Effect of tidal volume on gas exchange during rescue ventilation.

Tidal volume VT required for mouth-to-mouth (MTM) and bag-valve-mask (BVM) rescue ventilation remains debatable owing to differences in physiology and end-point objectives. Analysis of gas transport may clarify minimum necessary VT and its determinants. Alveolar and arterial O2 and CO2 responses to MTM and air BVM ventilation for VT between 0.4 and 1.2 liters were computed using a model of gas exchange that incorporates inspired gas concentrations, airway dead space, cardiac output, pulmonary shunt, blood gas dissociation curves, tissue compartments, and metabolic rate. Parameters were adjusted to match published human data. Steady state arterial oxygen saturation reached plateaus at VT above 0.7 liters with MTM and 0.6 liters with air ventilation at 12 breaths per minute. Increasing shunt shifted oxygenation plateaus downward, but larger tidal volumes did not improve oxygen saturation. Carbon dioxide retention occurred at VT below 2.3 liters for MTM ventilation and 0.6 liters for air ventilation. Results establish a physiological foundation for tidal volume requirements during resuscitation.

Lung compression effects on gas exchange in human breath-hold diving.

Lung compression during breath-hold diving reduces gas exchanging surface area. Beyond a critical depth, collapse of all alveoli should result in total pulmonary shunt and a drop in arterial oxygen partial pressure toward the mixed-venous level. The effect of lung collapse on human breath-hold diving capability is analysed using a computational model of the lungs and circulation that simulates oxygen, carbon dioxide, and nitrogen exchange between alveoli, blood, and tissues. Gas uptake during descent becomes limited by lung compression when the ratio of diffusing capacity to the product of perfusion and gas solubility in blood drops below one. An equation is derived for estimating collapse depth due to direct alveolar compression and time-dependent absorption atelectasis. Oxygen dissolved in blood during descent builds a limited capacitive store for supporting metabolism during the period of lung collapse. Hypoxemia with loss of consciousness prior to alveolar re-opening on ascent is predicted to occur on dives beyond 300 m, depending on initial lung volume.

Fast or Slow Rescue Ventilations: A Predictive Model of Gastric Inflation.

BACKGROUND: Rescue ventilations are given during respiratory and cardiac arrest. Tidal volume must assure oxygen delivery; however, excessive pressure applied to an unprotected airway can cause gastric inflation, regurgitation, and pulmonary aspiration. The optimal technique provides mouth pressure and breath duration that minimize gastric inflation. It remains unclear if breath delivery should be fast or slow, and how inflation time affects the division of gas flow between the lungs and esophagus. METHODS: A physiological model was used to predict and compare rates of gastric inflation and to determine ideal ventilation duration. Gas flow equations were based on standard pulmonary physiology. Gastric inflation was assumed to occur whenever mouth pressure exceeded lower esophageal sphincter pressure. Mouth pressure profiles that approximated mouth-to-mouth ventilation and bag-valve-mask ventilation were investigated. Target tidal volumes were set to 0.6 and 1.0 L. Compliance and airway resistance were varied. RESULTS: Rapid breaths shorter than 1 s required high mouth pressures, up to 25 cm H2O to achieve the target lung volume, which thus promotes gastric inflation. Slow breaths longer than 1 s permitted lower mouth pressures but increased time over which airway pressure exceeded lower esophageal sphincter pressure. The gastric volume increased with breath durations that exceeded 1 s for both mouth pressure profiles. Breath duration of ∼1.0 s caused the least gastric inflation in most scenarios. Very low esophageal sphincter pressure favored a shift toward 0.5 s. High resistance and low compliance each increased gastric inflation and altered ideal breath times. CONCLUSIONS: The model illustrated a general theory of optimal rescue ventilation. Breath duration with an unprotected airway should be 1 s to minimize gastric inflation. Short pressure-driven and long duration-driven gastric inflation regimens provide a unifying explanation for results in past studies.

Breath-Hold Diving.

Breath-hold diving is practiced by recreational divers, seafood divers, military divers, and competitive athletes. It involves highly integrated physiology and extreme responses. This article reviews human breath-hold diving physiology beginning with an historical overview followed by a summary of foundational research and a survey of some contemporary issues. Immersion and cardiovascular adjustments promote a blood shift into the heart and chest vasculature. Autonomic responses include diving bradycardia, peripheral vasoconstriction, and splenic contraction, which help conserve oxygen. Competitive divers use a technique of lung hyperinflation that raises initial volume and airway pressure to facilitate longer apnea times and greater depths. Gas compression at depth leads to sequential alveolar collapse. Airway pressure decreases with depth and becomes negative relative to ambient due to limited chest compliance at low lung volumes, raising the risk of pulmonary injury called "squeeze," characterized by postdive coughing, wheezing, and hemoptysis. Hypoxia and hypercapnia influence the terminal breakpoint beyond which voluntary apnea cannot be sustained. Ascent blackout due to hypoxia is a danger during long breath-holds, and has become common amongst high-level competitors who can suppress their urge to breathe. Decompression sickness due to nitrogen accumulation causing bubble formation can occur after multiple repetitive dives, or after single deep dives during depth record attempts. Humans experience responses similar to those seen in diving mammals, but to a lesser degree. The deepest sled-assisted breath-hold dive was to 214 m. Factors that might determine ultimate human depth capabilities are discussed. © 2018 American Physiological Society. Compr Physiol 8:585-630, 2018.

Mechanics of airway and alveolar collapse in human breath-hold diving.

A computational model of the human respiratory tract was developed to study airway and alveolar compression and re-expansion during deep breath-hold dives. The model incorporates the chest wall, supraglottic airway, trachea, branched airway tree, and elastic alveoli assigned time-dependent surfactant properties. Total lung collapse with degassing of all alveoli is predicted to occur around 235 m, much deeper than estimates for aquatic mammals. Hysteresis of the pressure-volume loop increases with maximum diving depth due to progressive alveolar collapse. Reopening of alveoli occurs stochastically as airway pressure overcomes adhesive and compressive forces on ascent. Surface area for gas exchange vanishes at collapse depth, implying that the risk of decompression sickness should reach a plateau beyond this depth. Pulmonary capillary transmural stresses cannot increase after local alveolar collapse. Consolidation of lung parenchyma might provide protection from capillary injury or leakage caused by vascular engorgement due to outward chest wall recoil at extreme depths.

Computer simulation of human breath-hold diving: cardiovascular adjustments.

The world record for a sled-assisted human breath-hold dive has surpassed 200 m. Lung compression during descent draws blood from the peripheral circulation into the thorax causing engorgement of pulmonary vessels that might impose a physiological limitation due to capillary stress failure. A computer model was developed to investigate cardiopulmonary interactions during immersion, apnea, and compression to elucidate hemodynamic responses and estimate vascular stresses in deep human breath-hold diving. The model simulates active and passive cardiovascular adjustments involving blood volumes, flows, and pressures during apnea at diving depths up to 200 m. Redistribution of blood volume from peripheral to central compartments increases with depth. Pulmonary capillary transmural pressures in the model exceed 50 mm Hg at record depth, producing stresses in the range known to cause alveolar capillary damage in animals. Capillary pressures are partially attenuated by blood redistribution to compliant extra-pulmonary vascular compartments. The capillary pressure differential is due mainly to a large drop in alveolar air pressure from outward elastic chest wall recoil. Autonomic diving reflexes are shown to influence systemic blood pressures, but have relatively little effect on pulmonary vascular pressures. Increases in pulmonary capillary stresses are gradual beyond record depth.