Goljan - Cellular Reaction To Injury

Front 1

Hypoxia

Back 1

Inadequate oxygenation of tissue (same definition of as shock).

Front 2

What is oxygen needed for?

Back 2

Need O2 for oxidation phosphorylation pathway – where you get ATP from inner Mito membrane (electron transport system, called
oxidative phosphorylation).

Front 3

Oxidation phosphorylation pathway

Back 3

The last rxn is O2 to receive the electrons. Protons are being kicked off, go backinto the membrane, and form ATP, and ATP in formed in the mitochondria

Front 4

Oxygen Content

Back 4

Hb x O2 saturation + partial pressure of arterial oxygen (these are the 3 main things that carry O2 in our blood)

Front 5

Partial pressure of arterial O2 is

Back 5

O2 dissolved in plasma

Front 6

In RBCs Fe must be?

Back 6

Fe 2+ not Fe 3+

Front 7

Oxygen Saturation

Back 7

O2 IN the RBC is attached TO the heme group = (measured by a pulse oximeter)

Front 8

Partial pressure of oxygen

Back 8

O2 dissolved in PLASMA

Front 9

O2 flow

Back 9

From alveoli through the interphase, then dissolves in plasma, and increases the partial
pressure of O2, diffuses through the RBC membrane and attaches to the heme groups on the RBC
on the Hb, which is the O2 sa

Front 10

What happens if the partial pressure of oxygen is decreased?

Back 10

O2 sat’n HAS to be decreased (B/c O2 came from
amount that was dissolved in plasma)

Front 11

Ischemia

Back 11

Decrease in ARTERIAL blood flow ……NOT venous

Front 12

Most common cause of ischemia

Back 12

Thrombus in muscular artery (b/c this is the most common cause of death in USA = MI, therefore MI is
good example of ischemia b/c thrombus is blocking arterial blood flow, producing tissue hypoxia)

Front 13

Decrease in cardiac output leads to?

Back 13

Hypovolemia and cardiogenic shock b/c there is a decrease in arterial blood flow.

Front 14

Hypoxemia

Back 14

Cause of hypoxia (they are not the same); deals with the partial pressure of arterial O2 (O2 dissolved in arterial plasma, therefore, when the particle pressure of O2 is decreased, this is
called hypoxemia).

Front 15

Respiratory Acidosis

Back 15

in terms of Dalton’s law, the sum of the partial
pressure of gas must = 760 at atmospheric pressure (have O2, CO2, and nitrogen; nitrogen
remains constant – therefore, when you retain CO2, this is resp acidosis; when CO2 goes up, pO2
Therefore, every time you have resp acidosis, from ANY cause, you have hypoxemia b/c low arterial pO
HAS to go down b/c must have to equal 760;
2; increase CO2= decrease pO2, and vice versa in resp alkalosis).

Front 16

Ventilation Defects

Back 16

Best example is resp distress syndrome (aka hyaline membrane dz in children). In adults, this is called

Front 17

Adult RDS

Back 17

Adult RDS, and has a ventilation defect. Lost ventilation to the alveoli, but still have perfusion; therefore have created an intrapulmonary shunt.

Front 18

Pt with hypoxemia, given 100% of O2 for 20 minutes, and pO2 did not increase, therefore what has occurred?

Back 18

indicates a SHUNT, massive ventilation defect

Front 19

Perfusion Defects

Back 19

knock off blood flow
Most common cause of a perfusion defect = pulmonary embolus, especially in prolonged flights, with sitting down and not getting up. Stasis in veins of the deep veins, leads to propagation of a clot and 3-5 days later an embolus develops and embolizes. In this case, you have ventilation, but no perfusion;
therefore there is an increase in dead space. If you give 100% O2 for a perfusion defect, pO2 will go UP (way to distinguish vent from perfusion defect), b/c not every single vessel in the lung is not perfused.

Front 20

What do perfusion defects cause?

Back 20

increase in dead space

Front 21

What do ventilation defects cause?

Back 21

intrapulmonary shunts

Front 22

How would you tell the difference between a ventilation and a perfusion defect?

Back 22

Give 100% O2 and see whether the pO2 stays the
same, i.e does not go up (shunt) or increases (increase in dead space).

Front 23

Diffusion Defect

Back 23

Something in the interphase that O2 cannot get through…ie fibrosis.

Front 24

Sarcoidosis

Back 24

(a restrictive lung disease); O2 already have trouble getting through the membrane; with fibrosis it is worse.

Front 25

Pulmonary edema

Back 25

O2 cannot cross; therefore there is a diffusion defect.

Front 26

Four things that cause hypoxemia

Back 26

(resp acidosis, ventilation defects, perfusion
defects, and diffusion defects)

Front 27

Fluid from heart failure

Back 27

Leads to dyspnea, b/c activated the J reflex is initiated (innervated by CN10); activation of CN10, leads to
dyspnea (can’t take a full breath) b/c fluid in interstium of the lung, and the J receptor is irritated