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Pathophysiology > Patho- Mcarthy > Flashcards

Patho- Mcarthy Flashcards

1
Q

ABG: normal value: pH, pCO2, pO2

A

pH: 7.35-7.45
pCO2: 35-35
pO2: 80-100

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2
Q

ABG normal value: calculated HCO3- (aka CO2 content)

A

24

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3
Q

what is the normal value for CO2 content in venous blood? what equation does the lab use to calculate this?

A

24-31 … represents the HCO3-

CO2 +H2O H2CO3 H+ + HCO3-

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4
Q

what is the partial pressure of O2 in dry air? in inspired (humidified) air?

A

dry: 160mmHg
inspired: 150mmHg

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5
Q

PAO2 (alveolar), PVO2 (venous blood), and PaO2 (arterial)

A

PVO2: 40
PAO2: 100 (gains from inspiration)
PaO2: 100

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6
Q

PCO2 in dry air, inspired air, venous blood, alveoli and arterial blood

A 
dry air: 0
inspired air : 0
venous: 46
alveoli: 40 (loses from expiration)
arterial: 40
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7
Q

what kind of problem is it if HCO3- values are abnormal?

A

chronic (aka compensatory response)

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8
Q

what formula do you use to calc partial pressure of O2 in alveoli?

A

PAO2= PIO2 - (PACO2*1.25)

and PIO2=150mmHg

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9
Q

FVC

A

forced vital capacity = amount able to fully exhale after deepest inhalation

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10
Q

RV

A

residual volume: about 1200mL : amount leftover after forced exhalation - not measurable by spirometry

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11
Q

FRC

A

functional residual capacity: amount leftover in lungs after normal tidal volume exhale
(expiratory RV + RV) –>
(1200 + 1200mL = 2400mL)

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12
Q

what will result from low V/Q ratio?

A

this means low blood O2 (hypoxemia) so youll inc. resp rate (forcibly increasing the V/Q ratio) to compensate for inc pCO2

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13
Q

low V/Q ratio (hypoxemia) …your resp rate increases to compensate … but what will happen if the work of breathing is too much… what pts is this common in?

A

work of breathing too much means you’re requiring too much O2 … you will get hypercapnia where pCO2> 45mmHg (common with COPD pts)

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14
Q

PCO2 < 35 is what? PCO2 >45 is what?

A

<35 : hypocapnia, alveolar hyperventilation : alkalosis

>45: hypercapnia, alveolar hypoventilation : acidosis

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15
Q

what is minute ventilation? what is the equation?

A

total rate of air movement into and out of the lungs

Tidal Vol * breaths/min = minute vent.

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16
Q

what is alveolar ventilation and its equation?

A

corrects for physiological dead space

(tidal vol - physiological dead space) * breaths/min = alveolar vent.

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17
Q

what is the relationship between PCO2 and alveolar vent (and the more useful equation for alv vent)?

A

inverse relationship: inc alveolar vent = dec PCO2 (blowing off more CO2)
PCO2=VCO2/VA
VCO2= rate CO2 production and VA= alveolar vent.

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18
Q

what is PETCO2? what is it used for?

A

amount of CO2 in expired air (the partial pressure of it). this gives early warning signs of respiratory compromise b/c it can be continuously monitored (“ventilation vital sign”)

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19
Q

what is the normal range of PETCO2?

A

its 1:1 with arterial ABG PCO2 so its 35-35 mmHg

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20
Q

increasing PCO2 = ___ H+ = ____ pH ..which means the person has…

A

= increasing H+ = dec. pH (acidosis)

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21
Q

its important to maintain normal pCO2 b/c its in equilibrium with _____ and a change in PCO2 can …

A

weak acid : H2CO3

disturb the acid-base balance

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22
Q

as lung vol increases, pressure of gas ___

A

decreases

23
Q

increase in ____ causes ______ acidosis

decrease in _____ causes _____acidosis

A

inc. PCO2: respiratory

dec. HCO3- : metabolic

24
Q

what is a case when there may be respiratory compensation for metabolic acidosis

A

if the lungs are healthy and they have diabetic ketoacidosis (serum HCO3- drops in attempt to buffer ketoacids… buffer consumes HCO3- (levels drop), pH drops… respiratory responds with hyperventilation to minimize change in pH, brain tells body to increase resp. rate.

25
Q

central chemoreceptors: location, process, goal

A

location: brainstem
process: CO2 diffuses into CSF: inc PaCO2=inc PCO2 in CSF = dec. pH = hypervent. to dec. CO2
goal: keep arterial PCO2 in range by min-to-min control of breathing

26
Q

peripheral chemoreceptors: location, process, goal

A

location: carotid arteries and aortic arch
process: PaO2 <60mmHg or dec. arterial pH in carotid bodies = hypervent. to dec. CO2
goal: activate and contribute to resp. rate change ONLY if PaO2<60mmHg or theres an acid-base balance alteration IN CAROTID BODIES

27
Q

PO2: normal range, hypoxemia

SaO2 (saturation): normal range, hypoxemia

A

PO2: 80-100, hypox: <80
SaO2: >95%, hypox: <95

28
Q

PO2: 60-80 , 40-60, <40 … what are the equivalent numbers in SaO2 ?

A

PO2: 60-80 = SaO2: 90-95
40-60 = SaO2: 75-90
<40 = SaO2: <75

29
Q

what are the levels of PO2 and SaO2 when it is reccomended to start O2 therapy? and the target numbers?

A

PO2: = or <55 TARGET: at least 60
SaO2: 88 TARGET: at least 90

30
Q

A-a gradient : how do you use it? what does it mean if A-a is normal?

A

(age/4) + 4 … use in comparison with what is calc. from alveolar gas equation . PAO2- PaO2= calc. gradient

if A-a is normal, there is no V/Q mismatch and the hypoxia is just secondary to inc. pCO2

31
Q

ANS on lung: parasympathetic effect vs sympathetic

A

both act on bronchial smooth muscle
PSNS –Ach–>bronchoconstriction
SNS –B2–> bronchodilation

32
Q

airflow, pressure gradient and resistance equation

A

Q= deltaP/R
Q: airflow
delta P: pressure gradient
R: resistance

33
Q

___ is the driving force of airflow (Q)

A

pressure difference (deltaP)

34
Q

recommendations for O2 therapy: hypoxic but NOT hypercapnic?

A

O2 therapy!

35
Q

recommendations for O2 therapy: hypoxic AND hypercapnic?

A

O2 therapy risks worse PCO2 retention .. monitor response to O2 w/ ABGs not with O2 Saturation (ABGs looks at pCO2)

36
Q

what is O2 saturation? vs paO2

A

% Hgb binding sites that carrying O2

paO2: represents actual O2 content in the blood

37
Q

explain the increase and rapid rise in the O2-Hgb dissosciation curve

A

as partial pressure inc, there are more O2 molecules available to bind. More O2 bound to Hgb, the easier it is for the next one to bind = speed inc and rapid rise in curve.. until all are filled and Hgb is saturated (getting close to saturation when O2 about 90% and paO2 60, curve begins to level off).
phenomenon: “positive cooperativity”

38
Q

minimum amount of O2 conc. needed to prevent ischemia in tissues…

A

O2 saturation of 90% and paO2 of 60 mmHg

39
Q

tissue hypoxia from inadequate tissue perfusion like HF: O2 delivery to tissues is determined by ___ and ____

A

blood flow (aka cardiac output) and O2 content in blood (dissolved O2 + Hgb bound O2)

40
Q

most of O2 delivered to tissues is ____

A

attached to Hgb (99%)

41
Q

when you measure PO2 from ABGs, youre measuring …

A

amount of O2 dissolved in blood, not what is attachd to Hgb

42
Q

3 major causes of tissue hypoxia

A
  1. inadequate gas exchange in lungs (only one you can txt w/ O2 therapy)
  2. anemia
  3. inadequate tissue perfusion (HF)
43
Q

Hgb affinity for fourth molecule of O2 is highest and occurs at values … what does this mean for affinity in lungs vs tissues.

A

PO2: 60-100mmHg , when we are closest to saturation

lungs: affinity at peak, about 100% saturated PaO2=100mmHg
tissue: affinity lower, about 75% saturated, PaO2=40mmHg

44
Q

how do tissues maintain the pressure gradient of O2 so that it keeps perfusing

A

they use the O2, so that the PaO2 in capillaries is always higher than in tissues and therefore O2 diffuses across into tissues

45
Q

cause of polycythemia:

A

hypoxia –> inc synthesis of erythropoietin in kidney –> acts on bone marrow –> RBC production –> inc Hgb production –> inc. O2 carrying capacity –> inc. total O2 in blood!

46
Q

cor pulmonale

A

right sided heart failure caused by pulm. HTN (which is caused by some primary pulm disease like COPD or ILD) or pulm. vasculature (PE)

47
Q

how to distinguish cor pulmonale from rightHF cause by left HF

A

left HF will cause inc. in PCWP (pulmonary capillary wedge pressure)

48
Q

compliance explained in terms of a rubber band… disorders of high and low compliance

A

high compliance: thin rubber band = thin elastic “tissue”, easily stretched (i.e. emphysema)
low compliance: thick rubber band = thick elastic “tissue”, hard to stretch but stronger snapback (i.e. fibrosis)

49
Q

definition of compliance

A

distensibility of the system: describes change in lung vol. for given change in pressure
C= deltaV * deltaP
V: lung vol.
P: transpulmonary pressure

50
Q

what is transpulmonary pressure

A

diff between inside alveoli and pleural surface of lung

51
Q

the A-a gradient is high, what are the two possible reasons for this?

A
  1. V/Q mismatch

2. shunting (essentially extreme V/Q mismatch)

52
Q

The A-a gradient is low, what would this mean?

A

low OR normal would mean that something caused dec. CO2 (hyperventilation-panic attack or high altitude) - if alkalosis.
or other cause from inc. CO2 (if acidosis)

53
Q

metabolic acidosis or alkalosis is always acute or chronic?

A

always acute

Pathophysiology (28 decks)

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