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Dead Space and Shunt-Producing Pathology Cheat Sheet (DRAFT) by

Ventilation and Gas Exchange

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Key Terms

Alveolar deadspace
alveolar that are ventilated but not perfused, and where, as a result, no gas exchange occur.
Deadspace ventil­ation
ventil­ation in excess of perfusion; High V/Q
Shunt perfusion
perfusion in excess of ventil­ation; Low V/Q
Pathology
it is the cause and effect of diseases; the typical behavior of a disease

Example

A 60-yea­r-old, 48-kg woman with a 2-day history of thromb­oph­lebitis of the right calf suddenly complains of chest pain and SOB. While breathing a fraction of inspired oxygen (FI02) of 0.21, the following clinical data are available above.

Result: Acute alveolar hyperv­ent­ilation (respi­ratory alkalosis) with mild hypoxemia.

Example (cont)

After 20 minutes of oxygen therapy (FIO2 0.50):

Result: Acute alveolar hyperv­ent­ilation (respi­ratory alkalosis) secondary to hypoxemia.

Example (contt)

On further evalua­tion, this patient was found to have a left lower lobe pneumonia.

If the diagnosis were pulmonary embolus, the following clinical data would have been:

Example (conttt)

The minute ventil­ation is about three times normal, and yet the PACO2 is only slightly less than normal, suggesting an increased deadspace ventil­ation.

At 50% inspired O2, there is a signif­icant increase in the PAO2 without signif­icant changes in the ventil­atory status – a circum­stance that suggests deadsp­ace­-pr­oducing pathology.

A.

Increase dead space occurs in pulmonary embolism
Lung areas that are ventilated but not perfused form part of the dead space. Alveolar dead space is potent­ially large in pulmonary embolism.
Acute PE impairs the efficient transfer of oxygen and carbon dioxide across the lung (Tables 2).
Decreased arterial Po2 (hypox­emia) and increase in the alveol­ar-­art­erial oxygen tension gradient are the most common gas exchange abnorm­ali­ties. Total dead space increases.
Ventil­ation and perfusion become mismat­ched, with blood flow from obstructed pulmonary arteries redirected to other gas exchange units. Shunting of venous blood into the systemic circul­ation may occur.