Respiratory Physiology During Anesthesia

Respiratory Physiology During Anesthesia: Gas Exchange and Respiratory Mechanics 01 The respiratory system provides O2 to the body and expels CO2 from the body
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The functional unit of the lung is the alveoli; epithelial cells and endothelial cells form the thin alveolar walls, which are the interface for gas exchange between blood and air
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The power of gas in and out of the lung (ventilation) comes from the movement of respiratory muscles or the drive of the ventilator, while the resistance of breathing movement includes airway resistance and elastic resistance of lung and chest wall
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Mastering the basic physiological mechanism of regulating gas exchange is helpful to correctly interpret the monitoring indicators of patients during anesthesia and guide the parameter setting of ventilator
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02 Arterial partial pressure of oxygen (PaO2) How oxygen is transported from the air into the blood (Figure 2.
1)
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Inhaled air is about 21% oxygen
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At sea level, the atmospheric pressure is 760mmHg; inhaling air in a fully saturated state of water vapor (47mmHg), the oxygen partial pressure (PO2) is calculated as follows: PO2=(760-47) mmHg*0.
21=150mmHg One unit (such as moles) of CO2 (CO2 production: VCO2) needs to consume slightly more O2 (O2 consumption: VO2), and the normal value of respirator quotient (RQ) (VCO2/VO2) is 0.
8
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In the alveoli, 1 volume of O2 is exchanged with 1.
2 volumes of CO2
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Therefore, when the arterial blood carbon dioxide partial pressure (PaCO2) is the normal value of 40mmHg, the alveolar oxygen partial pressure (PAO2) is: PAO2=PIO2-PACO2 x1.
2≈102mmHg The arterial blood will be mixed with a small amount of venous after flowing through the alveolar capillaries Blood, these venous blood comes from the smallest alveolar shunt (2%-3%, increasing with age) and pulmonary circulation shunt (such as some bronchial veins and phrenic veins) blood, so the actual PaO2 is slightly lower than 102mmHg Hypoxemia Cause: low PIO2 , Low PAO2, diffusing dysfunction, low PaO2 (shunt, low V/Q value), low PvO2 The fatal treatment of hypoxemia must be rapid.
For patients with uncomplicated conditions during anesthesia, only increasing FO2 Yes! However, for patients with complex conditions, the treatment methods for hypoxemia are different, such as ICU patients with respiratory failure, or surgical patients with severe respiratory diseases, and patients with some special surgical operations such as one-lung ventilation, thoracic surgery.
Trauma and pulmonary hemorrhage,
etc.

The fatal cause of hypoxemia is insufficient oxygen supply to cells: when PaO2 decreases significantly, it drives the transport of oxygen from the blood to the interstitium (PO2≈20~30mmHg), and then from the interstitium to the cells (PO2<20mmHg).
The pressure gradient is also reduced
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It is worth noting that this pressure gradient change is determined by PO2, not oxygen content, therefore, effective treatment of hypoxemia should aim to increase PaO2 rather than oxygen content
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03PaCO2CO2 and water are the end products of aerobic metabolism
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CO2 reaches equilibrium with hydrogen ions, bicarbonate and carbonic acid in plasma, and is excreted from the lungs in the form of gas
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So far, respiratory regulation is the most important way for the body to remove metabolic acids, far exceeding the amount of hydrogen ions removed by the kidneys
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In a steady state, PaCO2 is the value at which the CO2 (VCO2) produced by cell metabolism and the CO2 excreted through minute ventilation (VE) reach equilibrium PaCO2=VCO2/VEPaCO2 is a strong stimulus for ventilation: every increase in PaCO2 by 1 mmHg immediately caused an average increase in VE of 1-2 min
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Changes in this relationship are the most common causes of hypercapnia.
Hypercapnia increases CO2 production.
Increased CO2 production is seen in fever, chills, excessive caloric/carbohydrate intake, and in malignant hyperthermia , MH) and neuroleptic malignant syndrome (NMS), the maximum limit can be reached
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Decreased excretion of cO2 The most common cause of hypercapnia is decreased excretion of CO2
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The reduction of CO2 excretion includes two main reasons (1) hypoventilation: the limited excretion of CO2 increases PaCO2
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The common causes of hypoventilation are: ①Respiratory center depression: such as when sedative-hypnotics and opioids are used; ②Respiratory muscle weakness: such as Guillain Bare syndrome and severe polyneuropathy; ③Decreased chest and lung compliance or significant ventilation resistance Increased (see below): seen in severe asthma or bloating
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Emergency treatment of hypoventilation includes ventilatory support and supplemental oxygen (see Hypoxemia) (2) Dead space ventilation and high v/Q values ​​04 During general anesthesia and hypoxemia, a number of factors can lead to a decrease in PaO2 (Fig.
2.
5) 1 Lung volume reduction Regardless of whether muscle relaxants are used or not, the functional residual capacity (FRC) of patients decreases within minutes after induction of general anesthesia; when combined with reduced FRC, such as morbid obesity, pregnancy, and combined Acute respiratory dysfunction with reduced lung compliance, such as ARDS, will exacerbate the decline in FRC
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Significant oxygen desaturation may occur immediately after induction of anesthesia, and if rapid endotracheal intubation cannot be performed at this time, oxygen desaturation will drop rapidly
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Ideally, based on FRC oxygen content and average oxygen consumption, the body can tolerate hypoxia for 8 min before severe hypoxemia occurs
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However, when the patient is combined with the above conditions, the tolerance time of hypoxia will be shortened, and preparations should be made in advance to make full use of this short time
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If ventilatory support is inadequate, lung volumes, including FRC and tidal volumes, may continue to decrease throughout the maintenance of anesthesia
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Returning the patient to spontaneous breathing for other reasons may help improve hypoxemia, but support ventilation with a level of inspiratory pressure to provide adequate tidal volume and the use of positive end expiratory pressure (PEEP) is the key to optimal gas exchange
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2 During atelectasis anesthesia, atelectasis can occur due to reduced lung volume and/or inhalation of high concentrations of oxygen
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Nitrogen does not participate in gas exchange and can keep the alveoli open at the end of expiration, but inhaling high concentrations of oxygen can reduce the nitrogen concentration in the alveoli
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Therefore, it is called "absorptive atelectasis"; in addition to treating severe hypoxemia, inhalation of extremely high concentrations of oxygen should be avoided
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It has been calculated that 20% nitrogen in the alveoli can limit the collapse of the alveoli caused by inhaling high concentrations of oxygen
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3 Perioperative oxygen poisoning inhalation of high concentrations of oxygen can generate reactive oxygen species (ROS), ROS can cause lipid peroxidation in biofilms, damage the nucleus and cell membrane and denature DNA, thereby causing local and systemic damage.
damage
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