h e wide s c a t t e r of data in the pulse-systolic blood pressure scatterplot (Fig-

ureJ. CONCLUSION In a large series of patients, a 3.1% i n c i d e n c e of r e l a t i v e b r a d y c a r d i a in isolated penetrating abdominal t r a u m a and 1.8% in i s o l a t e d severe e x t r e m i t y injury was documented. A pulse rate of less than 100 was present in 35.2% of all patients presentAnnals of Emergency Medicine

ing w i t h a systolic blood pressure of less than 100 m m Hg. Relative bradycardia has n o w been d o c u m e n t e d in c i v i l i a n and b a t t l e f i e l d p e n e t r a t i n g a b d o m i n a l t r a u m a as well as in other etiologies of hypovolemia. Previously d e s c r i b e d as a p r e t e r m i n a l e v e n t , there was no increased m o r t a l i t y ass o c i a t e d w i t h t h i s p h e n o m e n o n in our study. T h e r e was no s t a t i s t i c a l l y signific a n t difference in pulse rates in patients w i t h h e m o r r h a g i c shock from isolated a b d o m i n a l t r a u m a compared w i t h patients w i t h isolated e x t r e m i t y trauma. This result does n o t support t h e previously theorized vagal-mediated response unique to intrap e r i t o n e a l bleeding. Traditionally, tachycardia has been t h o u g h t to be a good indicator of volume status in hemorrhagic shock. We c o n c l u d e t h a t t h e p u l s e rate in t h e p a t i e n t w i t h hemorrhage often is a n u n r e l i a b l e i n d i c a t o r of h y p o v o l e m i a , A g r e a t e r a p p r e c i a t i o n of the p h e n o m e n o n of relative bradycardia is needed, both in clinical practice and in textbooks discussing the hemodynamics of h e m o r r h a g i c shock. The authors are indebted to Michele A Parker, RN, of Northwestern Memorial Hospital for her assistance with statistical analysis and to Charles Sheaff, MD, of Cook County Hospital, for his assistance in obtaining the data from the computerized trauma registry. They also are appreciative of assistance given by Joan Duda, RN, of Cook County Hospital, in data collection.

REFERENCES

1. Shoemaker WC: Pathophysiology and therapy of hemorrhage and trauma states, in Cowley RA, Trump BF (eds}: Pathophysiology of Shock, Anoxia, and Ischemia. Baltimore, Waverly Press, 1982, p 439-445. 2. American College of Surgeons: Advanced 7¥auma Life Support Course For Physicians.

Chicago, ACS, 1985. 3. Abraham E: Approach to the patient in shock, in Callaham ML (ed}:Current Therapy in Emergency Medicine. Philadelphia, BC Decker Inc, 1987, p 52-53. 4. Jorden R: Shock, in Tintinalli JE, Krome RL, Ruiz E (eds): Emergency Medicine: A Comprehensive Study Guide. New York, McGraw-Hill Book Co, 1988, p 111. 5. Mannix FL: Hemorrhagic shock, in Rosen P (ed): Emergency Medicine. St Louis, CV Mosby Co, 1988, p 187. 6. Wiener 8L, Barrett J: Trauma Management. Philadelphia, WB Saunders, 1986, p 37-39, 5l. 7. Millikan JS, Moore EE, Den EL, et al: Tempo274/87

RELATIVE BRADYCARDIA Thompson, Adams & Barrett

rary cardiac pacing in traumatic arrest victims. Ann Emerg Med 1980~9:591-593. 8. |ansen RP8: Relative bradycardia: A sign of acute intraperitoneal bleeding. Aust N Z Obstet Gynaecol 1978;18:206-208. 9. Secher NH, Kare SJ, Werner C, et al: Bradycardia during severe but reversible shock in man. Circ Shock 1984;14:267-274. 10. Adams SL, Greene J8: Absence of a tachycardic response to intraperitoneal hemorrhage. J Emerg Med 1986;4:383-389. 11. Barriot P, Riou B: Hemorrhagic shock with paradoxical bradycardia. Intens Care Med 1987;13:203-207. 12. Vayer JS, Henderson JV, Bellamy RF, et al: Absence of a tachycardic response to shock in penetrating intraperitoneal injury. Ann Emerg Med 1988;17:227-231.

15. Hopkins RW, Sabga G, Penn I, et ah Hemodynamics aspects of hemorrhagic and septic shock. JAMA 1965;191:731-735. 16. Hoffman RL: Rupture of the spleen. A m J Obstet Gynecol 1972;113:524-530. 17. Hyun BH, Varga CF, Rubin RJ: Spontaneous and pathologic rupture of the spleen. Arch Surg 1972;104:652-657. 18. Moir JC, Myerscough PR: Munro Kerr's Operative Obstetrics, ed 8. London, Tindell and Cassell, 1971, p 840. 19. Burri C, Henkerneyer H, Passler HH, et ah Evaluation of acute blood loss by means of simple h e m o d y n a m i c p a r a m e t e r s . Prog Surg 1973;11:108-131. 20. Mengert WF, Cobb 8W, Brown WW: Introduction of blood into the peritoneal cavity. JAMA 1951;147:34-37.

13. 8nyder HS, Dresnick SJ: Lack of taehycardic response to hypotension in penetrating abdominal trauma {abstract). Ann Emerg Med 1988~ 17:879.

21. Pritchard JA, Adams RH: The fate of blood in the abdominal cavity. Surg Gynecol Obstet 1957;105:621-629.

14. Emerson CP, Ebert RV: A study of shock in battle casualities: Measurements of the blood volume changes in response to therapy. Ann Surg 1945;122:745-772.

22. Florey H, Witts LJ: Absorption of blood from the peritoneal cavity. Lancet 1928;1: 1323-1325.

88/275

23. Hahn PF, Miller LL, Robscheitt-Robbins FS,

Annals of Emergency Medicine

et ah Peritoneal absorption. J Exper Med 1944;80:77-82. 24. Cole WCC, Montgomery JC: Intraperitoneal blood transfusion: Report of two hundred and thirty seven transfusions in one hundred and seventeen patients in private practice. A m J Dis Child 1929;37:497-510. 25. Barcroft H, Edholm OG, McMichael J, et ah Posthaemorrhagic fainting, study by cardiac output and forearm flow. Lancet 1944;1:489-491. 26. Secher NH, Bie P: Bradycardia during reversible haemorrhagic shock - A forgotten ob k servation.2 Clin Physiol 1985;5:315-323. 27. Murray RH, Thompson LJ, Bowers JA, et ah Hemodynamie effects of graded hypovolemia and vascodepressor syncope induced by lower body negative pressure. A m Heart J 1968;76: 799-811. 28. Hamburger SA, Henry DP: Mechanism of hemorrhage induced bradycardia in the rat (abstract 1. FASEB [ 1988;2:498. 29. Oberg B, Thoren P: Increased activity in vagal cardiac afferents correlated to the appearance of reflex bradycardia during severe hemorrhage in cats. Acta Physiol Scand 1970;80: 22A-23A.

19:3 March 1990