Respiratory - FA p646-656 Flashcards

(51 cards)

1
Q
A
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2
Q

Formula to find O2 content of blood?

A

(1.34 × Hb × Sao2) + (0.003 × Pao2)

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3
Q

Formula for minute ventilation

A

Total volume of gas entering lungs per minute
VE = VT × RR

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4
Q

How does O2 sat and PAO2 change with dec Hgb?

A

There is no change in either one, the only change is with normal O2 content in arterial blood (PaO2).

Hb decreased

PaO2 is normal

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5
Q

Alveolar ventilation

A

Volume of gas that reaches alveoli each minute

VA = (VT − VD) × RR

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6
Q

What disease cause an increase in total O2 content?

A

Polycythemia

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7
Q

In which disease will there be dec O2 sat’n but normal Hgb?

A

CO poisoning

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8
Q

Diffusion equation

A

Diffusion:

V˙ gas = A × Dk × [(P1 – P2)/T]

A = area,

T = alveolar wall thickness,

Dk(P1 – P2) ≈ difference in partial pressures:

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9
Q

When is area decreased? when is alveolar wall thickness inc?

A

Emphysema, Pulm fibrosis

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10
Q

At ___, inward pull of lung is balanced by outward pull of chest wall, and system pressure is _________.

A

At FRC, inward pull of lung is balanced by outward pull of chest wall, and system pressure is atmospheric.

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11
Q

Dec in paO2 causes what in lung a/v?

A

VC (diff from systemic circ)

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12
Q

PVR formula (pulm vas resistance)

A

PVR =( Ppulm artery – P L atrium)/Cardiac Output

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13
Q

T or F Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung.

A

True

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14
Q

How does ventilation and perfusion change with exercise?

A

With exercise (INC cardiac output), there is vasodilation of apical capillaries –> Ž V˙/Q˙ ratio approaches 1.

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15
Q

Respiratory rate (RR)

A

12–20 breaths/min

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16
Q

Tidal volume

A

500 mL/breath

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17
Q

Physiological dead space

A

150 mL/breath

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18
Q

Formula to determine dead space, define dead space

A

.VD = physiologic dead space = anatomic dead space of conducting airways plus alveolar dead space; apex of healthy lung is largest contributor of alveolar dead space. Volume of inspired air that does not take part in gas exchange. VT = tidal volume. Paco2 = arterial Pco2. Peco2 = expired air Pco2

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19
Q

Cl−, H+, CO2, 2,3-BPG, and temperature cause what change in Hgb and O2?

A

favor taut form over relaxed form (shifts dissociation curve right O2 unloading).

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20
Q

T or F Myoglobin has higher affinity for O2 > Hgb

A

True

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21
Q

MoA of Cyanide/CO poisoning

A

Both inhibit aerobic metabolism via inhibition of complex IV (cytochrome c oxidase) –> hypoxia unresponsive to supplemental O2 and inc anaerobic metabolism

22
Q

Treatment of CN poisoning?

A

Hydroxocobalamin (forms cyanocobalamin) or induced methemoglobinemia with nitrites and sodium thiosulfate.

23
Q

Cyanide is found in ?

A

synthetic product combustion, ingestion of amygdalin (cyanogenic glucoside found in apricot seed)

24
Q

Presentation of CO poisoning?

A

headaches, dizziness, and cherry red skin.

25
Treatment for CO poisoning?
100% O2, Hyperbaric O2
26
What CNS lesion is seen with CO poisoning?
Classically associated with bilateral globus pallidus lesions on MR
27
What is methemoglobin?
Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily, but has inc affinity for cyanide.
28
Methemoglobinemia - presentation and Tx?
Methemoglobinemia may present with cyanosis and chocolate-colored blood methylene blue and vitamin C.
29
R shift of O2 curve - what does it mean? causes?
dec Hb affinity for O2 (facilitates unloading of O2 to tissue) **R** shift = get **Rid** of O2 Inc H+ ( dec pH, Acid) Inc PCO₂ Inc 2,3–BPG Exercise High Altitude Inc Temperature
30
L shift of O2 curve means? Causes?
dec unloading into tissues inc pH dec PCO2 dec temp dec 2,3 BPG Inc CO, Met Hb, HbF
31
How does the body compensate for left shift?
dec O2 unloading --\> renal hypoxia --\> inc EPO synthesis --\> erythrocytosis
32
Dec of PAO2 causes what?
DEC in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung.
33
Which gases are perfusion limited and which are diffusion limited?
Perfusion - O2 (normally), CO2, N2 - exchange can only inc if blood flow inc Diffusion limited - O2 (emphysema, fibrosis, exercise) & CO
34
Why does fetal Hgb shift the curve L?
Fetal Hb has higher affinity for O2 than adult Hb (due to low affinity for 2,3-BPG), so its dissociation curve is shifted left.
35
Increased parameters in elderly
Lung compliance (loss of elastic recoil) RV V ˙/Q ˙ mismatch A-a gradient
36
Decreased parameters in the elderly
Chest wall compliance (inc chest wall stiffness) FVC and FEV1 Respiratory muscle strength (can impair cough) ventilatory response to hypoxia/hypercapnia
37
How does CN/CO affect the O2 Sat curve?
CN - Curve normal; oxygen saturation may appear normal initially. CO - inc oxygen-binding capacity with left shift in curve, dec O2 unloading in tissues. ( Binds competitively to Hb with 200× greater affinity than O2 to form carboxyhemoglobin. )
38
When is A-a gradient normal / Inc?
Normal A-a gradient = 10-15 nmHg A-a gradient may occur in hypoxemia; causes include R--\> L shunting, V˙/Q˙ mismatch, fibrosis (impairs diffusion)
39
Causes of Hypoxia
DEC cardiac output Hypoxemia Anemia CO poisoning
40
Causes of Hypoxemia (DEC PaO2)
Normal A-a gradient ƒHigh altitude ƒHypoventilation (eg, opioid use) INC A-a gradient ƒ V˙/Q˙ mismatch ƒDiffusion limitation (eg, fibrosis) ƒ Right-to-left shunt
41
Ischemia (loss of blood flow)
Impeded arterial flow dec venous drainage
42
CO2 is transported from tissues to lungs in what forms?
HCO3− (90%). ƒƒ Carbaminohemoglobin or HbCO2 (5%). CO2 bound to Hb at N-terminus of globin (not heme). CO2 binding favors taut form (O2 unloaded). ƒƒ Dissolved CO2 (5%).
43
Bohr Effect?
In peripheral tissue, inc H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect).
44
haldane effect?
In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs
45
Majority of blood CO2 is carried as _____ in the plasma.
Majority of blood CO2 is carried as _HCO3−_ in the plasma.
46
Initial Body response to high altitude - what metabolic disturbance
dec atmospheric oxygen DEC (PiO2) --\> dec PaO2 --\> INC ventilation --\> PaCO2 --\> respiratory alkalosis --\> altitude sickness.
47
Other body responses to high altitude What two things do we produce more of? What happens in the kidney? on a cellular level?
* Inc erythropoietin --\> Inc hematocrit and Hb (chronic hypoxia). * Inc 2,3-BPG (binds to Hb so that Hb releases more O2). * Cellular changes ( Inc mitochondria). * Inc renal excretion of HCO3− to compensate for respiratory alkalosis (can augment with acetazolamide). * Chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH.
48
Response to Exercise
INC CO2 production. INC O2 consumption. INC ventilation rate to meet O2 demand. V ̇/Q ̇ ratio from apex to base becomes more uniform. INC pulmonary blood flow due to INC cardiac output.
49
What happens to pH in exercise?
Dec due to lactic acid
50
How do gas values change in exercise? (PaO2, PaCO2, v CO2/o2 content)
No change in paO2, and PaCO2, but INC venous CO2, and dec venous O2
51