SLEEP APNEA (SA) SYNDROMES

Types:

1. Obstructive (OSAS) - Cessation of airflow, but maintenance of respiratory efforts.
2. Central - Cessation of both airflow AND respiratory efforts.
3. Pickwickian - Related to morbid obesity, severe chronic obstructive SA leading to right heart failure.

Dx:

Pathophysiology:

• Normally: respiratory neurons innervate the larynx/genioglossus muscle and maintain airway tone/patency during sleep.
  
• In those with OSAS{1}: EMG shows loss of this activity --> airway collapse during sleep --> decreased gas exchange --> carbon dioxide (CO2) retention --> stimulates respiration --> increases negative intrathoracic pressure--> worsens airway collapse during sleep --> etc.
• can result in:
  1. protracted hypoxemia, in turn resulting in:
     • hypoxic pulmonary vasoconstriction --> chronic Pulmonary Htn ---> R-Heart Failure.
     • increased circulating catecholamines --> systemic hypertension (Htn).
  2. Chronic CO2 retention (R-shift CO2/response curve), possibly secondary to mechanical disadvantage of breathing in severe obesity{2}.
  3. During apnea: bradycardia, atrioventricular (AV) block, premature ventricular contractions (PVCs), ventricular tachycardia, asystole --> possibly explains the increased incidence of sudden death seen in SA patients.
  4. Post-extubation pulmonary edema {3} (if surgery does not effectively relieve obstruction).
     • Inspiration against upper airway obstruction --> marked increase in negative intrathoracic pressure --> favors hydrostatic translocation of fluids into the interstitium.
     • Cor Pulmonale/increased R-sided pressures --> impedes lymphatic drainage --> delays clearing & favors fluid accumulation.
     • Lack of airflow --> hypoxemia --> alpha-adrenergic stimulation --> increased systemic vascular resistance (SVR) --> shunts blood volume centrally -> increased central pressures that also favor translocation of fluids into interstitium.
     • Usually resolves quickly once obstruction is relieved --> aggressive treatment in usually not needed (but, rule out other diagnoses first!)

Evaluation:

1. Detailed history - look for signs of: systemic Htn, excessive daytime sleepiness, loud snoring, morning headaches, diabetes, coronary artery disease (CAD).
2. Physical exam/History for signs of right heart failure: dyspnea on exertion., syncope, chest pain.
3. Thorough airway exam. Flexible nasopharyngoscopy may help to identify redundant tissue.
4. Chest X-ray (CXR): look for cardiomegaly, plump pulmonary arteries indicating pulmonary htn.
5. Electrocardiogram (EKG): arrhythmias, right ventricular hypertrophy (RVH) strain pattern/Cor Pulmonale, right bundle branch block (RBBB), P. Pulmonale.
6. Echocardiogram: evaluate extent of cardiac function, estimate pulmonary arterial pressure, presence of tricuspid insufficiency.
7. Pulmonary function tests (PFT's) useful to delineate the extent of pulmonary/respiratory compromise. Helpful for planning post-operative management.

Management:

Pre-op: {4}

• Obese patients are at increased risk for aspiration, so precautions are appropriate: metoclopromide, H2 blocker (ranitidine may better than cimetadine, which has hepatic microsomal enzyme suppression, and may therefore delay clearance of certain anesthetics).
• NO SEDATIVES WHATSOEVER!!! Any sedatation will likely result in (potentially complete) airway obstruction. If this happens unobserved on the wards or during transport, the pt. could become hypoxic and go into cardiac arrest.
• Impress upon patient extreme the risks of anesthesia, including: awake & post-op intubation, possible need for tracheostomy, and other possible complications (including death).
• Night time nasal continuous positive airway pressure (CPAP), 10-15 cm H2O.

During Anesthesia:

• Regional technique (without sedation if possible, awake un-sedated intubation, consider fiberoptic intubation ; Minimize or avoid intra-op opioids. Try to use all short acting agents. {1,4}
• Consider beta-blockers/antihypertensives to blunt response to intubation if needed.
• Fat compresses abdomen --> stretches diaphragm, making breathing difficult to impossible in supine position (diaphragm simply cannot lift abdominal weight) ==> solution may be a crane (no joke!){5}
• Intubate in sitting position, then slowly recline patient AFTER intubation, maintain spontaneous respiration to be certain patient CAN breathe supine, BEFORE giving paralyzing agents.

Post-op:

• Avoid sedation/narcotics (these patients tend to be extremely sensitive to even small doses).
  • Also avoid perchlorperazine, hydroxyzine, clonidine, prazosin (also have sedative effects).
  • Propranolol may blunt responsiveness to CO2, carefully consider when using.
• Observe closely. Surgical relief of obstruction may unmask a central apnea syndrome not previously appreciated.
• Extubate only when fully awake -- consider having surgeon with tracheostomy set standing by (especially if pt. was a difficult intubation).
• Nasal CPAP and or nasopharyngeal airway may be helpful post extubation.
• Intensive care unit (ICU) monitoring overnight is strongly recommended. Watch for apnea & arrhythmias.

References:

1. Connolly LA. "Anesthetic Management of Obstructive Sleep Apnea Patients". J. Clin Anesth. 3:461-9, 1991
2. Rappaport DM. "Hypercapnia in the OSA Syndrome". Chest. 89:627-35, May 1986
3. Lorch DG, et.al. "Post-Extubation Pulmonary Edema Following Anesthesia Induced by Upper Airway Obstruction". Chest. 90(6): Dec. 1986
4. Chung F. "Sleep Apnoea Syndrome and Anesthesia". Can. J. Anaesth. 29(5):439-45, 1982
5. Neuman G. "Periop Management of a 430 Kg Patient with Pickwickian Syndrome". A & A. 65:985-7, 1986

Return to the NYU Writings Sub-Page