Common misconceptions and mistakes
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Hypoxemia is a significant cause of dyspnea
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A cutaneous O 2 sat ≥ 92% predicts adequate oxygenation and is the appropriate target for O 2 orders
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100% O 2 suppresses respiratory drive in CO 2 retainers
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O 2 supplementation for patients with COPD is given to improve exercise tolerance
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Confusing failure of oxygen delivery to tissues, hypoxia (the job of the circulatory system) with hypoxemia, and failure to maintain an adequate Pa o 2 (the job of the respiratory system)
Oxygenation
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Normal oxygenation (at sea level) predicts:
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A partial pressure of oxygen (Pa o 2 ) of 75–100 mm Hg with 21% Fi o 2 (room air) and a Pa o 2 of ~ 660 mm Hg with 100% Fi o 2
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Impaired oxygenation exists on a spectrum from mild (abnormal A-a gradient) to severe (shunt):
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Pa o 2 < 200 mm Hg on Fi o 2 of 100% = “shunt physiology”
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Without “shunt physiology” an Fi o 2 > 40% (~ > 6 L/min via nasal cannula (NC)) should give a Pa o 2 > 60 mm Hg , despite pathology causing an abnormally increased A-a gradient
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Patients demonstrating shunt physiology are at high risk for hypoxemic respiratory failure, necessitating a search for the underlying cause, as well as close observation and aggressive support (e.g. chest imaging, 100% Fi0 2 )
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What defines adequate oxygenation Pa o 2 , O 2 sat, or it depends? Correct answer, Pa o 2 :
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Tissue oxygenation is a function of the circulatory system (primarily cardiac output (CO) and hemoglobin (Hb))
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Systemic hypox ia , the result of failed oxygen delivery to tissue (e.g. distributive shock), leads to systemic lactic acidosis
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Increasing Pa o 2 does not meaningfully increase oxygen delivery to tissues or decrease lactate
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The job of the respiratory system is to maintain a Pa o 2 > 60 mm Hg
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When Pa o 2 drops acutely to < 60 mm Hg (hypox emia ), organ specific symptomatic hypox ia may occur
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Especially in the brain, heart , and kidney (high metabolic demand)
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When treating hypoxemia hypox emia target, a Pa o 2 > 60 mm Hg
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Hypoxemic respiratory failure is practically defined as a Pa o 2 < 60 mm Hg
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An acute drop in Pa o 2 < 60 mm Hg (but > 54 mm Hg), ie, “mild hypoxemia,” may cause a range of symptoms:
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Tachypnea (hypoxic hyperventilation reflex)
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Designed to increase alveolar O 2 by decreasing alveolar CO 2 , thereby increasing work of breathing
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Tachycardia
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The right ventricle (RV) attempts to maintain CO in the face of rising pulmonary artery pressure (PAP) (hypoxic vasoconstriction) and decreased stroke volume (SV) by increasing heart rate (HR)
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Mental status changes (agitation, confusion, and decreased sensorium)
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Increased left ventricular end-diastolic pressure (LVEDP) (a.k.a. heart failure) from diastolic dysfunction
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Hypoxia stiffens the left ventricle (LV) and tachycardia shortens diastole, both impairing ventricular filling
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Decreased glomerular filtration rate (GFR) from increased LVEDP (cardio-renal physiology) or hypoxic renal injury
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Additionally, asymptomatic patients with an acute drop in Pa o 2 ( < 60 mm Hg ) are at increased risk for sudden profound/life-threatening desaturations (steep portion of the hemoglobin–oxygen [Hb–O 2 ] dissociation curve)
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When patients in hypoxemic respiratory failure achieve a Pa o 2 > 60 mm Hg (without hyperventilation) no further increase in respiratory support aimed at improving oxygenation is required
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Efforts then focus on resolution of the underlying cause of hypoxemia
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A low O 2 saturation, occurring with a Pa o 2 > 60 mm Hg , indicates acidosis (causing Hb desaturation), not hypoxemic respiratory failure
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Efforts then focus on resolving the acidosis (eg, renal replacement therapy)
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Symptomatic hypoxemia can be effectively ruled out by demonstrating a Pa o 2 > 60 mm Hg
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And, to a lesser extent, screened for by a cutaneous O 2 saturation (with a good wave form) > 94%
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Pulse oximeter readings > 92% (but < 95%) may mask a Pa o 2 < 60 mm Hg because of alkalosis or error ( Figs. 1.1 and 1.2 )
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Hb is designed to bind O 2 tightly (increase O 2 sat) in the alkalotic lungs and unload O 2 (decrease O 2 sat) in acidotic muscle
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Alkalemia elevates Hb sat (steepening the Hb–O 2 dissociation curve, increasing the risk of rapid desaturation)
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Acidemia decreases Hb sat (flattening the Hb–O 2 dissociation curve buffering against rapid desaturation)
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Alkalosis occurs commonly in:
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Hypoxemia (hypoxic hyperventilation reflex)
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Resolving acute on chronic hypercapnic failure (eg, posthypercapnic alkalosis), as ventilation improves and the previously compensatory metabolic alkalosis becomes the primary disorder
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Aggressive diuresis (contraction alkalosis)
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Error occurs commonly:
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Secondary to a poor signal (e.g. inadequate wave form)
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Even with a good waveform, pulse oximetry devices have a ± 3 point error range
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Fig. 1.1
Hemoglobin–oxygen dissociation curve. Shown is the Bohr effect (eg, shift in Hb saturation based on pH) where, for any given Pa o 2 value, alkalosis promotes increased saturation and acidosis decreases it. The shaded area in red shows individuals whose cutaneous pulse oximetry readings will be > 92% but whose Pa o 2 values will be < 60 mm Hg (because of alkalemia). Pulse oximetry readings of > 94% ensure a Pa o 2 > 60 mm Hg over a wide range of pH values, making it a more appropriate target for pulse oximetry orders (aimed at screening for hypoxemia, ie, a Pa o 2 < 60 mm Hg)
Fig. 1.2
Encapsulated case. Worsening pulmonary edema, despite aggressive diuresis because of diastolic dysfunction provoked by hypoxemia during oxygen weaning, targeting a cutaneous O 2 saturation of 92%. Because of error and alkalosis, the patient had Pa o 2 values < 60 mm Hg, leading to subendocardial hypoxia, left-ventricular (LV) stiffening, impaired filling, and increased left-ventricular end-diastolic pressure (LVEDP) physiology despite a 4 L negative fluid balance.
Teaching point: pulse oximetry readings should be used to screen for hypoxemia (Pa o 2 values < 60 mm Hg), and thus one should target cutaneous O 2 saturations > 94%.
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Acute hypoxemic respiratory failure
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An acute drop in Pa o 2 < 60 mm Hg
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Typically occurs from the spectrum of low VQ to shunt ( Fig. 1.3 )
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Sudden decrease or absent ventilation to an area of lung with relatively preserved perfusion
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