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GENERAL ARTICLES

The Hemodynamic and Metabolic Effects of Tourniquet Application During Knee Surgery

Massimo Girardis, MD^*, Stefania Milesi, MD^*, Stefano Donato, MD^*, Michela Raffaelli, MD^*, Alessandra Spasiano, MD^*, Guglielmo Antonutto, MD, Alberto Pasqualucci, MD^*, and Alberto Pasetto, MD^*

*Cattedra di Anestesiologia e Rianimazione and Cattedra di Fisiologia Umana, Università degli Studi di Udine, Udine, Italy

Address correspondence and reprint requests to Massimo Girardis, Cattedra di Anestesiologia e Rianimazione, University of Udine, P. le S. Maria della Misericordia, 33100-Udine, Italy. Address e-mail to m.girardis{at}med.uniud.it

	Abstract

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We evaluated the effects of tourniquet application on the cardiovascular system and metabolism in 10 young men undergoing knee surgery with general anesthesia. The duration of inflation was from 75 to 108 min. Heart rate, mean arterial pressure, cardiac index (CI) by pulse contour method, and systemic vascular resistance were measured before, during, and after tourniquet inflation. pH, PaO₂, PaCO₂, and lactate blood concentrations were also measured. O₂ and CO₂ were assessed every minute from tracheal intubation up to 15 min after tourniquet deflation and O₂ in excess of the basal value over the 15 min after deflation (O₂exc) was calculated. Mean arterial pressure increased 26% (P < 0.05) during inflation and returned to basal values after deflation. CI did not change immediately after inflation; although, thereafter, it increased 18% (P < 0.05). Five minutes after deflation, CI further increased to a value 40% higher than the basal value. Therefore, systemic vascular resistance increased 20% suddenly after inflation (P < 0.05) and decreased 18% after deflation (P < 0.05). O₂ and CO₂ remained stable during inflation and increased (P < 0.05) after deflation. O₂exc depended on duration of tourniquet inflation time (Tisch) (P < 0.05). After deflation, PaCO₂ and lactate increased (P < 0.05) while Tisch increased. We conclude that tourniquet application induces modifications of the cardiovascular system and metabolism, which depend on tourniquet phase and on Tisch. Whether these modifications could be relevant in patients with poor physical conditions is not known.

Implications: The clinical effects of tourniquet application were evaluated in 10 young men undergoing knee surgery. Our data indicate that tourniquet application causes hemodynamic and metabolic changes which may become clinically relevant after a long period of tourniquet inflation, particularly in patients with concomitant cardiovascular diseases.

	Introduction

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Orthopedic surgery of the extremities often requires a bloodless field normally obtained by tourniquet application (1). This procedure causes hemodynamic and metabolic changes whose entity depends on the tourniquet phase (inflation-deflation), the time duration of tourniquet inflation, the extension of the ischemic area, the anesthesia method (i.e., general, epidural, or spinal), and the cardiovascular conditions of the patient. The variations of arterial blood pressure and heart rate occurring after tourniquet inflation (INF) and deflation (DEF) have been described in detail (2–4). On the contrary, little is known about cardiac output (CO) changes. Therefore, the hemodynamic mechanisms underlying blood pressure changes occurring during tourniquet application are unclear. In addition, numerous studies have investigated the metabolic effects of DEF (4–8), whereas oxygen consumption and carbon dioxide elimination during INF have been rarely reported. The purpose of this clinical study was to quantify the effects of INF and DEF on the cardiovascular system and metabolism of young male patients undergoing knee surgery during general anesthesia.

	Methods

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Ten young men were investigated during cruciate ligament reconstruction with general anesthesia. All of the subjects gave informed consent and had no signs of cardiopulmonary disease (ASA physical status I). Body surface area (BSA) was calculated according to Du Bois and Du Bois (9). Our study protocol was approved by the ethical committee of our university.

Ten minutes before anesthesia induction, patients received 0.7 mg/kg IV diazepam. Anesthesia was induced with 5 µg/kg fentanyl, 0.1 mg/kg vecuronium, and 2.5 mg/kg propofol, and maintained with 6–10 mg · kg^-1 · h^-1 propofol and 1 µg · kg^-1 · min^-1 vecuronium after tracheal intubation. Ventilation was controlled by using an O₂/air mixture with O₂ inspired fraction between 0.30 and 0.35 (Servo 900C; Siemens-Elma, Solna, Sweden). The inspired ventilation was adjusted to obtain an end-tidal CO₂ partial pressure between 30 and 35 mm Hg starting 15 min after anesthesia induction and for the duration of the study. After anesthetic induction, a 20-gauge catheter was placed in the radial artery. A pneumatic thigh tourniquet was applied as proximal as possible to limb radix and it was inflated to a pressure of 350 mm Hg for the entire surgical time. Surgical procedures started after tourniquet INF.

Invasive arterial pressure, heart rate (HR), end-tidal CO₂ partial pressure, and peripheral O₂ saturation were continuously monitored by means of a monitoring system (M1156A; Hewlett-Packard, Palo Alto, CA). A metabolic unit (Deltatrac; Datex, Helisinki, Finland) measured expired ventilation, mixed expired CO₂ fraction, FIO₂, and mixed expired O₂ fraction and also calculated oxygen consumption (O₂), CO₂ pulmonary elimination (CO₂), and respiratory quotient. The arterial pressure profile was digitized (MP 100; Biopac System, Goleta, CA) and recorded on magnetic disk.

Data were collected seven times during general anesthesia, as follows: 15 min after anesthetic induction (T0); 15, 30, and 60 min after INF (Ti15, Ti30, and Ti60, respectively); and 5, 10, and 15 min after DEF (Td5, Td10, and Td15, respectively). During each collection (Table 1), we recorded 20 s of arterial blood pressure profile and drew 3 mL of blood from the radial artery for measurement of hemoglobin (Hb) concentration (CellDyn 1700; Abbott Diagnostics, Abbott Park, IL), pH, PaO₂, PaCO₂, and lactate (La) concentration (Stat Profile Ultra; Nova Biomedical, Waltham, MA). O₂ and CO₂ were measured every minute from tracheal intubation up to 15 min after DEF. We calculated the O₂ in excess of the basal value (at T0) over the 15 min after cuff DEF (VO₂exc). Stroke volume (SV) of the left ventricle was estimated by using the pulse contour method (10). This method is based on the following relationship:

between SV and the area underneath the systolic portion (and above the diastolic value) of the peripheral arterial profile (As) and where Z is a calibration factor dimensionally equal to aortic impedance. Z changes with the age and with the cardiovascular conditions (HR and mean arterial pressure [MAP]) of the patient, and it was estimated by means of the algorithm proposed by Wesseling et al. (10). For each data collection we measured MAP, HR, and the arterial profile over 10 heart cycles. This allowed us to calculate SV from the above equation and cardiac output (CO = SV · HR). Then, we calculated cardiac index (CI) dividing CO by BSA and systemic vascular resistance index (SVRI) from the ratio of MAP to CI. O₂ and CO₂ were also normalized by BSA (O₂I and CO₂I).

	Results

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Patient mean age and BSA were 25.7 ± 6.8 yr (range 18–38 yr) and 1.97 ± 0.14 m² (range 1.82–2.25 m²), respectively. The average duration of INF (Tisch) was 93.0 ± 10.1 min (range 75–108 min). A bloodless surgical field was obtained in all cases.

During tourniquet INF, HR did not change, whereas MAP was higher (P < 0.05) than at T0 by approximately 27% (Figure 1). CO slightly decreased 15 min after INF and, thereafter, it increased (P < 0.05) in all patients to a mean value 18% higher than at T0. Consequently, at Ti15, SVRI values were higher (P < 0.05) than those collected at T0 by 38% and, then, they returned to basal values (Figure 2). During INF, CO₂ and PaCO₂ slightly decreased compared with T0 (P > 0.05) and O₂, PaO₂, pH, Hb, and La remained stable (Table 1).

View larger version (21K): [in this window] [in a new window]   Figure 1. Mean arterial pressure (MAP) () and heart rate (HR) () before (T0); 15, 30, and 60 min after tourniquet inflation (Ti); and 5,10, and 15 after tourniquet deflation (Td).

View larger version (25K): [in this window] [in a new window]   Figure 2. Cardiac index (CI) (•) and systemic vascular resistances index (SVRI) () before (T0); 15, 30, and 60 min after tourniquet inflation (Ti); and 5,10, and 15 after tourniquet deflation (Td). *P < 0.05 compared with T0.

After DEF, O₂I and CO₂I increased (P < 0.05) and achieved the peak value within 5 min in all patients. The differences between O₂ and CO₂ values at Td5 and at T0 (in mL/min^-1) were not correlated to BSA; however, when normalized by BSA (mL · min^-1 · m^-2) they increased when Tisch increased (P < 0.05) (slope = 1.5 mL · min^-2 · m^-2 and r = 0.80 for O₂I; slope = 0.8 mL · min^-2 · m^-2 and r = 0.72 for CO₂I). O₂exc was linearly correlated to Tisch (Figure 3). PaCO₂ and La increased after DEF (P < 0.05) and the peak values were observed in all patients at Td5. The differences between PaCO₂ and La measured at Td5 and those measured at T0 increased as Tisch increased (P < 0.05) (slope = 0.3 mm Hg/min^-1 and r = 0.70 for PaCO₂; slope = 0.05 mM/min^-1 and r = 0.68 for La). At Td5, pH was lower than that observed at T0 and at Ti60 (P < 0.05). The difference between pH at Td5 and T0 depended on Tisch (slope = -0.003 U/min^-1; r = 0.72; P < 0.05). Fifteen min after DEF, CO₂I and PaCO₂ returned to basal values; however, O₂I and La remained larger than at T0 (P < 0.05).

View larger version (11K): [in this window] [in a new window]   Figure 3. The relationship between oxygen consumption in excess of basal oxygen consumption over 15 min after cuff deflation (VO2exc, mL/m-2) and ischemia time (Tisch, min). The regression line is described by the following equation: O2exc = 13.3 · Tisch - 647. r = 0.74, P < 0.05.

	Discussion

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The use of invasive (flow-directed pulmonary catheter) and expensive (pulsed Doppler echocardiography) methods to evaluate hemodynamic variables does not appear clinically justified in patients without cardiopulmonary diseases undergoing orthopedic surgery of the lower limbs. A useful alternative, in view of its low invasiveness and cost, is the measure of CO from the arterial pressure profile. This method is based on the relationship among the SV of the left ventricle, the area subtended by the systolic phase of the arterial pressure profile and the calibration factor (Z) dimensionally and conceptually equal to the impedance of the arterial tree (10). To calculate Z, we used an algorithm previously validated comparing CO values obtained by this algorithm with those obtained by reference methods. The comparison yielded correlation coefficients ranging between 0.81 and 0.96 and mean percentage differences ranging between 8.1 and 11.0% (11,12). The development of an automated system (PICCO^TM; Pulsion, München, Germany) has increased the use of the pulse contour method in anesthesia and critical care practices. Comparison of the pulse contour method and thermodilution has indicated a good correlation between the two methods when used with critical patients (13,14).

In anesthetized patients, the tourniquet INF produces an increase of MAP which has been attributed to the increase of SVRI by the reduction of the vascular bed, an expansion of central venous blood by exsanguination of the limb before INF, and pain sensation by tourniquet compression and ischemia (1–3). The two former mechanisms are responsible for the increase of MAP occurring immediately after INF. Indeed, expansion of central blood volume could not be taken into account in our patients because exsanguination was not performed. Pain sensation, on the contrary, would be the cause of hypertension occurring 30–45 min after INF (2,3). Our data support this hypothesis. In fact, at Ti15 hypertension was entirely sustained by an increase of SVRI, whereas it was associated with CI increasing in the following time points of INF. Therefore, the increase in MAP occurring later during tourniquet INF cannot be explained by a pure hemodynamic effect of the tourniquet (decrease of vascular bed), but it is probably sustained by pain sensation. In accordance with others (4), hypertension in the later phases of INF was not associated with an increase in HR. The reasons for this controversial finding are unclear. In addition, the effects of anesthetics on the heart and on the physiological cardiovascular reflexes may be involved in the hemodynamic response to tourniquet application and in the lack of HR increasing during INF (2).

As far as metabolism during INF is concerned, an immediate reduction of O₂ and CO₂ should be observed after cuff INF caused by no arterial and venous blood flow in the limb. In contrast, in our study CO₂ slightly decreased and O₂ did not vary after INF. These data are partially explained by an increase of total body metabolic rate caused by pain sensation after cuff INF. Alternatively, the bias of the method used to measure O₂ and CO₂ (Deltatrac) must be taken into account. In fact, during general anesthesia the O₂ of one limb is smaller than 10% of total body O₂. Therefore, the entity of O₂ reduction after cuff INF is probably lower than the measurement accuracy of the Deltatrac (15). Inhaled anesthetics and fluctuations of FIO₂, which could cause problems in gas exchange measurements by Deltatrac, were excluded from the anesthetic protocol.

Tourniquet DEF causes a decrease of MAP that depends on the anesthetic method used (4). In our patients, decreased MAP was similar to that observed by others during general anesthesia (6). A postischemic reactive vasodilation and the release of metabolites from ischemic area to systemic circulation were considered the mechanisms responsible for the decreased MAP (6,7). Accordingly, we observed a marked reduction of SVR after DEF. As a compensatory mechanism, CI increased to maintain normotension. In fact, MAP values at Td5 were equal to basal values, whereas CI and SVRI were significantly different. As expected, the compensatory increase of CI was mainly sustained by an increase of myocardial inotropic state and, thereby, by an increase of SV (16). Because SVRI reduction directly depends on Tisch, this compensatory mechanism is larger, the longer the Tisch period. These events could be clinically relevant in a patient with a poor cardiac reserve whose compensatory response cannot be sufficient to avoid severe reduction of MAP, particularly after a long period of Tisch. Parmet et al. (17) reported a slight increase of CI and stable values of MAP and SVRI after tourniquet DEF in 34 patients undergoing knee arthroplasty during general anesthesia. These differences with our data can be explained by the fact that in the Parmet study, patients were aged and had cardiovascular diseases and each patient received 1 unit of autologous blood before tourniquet release to improve preload. We did not infuse red blood cells because Hb was in the normal range in all patients before DEF.

After DEF, lactate b (Lab), O₂, and CO₂ time courses were similar to those observed by others (5–7). Because O₂ is not supplied during INF, the energy for cellular metabolism is provided by O₂ stores, alactic (high energy phosphate) and lactic anaerobic processes in the ischemic area. These mechanisms lead to an increase of Lab and to VO₂exc after tourniquet release. The VO₂exc provides the energy needed to replenish high energy phosphate pool and O₂ stores depleted during ischemia (fast component) and the energy needed to resyntetize glycogen from La (slow component) (18). Therefore, VO₂exc ought to increase with the increase of Tisch. This was the case in our patients (see Figure 3). Others did not observe any relationship between VO₂exc and Tisch (5,7). This finding was attributed to a progressive decrease of temperature in the nonperfused extremity, which causes the reduction of metabolic rate of skeletal muscle. If this is true, the La increasing after reperfusion would not depend on Tisch. By contrast, in our patients increased Lab correlated with Tisch after DEF. Others also observed this relationship during both general anesthesia and spinal anesthesia (6,7,19).

Along with La, O₂ and CO₂, PaCO₂, and pH variations at Td5 depended on Tisch. Increased K⁺ plasma levels depending on Tisch have also been reported (7). These changes did not cause any significant clinical problem in our healthy young patients. Nevertheless, these transient changes can become relevant in certain patients. For instance, in patients with a head injury, the sudden increase of PaCO₂ may worsen intracranial pressure, especially after long periods of tourniquet INF.

In summary, our study indicates that the systemic arterial pressure variations observed during tourniquet INF and after DEF, are sustained by significant variations of CO and SVR. The hemodynamic and metabolic changes occurring after tourniquet DEF depend on the time of ischemia and, therefore, the tourniquet INF period should be as short as possible in patients in poor physical condition.

	References

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999