A6 Respiratory/Circulatory Failure

Topic

Respiratory and circulatory insufficiency represents a failure in the oxygen transport chain extending from the environment to the muscle mitochondria—a chain integrating three mutually coupled physical subsystems: pulmonary ventilation, which moves gas into and out of the lungs; cardiovascular circulation, which moves blood throughout the body; and tissue diffusion, which transports oxygen molecule by molecule between the blood and the tissue. In quadrupeds, there is also a notable mechanical coupling between pulmonary ventilation and locomotion: the deformation of the trunk caused by the impact of the limbs against the ground mechanically synchronizes the respiratory cycle with the gait cycle, thereby reducing the metabolic cost of breathing. When pathology arises, this coupling between ventilation and locomotion is lost.

Pulmonary ventilation is modeled as a pulsatile gas flow moving through a network of elastic conduits—analogous to a network of pipes that expand and contract with each respiratory cycle. Within this flow, a dimensionless number compares the relative importance of the inertial forces of the moving gas against the viscous forces that retard it against the conduit walls; this relationship between inertia and viscosity determines the uniformity or pulsatility of the airflow profile within the lung.

Oxygen delivered to the alveoli via pulmonary ventilation must subsequently cross—molecule by molecule—into the blood circulating through the capillaries surrounding each alveolus. This process is known as tissue diffusion, and the rate at which oxygen traverses the alveolo-capillary barrier is directly proportional to the difference in oxygen partial pressure between the two sides; thus, the greater the pressure difference, the more rapidly oxygen is transferred into the blood. Once oxygen enters the bloodstream, the fraction of hemoglobin that actually carries it—its oxygen saturation—does not increase in direct proportion to the available partial pressure of oxygen; instead, it follows an S-shaped curve: flattening out at the extremes (both very low and very high pressures) and rising steeply across the intermediate pressure range. Furthermore, this curve shifts depending on blood temperature, acidity, and dissolved carbon dioxide levels: when blood warms up, becomes more acidic, or accumulates more carbon dioxide, hemoglobin releases oxygen more readily at a given pressure level—a shift with critical consequences when an animal experiences severe hypoxia.

The cardiovascular circulation that moves this oxygenated blood through the body depends, first and foremost, on the amount of blood the heart pumps with each beat: the volume of blood ejected during systole increases with preload—that is, the volume of blood filling the heart at the end of the preceding diastole (the more the heart fills before contracting, the more blood it subsequently ejects). Mean arterial pressure, in turn, is jointly determined by the resistance peripheral blood vessels offer to blood flow and the total volume of blood the heart pumps per unit of time.

In response to prolonged exposure to high altitude or underwater immersion, the body chronically alters this oxygen transport chain: it increases the number of circulating red blood cells and changes hemoglobin's affinity for oxygen, thereby permanently adjusting the saturation curve—described in the previous mechanism—to the conditions of the new environment. When the chain of oxygen transport to muscle mitochondria fails to meet the demands of movement, the maximum oxygen consumption the body can sustain falls below that locomotor demand; this drop compels the animal to slow down or stop completely. In diving mammals, this same chain imposes the limit on breath-holding: the breath is held as long as blood carbon dioxide levels remain low, and the dive ends the moment that concentration rises enough to trigger the respiratory reflex, forcing the animal to breathe again.

ID:2623