eMedicine Specialties > Pulmonology > Sleep-Related Disorders

Hypoventilation Syndromes: Treatment & Medication

Author: Jazeela Fayyaz, DO, Senior Fellow, Department of Pulmonology, Lenox Hill Hospital
Coauthor(s): Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Contributor Information and Disclosures

Updated: Sep 18, 2009

Treatment

Medical Care

The treatment of hypoventilation primarily is directed at correcting the underlying disorder. Use caution when correcting chronic hypercapnia. Rapid correction of the hypercapnia can alkalinize the cerebrospinal fluid, which may cause seizures, and can induce a metabolic alkalosis placing the patient at risk for cardiac dysrhythmias. Infusion of sodium HCO3 is not indicated for chronic hypoventilation syndromes.

  • Bronchodilators such as beta-agonists (eg, albuterol, salmeterol), anticholinergic agents (eg, ipratropium bromide), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive lung disease and severe bronchospasm. Additionally, theophylline may improve diaphragm muscle contractility and stimulate the respiratory center.
  • Treatment also is aimed at assisting ventilation. Therapies that may be beneficial are endotracheal intubation with mechanical ventilation and noninvasive ventilatory techniques such as bilevel positive-pressure ventilation. Ventilatory assistance may be required in patients for the following indications:
    • Symptoms of nocturnal hypoventilation such as daytime hypersomnolence, morning headaches, fatigue, nightmares, and enuresis
    • Dyspnea at rest
    • Hypoventilation that causes pulmonary hypertension and cor pulmonale
    • Nocturnal hypoxia (arterial oxygen saturation <88%) despite supplemental oxygen
  • Noninvasive ventilation using nocturnal positive-pressure ventilation (PPV) is widely accepted as the ventilatory mode of choice in patients with chronic respiratory failure related to chronic obstructive pulmonary disease (COPD), neuromuscular disease, thoracic deformities, and idiopathic hypoventilation. Nocturnal PPV may obviate the need for tracheotomy and has improved many patient-oriented outcomes. Bilevel positive-pressure ventilation is the preferred method of noninvasive ventilation.
    • Based on the available literature, the indications for noninvasive PPV for nocturnal hypoventilation syndromes have been formulated. Patients considered for this therapy should have the following: a disease known to cause hypoventilation; symptoms and signs of hypoventilation present; failure to respond to first-line therapies in mild cases of hypoventilation (ie, treatment of primary underlying disease with bronchodilators, respiratory stimulants, weight loss, supplemental oxygen, or CPAP); or moderate-to-severe hypoventilation.
    • Nocturnal PPV is indicated for use in patients with neuromuscular disorders who exhibit morning headache, daytime hypersomnolence, sleep difficulties, or cognitive dysfunction.
    • In the absence of symptoms, nocturnal PPV is recommended when the partial pressure of alveolar carbon dioxide (PaCO2) is greater than 45 mm Hg or when the partial pressure of arterial oxygen (PaO2) is less than 60 mm Hg on a morning blood gas measurement.11
    • Daytime ventilation should be used when these patients have PaCO2 greater than 50 mm Hg or oxygen saturation of less than 92%.9
    • Studies in obesity hypoventilation syndrome (OHS) patients have shown that 1 year of treatment with nocturnal PPV improves blood gas values.12
    • Nocturnal hypoventilation acts by improving nocturnal hypoventilation and improving carbon dioxide responsiveness.11
    • See the related clinical guideline summary from the American Academy of Sleep Medicine, Practice parameters for the use of continuous and bilevel positive airway pressure devices to treat adult patients with sleep-related breathing disorders.13
    • Also see Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease, a clinical guideline summary from the Global Initiative for Chronic Obstructive Lung Disease (GOLD).14
  • Consideration for intubation and invasive mechanical ventilation should be undertaken if attempts at noninvasive ventilation fail to benefit the patient.
  • Drugs aimed at reversing the effects of certain sedative drugs also may be helpful in the event of an overdose. Naloxone (Narcan) may be used to reverse the effects of narcotics, and flumazenil (Romazicon) may be used to reverse the effects of benzodiazepines.
  • Because many patients with hypercapnia also are hypoxemic during the day, oxygen therapy may be indicated.
    • Oxygen therapy is indicated to prevent the sequelae of long-standing hypoxemia. Patients with COPD who meet the criteria for oxygen therapy have a decreased mortality when treated with oxygen. Oxygen therapy also has been shown to reduce pulmonary hypertension. Oxygen use alone is an inadequate therapy for obesity hypoventilation syndrome (OHS).
    • Use oxygen therapy with caution because it may worsen hypercapnia in some situations. In patients with COPD, the presence of worsening hypercapnia following oxygen therapy is a consequence of ventilation-perfusion mismatching rather than reduced ventilatory drive secondary to reduction in hypoxia. Hypercapnia is best avoided by titration of oxygen delivery to maintain oxygen saturations in the range of 90-94% and a PaO2 between 60 and 65 mm Hg.
    • Approximately half the patients with OHS require oxygen therapy in addition to nocturnal PPV.3
    • Patients with neuromuscular disease should not be given oxygen therapy without ventilatory support.
  • Respiratory stimulants have been used but have limited efficacy in alveolar hypoventilation.
    • Medroxyprogesterone increases the central respiratory drive, and it has been shown to be effective in OHS. Medroxyprogesterone also has been shown to stimulate ventilation in patients with COPD and alveolar hypoventilation. Initial studies documenting a reduction in hypercapnia with treatment with medroxyprogesterone were performed in the 1960s.15 More recent studies also have documented a decrease in hypercapnia in patients with OHS and COPD with associated hypercapnia while receiving total daily doses of 60 mg of medroxyprogesterone in divided doses 2-3 times per day.16 However, it does not improve apnea frequency or symptoms of sleepiness. In addition, the risk of venous thromboembolism is increased with progestational agents.6 Many experts do not currently recommend progesterone therapy.
    • Acetazolamide is a diuretic that inhibits carbonic anhydrase, increases HCO3 excretion, and causes metabolic acidosis. The metabolic acidosis subsequently stimulates ventilation. However, this medication must be used with caution. If the patient's respiratory system cannot compensate for the metabolic acidosis it induces, the patient may suffer hyperkalemia and, potentially, a cardiac dysrhythmia.
    • Theophylline increases diaphragm muscle strength and stimulates the central ventilatory drive.
  • Weight loss should be encouraged in patients with OHS. Diet regulation and exercise are prudent recommendations, and supervised weight loss programs should be offered to these patients. Unfortunately, many of these patients have numerous comorbidities that prevent them from performing an adequate level of exercise to facilitate significant weight loss. Bariatric surgical procedures such as gastric bypass procedures should be offered to patients who are appropriate surgical candidates and who are willing to accept the risk of the surgical procedure. OHS is associated with a higher operative mortality.3

Surgical Care

  • The numerous surgical options available today can be grouped into 2 categories based on their weight loss mechanism. Gastric restrictive procedures include vertical banded gastroplasty (VBG), adjustable gastric banding (AGB), and Roux-en-Y gastric bypass (RYGB). The procedures causing malabsorption include biliopancreatic diversion (BPD) and biliopancreatic diversion with duodenal switch (BPD-DS). All of the procedures have been successful in improving the comorbidities associated with obesity. The most commonly performed procedure is RYGB because it has the best short- and long-term results for safety, efficacy, and durability, and it has been shown to be superior to AGB. RYBG is generally performed laparoscopically. All the procedures require long-term dietary compliance and careful nutritional follow-up.17
  • The National Institutes of Health consensus statement addresses the issue of surgical treatment for obesity and obesity with associated comorbid conditions. According to these guidelines, patients with a body mass index greater than 35 kg/m2 and an obesity-related comorbid condition (including obesity hypoventilation syndrome) or patients with a body mass index greater than 40 kg/m2 are recommended for surgical treatment.
  • Some patients with thoracic deformities such as kyphoscoliosis may be candidates for corrective surgical procedures if they are acceptable candidates for thoracic surgery.
  • Diaphragm pacing in appropriate patients with primary alveolar hypoventilation may allow for a more normal lifestyle. This requires surgical placement of an electrode onto the phrenic nerve, which is connected to a subcutaneous receiver. An external battery-operated transmitter and antenna are placed on the skin over the receiver. This phrenic nerve is stimulated by the electric current thereby resulting in a diaphragmatic contraction. The transmitter settings may be adjusted for respiratory rate and to give enough tidal volume to allow for adequate oxygenation and ventilation. Unfortunately, phrenic nerve stimulation results in irreversible injury to the nerve. Thus, over time, pacing of the phrenic nerve becomes ineffective.18
  • More recently, direct pacing of the diaphragm in patients with phrenic nerve paralysis has been of interest. Studies are ongoing to determine the utility of this treatment modality.19

Consultations

  • Consider consultation with experts in certain medical specialties for assistance with evaluation and management of hypoventilation syndromes. The patient's history, physical examination findings, and available laboratory studies should guide the selection of consultation.20 Specialists who should be considered include the following:
    • Pulmonary medicine specialist
    • Neurologist
    • Physical and rehabilitation medicine specialist

Diet

Weight loss is an ideal treatment in OHS and improves the abnormal physiology and restores normal daytime gas exchange. Even a modest weight loss of 10 kg improves minute ventilation and normalizes daytime PaCO2. In concomitant obstructive sleep apnea (OSA), weight loss has been shown to decrease the number of sleep-disordered breathing events (apneas and hypopneas) and severity of hypoxemia.

Medication

Several drugs may be used to treat hypoventilation syndromes. Most produce the desired effect by stimulating the central respiratory drive, by reversing the effects of other medications that can depress central respiratory drive, and by inducing bronchial dilatation.

Bronchodilators

Act to decrease the muscle tone in both small and large airways in the lungs, thereby increasing ventilation. Include beta adrenergic, methylxanthines, and anticholinergic agonists.


Albuterol (Proventil, Ventolin)

Beta-agonist for reversal of bronchospasm.
Relaxes bronchial smooth muscle by its action on beta2-receptors, with little effect on cardiac muscle contractility.

Adult

2-4 mg/dose PO divided tid/qid; not to exceed 32 mg/d
MDI: 1-2 puffs q4-6h; not to exceed 12 puffs/d
Nebulizer: Dilute 0.5 mL (2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS; administer 2.5-5 mg q4-6h, diluted in 2-5 mL NS or water via nebulizer

Pediatric

<2 years: Not established
2-5 years: 0.1-0.2 mg/kg/dose PO divided tid; not to exceed 12 mg/d
5-12 years: 2 mg/dose PO divided tid/qid; not to exceed 24 mg/d
>12 years: Administer as in adults
MDI
<12 years: 1-2 puffs qid with tube spacer
>12 years: Administer as in adults
Nebulizer
<5 years: Dilute 0.25-0.5 mL (1.25-2.5 mg) of 0.5% inhalation solution in 1-2.5 mL of NS and administer q4-6h in equally divided doses
>5 years: Administer as in adults

Beta-adrenergic blockers antagonize effects; inhaled ipratropium may increase duration of bronchodilatation; cardiovascular effects may increase with MAOIs, inhaled anesthetics, TCAs, and sympathomimetic agents

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hyperthyroidism, diabetes mellitus, and cardiovascular disorders


Metaproterenol (Alupent, Metaprel)

Beta2-adrenergic agonist that relaxes bronchial smooth muscle with little effect on heart rate.

Adult

0.3 mL of 5% solution diluted in 2.5 mL of 0.45% or 0.9% NS, nebulized over 5-15 min q4h

Pediatric

0.1-0.2 mL of 5% solution diluted in 3 mL of 0.45% or 0.9% NS, over 5-15 min q4h

Decreases effect of beta-receptor blockers; increases toxicity of MAOIs, TCAs, and sympathomimetics

Documented hypersensitivity; arrhythmia associated with tachycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in hypertension, cardiovascular disease, congestive heart failure, hyperthyroidism, diabetes, and seizures; not recommended for breastfeeding mothers; adverse reactions include tachycardia, headache, nervousness, dizziness, tremor, gastrointestinal upset, hypertension, paradoxical bronchospasm, and cough


Ipratropium (Atrovent)

Anticholinergic bronchodilator chemically related to atropine.

Adult

MDI: 2-4 puffs q4-6h
Nebulizer: 250 mcg diluted with 2.5 mL NS q4-6h

Pediatric

MDI: 1-2 puffs tid; not to exceed 6 puffs/d
Nebulizer: 250 mcg tid

Drugs with anticholinergic properties (eg, dronabinol) may increase toxicity; albuterol may increase effects

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in narrow-angle glaucoma, prostatic hypertrophy, or bladder neck obstruction


Theophylline (Theo-Dur, Slo-bid, Theo-24, Aminophyllin, Theolair)

Potentiates exogenous catecholamines, stimulates endogenous catecholamine release, and stimulates diaphragmatic muscular relaxation, which, in turn, stimulates bronchodilation. Popularity has decreased because of narrow therapeutic range and frequent toxicity.
Therapeutic range is 10-20 mg/dL, but bronchodilation may require near-toxic (>20 mg/dL) levels. Clinical efficacy is controversial, especially in acute setting.

Adult

Initial: 10 mg/kg/d PO divided q8-12h; IV loading dose is 5.6 mg/kg (based on aminophylline) IV over 20 min, followed by maintenance infusion of 0.1-1.1 mg/kg/h
Maintenance: 10 mg/kg/d PO qd or divided bid; adjust dose in 25% increments to maintain serum theophylline level of 5-15 mcg/mL; not to exceed 800 mg/d

Pediatric

<6 weeks: Not established
6 weeks to 6 months: 0.5 mg/kg/h loading dose IV in first 12 h (based on aminophylline), followed by maintenance infusion of 12 mg/kg/d thereafter; may administer continuous infusion by dividing total daily dose by 24 h
6 months to 1 year: 0.6-0.7 mg/kg/h loading dose IV in first 12 h, followed by maintenance infusion of 15 mg/kg/d; may administer as continuous infusion, as above
>1 year: Administer as in adults

Aminoglutethimide, barbiturates, carbamazepine, ketoconazole, loop diuretics, charcoal, hydantoins, phenobarbital, phenytoin, rifampin, isoniazid, and sympathomimetics may decrease effects; effects may increase with allopurinol, beta-blockers, ciprofloxacin, corticosteroids, disulfiram, quinolones, thyroid hormones, ephedrine, carbamazepine, cimetidine, erythromycin, macrolides, propranolol, and interferons

Documented hypersensitivity; uncontrolled arrhythmias; peptic ulcers; hyperthyroidism; uncontrolled seizure disorders

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in peptic ulcer disease, hypertension, tachyarrhythmias, hyperthyroidism, and compromised cardiac function; not to inject IV solution >25 mg/min; patients diagnosed with pulmonary edema or liver dysfunction are at greater risk of toxicity because of reduced drug clearance

Opioid antagonists

Opioid abuse, toxicity, and overdose are potential etiologies of hypoventilation. Opioid antagonists can be used to reverse the effects of opiates and to improve ventilation.


Naloxone (Narcan)

Pure opioid antagonist. Prevents or reverses opioid effects (eg, hypotension, respiratory depression, sedation), possibly by displacing opiates from their receptors. Used to reverse opioid intoxication.

Adult

0.4-2 mg IV/IM/SC q2-3min prn; use increments of 0.1-0.2 mg in patients dependent on opioids; may need to repeat dose q20-60min; if no response after administering 10 mg, question diagnosis

Pediatric

0.1 mg/kg IV/IM/SC, repeat q2-3min prn

Decreases analgesic effects of narcotics

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in cardiovascular disease; may precipitate withdrawal symptoms in patients who are opioid dependent

Benzodiazepine antagonists

Used in reversing the CNS-depressant effects of benzodiazepine overdose. Ability to reverse the benzodiazepine-induced respiratory depression is less predictable.


Flumazenil (Romazicon)

Reverses effects of benzodiazepines in an overdose by selectively antagonizing GABA/benzodiazepine receptor complex. If patient who is overdosed has not responded after 5 min of administering a cumulative dose of 5 mg, cause of sedation is not likely due to benzodiazepines. Short acting, with a half-life of 0.7-1.3 h. However, because most benzodiazepines have longer half-lives, multiple doses should be administered to avoid relapse into sedative state.

Adult

0.2 mg IV over 30 seconds initially; repeat at 1-min intervals with 0.5 mg over 30 seconds until satisfactory response attained or 3 mg administered; may require additional titration to a total 5 mg

Pediatric

0.01 mg/kg IV over 15 seconds initially; repeat at 1-min intervals with 0.005-0.01 mg/kg; not to exceed 0.2 mg/dose

Caution in cases of mixed-drug overdose; toxic effects due to other drugs taken in overdose (eg, tricyclic antidepressants) may occur with reversal of benzodiazepine effects

Documented hypersensitivity; serious cyclic antidepressant overdosage; patients taking a benzodiazepine for control of potentially life-threatening condition (eg, intracranial pressure, status epilepticus)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for resedation (at least 2 h); respiratory depression, seizures, or other benzodiazepine residual effects; caution in drug or alcohol dependence, head injury, hepatic disease, and panic disorder; patients on benzodiazepines for prolonged periods may experience seizures

Carbonic anhydrase inhibitors

Inhibit the enzyme carbonic anhydrase, which, in turn, increases HCO3 excretion and causes metabolic acidosis. The metabolic acidosis subsequently stimulates ventilation.


Acetazolamide (Diamox)

Improves symptomatic periodic breathing and hypoxia.

Adult

250 mg PO qd/qid or 500 mg SR cap PO bid; 250 mg IV q8-12h

Pediatric

8-30 mg/kg/d PO or 300-900 mg/m2/d PO divided q8h; alternatively, 20-40 mg/kg/d PO divided q6h; not to exceed 1 g/d

Can decrease therapeutic levels of lithium and alter excretion of drugs (eg, amphetamines, quinidine, phenobarbital, salicylates) by alkalinizing urine

Documented hypersensitivity; hepatic disease; severe renal disease; adrenocortical insufficiency; severe pulmonary obstruction

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Patients with impaired hepatic function may go into coma; may cause substantial increase in blood glucose in some patients with diabetes

Progestins

These agents stimulate central respiratory drive and may be beneficial in patients with hypoventilation.


Medroxyprogesterone acetate (Provera)

Increases central respiratory drive and stimulates ventilation. May increase upper airway muscular tone.
For treatment of hypoventilation, higher doses than usual of medroxyprogesterone acetate required to induce significant reductions in hypercapnia.

Adult

60 mg PO divided bid/tid

Pediatric

Not recommended

May decrease effects of aminoglutethimide

Documented hypersensitivity; cerebral apoplexy, undiagnosed vaginal bleeding, thrombophlebitis, and liver dysfunction

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Caution in asthma, depression, renal or cardiac dysfunction, or thromboembolic disorders

More on Hypoventilation Syndromes

Overview: Hypoventilation Syndromes
Differential Diagnoses & Workup: Hypoventilation Syndromes
Treatment & Medication: Hypoventilation Syndromes
Follow-up: Hypoventilation Syndromes
References
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Further Reading

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Keywords

hypoventilation syndrome, primary alveolar hypoventilation, alveolar ventilation, VA, obesity hypoventilation syndrome, OHS, chronic obstructive pulmonary disease with hypercapnia, hypercapnia, chronic obstructive pulmonary disease, COPD, chronic lung disease, hypoxemia, hypoxia, respiratory system, respiratory failure, obstructive sleep apnea, sleep apnea, OSA, chest wall deformities, respiratory insufficiency, myasthenia gravis, amyotrophic lateral sclerosis, Guillain-Barre syndrome, Guillain-Barré syndrome, muscular dystrophy, kyphoscoliosis, dyspnea, central respiratory drive depression, pickwickian syndrome

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Contributor Information and Disclosures

Author

Jazeela Fayyaz, DO, Senior Fellow, Department of Pulmonology, Lenox Hill Hospital
Jazeela Fayyaz, DO is a member of the following medical societies: American College of Physicians and American Thoracic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Klaus-Dieter Lessnau, MD, FCCP, Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital
Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Society for Artificial Internal Organs, American Thoracic Society, Physicians for Social Responsibility, and Society of Critical Care Medicine
Disclosure: sepracor Ownership interest None

Medical Editor

Ryland P Byrd Jr, MD, Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University; Chief of Pulmonary Medicine, Medical Director of Respiratory Therapy, Intensive Care Unit, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, James H Quillen Veterans Affairs Medical Center
Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society, and Southern Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Om Prakash Sharma, MD, FRCP, FCCP, DTM&H, Professor, Department of Medicine, Division of Pulmonary and Critical Care Medicine, University of Southern California Keck School of Medicine
Om Prakash Sharma, MD, FRCP, FCCP, DTM&H is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Osler Society, American Thoracic Society, New York Academy of Medicine, and Royal Society of Medicine
Disclosure: Keck School of Medicine, USC None None

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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