Vosko Michels CIS Flashcards
major differences between NREM and REM sleep
REM– Even more Decreased postural muscle tone***
NREM (SWS) Increased arousal thresholds Decreased thermoregulation Decreased postural muscle tone 4 stages Synchronous EEG 75% of Total Sleep Time Prominent in early phases of sleep
REM (PS) Increased arousal thresholds Decreased thermoregulation Decreased postural muscle tone Rapid Eye Movements Vivid recall of dreams Asynchronous EEG 25% of Total Sleep Time Prominent in later phases of sleep
Benzodiazepines
suppress NREM sleep
(Valium)
*Most sedative hypnotics are benzodiazepines (GABA-ergic agonists)
Anti-depressants
suppress REM sleep
(Fluoxetine): Prozac Eyes
Withdrawal from drug causes
rebound of the sleep it normally suppresses
Process S
homeostatic control of sleep
things like adenosine build up in the brain and cause even more fatigue
Process C
circadian control of sleep
main one: cortisol (cortisol spike in the morning)
circadian misalignments occur with genetics, shift work, jet lag, etc.
Featues of sleep stages
Stage 1- transition phase. Low amplitude, high frequency. Occasional slow waves getting in.
Stage 2- K complexes- large deflections with sawtooth shape,
Sleep spindles- low amplitude blurbs
MOST of our sleep here
Stage 3- transitioning into stage 4, more delta waves
Stage 4- mostly delta waves. Number of delta waves is indicative of level of sleep deprivation.
Polysomnography
EOG- oculograms.
chest and abdomen movement tell you how much effort is going into the breathing
chin muscle tone is cyclic in stage 1, drops dramatically to stage 3 and 4.
when are you better at regulating your autonomics?
NREM, as opposed to REM sleep
eye movments characteristic of REM movements? Other clues?
opposing wave directions between R and L eye
going with no muscle tone in the chin, definitely tells you REM.
EEG waves should look a lot like being awake.
Heart rate can be increasing.
With obstructive sleep apnea, which phase of sleep is most disrupted? Why?
REM
autonomics aren’t as well controlled, postural muscles lose tone but are also serving as respiratory muscles in sleep apnea
If there is respiratory distress of any origin, it will likely first show up
during sleep. REM is the most sensitive period in sleep to show any respiratory dysfunction.
56 y/o Male Extreme Daytime Fatigue Awakens every 10 minutes during sleep Takes triazolam (Halcion) before bed Slurred Speech
Start with what?
Start with Epworth sleep scale.
clue that you can rule out insomnia is the sleeping pill doesn’t help. To surely rule it out you need a sleep lab study.
parasomnia- usually you think you’re sleeping, other people complain of your behaviors
sleep disordered breathing- need a sleep lab. Epidemiology can help- obesity, bed partner complaining of snoring
Both wake and sleep are coordinated by
specific brainstem and hypothalamic nuclei
Brainstem nuclei promote excitatory tonic input to motor neurons during wakefulness. Provides “muscle tone”
Definition and Epidemiology of OSA
Definition
Usually defined as 15 or more apneic events per hour of sleep lasted a duration of 10 s or more
Obstruction occurs despite central drive to breathe and inspiratory muscle activity
Predisposing factors Increased BMI Increased age Higher prevalence in men than women Higher prevalence in 3- to 5-year old children
OSA- Predisposing factors during sleep
Intermittent periods of upper airway occlusion that occur upon inspiration
Predisposing factors during sleep
Altered sleep position
Decreased tone of pharyngeal muscles
Depression of respiratory drive during NREM sleep
Depression of respiratory protective reflexes during NREM sleep
Complications of OSA
polycythemia
right-sided heart failure
increased risk of aortic dissection
increased risk for pulmonary hypertension
Causes of OSA
obesity (adipose tissue deposition can decrease the tone of pharyngeal muscles)
excessive compliance of the hypopharynx
upper airway edema
structural abnormalities of the upper airway
Symptoms and Signs of OSA
Symptoms: Snoring Hypersomnolence Changes in personality Headaches upon waking Nocturia
Signs: Systemic hypertension Polycythemia Right axis deviation on ECG Signs of cor pulmonale Bradycardia during the apneic event followed by tachycardia
Signs and Symptoms Hypersomnolence Nocturia Snoring and witness to apneic events Increased BMI Headaches upon waking Systemic hypertension
Diagnosis of OSA- Polysomnography
Gold standard
Overnight study
Three groups of physiologic signals are monitored
Sleep (EEG, electrooculogram, submental electromycogram)
Cardiac arrhythmia monitoring (ECG)
Respiration (airflow, thoracoabdominal effort and oximetry)
For a quiet respiration cycle, describe normal alveolar and intrapleural pressures.
end expiration: intrapleural pressure: -5
during inspiration- intrapleural pressure -30
What are examples of flow-limitation through tubes?
Flow-limitation through tubes:
- Pulmonary blood flow through zones of the lung.
- Airway obstruction during forced exhalation.
- Cardiac function.
How do blood gas levels change during an apneic event?
Which sequence of events occur to trigger arousal from sleep and breathing?
CO2 goes up and O2 goes down
chemoreceptors (via Vagus nerve) send info to brainstem –> surge in sympathetic activity
People die from apnea due to the huge surge in blood pressure and heart rate (apnea causes heart attacks through this pathway!)
How will repeated apneic events affect the acid-base status?
respiratory acidosis
could lead to metabolic alkalosis from renal compensation (holding onto bicarb). During the day the CO2 levels go back to normal but the renal compensation remains
Morning headache
Individuals with OSA will often wake with headaches in the morning. Changes in CO2 have an impact in cerebral blood flow
Pulmonary Hypertension and OSA
reduction in O2 –> vasoconstriction (hypoxic vasoconstriction) in regions of the lung to regions that are better ventilated
repeated incidents –> chronic pulmonary hypertension/ vascular remodeling
erythropietin is released from the kidney
Pulmonary hypertension and increased hematocrit increase the afterload of the right ventricle. Hypertrophy of the right ventricle is possible with the final stage of cor pulmonale.
An increase in right ventricular end-diastolic pressure can lead to increased atrial volume, which increases secretion of atrial natriuretic peptide. ANP results in sodium secretion. Increased atrial volume can also suppress ADH (increase in urine volume).
Systemic Hypertension
Acute
During hypoxic periods, stimulation of the chemoreflex increases sympathetic stimulation.
Individuals with OSA have a heightened chemoreflex response to hypoxemic stimulation.
In OSA, apneic periods are associated with acute peripheral vasoconstriction and an increase in arterial blood pressure.
Chronic
OSA is further associated with systemic hypertension. Increased sympathetic tone and systemic blood pressure during acute episodes may trigger vascular remodeling and changes in endothelial function.
Treatment of OSA
Oral appliances
Surgery
Lifestyle changes
Continuous positive airway pressure (CPAP)- holds the airways open during sleep.
