What are factors which affect arterial hypoxemia in the post operative care unit and what are the differential diagnosis?
Post operative hypoxemia
Atelectasis and alveolar hypoventilation are the most common causes of transient postoperative arterial hypoxemia in the immediate postoperative period
Factors leading to Postoperative Arterial Hypoxemia
Right-to-left intrapulmonary shunt (atelectasis)
Mismatching of ventilation to perfusion (decreased functional residual capacity)
Congestive heart failure
Pulmonary edema (fluid overload, postobstructive)
Alveolar hypoventilation (residual effects of anesthetics and/or neuromuscular blocking drugs)
Diffusion hypoxia (unlikely if receiving supplemental oxygen)
Inhalation of gastric contents (aspiration)
Pulmonary embolus
Pneumothorax
Increased oxygen consumption (shivering)
Sepsis
Transfusion-related lung injury
Adult respiratory distress syndrome
Advanced age
Obesity
1) ALVEOLAR HYPOVENTILATION
In the immediate postoperative period, the residual effects of inhaled anesthetics, opioids, and sedative-hypnotics depress the ventilatory response to carbon dioxide. The differential diagnosis of postoperative hypoventilation includes generalized weakness due to residual neuromuscular blockade or underlying neuromuscular disease. The presence of restrictive pulmonary conditions, such as preexisting chest wall deformity, postoperative abdominal binding, or abdominal distention, obesity can also contribute to inadequate ventilation.
2) Decreased Pao2
Diffusion hypoxia refers to the rapid diffusion of nitrous oxide into alveoli at the end of a nitrous oxide anesthetic. Nitrous oxide dilutes the alveolar gas and produces a transient decrease in Pao2 and Paco2. In the absence of supplemental oxygen administration, diffusion hypoxia can persist for 5 to 10 minutes after discontinuation of a nitrous oxide anesthetic in the post operative period.
3) Ventilation-Perfusion Mismatch and Shunt
Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood flow to well-ventilated alveoli. In the PACU, the residual effects of inhaled anesthetics and vasodilators such as nitroprusside and dobutamine used to treat systemic hypertension or improve hemodynamics will blunt hypoxic pulmonary vasoconstriction and contribute to arterial hypoxemia.Causes of postoperative pulmonary shunt include atelectasis, pulmonary edema, gastric aspiration, pulmonary emboli, and pneumonia.
4) Increased Venous Admixture
Increased venous admixture typically refers to low cardiac output states. It is due to the mixing of desaturated venous blood with oxygenated arterial blood. Normally, only 2% to 5% of cardiac output is shunted through the lungs,in low cardiac output states, blood returns to the heart severely desaturated. Additionally, the shunt fraction increases significantly in conditions that impede alveolar oxygenation, such as pulmonary edema and atelectasis.
5)Decreased Diffusion Capacity
A decreased diffusion capacity may reflect the presence of underlying lung disease such as emphysema, interstitial lung disease, pulmonary fibrosis, or primary pulmonary hypertension.
6) Pulmonary Edema
Pulmonary edema in the immediate postoperative period is often cardiogenic in nature secondary to intravascular volume overload or congestive heart failure. Less frequently, pulmonary edema may result from airway obstruction (postobstructive pulmonary edema), sepsis, or transfusion (transfusion-related lung acute lung injury [TRALI]).
Postobstructive Pulmonary Edema
. Postobstructive pulmonary edema is a transudative edema produced by the exaggerated negative intrathoracic pressure generated by an inspiratory effort against a closed glottis. The resulting negative intrathoracic pressure and increased venous return increase the hydrostatic pressure gradient across the pulmonary vascular bed, promoting the transudation of fluid. Muscular healthy patients are at increased risk of postobstructive pulmonary edema because of their ability to generate significant inspiratory force.
Laryngospasm is likely the most common cause of postobstructive pulmonary edema in the PACU, but postobstructive pulmonary edema may result from any condition that occludes the upper airway. The resultant arterial hypoxemia is usually manifested within 90 minutes of the upper airway obstruction.
Transfusion-Related Lung Injury
The differential diagnosis of pulmonary edema in the PACU should include transfusion-related lung injury in any patient who received blood products intraoperatively.Transfusion-related lung injury is typically manifested within 1 to 2 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets. Because reactions can occur up to 6 hours after transfusion, the syndrome may develop during the patient's stay in the PACU after a transfusion in the operating room.
Post operative hypoxemia
Atelectasis and alveolar hypoventilation are the most common causes of transient postoperative arterial hypoxemia in the immediate postoperative period
Factors leading to Postoperative Arterial Hypoxemia
Right-to-left intrapulmonary shunt (atelectasis)
Mismatching of ventilation to perfusion (decreased functional residual capacity)
Congestive heart failure
Pulmonary edema (fluid overload, postobstructive)
Alveolar hypoventilation (residual effects of anesthetics and/or neuromuscular blocking drugs)
Diffusion hypoxia (unlikely if receiving supplemental oxygen)
Inhalation of gastric contents (aspiration)
Pulmonary embolus
Pneumothorax
Increased oxygen consumption (shivering)
Sepsis
Transfusion-related lung injury
Adult respiratory distress syndrome
Advanced age
Obesity
1) ALVEOLAR HYPOVENTILATION
In the immediate postoperative period, the residual effects of inhaled anesthetics, opioids, and sedative-hypnotics depress the ventilatory response to carbon dioxide. The differential diagnosis of postoperative hypoventilation includes generalized weakness due to residual neuromuscular blockade or underlying neuromuscular disease. The presence of restrictive pulmonary conditions, such as preexisting chest wall deformity, postoperative abdominal binding, or abdominal distention, obesity can also contribute to inadequate ventilation.
2) Decreased Pao2
Diffusion hypoxia refers to the rapid diffusion of nitrous oxide into alveoli at the end of a nitrous oxide anesthetic. Nitrous oxide dilutes the alveolar gas and produces a transient decrease in Pao2 and Paco2. In the absence of supplemental oxygen administration, diffusion hypoxia can persist for 5 to 10 minutes after discontinuation of a nitrous oxide anesthetic in the post operative period.
3) Ventilation-Perfusion Mismatch and Shunt
Hypoxic pulmonary vasoconstriction refers to the attempt of normal lungs to optimally match ventilation and perfusion This response constricts vessels in poorly ventilated regions of the lung and directs pulmonary blood flow to well-ventilated alveoli. In the PACU, the residual effects of inhaled anesthetics and vasodilators such as nitroprusside and dobutamine used to treat systemic hypertension or improve hemodynamics will blunt hypoxic pulmonary vasoconstriction and contribute to arterial hypoxemia.Causes of postoperative pulmonary shunt include atelectasis, pulmonary edema, gastric aspiration, pulmonary emboli, and pneumonia.
4) Increased Venous Admixture
Increased venous admixture typically refers to low cardiac output states. It is due to the mixing of desaturated venous blood with oxygenated arterial blood. Normally, only 2% to 5% of cardiac output is shunted through the lungs,in low cardiac output states, blood returns to the heart severely desaturated. Additionally, the shunt fraction increases significantly in conditions that impede alveolar oxygenation, such as pulmonary edema and atelectasis.
5)Decreased Diffusion Capacity
A decreased diffusion capacity may reflect the presence of underlying lung disease such as emphysema, interstitial lung disease, pulmonary fibrosis, or primary pulmonary hypertension.
6) Pulmonary Edema
Pulmonary edema in the immediate postoperative period is often cardiogenic in nature secondary to intravascular volume overload or congestive heart failure. Less frequently, pulmonary edema may result from airway obstruction (postobstructive pulmonary edema), sepsis, or transfusion (transfusion-related lung acute lung injury [TRALI]).
Postobstructive Pulmonary Edema
. Postobstructive pulmonary edema is a transudative edema produced by the exaggerated negative intrathoracic pressure generated by an inspiratory effort against a closed glottis. The resulting negative intrathoracic pressure and increased venous return increase the hydrostatic pressure gradient across the pulmonary vascular bed, promoting the transudation of fluid. Muscular healthy patients are at increased risk of postobstructive pulmonary edema because of their ability to generate significant inspiratory force.
Laryngospasm is likely the most common cause of postobstructive pulmonary edema in the PACU, but postobstructive pulmonary edema may result from any condition that occludes the upper airway. The resultant arterial hypoxemia is usually manifested within 90 minutes of the upper airway obstruction.
Transfusion-Related Lung Injury
The differential diagnosis of pulmonary edema in the PACU should include transfusion-related lung injury in any patient who received blood products intraoperatively.Transfusion-related lung injury is typically manifested within 1 to 2 hours after the transfusion of plasma-containing blood products, including packed red blood cells, whole blood, fresh frozen plasma, or platelets. Because reactions can occur up to 6 hours after transfusion, the syndrome may develop during the patient's stay in the PACU after a transfusion in the operating room.
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