KEY NOTES WK 4 lec 3 Flashcards

1
Q

gas exhange is determined by

A

partial pressure gradient across the alveolar–capillary membrane.

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2
Q

oxygen transported in systemic circulation bound to

A

hemoglobin = oxyhemoglobin

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3
Q

gas transfer in lungs affected by

A

(uptake of O2 and the unloading of CO2) are affected primarily by blood flow.

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4
Q

pulmonary vs systemic circulation

A

pulmonary gets all cardiac output

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5
Q

pulmonary circulation

A

superior and inferior vena cava to alveoli for gas exhange

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6
Q

pulmonary circulation functions

A
  1. it serves as a filter (trap thrombi and emboli, has fibrinolytic substances)
  2. a metabolic organ (angiotensin II for vasoconstriction, bradykinin, serotonin, prostaglandin, If acute injury release histamine and prostaglandins)
  3. a blood reservoir. (10% of blood volume, mobilize blood to improve cardiac output if hemorrhagic shock)
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7
Q

conducting airways and bronchial circulation

A

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.

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8
Q

what can undergo angiogenesis

A

bronchial circulation

i.e. make collateral circulation if clot or embolus

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9
Q

flow, pressure and resistnace in pulmonary circulation

A

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

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10
Q

pulmonary vs systemic circulation: dilated and constricted

A

pulmonary= dilated

systemic= constricted

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11
Q

Pulmonary Capillary Wedge Pressure:
 Swan Ganz Catheter


A

direct measurement of pulmonary artery pressures and indirect measurement of left heart pressures

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12
Q

pulmonary vascular resistnace is low to reduce workload of

A

right ventricle

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13
Q

pulmonary vascular resistance decreases with

A

increased cardiac output

DIF FROM SYSTEMIC where an increase in perfusion pressure increases vascular resistance.

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14
Q

how pulmonary vascular resistance decreases with increased cardiac ouput

A
  1. recruit capillaries
  2. distend capillaries (widen)
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15
Q

enhancing gas exchange in lungs with higher cardiac output benefits

A

adequate time to uptake oxygen and get rid of CO2 (no increase in capillary blood flow)

increase capillary surface area to help gas exhange

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16
Q

when cardiac output increases but resistance doesnt what can it protect from

A

lung edema (bc low pressure)

pulmonary edema if high pressure (fluid accumulate in alveoli)

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17
Q

pulmonary vascular resistnace is optimal around _____

resistance increases at ______

A

optimal = functional residual capacity

more resistant at high (i.e. emphysema lose elasticity and diameter) or low lung (i.e. restrictive lung disease) volume

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18
Q

smoking effects on lungs

A

decreasing the pulmonary capillary cross-sectional area (destroy alveolar membrane)

increased pulmonary artery pressure.

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19
Q

vasoconstriction and vasodilation hormones affecting pulmonary vascular resistnace

A

Vasoconstrictors: Serotonin, norepinephrine, histamine, thromboxane A2, and leukotrienes (esp at low lung volumes)

Vasodilators: adenosine, acetylcholine, prostacyclin (prostaglandin I2), and isoproterenol.

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20
Q

drugs that relieve pulmonary hypertension via vasodilation

A

Nitric oxide and phosphodiesterase type V inhibitors such as sildenafil

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21
Q

Hypoxia Increases Pulmonary Vascular Resistance

A

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

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22
Q

what accentuates Hypoxia Increases Pulmonary Vascular Resistance

A

high CO2 and low blood pH

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23
Q

regional hypoxia in lungs vs generalized hypoxia

A

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)

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24
Q

generalized hypoxia examples

A

pulmonary hypertension

right ventricular hypertrophy

(increase pressure and resistance)

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25
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
26
gravity and blood flow to lungs
underperfused at apex (top) overperfused at base (bottom)
27
3 lung zones depend on relationship between which 3 factors
pulmonary arterial pressure (Pa), pulmonary venous pressure (PV), and alveolar pressure (PA)
28
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
29
which muscles require nervous stimulation to contract for breathing
diaphragm and intercostals
30
where is the respitarpy control center/ central pattern generator
pons and medulla
31
inputs to the respiratory control center (pons and medulla)
1. mechanoreceptors (stretch, j receptors, irritants) 2. central chemoreceptors 3. peripheral chemoreceptors (carotid and aortic) 4. muscle proprioceptors
32
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)
33
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
34
DRG vs VRG
DRG (inspiration) -nucleus of tracts solitarius VRG (active expiration and inspiration) - pre-botzinger complex (rhythogenesis)
35
2 pontine respiratory groups
1. apneustic centers: (stimulate DRG) for controlling deep inspiration 2. pneumotaxic centers: (inhibit DRG) for relaxation after inspiration
36
central inspiratory activity (CIA) gets switched off by
expiration - neurons in VRG and rostral pons
37
stretch receptors initiate which reflex
hering-breuer reflex (lung inflation reflex) to increase breathing frequency and prevent hyperinflation
38
juxtapulmonary capillary J receptors function
increase ventilation in lung edema (give feedback about fluid volume adjacent to alveoli and pulmonary capillaries)
39
how muscles impact rate of breathing
limb velocity, movement, weight load on limb
40
arterial PCO2 increases or if the arterial PO2 decreases or if pH decreases. then ventilation
increases
41
central and peripheral chemoreceptors affecting respiration (PaO2, PaCO2, pH)
central: CO2/ph changes in the lower brainstem peripheral: carotid arteries and aortic arch
42
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.
43
Hypoxic-induced Ventilatory Response what is it mediated by
increase in ventilation triggered by low arterial oxygen levels (PaO₂) via peripheral chemoreceptors
44
what are the only receptors that response to PaO2
peripheral chemoreceptors *hypoxemia
45
4 causes of reduced PO2 in arterial blood
1. hypoventilation 2. diffusion impairment 3. shunt 4. ventilation-perfusion inequality
46
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)
47
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.
48
diffusion impairment causing hypoxemia
thickened blood gas barrier slows diffusion i.e. interstitial fibrosis (widen walls), hypoxemia worse during exericse
49
shunt definition
unventilated but perfused area of the lung
50
shunts causing hypoxemia
anatomic shunt: bypass alveoli through a channel i.e. from right to left heart
51
what wont help a shunt
if just give oxygen it wont help increase arterial PO2
52
intrapulmonary shunts
alveoli are perfused but not ventilated i.e. respiratory distress syndrome, pneumonia, pulmonary edeme
53
extra pulmonary shunts
congenital heart disease (atrial or ventricular septal defects) i.e. right to left shunt
54
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
55
ventilation-perfusion inequalities causing hypoxemia what ratio causes
~1 COPD, parenchymal lung disease, pulmonary embolism, pulmonary hypertension
56
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
57
exercise induced hyperpnea (increase depth and breath rate) is not Fromm
Arterial PCO2, pH, or PaO2 are not involved
58
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)
59
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)
60
intermittent hypoxemia in sleep 2 types
apnea and hypopneas apnea: >90% for >10secs hypopnea >50% for >10 secs
61
obstructive sleep apnea
Respiratory center remains active Paradoxical movement of chest and abdomen upper airway collapse (tongue move back, pharyngeal walls collapse, enlarge tonsils)
62
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
63
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
64
central sleep apnea in heart failure: cheyne strokes respiration
periodic breathing: apnea and hyperpnea respiration waxes and wanes in crescendo-decresendo pattern
65
cheynes stokes respiration pathogenesis
lung congestion stimulates the j receptors hyperventilate reduce PaCO2 central apnea
66
congenital central hypoventilation
box shapes face, decreased forehead lobe, PHOX2B gene
67
central sleep apnea
idiopathic neurologic disease (i.e. myasthenia gravis, encephalisitis)
68
obesity hypoventilation syndrome (pickwickian syndrome)
obese, hyperventilate and daytime hypercapnia
69
Nocturnal Oximetry
 Obesity Hypoventilation Syndrome
severe OSA resolved with CPAP machine from prolonged obesity hypoventilation syndrome
70
pulmonary edema
accumulate fluid in interstial and alveolar spaces (from heart or lung disease)
71
2 stages of pulmonary edema
2. interstitial (widen alveolar wall interstitium, fluid leaked to perivascular and peribronchial spaces) 2. alveolar (fluid crosses epithelium causing alveolar edema)
72
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
73
interstitial vs alveolar edema
interstitial doesnt effect pulmonary function much alveolar prevents ventilation --> hypoxemia
74
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)
75
alveolar edema sx
dyspnea, orthopnea, cough up pink fluid hypoxemia
76
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
77
check for pulmonary edema via
radiograph
78
pulmonary embolism
thrombi in large veins travel to lungs and occlude pulmonary circulation
79
2 types of pulmonary emblism
1. venous thrombi 2. nonthrombotic emboli: fat, air, amniotic fluid
80
venous trombi ____ triad
from deep veins in lower (or upper) virchows triad: stasis of blood, hyper coagulability, abnormal vessel wall
81
dif sized emboli
small= asymptomatic massive= shock, pallor, cardiac arrest, hypotension
82
cor pulmonale
right ventricular failure from high pulmonary artery pressures (i.e. pulmonary emboli, pulmonary vascular disease, or parenchymal disease like COPD)