Ulrich C. Luft

Comparison of noninvasive pulsed Doppler and Fick measurements of stroke volume in cardiac patients

We compared simultaneous measurements of stroke volume by direct Fick (SVF) and noninvasive pulsed Doppler (SVD) techniques in 15 resting, supine cardiac patients. Doppler measurements of ascending aorta blood velocity were obtained from the suprasternal notch with a single crystal transducer. The systolic velocity integral of the spatial-average velocity waveform was multiplied by cross-sectional area from the systolic aortic diameter, obtained independently by M-mode echocardiography, to determine absolute values for SVD. The resulting linear regression equation was SVD = -1.14 + 0.95SVF, r = +0.91, p less than 0.0001. The mean SVD and SVF values were 68 and 73 cm3, respectively. These results in consecutive patients serve to validate empirically the pulsed Doppler method at rest. It is a convenient, safe, and painless procedure which appears appropriate for clinical diagnostic screening where serial measurements would be useful. However, this noninvasive technique does require technical experience and an understanding of anatomy and flow waveforms by the operator to obtain valid measurements.

Quantitative description of whole blood CO2 dissociation curve and Haldane effect

A simple procedure is presented to describe accurately the whole blood CO2 dissociation curve on linear content (CCO2) and pressure (PCO2) coordinates with an exponential equation (CCO2 = K . PCO2b). A single coordinate and the hemoglobin concentration, Hb, are required. Whole blood CCO2 can be calculated from values for pH, PCO2, Hb and O2 saturation by empirically accurate equations. The mathematical description of the CO2 curve was employed to quantitate the in vivo Haldane factor (fH) from simultaneous arterial and mixed venous blood samples in 20 healthy exercising subjects. The mean +/- SE was 0.28 +/- 0.03 (vol. % delta CCO2/vol. % delta HbO2). In 20 patients with severe obstructive lung disease fH was 0.29 +/- 0.08 when calculated from arterial samples while breathing air and 100% O2. Values for fH were not related significantly to acid-base status or Hb as suggested by previous workers. By assuming these or other values for fH, the in vivo change in blood PCO2 resulting from a given change in oxygenation can be predicted.

Pathophysiological Changes in the Lungs During Extracorporeal Circulation

An attempt has been made to determine the optimal method of managing the lungs during cardiopulmonary bypass. The chemical behavior (oxygen saturation, acid-base balance) of the pulmonary venous blood indicates (a) that static inflation of the lungs with either a gas mixture of high oxygen content or ambient air is sufficient to maintain a proper internal milieu for the pulmonary vasculature when the bronchial collateral flow is the sole pulmonary perfusate, and (b) that in adult human beings artificial respiration up to 2 L./min. is necessary when the pulmonary perfusate consists of the coronary venous blood in addition to the bronchial collateral flow. The effective application of the heart-lung bypass procedure in physiological investigation is depicted by the studies on metabolic rate of the lung tissues and the measurement of bronchial flow. It is estimated that the bronchial collateral flow amounts to 8.8 ml./ min. or 0.7 per cent of the total systemic flow, and that the oxygen consumption of the lungs averages 1.6 ml./min. or 1 to 2 per cent of the total metabolic rate in the open-chest dogs. The pulmonary compliance did not change following either passive deflation or static inflation, but is transiently reduced after artificial respiration.

Contribution of the Haldane effect to the rise of arterial Pco2 in hypoxic patients breathing oxygen.

Arterial (Paco2), alveolar (Paco2), mixed expired (Peco2) CO2 pressures, CO2 production (Vco2) as well as arterial O2 saturation (Sao2) were measured on 20 severely hypoxic and hypercapnic patients breathing air (A) and 100% O2 (HO). On HO, mean Paco2 increased to 56.6 torr from 50.8 torr on A, whereas there was no significant change in Paco2 (38.3 on A, 38.6 on HO), so that the arterial-alveolar gradient (aADCO2) increased from 12.5 to 18.0 torr. Peco2 remained essentially the same. There was a statistically significant correlation between the increase in Paco2 on HO and the arterial unsaturation (100 - Sao2) on A and also between Paco2 on A and its increment on HO. When the rise in Paco2 and aADCO2 were estimated which resulted from the shift in the Co2 dissociation curve due to complete oxygen-ation of hemoglobin on HO (Haldane effect), 78% of the observed change in Paco2 could be accounted for. The deadspace/tidal volume ratio (Vd/Vt) increased from 0.59 on A to 0.64 on HO and 87% of this difference could be attributed to the Haldane effect. The results emphasize the importance of considering this effect when interpreting alterations in Paco2, aADCO2 and Vd/Vt on transition from air to hyper-oxia, particularly in patients with severe hypoxemia and hypercapnia.

Relationship between whole blood base excess and CO2 content in vivo

Empirical relationships are demonstrated for whole blood base excess (BE) and CO2 content (CCO2), both calculated from in vivo measurements of PCO2, pH, hemoglobin concentration and O2 saturation. Comparisons are provided by measurements from three separate studies: (1) supine exercise (arterial and mixed venous samples); (2) chronic obstructive disease patients (arterial samples) breathing air and 100% O2; and (3) maximal seated exercise on a bicycle ergometer with and without added inspired CO2 (arterial samples before, during and after). Two standardized values of CCO2 (vol.%) are derived which closely relate to BE (mmol/l). The CCO2 at a PCO2 of 40 mmHG [CCO2(40)] for all samples (n = 220) demonstrated a curvilinear relationship: CCO2 (40) = 45.37 + 1.48(BE) + 0.0156(BE)2, r = + 0.996, SEE = 0.88 vol.%. The CCO2 at a pH of 7.4 [CCO2(7.4)] gave a linear relationship: CCO2(7.4) = 45.09 + 2.58(BE), r = + 0.998, SEE = 1.19 vol.%. Empirical computations for the Haldane factor from studies 1 and 2 gave values of 0.285 in terms of CCO2 (vol.%/vol.%) and 0.266 for BE (mmol/l/mmol reduced Hb). The BE values can serve as useful estimates of lactate concentrations during exercise and the excellent relationships between standardized CCO2 and BE demonstrate their equivalency and either can be utilized, depending on whether quantification of the CO2 dissociation curve or acid-base status is desired.

Effect of lower body negative pressure release on hyperpnea induced by inhaled gas

Transient breath-by-breath ventilation (VI) and end-tidal gases were measured on 6 men in response to: (1) the release of lower body negative pressure (LBR); (2) the one-min inhalation of a gas mixture (GAS) containing 5.4% CO2, 14% O2, balance N2; (3) the two combined (LBR + GAS) with LBR preceding GAS inspiration by 5 sec. With LBR a + 29% peak response in VI occurred after 20 sec whereas with GAS and LBR + GAS, VI tended to level off after 25 sec at + 100% and + 180%, respectively. Simultaneously, PETCO2 had risen 2, 5 and 8 mm Hg and PETO2 had fallen 7, 14 and 19 mm Hg, respectively. LBR accelerated and potentiated the VI response to GAS. Leg volume indicated that 50% of the pooled blood returned from the legs after 4 sec, presumably with high PCO2 and low PO2 contributing an endogenous respiratory stimulus to the exogenous one of GAS. VI with LBR + GAS was greater than the sum of each, suggesting an enhancement of the chemoreceptor response by returning pooled blood.

Circulation and respiration response to arm exercise and lower body negative pressure

The effects of supine arm exercise and lower body negative pressure (LBNP) were studied in six subjects with 10 min of LBNP at -40 mmHg (L), arm cranking for 8 min at a work load of 225 kpm/min (E) and both combined (L + E) preceded by 2 min of LBNP. Initial responses of ventilation (VI) and VO2 were curtailed and heart rate was significantly higher after the first min of L + E than E, reflecting the less accessible venous reservoir and reduced stroke volume due to L. Leg volume was significantly reduced after 30 s of E and continued to decline and remained below baseline during 6 min of recovery. With L + E, leg volume remained constant after E began, indicating both a shift of blood from legs to arms and reduced extra-vasation with LBNP. End-tidal PO2, VI and VI/VO2 were higher and PCO2 lower during the latter stages of L + E than during E, indicating less effective lung perfusion and greater alveolar deadspace caused by LBNP. The release of pooled blood from the lower body after L + E caused a greater VI, VO2 and lower RE than after E and produced marked transients in PCO2 and PO2, thereby slowing the recovery of gas exchange.

Thermal Homoiostasis Under Hypoxia in Man

The complex regulatory mechanisms involved in maintaining optimal thermal conditions for the vital functions in the homoiothermic organism provide functional integrity over a limited range of variation in the temperature of the environment. These adaptations to thermal stress are mediated by humoral and neural pathways which are known to be susceptible to oxygen deprivation. Moreover, certain physiological responses elicited by heat or cold may be in conflict with others engaged to counteract hypoxia and vice versa. Human subjects were exposed to cold (4°C RH 30%), warm (40. 5°C RH 80%) and neutral (27°C RH 30%) environmental conditions for two hours while breathing gas mixtures simulating an altitude of 6000 m (inspired PO2: 65 mm Hg and for a control period of the same duration breathing air. In the cold, no difference was observed in the course of skin temperature between the hypoxic and eupoxic tests. Core temperatures were maintained constant in the presence of vigorous shivering whereby metabolic rate was increased 2 to 3 fold. In the warm environment, the core temperatures (rectal and gastric) were consistently higher with oxygen lack than in the controls, but the rate of increase in temperature was the same. At the end of the tests rectal temperature was an average 39°C. The effects of combined thermal and hypoxic stress on cardiovascular and respiratory activity appeared to be additive. Subsequently, similar experiments were performed on lightly anesthetized dogs where hypoxia of a more severe degree (inspired PO2: 52, 41 and 29 mm Hg) was employed. In these animals hypoxia invariably inhibited or entirely suppressed shivering and in the cold they suffered a more rapid fall of mean body temperature under hypoxia than on air. Experiments in which a normal partial pressure of CO2 was maintained by partial rebreathing suggest that hypocapnia may contribute to the suppression of shivering in the cold. During the exposure to heat there was a marked facilitation of panting under hypoxia, giving rise to extreme hyperpnea with hypocapnia. The animals were sacrificed in hypoxia by progressive rebreathing to determine the critical oxygen tension. Under heat stress the animals succumbed at significantly higher oxygen tensions than in the cold or neutral environment. This may be due to the compound stress of heat, hypoxia and hypocapnia.

Funktionelle Orthologie der Atmung. Die Lungenbelüftung und der alveolare Gasaustausch

Die Atmung umfast im weiteren biologischen Sinne alle Vorgange, welche zum oxydativen Stoffwechsel der lebenden Zelle mittelbar oder unmittelbar bei tragen. Im Warmbluterorganismus gehort dazu eine ganze Kette eng ineinandergreifender Funktionen. Zunachst der Gasaustausch der Zelle mit dem sie umgebenden Gewebe und dem Blut, ferner der Gastransport durch den Blutkreislauf, der Gaswechsel zwischen dem Pulmonalblut und dem Gasraum der Lunge und schlieslich die standige Erneuerung der Lungenluft mit Ausenluft. All diese Vorgange sind im gesunden Individuum fein aufeinander abgestimmt und werden je nach den Bedurfnissen des Gesamtstoffwechsels oder der Umweltbedingungen mittels chemischer, physikalisch-nervoser und hormonaler Regulationen gesteuert. In pathologischen Zustanden, welche dieses oder jenes Glied dieser Funktionskette beeintrachtigen, ist in gewissen Grenzen ein Ausgleich moglich durch kompensatorische Mehrleistung anderer Glieder. Im allgemeinen wird dies jedoch nicht ohne Einschrankung der Belastungsbreite der Atemfunktionen moglich sein1.