Module 1 - Respiratory & Cardiovascular Control During Sleep Flashcards
Where is the velopharyngeal segment of the upper airway?
Behind the soft palette
Where is the oropharyngeal segment of the upper airway?
Behind the tongue
Where is the hypopharyngeal segment of the upper airway?
Above the larynx
What segments of the upper airway form a hollow muscular tube?
oropharyngeal and velopharyngeal
How does the hollow part of the upper airway stay open?
No bony or cartilaginous support on anterior wall so requires upper airway muscle activity
When and how are the upper airway muscles activated?
During inspiration, rhythmically
What is the main difference between the upper airway regions; nasal passage, larynx, nasopharynx?
The former have cartilaginous support to help tone, the nasopharynx has no bony support on anterior edge so needs muscle tone
What types of forces promote upper airway latency?
Collapsing and dilating forces
What is the collapsing force in the upper airway?
Negative airway pressure generated by the inspiratory activity of the diaphragm
What is the dilating force in the upper airway?
Upper airway dilator muscle activity
How does collapse occur in the upper airway, with reference to the collapsing and dilating forces?
When the force produced by dilating muscles is exceeded by the negative airway pressure (collapsing force), for a given cross-sectional area
Describe how airflows into airway in terms of the negative pressure gradient
- Breathe in, diaphragm contracts
- This decreases pressure in the plural space, causing a negative pressure gradient
- Air then flows from airway into lungs
What factors promote pharyngeal airway obstruction?
- Anatomical narrowing of the pharyngeal airway
- Excessive lose of pharyngeal airway muscle tone
- Defective upper airway protective reflexes
- Increased loop gain promotes unstable airway (brain ventilatory responses)
- Frequent arousals destabilise airway
What is the shape of the pharyngeal region in OSA compared to controls?
OSA is round
Control very small but lateral shape
In which regions can airway obstruction happen?
Always between choanae (back nose) and epiglottis (upper laryngeal cartilage)
Usually behind uvula and soft palate (nasopharynx) or behind the tongue (oropharynx)
Collapse at the level of epiglottis is unusual, but multi-level collapse is usual.
What 6 factors promote OSA?
- Sex (men have higher pharyngeal resistance, narrow pharynx and maybe hormonal factor or longer airway)
- Age (pharyngeal resistance increases with age due to decreasing elasticity)
- Obesity (fat deposition in pharyngeal walls, neck or abdomen and/or increased mass, decreases lunch volume so more prone to collapse)
- Genetics (polygenic, mb obesity too)
- Ethanol
- Cranio-Facial Anatomy
What does higher pharyngeal resistance mean for the airway?
Narrower pharynx
Why do males have higher OSA risk?
Higher pharyngeal resistance
Possible hormonal factor or longer airway
How is does ethanol related to OSA?
Secondary cause
Increases frequency and duration of apnoeas
Reduces upper airway muscle tone
What are 2 types of crania-facial anatomy that are related to OSA?
Retrognathia (small mandible = smaller space for muscles)
Enlarged tonsils (so big they fall back and cause obstruction)
How does a smaller airway lead to more obstruction?
- Smaller airway = increased upper airway resistance (Resistance ~ length/radius^4)
More negative pharyngeal pressure during inspiration (Bernoulli principle)
->
Increased transmural collapsing pressure
->
Pharyngeal airway occlusion during slee0
What is Poiseuille’s law?
R ~ l/r^4
Resistance is proportional to length of tube divided by radius ^4
Longer and smaller the tube, the increased resistance
Is the length or radius of the airway tube the stronger in determining resistance?
Radius
What happens to velocity when a tube narrows (but is equal at either end)?
Velocity increases to conserve mass (flow)
When velocity increases in a tube that narrows, what occurs to pressure in that space?
Need more negative pressure so collapsing pressures increase
Driving force for increased velocity is negative airway pressure gradient
When narrowing occurs in the nasal passage, what force does it have a significant impact on?
Collapsing force increases
How do you measure breathing?
Spirometer
What is Tidal Volume?
The amount of air that moves in or out of lungs in each respiratory cycle
What is the Vital Capacity?
Breathe in all the way and all the way out
What is the total lung capacity made up of?
Vital capacity + residual volume
What is residual volume?
The air you can’t breathe out
What is IRV & ERV?
Inspiratory and expiratory reserve volume
Difference between tidal volume and vital capacity
What is the relationship between PaO2 and SaO2?
Curved
Can drop PaO2 to 60 and it will stay relatively stable, Sa will drop below PaO2<60
What is the relationship between PaO2 and ventilation?
PaO2 increases with increased ventilation
What is the relationship between PaCO2 and ventilation?
PaCO2 decreases with increasing ventilation
What is the normal alveolar ventilation that keeps PaCO2 at 40mmHg?
5-6L
What is the relationship between pH and ventilation?
Increasing pH increases ventilation
How many L/min is normal ventilation?
6-7L but at alveoli it’s 5L/min
Describe the key features of arousal responses in sleep
State-specific (wake vs non rem vs rem)
Plastic
Stimulus specific
What is the main difference between wake and sleep in terms of drive to breathe
During wakefulness, behavioural activities provide input drive to central oscillator which overrides automatic brainstem oscillator.
So, rhythm of breathing generated in the brainstem but wakeful neural activity provides significant drive to breathe.
What is the normal rate, tidal volume and minute ventilation for an adult?
14/min
350mL
7L/min
What are the normal resting PaCO2 and PaO2 levels?
PaCO2 = 40mmHg
PaO2 = 95-100mmHg
What is the true baseline of breathing?
Non-REM sleep, but we measure at rest in research
What are the features of breathing in NonREM sleep?
Clockwork, due to brainstem oscillator
Steady rate and tidal volumes
PaCO2 = 40mmHg
Has apnea threshold (breathing stops if CO2 is reduced)
What is an apnea threshold?
Breathing stops if CO2 reduces
What are the features of arousal responses in Non-REM sleep?
Strong, clear and stimulus-specific
Why does breathing stop when CO2 is reduced in non-REM sleep?
Has an apneic threshold, which triggers abnormal breathing events as you’re dependent on the central oscillator in nonREM sleep, which is sensitive to CO2
What are the features of breathing in REM sleep?
Breathing is co-opted by brain activity, so changes with dream content
Variable rate and tidal volumes (similar to when talking) with short central apneas
Reduced ventilatory responses
No clear apnea threshold
Why are ventilatory responses apparently reduced in REM sleep?
Through enabling the behavioural drive to control breathing, similar to when awake which switches off the brainstem oscillator
What is the difference with PaCO2 levels in Non-REM and REM sleep?
NonREM - 40
REM - 40 or lower
What are the features of arousal thresholds in REM sleep?
Variable and stimulus specific
e.g. some reflexes are lower and some are higher
What is the difference between arousal thresholds in non-REM and REM sleep?
nonREM: clear, strong and stimulus specific
REM: variable and stimulus specific
What are the main changes to breathing between sleep/wake states?
Wake to nonREM: gain switching with arousals decreases ventilatory response, and periodic breathing
nonREM to REM: major muscle tone changes, lose inhibition of postural muscles, breathing pattern changes from regular to irregular and central apneic events
What happens to the mechanics of breathing when transitioning from wake to nonREM sleep?
- Reduced upper airway dilator muscle tone (which increases resistance from 2cm to 5-10cm)
- pre-snore breathing noise, sound of narrowing
- balanced activity of breathing muscles
What happens to the mechanics of breathing when transitioning from nonREM to REM sleep?
- active inhibition on postural muscles
- further reduction of upper airway tone
- loss of intercostal and abdominal muscle activity
- dependence on diaphragm (fully brainstem controlled)
- unbalanced activity of breathing muscles
Why does REM sleep show even mild OSA?
Loss of all muscles with the exception of the diaphragm
Why do newborns exhibit very shallow, quick breaths in REM?
Loss of intercostal and abdominal muscle activity decreases lung volume dramatically so they breathe faster to increase ventilation
What happens to the central chemoreceptors in hypocapnia in each sleep stage?
All, increase PaCO2 increases ventilation
Reduced response in non-REM and even more in REM
What happens to the central chemoreceptors in hypoxia in each sleep stage?
All, decrease SaO2, increase ventilation
Reduced response in non-REM and even more in REM. Much higher arousal threshold in REM (lower SaO2)
What is the difference in arousal thresholds for hypercapnia and hypoxia in nonREM and REM sleep?
Higher arousal thresholds from REM sleep.
More hypercapnia (higher PaCO2) and hypoxia (lower SaO2)
What happens in the diseased lung in the transition to sleep that differs from a healthy lung?
A more severe drop in saturation with the same drop in PaO2.
Which response curve is easier to look at with SaO2 than PaO2?
Ventilatory response to hypoxia
What region of the brain responds with increased sensitivity when CO2 increases slightly?
carotid body
To increase arousal response
When does the diaphragm contract?
Inspiration, increasing intrathoracic volume
List what FRC, TLC, RV, VC and Vt are
- Functional Residual Capacity (FRC) is the resting lung volume.
- Total Lung Capacity (TLC) is maximal volume, and Residual Volume (RV) is remaining volume.
- Vital Capacity (VC) is max air expelled after full inflation.
- Tidal Volume (Vt) is volume in each quiet breathing cycle.
Describe how air flows into the lungs in terms of pressure gradients
Inspiration involves diaphragm and intercostal muscle contraction, leading to a negative pressure gradient.
Is expiration passive or active?
Expiration is passive during rest but active during exercise.
How does body position impact Functional Residual Capacity (FRC) and TLC?
Supine position reduces FRC and TLC due to increased intrathoracic blood volume or abdominal pressure.
How does sleep impact Functional Residual Capacity (FRC)?
- FRC decreases during sleep, impacting lung volumes and minute ventilation.
How does sleep impact tidal volume?
- Reduction in tidal volume during NREM and REM sleep compared to wakefulness.
How is glottal closure related to apneas in infants and why is it relevant to infants?
- Glottal closure is observed during central apneas, contributing to inspiratory breath-holding.
- The physiological relevance includes maintaining high lung volume, positive sub-glottal pressure, and minimizing aspiration of secretions.
How are Laryngeal Chemoreflexes related to apneas in infants?
Laryngeal chemoreflexes are triggered by contact with liquids on laryngeal mucosa, eliciting protective reflexes like swallowing and coughing.
The apnea component of laryngeal chemoreflexes can be influenced by central respiratory drive and various drugs.
What are the three swallowing phases in infants?
Three phases: sucking, pharyngeal, and esophageal.
When does the coordination of swallowing develop in infants?
Coordination matures between 32-36 weeks postconceptional age.
What influences the frequency of Non-Nutritive Swallowing?
- States of alertness: Highest in REM sleep.
- Gestational age: Higher frequency in preterm newborns.
- Neonatal conditions impacting NNS activity may affect swallowing maturation
What influences the coordination of non-nutritive sucking with the breathing cycle?
- States of alertness: i-type most frequent, e-type least frequent.
- Age: Similar NNS distribution in preterm and full-term newborns.
What coordinates breathing and sucking functions in infants?
Competing functions, coordinated by central pattern generators.
What type of apneas are associated with non-nutritive sucking?
Majority of apneas associated with NNS are obstructive or mixed.
What may contribute to respiratory issues in infants?
Immaturity of reflexes like laryngeal chemoreflexes and NNS
How do you measure the performance of the gas exchange from the respiratory system?
Directly measure arterial blood gasses
What levels for PaO2, PaCO2, pH, BE and HCO3- would you expect from arterial blood gasses in a healthy respiratory system?
- PaO2 80-100mmHg
- PaCO2 35-43
- ph 7.38-4.2
- BE 0+- 2
- HCO3- 24+-2 mmol
What is a bodily system with no feedback called?
Open loop control
What happens in an open loop control system when a disturbance occurs?
No output/behavioural modification can occur so the system doesn’t work properly.
How does a closed loop control system work?
Feedback is provided from the output/behaviour to modify the controller which will subsequently modify the output
Explain how the control of breathing is a closed loop system (controllers, system, behaviour)
Chemical, Behavioural and Mechanical inputs to the respiratory centre in the brainstem which control the respiratory muscles. The muscles then feed back to the c, b, and m inputs to modify output.
Where is the respiratory control centre and what does it control?
Group of cells within the brainstem that provide output to respiratory muscles to move the chest wall and allow ventilation to occur
Within the respiratory centre, there are respiratory neurons. There are 3 types of these, what are they called and where are they found?
Pontine Respiratory Group (PRG) in the pons
Ventral and Dorsal Respiratory Group (VRG AND DRG) in the medulla
What do the respiratory neurons control?
PRG, VRG and DRG have a complex interaction with respiratory muscles to control the phase and timing of respiration
If you sever the spinal cord, what happens to the respiratory output?
The lower (more distal) the severing, the greater the effect on respiratory output. Below the VRG, all respiration ceases.
There are two main motor outputs from the respiratory control centre. What are their called and what do they control?
Pump muscles
- Cranial nerves to the upper airway (larynx, pharynx)
- Spinal tracts to thoracic pump muscles (Output of C3,C4,C5 to phrenic nerve to stimulate diaphragm and intercostals)
Bronchial airway muscles
What are the three inputs to the respiratory centre?
Chemical (chemoreceptors)
Behavioural (sleep/wake/activity)
Mechanical (breathing receptors)
What is the name of chemoreceptors that are located in the carotid body?
Peripheral
What is the name of chemoreceptors that are located in the medulla?
Central
Where are the central and peripheral chemoreceptors located and what do they respond to?
Peripheral: Carotid, SaO2 and PaCO2
Central: medulla: CO2
How does the peripheral chemoreceptors respond to decreasing SaO2?
Linearly increase output (rapidly) to increase ventilation (PaO2 is a curve)
How does the peripheral chemoreceptors respond when there is high oxygen saturation?
Still low level of activity
How does PaCO2 influence the activity of the peripheral chemoreceptors when oxygen decreases?
Increase in ventilation with decreasing SaO2, but this is less pronounced when paCO2 is lower.
How does the central chemoreceptors respond to increasing pCO2?
Increased response to increase ventilation with increasing PaCO2
How do central chemoreceptors differ from person to person?
The level of ventilation response changes between people (some have a stronger slope)
Chronic environmental changes or disease processes can also differ
What can influence the body’s response to increasing PaCO2?
Sleep
Chronic environmental changes
Disease processes
What happens when there is damage to any chemoreceptors?
Alter ventilatory responses to hypoxia, hypercapnia or acidodis.
Theses changes may only be seen in sleep
What occurs to an individual’s resting arterial blood gasses if they experience sustained hypoxia or hypercapnia?
Altered respiratory control through chemoreceptor mechanism
Can even occur in just episodic hypoxia/hypercapnia
What are examples of behavioural inputs to the respiratory centre?
Non-Respiratory functions: laughing, crying, singing. Can override metabolic and homeostatic function
Wakefulness/Sleep State
How does each wake/sleep state influence respiration?
Sleep onset has unsteady respiration as they cycle between Stage I and II and wake..
Stage II and SWS has steady respiration
REM has erratic and shallow, highly variable breathing
How does REM sleep impact breathing?
Only controlled by the diaphragm
Variable respiratory state. Erratic and shallow breathing.
Irregularities in both amplitude and frequency synchronous to REM bursts (probably of central origin)
How is hypoxemia different in REM vs nonREM sleep?
Hypoxaemia in REM is equal to (or greater than) that seen in NREM results mainly from hypoventilation.
When transitioning to sleep and then deeper stages of sleep, how does ventilation change?
Relative hypoventilation
A reduction in ventilation characterised by a rise in CO2 and fall of O2 levels
How does chemoreceptor responsiveness change during sleep?
Reduced sensitivity to hypocapnia in NREM and even more in REM
Lower responsiveness to increase ventilation with increasing PaCO2 in nonREM and more in REM
What sources of information does the mechanical inputs send to the respiratory centre?
State of inflation/deflation lung tissue, expansion of muscle wall, airflow and mechanics of upper airway
What information do the Upper airway receptors send to the respiratory centre to control breathing? (mechanical input)
- information on flow of air through larynx, pharynx, nasopharynx → influences phase and timing of respiration
- information of threatening or noxious stimuli from within upper airway such as foreign bodies → triggers reflex to protect airway (coughing sneezing, gagging). complex reflex
What information do the lung receptors send to the respiratory centre to control breathing? (mechanical input)
- Provide information on the state of inflation or deflation of chest and lung → influence timing and phase of respiration
- And irritation → trigger a cough
What information do the chest wall receptors send to the respiratory centre to control breathing? (mechanical input)
in intercostal, joints of chest → influence timing and phase of respiration
What are the three key components that contribute to sleep disordered breathing?
- increased upper airway resistance
- hypoventilation
- control of breathing
all are influenced in a complex way by sleep
also, obesity, extraneous factors (alcohol, neuromuscular disease)
What is the best way to prevent the airway from closure?
Arousal
How does obesity lead to sleep disordered breathing?
- extra weight on diaphragm
- extra mass load on respiratory muscles
- hypoventilation can become more pronounced as well
How does alcohol contribute to sleep disordered breathing?
muscle relaxant and diminishes arousability
What are normal changes that occur in sleep that contribute to sleep disordered breathing?
- decrease in upper airway muscle tone/increased work of breathing and upper airway resistance
- change in chemoreceptor sensitivity
- changes in respiratory drive
- alteration in lung volumes
- change in metabolic rate
How does CPAP support sleep disordered breathing?
Adding positive pressure to overcome the suction forces that cause the upper airway to close.
-> Mechanical input
For some this isn’t sufficient
What muscles work to maintain the upper airway to be open?
Upper airway dilator muscles (accessory respiratory muscles) to make the airway more rigid.
What’s the problem associated with the difference in timing between the drive of the upper airway dilator muscles and inspiratory pump muscles?
if inspiration is initiated before the activation of dilator muscles, the upper airway is at risk of closure by the suction
What is the relationship between upper airway flow, resistive loading and ventilation?
Increased airway flow increases resistance (result of narrowing airway) reductes ventilation
What happens if someone has naturally lower ventilatory responses?
Predisposed to sleep apnea
What is the Pre-Bötzinger Complex and how is it related to breathing?
A region with neurons that contribute to respiratory rate and rhythm have pacemaker-like properties.
Their expiratory neurons inhibit inspiratory pre-motoneurons during expiration.
What happens if there’s a loss of pre-Botzinger complex neurons?
Loss of pre-Bötzinger complex neurons may lead to abnormal breathing and central apneas, relevant in aging and neurodegenerative diseases.
Does the brainstem reticular neurone provide tonic or phasic input to the respiratory system in sleep?
Tonic drive
How is the input to the pharyngeal muscles different in wake and sleep?
Tonic drive is prominent in wakefulness but withdrawn in sleep, contributing to vulnerability in airway collapse during sleep.
How are the hypoglossal motoneurons stimulated differently in inhalation and exhalation?
Not actively inhibited in expiration.
Which chemical systems contribute to wakefulness?
- Cholinergic and aminergic systems
Which chemical systems contribute to sleep?
GABA-containing neurons from ventrolateral preoptic (VLPO) inhibit the ascending arousal system, promoting sleep.
How do the neurons from the VLPO actively generate sleep?
Become active in non-REM sleep, influenced by the thermal stimulus from the CR-mediated decline in body temperature at bedtime.
This decline in body temperature is also mediated by a change in the set point of hypothalamic temperature-regulating neurons leading to a “warm stimulus” because body temperature is at first higher than the new set point
The warm stimulus actives NREM sleep-active hypothalamic neurons and so promotes sleep onset
Also suppresses cortical arousal and inhibits brainstem arousal neurons via GABA
What neural influences promote REM sleep?
Decreased serotonergic and noradrenergic activity facilitates acetylcholine release into pontine reticular formation
motor suppression involves descending pathways from pontine neurons inhibiting spinal motoneurons via glycine release.
Glutamatergic-GABAergic mechanism in REM sleep induction involves suppression of spinal motoneuron activity.
How do the inputs that modify breathing change between sleep and wakefulness?
- Most inputs modifying breathing are absent or downregulated during sleep.
- Chemical control, particularly CO2 levels, becomes the dominant driver of breathing during sleep.
How does chemoreceptor sensitivity change in stable sleep?
Chemoreceptor sensitivity is reduced during N2 and slow-wave sleep (N3), with CO2 being the main regulator of breathing.
What happens to minute ventilation and PaCO2 at sleep onset?
There is a rapid reduction in minute ventilation (from 7 to 5 L/min). There is delay between the reduction in ventilation and changes in Paco2.
As PaCO2 rises, upper airway muscles may be recruited and minute ventilation may increase somewhat
What does the ventilatory response to after an arousal?
Ventilatory response to arousal reinstates wakefulness chemical control of breathing, resolving sleep-related upper airway resistance as CO2 levels tolerated during sleep become excessive.
Arousal from sleep is associated with a rapid increase in breathing.
What is an apnea threshold?
When PaCO2 falls, breathing ceases. It is dependent on peripheral chemoreceptors.
What is the CO2 reserve?
The difference between wakefulness PaCO2 and apnea threshold
What is loop gain?
Quantifies overall sensitivity of ventilatory control system during sleep.
Includes plant gain (efficiency of breathing to remove CO2), mixing and circulation delays, and controller gain (chemoreceptor sensitivity).
How is progesterone related to sleep disordered breathing?
Is a respiratory stimulant, so SDB is more common postmenopausal women.
Is steady state loop gain different between men and women?
No
How does respiration in sleep differ between the sexes?
in breathing during sleep onset, ventilatory response to arousal, and apnea threshold.
When is respiratory activity first detected in utero?
11 weeks
When is sleep activity first detected in utero?
25 weeks
When does the wake and sleep circadian rhythm develop?
Wake: By 45 days old
Sleep: 4-8 weeks is evident
How do arousal responses change in childhood?
Change with age, influenced by a range of factors.
Is a protective mechanism
When are breathing movements first observed in utero?
10 weeks gestation
What are metal breathing movements generated by in the brain?
neural-based respiratory rhythm generator.
How does respiratory rate change with age?
Decrease with increasing age
What apnea events are more common in healthy infants?
Central
Frequency and duration decrease with age
What is periodic breathing?
Pauses in breathing
Common in healthy infants, even with oxygen desaturation
Are respiratory events common in children?
Yes, but less common after 1
Why are vascular responses to sleep important?
major long term outcomes of SDB are vascular
How do we assess vascular responses in sleep?
heart rate and blood pressure, but they are inadequate.
Want to measure tissue perfusion is critical but invisible
Describe the hemodynamic response to an apnea
blood pressure + flow drops followed by marked increase
blood flow to regional areas almost completely stops during apnea
What happens to nervous system response in the first sleep cycle of the night?
Relative autonomic stability due to vagus nerve dominance and heightened baroreceptor gain
What changes happen to heart beats during NREM sleep?
Sinus variability/arrhythmia during NREM sleep = good heart health
What is an indicator of poor cardiac health during non-REM sleep?
Absence of intrinsic variability is associated with cardiac pathology and aging
What happens to reflex adaptions during sleep that influence respiratory rate?
Reduced arterial blood pressure increases respiratory rates
How does the cardiovascular system compensate for breathing pauses?
Increased respiratory rate to normalise arterial blood pressure
What are some clinical features in children associated with breathing and heart rate variation?
- SIDS = reduced breathing variation and absence of normal breathing pauses
- Congenital central hypoventilation syndrome = reduced heart rate variability
- OSA = exaggerated heart rate variation and enhanced bradycardia/tachycardia during apnea
What clinical features do people with heart failure have in terms of their respiratory function?
diminished respiratory function-related heart rate variation.
How does the sympathetic nerve activity respond to being in NREM sleep?
Relatively stable (+ autonomic stable too)
What happens to vagus nerve activity its between NREM-REM sleep transitions?
Vagus nerve activity bursts
Possibility of pauses in heart rhythm and frank asystole during transitions.
How does being in REM sleep change cardiorespiratory functions?
REM sleep disrupts cardiorespiratory homeostasis due to brain neurochemical functions and behavioral adaptations.
What are the features of cardiorespiratory functions in REM sleep?
- Increased excitability leads to surges of cardiac sympathetic nerve activity.
- Reduced baroreceptor gain during REM sleep.
- Heart rate fluctuations with marked tachycardia and bradycardia episodes.
- Suppressed cardiac efferent vagus nerve tone during REM sleep.
- Irregular breathing patterns during REM sleep can lead to lower oxygen levels, especially in pulmonary or cardiac disease patients.
Which brain regions are associated with cardiorespiratory response, particularly in sleep?
Pontine and medullary raphe nuclei, as well as rostral ventrolateral medulla (RVLM)
Which brain regions are damaged in OSA leading to increased sympathetic nerve activity?
multiple brain structures, especially raphe and RVLM, are damaged
What brain regions are crucial for cardiovascular and respiratory control?
- Cerebellum is crucial for cardiovascular and respiratory control; damage in heart failure, OSA, and SUDEP.
- Cerebellar role in blood pressure coordination and termination of apnea.
How does CPAP influence blood pressure?
CPAP can partially normalize blood pressure in apnea-induced hypertension.
What does stopping sympathetic activity to the heart do for REM sleep?
Stops the acceleration that’s seem in REM sleep
What happens to heart rate in REM sleep?
Surges, associated with increase blood pressure rise
Also decelerations during tonic REM sleep, could be just before REM movements
What happens to coronary blood flow during sleep?
Increases in sleep
REM sleep: surges of blood flow with heart rate during eye movements
What is the cardiovascular autonomic nervous system?
The CANS is a highly integrated network controlling visceral functions, making rapid adjustments in heart rate (HR), arterial blood pressure (BP), and blood flow redistribution based on behavior, environment, and emotions.
How do the parasympathetic and sympathetic nervous systems stimulate the heart differently?
- Parasympathetic neurons stimulate the heart primarily via the vagus nerve, resulting in bradycardia.
- Sympathetic neurons stimulate the heart and blood vessels, inducing tachycardia, increased contractility, vasoconstriction, and vasodilation.
Where do the autonomic impulses from the brain to the heart and veins originate from?
vasomotor center in the brainstem.
How do the baroreceptors adjust the cardiovascular system with an increased blood pressure?
Increased BP results in bradycardia, reduced contractility, and peripheral vasodilation
How do the baroreceptors adjust the cardiovascular system with a decreased blood pressure?
decreased BP leads to reflex tachycardia and increased peripheral vasoconstriction.
What are the three cardiovascular reflexes and what do they respond to?
Arterial baroreflex (BP)
Cardiopulmonary Reflex (low pressure receptors)
Chemoreflexes (peripheral -> o2 tension, central -> ph)
What is the diving reflex?
a protective mechanism during apnea, preserving blood flow to the heart and brain while limiting cardiac oxygen demand.
