KEY NOTES WK 4 lec 3 Flashcards
gas exhange is determined by
partial pressure gradient across the alveolar–capillary membrane.
oxygen transported in systemic circulation bound to
hemoglobin = oxyhemoglobin
gas transfer in lungs affected by
(uptake of O2 and the unloading of CO2) are affected primarily by blood flow.
pulmonary vs systemic circulation
pulmonary gets all cardiac output
pulmonary circulation
superior and inferior vena cava to alveoli for gas exhange
pulmonary circulation functions
- it serves as a filter (trap thrombi and emboli, has fibrinolytic substances)
- a metabolic organ (angiotensin II for vasoconstriction, bradykinin, serotonin, prostaglandin, If acute injury release histamine and prostaglandins)
- a blood reservoir. (10% of blood volume, mobilize blood to improve cardiac output if hemorrhagic shock)
conducting airways and bronchial circulation
The bronchial circulation is responsible for supplying oxygen and nutrients to the lung tissue itself (the bronchi, bronchioles, and pleura)—it does not participate in gas exchange.
what can undergo angiogenesis
bronchial circulation
i.e. make collateral circulation if clot or embolus
flow, pressure and resistnace in pulmonary circulation
Unlike the systemic circulation, the pulmonary circulation is a high flow, low-pressure and low- resistance system.
pulmonary artery has thinner wall, less elastin and smooth muscle that aorta = more compliant
pulmonary arterioles less ability to constrict than systemic
pulmonary vs systemic circulation: dilated and constricted
pulmonary= dilated
systemic= constricted
Pulmonary Capillary Wedge Pressure: Swan Ganz Catheter
direct measurement of pulmonary artery pressures and indirect measurement of left heart pressures
pulmonary vascular resistnace is low to reduce workload of
right ventricle
pulmonary vascular resistance decreases with
increased cardiac output
DIF FROM SYSTEMIC where an increase in perfusion pressure increases vascular resistance.
how pulmonary vascular resistance decreases with increased cardiac ouput
- recruit capillaries
- distend capillaries (widen)
enhancing gas exchange in lungs with higher cardiac output benefits
adequate time to uptake oxygen and get rid of CO2 (no increase in capillary blood flow)
increase capillary surface area to help gas exhange
when cardiac output increases but resistance doesnt what can it protect from
lung edema (bc low pressure)
pulmonary edema if high pressure (fluid accumulate in alveoli)
pulmonary vascular resistnace is optimal around _____
resistance increases at ______
optimal = functional residual capacity
more resistant at high (i.e. emphysema lose elasticity and diameter) or low lung (i.e. restrictive lung disease) volume
smoking effects on lungs
decreasing the pulmonary capillary cross-sectional area (destroy alveolar membrane)
increased pulmonary artery pressure.
vasoconstriction and vasodilation hormones affecting pulmonary vascular resistnace
Vasoconstrictors: Serotonin, norepinephrine, histamine, thromboxane A2, and leukotrienes (esp at low lung volumes)
Vasodilators: adenosine, acetylcholine, prostacyclin (prostaglandin I2), and isoproterenol.
drugs that relieve pulmonary hypertension via vasodilation
Nitric oxide and phosphodiesterase type V inhibitors such as sildenafil
Hypoxia Increases Pulmonary Vascular Resistance
small arteries constrict (stimulate smooth muscle cells) in response to low alveolar oxygen (hypoxia and hypoxemia)
increases resistnace
helps optimize gas exhange by diverting blood away from poorly ventilated alveoli to well ventilated one
Reminder: Hypoxemia causes vasodilation in systemic vessels
what accentuates Hypoxia Increases Pulmonary Vascular Resistance
high CO2 and low blood pH
regional hypoxia in lungs vs generalized hypoxia
localize vasoconstriction to specific lung regions and divert blood away (little effect on pulmonary arterial pressure or resistance)
general increases resistnace and pulmonary artery pressure (i.e. asthma, emphysema, cystic fibrosis, high altitude)
generalized hypoxia examples
pulmonary hypertension
right ventricular hypertrophy
(increase pressure and resistance)
Hypoxic Pulmonary Vasoconstriction
fetal vs after birth
fetal: dont need lungs for gas exhange so blood shunted away from lungs
1st breath: pulmonary arterioles dilate and resistnace decrasees
then after birth HPV will shunt blood away from poorly ventilated regions –> improve ventilation to perfusion matching
gravity and blood flow to lungs
underperfused at apex (top)
overperfused at base (bottom)
3 lung zones depend on relationship between which 3 factors
pulmonary arterial pressure (Pa), pulmonary venous pressure (PV), and alveolar pressure (PA)
3 lung zones
pulmonary arterial pressure (Pa), pulmonary venous pressure (PV), and alveolar pressure (PA)
zone 1 (least perfused @ apex)
PA > Pa > Pv
–> if alveolar pressure greater than arterial pressure then no blood flow (bc want to go high to low pressure)
–> alveolar dead space (ventilated but not perfused)
zone 2
Pa > PA > Pv
zone 3 (most perfused)
Pa > Pv > PA
capillaries become more distended and resistance decreases as go down
which muscles require nervous stimulation to contract for breathing
diaphragm and intercostals
where is the respitarpy control center/ central pattern generator
pons and medulla
inputs to the respiratory control center (pons and medulla)
- mechanoreceptors (stretch, j receptors, irritants)
- central chemoreceptors
- peripheral chemoreceptors (carotid and aortic)
- muscle proprioceptors
which emotions and which brain areas are descending inputs on lung function at respiratory control center (pons and medulla)
rage and fear in hypothalamic and limbic system for voluntary control (cerebrum)
medulla has 2 groups for which breathing
DRG (dorsal respiratory group) for inspiration
–> diaphragm and intercostal muscles
–> nucleus of tractus solitarius
VRG (ventral respiratory group) for active respiration
–> pre-botzinger complex (rhythogenesis)
cross communication between VRG and DRG for synchrony and rhythmic movement s
DRG vs VRG
DRG (inspiration)
-nucleus of tracts solitarius
VRG (active expiration and inspiration)
- pre-botzinger complex (rhythogenesis)
2 pontine respiratory groups
- apneustic centers: (stimulate DRG) for controlling deep inspiration
- pneumotaxic centers: (inhibit DRG) for relaxation after inspiration
central inspiratory activity (CIA) gets switched off by
expiration - neurons in VRG and rostral pons
stretch receptors initiate which reflex
hering-breuer reflex (lung inflation reflex) to increase breathing frequency and prevent hyperinflation
juxtapulmonary capillary J receptors function
increase ventilation in lung edema (give feedback about fluid volume adjacent to alveoli and pulmonary capillaries)
how muscles impact rate of breathing
limb velocity, movement, weight load on limb
arterial
PCO2 increases or if the arterial PO2 decreases or if pH decreases. then ventilation
increases
central and peripheral chemoreceptors affecting respiration (PaO2, PaCO2, pH)
central: CO2/ph changes in the lower brainstem
peripheral: carotid arteries and aortic arch
what is not sensed in the brain (because of blood brain barrier preventing H+ from crossing) and rely on input from peripheral chemoreceptors
arterial PO2 and arterial pH
The BBB is impermeable to charged ions like H⁺, preventing direct entry into the brain.
However, CO₂ is highly lipid-soluble and CAN cross the BBB freely.
Hypoxic-induced Ventilatory Response
what is it mediated by
increase in ventilation triggered by low arterial oxygen levels (PaO₂)
via peripheral chemoreceptors
what are the only receptors that response to PaO2
peripheral chemoreceptors
*hypoxemia
4 causes of reduced PO2 in arterial blood
- hypoventilation
- diffusion impairment
- shunt
- ventilation-perfusion inequality
central and peripheral causes of hypoventilation
central- outside of lung (drugs, medulla encephalitis, cervical spine injury, hangman fracture C2 spine, C4 spine quadriplegia)
peripheral- lung disease (COPD, Duchenne, Gillian barre, myasthenia gravis, obesity hurts thoracic cage)
hypoventilation will cause a rise in
diagnostic feature
sx
what is not a feature
diagnostic: PCO2
respiratory acidosis - pH 7.2, altered mental state
Hypoxemia is not the dominant feature of hypoventilation.
diffusion impairment causing hypoxemia
thickened blood gas barrier slows diffusion
i.e. interstitial fibrosis (widen walls),
hypoxemia worse during exericse
shunt definition
unventilated but perfused area of the lung
shunts causing hypoxemia
anatomic shunt: bypass alveoli through a channel i.e. from right to left heart
what wont help a shunt
if just give oxygen it wont help increase arterial PO2
intrapulmonary shunts
alveoli are perfused but not ventilated i.e. respiratory distress syndrome, pneumonia, pulmonary edeme
extra pulmonary shunts
congenital heart disease (atrial or ventricular septal defects) i.e. right to left shunt
shunts and dead space relationship
Both shunts and dead space cause ventilation-perfusion (V/Q) mismatches but in opposite ways.
shunt: Blood reaches the alveoli without gas exchange due to absent or impaired ventilation.
shunt: unventilated but perfused area of lung
deadspace: Air reaches alveoli, but no blood flow is available for gas exchange.
Dead space refers to areas of the respiratory system where ventilation occurs, but no gas exchange takes place
ventilation-perfusion inequalities causing hypoxemia
what ratio
causes
~1
COPD, parenchymal lung disease, pulmonary embolism, pulmonary hypertension
COPD have elevated ____ but they _____
what should you not do
CO2 (hypercapnia) but they adapt to tolerate high arterial PCO2 and rely on hypoxemia to drive ventilation
supplemental O2 may cause these patients to stop breathing because arterial PO2 is increased abruptly, removing their drive to breathe
exercise induced hyperpnea (increase depth and breath rate) is not Fromm
Arterial PCO2, pH, or PaO2 are not involved
3 mechanisms of breathing during exercise
phase 1 neurological phase (medullary generator)
phase 2 metabolic phase (increase alveolar ventilation, no change in PaCO2)
phase 3 compensatory phase (shift from aerobic to anaerobic; lactic acid by product instead of CO2)
sleep via
breathing
small rise in
vulnerable if
withdrawal from wakefulness stimuli via brainstem reticular formation
depressed breathing
small rise in PaCO2
vulnerable if have respiratory muscle weakness, impaired gas exhange etc. (nocturnal before diurnal problems)
intermittent hypoxemia in sleep
2 types
apnea and hypopneas
apnea: >90% for >10secs
hypopnea >50% for >10 secs
obstructive sleep apnea
Respiratory center remains active
Paradoxical movement of chest and abdomen
upper airway collapse (tongue move back, pharyngeal walls collapse, enlarge tonsils)
central sleep apnea (i.e. from CNS injury or if healthy in high altitude)
Respiratory center is inactive
The absence of paradoxical movement of chest and abdomen
obstructive vs central sleep apnea
both have cessation of airflow, oxygen desaturation and arousal from sleep
in OSA:respiratory center active and theres paradoxical chest and ab mvoemtns
in CSA: respiratory center inactive and absence of paradoxical movements
central sleep apnea in heart failure: cheyne strokes respiration
periodic breathing: apnea and hyperpnea
respiration waxes and wanes in crescendo-decresendo pattern
cheynes stokes respiration pathogenesis
lung congestion stimulates the j receptors
hyperventilate
reduce PaCO2
central apnea
congenital central hypoventilation
box shapes face, decreased forehead lobe,
PHOX2B gene
central sleep apnea
idiopathic
neurologic disease (i.e. myasthenia gravis, encephalisitis)
obesity hypoventilation syndrome (pickwickian syndrome)
obese, hyperventilate and daytime hypercapnia
Nocturnal Oximetry
Obesity Hypoventilation Syndrome
severe OSA resolved with CPAP machine
from prolonged obesity hypoventilation syndrome
pulmonary edema
accumulate fluid in interstial and alveolar spaces (from heart or lung disease)
2 stages of pulmonary edema
- interstitial (widen alveolar wall interstitium, fluid leaked to perivascular and peribronchial spaces)
- alveolar (fluid crosses epithelium causing alveolar edema)
transition from interstitial to alveolar edema
lymphs are overloaded
pressure in interstitial spaces increases and fluid spills into alveoli
alveolar epithelium also damaged and increased permeability
protein and red cells in alveolar fluid
interstitial vs alveolar edema
interstitial doesnt effect pulmonary function much
alveolar prevents ventilation –> hypoxemia
Edema in the Perivascular or Peribronchial Region Reduces ___
the Caliber of Vessels & Airways
compresses vasculature (reduce caliber and lead to pulmonary vascular resistnace) and compress airways (narrow bronchioles and airways)
alveolar edema sx
dyspnea, orthopnea, cough up pink fluid
hypoxemia
causes of pulmonary edema
increased capillary hydrostatic pressure (i.e. heart failure, myocardial infarction)
increased capillary permeability (i.e toxin, sepsis)
reduced lymph drainage
decreased interstitial pressure
decrease colloid osmotic pressure
check for pulmonary edema via
radiograph
pulmonary embolism
thrombi in large veins travel to lungs and occlude pulmonary circulation
2 types of pulmonary emblism
- venous thrombi
- nonthrombotic emboli: fat, air, amniotic fluid
venous trombi
____ triad
from deep veins in lower (or upper)
virchows triad: stasis of blood, hyper coagulability, abnormal vessel wall
dif sized emboli
small= asymptomatic
massive= shock, pallor, cardiac arrest, hypotension
cor pulmonale
right ventricular failure from high pulmonary artery pressures (i.e. pulmonary emboli, pulmonary vascular disease, or parenchymal disease like COPD)
