Physiology Flashcards
Physiologic dead space = ………….+…………..
anatomic dead space + physiologic dead space
What is minute ventilation? formula
Volume of the gases that enter the lungs per minute
Ve = V tidal x RR
What is alveolar ventilation? formula
Volume of the gases that reach alveoli+resp bronchioli per minute
Va = (Vt - Vd) x RR
What part of the lungs is the largest contributor of alveolar dead space? Why?
Apex. Due to low perfusion [well-ventilated, but poorly perfused alveoli]
What is the formula of physiologic dead space?
Vd= tidal volue - ([paCO2-peCO2]/paCO2)
Resting equilibrium of the respiratory system is …….
collapsing force of the lungs is equivalent to the expanding force of the chest wall
What is alveolar pressure and volume at resting equilibrium of the respiratory system?
Alveolar = 0 cm mmHg (same as atmospheric)
lung volume: FRC
Highly compliant container is able to stretch to accommodate large increases in volume with little change in …………
pressure
chest wall has …. compliance at ….. lung volumes
chest wall has low compliance at low lung volumes
lung compliance is the greatest at ………….
It decreases at ………. or ……….
around FRC
At very high or very low volumes
During inspiration , …………. and the lungs outward.
intrapleural negative pressure
Intrapleural negative pressure peaks at …………. at a value of approximately -8 cm H2O.
Maximal inspiration
Intrapleural negative pressure peaks at …………. at a value of approximately …… cm H2O.
Maximal inspiration; -8
at equilibrium IPP is …………….
-5 cm H2O
The lungs at all volumes tend to ……….. toward a smaller volume
recoil
Hemoglobin carries CO2 in the form of …………………
Carbaminohemoglobin
Formula, how is created carbaminohemoglobin
CO2 + Hb-NH3 –> 2H + HbNH-CO2
Blood CO2 carries as ……….
in plasma as bicarbonate ion
HCO-3 exchange to Cl in RBCs. What protein participates?
Band 3 protein
3 steps to carry HCO-3 in plasma from CO2 in tissue
- CO2 enters RBC. CO2+H2O –> H2CO3 by CA
- H2CO3 –>spontaneous conversion –> H+ + HCO-3
- H+ + Hb –> HHb and HCO-3 is transfered to plasma via band 3 protein in exchange for chloride
Why is important to exchange HCO-3 to Cl in RBC?
to maintain electrical neutrality
What makes high RBC cloride content in venous blood?
HCO-3 goes to plasma in exchange to Cl. Cl is in RBC. This change is ,,chloride shift”
When HCO-3 is transfered from RBC?
When there is excess inside the RBC
What are changes in pulmonary vessels - resistance and pressure (2) in high altitude?
Hypoxic vasoconstriction leads to increase PVR and PAP
PaO2 and PaCO2 in high altitude in lungs?
increased minute ventilation: inc. PaO2 (slightly, because there is lack of oxygen in the air despite increased ventilation) and decreased PaCO2
The decreased atmospheric pressure at high altitude reduces the ………………….
Partial pressure of inspired oxygen (PiO2).
Why there is increased HCO-3 excretion in lungs?
Due to increased ventilation - resp. alkalosis. Therefore, the body body excretes HCO-3 to compensate resp. alkalosis
In high altitude, peripheral ……………….. stimulate ………… in an effort to increase ………….
chemoreceptors in the aorta and carotid body; hyperventilation;
to increased arterial oxygenation (PaO2)
Initially, high altitude induced alkalosis shifts Hb-oxygen curve to …….. Why?
Left. To increased O2 uptake in the lungs (left - increased Hb affinity to O2)
Increase pulmonary vascular resistance occurs in initial or late stage?
initial
What is function of SNS in high altitude?
In initial stage increases HR –> CO
What is effect of PaCO2 on cerebral blood flow? What happens in high altitude?
Incr. PaCO2 –> decr. pH –> vasodilation;
In high altitude - decr. PaCO2 due to increased ventilation - technically, should be brain vasoconstriction.
BUT reduced PaO2 and marked tissue ischemia lead to overall cerebral vasodilation
When occurs changes that help to accommodate to high altitude in brain? initially or later?
initially
When occurs compensatory metabolic acidosis in high altitude? Why it happens?
over next 24-48 hours (late stage)
kidney excretes HCO-3 in response to resp. alkalosis
Central chemoreceptors inhibit ventilation when pH …………, therefore the …………. excretion allows for additional hyperventilation in high altitude
gets too high;
HCO-3
Why there is body volume loss in high altitude?
because hypoxemia supresses aldosterone activity + there is increased excretion of HCO-3 ——-> diuresis
Why there is decreased of myocardial O2 demand in high altitude?
Hypoxia –> suppresed aldosterone and incr HCO-3 excretion –> diuresis –> volume depletion –> decreased preload –> decreased cardiac work –> decreased oxygen demand
Volume depletion leads to decreased cardiac preload –> decr. SV. Why CO is still slightly increased?
Due to increased HR via SNS
What is important factor produced by RBC in late altitude stage to supply enough oxygen in tissues?
RBCs produce 2,3BPH, which shifts Hb-oxygen curve to right –> facilitated unload of oxygen in tissues
What 2 factors promotes erythropoesis in high altitude?
Erythropoetin from kidney and hypoxia inducable factor (HIF) in cells throughout the body
What stimulates angiogenesis in tissues in high altitude? Why angiogenesis is important?
Hypoxia induced factor (HIF) which is released from cells throughout the body. To improve oxygen delivery.
In what stage of high altitude there is increase in 2,3BPG and HIF?
later (24-48h after the initial stage)
Why there is needed aldosterone suppression in high altitude?
To decrease blood volume –> increase in Ht
When people in prolonged stay in high altitude exprecience the full benefit of increased erythropoesis and HIF?
Several weeks later
What what pressure PaO2 has important influence on cerebral blood flow?
If PaO2 drops below 50 mmHg –> rapid increase in CBF. Otherwise - PaO2 has little influence on CBF
What is the main factor affecting cerebral blood flow?
incr. PaCO2 –> decr. pH
What is effect of panic attack for cerebral blood flow? Why?
Hyperventilation – decr. PaCO2 = hypocapnia –> with decreased PaCO2 - decreased CBF. CBF increased when there is increase in PaCO2
What disturbances increase A-a O2 gradient?
V/Q mismatch (eg, pulmonary embolism), diffusion limitation, and right-to-left shunting
What is effect of hypo/hyperventilation on A-a gradient?
no effect
What is a sign on tissues hypoxia?
Increased arterial lactacic acid
Elastic resistance/recoil increases at ………
higher tidal volumes
What disturbances insrease elastic resistance?
Restrictive lung diseases.
Interstitial fibrosis increase …………… and obesity increase …………
Lung stiffness; chest wall stiffness
restrictive and obstructive diseases are related to what resistances?
Restrictive - elastic resistance
Obstructive - airflow resistance
What (2) causes airflow resistance?
Limited airway diameter and turbulent airflow
Airflow resistance. Turbulent airflow mechanism.
Higher respiratory rates –> faster airflow –> turbulent airflow
Airflow resistance. Airway diameter mechanism.
Low lung volumes –> reduced airway diameter
To reduced WOB, what is optimized? (2)
Tidal volume and respiratory rate
In restrictive lung diseases, there is ………….. lung volumes. How it affects RR?
Low lung volume (increased elasticity) –> rapid, shallow breathing to compensate those low lung volumes
In obstructive lung diseases, there is ………….. lung volumes. How it affects RR?
High lung volumes –> slow, deep breathing (because we have enough total oxygen volume)
Why obstructive lung diseases cause increased airflow resistance?
Bronchoconstriction and/or airway collapse
Alpha-1 antitripsin deficiency. WOB?
It causes emphysema = COPD
Increased airflow resistance –> slow, deep breathing
Anxiety. WOB?
High breathing rate –> increased airway turbulence (its airway resistance group)
A fixed upper airway obstruction (eg, caused by a large goiter) leads to ……………. and favors slow, deep breaths to minimize the
increased air flow resistance
As blood moves through the pulmonary capillaries, it becomes progressively more oxygenated until …………….
It equilibrates with the alveolar pO2 (~104 mm Hg when breathing room air).
LA and LV has slightly lower pO2 than blood in pulmonary capilaries. Why?
Because deoxygenated blood from bronchopulmonary + thebesian veins flows to pulmonary veins, which carries already oxygenated blood from alveoli
What are thebesian veins?
Thebesian veins – smallest cardiac veins that drain the inner suurface of the myocardium.
thebesian veins drains to ………
left atria and ventricle
wasted ventilation is called as …………..
dead space ventilation
Dual circulation in the lung consists of ………………
Pulmonary arteries and bronchial arteries
Dual circulation of the lung protects against …………
Protects against lung infarction as a complication of pulmonary embolism
Pulmonary arteries provide a blood to the lungs for ………………
gas exchange
Bronchial arteries provide a blood to the lungs for ………………
lung parenchyma with nutrients, remove waste from bronchi and provide collateral blood
When a clot occludes the pulmonary system, the …………….. continue blood supply to bronchial system/parenchyma.
bronchial arteries
In what arteries PE more likely to cause infarction?
In small arteries (≤3 mm)
Why distal PE ie in small arteries more likely can cause lung infarction?
Because distal PE can occlude areas which are distal to the pulmonary-bronchial anastomoses
Pulmonary infarction is more common hemorrhagic or ischemic? Why?
Hemorrhagic
Dual blood supply + low density of lung tissue
Alveolar inflammation triggered by PE can eventually lead to ……………..
Decreased surfactant and some degree of atelectasis.
To decrease surfactant due to alveolar inflammation caused by PE occurs within …………..
Takes up to 2 days to develops
endothelial-derived TPA is limited primarily to ……………….
Bronchial circulation
what drug may be used to treat PE which is hemodinamically unstable?
Recombinant tissues plasminogen activator (TPA)
Why endothelial derived TPA would cause slow recanalization of the pulmonary artery?
Because it is predominantly limited to the bronchial circulation.
Recombinant TPA would use to threat PE
Why endothelial derived TPA would cause slow recanalization of the pulmonary artery?
Because it is predominantly limited to the bronchial circulation.
Recombinant TPA would use to threat PE in pulmonary circulation
Intrapulmonary shunting occurs when an area of the lung is ……………….. but …………… ventilated
Adequately perfused but poorly ventilated
PE causes intrapulmonary shunting due to ……………………….
Redistribution of blood away from segments directly affected by the clot;
The remaining accessible alveoli after intrapulmonary shunting in PE are unable to ……………….
Unable to fully oxygenate all the blood passing through the pulmonary circulation, resulting in hypoxemia
Why in PE there is hypoxia’?
Alveoli, that get intrapulmonary shunting from the areas affected by the clot, cannot fully oxygenate blood passing through –> hypoxia
Areas distal to the clot receive ……………….ventilation but …………. perfusion
adequate ventilation but poor perfusion
Regional differences in ventilation and perfusion occur vertically in the lungs due to …………………
Gravity
Ventilation is lowest in the …………….and highest in the …………….. Why?
Ventilation is lowest in the apex and highest in the base.
Gravity stretch alveoli in the apex more than in the base
How is called effect of the gravity when alveoli in the apex are stretched more than in the base?
Slinki effect
During inspiration a small amount of air goes to ……………..where alveoli are distended and less compliant, while more air goes to ……………. where alveoli have ample potential space to fill and are more compliant.
less air to the apex - less compliant alveoli;
more air to the base - more compliant alveoli
Perfusion is lowest in the ………… and highest in the …………….
apex; base
Why perfusion is lowest in the apex and highest in the base?
Increased hydrostatic pressure in the lower lung regions facilitates increased blood flow.
What is denser - blood or air/lung tissue?
blood
Why gravitation effect is more pronounced on blood flow and ventilation?
because blood is denser than air/lung tissue
V/Q is lowest at the ………….. and highest at the ………
base; apex
Increased tissue oxygen extraction would cause venous oxygen levels to ……….. but would not …………… the arterial oxygen content.
decrease; would not affrect
Increased tissue oxygen extraction would cause venous oxygen levels to ……….. but would not …………… the arterial oxygen content.
decrease; would not affect
in hyperventilation - high V/Q regions have ………………. capacity too absorb additional O2 and compensate for low V/Q regions
little
CO2 removal is directly dependent on ………….
ventilation
How rapidly decreases CO2 and increases O2 in arterial blood with hyperventilation?
CO2 rapidly decreases;
O2 increase just little bit
High V/Q regions …………. compensate O2 in relation to low V/Q regions, and high V/Q regions …………… compensate increased CO2 in relation to low V/Q regions.
High V/Q regions just little bit increase O2 as compensation to low V/Q regions. But, high V/Q regions effectively can exhale additional CO2 which cannot be exhaled in low V/Q region
Immobilization increases risk for PE due to …………
venous stasis
Recent surgery increases risk for PE due to …………
inflammation induced hypercoagulable state
Where originate thrombi after orthopedic proocedures? (2)
Deep veins of pelvis or deep veins in lower extremities
How manifest fat embolism?
follows long-bone fracture + skin rash + neurologic findings
Thrombotic occlusion of the pulmonary circulation leads to ……………………….. of blood flow in the lungs
redistribution
in PE, part alveoli are not perfused, but ventilated. Other normal alveoli are ventilated and have perfusion. What is the capability to oxygenate the blood of those well ventilated and well perfused alveoli?
The remaining accessible alveoli are unable to fully oxygenate the volume of blood that continues to flow through the pulmonary circulation, and hypoxemia results.
As in PE, V/Q mismatch affects only part of the lungs. How can it be managed? Why?
Supplemental oxygen can help correct the hypoxemia by increasing the alveolar partial pressure of oxygen, allowing accessible alveoli to transfer additional oxygen to the blood.
Obstruction of the pulmonary circulation by an embolus causes increased ………………. ventilation
dead space (alveoli are ventilated but not perfused
How diffusion capacity is affected in PE?
It is not affected in PE. It is affected in states that disrupt the alveolar-capillary interface eg pulmonary fibrosis
Lower extremities deep vein thrombosis manifest as ……………. (local symptoms)
Calf swelling
What stimulates central respiratory drive (hyperventilation) in PE? (2)
Dyspnea and inflammatory mediators released by ischemic pulmonary tissue
Why high V/Q regions just little bit increase oxygenation of the blood?
Because Hb is nearly fully saturated in normal V/Q regions. When in high V/Q - capacity increased just little bit.
CO2 removal is more directly dependent on …………………, and high V/Q regions have large capacity to exhale additional CO2
ventilation
Hyperventilation leads to ………..capnia and hypoventilation to ……….capnia
Hyper to hypocapnia;
hypo to hypercapnia
What is serum level of HCO-3 in initial stage in PE? When it changes?
Initial - normal. Since PE leads to resp. alkalosis due to hyperventilation, metabolic compensation with renal HCO-3 excretion takes place over next 72h
Diagnostic test for PE?
CT angiography, which requires intravenous contrast administration.
What precautions should be considered in case we need to do CT angiography in PE when IV contrast is needed?
CT studies should be avoided in patients with chronic kidney disease due to the increased risk of contrast-induced nephropathy
What is alveolar hypoventilation?
Global decrease in alveolar partial pressure of oxygen
What 2 mechanisms cause alveolar hypoventilation?
Decrease in tidal volume or respiratory rate
What metabolic disorder manifests in alveolar hypoventilation?
Decreased CO2 excretion –> respiratory acidosis
What disorders cause diffusion impairment?
Chronic lung diseases such pulmonary fibrosis and emphysema
What is normal response to local alveolar hypoxia in lungs?
hypoxic pulmonary vasoconstriction
By what mechanism is caused hypoxic vasoconstriction in lungs?
Hypoxia detected by mitochondria in pulmonary vascular cells –> stimulates smooth muscle contraction
Hypoxic vasoconstriction is impaired//released by …………. in such states as ………. or ……….
by inflammatory states such acute pneumonia or sepsis
What molecules cause regional vasodilation in inflammatory states in lungs?
proinflammatory cytokines
inflammatory states lead to regional vasodilation in lungs and it lowers ……. and worsens ………
lowers V/Q ration and worsening the hypoxemia
Once treatment for inflammatory states is initiated, vasoactive inflammatory mediators are downregulated over the ensuing hours to days and …………….is restored.
hypoxic vasoconstriction
Why radiographic clearance of pneumonic infiltrates often lags weeks behind clinical improvement in oxygenation?
Once treatment for inflammatory states is initiated –> decreased proinflammatory cytokines –> restores hypoxic vasocontriction. It occurs prior to resorption of alveolar debris, which is carried by macrophages and is slow process. So xray would show infiltrates weeks behind resolved oxygenation
Changes due to chronic hypoxemia ……………….. for hypoxemia, but do not …………….
compensate, but do not resolve
What is reduced compliance?
For any given volume the pressure will be significantly increased/for any given change in pressure less air will flow
What are 3 base changes in aging in the respiratory system?
Decr. lung elastin;
Incr. chest wall stiffness
Decr. diaphragm strength
Why increases lung compliance in aging?
due to loss of elastin
Loss of elastin with aging leads to ……….
increased compliance
incr. lung compliance with aging leads to ……. (3)
resembles mild emphysema and leads to dynamic expiratory airflow obstruction, premature airway closure, progressive hyperinflation
with aging, chest wall compliance …………… due to ………. (2)
decreases due to degenerative changes (ossification, arthritis) of the costovertebral/sternocostal joints and kyphosis of the thoracic spine
Total respiratory system compliance with aging is …………
decreased
why total respiratory system compliance is decreased in elderly, if lung compliance increased?
Stiffness of the chest wall dominates over the increased laxity of the lungs
How changes dead space ventilation with aging? why?
increases due to mechanical changes (lung compliance, chest wall compliance and total resp system compliance)
in which site there is dead space increase with aging?
Anatomic - constant
Alveolar - increases
Why alveolar dead space increases with aging? (3)
progressive elastin degeneration, alveolar simplification, capillary dropout
What is net result (2) of lung with aging’?
lower compliance with increased ded space
WOB with aging? why?
increased, because need to maintain normal minute ventilation
why elderly less tolerate illnesses that impair resp. compliance and/or gas exchange?
due to mechanical changes and inc. alveolar dead space with aging
decr ventilatory efficiency with aging results from combination of 2 components?
Incr. V/Q mismatch + inc. WOB
During aerobic exercise, respiratory activity changes to help meet the body’s ……………..
increased metabolic demand
how changes minute ventilation in athletes?
increased
Increased minute ventilation in athletes occurs via …………. (2)
incr RR and tidal volume
Increased minute ventilation facilitates ……………… (2)
increased rate of oxygen uptake and CO2 removal
What increases alveolar ventilation in athletes?
increased minute ventilation
How increased minute ventilation changes alveolar ventilation?
increases
V/Q changes in athletes?
increased
how changes pulmonary vascular resistance and CO in athletes?
resistance - decreased
CO - increased
What influence is due to reduced pulm. vasc. resistance and incr. CO on physiologic dead space in lungs?
Those 2 changes allow for more evenly distributed blood flow throughout the lungs and reduces physiological dead space
Why there is increa in V/Q in atheltes?
blood flow through the lungs and incr. alveolar ventilation is increased. BUT ALVEOLAR VENTILATION IS MORE INCREASED than BLOOD FLOW –> inc. V/Q
What metabolic changes facilitates oxygen unloading in atheltes?
Lactatic acid –> decr. blood pH –> rightward shift –> incr. unloading of oxygen
In exercises there is inc. CO but decr. time of oxygen unloading in skeletal muscles. Why anyway is enough provided oxygen?
arterial oxygen extraction by skeletal muscle markedly increased during exercise, outpacing CO, which is the reason of fast bloow flow through skeletal muscle vessels.
mixed venous oxygen content in athletes?
decreased; due to increased extraction of oxygen
What is the primary limitation to the aerobic exercise in athletes?
CO
What mechanism leads to incr. WOB in aging?
respiratory mechanics changes
What mechanism leads to incr. V/Q in aging?
gas exchange changes
What mechanism increases physiological dead space in aging?
decr. alveolar surface area
What mechanism increases A-a gradient in aging?
Micro-atelectasis (incr. shunt effect)
What mechanism decr. FVC in aging? (2)
Incr. RV (dinamic obstruction)
note - TLC unchanged
What mechanism decr. total system compliance in aging? (2)
Incr. lung compliance
very decr. chest wall compliance
what obstruction causes loss of elastic fibers?
dynamic airflow obstruction resembling emphysema –> hyperinflation
What change is in diaphragm with aging?
atrophy of fast-twitching muscle fibers
Changes in diaphragm with aging leads to ……………..
lower peak force production for maneuvers such deep inspiration or coughing
Combination of what 2 mechanisms cause microatelectasis with aging?
Chest wall stiffening + lower peak force production due to atrophy of diaphragm
microatelectasis with aging leads to …………….
intrapulmonary shunting
What leads to incr. A-a gradient with aging?
ventilation-perfusion mismatch
what is expected A-a gradient in relation to age?
expected A-a gradient = age/3mmHg
How changes PaO2 and PaCO2 with aging?
PaO2 - decreased;
PaCO2 - not significantly changed
Why elderly people are prone to hypercapnia when acutely ill
Elderly persons are less able to compensate for high minute ventilation loads
Normal aging is characterized by a gradual increase in …………….. (due to …………………….) and increased……………….. (……………………).
Normal aging is characterized by a gradual increase in ventilation-perfusion mismatch (due to basilar microatelectasis causing shunt effect) and increased dead space (loss of alveolar surface area).
Normal aging is characterized by a gradual increase in ventilation-perfusion mismatch (due to basilar microatelectasis causing shunt effect) and increased dead space (loss of alveolar surface area). This manifests as a wider ………….. (ie, decline in ………..) without ………………….. (normal …….)
This manifests as a wider alveolar-arterial oxygen gradient (ie, decline in PaO2) without hypoventilation (normal PaCO2).
At what age starts changes in lungs?
age > 35
Loss of elastic recoil occurs particularly in ……….
alveolar ducts
How changes residual volume with aging? why?
Increased; due to loss of elastic recoil
How changes total incr capacity with aging? why?
remains normal; decreased chest wall compliance counterbalances increases in lung compliance
How changes FVC and FEV1 with aging?
Both decreases
TLC stays unchanged with aging, but proportion of ……….. increases
residual volume
What is normal FEV1?
> 80proc (of predicted)
What is normal FEV1/FVC?
> 70proc
What is normal FVC?
> 80proc (of predicted)
Obstructive LD. FEV1?
decreased
Obstructive LD. FEV1/FVC ratio?
decreased
Obstructive LD. FVC?
normal to decreased
Restrictive LD + obesity. FEV1?
decreased
Restrictive LD + obesity. FEV1/FVC ratio?
normal to decreased
Restrictive LD + obesity. FVC?
decreased
What is FEV1?
volume of air expelled during the first second
What is FVC?
total volume of expelled air
Neuromuscular weakness and obesity hypoventilation syndrome demonstrates what pattern on spirometry?
restrictive pattern
How to differentiate asthma and COPD?
bronchodilator testing.
Asthma has higher degree of reversibility than that due to COPD
How changes RV/TLC in COPD? Why?
Increased
RV increases more than TLC –> therefore RV/TLC ratio is increased
ERV in COPD?
Decreased
Why FRC is increased, if ERV is decreased in COPD?
Increase in RV is greater than decrease in ERV
Why FEV1/FVC ratio in COPD is decreased, if both of those numbers decreased?
FEV1 is decreased more than FVC
TLC, RV, FVC, and FEV1 in restrictive. FEV1/FVC ratio?
All decreased. FEV1/FVR ratio normal or increased
In what population increased TLC and FVC with normal RV?
elite athletes
In elite athletes what TLC and FVC and RV?
TLC and FVC increased;
RV normal
What is the main stimulator for respiratory drive?
PaCO2;
PaO2 exects minimal effect on drive, unless drops below 60-70mmHg
Why patients with COPD have decreased sensitivity to PaCO2?
due to chronic CO2 retention
What levels of PaO2 may be in COPD?
it may drop below 60mmHg and then it would be a stimulator for respiratory drive
The depth and rate of respirations are controlled by …………………….
the medullary respiratory center
The depth and rate of based on ………………… (2)
Input from central and peripheral chemoreceptors and airway mechanoreceptors
Peripheral chemoreceptors found in ………………..
carotid and aortic bodies
Peripheral chemoreceptors sense …………. and are stimulated by ………….
sense PaO2 and are stimulated by hypoxemia
What method can reduce peripheral chemoreceptor stimulation when low PaO2?
Supplemental oxygen –> incr. PaO2 –> reduced perif.chem. stimulation –> reduced respiratory rate
oxygen-induced hypercapnia (oxygen –> decr. RR –> accummulation of CO2) in COPD. What is minor and major factors?
Minor - reduced RR
Major - V/Q mismatch by alleviation of pulmonary vasoconstriction in poorly ventilated areas
Central chemoreceptors, located in the medulla, are more involved in the respiratory response to …………….. than to …………….
hypercapnia than to hypoxemia
CO2 diffuses through BBB. Where it forms hydrogen ions?
in CSF –> decr pH –> sensed by medullary neurons –> triggered and increase in respiration
Why blood pH has little effect on central receptors?
Because BBB is relatively impermeable to hydrogen ions. But they are sensed in CSF when formed from CO2
What include pulmonary stretch receptors? (2)
myelinated and unmyelinated C fibers
Where are pulmonary stretch receptors?
in lungs and airways
What is the function of pulmonary stretch receptors?
regulate the duration of inspiration depending on the degree of lung distension
How is called reflex: duration of inspiration depending on the degree of lung distension?
Hering-Breuer reflex
What is Hering Breuer reflex?
Duration of inspiration depending on the degree of lung distension
In patients with COPD, the response to PaCO2 is ……….. and ………… can contribute to respiratory drive
blunted;
hypoxemia
Chest x ray of COPD? (2)
hyperinflated lungs and flattened diaphragm
