Sequential gas delivery provides precise control of alveolar gas exchange.

Of the factors determining blood gases, only alveolar ventilation (VA) is amenable to manipulation. However, current physiology text books neither describe how breath-by-breath VA can be measured, nor how it can be precisely controlled in spontaneously breathing subjects. And such control must be effected independent of minute ventilation (VE) and the pattern of breathing.

CPAP reduces hypercoagulability, as assessed by thromboelastography, in severe obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is associated with increased cardiovascular morbidity and mortality and hypercoagulability may be an underlying factor. We tested the hypotheses that patients with severe OSA are hypercoagulable and that two weeks of continuous positive airway pressure (CPAP) treatment reduces this hypercoagulability. In a prospective crossover study, twelve patients were randomized to either CPAP or no-CPAP for two weeks, a one week washout period, and then the other testing period for two weeks.

Rapid elimination of CO through the lungs: coming full circle 100 years on.

At the start of the 20th century, CO poisoning was treated by administering a combination of CO(2) and O(2) (carbogen) to stimulate ventilation. This treatment was reported to be highly effective, even reversing the deep coma of severe CO poisoning before patients arrived at the hospital. The efficacy of carbogen in treating CO poisoning was initially attributed to the absorption of CO(2); however, it was eventually realized that the increase in pulmonary ventilation was the predominant factor accelerating clearance of CO from the blood.

Supplementary oxygen for nonhypoxemic patients: O2 much of a good thing?

Supplementary oxygen is routinely administered to patients, even those with adequate oxygen saturations, in the belief that it increases oxygen delivery. But oxygen delivery depends not just on arterial oxygen content but also on perfusion. It is not widely recognized that hyperoxia causes vasoconstriction, either directly or through hyperoxia-induced hypocapnia.

A simple and portable breathing circuit designed for ventilatory muscle endurance training (VMET).

Background: Ventilatory muscle endurance training (VMET) involves increasing minute ventilation (V (E)) against a low flow resistance at rest to simulate the hyperpnea of exercise. Ideally, VMET must maintain normocapnia over a wide range of V (E). This can be achieved by providing a constant fresh gas flow to a sequential rebreathing circuit.

Hyperinflation-induced cardiorespiratory failure in rats.

We previously showed that severe inspiratory resistive loads cause acute (<1 h) cardiorespiratory failure characterized by arterial hypotension, multifocal myocardial infarcts, and diaphragmatic fatigue. The mechanisms responsible for cardiovascular failure are unknown, but one factor may be the increased ventricular afterload caused by the large negative intrathoracic pressures generated when breathing against an inspiratory load. Because expiratory threshold loads increase intrathoracic pressure and decrease left ventricular afterload, we hypothesized that anesthetized rats forced to breathe against such a load would experience only diaphragmatic failure.

Repeated inspiratory occlusions acutely impair myocardial function in rats.

Repeated episodes of hypoxia and sympathetic activation during obstructive sleep apnoea are implicated in the initiation and progression of cardiovascular diseases, but the acute effects are unknown. We hypothesized that repeated inspiratory occlusions cause acute myocardial dysfunction and injury. In 22 spontaneously breathing pentobarbital-anaesthetized rats, inspiration was occluded for 30 s every 2 min for 3 h.

Cardiorespiratory failure in rat induced by severe inspiratory resistive loading.

The mechanisms underlying acute respiratory failure induced by respiratory loads are unclear. We hypothesized that, in contrast to a moderate inspiratory resistive load, a severe one would elicit central respiratory failure (decreased respiratory drive) before diaphragmatic injury and fatigue. We also wished to elucidate the factors that predict endurance time and peak tracheal pressure generation.

Calculation of O2 consumption during low-flow anesthesia from tidal gas concentrations, flowmeter, and minute ventilation.

We present the principles of a new method to calculate O2 consumption (V*O2) during low-flow anesthesia with a circle circuit when the source gas flows, end-tidal O2 concentrations and patient inspired minute ventilation are known. This method was tested in a model with simulated O2 uptake and CO2 production. The difference between calculated V*O2 and simulated V*O2 was 0.

Fast and slow skeletal troponin I in serum from patients with various skeletal muscle disorders: a pilot study.

Background: Detection of skeletal muscle injury is hampered by a lack of commercially available assays for serum markers specific for skeletal muscle; serum concentrations of skeletal troponin I (sTnI) could meet this need. Moreover, because sTnI exists in 2 isoforms, slow (ssTnI) and fast (fsTnI), corresponding to slow- and fast-twitch muscles, respectively, it could provide insight into differential injury/recovery of specific fiber types. The purpose of this study was to investigate whether the 2 isoforms of sTnI and their modified forms are present in the blood of patients with various skeletal muscle disorders.

Respiratory muscle injury, fatigue and serum skeletal troponin I in rat.

To evaluate injury to respiratory muscles of rats breathing against an inspiratory resistive load, we measured the release into blood of a myofilament protein, skeletal troponin I (sTnI), and related this release to the time course of changes in arterial blood gases, respiratory drive (phrenic activity), and pressure generation. After approximately 1.5 h of loading, hypercapnic ventilatory failure occurred, coincident with a decrease in the ratio of transdiaphragmatic pressure to integrated phrenic activity (P(di)/ integral Phr) during sighs.

Normocapnia improves cerebral oxygen delivery during conventional oxygen therapy in carbon monoxide-exposed research subjects.

Study Objective: We determine whether maintaining normocapnia during hyperoxic treatment of carbon monoxide-exposed research subjects improves cerebral oxygen delivery.

Methods: This experiment used a randomized, single-blinded, crossover design. We exposed 14 human research subjects to carbon monoxide until their carboxyhemoglobin levels reached 10% to 12%.

Hypercapnia improves tissue oxygenation.

Background: Wound infections are common, serious, surgical complications. Oxidative killing by neutrophils is the primary defense against surgical pathogens and increasing intraoperative tissue oxygen tension markedly reduces the risk of such infections. Since hypercapnia improves cardiac output and peripheral tissue perfusion, we tested the hypothesis that peripheral tissue oxygenation increases as a function of arterial carbon dioxide tension (PaCO(2)) in anesthetized humans.

Direct effect of Pa(CO2) on respiratory sinus arrhythmia in conscious humans.

Respiratory sinus arrhythmia (RSA) may improve the efficiency of pulmonary gas exchange by matching the pulmonary blood flow to lung volume during each respiratory cycle. If so, an increased demand for pulmonary gas exchange may enhance RSA magnitude. We therefore tested the hypothesis that CO2 directly affects RSA in conscious humans even when changes in tidal volume (V(T)) and breathing frequency (F(B)), which indirectly affect RSA, are prevented.