Is central sleep apnea-Cheyne-Stokes respirations (CSA-CSR) in the setting of heart failure (HF) detrimental?

CSA-CSR is characterized by a crescendo-decrescendo pattern of 20-30 second hyperventilation followed by 10- 40 second hypopneas or apneas during exercise, wakefulness or stages 1 and 2 non-rapid eye movement sleep (1,2).

CSA-CSR is associated with elevated pulmonary capillary wedge pressure, ventricular dilatation, atrial fibrillation, and increased central and peripheral chemosensitivity to arterial C02 levels (1).

In contrast to obstructive sleep apnea whose detrimental impact is widely accepted, CSA-CSA has not consistently been shown to be associated with higher mortality rates.  Some even argue that it may be beneficial in HF by providing intrinsic positive end-expiratory pressure (PEEP), augmented stroke volume, avoidance of hypercapnic acidosis, attenuated sympathetic activity, bronchodilation and cyclic respiratory muscle rest, akin to those seen with episodic CPAP (2).

Wow! Is CSA-CSR nature’s CPAP? This is an interesting way of looking at CSA-CSR, and underscores the importance of addressing the underlying problem (e.g. HF) rather than the symptoms alone.

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References

1. Rosen D, Roux FJ, Shah N. Sleep and breathing in congestive heart failure. Clin Chest Med 2014, 35: 521–534. https://www.ncbi.nlm.nih.gov/pubmed/25156768

2. Naughton MT. Cheyne-Stokes respiration: friend or foe. Thorax 2012;67:357-360. http://thorax.bmj.com/content/thoraxjnl/67/4/357.full.pdf

Is central sleep apnea-Cheyne-Stokes respirations (CSA-CSR) in the setting of heart failure (HF) detrimental?

How good are arterial blood gases in ruling out pulmonary embolism (PE)?

Not as good as one would hope! 

In an often quoted study involving 768 patients with suspected PE who underwent angiography, a combination of normal A-a gradient (<20 mm Hg ), normal PaO2 (>80 mm Hg), and normal PaCO2 (>35 mm Hg) was examined to help exclude PE (1). Among patients with no known cardiopulmonary disease and normal values in all 3 parameters,  over 30% still had PE, while among those with cardiopulmonary disease and normal parameters 17% had PE.  

In short, normal arterial blood gases may make PE less likely, they do not by any means exclude the possibility of PE.

Reference

  1. Stein PD, Goldhaber SZ, Henry JW, et al. Arterial blood gas analysis in the assessment of suspected acute pulmonary embolism. CHEST 1996; 109:78-81. https://www.ncbi.nlm.nih.gov/pubmed/8549223

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How good are arterial blood gases in ruling out pulmonary embolism (PE)?