Introduction to Obstructive Sleep Apnea

Table of Contents:

Introduction to Obstructive Sleep Apnea
Symptoms
Cardiovascular Consequences
Pathophysiology
Polysomnography
Behavioral Consequences
Medical Management
Surgical Management





Introduction To Obstructive Sleep Apnea



Obstructive Sleep Apnea is characterized by repetitive episodes of upper airway obstruction that occur during sleep, usually associated with a reduction in blood oxygen saturation.




Symptoms



Patients of OSA may endure the following:

    Excess Sleepiness
    Snoring
    Apneic Episodes
    Choking or gasping in sleep
    Nocturia
    Tiredness upon Awakening



Features that OSA may cause, include:

    Motor Vehicle Crashes
    Work Related Accidents
    Impaired school or work performance
    Social Embarrassment
    Marital problems
    Memory or concentration difficulties
    Depression
    Impaired quality of life



Children may suffer the following:

    Hyperactivity or excessive sleepiness
    Noisy breathing during sleep
    Irregular body positions in sleep
    Rib cage retractions
    Flaring of ribs



The prevalence of habitual snoring in children ranges from 3.2% to 12.1%. All children should be screened for snoring. The prevalence of OSAS ranges from 0.7% to 10.3%.

Children with sleep disorders breathing are at increased risk of hyperactivity and learning problems. The combined odds ratio of neurobehavioral abnormalities in snoring children is 2.93%. Decreased somatic growth can occur in children with OSAS. Right ventricular dysfunction and systemic hypertension have been reported in children with OSAS.

Adenotonsillectomy is the first-line treatment for children with OSAS.
Adenotonsillectomy is usually curative.

Careful postoperative monitoring because of the high risk of respiratory complications. Children with persistent snoring (and perhaps with severely abnormal preoperative PSG results) should have PSG repeated postoperatively.

  Sleep Apnea Controls p Value
  29 35  
Accident Rate 0.41 0.06 <0.01

Accident - At
fault rate.

 0.24 0.03 <0.01
At least 1 accident. 31% 6% <0.01
Citation Rate 0.86 0.34 <0.05


Driving and Sleep Apnea


In Spain, a study of professional drivers showed that 25.2% had an AHI of >5 , and 8.6% had symptomatic sleep apnea.

In Poland, 31.2% of 503 drivers admitted to fall asleep at least once while driving.

In Switzerland, the accident rate was 13.0/million km traveled in patients with moderate to severe OSA cf. 0.78 in a control group.

In Japan, 8.9% of patients with OSAS had 1 or more MVA's in 5 years.

In Canada, in severe OSAS, the rate of MVA's per year was 0.11 cf. 0.08 in controls and in OSAS the citation was double.

Predisposing Factors


    Age (40-60 years)
    Obesity
    Gender (male:female - 2:1)
    Anatomical abnormalities
      Upper airway obstruction
      Craniofacial abnormalities
    Medications
    Alcohol
    Smoking
    Family History


Examination Findings


    Short, fat neck
    Obesity
    Upper airway narrowing:
      Large tonsils/adenoids
      Enlarged Uvula
      Long, soft palate
    Micrognathia/retrognathia

 



Sleep Apnea and Insulin Resistance


OSA patients have higher levels of fasting insulin.

The fasting insulin levels correlate with sleep variables such as RDI and lowest oxygen saturation. AHI is associated with insulin medicated glucose uptake.

OSA subjects are insulin resistant.

Plasma Leptin is increased in OSA.

Insulin resistant cytokines tumor necrosis factor-alpha and interleukin-6 are increased in OSA.

Associated Disorders


Disorders affiliated with OSA are:
    Hypothyroidism
    Acromegaly
    Marfan's Syndrome
    Amyloidosis
    Shy Drager Disorder
    Myotonic Dystrophy

 



Physiological Consequences of Sleep Apnea


Asphyxia - hypoxemia, hypercapnia, acidosis:
    Cardiac dysrhythmias
    Hypertension - systemic, pulmonary artery
    Hypotension - in older patients
Sleep Fragmentation:
    Excessive daytime sleepiness

 


Hemodynamic Consequences


    Blood Pressure: Cyclical variations in systemic and pulmonary hypertension.
    Cardiac Output: Cyclical reductions due to bradycardia and negative inthrathordic pressure.
    Cor Pulmonale: Can occur in presence of hypoxemia during wakefulness.




Cardiovascular Consequences


    Systemic hypertension
    Pumonary hypertension
    Cor pulmonale
    Brady-tachycardia
    Sinus Arrest
    Complete heart block
    Atrial and ventricular arrhythmias
    Mydocardial infarction
    Sudden Death

 


Systemic Hypertension


33% of OSA patients have systemic hypertension.
33% of Hypertensive patients have OSA.

Variable
Adjusted for Demographics Odd Ratio
BMI, Alcohol, smoking Odds Ratio
Apnea-Hyponea Index
>+30
2.27 (1.76-2.92)
1.37 (1.03-1.83)
% Time below 90% Sat
2.03 (1.62-2.53)
1.45 (1.12-1.88)


A study of 6132 patients over 40 years of age were assessed by portable PSG and associations with blood pressure and hypertension were examined while controlling for demographic variables including body weight. The findings indicated an association between sleep-disordered breathing and hypertension.

   Untreated Hypertensives  Treated Hypertensives  Normotensive
Number  34  34  25
Age (SEM)  58.0 (2.1)  60.9 (2.0)  54.6 (2.6)
Lowest SaO2  86.0 (1.4)  87.3 (1.2)  90.7 (0.5)
       
AHI (mean) (SEM)  8.3 (2.5)  9.0 (2.3)  1.2 (0.3)
       
AHI >5 (%)  13 (38)  12 (38) 1 (4)
AHI >10 (%)  8 (23)  8 (23)  0
AHI >15 (%)  5 (15) 8 (23)  0



Pulmonary Hypertension


17% of OSA patients have pulmonary hypertension.

Pulmonary hypertension is more likely to occur in sleep apnea patients who have daytime oxygen desaturation.



17% of patients with OSAS have Pulmonary Hypertension

Variable

n
Age
BMI kg/m²
FEV1
PaO2
PAP rest, mmHg
AHI
Mean SaO2

Group 1

37
52
34
1,830
64.4
26.0
100
88.5

 Group 2

183
53
31
2,890
74.7
13.7
73
94.2

p Value


NS
<.001
<.001
<.001
<.001
<.001
<.001


Group 1 = Pulmonary Hypertension (PAP 20 or greater)
Group 2 = PAP less than 20 mmHg


Cardiac Arrhythmias


Bradyarrhythmias:
    Bradycardia
    Bradytachycardia
    Sinus arrest
    Heart block - Mobitz type 1
      Secondary heart block


Tackyarrhythmias:

    Ventricular ectopy
    Supraventricular tachycardia
    Ventricular tachycardia


 

Cerebral Blood Flow


Single photon emission computer tomography (SPECT) studies have shown that patients with severe sleep apnea syndrome have reduced cerebral blood flow while awake.
Systolic (VC) and mean (VM) cerebral blood flow velocities are significantly lower in patients with SAS than in control subjects.
Dramatic increases in Cerebral blood flow can be observed during apnoeic episodes, with maximum increases during REM sleep.
CO2 reactivity and changes in CBFV related apnea duration were markedly increased during sleep compared with the waking state of SAS patients.


Pathophsyiology




Polysomnography




Behavioral Treatment


1. Attain an ideal body weight
2. Sleep on the side
3. Avoid sedative medications before sleep
4. Avoid being sleep deprived
5. Avoid alcohol before sleep
6. Elevate the head of bed
7.Promptly treat colds and allergies
8. Avoid large meals before bedtime
9. Stop smoking




Medical Management


1. Weight Loss
2. Pharmacological
3. Oxygen Therapy
4. Nasopharyngeal intubation
5. Nasal CPAP
6. BiLevel CPAP
7. Oral Appliances
8. Atrial Pacing





Surgical Management