Common misconceptions and mistakes
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Attempting to force awake patients with central hypoventilation and no increased work of breathing to use bilevel positive airway pressure (BiPAP)
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Diagnosing a chronic obstructive pulmonary disease (COPD) patient with end-stage COPD because they present with a compensated severe respiratory acidosis (failing to notice that it developed over weeks to months)
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Failing to work up an elevated serum HCO 3 with an arterial blood gas (ABG) (instead assuming it represents a primary metabolic alkalosis)
Obesity hypoventilation syndrome
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Obesity is a common cause of blunted ventilatory drive (unknown mechanism) and thus chronic hypoventilation
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Individuals typically experience mild-moderate hypoventilation, with P co 2 values in the 45–55 mm Hg range
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This leads to renal compensation and serum HCO 3 elevations in the 30–34 mmol/L range
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Assuming no renal tubular acidosis (RTA) or end-stage renal disease (ESRD)
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Patients with RTA or ESRD may have an uncompensated respiratory acidosis (despite chronicity), giving them an ABG with the appearance of acute hypercarbic respiratory failure
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Clinically they have no acute respiratory complaints, which:
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Distinguishes them from patients with true acute hypercarbic respiratory failure, and
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Demonstrates their tolerance to acidosis, with regards to dyspnea (ie, blunted ventilatory drive), and hypercarbia, with regard to CO 2 narcosis
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Patients obese enough to suffer from hypoventilation almost always have concomitant obstructive sleep apnea (OSA)
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Hypoventilation is always worse during sleep; therefore poorly treated OSA exacerbates chronic hypoventilation
Exacerbation of Obesity Hypoventilation Syndrome
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An exacerbation of obesity hypoventilation syndrome (OHS) describes a subacute presentation in which patients gradually retain CO 2 (20–40 mm Hg) over weeks to months, allowing for renal compensation and central tolerance to CO 2 narcosis
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Ultimately they present complaining of shortness of breath and/or worsening exercise limitation
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Occasionally they present with lethargy secondary to symptomatic CO 2 narcosis (because of the absolute magnitude of the P co 2 elevation or the rapidity of its rise)
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The syndrome often presents as a “cor pulmonale” mimic, with:
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Severe, chronic, compensated respiratory acidosis (P co 2 often > 60 mm Hg)
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Peripheral edema
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Cardiac echo cardiogram suggesting pulmonary hypertension and isolated right-sided heart failure (ie, preserved left-ventricular (LV) function ± normal left artery (LA) size)
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Profound exercise limitation
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Unlike true cor pulmonale, the phenomena are potentially reversible in weeks to months with diuresis to euvolemia, supplemental O 2 use, and OSA treatment (nocturnal positive airway pressure therapy)
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The chest x-ray (especially portable) is often difficult to interpret, given obesity:
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Soft tissue veil may represent effusion or adipose
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Increased interstitial markings with hilar fullness may represent cardiogenic edema or low lung volumes
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Decompensated heart failure (commonly heart failure with a preserved ejection fraction [HFpEF]), with gross total body volume overload (> 15 L/30 lbs), is central to the pathophysiology of the OHS exacerbation:
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Volume overload (pulmonary edema and pleural effusion) decrease compliance, increasing the work of breathing required to maintain the patient’s baseline P co 2
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Individuals with blunted ventilation choose, instead, to maintain the same work of breathing, hypoventilating (gradually) and allowing their P co 2 to rise, thereby triggering both renal and central compensation
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A viscous cycle ensues where Hypoventilation and pulmonary edema cause hypoxemia, which worsens diastolic dysfunction leading to decompensated HFpEF, pulmonary edema, worse compliance, and further hypoventilation (worse during sleep)
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When looked at over time, HCO 3 levels and patient weight can be seen to increase and decrease together, as episodes of heart failure (as evidenced by fluid mediated weight gain), provoke episodes of hypoventilation (as evidenced by HCO 3 rise) OHS ( Fig. 8.1 ).
Fig. 8.1
Graphical display of an obese individual’s weight and HCO 3 values over a 1-year period, showing three points in time (red arrows) when they were admitted with acute respiratory failure secondary to chronic obstructive pulmonary disease (COPD) and heart failure (HF). The episodic dramatic elevations in weight reflect heart failure and volume overload, whereas the elevation of HCO 3 reflects renal compensation for subacute hypoventilation. This pattern is typical of patients with obesity hypoventilation syndrome and HF.
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Patients present on a spectrum of acuity :
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Worsening exercise limitation and dyspnea on exertion ( Fig. 8.2 )
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ABG suggests chronic hypercapnic respiratory failure
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Acidic pH in the normal range (7.35–7.39) and a severe respiratory acidosis
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Fig. 8.2
Encapsulated case of a patient with obesity, obstructive sleep apnea, chronic kidney disease 3, and heart failure with preserved ejection fraction (HFpEF) who presented complaining of shortness of breath and diminished exercise capacity and was admitted for an exacerbation of HFpEF. His echocardiogram showed normal systolic function, an increased pulmonary artery systolic with right-arterial dilation, and right-ventricular hypokinesis, but his chest x-ray showed interstitial edema with probable bilateral pleural effusion. He had a VQ scan that was low probability for pulmonary embolism (PE). His admission chemistry was notable for a HCO 3 of 42 mmol, which had been normal 1 month prior. His arterial blood gas (ABG) showed a chronic compensated respiratory acidosis with a P co 2 of 76 mm Hg, occurring over the past month based on his last normal HCO 3 . His preadmission (baseline) pulmonary function tests (PFTs) showed a restrictive pattern (likely from cardiogenic pulmonary edema). The patient was supported with oxygen, nocturnal bilevel positive airway pressure (BiPAP) (though poorly compliant), and diuresis with loop diuretics and intermittent acetazolamide (on any day that his pH was alkalotic). After diuresis of 17 L, he left the hospital 2 weeks later with a near normalization of his ventilation. This case illustrates how individuals with blunted ventilation, like the morbidly obese, may suffer subacute hypoventilation when they experience worsening respiratory mechanics, such as the decreased compliance associated with cardiogenic pulmonary edema. Ventilation returns to normal as the pulmonary edema resolves and respiratory mechanics return to baseline. The patient was not taking narcotics, sedatives, or other centrally acting medications or drugs (urine toxicology screen negative).
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Acute on chronic hypercapnic failure with shortness of breath (often with no increased work of breathing)
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ABG suggests acute on chronic hypercapnic respiratory failure
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Acidotic pH (< 7.35) and a mostly compensated severe respiratory acidosis
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Lethargy to obtundation (symptomatic CO 2 narcosis) with no increased work of breathing
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ABG shows either an extremely high P co 2 (> 90 mm Hg) or a mostly uncompensated severe respiratory acidosis (ie, evidence of rapid P co 2 rise)
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Acute hypoxemic respiratory failure from hypoventilation and alveolar edema (often with increased work of breathing)
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ABG suggests mixed hypoxemic hypercapnic respiratory failure with at least a partially compensated severe respiratory acidosis
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Recent history shows weight gain (often 15–30 lbs of fluid weight)
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Physical examination reveals peripheral edema, often with pulmonary edema (ie, crackles and diminished basilar breath sounds with dullness to percussion)
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Serum chemistry shows a dramatically elevated serum HCO 3
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Prior laboratory results show serum HCO 3 close to normal (or normal) in the recent past, before the onset of volume overload
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Chest x-ray shows interstitial edema, pleural effusion, and varying degrees of alveolar edema
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Narcotics and sedatives (often poorly cleared in the setting of decompensated HF with cardiorenal physiology) may complicate the picture, worsening hypoventilation
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Underlying COPD and baseline CO 2 retention also increase the propensity for hypoventilation
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Doctors may erroneously attribute these patients’ severe respiratory acidosis to progression of their obstructive lung disease, labeling them as end-stage COPD with cor pulmonale
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This happens despite the fact that their CO 2 retention occurred over weeks to months, not years as is the case with COPD ( Fig. 8.3 )
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