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1 STEP Uworld pulmo > Physiology > Flashcards

Physiology Flashcards

1
Q

Physiologic dead space = ………….+…………..

A

anatomic dead space + physiologic dead space

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2
Q

What is minute ventilation? formula

A

Volume of the gases that enter the lungs per minute

Ve = V tidal x RR

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3
Q

What is alveolar ventilation? formula

A

Volume of the gases that reach alveoli+resp bronchioli per minute
Va = (Vt - Vd) x RR

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4
Q

What part of the lungs is the largest contributor of alveolar dead space? Why?

A

Apex. Due to low perfusion [well-ventilated, but poorly perfused alveoli]

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5
Q

What is the formula of physiologic dead space?

A

Vd= tidal volue - ([paCO2-peCO2]/paCO2)

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6
Q

Resting equilibrium of the respiratory system is …….

A

collapsing force of the lungs is equivalent to the expanding force of the chest wall

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7
Q

What is alveolar pressure and volume at resting equilibrium of the respiratory system?

A

Alveolar = 0 cm mmHg (same as atmospheric)
lung volume: FRC

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8
Q

Highly compliant container is able to stretch to accommodate large increases in volume with little change in …………

A

pressure

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9
Q

chest wall has …. compliance at ….. lung volumes

A

chest wall has low compliance at low lung volumes

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10
Q

lung compliance is the greatest at ………….
It decreases at ………. or ……….

A

around FRC
At very high or very low volumes

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11
Q

During inspiration , …………. and the lungs outward.

A

intrapleural negative pressure

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12
Q

Intrapleural negative pressure peaks at …………. at a value of approximately -8 cm H2O.

A

Maximal inspiration

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13
Q

Intrapleural negative pressure peaks at …………. at a value of approximately …… cm H2O.

A

Maximal inspiration; -8

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14
Q

at equilibrium IPP is …………….

A

-5 cm H2O

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15
Q

The lungs at all volumes tend to ……….. toward a smaller volume

A

recoil

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16
Q

Hemoglobin carries CO2 in the form of …………………

A

Carbaminohemoglobin

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17
Q

Formula, how is created carbaminohemoglobin

A

CO2 + Hb-NH3 –> 2H + HbNH-CO2

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18
Q

Blood CO2 carries as ……….

A

in plasma as bicarbonate ion

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19
Q

HCO-3 exchange to Cl in RBCs. What protein participates?

A

Band 3 protein

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20
Q

3 steps to carry HCO-3 in plasma from CO2 in tissue

A
  1. CO2 enters RBC. CO2+H2O –> H2CO3 by CA
  2. H2CO3 –>spontaneous conversion –> H+ + HCO-3
  3. H+ + Hb –> HHb and HCO-3 is transfered to plasma via band 3 protein in exchange for chloride
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21
Q

Why is important to exchange HCO-3 to Cl in RBC?

A

to maintain electrical neutrality

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22
Q

What makes high RBC cloride content in venous blood?

A

HCO-3 goes to plasma in exchange to Cl. Cl is in RBC. This change is ,,chloride shift”

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23
Q

When HCO-3 is transfered from RBC?

A

When there is excess inside the RBC

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24
Q

What are changes in pulmonary vessels - resistance and pressure (2) in high altitude?

A

Hypoxic vasoconstriction leads to increase PVR and PAP

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25
Q

PaO2 and PaCO2 in high altitude in lungs?

A

increased minute ventilation: inc. PaO2 (slightly, because there is lack of oxygen in the air despite increased ventilation) and decreased PaCO2

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26
Q

The decreased atmospheric pressure at high altitude reduces the ………………….

A

Partial pressure of inspired oxygen (PiO2).

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27
Q

Why there is increased HCO-3 excretion in lungs?

A

Due to increased ventilation - resp. alkalosis. Therefore, the body body excretes HCO-3 to compensate resp. alkalosis

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28
Q

In high altitude, peripheral ……………….. stimulate ………… in an effort to increase ………….

A

chemoreceptors in the aorta and carotid body; hyperventilation;
to increased arterial oxygenation (PaO2)

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29
Q

Initially, high altitude induced alkalosis shifts Hb-oxygen curve to …….. Why?

A

Left. To increased O2 uptake in the lungs (left - increased Hb affinity to O2)

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30
Q

Increase pulmonary vascular resistance occurs in initial or late stage?

A

initial

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31
Q

What is function of SNS in high altitude?

A

In initial stage increases HR –> CO

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32
Q

What is effect of PaCO2 on cerebral blood flow? What happens in high altitude?

A

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

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33
Q

When occurs changes that help to accommodate to high altitude in brain? initially or later?

A

initially

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34
Q

When occurs compensatory metabolic acidosis in high altitude? Why it happens?

A

over next 24-48 hours (late stage)
kidney excretes HCO-3 in response to resp. alkalosis

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35
Q

Central chemoreceptors inhibit ventilation when pH …………, therefore the …………. excretion allows for additional hyperventilation in high altitude

A

gets too high;
HCO-3

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36
Q

Why there is body volume loss in high altitude?

A

because hypoxemia supresses aldosterone activity + there is increased excretion of HCO-3 ——-> diuresis

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37
Q

Why there is decreased of myocardial O2 demand in high altitude?

A

Hypoxia –> suppresed aldosterone and incr HCO-3 excretion –> diuresis –> volume depletion –> decreased preload –> decreased cardiac work –> decreased oxygen demand

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38
Q

Volume depletion leads to decreased cardiac preload –> decr. SV. Why CO is still slightly increased?

A

Due to increased HR via SNS

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39
Q

What is important factor produced by RBC in late altitude stage to supply enough oxygen in tissues?

A

RBCs produce 2,3BPH, which shifts Hb-oxygen curve to right –> facilitated unload of oxygen in tissues

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40
Q

What 2 factors promotes erythropoesis in high altitude?

A

Erythropoetin from kidney and hypoxia inducable factor (HIF) in cells throughout the body

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41
Q

What stimulates angiogenesis in tissues in high altitude? Why angiogenesis is important?

A

Hypoxia induced factor (HIF) which is released from cells throughout the body. To improve oxygen delivery.

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42
Q

In what stage of high altitude there is increase in 2,3BPG and HIF?

A

later (24-48h after the initial stage)

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43
Q

Why there is needed aldosterone suppression in high altitude?

A

To decrease blood volume –> increase in Ht

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44
Q

When people in prolonged stay in high altitude exprecience the full benefit of increased erythropoesis and HIF?

A

Several weeks later

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45
Q

What what pressure PaO2 has important influence on cerebral blood flow?

A

If PaO2 drops below 50 mmHg –> rapid increase in CBF. Otherwise - PaO2 has little influence on CBF

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46
Q

What is the main factor affecting cerebral blood flow?

A

incr. PaCO2 –> decr. pH

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47
Q

What is effect of panic attack for cerebral blood flow? Why?

A

Hyperventilation – decr. PaCO2 = hypocapnia –> with decreased PaCO2 - decreased CBF. CBF increased when there is increase in PaCO2

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48
Q

What disturbances increase A-a O2 gradient?

A

V/Q mismatch (eg, pulmonary embolism), diffusion limitation, and right-to-left shunting

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49
Q

What is effect of hypo/hyperventilation on A-a gradient?

A

no effect

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50
Q

What is a sign on tissues hypoxia?

A

Increased arterial lactacic acid

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51
Q

Elastic resistance/recoil increases at ………

A

higher tidal volumes

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52
Q

What disturbances insrease elastic resistance?

A

Restrictive lung diseases.

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53
Q

Interstitial fibrosis increase …………… and obesity increase …………

A

Lung stiffness; chest wall stiffness

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54
Q

restrictive and obstructive diseases are related to what resistances?

A

Restrictive - elastic resistance
Obstructive - airflow resistance

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55
Q

What (2) causes airflow resistance?

A

Limited airway diameter and turbulent airflow

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56
Q

Airflow resistance. Turbulent airflow mechanism.

A

Higher respiratory rates –> faster airflow –> turbulent airflow

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57
Q

Airflow resistance. Airway diameter mechanism.

A

Low lung volumes –> reduced airway diameter

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58
Q

To reduced WOB, what is optimized? (2)

A

Tidal volume and respiratory rate

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59
Q

In restrictive lung diseases, there is ………….. lung volumes. How it affects RR?

A

Low lung volume (increased elasticity) –> rapid, shallow breathing to compensate those low lung volumes

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60
Q

In obstructive lung diseases, there is ………….. lung volumes. How it affects RR?

A

High lung volumes –> slow, deep breathing (because we have enough total oxygen volume)

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61
Q

Why obstructive lung diseases cause increased airflow resistance?

A

Bronchoconstriction and/or airway collapse

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62
Q

Alpha-1 antitripsin deficiency. WOB?

A

It causes emphysema = COPD
Increased airflow resistance –> slow, deep breathing

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63
Q

Anxiety. WOB?

A

High breathing rate –> increased airway turbulence (its airway resistance group)

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64
Q

A fixed upper airway obstruction (eg, caused by a large goiter) leads to ……………. and favors slow, deep breaths to minimize the

A

increased air flow resistance

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65
Q

As blood moves through the pulmonary capillaries, it becomes progressively more oxygenated until …………….

A

It equilibrates with the alveolar pO2 (~104 mm Hg when breathing room air).

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66
Q

LA and LV has slightly lower pO2 than blood in pulmonary capilaries. Why?

A

Because deoxygenated blood from bronchopulmonary + thebesian veins flows to pulmonary veins, which carries already oxygenated blood from alveoli

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67
Q

What are thebesian veins?

A

Thebesian veins – smallest cardiac veins that drain the inner suurface of the myocardium.

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68
Q

thebesian veins drains to ………

A

left atria and ventricle

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69
Q

wasted ventilation is called as …………..

A

dead space ventilation

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70
Q

Dual circulation in the lung consists of ………………

A

Pulmonary arteries and bronchial arteries

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71
Q

Dual circulation of the lung protects against …………

A

Protects against lung infarction as a complication of pulmonary embolism

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72
Q

Pulmonary arteries provide a blood to the lungs for ………………

A

gas exchange

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73
Q

Bronchial arteries provide a blood to the lungs for ………………

A

lung parenchyma with nutrients, remove waste from bronchi and provide collateral blood

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74
Q

When a clot occludes the pulmonary system, the …………….. continue blood supply to bronchial system/parenchyma.

A

bronchial arteries

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75
Q

In what arteries PE more likely to cause infarction?

A

In small arteries (≤3 mm)

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76
Q

Why distal PE ie in small arteries more likely can cause lung infarction?

A

Because distal PE can occlude areas which are distal to the pulmonary-bronchial anastomoses

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77
Q

Pulmonary infarction is more common hemorrhagic or ischemic? Why?

A

Hemorrhagic
Dual blood supply + low density of lung tissue

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78
Q

Alveolar inflammation triggered by PE can eventually lead to ……………..

A

Decreased surfactant and some degree of atelectasis.

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79
Q

To decrease surfactant due to alveolar inflammation caused by PE occurs within …………..

A

Takes up to 2 days to develops

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80
Q

endothelial-derived TPA is limited primarily to ……………….

A

Bronchial circulation

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81
Q

what drug may be used to treat PE which is hemodinamically unstable?

A

Recombinant tissues plasminogen activator (TPA)

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82
Q

Why endothelial derived TPA would cause slow recanalization of the pulmonary artery?

A

Because it is predominantly limited to the bronchial circulation.
Recombinant TPA would use to threat PE

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83
Q

Why endothelial derived TPA would cause slow recanalization of the pulmonary artery?

A

Because it is predominantly limited to the bronchial circulation.
Recombinant TPA would use to threat PE in pulmonary circulation

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84
Q

Intrapulmonary shunting occurs when an area of the lung is ……………….. but …………… ventilated

A

Adequately perfused but poorly ventilated

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85
Q

PE causes intrapulmonary shunting due to ……………………….

A

Redistribution of blood away from segments directly affected by the clot;

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86
Q

The remaining accessible alveoli after intrapulmonary shunting in PE are unable to ……………….

A

Unable to fully oxygenate all the blood passing through the pulmonary circulation, resulting in hypoxemia

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87
Q

Why in PE there is hypoxia’?

A

Alveoli, that get intrapulmonary shunting from the areas affected by the clot, cannot fully oxygenate blood passing through –> hypoxia

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88
Q

Areas distal to the clot receive ……………….ventilation but …………. perfusion

A

adequate ventilation but poor perfusion

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89
Q

Regional differences in ventilation and perfusion occur vertically in the lungs due to …………………

A

Gravity

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90
Q

Ventilation is lowest in the …………….and highest in the …………….. Why?

A

Ventilation is lowest in the apex and highest in the base.
Gravity stretch alveoli in the apex more than in the base

91
Q

How is called effect of the gravity when alveoli in the apex are stretched more than in the base?

A

Slinki effect

92
Q

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.

A

less air to the apex - less compliant alveoli;
more air to the base - more compliant alveoli

93
Q

Perfusion is lowest in the ………… and highest in the …………….

A

apex; base

94
Q

Why perfusion is lowest in the apex and highest in the base?

A

Increased hydrostatic pressure in the lower lung regions facilitates increased blood flow.

95
Q

What is denser - blood or air/lung tissue?

A

blood

96
Q

Why gravitation effect is more pronounced on blood flow and ventilation?

A

because blood is denser than air/lung tissue

97
Q

V/Q is lowest at the ………….. and highest at the ………

A

base; apex

98
Q

Increased tissue oxygen extraction would cause venous oxygen levels to ……….. but would not …………… the arterial oxygen content.

A

decrease; would not affrect

99
Q

Increased tissue oxygen extraction would cause venous oxygen levels to ……….. but would not …………… the arterial oxygen content.

A

decrease; would not affect

100
Q

in hyperventilation - high V/Q regions have ………………. capacity too absorb additional O2 and compensate for low V/Q regions

A

little

101
Q

CO2 removal is directly dependent on ………….

A

ventilation

102
Q

How rapidly decreases CO2 and increases O2 in arterial blood with hyperventilation?

A

CO2 rapidly decreases;
O2 increase just little bit

103
Q

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.

A

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

104
Q

Immobilization increases risk for PE due to …………

A

venous stasis

105
Q

Recent surgery increases risk for PE due to …………

A

inflammation induced hypercoagulable state

106
Q

Where originate thrombi after orthopedic proocedures? (2)

A

Deep veins of pelvis or deep veins in lower extremities

107
Q

How manifest fat embolism?

A

follows long-bone fracture + skin rash + neurologic findings

108
Q

Thrombotic occlusion of the pulmonary circulation leads to ……………………….. of blood flow in the lungs

A

redistribution

109
Q

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?

A

The remaining accessible alveoli are unable to fully oxygenate the volume of blood that continues to flow through the pulmonary circulation, and hypoxemia results.

110
Q

As in PE, V/Q mismatch affects only part of the lungs. How can it be managed? Why?

A

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.

111
Q

Obstruction of the pulmonary circulation by an embolus causes increased ………………. ventilation

A

dead space (alveoli are ventilated but not perfused

112
Q

How diffusion capacity is affected in PE?

A

It is not affected in PE. It is affected in states that disrupt the alveolar-capillary interface eg pulmonary fibrosis

113
Q

Lower extremities deep vein thrombosis manifest as ……………. (local symptoms)

A

Calf swelling

114
Q

What stimulates central respiratory drive (hyperventilation) in PE? (2)

A

Dyspnea and inflammatory mediators released by ischemic pulmonary tissue

115
Q

Why high V/Q regions just little bit increase oxygenation of the blood?

A

Because Hb is nearly fully saturated in normal V/Q regions. When in high V/Q - capacity increased just little bit.

116
Q

CO2 removal is more directly dependent on …………………, and high V/Q regions have large capacity to exhale additional CO2

A

ventilation

117
Q

Hyperventilation leads to ………..capnia and hypoventilation to ……….capnia

A

Hyper to hypocapnia;
hypo to hypercapnia

118
Q

What is serum level of HCO-3 in initial stage in PE? When it changes?

A

Initial - normal. Since PE leads to resp. alkalosis due to hyperventilation, metabolic compensation with renal HCO-3 excretion takes place over next 72h

119
Q

Diagnostic test for PE?

A

CT angiography, which requires intravenous contrast administration.

120
Q

What precautions should be considered in case we need to do CT angiography in PE when IV contrast is needed?

A

CT studies should be avoided in patients with chronic kidney disease due to the increased risk of contrast-induced nephropathy

121
Q

What is alveolar hypoventilation?

A

Global decrease in alveolar partial pressure of oxygen

122
Q

What 2 mechanisms cause alveolar hypoventilation?

A

Decrease in tidal volume or respiratory rate

123
Q

What metabolic disorder manifests in alveolar hypoventilation?

A

Decreased CO2 excretion –> respiratory acidosis

124
Q

What disorders cause diffusion impairment?

A

Chronic lung diseases such pulmonary fibrosis and emphysema

125
Q

What is normal response to local alveolar hypoxia in lungs?

A

hypoxic pulmonary vasoconstriction

126
Q

By what mechanism is caused hypoxic vasoconstriction in lungs?

A

Hypoxia detected by mitochondria in pulmonary vascular cells –> stimulates smooth muscle contraction

127
Q

Hypoxic vasoconstriction is impaired//released by …………. in such states as ………. or ……….

A

by inflammatory states such acute pneumonia or sepsis

128
Q

What molecules cause regional vasodilation in inflammatory states in lungs?

A

proinflammatory cytokines

129
Q

inflammatory states lead to regional vasodilation in lungs and it lowers ……. and worsens ………

A

lowers V/Q ration and worsening the hypoxemia

130
Q

Once treatment for inflammatory states is initiated, vasoactive inflammatory mediators are downregulated over the ensuing hours to days and …………….is restored.

A

hypoxic vasoconstriction

131
Q

Why radiographic clearance of pneumonic infiltrates often lags weeks behind clinical improvement in oxygenation?

A

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

132
Q

Changes due to chronic hypoxemia ……………….. for hypoxemia, but do not …………….

A

compensate, but do not resolve

133
Q

What is reduced compliance?

A

For any given volume the pressure will be significantly increased/for any given change in pressure less air will flow

134
Q

What are 3 base changes in aging in the respiratory system?

A

Decr. lung elastin;
Incr. chest wall stiffness
Decr. diaphragm strength

135
Q

Why increases lung compliance in aging?

A

due to loss of elastin

136
Q

Loss of elastin with aging leads to ……….

A

increased compliance

137
Q

incr. lung compliance with aging leads to ……. (3)

A

resembles mild emphysema and leads to dynamic expiratory airflow obstruction, premature airway closure, progressive hyperinflation

138
Q

with aging, chest wall compliance …………… due to ………. (2)

A

decreases due to degenerative changes (ossification, arthritis) of the costovertebral/sternocostal joints and kyphosis of the thoracic spine

139
Q

Total respiratory system compliance with aging is …………

A

decreased

140
Q

why total respiratory system compliance is decreased in elderly, if lung compliance increased?

A

Stiffness of the chest wall dominates over the increased laxity of the lungs

141
Q

How changes dead space ventilation with aging? why?

A

increases due to mechanical changes (lung compliance, chest wall compliance and total resp system compliance)

142
Q

in which site there is dead space increase with aging?

A

Anatomic - constant
Alveolar - increases

143
Q

Why alveolar dead space increases with aging? (3)

A

progressive elastin degeneration, alveolar simplification, capillary dropout

144
Q

What is net result (2) of lung with aging’?

A

lower compliance with increased ded space

145
Q

WOB with aging? why?

A

increased, because need to maintain normal minute ventilation

146
Q

why elderly less tolerate illnesses that impair resp. compliance and/or gas exchange?

A

due to mechanical changes and inc. alveolar dead space with aging

147
Q

decr ventilatory efficiency with aging results from combination of 2 components?

A

Incr. V/Q mismatch + inc. WOB

148
Q

During aerobic exercise, respiratory activity changes to help meet the body’s ……………..

A

increased metabolic demand

149
Q

how changes minute ventilation in athletes?

A

increased

150
Q

Increased minute ventilation in athletes occurs via …………. (2)

A

incr RR and tidal volume

151
Q

Increased minute ventilation facilitates ……………… (2)

A

increased rate of oxygen uptake and CO2 removal

152
Q

What increases alveolar ventilation in athletes?

A

increased minute ventilation

153
Q

How increased minute ventilation changes alveolar ventilation?

A

increases

154
Q

V/Q changes in athletes?

A

increased

155
Q

how changes pulmonary vascular resistance and CO in athletes?

A

resistance - decreased
CO - increased

156
Q

What influence is due to reduced pulm. vasc. resistance and incr. CO on physiologic dead space in lungs?

A

Those 2 changes allow for more evenly distributed blood flow throughout the lungs and reduces physiological dead space

157
Q

Why there is increa in V/Q in atheltes?

A

blood flow through the lungs and incr. alveolar ventilation is increased. BUT ALVEOLAR VENTILATION IS MORE INCREASED than BLOOD FLOW –> inc. V/Q

158
Q

What metabolic changes facilitates oxygen unloading in atheltes?

A

Lactatic acid –> decr. blood pH –> rightward shift –> incr. unloading of oxygen

159
Q

In exercises there is inc. CO but decr. time of oxygen unloading in skeletal muscles. Why anyway is enough provided oxygen?

A

arterial oxygen extraction by skeletal muscle markedly increased during exercise, outpacing CO, which is the reason of fast bloow flow through skeletal muscle vessels.

160
Q

mixed venous oxygen content in athletes?

A

decreased; due to increased extraction of oxygen

161
Q

What is the primary limitation to the aerobic exercise in athletes?

A

CO

162
Q

What mechanism leads to incr. WOB in aging?

A

respiratory mechanics changes

163
Q

What mechanism leads to incr. V/Q in aging?

A

gas exchange changes

164
Q

What mechanism increases physiological dead space in aging?

A

decr. alveolar surface area

165
Q

What mechanism increases A-a gradient in aging?

A

Micro-atelectasis (incr. shunt effect)

166
Q

What mechanism decr. FVC in aging? (2)

A

Incr. RV (dinamic obstruction)
note - TLC unchanged

167
Q

What mechanism decr. total system compliance in aging? (2)

A

Incr. lung compliance
very decr. chest wall compliance

168
Q

what obstruction causes loss of elastic fibers?

A

dynamic airflow obstruction resembling emphysema –> hyperinflation

169
Q

What change is in diaphragm with aging?

A

atrophy of fast-twitching muscle fibers

170
Q

Changes in diaphragm with aging leads to ……………..

A

lower peak force production for maneuvers such deep inspiration or coughing

171
Q

Combination of what 2 mechanisms cause microatelectasis with aging?

A

Chest wall stiffening + lower peak force production due to atrophy of diaphragm

172
Q

microatelectasis with aging leads to …………….

A

intrapulmonary shunting

173
Q

What leads to incr. A-a gradient with aging?

A

ventilation-perfusion mismatch

174
Q

what is expected A-a gradient in relation to age?

A

expected A-a gradient = age/3mmHg

175
Q

How changes PaO2 and PaCO2 with aging?

A

PaO2 - decreased;
PaCO2 - not significantly changed

176
Q

Why elderly people are prone to hypercapnia when acutely ill

A

Elderly persons are less able to compensate for high minute ventilation loads

177
Q

Normal aging is characterized by a gradual increase in …………….. (due to …………………….) and increased……………….. (……………………).

A

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).

178
Q

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 …….)

A

This manifests as a wider alveolar-arterial oxygen gradient (ie, decline in PaO2) without hypoventilation (normal PaCO2).

179
Q

At what age starts changes in lungs?

A

age > 35

180
Q

Loss of elastic recoil occurs particularly in ……….

A

alveolar ducts

181
Q

How changes residual volume with aging? why?

A

Increased; due to loss of elastic recoil

182
Q

How changes total incr capacity with aging? why?

A

remains normal; decreased chest wall compliance counterbalances increases in lung compliance

183
Q

How changes FVC and FEV1 with aging?

A

Both decreases

184
Q

TLC stays unchanged with aging, but proportion of ……….. increases

A

residual volume

185
Q

What is normal FEV1?

A

> 80proc (of predicted)

186
Q

What is normal FEV1/FVC?

A

> 70proc

187
Q

What is normal FVC?

A

> 80proc (of predicted)

188
Q

Obstructive LD. FEV1?

A

decreased

189
Q

Obstructive LD. FEV1/FVC ratio?

A

decreased

190
Q

Obstructive LD. FVC?

A

normal to decreased

191
Q

Restrictive LD + obesity. FEV1?

A

decreased

192
Q

Restrictive LD + obesity. FEV1/FVC ratio?

A

normal to decreased

193
Q

Restrictive LD + obesity. FVC?

A

decreased

194
Q

What is FEV1?

A

volume of air expelled during the first second

195
Q

What is FVC?

A

total volume of expelled air

196
Q

Neuromuscular weakness and obesity hypoventilation syndrome demonstrates what pattern on spirometry?

A

restrictive pattern

197
Q

How to differentiate asthma and COPD?

A

bronchodilator testing.
Asthma has higher degree of reversibility than that due to COPD

198
Q

How changes RV/TLC in COPD? Why?

A

Increased
RV increases more than TLC –> therefore RV/TLC ratio is increased

199
Q

ERV in COPD?

A

Decreased

200
Q

Why FRC is increased, if ERV is decreased in COPD?

A

Increase in RV is greater than decrease in ERV

201
Q

Why FEV1/FVC ratio in COPD is decreased, if both of those numbers decreased?

A

FEV1 is decreased more than FVC

202
Q

TLC, RV, FVC, and FEV1 in restrictive. FEV1/FVC ratio?

A

All decreased. FEV1/FVR ratio normal or increased

203
Q

In what population increased TLC and FVC with normal RV?

A

elite athletes

204
Q

In elite athletes what TLC and FVC and RV?

A

TLC and FVC increased;
RV normal

205
Q

What is the main stimulator for respiratory drive?

A

PaCO2;
PaO2 exects minimal effect on drive, unless drops below 60-70mmHg

206
Q

Why patients with COPD have decreased sensitivity to PaCO2?

A

due to chronic CO2 retention

207
Q

What levels of PaO2 may be in COPD?

A

it may drop below 60mmHg and then it would be a stimulator for respiratory drive

208
Q

The depth and rate of respirations are controlled by …………………….

A

the medullary respiratory center

209
Q

The depth and rate of based on ………………… (2)

A

Input from central and peripheral chemoreceptors and airway mechanoreceptors

210
Q

Peripheral chemoreceptors found in ………………..

A

carotid and aortic bodies

211
Q

Peripheral chemoreceptors sense …………. and are stimulated by ………….

A

sense PaO2 and are stimulated by hypoxemia

212
Q

What method can reduce peripheral chemoreceptor stimulation when low PaO2?

A

Supplemental oxygen –> incr. PaO2 –> reduced perif.chem. stimulation –> reduced respiratory rate

213
Q

oxygen-induced hypercapnia (oxygen –> decr. RR –> accummulation of CO2) in COPD. What is minor and major factors?

A

Minor - reduced RR
Major - V/Q mismatch by alleviation of pulmonary vasoconstriction in poorly ventilated areas

214
Q

Central chemoreceptors, located in the medulla, are more involved in the respiratory response to …………….. than to …………….

A

hypercapnia than to hypoxemia

215
Q

CO2 diffuses through BBB. Where it forms hydrogen ions?

A

in CSF –> decr pH –> sensed by medullary neurons –> triggered and increase in respiration

216
Q

Why blood pH has little effect on central receptors?

A

Because BBB is relatively impermeable to hydrogen ions. But they are sensed in CSF when formed from CO2

217
Q

What include pulmonary stretch receptors? (2)

A

myelinated and unmyelinated C fibers

218
Q

Where are pulmonary stretch receptors?

A

in lungs and airways

219
Q

What is the function of pulmonary stretch receptors?

A

regulate the duration of inspiration depending on the degree of lung distension

220
Q

How is called reflex: duration of inspiration depending on the degree of lung distension?

A

Hering-Breuer reflex

221
Q

What is Hering Breuer reflex?

A

Duration of inspiration depending on the degree of lung distension

222
Q

In patients with COPD, the response to PaCO2 is ……….. and ………… can contribute to respiratory drive

A

blunted;
hypoxemia

223
Q

Chest x ray of COPD? (2)

A

hyperinflated lungs and flattened diaphragm

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