Physiological response to the six-minute walk test in pulmonary arterial hypertension.

The 6-min walk test (6MWT) is commonly used to evaluate exercise capacity in patients with pulmonary arterial hypertension (PAH). However, little is known about the corresponding metabolic stress as measured by cardiopulmonary exercise testing. The present study, therefore, measured ventilatory variables and heart rate during the 6MWT and symptom-limited incremental maximal exercise testing in 20 patients with PAH. The distance walked in 6 min was 450+/-22 m (mean+/-se). During the 6MWT, ventilation, O2 consumption, CO2 production and heart rate increased during the first 3-4 min, and then remained stable. As compared with the maximum values measured during the cardiopulmonary exercise test, O2 consumption tended to be higher (14.2+/-0.6 versus 12.9+/-0.7 mL.kg-1.min-1), while maximum ventilation (46+/-3 versus 57+/-4 L.min-1), respiratory quotient (0.90+/-0.02 versus 1.15+/-0.02) and heart rate (119+/-4 versus 135+/-4 beats.min-1) remained lower. In conclusion, patients with pulmonary arterial hypertension exercise at higher aerobic capacity and lower metabolic stress during the 6MWT than during a cardiopulmonary exercise test.

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

OBJECT: Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury. METHODS: The effect of 0 degrees, 15 degrees, 30 degrees, and 45 degrees head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro - Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45 degrees, from 46.3+/-4.8 to 28.7+/-2.3 ml x min(-1) x 100 g(-1) (mean +/- standard error, p<0.01), and the PsaMonro - Pj from 80+/-3 to 73+/-3 mm Hg (p< 0.01). The CPP remained stable between 0 degrees and 30 degrees of head elevation, at 62+/-3 mm Hg, and decreased from 62+/-3 to 57+/-4 mm Hg between 30 degrees and 45 degrees (p<0.05). A simulation showed that the 38% decrease in CBF between 0 degrees and 45 degrees resulted from PsaMonro - Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%. CONCLUSIONS: During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45 degrees of head elevation.

Cerebral blood flow velocity responses to hypoxia in subjects who are susceptible to high-altitude pulmonary oedema.

Cerebral blood flow increases on exposure to high altitude, and perhaps more so in subjects who develop acute mountain sickness. We determined cerebral blood flow by transcranial Doppler ultrasound of the middle cerebral artery at sea level, in normoxia (fraction of inspired O2, F(I)O2 0.21), and during 15-min periods of either hypoxic (F(I)O2 0.125) or hyperoxic (F(I)O2 1.0) breathing, in 7 subjects with previous high-altitude pulmonary oedema, 6 climbers who had previously tolerated altitudes between 6000 m and 8150 m, and in 20 unselected controls. Hypoxia increased mean middle cerebral artery flow velocity from 69 (3) to 83 (4) cm x s(-1) (P<0.001) in the controls, from 63 (3) to 75 (3) cm x s(-1) (P<0.001) in the high-altitude pulmonary-oedema-susceptible subjects, and from 58 (4) to 70 (4) cm x s(-1) (P<0.001) in the successful high-altitude climbers. Hyperoxia decreased mean middle cerebral flow velocity to 60 (3) cm x s(-1) (P<0.001), 53 (3) cm x s(-1) (P<0.01), and 49 (3) cm x s(-1) (P<0.01) in the controls, high-altitude pulmonary-oedema-susceptible, and high-altitude climbers, respectively. We conclude that a transcranial Doppler-based estimate of cerebral blood flow is affected by hypoxic and hyperoxic breathing, and that it is not predictive of tolerance to high altitude.

Cerebral CO2 vasoreactivity evaluation with and without changes in intrathoracic pressure in comatose patients.

It is well established that cerebral blood flow (CBF) is sensitive to variations in arterial PCO2 (PaCO2) and can be influenced by changes in jugular venous return due to elevated intrathoracic pressure. Therefore, we compared cerebral CO2 vasoreactivity when PaCO2 was altered either by changing inspired PCO2 or tidal volume. In addition, we sought to determine if noninvasive transcranial Doppler ultrasonography can be used instead of invasive CBF measurement to determine cerebral CO2 vasoreactivity. In 36 mechanically ventilated patients in coma due to acute brain lesion, we evaluated CBF by continuous jugular thermodilution, middle cerebral artery flow velocity (Vm) by transcranial Doppler ultrasonography, intracranial pressure (ICP; in only 23 of them) by intraventricular catheter, systemic and pulmonary hemodynamic variables, and arterial and jugular bulb blood gases. Measurements were taken at four levels of PaCO2 (25, 30, 35, and 40 mmHg) by modifying in a random order either tidal volume or inspired PCO2. Cerebral, pulmonary, and systemic hemodynamic changes were similar in magnitude during both methods of altering PaCO2. From the highest to the lowest PaCO2, CBF decreased from 61+/-7 to 36+/-4 ml/min/100 g (p < 0.001, mean +/- SE), Vm from 89+/-7 to 65+/-5 cm/s (p < 0.001), and ICP from 29+/-2 to 12+/-2 mmHg (p < 0.001), but cerebral perfusion pressure remained constant, ranging from 65+/-3 to 67+/-4 mmHg (p = NS). Arteriojugular oxygen content difference increased from 3.2+/-0.2 to 5.7+/-0.4 ml/dl (p < 0.001). Eleven of the 20 patients with a preserved CBF response to CO2 survived to 6 months, whereas only two of the 16 patients with an altered response were alive at 6 months (p < 0.05). When compared with CBF by jugular thermodilution, the rates of sensitivity and specificity of transcranial Doppler ultrasonography to detect impaired cerebral CO2 vasoreactivity were 69% and 65%, respectively. In conclusion, the reduction of PaCO2 from 40 to 25 mmHg by modifying either tidal volume or inspired PCO2 resulted in similar effects on cerebral, pulmonary, and systemic circulations. Cerebral CO2 vasoreactivity is of prognostic value in brain-injured patients when determined using CBF but may be misleading when evaluated using velocities measured by transcranial Doppler ultrasonography.

Effects of positioning and exercise on intracranial pressure in a neurosurgical intensive care unit.

BACKGROUND AND PURPOSE: The purpose of the study was to assess the safety of physical therapy by investigating its effects on intracranial pressure (ICP) and cerebral perfusion pressure. SUBJECTS: The subjects were 65 patients in a neurosurgical intensive care unit who had normal ICP (< 15 mm Hg) or increased ICP (> 15 mm Hg). METHODS: Intraventricular ICP was measured in a 30-degree head-up position (all patients) and in supine and 45-degree head-up positions (patients with normal ICP) during passive range of motion (comatose patients) and exercises involving limb movement (awake patients). RESULTS: In patients with normal ICP, passive range of motion decreased mean ICP by 1 mm Hg in the supine position but not in the head-up position. In patients with high ICP, it decreased ICP by 2 mm Hg. Limb exercises left the mean ICP essentially unchanged in both the patients with normal ICP and the patients with high ICP. Isometric hip adduction increased mean ICP by 4 mm Hg in patients with normal ICP. It did not affect ICP in patients with high ICP. Limb movement was associated with suppression of abnormal ICP waves and improvement of consciousness in 13 patients. CONCLUSION AND DISCUSSION: Physical therapy can be used safely in patients with normal or increased ICP provided that Valsalva-like maneuvers are avoided. [Brimioulle S, Moraine J-J, Norrenberg D, Kahn RJ. Effects of positioning and exercise on intracranial pressure in a neurosurgical intensive care unit.

Dobutamine increases cerebral blood flow velocity and jugular bulb hemoglobin saturation in septic patients.

OBJECTIVE: To evaluate the effects of dobutamine on cerebral hemodynamics in septic patients with stable hemodynamic status. DESIGN: Open-label, prospective study. SETTING: Multidisciplinary department of intensive care in a university hospital. PATIENTS: Fourteen mechanically ventilated septic patients with altered mental status and stable hemodynamic status. INTERVENTIONS: Dobutamine infusion, in incremental doses of 2 micrograms/kg/min every 10 mins, for < or = 10 micrograms/kg/min. MEASUREMENTS AND MAIN RESULTS: Mean flow velocity in the right middle cerebral artery, as measured by transcranial Doppler, increased from 68 +/- 6 (SEM) cm/sec at baseline to 80 +/- 7 cm/sec (p < .001) with 10 micrograms/kg/min of dobutamine. Cerebral arterial-venous oxygen content difference and cerebral oxygen extraction ratio concurrently decreased from 4.1 +/- 0.2 to 3.4 +/- 0.3 mL/dL (p < .05) and from 46 +/- 3% to 36 +/- 4% (p < .05), respectively. Dobutamine also increased cardiac index from 3.8 +/- 0.3 to 6.3 +/- 0.5 L/min/m2 (p < .001) and systemic oxygen delivery (DO2) from 497 +/- 35 to 817 +/- 55 mL/min/m2. Mean arterial pressure increased slightly from 77 +/- 3 mm Hg to a maximum value of 86 +/- 4 mm Hg (p < .05). Relative changes in mean flow velocity were better correlated with cardiac index (r2 = .52, p < .001) than with arterial pressure (r2 = .20; p < .001). Cerebral DO2 (estimated by the product of mean flow velocity and arterial oxygen content) increased by 12% with dobutamine, whereas estimated cerebral oxygen consumption (VO2) did not. CONCLUSION: These measurements of middle cerebral artery flow velocity and jugular bulb oximetry suggest that dobutamine increases cerebral blood flow but not cerebral VO2 in stable septic patients.

Incentive spirometry performance. A reliable indicator of pulmonary function in the early postoperative period after lobectomy?

OBJECTIVES: The purpose of our study was to validate the incentive spirometry (IS) as a simple mean to follow pulmonary function at the bedside after lung surgery. MATERIALS AND METHODS: We studied prospectively 19 patients (16 men, 3 women; mean +/- SE age, 60 +/- 2.8 years) undergoing lobectomy for lung cancer. All the patients had an obstructive pattern with FEV1/FVC below 75%. Lung volumes, including functional residual capacity (FRC) and residual volume (RV), measured using spirometry and the helium dilution technique, and IS were measured preoperatively and postoperatively at days 1, 2, 3, and 8, and at 2 months. RESULTS: Our results showed that in the postoperative period after lung resection, IS performance was well correlated (R) during the first 8 postoperative days with vital capacity (VC) (R between 0.667 and 0.870) mainly due to the excellent correlation with the inspiratory reserve volume (IRV, R between 0.680 and 0.895) but was poorly correlated with expiratory reserve volume (R below 0.340), RV (R below 0.180), and FRC (R below 0.470). CONCLUSIONS: IS can be used as a simple mean to follow lung function, especially VC and IRV, in the postoperative period in spontaneously breathing patients. IS is noninvasive and can be performed repeatedly at the bedside in the intensive care setting.

Estimation of cerebral blood flow at bedside by continuous jugular thermodilution.

The Kety-Schmidt technique can be regarded as the reference method for the measurement of cerebral blood flow (CBF). However, the method is somewhat cumbersome for routine use in the intensive care unit (ICU) at the beside. The continuous thermodilution technique developed many years ago for the measurement of coronary sinus blood flow can be applied for the measurement of jugular blood flow (JBF). However, the measurement of JBF by thermodilution has never been validated using the Kety-Schmidt reference method. We first validate the continuous thermodilution in vitro by comparison with a volumetric flow. The thermodilution method is accurate for flows between 50 and 900 ml min-1 with a mean difference volumetric-thermodilution flow of -1 +/- 18 ml min-1 (mean +/- SD), and precise with a coefficient of variability ranging between 1.21% and 2.50%. In vivo accuracy was assessed by comparing in 15 comatose patients CBF measured using the Kety-Schmidt (CBFKS) method and estimated from JBF measured by thermodilution (CBFTH) at four levels of arterial PaCO2 (25, 30, 35, and 40 mm Hg). The mean difference CBFKS-CBFTH is -0.9 +/- 3.6 ml min-1 100 g-1. In vivo precision of the method was good, with a coefficient of variability of 4.1% in mean. We conclude that jugular continuous thermodilution technique is a reliable method for estimating CBF at the bedside. This technique allows repeated measurements jugular bulb blood sampling for brain metabolic studies.

Effects of dobutamine on the relationship between oxygen consumption and delivery in healthy volunteers: comparison with sodium nitroprusside.

1. Dobutamine has been used to study the relationship between oxygen consumption (VO2) and oxygen delivery (DO2) in critically ill patients, but this has led to concerns that it could consistently increase VO2 in all patients. Although a direct thermogenic effect of the catecholamine has been primarily implicated in this increase in VO2, an increase in blood flow may contribute significantly by increasing the oxygen requirements of the heart and other organs such as the kidney and the liver. If this mechanism is predominant, it should also be observed when blood flow increases during the infusion of non-adrenergic agents. To separate the two mechanisms, we compared the effects of dobutamine with those of sodium nitroprusside on VO2/DO2 relationships in healthy volunteers. 2. Eight healthy volunteers received infusions of dobutamine at doses of 2, 4 and 6 micrograms min-1 kg-1 and nitroprusside at doses of 0.5, 1 and 2 micrograms min-1 kg-1 in an alternate order. 3. VO2 was determined by indirect calorimetry and cardiac output by electrical bioimpedance. Data were analysed by analysis of variance for repeated measurements and individual VO2/DO2 slopes were determined by linear regression. 4. VO2 increased more with dobutamine than with nitroprusside (from 138 +/- 14 to 149 +/- 20 ml min-1 m-2, P < 0.001, and from 131 +/- 14 to 138 +/- 17 ml min-1 m-2, P < 0.001, respectively). However, DO2 also increased more with dobutamine than with nitroprusside (from 531 +/- 186 to 702 +/- 274 ml min-1 m-2, P < 0.001, and from 523 +/- 107 to 610 +/- 122 ml min-1 m-2, P < 0.001, respectively). Individual VO2/DO2 slopes were similar with dobutamine and nitroprusside (6.5 +/- 3.5 compared with 7.1 +/- 4.6%, P not significant). 5. At the doses used, DO2 and VO2 increased more with dobutamine than with nitroprusside in healthy volunteers. However, the VO2/DO2 slopes were similar for both substances. Thus, an increase in VO2 is not exclusively observed with catecholamines. Studies of the effects of therapeutic interventions on oxygen-derived variables should report not only changes in VO2 but also VO2/DO2 slopes.

Doppler assessment of hypoxic pulmonary vasoconstriction and susceptibility to high altitude pulmonary oedema.

BACKGROUND: Subjects with previous high altitude pulmonary oedema may have stronger than normal hypoxic pulmonary vasoconstriction. Susceptibility to high altitude pulmonary oedema may be detectable by echo Doppler assessment of the pulmonary vascular reactivity to breathing a hypoxic gas mixture at sea level. METHODS: The study included 20 healthy controls, seven subjects with a previous episode of high altitude pulmonary oedema, and nine who had successfully climbed to altitudes of 6000-8842 m during the 40th anniversary British expedition to Mount Everest. Echo Doppler measurements of pulmonary blood flow acceleration time (AT) and ejection time (ET), and of the peak velocity of the tricuspid regurgitation jet (TR), were obtained under normobaric conditions of normoxia (fraction of inspired oxygen, FIO2, 0.21), of hyperoxia (FIO2 1.0), and of hypoxia (FIO2 0.125). RESULTS: Hypoxia decreased AT/ET by mean (SE) 0.06 (0.01) in the control subjects, by 0.11 (0.01) in those susceptible to high altitude pulmonary oedema, and by 0.02 (0.02) in the successful high altitude climbers. Hypoxia increased TR in the three groups by 0.22 (0.06) (n = 14), 0.56 (0.13) (n = 5), and 0.18 (0.1) (n = 7) m/s, respectively. However, AT/ET and/or TR measurements outside the normal range, defined as mean +/- 2 SD of measurements obtained in the controls under hypoxia, were observed in only two of the subjects susceptible to high altitude pulmonary oedema and in five of the successful high altitude climbers. CONCLUSIONS: Pulmonary vascular reactivity to hypoxia is enhanced in subjects with previous high altitude pulmonary oedema and decreased in successful high altitude climbers. However, echo Doppler estimates of hypoxic pulmonary vaso-constriction at sea level cannot reliably identify subjects susceptible to high altitude pulmonary oedema or successful high altitude climbers from a normal control population.

Effects of dobutamine on oxygen consumption in septic patients. Direct versus indirect determinations.

Dobutamine has been proposed as a means of disclosing a pathologic oxygen supply (DO2) dependency in critically ill patients. Like other catecholamines, however, dobutamine might increase cellular metabolism, so that oxygen consumption (VO2) would increase regardless of the presence or absence of a supply dependency. This study investigated the effects of graded doses of dobutamine on VO2 in stable, septic patients. Since it has been suggested that the use of reverse Fick equation to determine VO2 can induce a spurious VO2/DO2 dependency owing to a mathematical coupling of data, we determined VO2 both by respiratory gas analysis (VO2DIR) and from the reverse Fick equation (VO2INDIR). In 12 adult patients with signs of sepsis but an otherwise stable hemodynamic status (normal blood lactate levels, and no change in vasoactive drugs or fluid administration for at least 2 h), a dobutamine infusion was administered at a dose of up to 10 micrograms/kg/min in increments of 2 micrograms/kg/min every 10 min. Complete hemodynamic and gas measurements were obtained at baseline, at each dose of dobutamine, and 20 min after discontinuation of the infusion. All of the measured parameters were similar at baseline and after discontinuation of the dobutamine infusion. Dobutamine induced a dose-related increase in the cardiac index (from 3.84 +/- 0.97 to 6.19 +/- 1.56 L/min/m2, p < 0.01) and DO2 (from 501 +/- 123 to 801 +/- 219 ml/min/m2, p < 0.01). Both VO2DIR and VO2INDIR increased, from 161 +/- 37 to 183 +/- 40 ml/min/m2 and from 140 +/- 29 to 168 +/- 42 ml/min/m2, respectively (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dobutamine and prostacyclin on cerebral blood flow velocity in septic patients.

PURPOSE: Both dobutamine and prostacyclin (PGI2) have been used to increase oxygen delivery in septic patients, but their effects on cerebral blood flow have not been well studied. METHODS: In 10 septic patients with altered mental status, stable hemodynamic status, and normal lactatemia, we investigated the effects of successive infusions of dobutamine at 5 micrograms/kg/min and PGI2 at 5 ng/kg/min on mean blood flow velocity in a middle cerebral artery, using transcranial Doppler flowmetry. RESULTS: Mean flow velocity increased with dobutamine (from 52 +/- 4 to 62 +/- 6 cm/s, P < .005) but not with PGI2 (from 55 +/- 5 to 57 +/- 5 cm/s, P = not significant). Each substance significantly increased cardiac index. Dobutamine increased arterial pressure from 85 +/- 6 to 91 +/- 5 mm Hg (P < .05), but PGI2 decreased it from 87 +/- 6 to 77 +/- 5 mm Hg (P < .005). With each agent, mean flow velocity was correlated with cardiac index (r = .51, P < .001) but not with arterial pressure. PGI2 reduced PaO2 from 103 +/- 10 to 82 +/- 6 mm Hg (P < .005). Cerebral oxygen delivery (estimated by the product of mean flow velocity and arterial oxygen content) increased by 19% with dobutamine but remained unchanged with PGI2. CONCLUSIONS: Dobutamine and PGI2 at the administered doses exert different effects on arterial pressure and middle cerebral artery flow velocity in septic patients. According to these data, dobutamine increases cerebral oxygen delivery more than PGI2.

Relationship of middle cerebral artery blood flow velocity to intensity during dynamic exercise in normal subjects.

Cerebral blood flow has been reported to increase during dynamic exercise, but whether this occurs in proportion to the intensity remains unsettled. We measured middle cerebral artery blood flow velocity (vm) by transcranial Doppler ultrasound in 14 healthy young adults, at rest and during dynamic exercise performed on a cycle ergometer at a intensity progressively increasing, by 50 W every 4 min until exhaustion. Arterial blood pressure, heart rate, end-tidal, partial pressure of carbon dioxide (PETCO2), oxygen uptake (VO2) and carbon dioxide output were determined at exercise intensity. Mean vM increased from 53 (SEM 2) cm.s-1 at rest to a maximum of 75 (SEM 4) cm.s-1 at 57% of the maximal attained VO2 (VO2max), and thereafter progressively decreased to 59 (SEM 4) cm.s-1 at VO2max. The respiratory exchange ratio (R) was 0.97 (SEM 0.01) at 57% of VO2max and 1.10 (SEM 0.01) at VO2max. The PETCO2 increased from 5.9 (SEM 0.2) kPa at rest to 7.4 (SEM 0.2) kPa at 57% of VO2max, and thereafter decreased to 5.9 (SEM 0.2) kPa at VO2max. Mean arterial pressure increased from 98 (SEM 1) mmHg (13.1 kPa) at rest to 116 (SEM 1) mmHg (15.5 kPa) at 90% of VO2max, and decreased slightly to 108 (SEM 1) mmHg (14.4 kPa) at VO2max. In all the subjects, the maximal value of vm was recorded at the highest attained exercise intensity below the anaerobic threshold (defined by R greater than 1). We concluded that cerebral blood flow as evaluated by middle cerebral artery flow velocity increased during dynamic exercise as a function of exercise intensity below the anaerobic threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin E1 in the adult respiratory distress syndrome. Benefit for pulmonary hypertension and cost for pulmonary gas exchange.

Prostaglandin E1 (PGE1) has been reported to improve survival in patients with the adult respiratory distress syndrome (ARDS). However, the effects of this pulmonary vasodilating compound on gas exchange have been little documented. We therefore measured hemodynamics, blood gases, and the distributions of ventilation-perfusion ratios (VA/Q), using the multiple inert gas elimination technique, at baseline and during infusion of PGE1 0.02 to 0.04 microgram.kg-1.min-1 in six patients with pulmonary hypertension secondary to ARDS ventilated with 10 cm H2O positive end-expiratory pressure. PGE1 decreased systemic arterial mean pressure (-16%) and pulmonary arterial mean pressure (-15%) and increased cardiac index (+20%) and heart rate (+11%). Arterial PO2 decreased from 99 +/- 6 to 77 +/- 8 mm Hg (p less than 0.01, mean +/- SEM) with no change in mixed venous PO2 and in O2 consumption. PGE1 increased true shunt from 21 +/- 4 to 32 +/- 5% of total blood flow (p less than 0.01) with no significant modification in the pattern of VA/Q distribution. Thus, in ARDS, pulmonary hypertension is reduced by PGE1 at the price of a deterioration in pulmonary gas exchange. The clinical relevance of these findings remains to be evaluated.

Toe temperature versus transcutaneous oxygen tension monitoring during acute circulatory failure.

Measurements of toe temperature and transcutaneous PO2 (PtcO2) have been both suggested for non-invasive assessment of peripheral blood flow in acute circulatory failure. The underlying principle of the two methods is that cutaneous vasoconstriction occurs early when tissue perfusion is altered. In 15 patients, we compared the two measurements during cardiogenic shock (27 measurements) or septic shock (29 measurements). Toe-ambiant temperature gradient and PtcO2 correlated well together (r = 0.66, p less than 0.001) especially in hyperkinetic septic shock (r = 0.79, p less than 0.001). In cardiogenic shock, toe-ambiant temperature correlated well with cardiac index (r = 0.63), stroke index (r = 0.64) and oxygen transport (r = 0.65), and these correlations were stronger than for PtcO2. In septic shock, both techniques were poor indicators of blood flow indexes but PtcO2 rather correlated with arterial pressure (r = 0.66) and left ventricular work (r = 0.66). Trend evaluation of data revealed in cardiogenic shock that the increase in toe temperature usually preceded the increase in PtcO2. Since measurement of PtcO2 is technically more complicated, correlates less well with standard hemodynamic parameters and later reflects cardiovascular improvement, it has no advantage over measurement of toe temperature in circulatory shock. In cardiogenic shock, measurements of toe temperature can reliably track cardiac output changes. In septic states, however, non-invasive assessment of skin perfusion is of limited interest.