Common misconceptions and mistakes
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100% O 2 sat is reassuring with regard to impending respiratory failure in a tachypneic, dyspneic patient
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Hypercapnic respiratory failure is ruled out by P co 2 < 45 mm Hg
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Chronic CO 2 retention in chronic obstructive pulmonary disease (COPD) is caused by the severity of the obstructive defect
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Ventilation is driven by P co 2 alone
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Thinking about (and reporting) pH as either normal or abnormal when in actuality it is always acidemic, pH < 7.40, or alkalemic pH ≥ 7.40
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Diagnosing (or worse, treating) a primary anxiety disorder in a tachypneic patient without an arterial blood gas (ABG) measurement
Normal ventilation
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The role of ventilation is to remove dissolved CO 2 (the ultimate metabolic waste product of all metabolism) from the blood
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Dissolved CO 2 acidifies blood, threatening to decrease pH (a big problem)
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pH is one of the mostly tightly regulated parameters in humans
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The “cost–benefit” ratio of evolution has selected for enzymes that function extremely efficiently (benefit) but do so over a tiny range of pH (cost)
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The minute-to-minute regulation of blood pH is controlled by, the medullary respiratory center, in the brainstem
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Under normal physiologic conditions, the respiratory center aggressively targets P co 2 ≈ 40 mm Hg (normal range 35–45 mm Hg), yielding a pH of ≈ 7.4 (normal range 7.35–7.45)
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To maintain tight control over CO 2 and pH, minute ventilation (MV), defined as tidal volume x respiratory rate, varies widely throughout the day (between 5 and 10 L/min) based on metabolic activity (mainly body temperature and the degree of skeletal muscle activity)
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As temperature increases (ie, fever), or more muscle groups are activated (ie, physical activity), more glucose is metabolized to CO 2 , which threatens to increase P co 2 above 40 mm Hg
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This triggers the respiratory center to increase MV
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This is achieved by effortlessly increasing tidal volume and rate (ie, not noticed by the individual)
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When pH is in the normal range, normal , MV varies, targeting P co 2 ≈ 40 mm Hg
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When pH is abnormal, MV varies targeting the normal pH range
Compensatory ventilatory responses to acidemia and alkalemia (A.K.A. ABG interpretation)
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Protecting a normal pH is more important physiologically than protecting a normal P co 2 (ie, pH trumps P co 2 ) with regard to control of ventilation
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Metabolic acidosis increases ventilation , decreasing P co 2 , increasing pH toward, but never > 7.35
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Metabolic alkalosis inhibits ventilation , increasing P co 2 , decreasing pH toward, but never < 7.45
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When a metabolic process occurs that either lowers pH (eg, lactic acidosis) or raises pH (eg, contraction alkalosis) MV either increases (acidosis) or decreases (alkalosis) in an attempt to compensate, without overcompensating
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No overcompensation means the pH defines the primary disorder
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If the pH is ≥ 7.40 the primary disorder is the one producing the alkalemia
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If the pH is < 7.40 the primary disorder is the one producing the acidemia
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P co 2 determines whether or not respiratory compensation is appropriate
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Appropriate compensation suggests a single acid–base disorder
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Inappropriate compensation implies a mixed acid–base disorder
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Checking for appropriate respiratory compensation without math, equations, or the “nomogram”
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Ensuring that respiratory compensation is appropriate for the degree of metabolic acidosis is crucial, since inappropriate compensation may signal impending respiratory failure
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The last two digits of the pH are the predicted P co 2 (spectacularly convenient), observe:
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Appropriate compensation for metabolic acidosis with a pH of 7.32 is P co 2 ≈ 32 mm Hg (± 1–2 mm Hg)
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Appropriate compensation for metabolic acidosis with a pH of 7.27 is P co 2 ≈ 27 mm Hg (± 1–2 mm Hg)
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Note that this rule begins to fall apart when pH is < 7.20 because the maximum ventilation a normal person can achieve is P co 2 ≈ 20–25 mm Hg (even though some young individuals with diabetic ketoacidosis [DKA] can do much better, ie, P co 2 < 10 mm Hg)
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The appropriate respiratory compensation for a pH of 7.16 should be “maximum ventilation,” which should generate a P co 2 in the low 20s mm Hg (not necessarily 16 mm Hg as the rule implies)
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Example: metabolic acidosis with a serum HCO 3 of 18 mEq/L will give a pH of 7.35 and a P co 2 of 35 mm Hg
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Because the pH is < 7.40 we know the primary disorder is an acidosis; Because the P co 2 < 40 mm Hg we know that the acidosis is metabolic
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Since a pH of 7.35 should drive the P co 2 down to 35 mm Hg, compensation is appropriate, which means there is a single acid–base disorder present
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Overcompensation (which does not occur) would suggest that an HCO 3 of 18 mEq/L could give you a pH of 7.41 and a P co 2 of 30 mm Hg
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Instead, this ABG represents a primary respiratory alkalosis, obvious by the fact that the pH is > 7.40 (alkalosis) and the P co 2 is < 35 mm Hg (low)
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Ensuring that respiratory compensation is appropriate for the degree of metabolic alkalosis is also crucial, since inappropriate compensation may signal superimposed hypercapnic respiratory failure
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The last two digits of the pH are still the predicted P co 2 (with more variability [± 5 mm Hg])
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Often more helpful is the fact that a metabolic alkalosis with compensatory respiratory hypoventialtion will never yield a pH < 7.45 (overcompensation dos not occur):
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A pH < 7.45 in a patient with metabolic alkalosis always implies a superimposed respiratory acidosis (lowering the pH to the normal range)
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Example: A metabolic alkalosis with a serum HCO 3 of 38 mEq/L will give a pH of 7.49 and cause compensatory hypoventilation (ie, decreased MV) giving a P co 2 of ≈49 mm Hg
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Because the pH is > 7.40, a primary alkalosis has occurred; Because the P co 2 > 40 mm Hg we know the alkalosis is metabolic
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Since a pH of 7.49 should cause the P co 2 to rise to 49 mm Hg, compensation is appropriate, which means there is a single acid–base disorder present
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Overcompensation (which does not occur) would suggest that an HCO 3 of 38 mEq/L could give a pH of 7.42 and a P co 2 of 55 mm Hg
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Instead, this ABG represents primary metabolic alkalosis (pH > 7.40) with a superimposed respiratory acidosis
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Because a metabolic alkalosis should give a pH > 7.45, the P co 2 must be higher than expected which implies additional hypoventilation = , or hypercapnic respiratory failure (often central, from CO 2 narcosis)
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Relevant mixed acid–base disorders (a.k.a. never missing a “hidden” acidosis):
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The most important thing not to miss in a mixed acid–base disorder is a “ hidden” acidosis , either:
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Metabolic acidosis:
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A P co 2 <35 mm Hg occurring with a normal pH reveals a hidden metabolic acidosis
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As occurs when there is a superimposed respiratory alkalosis (eg, pH 7.38, P co 2 29 mm Hg)
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No equations or math required to spot the metabolic acidosis
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pH is < 7.40, so the primary disorder is an acidosis; P co 2 < 40 mm Hg, so it is not a respiratory acidosis (lactate was elevated)
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Furthermore a P co 2 > 35 mm Hg should yield a pH > 7.45
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Respiratory acidosis:
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A P co 2 > 45 mm Hg occurring with a normal pH reveals a hidden acute respiratory acidosis
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As occurs when there is a superimposed metabolic alkalosis (eg, pH 7.42, P co 2 55 mm Hg)
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No equations or math required to spot the respiratory acidosis
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pH is > 7.40, so the primary disorder is an alkalosis; P co 2 > 40 mm Hg, so there is an additional respiratory acidosis
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The question is, “Is the respiratory acidosis an appropriate compensation for the metabolic alkalosis, or does it represent superimposed hypoventilation?”
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The answer is, “A compensatory respiratory acidosis never gives a pH < 7.45; therefore hypoventilation is present” (the patient was lethargic and required intubation for hypercapnic failure)
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“Failing to compensate” for a metabolic acidosis = implies hypercapnic failure, often occurring with a normal (or occasionally low) P co 2 (important not to miss)
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For a patient without chronic CO 2 retention “failing to compensate” = is detected by a P co 2 that is higher than anticipated:
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Example: DKA patient has an ABG showing a pH of 7.19 and a P co 2 of 33 mm Hg
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Even though the P co 2 is low (with regard to the normal range), it represents significant hypoventilation (expected P co 2 < 25 mm Hg)
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If this patient demonstrates increased work of breathing (WOB), intubation should be considered for impending hypercapnic respiratory failure
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If the patient does not demonstrate increased WOB it implies the patient has blunted ventilation (ie, a central component to their hypoventilation), as seen in narcotic use, obesity, and CO 2 -retaining COPD patients
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This is a more stable situation than the individual with the same ABG who demonstrates an increased WOB, because it is less likely to progress to respiratory failure
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Individuals with chronic CO 2 retention tend to not fully compensate for their metabolic acidemia
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The decision to support them should be made on clinical grounds or when their pH is < 7.35
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Evaluation of tachypnea and increased WOB
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Patients with an intact respiratory drive suffering impending respiratory failure experience extreme anxiety
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The anxiety is not the primary problem; the respiratory failure is
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Treating the anxiety of respiratory failure with “anxiolytics” precipitates respiratory arrest
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This should only be done in patients in whom comfort is the primary goal
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It is not possible to determine whether an anxious tachypneic patient is in respiratory failure or suffering a panic attack without an ABG
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Alkalemia = anxiety
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Acedemia = threatened or actual respiratory failure
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Obtain an arterial blood gas to check pH, P co 2 , and PaO 2 ( Fig. 2.1 )
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Even if the pH is in the “normal range” decide if it is acidemic (ie, pH < 7.40) or alkalemic (ie, pH ≥ 7.40)
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Then decide if the P co 2 is high (ie, > 45 mm Hg) or low (ie, < 35 mm Hg)
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Patients with visibly increased WOB and tachypnea rarely have a normal P co 2
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Acidemic patients with a high P co 2 have acute hypercapnic respiratory failure
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Acidemic patients with a low P co 2 are attempting to, or adequately compensating for their acidosis (± additional hyperventilation component)
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Alkalemic patients with a high P co 2 (and tachypnea) have chronic hypercapnic respiratory failure with superimposed acute respiratory alkalosis (driven by either hypoxemia or anxiety/pain)
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Alkalemic patients with a low P co 2 have acute respiratory alkalosis (driven by either hypoxemia or anxiety/pain)
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