RESP PART 4

8/8/2019 RESP PART 4

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CONTROL OF

RESPIRATION


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CONTROL OF

BREATHING volume of air inspired and expired per

unit time is tightly controlled, both with

respect to frequency of breaths and totidal volume.

Breathing is regulated so the lungs

can maintain the PaO2 and PaCO2within the normal range, even under

widely varying conditions such as

exercise.


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BREATHING CONTROL

SYSTEM: four components :

1. chemoreceptors for O2 or CO2

2. mechanoreceptors in the lungs and

joints

3. control centers for breathing in the

brain stem (medulla and pons)4. the respiratory muscles, whose activity

is directed by the brain stem

centers


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Initiation and regulation of

breathing in the CNSA. Voluntary control

> can also be exerted by commands from thecerebral cortex (e.g., breath-holding orvoluntary hyperventilation), which cantemporarily override the brain stem.

B. Automatic controlI. NEURAL CONTROL

II. CHEMICAL CONTROL


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CEREBRAL CORTEX

originates in the motor cortex, and

signaling passes directly to motor neurons

in the spine through the corticospinaltracts

responsible for conscious,voluntary

control


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CEREBRAL CORTEX

can temporarily override the automaticbrain centers (talking, eating, drinking)

Limited to short-term

Involuntary system remains the master


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BRAIN STEM CONTROL

OF BREATHING involuntary

controlled by the medulla and pons of

the brain stem


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BRAINSTEM CONTROL

OF BREATHING three groups of neurons orbrainstem

centers:

the medullary respiratory center DRG

VRG

the apneustic center

the pneumotaxic center


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DORSAL RESPIRATORY

GROUP Extends most of the

length of medulla

MOSTLY: Neurons arelocated within the

tractus solitarius

some - reticular

substance of medulla


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Nucleus Tractus Solitarius

Sensory termination of CN X and IX

Transmit sensory signals into the

respiratory center from:

1. peripheral chemoreceptors

2. baroreceptors

3. lung receptors


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DRG

Generates basic rhythm of respiration

contains inspiratory neurons that

innervate the diaphragm and the externalintercostals

Despite transection at the level of medulla

still emits repetitive bursts ofinspiratory neuronal action potentials


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INSPIRATORY RAMP

SIGNALAction potential begins weakly and

increases steadily in a ramp manner for

about 2 seconds, then ceases abruptlyfor the next 3 seconds

Advantage: promotes steady increase in

the lung volume during

inspiration, rather than

inspiratory gasps


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INSPIRATORY RAMP SIGNAL

Rhythmic breathing


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INSPIRATORY RAMP SIGNAL

Rhythmic breathing


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2 qualities of the inspiratory

ramp that are controlled:1. Controloftherateofincreaseoftheramp

signal

> so that during heavy respiration, the rampincreases rapidly and therefore fills the lungsrapidly.

2. Controlofthelimitingpointat whichtherampsuddenlyceases

This is the usual method for controlling the rate ofrespiration; that is, the earlier the ramp ceases,the shorter the duration of inspiration. This alsoshortens the duration of expiration. Thus, thefrequency of respiration is increased.


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VENTRAL RESPIRATORY

GROUP Located in each side of

medulla

Found in the nucleusambiguus rostrally and

nucleus retroambiguus

caudally


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VENTRAL RESPIRATORY

GROUP The ventral respiratory neurons do not appear to

participate in the basic rhythmical oscillation that

controls respiration. When the respiratory drive for increased

pulmonary ventilation becomes greater than

normal, respiratory signals spill over into the

ventral respiratory neurons from the basic

oscillating mechanism of the dorsal respiratory

area. As a consequence, the ventral respiratory

area contributes extra respiratory drive as well.


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VENTRAL RESPIRATORY

GROUP these neurons contribute to both

inspiration and expiration.

They are especially important inproviding the powerful expiratory signalsto the abdominal muscles during veryheavy expiration. Thus, this area

operates more or less as an overdrivemechanism when high levels ofpulmonary ventilation are required,especially during heavy exercise.


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DRG


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DRG

VRG


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PNEUMOTAXIC CENTER

Located dorsally in the nucleus

parabrachialis of the upperpons

Switches off the inspiratory ramp Shortens inspiratory time decrease

lung filling

PRIMARY EFFECT: limitinspiration increase RR


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Pneumotaxic Center

turnsoffinspiration

limits the size of the tidal volume,

regulates the respiratory rate controls rate and depth of breathing.

A normal breathing rhythm persists in

the absence of this center.


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APNEUSIS

is an abnormal breathing pattern with

prolonged inspiratorygasps,

followed by brief expiratory movement Produced when apneustic center is

stimulated


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Apneustic Center

Located in the lowerpons

Stimulation of these neurons apparently

excites the inspiratory center in themedulla, prolonging the period of action

potentials in the phrenic nerve, and

thereby prolonging the contraction of the

diaphragm.


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CHEMICALCONTROL OF

RESPIRATION


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CENTRAL

CHEMORECEPTORS located in the brain stem, are the most

important for the minute-to-minute

control of breathing located on the ventral surface of the

medulla, near the point of exit of the

glossopharyngeal (CN IX) and vagus(CN X) nerves and only a short distance

from the medullary inspiratory center.


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Chemosensitive Areaof

the Respiratory Center The medullary chemoreceptors respond

directly to changes in the pH of CSF

and indirectly to changes in arterial Pco2 communicate directly with the

inspiratory center

exquisitely sensitive to changesinthepH ofcerebrospinalfluid (CSF).


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CENTRAL

CHEMORECEPTORS communicate directly with the inspiratory center

Decreases in the pH of CSF produce increasesin breathing rate (hyperventilation)

Increases in the pH of CSF produce decreasesin breathing rate (hypoventilation).


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Chemosensitive Areaof

the Respiratory Center Primary direct stimulus:

H+ ions

BUT H+ ions do not cross

BBB indirect effect: CO2

react with the water of thetissues to form carbonicacid, which dissociates into

hydrogen and bicarbonateions; the hydrogen ionsthen have a potent directstimulatory effect onrespiration


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ROLE OF CENTRAL

CHEMORECEPTORS

about75-85%of respiratory

drive undernormal conditionsis due to centralchemoreceptor

stimulation byCO2


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Quantitative Effects of Blood PCO2

and Hydrogen Ion Concentration on

Alveolar Ventilation

marked increase in

ventilation caused by

an increase in Pco2 in

the normal range

between 35 and 75 mm

Hg.

This demonstrates the

tremendous effect that

carbon dioxide changes

have in controlling

respiration.


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Quantitative Effects of Blood PCO2

and Hydrogen Ion Concentration on

Alveolar Ventilation

the change in

respiration in the

normal blood pH range

between 7.3 and 7.5 is

less than one-tenth as

great


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EffectofCO2:

Increases RR but only for 1-2 days

After which renal adjustment of the

H+ ion concentration by increasingblood HCO3


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A changeinblood CO2concentrationhasapotentacute

effectoncontrollingrespiratorydrive BUT onlya weakchronic

effectafterafew daysadaptation


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PERIPHERAL

CHEMORECEPTORS Primarily detect

changes in PO2

1. carotid bodies2. aortic bodies


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CAROTID BODIES

located bilaterally in the

bifurcation of the common

carotid arteries

Afferent nerve fibers pass

thru Herings nerves

CN IX dorsal respiratory

area of medulla Contains most of the

receptors


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AORTIC BODIES

Located along the arch of

aorta

Afferent fibers pass thruthe CN X to the dorsal

medullary respiratory area


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CAROTID BODIES

comprise glomus cells that containoxygen-sensitive potassium channels

located at sites of high arterial bloodflow

designed to detect changes in the

amount of dissolved oxygen in thearterial blood supply


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Basic Mechanismofstimulationof

theperipheralchemoreceptors

GLOMUS CELLS

- which synapse directly or indirectly with

the nerve endings- might function as the chemoreceptors

and then stimulate the nerveendings

- other studies suggest that the nerveendings themselves are directlysensitive to the low Po2.

C


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Carotid body oxygen sensor releases

neurotransmitterwhen decrease in PO2


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ARTERIAL PO2 & IMPULSES

IN AORTIC BODY

Respond weakly than carotid bodies

PO2 especially between

60 and 30mm Hg strongly stimulates

the carotid bodies.

This is the range wherein the Hbsaturation decreases.


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no effect on ventilation as

long as the arterial Po2remains greater than 100mm Hg

But at pressures lowerthan 100 mm Hg,ventilation approximatelydoubles when the arterialPo2 falls to 60 mm Hg


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Changes in arterial blood composition detectedby peripheral chemoreceptors increaseinbreathingrate:

1. Decreasesinarterial Po2

if arterial Po2 is between 100 mm Hg and 60mm Hg, the breathing rate is virtually

constant.

if arterial Po2 is lessthan 60 mm Hg, thebreathing rate increases in a very

steep and linear fashion


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Changes in arterial blood composition detected

by peripheral chemoreceptors increaseinbreathingrate:

2. Increasesinarterial Pco2

- effect is less important than theirresponse to decreases in Po2.


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Changes in arterial blood composition detected

by peripheral chemoreceptors increasein

breathingrate:

3. DecreasesinarterialpH

This effect is independent of changes in the arterial

Pco2 and is mediated onlyby chemoreceptors in thecarotid bodies (not by those in the aortic bodies).

Thus, in metabolic acidosis, in which there is

decreased arterial pH, the peripheral chemoreceptors

are stimulated directly to increase the ventilation rate(the respiratory compensation for metabolic acidosis


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PERIPHERAL

CHEMORECEPTORS

responsive to decreased arterial PO2 responsive to increased arterial PCO2 responsive to increased H+ ion

concentration.

HYPERVENTILATION


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MECHANICAL CONTROL OF

BREATHING

Sensory receptors in the lung andairways are stimulated by irritation of

the mucosa and changes in thedistending pressure.

Afferent (sensory) neurons travel upthe vagus to the brainstem areascontrolling respiration.


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1. LUNG STRETCH

RECEPTORS Mechanoreceptors located in the

muscular portions of the walls of the

bronchi and bronchioles throughout thelungs

transmit signals through the vagi into the

dorsal respiratory group of neurons when

the lungs become overstretched.


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Hering-Breuer inflation

refl

ex

not activated until the tidal volume

increases to more than three times

normal (> 1.5 liters per breath).Therefore, this reflex appears to be

mainly a protective mechanism for

preventing excess lung inflation rather

than an important ingredient in normalcontrol of ventilation.


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2. Jointandmuscle

receptors Mechanoreceptors located in the joints

and muscles detect the movement of

limbs and instruct the inspiratory center toincrease the breathing rate.

Information from the joints and muscles is

important in the early (anticipatory)

ventilatory response to exercise.


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3. Irritantreceptors

Irritant receptors for noxious chemicals and

particles are located between epithelial cells

lining the airways.

Information from these receptors travels to themedulla via myelinated CN X and causes a

reflex constriction of bronchial smooth muscle

and an increase in breathing rate.

cause coughing and sneezing They may also cause bronchial constriction in

such diseases as asthma and emphysema

These receptors are rapidlyadapting


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Inhaled dust, noxious gases, or

cigarette smoke stimulates irritant

receptors in the trachea and largeairways that transmit information

through myelinated vagal afferent

fibers.

These receptors are also known asrapidlyadaptingreceptors


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4. J RECEPTORS

Juxtacapillary (J) receptors are located in

the alveolar walls and, therefore, are near

the capillaries.

transmit their afferent input throughunmyelinated, vagal C fibers.


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J RECEPTORS

Engorgement of pulmonary capillaries with

blood and increases in interstitial fluid

volume may activate these receptors and

produce an increase in the breathing rate. For example, in left-sidedheartfailure,

blood "backs up" in the pulmonary

circulation, and J receptors mediate a

change in breathing pattern, including rapid

shallow breathing and dyspnea (difficulty in

breathing).


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OTHER FACTORS AFFECTING

BREATHING:

Other parts of the brain (limbic system,hypothalamus) can also alter the breathingpattern

e.g. affective states, strong emotions such

as rage and fear.

In addition, stimulation of touch, thermal andpain receptors can also stimulate therespiratory system.


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Other factors affecting breathing:

Reticularactivatingsystem:modulates the brainstem controller byaffecting the state of alertness

In the alert, conscious humanexternal stimuli act reflexly at thebrain centers to affect breathing.


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Regulation of Respiration

during exercise Increase in ventilation during exercise

Results from neurogenic signals

transmitted directly into the brain stemrespiratory center at the same time

that signals go to the body muscles to

cause muscle contraction


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Ventilationand Exercise:

To make up for the increased demand for O2 bothperfusion and ventilation are increased.

1. Increased recruitment of capillaries to increase thearea for gas diffusion.

2. Increased tidal volume to increase the distensionof the airways.

3. Increase the rate of breathing4. Increase the utilization coefficient

5. Increase cardiac output


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Responsesto High Altitude

Acute responses:hypoxemia hyperventilation thru

stimulation of peripheral receptors

Chronic responses:

increased erythropoietin

increased Hct raising the oxygencarrying capacity


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Chronic Breathing of Low Oxygen

Stimulates Respiration Even More-The

Phenomenon of "Acclimatization" on ascent to a mountain slowly, over a

period of days rather than a period ofhours, they breathe much more deeply

and therefore can withstand far loweratmospheric oxygen concentrations thanwhen they ascend rapidly. This is calledacclimatization.


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"Acclimatization"

The reason for acclimatization is that,within 2 to 3 days, the respiratory centerin the brain stem loses about four fifths

of its sensitivity to changes in Pco2 andhydrogen ions.


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"Acclimatization"

Instead of the 70 percent increase inventilation that might occur after acute

exposure to low oxygen, the alveolarventilation often increases 400 to 500percent after 2 to 3 days of low oxygen;this helps immensely in supplying

additional oxygen to the mountainclimber.


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ABNORMALPATTERNS OF

BREATHING


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Cheyne-Stokes Breathing

The person breathes deeply for a short interval

and then breathes slightly or not at all for an

additional interval, with the cycle repeating

itself over and over

is characterized by slowly waxing and waning

respiration occurring about every 40 to 60

seconds


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Cheyne-Stokes breathing


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CHEYNE-STOKES BREATHING

Two situations where it can occur:

1. Long delay in transport of blood from thelungs to the brain

When a person overbreathes, thus blowing

off too much carbon dioxide from the

pulmonary blood while at the same time

increasing blood oxygen, it takes several

seconds before the changed pulmonary

blood can be transported to the brain and

inhibit the excess ventilation.


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Long delay in transport of blood from the lungs to thebrain..

Therefore, when the overventilated blood finally

reaches the brain respiratory center, the centerbecomes depressed to an excessive amount. Then

the opposite cycle begins. That is, carbon dioxide

increases and oxygen decreases in the alveoli.

Again, it takes a few seconds before the brain can

respond to these new changes. When the brain

does respond, the person breathes hard once again

and the cycle repeats


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CHEYNE-STOKES

BREATHING

Long delay in transport of blood from thelungs to the brain..

occurs in patients with severe cardiac failurebecause blood flow is slow, thus delaying the

transport of blood gases from the lungs to the

brain


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2. Increased negative feedback gain in therespiratory control areas.

hypersensitivity to changes in arterial PCO2

and PO2 This means that a change in blood carbon

dioxide or oxygen causes a far greater

change in ventilation than normally

can occur in brain damage This means that a change in blood carbon

dioxide or oxygen causes a far greater

change in ventilation than normally


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BIOTS BREATHING

characterized by prolonged periods ofapnea interrupting normal respiratorycycles

represents a form of cheyne-stokesbreathing, resulting from CNS disease


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KUSSMAUL BREATHING

increased depth in breathing

seen most commonly in diabetic

ketoacidosis


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DURING SLEEP

approximately a third of normal individuals

have brief episodes of apnea or

hypoventilation that have no significanteffects on arterial Po2 or Pco2. The apnea

usually lasts less than 10 seconds, and it

occurs in the lighter stages of slow-wave

and rapid eye movement (REM) sleep.


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CLINICAL ABNORMALITIES

OF BREATHING

Related to sleep apnea

1. obstructive sleep apnea

2. central sleep apnea

S


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SLEEP APNEA

SYNDROME the duration of apnea is abnormally prolonged,

and it changes arterial Po2 and Pco2.

two major categories of sleep apnea

1. obstructivesleepapnea- the most common of the sleep apnea

syndromes

- it occurs when the upper airway (generally thehypopharynx) closes during inspiration.

Although the process is similar to whathappens during snoring, it is more severe,obstructs the airway, and causes cessation ofairflow.

SLEEP APNEA


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SLEEP APNEA

SYNDROME 2. centralsleepapnea

- occurs when the ventilatory drive to therespiratory motor neurons decreases

- The degree of hypercapnia andhypoxemia in individuals with centralsleep apnea is less than that inindividuals with OSA, but the samecomplications (polycythemia, etc.)

can occur when central sleep apneais recurrent and severe.

CENTRAL ALVEOLAR


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CENTRAL ALVEOLAR

HYPOVENTILAT

ION

also known as Ondine's curse

is a rare disease in which voluntary breathing isintact but abnormalities in automaticity exist.

the most severe of the central sleep apneasyndromes. As a result, people with CAH canbreathe as long as they do not fall asleep. Forthese individuals, mechanical ventilation or, more

recently, bilateral diaphragmatic pacing (similar to acardiac pacemaker) can be lifesaving.


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Hypoxemia and Hypoxia

Hypoxemia - a decrease in arterial Po2.

Hypoxia - decrease in O2 delivery to, or

utilization by, the tissues. Hypoxemia is one cause of tissue hypoxia,

although it is not the only cause.


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Highaltitude barometric pressure (Pb) is decreased, whichdecreases the Po2 of inspired air (PiO2) and

of alveolar air (PaO2).

At high altitude, breathing supplemental O2raises arterial Po2 by raising inspired and

alveolar Po2.


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Hypoventilation decrease alveolar Po2 (less fresh inspired air

is brought into alveoli).

breathing supplemental O2 raises arterial Po2

by raising the alveolar Po2.


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Diffusiondefects (e.g., fibrosis,

pulmonary edema)

increase diffusion distance or decrease

surface area for diffusion. Equilibration of O2

is impaired, PaO2 is less than PAO2, and theA - a gradient is increased, or widened.

breathing supplemental O2 raises arterial

Po2 by raising alveolar Po2 and increasing

the driving force for O2 diffusion.


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V/Qdefects always cause hypoxemia andincreased A - a gradient.

high V/Q

regions - high Po2 low V/Q regions - low Po2

high V/Q regions have blood with a high Po2,blood flow to those regions is low (i.e., highV/Q ratio) and contributes little to total blood

flow. Low V/Q regions, where Po2 is low, have the

highest blood flow and the greatest overalleffect on Po2 of blood leaving the lungs. InV/Q defects

supplemental O2 can be helpful, primarilybecause it raises the Po2 of low V/Q regionswhere blood flow is highest.

Ri ht t l ft h t ( i ht t l ft di h t


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Right-to-leftshunts (right-to-left cardiac shunts,intrapulmonary shunts) always cause hypoxemiaand increased A - a gradient.

Shunted blood completely bypasses ventilatedalveoli and cannot be oxygenated. Becauseshunted blood mixes with, and dilutes, normallyoxygenated blood (nonshunted blood), the Po2of blood leaving the lungs must be lower thannormal.

Supplemental O2 has a limited effect on thePo2 of systemic arterial blood because it can

only raise the Po2 of normal nonshunted blood;the shunted blood continues to have a dilutionaleffect.

B i Ed D th


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Brain Edema Depresses the

Respiratory Center

the damaged brain tissues swell,compressing the cerebral arteries against thecranial vault and thus partially blocking

cerebral blood supply.

Occasionally, can be relieved temporarily byintravenous injection of hypertonic solutionssuch as highly concentrated mannitol

solution. These solutions osmotically removesome of the fluids of the brain, thus relievingintracranial pressure and sometimes re-establishing respiration within a few minutes.


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Anesthesia

Perhaps the most prevalent cause of respiratorydepression and respiratory arrest is overdosagewith anesthetics or narcotics. For instance,

sodium pentobarbital depresses the respiratorycenter considerably more than many otheranesthetics, such as halothane. At one time,morphine was used as an anesthetic, but thisdrug is now used only as an adjunct to

anesthetics because it greatly depresses therespiratory center while having less ability toanesthetize the cerebral cortex.


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Respiratory Centers


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Brainstem Respiratory


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Brainstem Respiratory

Centers

Dorsal Respiratory Group - Quiet inspiration

Ventral Respiratory Group - Forceful

inspiration and active expiration

Pneumotaxic Center - Influences inspiration

to shut off

Apneustic Center - Prolongs inspiration


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