Lung Flashcards
Describe the indications/contraindications for PFT
Evaluate signs of lung disease
Assess progression of lung disease
Monitor the effectiveness of therapy
Evaluate preoperative patients in selected situations
Screen t risk of pulmonary disease such as smokers of occupational exposure
Monitor toxic effects of drugs (amiodarone, beryllium)
-NOT in others without symptoms-may be confusing when nonpulmonary diseases effect pulmonary system
Describe the components of pulmonary function test
Ok
Compare and contract obstructive and restrictive PFT
Obstructive-decreased to normal FVC, decreased FEV1, decreased FEV1/FVC ration
TLC normal or increased
Restrictive-decreased FVC, decreased or normal FEV1, normal FEV1/FVC, decreased total lung capacity
What is the body’s clock
Suprachiasmatic nucleus of the hypothalamus
Neurons discharge rates wax and wan as days go on
Genes control this
-strong genetic component
How set time in nucleus of SCN neuron (no circadian rhythm on its own)
Clock (CLK) on own no circadian rhythm with BMAL19has circadian rhythm increases at night (protein products are transcription factors->increase transcription/translation of:
Period genes:Per1, Per2, Per3 and cryptochrome genes: Cry1, Cry2
Also come back and inhibit Clocka Nd BAL 1 gene products,
Night
Increasing BMAL and CLOCK
Phase shift of CRY.PER bc made by them —-as accumulate at night get negative feedback on BMAL and CLOCK which triggers CRY and PER to fall off
Day
Decrease BMAL and CLOCK
Phase shift Cry/PER just a little behind bc caused by BAL and CLOCK
In nucleus
Two set of neurons fire at day break and another set active at dusk
Tell morning vs night
Morning vs night people
Genetically controlled
Ppl fall asleep at 7—-mutation in clock genes if homozygous had to fall asleep at 7 and wake up at 4
Genetic day
Longer than 24 days..genetic day longer than circadian
We match out active/inactive periods to the day.night cycle of the external env
Younger
Longer genetic day
Older
Shorter day
How long is genetic day
35 hours
How we do this
Retinal hypothalamic tract.. photoreceptors in retina that axons through ganglion travel directly to the SCN in hypothalamus, retino hypothalamic tract is separate from vision tract and it relays light and dark to SCN using 2 neurotransmitters
Glutatme (light
Melatonin (dark)
So SCN gets signal of light (glutamate)
Dark (melatonin)
How generate circadian rhythm, including genetic components
The circadian rhythm is set by the activity of clock, BMAL, Per and CRY gene products in neurons and SCN
Our natural circadian clock seems to be 25 hours long
Describe how entrainment of the genetically determined circadian rhythm to the env occurs
Our circadian clock is synchronized to physical day/night by the action of the retinohypothalamic pathway (glutamate) for day and melatonin for night
Action potential brain
By millions of neurons int he human brain create the EEG
Put electrodes on skull, eye monitors and EKG
*activity is not as regular as EKG-lower volatile
<200 microV
Frequency<1Hz->50 HZ
Differs over different parts of the brain
EEG changes
Degree of activity in brain
Arousal/awareness
Sensory input
Most of time no distinct astern
Clear patterns associated with pathology (epilepsy)
Normal EEG wave
Alpha waves Beta waves Gamma waves Theta waves Delta waves
Alpha waves
8-13 Hz
50 microvolts
Occurs during quiet wakefulness (thinking) when eyes are CLOSED
Over occipital cortex
Disappear during sleep
Origin alpha waves
Requires connection between thalamus and cortex
GABAergic neurons force coordination of neuronal activity (activated by thalamalcortical neurons)
Beta waves
14-80Hz
<50 microV
Awake and alert with eyes open
Alpha block
Eyes closed but awake
Open eyes show more beta waves
Open eyes prevents alpha waves
With sensor input alpha waves cease
-alpha block or alerting response
Where are beta waves
Frontal cortex (thinking’s) Parietal cortex too
But can occur elsewhere
Origin beta waves
Same as alpha
Sensory input disrupts the oscillation to some extent
Thalamus to frontal
Gamma waves
30-80 HZ
Occur when aroused or focused on something
Replaced by even more irregular activity if plan a motor response
May require hippocampus
Theta waves
;rage slow
4-7 HZ
100 microvolts
Normal in kids, particularly over parietal and frontal cortex
Adults frustration or disappointment if awake
-pathologic if not frustrated or disappointed if awake
See in sleeed
Origin theta
Probably hippocampus
Delta waves
Big slow
<3.5Hz
100-200 micro V
Deep sleep in adults
Infants awake and asleep
If in awake it is “serious organic brain disease”
Origin delta wave
Does not require connection between thalamus and cortex
-disconnection during sleep
If see when awake substantial dearangement
Feedback oscillation within cortex creates waves
Taken to indicate that the cortex is no longer connected to thalamus
Alpha
Awake, eyes closed
Beta
Wake, eyes open
High freq low amplitude
Frontal parietal
Gamma
Slower
Associated with attention.motor planning
Theta
Slower higher amplitude, frustration sleep
Delta
Slow large
Dissociation cortex and hypothalamus
Increased mental and neural activity
Increased EEG activity
Infant
Fast bets like activity, but over the occipital region there is slow .5-2 HZ activity
Babies delta wave can be normal
Occipital region slow was in infancy willl increase in childhood
Alpha wave patten will appear during adolescence
Alpha decreased
Hypoglycemia(brain activity dec)
Low body temp
Low adrenal glucocorticoids
High paCO2
Age
Infant-generally slower waves predominance even in wakefulness
Adolescence is when EEG topical adult pattern
52 yo female with insomnia and day time sleepiness but cant fall asleep at night , HTN, obesity, type I diabetes,
- Risk of dying in sleep or falling asleep at wheel
The hypothalamus controls both the circadian rhythm and sleep induction.arousal ___
Separately
Sleep
Cycle of deep to shallow sleep
Common to wake up briefly at end of cycles !!
Non rem sleep
Grey areas -
Earlier in night
Deeper sleep
Slow and bigger wave
Stages non rem
1(N1), 2(N2), deep sleep
Rem sleep
Black areas-top of bars eeg looks like away
Come into and out as go through the cycles
Nonrem
Msot time asleep
Three stages-1, 2, and deep
Slower and bigger EEG waves the deeper and less sensitive you are to external stimuli bc of the thalamus
Dreams do occur in non rem, but they are generally rehashing of days evens (boring)
Non rem dreams
Consolidation of short to long term memory occurs at night
Consolidate what need to remember activate papez circuit
REM
Rapid eye movement
Low amplitude high frequency
Eyes move rapidly l to r
Vivid dreams that you remember
-memory consolidation, brain is sifting through new things you learn and match to old things
Non rem
Bulk, slow rolling eye movements, eeg slow and increases in amp, dreams mundane but starting to consolidate to long term memory,
Rem sleep
Cycle through 90 mins, epoch is is longer into sleep more time
EEG eye movements dreams memorable(vivid and bizarre)
How prevent ourselves from acting out dreams in sleep
Ok
Inducing sleep
Circadian clock entrained to physical reality day and night drives part of need to sleep
1.sleep homeostasis “need for sleep”-loosely tied to circadian clock , gets stronger as night time approaches
NREM sleep
Alertness-tied to circadian clock
Circadian clock drives rem sleep
What drives rem sleep
Circadian clock
What drives non rem
Sleep homeostasis need for sleep
Ventral preoptic ares homeostatic need for sleep
Ventral Preoptic area of hypothalamus gets signals fromt he body
Daylight PGD2 made and released bind to cells of leptomeninges using DP receptor, leads to release of adenosine into CSF , adenosine bind cells in ventral preoptic region , VPO express adenosine 2a receptors which trigger you falling asleep,
Caffeine
Weak blocker of adenosine receptors keeps you awake
PGD2
Binds leptomeninges which secretes adenosine which binds A2a in VPO start sleep
Caffeine blocks this-caffeine 7 hour
What else causes sleep
IL1b and TNF-a
Cytokines-when sick, inflammation sick people are sleepy
NFKB->NO synthase->NO
When else do you sleep a lot
During growth,
Teens don’t get up!! Can sleep in till noon
GHRH
NF-Kb->NO synthase, NO
VPO neurons
Inhibit ascending reticular activating system and reduce sleep
That was all induction of NREM sleep
First o bed , nap
REM sleep
Initiated independently and separate mechanism
REM sleep structures
Cholinergic neurons in the lateral pontine tegmentum, release Ach in the geniculate body
Which then sends input to the occipital cortex
Lateral pontine tegmentum is also part of the brainstem arousal mechanism-the use f Ach to induce REM sleep as
Muscle paralysis in REM sleep
Anhistamines-drowsiness
Promotes induction of sleep into NREM , interfere with REM sleep bc of two different mechanisms
*mucsle paralysis
-crucial to prevent muscle activation during dreams 9if not we would act out, rem behavioral disorder ppl act out dream)
By inhibiting motor neurons
Locus cerulean: inhiibtory input to a motorneurons down spinal cord to paralyze large msucles (not small bc cant do harm)-spares diaphragms and respiratory
Sleep normal induction
PGD2 accumulation in periphery
Adenosine accumulation in CSF (triggered by PGD2)
Adenosine receptor activation in VPI
Leads to inhibition of ARAS
During special circumstance
Growth -GnRH and GH secretagogue receptors
Illness -TNF of IL1b
Any of these trigger NFKB
Induction of REM
Ach from lateral pontine tegmentum, release in geniculate body
Large muscle paralysis requires locus cerulean
When wake up
From REM
How wake up
Hypothalamus
Lateral hypothalamus controls appetite , and releases orexins which make you hungry (orexin a and b) (aka hypocretin 1 and 2) int he brain
Orexin
Makes you eat from lateral hypothalamus
Hypocretin
Hypothalamic for secretin
Triggers pancreatic secretions
Orexin
From lateral hypothalamic axons to tubulomamillary nucleus in hypothalamus, release histamine from tubulomamillary sent to locus ceruleus bind to H1 receipts and thesis neurons release NE and suppress sleep
_whi anti histamine makes you sleeps
REM sleep controlled by what
Circadian clock more active as more into night so stopping rem sleep
First cycle
70-100 minutes
Then moves to short REM and back to deep sleep
Later into night
Hardly in deep sleep, in shallow and rem
90 minute cycle
Children
Sleep a lot in deep and rem
More total sleep
Older elderly
Disruption of cycle
-fewer REM epochs(but they can be long)
Same amount of REM but different sequence
No deep sleep-where brain clears adenosine, so older feel increased need for sleep by not going through deep sleep adenosine not cleared
More frequent awakenings from different sleep stages (not just rem)
Less total sleep (more likely to nap)
Slow wave sleep
N1-N3
Slow eeg
REM sleep
RAM and eeg picks up high frequency
Paralysis of large muscles
N1
Drowsiness/earliest stage of sleeo
Physical-slow, rolling motions of eyes, EMG show muscle activity,
EEG-low voltage , slowing frequency
N2
Slower and bigger
“True sleep”
Physical-EMG show msucle activity, but relatively quiet
EEG-increasing voltage, slowing free, SLEEP SPINDLES(bring interruption with very fast activity)
Sleep spindles
Being in N1, but are most prominent in N2
Bursts of alpha like activity interrupting the slower EEG of sleeo
May be preceded by a sharp wave (K complex) BIG SHARP may preceded
N3
Deep
Large amplitude, slow, delta waves
———-disaccociation between thalamus and cortex, thalamocortical neurons are hypopolarized, cortex is free wheeling
Deep sleep
Quiet EMG,
EEG large slow,
REM
Rapid side to side movements
—DEFLECT IN OPPOSITE DIRECTIONS
EMG suppressed (locus ceruleus) Vivid dreams
EEG-rapid low voltage
Out patient
Obstructive sleep apnea
Increased sleep latency
Thorax bigger abdomen smaller
Paradoxical motion of thorax and abdomen no airflow in or out
Upper airway collapses-suppression of muscle during REM spares diaphragm and not other muscles of respiration collapse and negative pressure in trachea collapses, this person not moving air but moving muscles O sat falls, SNORING
Expiration
Internal inter coastal and abdominal recti
Upper middle lower zone
-10 top -2.5 bottom
Lowest ventilation top bigger at bottom
Insp to ex aVL and intrapleural pressure
-5, -8, -5 intrapleural
0, -1, 0, +1 alveolar pressure
Anatomic dead space
Respiratory bronchiole-has alveoli, anything with alveoli are not anatomic dead space
Trachea, right main, terminal bronchioles
Physiologic dead space
Anatomic+alveolar dead space=total
Total dead space
Usually same as
Pulmonary flow
Low resistance, high compliance
Hypoxia effect
Vasoconstriction
Hypocapnea what happens
Ok
Hypercapnea what happens
Ok
Acid base of respiratory system
PHa=7.48, PaO2 51, PaCO@ 27, HCO3
Acute respiratory alkalosis
Normal ph 7.4, PaO2 95-100, CO2 40, HCO3, 24
PH first 7.4 acid or alk
Cause?resp(CO2 down) or metabolic (HCO3 up)
CO2+H2O=H2CO2=H+HCO2
Decrease CO2 get less product
Central vs peripheral chemoreceptors *low O2 can trigger increased external respiration
Central-medullary neurons
Peripheral-carotid and aortic bodies
Arterial PO2<60, increase peripheral chemoreceptors and decrease central and medullary respiration center, peripheral chemoreceptors increase medullary respiratory center and central has no effect
Increases ventilation, increases arterial PO2
Peripheral chemoreceptors-decrease O2, increase CO2, increase H…very sensitive to reduction in partial pressure of oxygen. Send impulses to inspiration center to stimulate, increase rate and force of respiration and rectifies tha lack of oxygen
Central chemoreceptors increase CO2, increase H+, sensitive to increase in H, H cant cross BBB CO2 crosses and forms carbonic acid, as carbonic acid is unstable it dissociates to H and bicarbonate, , stimulates central which stimulate dorsal group of respiratory center and increase rate and force of breathing …need CO2 in , DONT CHANGE AS OXYGEN CHANES IN BLOOD. H not allowed into CSF so CO2 cross make cabinoc acid then H
Rapidly adapting stretch receptors
Nerve endings between airway epithelial close to the mucosal surface
Myelinated afferent fibers
Stimulated by a host of irritates: cigarette, gases
Depending not he stimulus may result in cough, rapid shallow breathing or mucus secretion
State dependent: reflex cough in awake state versus apnea when asleep/anesthetize
J receptors what stimulates central
In alveolar walls in juxtaposition to the pulmonary capillaries
Stimulated espicially when the pulmonary capillaries become engaged with blood
*pulmonary edema , microembolism
Excitation may give feeling of dyspnea
C fiber sensory nerve endings located within he alveolar walls in juxtaposition to the pulmonary capillaries of lung and innervated by vagus
Stimualtion of these receptors leads to inhibition of the skeletal muscles
Changes in compliance on response system
Increased compliance-filling easy, exhalation hard
Change in v/change in p=compliance
Chances on respiratory system
Ok
Equation flux
SAxDiffusion coefficient (P1-P2)/diffusion distance
Westmarkers sign reduced blood flow to an area what is blood like leaving that area
110, 30
V/q left lung 1.2 (.8 normal) Q down
V/q healthy lung= =.5 Q up!
High V/Q=alveoli with lots of O2, not getting in
PaO2 and PAO2 climb bc not removing O2 , decrease flow,
Bringing low CO2 bc little blood…decrease bc not delivering any.
