Peripheral
Vascular Tone in Sepsis*
Mark E. Astiz, M.D., F.C.C.P.; Elena Tilly, M.D.; Eric D. Rackow, M.D., F.C.C.P.; and Max H. Weil, M.D., Ph.D., F.C.C.P.
Septic shock is characterized as a distributive form of circulatory failure. We examined the relationship of changes in forearm arterial, ve1m0s, and microvascular tone to the severity of sepsis. The study population consisted of ten control patients, 15 patients with sepsis, and eight patients with sepsis and shock. Patients treated with inotropic, vasopressor, or vasodilator drugs were excluded from the study. Forearm venous capacity (MVC), forearm venous tone (F-VT), arterial blood ftow (FBF), forearm arterial resistance (FAR), and hyperemic response (FBF-RH) were measured using air plethysmography. MVC was decreased and VT increased in septic and septic shock patients. FBF was decreased with modest increases in FAR in septic and septic shock patients. FBF-RH was significantly reduced in
both septic and septic shock patients. Decreases in FVT and attenuation of the reactive response to hyperemia occurred early in sepsis in patients without clinical evidence ofhypoperfusion. In our patients, progressive vasodilatation in skeletal muscle was not associated with severe sepsis. These changes appear to be proportional to the severity of sepsis and are most pronounced in patients with circulatory (Chest 1991; 99:1072-75) failure.
septic shock is characterized as a distributive form of circulatory failure. 1 Alterations in peripheral arterial and venous tone have been implicated as major factors contributing to hemodynamic instability and mortality in patients with septic shock. 2-s Loss of normal microcirculatory control mechanisms has also been reported that may compromise tissue nutrient flow and contribute to the development of organ
perfusion and shock were identified by increases in arterial lactate >2.0 mmoVL and at least one other sign of organ dysfunction: (1) altered mentation; (2) oliguria (urine output rt> Lactate, mEq!L
Control n= 10
St>psis n= 1.'5
St>ptic Shock n=ll
64.3±3.1
102±3 4.69±0.12 7.33±0.44 14.1!9± 1.03 .'51.14±3.32 7.01±0.1.'5
61!.3± 2.4 31!.3 ± 0.4 30±2 101!±:3 91±3 2.1!6 ± 0.21lt'W 11.1!3 ± l.07t'W 14.(13 ± 1.34 34.6.'3±4.32t§ 7.91 ± l.Oil
72.2±2.9 37.9±0.7 34±4 12.'5±7 64±3t l.34±0.llt 2:3.4 ± l.9t 10.43± 1..53 1.'5.69 ± 2. 9St 1!.76± 1.02
1.91! ± 0.1.'5
3 ..'54 ± 1.60
.'5.61! ± 1.0t
ll.ll7±0.St'W 1.62 ± 0.17t'W
17.3.'5±2 ..'56t 4.73±0 ..'56t
*MVC =maximum vt>nous eapacity; FBF =forearm hlnnd Anw: FAR= fi>rearm arterial resistanct>; Rll =(during) reactiw hyperemia; FVT=fi>rearm vt>nous tone; and MAP=mt>;m arlt•rial pn•ssure. tpnous volume-prt>ssurt> eun·t> (complianee). Forearm blood flow at rest and during readive hypt>remia (RII) was determint>d by means of a vt•nous oedusion plethysmographie technique."·"·'·' Reactive hyperemia was prriod, the occluding cuff was rapidly dt>flatt>d to 0 mm llg and then reinflated to 30 mm Hg with flow mt>asurements takt>n evt•ry 1.'5 s until the peak flow response was observed. Forearm arterial resistanee during RH was calculated as above. The differences between groups were analyzed hy the Student's t test for paired and unpaired samplt>s. The Bnnft>rrnni method fur preplanned tests was used to adjust the analysis fi>r multiple comparisons. Differences were t-•msiden•d significant at pplit· Shock Day .'5 (n-.'5)
72.4±3.7 37.1l ± 1.2 36 ± 1 130± 7 61±3 1.42 ± 0.17 22 ..'50 ± 2.9:3 9.39± 1.29 11.42 ± 1.64 9.21 ± 1..'54 6.1l.'3± 1.31! 16.1l± 1.4 5.14±0.7
36.4±0.2St l9±2H llll±2t ll2±2t 2.1!0±0.61 12.64 ± 2.26t 14.0±2.4 3.'5.6±2.23t 7.10±1.19 2.31 ±O.Il7t 4.6±0.9* 1.13 ± 0.13t
*MVC =maximum venous capaeity; FBF = fort>ann hiadivt> hyperemia; F\T=Ii>rearm venous tont>; and I\IAP=nwan arterial pressure. tp
Vascular Tone in Sepsis*
Mark E. Astiz, M.D., F.C.C.P.; Elena Tilly, M.D.; Eric D. Rackow, M.D., F.C.C.P.; and Max H. Weil, M.D., Ph.D., F.C.C.P.
Septic shock is characterized as a distributive form of circulatory failure. We examined the relationship of changes in forearm arterial, ve1m0s, and microvascular tone to the severity of sepsis. The study population consisted of ten control patients, 15 patients with sepsis, and eight patients with sepsis and shock. Patients treated with inotropic, vasopressor, or vasodilator drugs were excluded from the study. Forearm venous capacity (MVC), forearm venous tone (F-VT), arterial blood ftow (FBF), forearm arterial resistance (FAR), and hyperemic response (FBF-RH) were measured using air plethysmography. MVC was decreased and VT increased in septic and septic shock patients. FBF was decreased with modest increases in FAR in septic and septic shock patients. FBF-RH was significantly reduced in
both septic and septic shock patients. Decreases in FVT and attenuation of the reactive response to hyperemia occurred early in sepsis in patients without clinical evidence ofhypoperfusion. In our patients, progressive vasodilatation in skeletal muscle was not associated with severe sepsis. These changes appear to be proportional to the severity of sepsis and are most pronounced in patients with circulatory (Chest 1991; 99:1072-75) failure.
septic shock is characterized as a distributive form of circulatory failure. 1 Alterations in peripheral arterial and venous tone have been implicated as major factors contributing to hemodynamic instability and mortality in patients with septic shock. 2-s Loss of normal microcirculatory control mechanisms has also been reported that may compromise tissue nutrient flow and contribute to the development of organ
perfusion and shock were identified by increases in arterial lactate >2.0 mmoVL and at least one other sign of organ dysfunction: (1) altered mentation; (2) oliguria (urine output rt> Lactate, mEq!L
Control n= 10
St>psis n= 1.'5
St>ptic Shock n=ll
64.3±3.1
102±3 4.69±0.12 7.33±0.44 14.1!9± 1.03 .'51.14±3.32 7.01±0.1.'5
61!.3± 2.4 31!.3 ± 0.4 30±2 101!±:3 91±3 2.1!6 ± 0.21lt'W 11.1!3 ± l.07t'W 14.(13 ± 1.34 34.6.'3±4.32t§ 7.91 ± l.Oil
72.2±2.9 37.9±0.7 34±4 12.'5±7 64±3t l.34±0.llt 2:3.4 ± l.9t 10.43± 1..53 1.'5.69 ± 2. 9St 1!.76± 1.02
1.91! ± 0.1.'5
3 ..'54 ± 1.60
.'5.61! ± 1.0t
ll.ll7±0.St'W 1.62 ± 0.17t'W
17.3.'5±2 ..'56t 4.73±0 ..'56t
*MVC =maximum vt>nous eapacity; FBF =forearm hlnnd Anw: FAR= fi>rearm arterial resistanct>; Rll =(during) reactiw hyperemia; FVT=fi>rearm vt>nous tone; and MAP=mt>;m arlt•rial pn•ssure. tpnous volume-prt>ssurt> eun·t> (complianee). Forearm blood flow at rest and during readive hypt>remia (RII) was determint>d by means of a vt•nous oedusion plethysmographie technique."·"·'·' Reactive hyperemia was prriod, the occluding cuff was rapidly dt>flatt>d to 0 mm llg and then reinflated to 30 mm Hg with flow mt>asurements takt>n evt•ry 1.'5 s until the peak flow response was observed. Forearm arterial resistanee during RH was calculated as above. The differences between groups were analyzed hy the Student's t test for paired and unpaired samplt>s. The Bnnft>rrnni method fur preplanned tests was used to adjust the analysis fi>r multiple comparisons. Differences were t-•msiden•d significant at pplit· Shock Day .'5 (n-.'5)
72.4±3.7 37.1l ± 1.2 36 ± 1 130± 7 61±3 1.42 ± 0.17 22 ..'50 ± 2.9:3 9.39± 1.29 11.42 ± 1.64 9.21 ± 1..'54 6.1l.'3± 1.31! 16.1l± 1.4 5.14±0.7
36.4±0.2St l9±2H llll±2t ll2±2t 2.1!0±0.61 12.64 ± 2.26t 14.0±2.4 3.'5.6±2.23t 7.10±1.19 2.31 ±O.Il7t 4.6±0.9* 1.13 ± 0.13t
*MVC =maximum venous capaeity; FBF = fort>ann hiadivt> hyperemia; F\T=Ii>rearm venous tont>; and I\IAP=nwan arterial pressure. tp
