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Step 1: Determine Whether the Primary Disorder is an Acidosis or Alkalosis by Reviewing the pH
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The low pH confirms the primary disorder is an acidosis.
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Step 2: Determine Whether the Primary Acidosis or Alkalosis is Metabolic or Respiratory by Reviewing the HCO3− and PaCO2
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Na+, 138 mEq/L; K+, 5.1 mEq/L; HCO3−, 27 mEq/L; Cl−, 102 mEq/L; BUN, 30 mg/dL; creatinine, 1.2 mg/dL.
The PaCO2 and HCO3− are both elevated. An elevated PaCO2 would lower pH and cause an acidemia (whereas an elevated HCO3− would cause alkalemia). Since the patient is acidemic, the primary process is a respiratory acidosis.
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Step 3: Explore the Differential Diagnoses of the Primary Disorder
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Respiratory acidosis may be caused by lung diseases, pleural diseases, or a variety of neuromuscular diseases (see Table 4-1). His prior history of COPD and acute pulmonary complaints of cough and fever clearly suggest that his respiratory acidosis is due to a pulmonary process. Specifically, Mr. R's history of very poor exercise tolerance at baseline suggests severe COPD. Such severe COPD could result in chronic carbon dioxide retention and chronic respiratory acidosis. A "must not miss" possibility is that his acute respiratory infection has precipitated acute respiratory failure (and acute respiratory acidosis). This is suggested by his worsening symptoms, respiratory distress, upright posture, pursed lip breathing, pulsus paradox, and decreased breath sounds. It is critical to distinguish acute respiratory acidosis from chronic respiratory acidosis because the former is more likely to progress rapidly to complete respiratory failure and respiratory arrest. Therefore, acute respiratory acidosis is both the leading hypothesis and the "must not miss" diagnosis. Table 4-7 ranks the differential diagnosis according to the available demographic information, risk factors, and symptoms and signs.
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Patients with a history of asthma or COPD should be asked about a prior history of intubation or ICU admission. Such patients are at greater risk for respiratory failure.
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Is the clinical information sufficient to make a diagnosis? If not, what other information do you need?
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Leading Hypothesis: Respiratory Acidosis
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Textbook Presentation
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The presentation of respiratory acidosis depends primarily on the underlying cause. The most common causes are severe underlying lung disease (eg, COPD, pneumonia, or pulmonary edema). Such patients are typically in extreme respiratory distress.
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Insufficient ventilation results in increasing levels of PaCO2. This in turn lowers arterial pH. Compensation occurs over several days, with increased renal HCO3− regeneration.
Ventilation is assessed by measuring the arterial PaCO2 and pH. Significant hypoventilation and acidosis may occur without significant hypoxia.
Etiology: Although most commonly due to lung disease, respiratory acidosis may result from any disease affecting ventilation—from the brain to the alveoli. (See differential diagnosis of acid-base disorders in Table 4-1.)
Manifestations are primarily CNS.
Severity depends on acuity. Patients with chronic hypercapnia have markedly fewer CNS effects than patients with acute hypercapnia.
Anxiety, irritability, confusion, and lethargy
Headache may be prominent in the morning due to the worsening hypoventilation that occurs with sleep.
Stupor and coma may occur when the PaCO2 > 70–100 mm Hg.
Tremor, asterixis, slurred speech, and papilledema may be seen.
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Evidence-Based Diagnosis
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Typically characterized by PaCO2 > 43 mm Hg.
Occasionally, a normal PaCO2 suggests respiratory failure.
For example, during asthma attacks, patients typically hyperventilate and present with a PaCO2 below normal. A normal PaCO2 in such a patient may reflect respiratory fatigue and herald the development of frank respiratory failure.
Patients with primary metabolic acidoses typically hyperventilate to compensate, lowering the PaCO2 below normal.
(1) A PaCO2 of ≥ 40 mm Hg is inappropriate in such cases and represents a respiratory acidosis.
(2) Inability to compensate for a metabolic acidosis (hyperventilate) is associated with an increased risk of respiratory failure and the subsequent need for mechanical ventilation.
The alveolar-arterial oxygen gradient (PaO2-PaO2) can help distinguish hypercapnia due to pulmonary disease from hypercapnia due to CNS disease (central hypoventilation).
This gradient compares the calculated alveolar partial pressure of oxygen (PaO2) with the measured arterial partial pressure of oxygen (PaO2).
(1) In the absence of lung disease, there is little difference between the alveolar and arterial O2.
(2) A normal A-a gradient is around 10 mm Hg.
Therefore, the A-a gradient is usually normal in hypoventilation due to CNS disease but increased in pulmonary disease.
The PaO2 is measured in an ABG whereas the PaO2 is calculated from the following formula:
PaO2 = FIO2 (pAtm – pH20) – PaCO2/R.
(FIO2 is the fraction of inspired oxygen: 0.21 for patients not on supplemental oxygen. pAtm = 760 at sea level, the partial pressure of H2O = 47 and PaCO2 is the arterial PCO2 measured in the blood gas. R refers to the respiratory quotient and is often estimated at 0.8.)
Pulsus paradox
Defined as > 10 mm Hg drop in systolic BP during inspiration
May be seen in patients using unusually strong inspiratory effort due to asthma, COPD, or other respiratory diseases
When elevated in patients with asthma, it is highly specific for a severe attack but has poor sensitivity (Table 4-8).
When pulsus paradox is marked, there is a high LR of severe disease.
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Treat underlying disease process (ie, bronchodilators for asthma, naloxone for opioid overdose).
Supplemental oxygen should be given as necessary to prevent hypoxemia.
Supplemental oxygen occasionally worsens hypercapnia in some patients with severe COPD, asthma, and sleep apnea but should never be withheld from hypoxic patients.
Avoid hypokalemia and dehydration that may worsen metabolic alkalosis, raise the serum pH, and inadvertently further suppress ventilation.
Mechanical ventilation with either intubation or biphasic positive airway pressure (BiPAP) is lifesaving in some patients.
Institution of mechanical ventilation is considered when pH < 7.1–7.25 or PaCO2 > 80–90 mm Hg.
In general, patients with acute hypoventilation require mechanical ventilation with milder hypercapnia than patients with chronic hypoventilation.
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Step 4: Diagnose Primary Disorder
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The patient's clinical picture and ABG clearly suggest the primary disorder is a respiratory acidosis.
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Step 5: Check for Additional Disorders
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Step 5A: Calculate Anion Gap (Even in Patients Without Acidosis) to Uncover Unexpected Anion Gap Metabolic Acidosis
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Another "must not miss" diagnosis for Mr. R would be sepsis. His symptoms of fever and cough suggest the possibility of pneumonia, which can be complicated by sepsis resulting in an anion gap metabolic lactic acidosis. Although his elevated HCO3− does not immediately suggest a metabolic acidosis from sepsis, the HCO3− may not be low if there is also a superimposed metabolic alkalosis generating HCO3−. These hidden acidoses can be discovered by evaluating the anion gap (which is usually elevated due the accumulation of lactate) or by measuring the serum lactate level.
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The anion gap = 138 − (102 + 27) = 9, and the serum lactate level is 0.8 mEq/L (normal 0.5–1.5 mEq/L).
Mr. R has a normal anion gap and normal lactate level, ruling out a coexistent hidden anion gap metabolic acidosis from sepsis.
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Step 5B: Calculate Whether Compensation is Appropriate
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In this case, it is critical to determine whether the PaCO2 is chronically elevated or whether this represents an acute decompensation. Acute respiratory acidosis can be distinguished from chronic respiratory acidosis by evaluating the degree of metabolic compensation (provided there are no other acidoses also effecting HCO3−). Because metabolic compensation takes time, chronic respiratory acidoses are associated with more complete compensation than acute respiratory acidoses. Table 4-2 shows the formulas that can be used to calculate the HCO3− levels. In acute respiratory acidosis, the HCO3− increases by only 1 mEq/L for every 10 mm Hg increase in PaCO2 whereas in chronic respiratory acidosis, the HCO3− increases by 4 mEq/L for every 10 mm Hg increase in PaCO2. In Mr. R's case, the PaCO2 is 70 mm Hg, up by 30 mm Hg (from a normal of 40 mm Hg), so if this were an acute respiratory acidosis, the HCO3− level would be expected to increase by only 3 mEq/L (from a normal of 24 mEq/L to 27 mEq/L). If, on the other hand, this is a chronic respiratory acidosis, an increase of 4 mEq/L of HCO3− per 10 mm Hg increase in PaCO2 would be expected. For a 30 mm Hg increase in PaCO2, the predicted increase in HCO3− would be 3 × 4 = 12 mEq.
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Mr. R's laboratory results reveal a HCO3− of 27 mEq/L, an increase of only 3 mEq/L from a normal baseline of 24 mEq/L. Other initial laboratory test results include WBC, 16,500/mcL with 62% granulocytes and 10% bands. Chest radiograph reveals hyperinflated lung fields and a left lower lobe infiltrate.
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Step 6: Reach Final Diagnosis
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The tiny metabolic compensation suggests that Mr. R is suffering from an acute respiratory acidosis with metabolic compensation. There is no evidence of a hidden anion gap acidosis. Therefore, Mr. R has an acute respiratory acidosis caused by pneumonia and COPD. He is at significant risk for complete respiratory failure and he is transferred him to the ICU.
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It is vital to distinguish acute from chronic respiratory acidoses.