N. H. Secher

Continuous stroke volume monitoring by modelling flow from non-invasive measurement of arterial pressure in humans under orthostatic stress

The relationship between aortic flow and pressure is described by a three-element model of the arterial input impedance, including continuous correction for variations in the diameter and the compliance of the aorta (Modelflow). We computed the aortic flow from arterial pressure by this model, and evaluated whether, under orthostatic stress, flow may be derived from both an invasive and a non-invasive determination of arterial pressure. In 10 young adults, Modelflow stroke volume (MFSV) was computed from both intra-brachial arterial pressure (IAP) and non-invasive finger pressure (FINAP) measurements. For comparison, a computer-controlled series of four thermodilution estimates (thermodilution-determined stroke volume; TDSV) were averaged for the following positions: supine, standing, head-down tilt at 20 degrees (HDT20) and head-up tilt at 30 degrees and 70 degrees (HUT30 and HUT70 respectively). Data from one subject were discarded due to malfunctioning thermodilution injections. A total of 155 recordings from 160 series were available for comparison. The supine TDSV of 113+/-13 ml (mean+/-S.D.) dropped by 40% to 68+/-14 ml during standing, by 24% to 86+/-12 ml during HUT30, and by 51% to 55+/-15 ml during HUT70. During HDT20, TDSV was 114+/-13 ml. MFSV for IAP underestimated TDSV during HDT20 (-6+/-6 ml; P<0.05), but that for FINAP did not (-4+/-7 ml; not significant). For HUT70 and standing, MFSV for IAP overestimated TDSV by 11+/-10 ml (HUT70; P<0.01) and 12+/-9 ml (standing; P<0.01). However, the offset of MFSV for FINAP was not significant for either HUT70 (3+/-8 ml) or standing (3+/-9 ml). In conclusion, due to orthostasis, changes in the aortic transmural pressure may lead to an offset in MFSV from IAP. However, Modelflow correctly calculated aortic flow from non-invasively determined finger pressure during orthostasis.

‘Liberal’ vs. ‘restrictive’ perioperative fluid therapy – a critical assessment of the evidence

Background: Several studies have assessed the effect of a ‘liberal’ vs. a ‘restrictive’ perioperative fluid regimen on post‐operative outcome. The literature was reviewed in order to provide recommendations regarding perioperative fluid regimens.

Monitoring of peri‐operative fluid administration by individualized goal‐directed therapy

Background:  In order to avoid peri‐operative hypovolaemia or fluid overload, goal‐directed therapy with individual maximization of flow‐related haemodynamic parameters has been introduced. The objectives of this review are to update research in the area, evaluate the effects on outcome and assess the use of strategies, parameters and monitors for goal‐directed therapy.

Cerebral desaturation during exercise reversed by O2 supplementation

The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation (ScO2) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 +/- 1 mmHg; mean +/- SE) and O2 pressure (77 +/- 2 mmHg) as well as the hemoglobin saturation (91.9 +/- 0.7%) were reduced (P < 0.05). ScO2 was reduced from 80 +/- 2 to 63 +/- 2% (P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (DeltaHb) and oxyhemoglobin (DeltaHbO2) of the vastus lateralis muscle increased 22 +/- 3 microM and decreased 14 +/- 3 microM, respectively (P < 0.05). Increasing the inspired O2 fraction to 0.30 did not affect ventilation (174 +/- 4 l/min), but arterial CO2 pressure (37 +/- 2 mmHg), O2 pressure (165 +/- 5 mmHg), and hemoglobin O2 saturation (99 +/- 0.1%) increased (P < 0. 05). ScO2 remained close to the resting level during exercise (79 +/- 2 vs. 81 +/- 2%), and although the muscle DeltaHb (18 +/- 2 microM) and DeltaHbO2 (-12 +/- 3 microM) were similar to those established without O2 supplementation, work capacity increased from 389 +/- 11 to 413 +/- 10 W (P < 0.05). These results indicate that an elevated inspiratory O2 fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.The combined effects of hyperventilation and arterial desaturation on cerebral oxygenation ([Formula: see text]) were determined using near-infrared spectroscopy. Eleven competitive oarsmen were evaluated during a 6-min maximal ergometer row. The study was randomized in a double-blind fashion with an inspired O2 fraction of 0.21 or 0.30 in a crossover design. During exercise with an inspired O2 fraction of 0.21, the arterial CO2 pressure (35 ± 1 mmHg; mean ± SE) and O2 pressure (77 ± 2 mmHg) as well as the hemoglobin saturation (91.9 ± 0.7%) were reduced ( P < 0.05).[Formula: see text] was reduced from 80 ± 2 to 63 ± 2% ( P < 0.05), and the near-infrared spectroscopy-determined concentration changes in deoxy- (ΔHb) and oxyhemoglobin (ΔHbO2) of the vastus lateralis muscle increased 22 ± 3 μM and decreased 14 ± 3 μM, respectively ( P < 0.05). Increasing the inspired O2fraction to 0.30 did not affect ventilation (174 ± 4 l/min), but arterial CO2 pressure (37 ± 2 mmHg), O2 pressure (165 ± 5 mmHg), and hemoglobin O2saturation (99 ± 0.1%) increased ( P < 0.05).[Formula: see text] remained close to the resting level during exercise (79 ± 2 vs. 81 ± 2%), and although the muscle ΔHb (18 ± 2 μM) and ΔHbO2 (-12 ± 3 μM) were similar to those established without O2 supplementation, work capacity increased from 389 ± 11 to 413 ± 10 W ( P < 0.05). These results indicate that an elevated inspiratory O2fraction increases exercise performance related to maintained cerebral oxygenation rather than to an effect on the working muscles.

Orthostatic Tolerance, Cerebral Oxygenation, and Blood Velocity in Humans With Sympathetic Failure

BACKGROUND AND PURPOSE Patients with orthostatic hypotension due to sympathetic failure become symptomatic when standing, although their capability to maintain cerebral blood flow is reported to be preserved. We tested the hypothesis that in patients with sympathetic failure, orthostatic symptoms reflect reduced cerebral perfusion with insufficient oxygen supply. METHODS This study addressed the relationship between orthostatic tolerance, mean cerebral artery blood velocity (V(mean), determined by transcranial Doppler ultrasonography), oxygenation (oxyhemoglobin [O(2)Hb], determined by near-infrared spectroscopy), and mean arterial pressure at brain level (MAP(MCA), determined by finger arterial pressure monitoring [Finapres]) in 9 patients (aged 37 to 70 years; 4 women) and their age- and sex-matched controls during 5 minutes of standing. RESULTS Supine MAP(MCA) (108+/-14 versus 86+/-14 mm Hg) and V(mean) (84+/-21 versus 62+/-13 cm. s(-1)) were higher in the patients. After 5 minutes of standing, MAP(MCA) was lower in the patients (31+/-14 versus 72+/-14 mm Hg), as was V(mean) (51+/-8 versus 59+/-9 cm. s(-1)), with a larger reduction in O(2)Hb (-11. 6+/-4 versus -6.7+/-4.5 micromol. L(-1)). Four patients terminated standing after 1 to 3.5 minutes. In these symptomatic patients, the orthostatic fall in V(mean) was greater (45+/-6 versus 64+/-10 cm. s(-1)), and the orthostatic decrease in O(2)Hb (-12.0+/-3.3 versus -7.6+/-3.9 micromol. L(-1)) tended to be larger. The reduction in MAP(MCA) was larger after 10 seconds of standing, and MAP(MCA) was lower after 1 minute (25+/-8 versus 40+/-6 mm Hg). CONCLUSIONS In patients with sympathetic failure, the orthostatic reduction in cerebral blood velocity and oxygenation is larger. Patients who become symptomatic within 5 minutes of standing are characterized by a pronounced orthostatic fall in blood pressure, cerebral blood velocity, and oxygenation manifest within the first 10 seconds of standing.

Management of major blood loss: An update

Haemorrhage remains a major cause of potentially preventable deaths. Trauma and massive transfusion are associated with coagulopathy secondary to tissue injury, hypoperfusion, dilution and consumption of clotting factors and platelets. Concepts of damage control surgery have evolved, prioritizing the early control of the cause of bleeding by non‐definitive means, while haemostatic control resuscitation seeks early control of coagulopathy. Haemostatic resuscitation provides transfusions with plasma and platelets in addition to red blood cells (RBCs) in an immediate and sustained manner as part of the transfusion protocol for massively bleeding patients. Transfusion of RBCs, plasma and platelets in a similar proportion as in whole blood prevents both hypovolaemia and coagulopathy. Although an early and effective reversal of coagulopathy is documented, the most effective means of preventing coagulopathy of massive transfusion remains debated and randomized controlled studies are lacking. Results from recent before‐and‐after studies in massively bleeding patients indicate that trauma exsanguination protocols involving the early administration of plasma and platelets are associated with improved survival. Furthermore, viscoelastic whole blood assays, such as thrombelastography (TEG)/rotation thromboelastometry (ROTEM), appear advantageous for identifying coagulopathy in patients with severe haemorrhage, as opposed to conventional coagulation assays. In our view, patients with uncontrolled bleeding, regardless of its cause, should be treated with goal‐directed haemostatic control resuscitation involving the early administration of plasma and platelets and based on the results of the TEG/ROTEM analysis. The aim of the goal‐directed therapy should be to maintain a normal haemostatic competence until surgical haemostasis is achieved, as this appears to be associated with reduced mortality.

Stroke volume of the heart and thoracic fluid content during head-up and head-down tilt in humans

Background:  The stroke volume (SV) of the heart depends on the diastolic volume but, for the intact organism, central pressures are applied widely to express the filling of the heart.

Functional intravascular volume deficit in patients before surgery

Background: Stroke volume (SV) maximization with a colloid infusion, referred to as individualized goal‐directed therapy, improves outcome in high‐risk surgery. The fraction of patients who need intravascular volume to establish a maximal SV has, however, not been evaluated, and there are only limited data on the volume required to establish a maximal SV before the start of surgery. Therefore, we estimated the occurrence and size of the potential functional intravascular volume deficit in surgical patients.

Reduced left ventricular diameters at onset of bradycardia during epidural anaesthesia

Pathophysiologic mechanisms of bradycardia during epidural anaesthesia (L3‐L4 with 1% lidocaine, 38 ml) were evaluated by studying changes in selected cardiovascular and hormonal parameters. Six of eight subjects (analgesia to T8‐T10) remained circulatory stable with no significant changes in heart rate (HR), mean arterial pressure (MAP) and thoracic impedance (TI). In one of two subjects MAP decreased after 25 min from 85 to 50 mmHg (11.3 to 6.7 kPa), HR from 80 to 45 beats · min‐1 while thoracic impedance increased from 25.5 to 26.5 ohm. End‐systolic diameter (ESD) and end‐diastolic diameter (EDD) of the left ventricle determined with echocardiography were reduced from 3.8 to 3.2 cm (17%) and 5.6 to 5.0 cm (11%), respectively. In the other subject MAP decreased after 25 min from 75 to 50 mmHg (10.0 to 6.7 kPa) and HR from 82 to 60 beats · min‐1 while thoracic impedance increased from 28.8 to 29.6 ohm. ESD was reduced from 3.8 to 3.3 cm (13%), and EDD from 5.6 to 5.0 cm (11%). Both subjects recovered after infusion of saline and being placed in the head‐down position. There were no consistent changes in plasma catecholamines, whereas pancreatic polypeptide increased from 5 and 3 to 152 and 69 pmol·1‐1, vasopressin from 3 and 2 to 152 and 46 pmol·1‐1, and aldosterone from 282 and 229 to 383 and 485 pmol·‐1, respectively. The established level of analgesia suggests that the changes in circulatory and hormonal variables as well as successful resuscitation of the subjects with saline in the head‐down position conform to central blood volume depletion leading to increased vagal tone. During epidural anaesthesia presyncopal symptoms were preceded by an approximately 13% reduction in left ventricular diameters.

Effect of Tubocurarine on Human Soleus and Gastrocnemius Muscles

The effect of a bolus injection of tubocurarine (0.1‐0.13 mg × kg‐1 i. v.) was followed in six young male subjects by registration of the rectified smoothed electromyogram (rsEMG) from them. soleus (71±5.1 (s.e.mean) % slow twitch muscle fibers) and from the m. gastrocnemius (54±3.1% slow twitch muscle fibers). Volitional muscle strength was recorded in isometric plantar flexions with the knee fully (0°) extended where m. soleus and m. gastrocnemius both are active, and with the knee bent 90° where m. soleus is dominating force development. During maximal action of the drug, the rsEMG from the soleus muscle was reduced to 30±4.0% of the control value, while the rsEMG from the gastrocnemius muscle was reduced to 53±5.2% (P<0.01). Muscle strength with the knee extended showed 53±7.5% force left, while 44±6.4% of the muscle strength remained when the knee was bent (P<0.01). The results suggest that tubocurarine aflects human muscles in proportion to their slow twitch muscle fiber content.