Hypoxic Respiratory Failure
Respiratory failure describes a set of conditions impairing delivery of oxygen to the tissues or removal of carbon dioxide from the tissues.
Respiratory failure can be classified under many different schemas, each having its advantages.
Classification by timing of onset, underlying etiology and/or anatomic area is useful when determining a differential diagnosis.
Understanding the pathophysiology of respiratory failure and applying physiologic principles can guide the physician in developing a differential diagnosis and administering timely treatment to the patient.
On the basis of pathophysiologic abnormalities, there are four types of respiratory failure.
Type 1: hypoxic respiratory failure.
Type 3: postoperative or atelectatic respiratory failure.
Type 4: circulatory shock-associated respiratory failure associated with hypoperfusion of respiratory muscles.
The primary derangement in acute hypoxic respiratory failure is an inability of the cardiopulmonary system to deliver adequate oxygen supply to the tissues.
Clinically, this can be further defined as the partial pressure of arterial oxygen (PaO2) <60 mm Hg.
It is also important to differentiate hypoxia from hypoxemia.
Hypoxia occurs when tissues are not adequately supplied with sufficient oxygen to accomplish cellular respiration.
Hypoxemia is characterized by a decrease in the content of oxygen in arterial blood. This includes both oxygen bound to hemoglobin and oxygen dissolved in the blood.
Hypoxemia is, therefore, a form of hypoxia.
There are four basic classes of hypoxia:
Hypoxemic hypoxia: low arterial oxygen content with impaired oxygen delivery.
Anemic hypoxia: low circulating hemoglobin concentration with impaired oxygen delivery.
Circulatory hypoxia: low cardiac output with impaired oxygen delivery.
Cytotoxic hypoxia: poisoning with cyanide where oxygen is delivered to the tissues but cannot be used.
Hypoxemia results from one of six basic pathophysiologic mechanisms.
Decreased inspired oxygen pressure
Low mixed venous oxygen content
Multiple pathophysiologic mechanisms may be at play in a single hypoxemic patient at any given time.
However, while all six mechanisms can contribute, typically, the only clinically significant mechanisms are ventilation/perfusion mismatch (V/Q mismatch), right-to-left shunting (shunt), and low mixed venous oxygen content.
Decreased Inspired Oxygen Pressure
In conditions of low atmospheric pressure (Patm), a decreased partial pressure of inspired oxygen (PiO2) occurs.
PiO2 is calculated as: PiO2 = FiO2 (Patm − PH2O)
Therefore, while the FiO2 (fraction of inspired oxygen) in the atmosphere is a constant 21%, the PiO2, and thus the driving pressure for oxygen diffusion across the alveolar membrane, is reduced in circumstances where atmospheric pressure is decreased (i.e., at altitude).
With a reduction in alveolar ventilation, partial pressure of arterial carbon dioxide (PaCO2) will increase.
Using the alveolar gas equation we can predict that with the increased CO2 resulting from hypoventilation, the partial pressure of alveolar oxygen (PAO2) will decrease:
PAO2 = (FiO2 × [Patm − PH2O]) − (PaCO2/0.8)
Hypoxemia related to hypoventilation can be reversed by an increase in FiO2 using supplementary oxygen, or an increase in alveolar ventilation.
Diffusion of oxygen across the alveolar–capillary membrane is rarely the sole reason for hypoxemia.
Diffusion of gas across a membrane is governed by Fick Law: Vgas + (A × D × [P1 − P2])/T
Vgas = volume of gas diffusing
A = surface area available for diffusion
D = diffusion coefficient of the gas
P1 − P2 = difference in partial pressures of the gas across the membrane
T = thickness of the membrane
In healthy subjects at rest, a single red blood cell will spend ∼0.75 seconds moving through a pulmonary capillary in contact with an alveolus.
Oxygen is a perfusion-limited gas. Therefore, the partial pressure of oxygen in the alveolus equilibrates quickly with that in the capillary. This takes ∼0.25 seconds.
Thus, there is considerable diffusion reserve if other variables in Fick Law are compromised.
However, in conditions where cardiac output is increased (i.e., exercise) the red blood cell spends significantly less time in contact with the alveolus. In these instances, impaired diffusion may contribute to the development of hypoxemia (e.g., interstitial lung disease).
Impaired diffusion is characterized by a widened Alveolar–arterial (A–a) gradient and will correct with supplemental oxygen.
V/Q mismatch is the most common cause of hypoxemic respiratory failure, owing to the wide variety of clinical conditions in which it occurs.
Ideally, ventilation of alveoli would perfectly match the perfusion of blood to those alveoli resulting in a V/Q ratio of 1.
However, even in healthy subjects, differential ventilation and perfusion of the lung from apex to base is not perfectly matched. Normally, the ventilation to perfusion ratio of the entire lung is around 0.8, accounting for the physiologic A–a gradient.
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