ライフサイエンスコーパス: cardiac output

1 excessively reduces central blood volume and cardiac output.

2 ssure, pulmonary arterial wedge pressure and cardiac output.

3 wering intrathoracic pressure and increasing cardiac output.

4 decisions when selecting a device to measure cardiac output.

5 with underfilling of the left heart and low cardiac output.

6 cular filling and contributes to maintaining cardiac output.

7 g smoking, oxygenation, and left ventricular cardiac output.

8 ricular end-diastolic pressure and increased cardiac output.

9 isassemble in response to acute increases in cardiac output.

10 pulmonary vascular resistance and increased cardiac output.

11 remained in this range after T3, similar to cardiac output.

12 ulation, restricting ventricular filling and cardiac output.

13 l effectors that are involved in determining cardiac output.

14 in the measurements for the magnitude of the cardiac output.

15 rmeability and hypotension despite increased cardiac output.

16 dilation and permeability, and also lowered cardiac output.

17 lic volume, high ejection fraction, and high cardiac output.

18 tal mortality attributable to persisting low-cardiac output.

19 ilation, mixed venous oxygen saturation, and cardiac output.

20 ion of VEGF in cardiac muscle did not affect cardiac output.

21 N1-deficient mice display a severely reduced cardiac output.

22 has acceptable agreement with thermodilution cardiac output.

23 ficant increase in cardiac contractility and cardiac output.

24 an attempt to counteract the restrictions of cardiac output.

25 iogenesis, lowered heart rate, and decreased cardiac output.

26 of extracellular fluid volume and increased cardiac output.

27 cardiac output monitoring and thermodilution cardiac output.

28 aintaining normal cardiac rhythm and optimal cardiac output.

29 sion of the right ventricle (RV) and reduced cardiac output.

30 rsus -31.8+/-20.3%; P=0.03) and increases in cardiac output (121.2+/-59.9% versus 88.7+/-53.3%; P=0.0

31 en groups, mean pulmonary artery pressure at cardiac output=13.8 L.min(-1) was 22.5 mm Hg in controls

32 L.min(-1) versus 1.95 L.min(-1), P=0.2; and cardiac output 17.9 L.min(-1) versus 13.8 L.min(-1), P=0

33 iled to adapt output with increased preload (cardiac output: 2.9 +/- 2.0 vs. 10.6 +/- 1.2 ml min(-1))

34 0 vs. 10.6 +/- 1.2 ml min(-1)) or afterload (cardiac output: -5.3 +/- 2.0 vs.1.4 +/- 1.2 ml min(-1));

35 Hypoxic piglets had cardiogenic shock (cardiac output 58% +/- 1% of baseline), hypotension (sys

36 d (48% +/- 7% to 49% +/- 5%, p = 0.4) as did cardiac output (6.3 +/- 1.3 to 5.9 +/- 3 L/min, p = 0.7)

37 - 4 vs 65 +/- 2 beats/min; all p < 0.05) and cardiac output (6.7 +/- 0.3 vs 6.1 +/- 0.3 vs 4.4 +/- 0.

38 ePVH patients had lower peak cardiac output (73+/-14% versus 103+/-18% predicted; P<0

39 r lobes, a significant increase in PBF after cardiac output adjustment remained: a 16% increase in th

40 The inodilator levosimendan increases cardiac output after cardiac surgery with cardiopulmonar

41 s to the mechanisms redistributing the fetal cardiac output, although the source of ROS is unknown.

42 athy, a condition characterized by increased cardiac output and a reduced ventricular response to str

43 at peak exercise (VO2 and VCO2), heart rate, cardiac output and arterial blood gas variables at peak

44 This requires additional assessment of cardiac output and arteriovenous oxygen content differen

45 SVR was higher and cardiac output and ascites volume were lower in rats wit

46 isovolumic time with concurrent increase of cardiac output and cardiac index in the overall populati

47 Cardiac output and cardiac index were increased signific

48 significant changes in ejection fraction and cardiac output and could prove to be a useful tool in cl

49 The absolute increase in cardiac output and CVC were similar between groups, wher

50 a hemodynamic perturbation by AF or reduced cardiac output and cycle length may have a significant i

51 ted within 3 hours, accompanied by preserved cardiac output and decreased expressions of connexin 43

52 sepsis and was only found in models with low cardiac output and decreased renal blood flow (p < 0.000

53 CA alone, producing additional increases in cardiac output and decreases in left atrial pressure and

54 ion revealed that even the earliest drops in cardiac output and DO2 during endotoxic shock did not pr

55 Cardiac output and ejection fraction were also equally c

56 ardiac contractility, ejection fraction, and cardiac output and elicited vasodilatation in rat in viv

57 Although reduced cardiac output and high burden of cardiovascular risk fa

58 ion, as illustrated by a drastically reduced cardiac output and impaired contractility and relaxation

59 pulmonary vascular resistance and increased cardiac output and index (P<0.01 for all).

60 inical relevance despite anemia-induced high cardiac output and less severely elevated pulmonary vasc

61 x is strongly associated with a reduction in cardiac output and may not be related to other pathophys

62 ed rapidly within 15 mins from a decrease in cardiac output and mean arterial pressure, whereas treat

63 ute chamber effects of CRT include increased cardiac output and mechanical efficiency and reduced mit

64 relation was found between echocardiographic cardiac output and MostCare cardiac output (r = 0.85; p

65 A total of 400 paired echocardiographic cardiac output and MostCare cardiac output measures were

66 CUs, the mean bias between echocardiographic cardiac output and MostCare cardiac output ranged from -

67 Research on the relative contributions of cardiac output and other factors is warranted to further

68 As impaired cardiac output and peripheral oxygen diffusion are the m

69 Exercise and saline each increased cardiac output and pressures in the right atrium, pulmon

70 ation whereby a micro-emulsion both improves cardiac output and rapidly ferries the drug away from or

71 uced increases in heart rate, stroke volume, cardiac output and reductions in mean arterial pressure

72 nimals [32.4%]) and only seen with decreased cardiac output and renal blood flow.

73 fibrillation (VF), which in turn compromise cardiac output and result in secondary global cardiac is

74 by multiple defects, including reductions in cardiac output and skeletal muscle diffusion capacity.

75 Two of these steps, cardiac output and skeletal muscle O2 diffusion, were im

76 lmonary exercise tests, with measurements of cardiac output and skeletal muscle oxygenation.

77 Cardiac output and splanchnic blood flow were reduced by

78 associated with an increase in both maximal cardiac output and stroke volume.

79 Cardiac output and stroke work was preserved in the MI h

80 ly instrumented for continuous monitoring of cardiac output and systemic arterial pressure.

81 essure and PP were continuously recorded and cardiac output and systemic vascular resistance (SVR) as

82 in an fluid challenge affect the changes in cardiac output and the proportion of responders and nonr

83 oup compared with the control group, whereas cardiac output and transcranial Doppler readings were si

84 ges in cardiovascular haemodynamics, such as cardiac output and vascular shear stress, that are simil

85 power output (mean arterial blood pressure x cardiac output) and functional capacity by peak exercise

86 within 12 hours of pacemaker optimization on cardiac output, and all patients were discharged from th

87 abnormal exercise patterns in oxygen uptake, cardiac output, and arteriovenous oxygen content differe

88 mes in critical care, including oxygenation, cardiac output, and blood pressure, have similarly faile

89 lar total isovolumic time and stroke volume, cardiac output, and cardiac index in all groups.

90 ty, ventricular geometry, ejection fraction, cardiac output, and contractility compared with controls

91 sustained increase in heart rate, increased cardiac output, and decreased contractility indices, as

92 EF units; p = 0.0009), as did stroke volume, cardiac output, and diastolic strain only in the combina

93 s, including systemic hypotension, increased cardiac output, and dilatory cardiomyopathy.

94 h ventricles accompanied by hypotension, low cardiac output, and high filling pressures occurring in

95 Furthermore, ejection fraction, cardiac output, and oxygen extraction ratio declined in

96 decreased ejection fraction, stroke volume, cardiac output, and peak ejection rate.

97 igoxin increases ejection fraction, augments cardiac output, and reduces pulmonary capillary wedge pr

98 t of heart rate on cardiac electromechanics, cardiac output, and stroke volume in the perioperative s

99 rements of hepatic venous pressure gradient, cardiac output, and systemic vascular resistance were ma

100 ermeability, circulatory collapse, decreased cardiac output, and various other biological effects.

101 r cm(-5) versus 91+/-33 dyne/s per cm(-5) at cardiac output approximately 10.6 L/min; P=0.04).

102 ior vena cava is predominantly determined by cardiac output, arterial oxygen content, and oxygen cons

103 an increased heart rate, stroke volume, and cardiac output, as well as increased LV volume and mass.

104 elocities of the middle cerebral artery, and cardiac output at baseline, 5 minutes, 1 hour, and 6 hou

105 on (Pearson) with fractional area change and cardiac output at day 7, this effect was lost by day 28.

106 Maximum oxygen uptake ( max) and cardiac output at rest and during exercise (C2H2 rebreat

107 ease oxygen consumption and redistribute the cardiac output away from peripheral vascular beds and to

108 disagreement between studies with regard to cardiac output because of the timing of echocardiography

109 Men had greater RV volumes and cardiac output before and after indexation to body size

110 r SD FEV1/FVC decline; P < 0.0001) and lower cardiac output (beta = -0.070 L/min per SD of FEV1/FVC d

111 r SD of FVC decline; P < 0.0001) and greater cardiac output (beta = 0.109 L/min per SD of FVC decline

112 dipose tissue was also associated with lower cardiac output (beta=-0.10, P<0.05) and higher systemic

113 body subcutaneous fat associated with higher cardiac output (beta=0.20, P<0.0001) and lower systemic

114 Accounting for differences in cardiac output between groups, mean pulmonary artery pre

115 ance and minimum septal curvature indexed to cardiac output both at baseline and during vasodilator t

116 not be dependent on moderate lung injury or cardiac output but on the metabolic production or capaci

117 dium nitrite (NaNO2) infusion would increase cardiac output but reduce systemic arterial blood pressu

118 improve ventricular filling and to maintain cardiac output, but also increases the susceptibility to

119 inal common pathway for autonomic control of cardiac output, but the neuroanatomy of this system is n

120 Sepsis increased cardiac output by 60%, renal blood flow by 35%, and arte

121 Mean arterial pressure, cardiac output, cerebral blood flow, skeletal muscular o

122 study setting and is able to reliably track cardiac output changes induced by cardiac output-modifyi

123 fference, whereas exercise training improved cardiac output, citrate synthase activity, and peak tiss

124 (MCA V(mean)), mean arterial pressure (MAP), cardiac output (CO) and partial pressure of arterial car

125 jection fraction (LVEF), heart rate (HR) and cardiac output (CO) both prior to and 10 days after drug

126 Cardiac output (CO) is a key indicator of cardiac functi

127 stroke volume (SV), ejection fraction (EF), cardiac output (CO), and myocardial mass values calculat

128 V), end systolic volume, stroke volume (SV), cardiac output (CO), LV mass, ejection fraction, LV mass

129 k (eFick) methods are widely used to measure cardiac output (CO).

130 increase in fractional area change (FAC) and cardiac output (CO).

131 ly higher LV mass, mass-to-volume-ratio, and cardiac output compared with those with normal tests (p

132 0.019 and p = 0.002) in the patients with a cardiac output decrease.

133 RV volumes and cardiac output decreased with advancing age.

134 the size of the stagnation zone increased as cardiac output decreased.

135 sures, pulmonary hypertension, and increased cardiac output, despite similar ejection fraction.

136 ed (p < 0.01) after the MgSO4 bolus, whereas cardiac output did not change.

137 ic resonance imaging-assessed cardiac index (cardiac output divided by body surface area) to incident

138 biventricular filling pressures and reduced cardiac output during early exercise.

139 cutaneous vasodilatation and the increase in cardiac output during passive heating.

140 eater levels of cutaneous vasodilatation and cardiac output during passive heating.

141 duction of pCa(50) at long SL may not reduce cardiac output during periods of high metabolic demand b

142 eptor (beta-AR) stimulation ensures adequate cardiac output during stress, it can also trigger life-t

143 Myocardial function, as measured by cardiac output, ejection fraction, and myocardial perfor

144 y with the pulse contour method MostCare for cardiac output estimation in a large and nonselected cri

145 respectively, noninvasive and less invasive cardiac output estimation.

146 try allows completely noninvasive continuous cardiac output estimation.

147 responsiveness was defined as an increase in cardiac output following intravenous fluid administratio

148 For example, our method implicates "abnormal cardiac output" for a patient with a longstanding family

149 nd may be driven by left heart failure, high cardiac output from arteriovenous fistula, hypoxic lung

150 LVAD support leads to alterations in cardiac output, functional status, neurohormonal activit

151 Patients were randomized to a cardiac output-guided hemodynamic therapy algorithm (goa

152 ing major gastrointestinal surgery, use of a cardiac output-guided hemodynamic therapy algorithm comp

153 Patients were randomly assigned to a cardiac output-guided hemodynamic therapy algorithm for

154 entricular stroke volume, ejection fraction, cardiac output, heart rate, diastolic filling function,

155 stolic dysfunction, lower blood pressure and cardiac output, higher pulmonary artery systolic pressur

156 We assessed cardiac output in 400 patients in whom an echocardiograp

157 nt bolus thermodilution over a wide range of cardiac output in an adult porcine model of hemorrhagic

158 Average o2 and cardiac output in controls and SIPE-susceptible subjects

159 e effectiveness of pacemaker optimization on cardiac output in critically ill patients with cardiogen

160 , augments both cutaneous vasodilatation and cardiac output in healthy older humans.

161 Elevated cardiac output in high-output HF patients was related to

162 an alternative to echocardiography to assess cardiac output in ICU patients with a large spectrum of

163 nous oxygen difference) is used to determine cardiac output in numerous clinical situations.

164 performed during heat stress would increase cardiac output in older adults without parallel increase

165 ents to maintain adequate blood pressure and cardiac output in patients with cardiogenic shock althou

166 riable effects of norepinephrine infusion on cardiac output in postoperative cardiac surgical patient

167 jection fraction, cardiac contractility, and cardiac output in severe hypoxia.

168 noninvasive devices are available to measure cardiac output in the critical care setting.

169 activated in the syndrome to try and sustain cardiac output in the face of decompensating function.

170 /- 0.4; p = 0.0002) associated with improved cardiac output (in n = 4; 3.0 +/- 0.6 l/min to 4.3 +/- 1

171 volume variation was higher in those in whom cardiac output increased (14.4 +/- 4.2% vs. 9.1 +/- 2.4%

172 mm Hg) was reached in both NE and AT-II, and cardiac output increased similarly (NE: from 64 mL/kg/mi

173 ped with hypotension, tachycardia, increased cardiac output, increased renal blood flow, oliguria, de

174 g sepsis-induced myocardial dysfunction when cardiac output index remains low after preload correctio

175 The change in cardiac output induced by norepinephrine is determined b

176 ardiography-guided pacemaker optimization of cardiac output is a feasible bedside therapeutic option,

177 Inadequate cardiac output is associated with a poor outcome followi

178 much more susceptible to acute rupture when cardiac output is increased.

179 he ultimate goal of treatments that increase cardiac output is to reduce tissue hypoxia.

180 romising left ventricular filling or forward cardiac output) is a rational, nonpharmacological strate

181 atively) to VO2 kg(-1) (r = -0.45, P< 0.05), cardiac output kg(-1) (QT kg(-1) , r = -0.54, P < 0.02),

182 en minor; on average, correcting a patient's cardiac output led to a 7+/-0.5% predicted improvement i

183 hocardiography was used to assess changes in cardiac output, left ventricular filling time, ejection

184 /Doppler parameters developing in the heart (cardiac output, left ventricular stroke volume, isovolum

185 ssure, arterial and central venous pressure, cardiac output (LiDCOplus; LiDCO, Cambridge, United King

186 ommunication with one another to ensure that cardiac output matches the dynamic process of regional b

187 No effect was found on cardiac output, mean 6.9 +/- 1.7 L/min at baseline versu

188 Cardiac output, mean pulmonary pressure, and mean diasto

189 system (Tensys Medical, San Diego, CA) with cardiac output measured by intermittent pulmonary artery

190 Continuous cardiac output measurement using the noninvasive applana

191 One echocardiographic cardiac output measurement was compared with the corresp

192 Thermodilution is relatively accurate for cardiac output measurements in both animals and humans w

193 The aim of the present study was to compare cardiac output measurements obtained with applanation to

194 The average of the three thermodilution cardiac output measurements was compared with the averag

195 sed on comparisons with thermodilution-based cardiac output measurements.

196 g three AT-CO values resulting in 150 paired cardiac output measurements.

197 chocardiographic cardiac output and MostCare cardiac output measures were compared.

198 In 13 patients, cardiac output-modifying maneuvers performed for clinica

199 ably track cardiac output changes induced by cardiac output-modifying maneuvers.

200 Noninvasive cardiac output monitoring and intermittent thermodilutio

201 trated a 97% concordance between noninvasive cardiac output monitoring and thermodilution cardiac out

202 Simultaneous noninvasive cardiac output monitoring and thermodilution measurement

203 study tests the hypothesis that noninvasive cardiac output monitoring based upon bioreactance (Cheet

204 and resuscitation in large pigs, noninvasive cardiac output monitoring has acceptable agreement with

205 Overall, noninvasive cardiac output monitoring percent bias was 1.47% (95% CI

206 From all published cardiac output monitoring studies reviewed, the animal m

207 ative outcomes may be improved by the use of cardiac output monitoring to guide administration of int

208 acute circulatory failure, having continuous cardiac output monitoring, and receiving controlled low

209 In seven patients who required cardiac output monitoring, continuous iliac arterial tem

210 database for articles describing the use of cardiac output monitors yielded 1,526 sources that were

211 f vasodilatation with hypotension and higher cardiac outputs necessitating greater use of vasoconstri

212 < 0.05 vs other groups) and improvements in cardiac output, neurological recovery, and survival (eig

213 < 0.05) but failed to significantly improve cardiac output, neurological recovery, and survival rate

214 d ability to couple ventricular filling with cardiac output on a beat-to-beat basis.

215 The echocardiography-driven cardiac output optimization protocol led to a significan

216 g-induced changes in flow variables, such as cardiac output or its direct derivatives (sensitivity of

217 reflected the presence of an associated low cardiac output or low renal blood flow syndrome.

218 either treatment could significantly restore cardiac output or prevent muscular compartment ischemia

219 Augmentation of cardiac output or related parameters following passive l

220 ssive leg raising followed by measurement of cardiac output or related parameters may be the most use

221 ed right atrial pressures, with no effect on cardiac output or stroke volume.

222 y elevated cardiac filling pressures and low cardiac output, or b) ongoing signs of hypoperfusion des

223 en changes in RR interval and stroke volume, cardiac output, or cardiac index in the overall populati

224 The Fick principle (cardiac output = oxygen uptake ( O2)/systemic arterio-ve

225 storage hearts, perfusion hearts had higher cardiac output (P = 0.004), LV dP/dt max (P = 0.003) and

226 ial, there was a main effect of haplotype on cardiac output (P = 0.04), as Arg16+Gln27 had the lowest

227 drial function significantly correlated with cardiac output (p<0.05, Spearman rank-correlation test).

228 essment of critical care parameters, such as cardiac output performance or likelihood of adverse even

229 Over the wide range of cardiac output produced by hemorrhage and resuscitation

230 poxia-induced QIPAVA is not simply increased cardiac output, pulmonary artery systolic pressure or sy

231 V(O2peak), peak cardiac output (Q(peak)), haemoglobin mass (Hb(mass)) an

232 Oxygen uptake (VO2; Douglas bag technique), cardiac output (Qc, foreign-gas rebreathing), ventricula

233 During 320 ADR cardiac output (QT) and pulmonary artery systolic pressu

234 chocardiographic cardiac output and MostCare cardiac output (r = 0.85; p < 0.0001).

235 chocardiographic cardiac output and MostCare cardiac output ranged from -0.40 to 0.45 L/min, and the

236 om 1.95 to 9.90 L/min, and echocardiographic cardiac output ranged from 1.82 to 9.75 L/min.

237 n; p = 0.002) and normalized the increase in cardiac output relative to oxygen consumption.

238 eadouts, including fractional shortening and cardiac output, remained unchanged.

239 ventricular filling pressures and depressed cardiac output reserve (both p < 0.0001).

240 Nitrite-enhanced cardiac output reserve improved with exercise (+0.5 +/-

241 y in people with severe TR is related to low cardiac output reserve relative to metabolic needs, coup

242 NO3(-) increased exercise vasodilatory and cardiac output reserves.

243 dant changes in visceral function, including cardiac output, respiration and digestion.

244 dant changes in visceral function, including cardiac output, respiration and digestion.

245 Reduced cardiac output response, rather than impaired peripheral

246 This leads to reduced cardiac output, right heart failure, and ultimately deat

247 ing RV systolic and end-diastolic pressures, cardiac output, RV size, and morbidity.

248 on use of inotropes and vasodilators for low cardiac output septic shock associated with elevated sys

249 The maximal change in cardiac output should be assessed 1 minute after the end

250 origin, including small aortic calibre, low cardiac output states, high vasopressor requirements cau

251 essure, heart rate, central venous pressure, cardiac output, stroke volume variation and, with use of

252 useful for guiding volume therapy, including cardiac output, stroke volume variation monitoring, and

253 PP, mean arterial pressure, cardiac output, SVR, and ascites volume were also measur

254 nfection (12.9% vs 29.7%; p = 0.002) and low cardiac output syndrome (6.5% vs 26.6%; p = 0.002).

255 Low cardiac output syndrome after cardiac surgery is associa

256 in small studies to prevent or treat the low cardiac output syndrome after cardiac surgery.

257 relationship was observed for stroke and low cardiac output syndrome but not for renal replacement th

258 Composite end point reflecting low cardiac output syndrome with need for a catecholamine in

259 nts after cardiac surgery because of the low cardiac output syndrome.

260 ve levosimendan to prevent postoperative low cardiac output syndrome.

261 Cardiac output, systemic vascular resistance, and mean a

262 ng greater than or equal to 50% reduction of cardiac output (T1), after initial resuscitation to base

263 to baseline (T2), and after optimization of cardiac output (T3).

264 cutaneous vasodilatation and the increase in cardiac output that healthy older adults can achieve dur

265 n the levels of cutaneous vasodilatation and cardiac output that healthy older adults can achieve dur

266 intervention, conversion to sternotomy, low cardiac output that required mechanical support, aortic

267 While inotropes successfully increase cardiac output, their use has been plagued by excessive

268 Cardiac output (thermodilution), forearm vascular conduc

269 Fallot patients had the largest increase in cardiac output, they had lower resting (3+/-1.2 L/min pe

270 However, after adjustment for cardiac output, this change was not evident anymore (inc

271 Arterial blood pressure, cardiac output, tissue oxygen tension and the circulatin

272 entions can tend to return venous return and cardiac output to appropriate values.

273 contraction and speeding relaxation to match cardiac output to changing circulatory demands.

274 gnaling, muscle vascularization, and percent cardiac output to muscle rather than insulin sensitizati

275 Blood pressure is determined by cardiac output (total flow) and total vascular resistanc

276 ulating the force of contraction to maintain cardiac output under changes of preload and afterload.

277 was compared with the corresponding MostCare cardiac output value per patient, considering different

278 MostCare cardiac output values ranged from 1.95 to 9.90 L/min, an

279 he applanation tonometry technology provides cardiac output values with reasonable accuracy and preci

280 n resting and in maximal heart rate, whereas cardiac output was completely preserved because of great

281 , and after the first round of measurements, cardiac output was increased by approximately 30% by con

282 Cardiac output was indexed to body surface area (cardiac

283 At the end of the protocol, cardiac output was lower in mild hypothermia than in nor

284 Cardiac output was measured simultaneously by pulmonary

285 Simultaneous cardiac output was measured using a real-time MR flow se

286 luid infusion MEASUREMENTS AND MAIN RESULTS: Cardiac output was measured with a calibrated LiDCOplus

287 The predicted maximal effect on cardiac output was observed at 1.2 minutes (95% credible

288 peripheral resistance were greater, whereas cardiac output was smaller, in LVAD patients compared wi

289 olic pulmonary artery pressure, and exercise cardiac output were all significantly (P<0.05) impaired

290 onitoring and thermodilution measurements of cardiac output were compared by Bland-Altman analysis.

291 , blood pressure, rate-pressure product, and cardiac output were greater with exercise compared with

292 ariations, and stroke volume variations; and cardiac output were obtained during controlled mechanica

293 Stroke volume and cardiac output were significantly increased versus sham.

294 hase; however, heart rate, stroke volume and cardiac output were similar between phases.

295 t monitoring and intermittent thermodilution cardiac output were simultaneously measured at nine time

296 urthermore, healthy older humans can augment cardiac output when cardiac pre-load is increased during

297 ization results in a significant increase in cardiac output when compared with clinically derived pac

298 ncreased afterload and preload and decreased cardiac output, whereas ventilatory consequences include

299 Conversely, the lack of an increase in cardiac output with passive leg raising identified patie

300 y potentially lead to an inappropriately low cardiac output, with a subsequent compromise of microvas