alveolar ventilation

In very general terms, hyperventilation is an increased alveolar ventilation.

This is because alveolar ventilation will increase more in the acclimated person.

One must also take care to consider the effect of dead space on alveolar ventilation, as seen below in "Relationship to other physiological rates".

If the alveolar ventilation is insufficient, there will not be enough oxygen delivered to the alveoli for the body's use.

Alveolar ventilation is under the control of the central respiratory centers, which are located in the pons and the medulla.

Hypoventilation exists when the ratio of carbon dioxide production to alveolar ventilation increases above normal values.

Minute volume comprises the sum of alveolar ventilation and dead space ventilation.

Mean airway pressure correlates with alveolar ventilation, arterial oxygenation, hemodynamic performance, and barotrauma.

Extrapulmonary restriction is a type of restrictive lung disease, indicated by decreased alveolar ventilation with accompanying hypercapnia.

Arterial chemical receptors are stimulated by exposure to a low partial pressure and hence increase alveolar ventilation, up to a maximum of 1.65 times.

In patients with lung disease, lungs may not be able to increase alveolar ventilation in the face of increased amounts of dissolved CO.

Subject 5a was modeled using the same procedure using the body weight (121 Kg), fat fraction (0.38) alveolar ventilation, and Kbair measured for this subject.

This is a result of stimulation to chemoreceptors, which increases alveolar ventilation, leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of hyperventilation).

Carbon dioxide is produced continuously as the body's cells respire, and this CO will accumulate rapidly if the lungs do not adequately expel it through alveolar ventilation.

All the other parameters required for the PBPK (organ volumes, blood flows, alveolar ventilation, organ/blood partition and volume, etc.) are determined simply by a call to "standardhuman".

This is an idealized case and it is known that even in normal humans the lung is heterogeneous, with different regions receiving different fractions of the cardiac output and the alveolar ventilation.

Likewise, for any given total body CO production rate, alveolar ventilation is inversely proportional to end-tidal CO concentration (since their mutual product must equal total body CO production rate).

DLCO corrected for alveolar ventilation (DLCO corr /VA) showed no differences between both HTLV groups and seronegatives in either the unadjusted or the multivariable analysis.

When alveolar ventilation (in liters of air per minute) and alveolar capillary blood flow (in liters of blood per minute) are approximately equal, oxygen equilibrates across the alveolar-capillary membrane well before the blood has traversed the alveolus.

Gas exchange is affected by increases in the dispersion of both alveolar ventilation and cardiac output because bronchial and vascular functions are altered by injury-related factors, such as the effects of inflammatory mediators on airway and vascular smooth muscle tone.

At the steady state, the rate of production of CO equals the net rate at which it is exhaled from the body, which (assuming no CO in the ambient air) is the product of the alveolar ventilation and the end-tidal CO concentration.

Excretion of carbon dioxide is also impaired, but a rise in the arterial partial pressure of carbon dioxide (paCO) is very uncommon because this leads to respiratory stimulation and the resultant increase in alveolar ventilation returns paCO to within the normal range.

The matched timing of alveolar ventilation and its perfusion with RSA within each respiratory cycle could save energy expenditure by suppressing unnecessary heartbeats during expiration and ineffective ventilation during the ebb of perfusion (delivery of blood from arteries to capillaries for oxygenation and nutrition).