Respiratory - FA p646-656 Flashcards

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
Q

Treatment for CO poisoning?

A

100% O2, Hyperbaric O2

26
Q

What CNS lesion is seen with CO poisoning?

A

Classically associated with bilateral globus pallidus lesions on MR

27
Q

What is methemoglobin?

A

Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily, but has inc affinity for cyanide.

28
Q

Methemoglobinemia - presentation and Tx?

A

Methemoglobinemia may present with cyanosis and chocolate-colored blood

methylene blue and vitamin C.

29
Q

R shift of O2 curve - what does it mean? causes?

A

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
Q

L shift of O2 curve means? Causes?

A

dec unloading into tissues

inc pH
dec PCO2
dec temp

dec 2,3 BPG
Inc CO, Met Hb, HbF

31
Q

How does the body compensate for left shift?

A

dec O2 unloading –> renal hypoxia –> inc EPO synthesis –> erythrocytosis

32
Q

Dec of PAO2 causes what?

A

DEC in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung.

33
Q

Which gases are perfusion limited and which are diffusion limited?

A

Perfusion - O2 (normally), CO2, N2 - exchange can only inc if blood flow inc

Diffusion limited - O2 (emphysema, fibrosis, exercise) & CO

34
Q

Why does fetal Hgb shift the curve L?

A

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
Q

Increased parameters in elderly

A

Lung compliance (loss of elastic recoil)
RV
V ˙/Q ˙ mismatch
A-a gradient

36
Q

Decreased parameters in the elderly

A

Chest wall compliance (inc chest wall stiffness)
FVC and FEV1
Respiratory muscle strength (can impair cough)

ventilatory response to hypoxia/hypercapnia

37
Q

How does CN/CO affect the O2 Sat curve?

A

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
Q

When is A-a gradient normal / Inc?

A

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
Q

Causes of Hypoxia

A

DEC cardiac output
Hypoxemia
Anemia
CO poisoning

40
Q

Causes of Hypoxemia (DEC PaO2)

A

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
Q

Ischemia (loss of blood flow)

A

Impeded arterial flow

dec venous drainage

42
Q

CO2 is transported from tissues to lungs in what forms?

A

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
Q

Bohr Effect?

A

In peripheral tissue, inc H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect).

44
Q

haldane effect?

A

In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs

45
Q

Majority of blood CO2 is carried as _____ in the plasma.

A

Majority of blood CO2 is carried as HCO3− in the plasma.

46
Q

Initial Body response to high altitude - what metabolic disturbance

A

dec atmospheric oxygen DEC (PiO2) –> dec PaO2 –> INC ventilation –> PaCO2 –> respiratory alkalosis –> altitude sickness.

47
Q

Other body responses to high altitude What two things do we produce more of? What happens in the kidney? on a cellular level?

A
  • 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
Q

Response to Exercise

A

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
Q

What happens to pH in exercise?

A

Dec due to lactic acid

50
Q

How do gas values change in exercise? (PaO2, PaCO2, v CO2/o2 content)

A

No change in paO2, and PaCO2, but INC venous CO2, and dec venous O2

51
Q
A