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Detection & Correction of Hypoxia During Anesthesia

Christine M. Egger, DVM, Diplomate ACVA

Anesthesiology & Pain Management

|September 2008|Peer Reviewed

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Hypoxia is a life-threatening condition in which oxygen delivery (DO2) is inadequate to meet metabolic demands. 

D O2 is the product of blood flow and oxygen content; thus, hypoxia may result from alterations in tissue perfusion, decreased oxygen partial pressure in the blood, or decreased oxygen-carrying capacity. Hypoxia may also result from restricted oxygen transport from the microvasculature to cells or impaired utilization within the cells. 

An inadequate supply of oxygen ultimately causes cessation of aerobic metabolism and oxidative phosphorylation, depletion of high-energy compounds, cellular dysfunction, and death. A systematic approach to diagnosis and treatment will save valuable time when dealing with this imminently life-threatening problem. 

Detection of Hypoxia
An arterial blood gas samplesuggests tissue hypoxia if:
The partial pressure of oxygen is < 90 mm Hg (hypoxemia)
The bicarbonate level is < 20 mEq/L
The base deficit is > -4
The serum lactate level is > 5 mmol/L.

If the latter 2 variables are increasing, this is highly suggestive of ongoing tissue hypoxia. Tissue hypoxia can also be inferred when the pulse oximetry reading is less than 97%. False hypoxemic readings are common with pulse oximeters, so any value less than 97% should prompt an immediate assessment of the patient's clinical signs before deciding whether a reading is spurious.

Clinical Signs of Hypoxia
Mild arterial hypoxemia
(SaO2, 94%-96%; PaO2, 70-90 mm Hg)

causes increased heart rate, cardiac output, and systemic vascular resistance. Mild hypertension may occur. 
Moderate arterial hypoxemia
(SaO2, 91%-94%; PaO2, 60-70 mm Hg)

results in local vasodilation and decreases in blood pressure. Heart rate may continue to increase if the baroreceptor reflex response is intact. 
Severe hypoxemia
(SaO2 < 91%; PaO2 < 60 mm Hg) 
allows local depressant effects to dominate; blood pressure falls rapidly, the heart rate slows, shock develops, and ventricular fibrillation or asystole follows. 
Hypoxemia promotes cardiac arrhythmias, stimulates respiration, and increases minute ventilation, although inadequate supply of oxygen to the brain stem eventually causes depressed respiration and apnea.
In sedated or anesthetized patients, the early sympathetic nervous system reactivity to hypoxemia may be reduced, and bradycardia, severe hypotension, cardiovascular collapse, and apnea may occur before a problem is detected, particularly if monitoring is inadequate.
Tissue hypoxia can be inferred if prolonged hypotension has occurred (mean arterial pressure < 60 mm Hg, systolic arterial pressure < 80 mm Hg for > 10 minutes).

Review of Oxygen Transport
Oxygenpasses from the atmosphere into the lungs, arterial circulation, extracellular fluid, interstitium, cytoplasm, and finally into the mitochondria, where it acts as the final electron acceptor in oxidative phosphorylation and production of adenosine triphosphate.
As oxygen moves from the atmosphere to the tissues, it moves down a series of pressure gradients from the atmosphere (Figure 1). · 1% to 2% of total oxygen in the blood is dissolved in plasma and is measured by PaO2, the rest is bound to hemoglobin (Figure 2). 
SaO2 in arterial blood under normal conditions is 97% to 100%; saturation of hemoglobin in venous blood is about 75%.
If metabolic tissue requirements are met, oxygen extraction is constant at around 25% in most tissues regardless of delivery (flow-independent); 75% is returned to the heart and lungs.
As DO2 decreases, oxygenextraction increases up to 75% and sympathetic nervous system stimulation results in venoconstriction, increased venous return, myocardial contractility, heart rate, and cardiac output in an attempt to maintain DO2
In many tissues, once 75% extraction has been reached, the DO2 becomes flow-dependent and there is a linear relationship between oxygen delivery and uptake.
The heart normally extracts about 70% of the oxygen in coronary arterial blood and cannot increase extraction much beyond that.

Thus, it must rely on increased coronary blood flow via sympathetic nervous system stimulation, simultaneously resulting in increased myocardial oxygen consumption, which makes the heart particularly susceptible to hypoxia.
The brain is another organ that is particularly susceptible to hypoxia-it has a very limited ability for anaerobic metabolism and neurons have very high metabolic activity.
Hypoxia can result from problems located anywhere along the oxygen pathway, and systematically considering the main categories of hypoxia can help to determine the cause and facilitate appropriate treatment.

Main Categories of Hypoxia
See Table for summary of etiology and treatment.

Hypoxic Hypoxia
Results from the inhalation of inadequate oxygen due to low partial pressure of inspired oxygen (PIO2) or low fraction of inspired oxygen (FIO2). 
Atmospheric oxygen partial pressure is determined by altitude, temperature, and other weather conditions. This pressure determines the PIO2 in patient's breathing room air (21% FIO2). At higher altitudes with lower barometric pressures, FIO2 is 21%, but it is 21% of 620 mm Hg (PIO2 = 130 mm Hg) instead of the sea level value of 21% of 760 mm Hg (PIO2 = 160 mm Hg); the result is a lower PIO2.
The pressure of oxygen in the breathing circuit determines PIO2 in patients receiving supplemental oxygen, either via mask or tracheal intubation.
Low FIO2 and PIO2 can occur when the oxygen flowmeter is turned down or off, the oxygen source is depleted, the patient is rebreathing carbon dioxide, or a hypoxic mixture of nitrous oxide or carbon dioxide and oxygenis administered.

Ventilatory Hypoxia
Occurs with inadequate delivery of oxygen to the alveolus due to hypoventilation
The PAO2 can be calculated from the alveolar gas equation:  PaO2 = FIO2 (PB-47) - 1.2 (PaCO2)
- PB = atmospheric pressure
- 47 = saturated vapor pressure of water (mm Hg)
- 1.2 = constant (based on respiratory quotient of 0.8)
- PaCO2 = partial pressure of carbon dioxide in arterial blood (assumed to equal the partial pressure of carbon dioxide in alveolar gas [PACO2])
As indicated by the equation, PAO2 is determined by the following: -FIO2 and PIO2 in the atmosphere or breathing circuit
- Humidification: The addition of water vapor reduces the PAO2 slightly compared with PIO2; humidificationdoes not occur in a tracheally intubated patient attached to a nonhumidified breathing circuit. 
- Minute ventilation (respiratory rate × tidal volume):

Hypoventilation reduces delivery of oxygen to the alveolus and can be caused by upper or lower airway obstruction, increased intraabdominal pressure (obesity, pregnancy, gastric distention), thoracic or upper abdominal pain, hypothermia, central or peripheral nervous system disease, paralysis, exhaustion, weakness, high doses of opioids, and brain stem depression due to severe hypotension or high doses of volatile and injectable anesthetics. -
Carbon dioxide production and elimination:Hypoventilation and increased production of carbon dioxide(ie, fever, malignant hyperthermia) result in increased PACO2, thereby displacing oxygen and decreasing PAO2

Diffusional Hypoxia
PaO2 isdetermined by the following:
The partial pressure gradient of oxygen from the alveolus to the arterial blood, called the PAO2-PaO2 gradient: 
· Carbon dioxide is 20 times as diffusible as oxygen, so the partial pressure gradient for carbon dioxide is much lower than for oxygen. 
Because oxygen is less diffusible, its uptake is greatly affected by alterations in the gradient (ie, low PAO2).
-The diffusion barrier: 
  Oxygen and carbon dioxide move across type I alveolar cells by simple diffusion, dependent on Fick's law of diffusion, which states that the volume of gas that moves across a sheet of tissue is directly proportional to its surface area and inversely proportional to its thickness.
  Pulmonary thromboembolism dramatically reduces surface area for gas exchange and negatively affects oxygen uptake and carbon dioxide elimination.
  Barrier thicknessincreases with pulmonary aspiration, pneumonia, pulmonary edema, and fibrosis and negatively affects oxygen diffusion.

Ventilation-Perfusion (V/Q) Mismatch Hypoxia
Ideally, ventilation is perfectly matched with perfusion (V/Q = 1) at the alveolus, but there is always some mismatch.
General anesthesia tends to increase mismatch in 2 possible ways:
High V/Q (> 1 to ∞) occurs when perfusion is low compared with ventilation because of increased dead space. Dead space in an anesthetized patient includes the following:
  Anatomic dead space, or airways not involved in gas exchange
  Mechanical dead space, or portions of the breathing circuit in which there is no separation of inspired and expired gas streams (excessively long endotracheal tubes or extensions of the Y-connector)
  Physiologic dead space, or alveoli that are being ventilated but not perfused due to low cardiac output, pulmonary arterial hypotension, cardiopulmonary arrest, or pulmonary thromboembolism; increased physiologic dead space can also be classified as a type of perfusional hypoxia (see category below).
Low V/Q (< 1 to 0) occurs when ventilation is low compared with perfusion, and effectively causes a right-to-left shunt. Shunt occurs whenever blood passes from the right to left side of the circulation without exposure to oxygen.
  Normal shunt fraction is about 5% because venous blood from the myocardial and bronchial circulations empties into the left ventricle.
  A congenital shunt-such as a ventricular septal defect, patent foramen ovale, or patent ductus arteriosus-shunts blood from the left side of the heart to the right side, as long as pulmonary vascular resistance, or right-heart afterload, is lower than systemic vascular resistance, or left-heart afterload. If pulmonary vascular resistance exceeds systemic vascular resistance, blood is shunted from the right side of the heart to the left side, resulting in reduced pulmonary blood flow and increased mixing of deoxygenated and oxygenated blood in the arterial circulation. Increases in pulmonary vascular resistance can result from hypoxemia, hypercarbia, and significant atelectasis during anesthesia. A significant decrease in systemic vascular resistance due to systemic arterial hypotension can also increase right-to-left shunting with congenital shunts.
  Recumbency, general anesthesia, and positive intrathoracic pressure (pneumothorax, pleural effusion) predispose to the development of atelectasis, which effectively causes shunting of blood from the right to the left side of the circulation without exposure to oxygen(these alveoli are perfused but not well ventilated).
  Oxygen uptake is greatly compromised by shunt, resulting in low PaO2, even with supplemental oxygen.
  Carbon dioxide elimination is not compromised until the shunt is very severe (> 50%) because of its high diffusibility.

Perfusional Hypoxia
Perfusional causes of hypoxia include the following:

- Pulmonary hypoperfusion: Increased physiologic dead space and V/Q mismatch

- Stagnant hypoxia: Tissue hypoperfusion and inadequate DO2 to cells due to low cardiac output and systemic arterial hypotension

- Anemic hypoxia:
  Oxygen content is determined by the amount dissolved in plasma (PaO2) and the amount bound to hemoglobin.
  The amount of oxygen bound to hemoglobin depends on the hemoglobin concentration, the affinity of the hemoglobin for oxygen, and the PaO2, which provides the "driving pressure" for oxygen binding to hemoglobin.
  SaO2 indicates how much of the hemoglobin is saturated with oxygen, but doesn't indicate whether hemoglobin concentration is adequate.
  Anemia and reduced oxygen-carrying capacity of hemoglobin (carboxy-hemoglobin or methemoglobin) result in anemic hypoxia.

Excessive Utilization or Inability to Use Oxygen
The final stage of oxygen delivery to tissues is diffusion from capillary blood into tissue cells and uptake by the mitochondria, which requires an intact mitochondrial enzyme system.
Histotoxic hypoxia can occur with cyanide poisoning and sepsis with multiple organ failure because both result in uncoupling of oxidative phosphorylation and inability of the cells to use oxygen.
Examples of excessive utilization of oxygen are malignant hyperthermia, fever, and excessive exercise.

Conclusion Timely detection and correction of hypoxia in sedated and anesthetized patients is imperative to avoid serious complications, including cardiac dysfunction, blindness, acute renal failure, and death.


Suggested Reading
Anesthesia for pediatric cardiac surgery. Greely WJ, Steven JM, Nicolson SC. In Miller RD (ed): Miller's Anesthesia, 6th ed-Philadelphia: Elsevier-Churchill Livingston, 2005, pp 2005-2042.
Cerebral blood flow, cerebral spinal fluid, and brain metabolism. In Guyton AC, Hall JE (eds): Textbook of Medical Physiology, 11th ed-Philadelphia: Elsevier Saunders, 2006,p767.
Gas exchange. Bellamy MC, Turner S. In Hemmings HC, Hopkins PM (eds): Foundations of Anesthesia: Basic Sciences for Clinical Practice, 2nd ed -Philadelphia: Mosby-Elsevier, 2006, pp 583-592.
Muscle blood flow and cardiac output during exercise. In Guyton AC, Hall JE (eds): Textbook of Medical Physiology, 11th ed-Philadelphia: Elsevier Saunders, 2006, pp 251-252.
Pulmonary gas exchange and blood transport of gases. In Stoelting RK, Hillier SC (eds): Pharmacology and Physiology in Anesthetic Practice, 4th ed-Philadelphia: Lippincott Williams & Wilkins, 2006, pp 783-793.
Redox pairs, tissue hypoxia, organ dysfunction, and mortality. Mizack B. Crit Care Med 28:270-272, 2000.
Respiratory physiology and respiratory function during anesthesia. Wilson WC, Benumof JL. In Miller RD (ed): Miller's Anesthesia, 6th ed -Philadelphia: Elsevier-Churchill Livingston, 2005, pp 679-722.
Ventilation and perfusion. Beadle MR, Lumb AB. In Hemmings HC, Hopkins PM (eds): Foundations of Anesthesia: Basic Sciences for Clinical Practice, 2nd ed-Philadelphia: Mosby-Elsevier, 2006, pp 573-582.

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