Respiratory Physiology Lecture 4

Front 1

What is P50?

Back 1

The index of hemoglobin's affinity for oxygen.

or the PO2 required to produce a saturation if 50%.

For conditions of normal systemic arterial blood (37 C, PCO2 40 mmHg, pH 7.4) the P50 is about 27mmHg.

Front 2

What is a left or right shift in the Oxyhemoglobin Dissociation Curve?

Back 2

A right shift indicates a decreased affinity of hemoglobin to oxygen requiring a higher PO2 to achieve P50. (Normal at the tissues)

A left shift indicates an increased affinity of hemoglobin to oxygen requiring a lower PO2 to achieve P50. (Normal in the Lungs)

Front 3

Back 3

Front 4

What is the Bohr Effect?

Back 4

When elevated CO2 and or H+ decreases Oxy-Hemoglobin Affinity.

Front 5

What conditions can cause a left shift?

Back 5

Decreased PCO2

Decreased H+

Decreased Temperature

Increased pH

Carbon Monoxide

Front 6

What conditions can cause a Right Shift?

Back 6

Increased PCO2

Increased H+

Increased Temperature

Increased 2,3 Diphosphorgycerate (2,3DPG)

Front 7

What factors can lead to an increase in 2,3 Diphosphoglycerate?

Back 7

Increase in Epinephrine, Growth Hormone, & Thyroid Hormone

Alkalosis

Chronic Tissue Hypoxia

Blood stored in a blood bank for as little as 1 Wk has a decrease in 2,3 DPG

Front 8

How is Hb F different than Hb A?

Back 8

Molecular difference in structure between Hb Fetal & Hb Adult causes a change in the Oxy-hemoglobin dissociation curve shifting it to the Left (Higher affinity).

Front 9

What is formed when Carbon Monoxide binds with Hemoglobin? What affect does it have on PO2? Does it have an effect on respiration rate?

Back 9

It forms carboxyhemoglobin (has 240 times affinity).

It has no effect on PO2 as that is determine by O2 dissolved in the blood.

No, Chemoreceptors in the blood monitor PO2 not total O2 concentrations.

Front 10

What are the symptoms of Carbon Monoxide poisoning and the corresponding levels?

Back 10

Front 11

How is CO2 transported in the plasma at the tissues? (4 ways and percentages)

Back 11

10% is dissolve in the plasma as CO2.

70% In Hb metabolized with H2O to into HCO3 and H+ then diffuses out of Hb into plasma Cl- shifts into Hb cell.

20% reversibly bound to Hb as Carbaminohemoglobin.

Small amt dissolve in Plasma converts to HCO3

Front 12

What happens to the CO2 when Blood reaches Pulmonary Capillaries?

Back 12

All processes are reversed caused by PCO2 gradients.

Front 13

How is the CO2 disassociation curve different than the O2 disassociation curve?

Back 13

CO2 disassociation curve is almost linear.

Front 14

What is the Haldane Effect?

Back 14

The more desaturated the hemoglobin is of oxygen the better able is that blood to carry CO2.

Front 15

What is a normal V/Q ratio

Back 15

4:5 or 0.8

Front 16

How are PO2 and PCO2 related through alveolar ventilation?

Back 16

Inversely

Front 17

How is Hyperventilation defined?

How is Hypoventilation defined?

Back 17

PACO2< 40 mmHg Increasing V/Q ratio produces Higher PAO2 and lower PACO2

PACO2>40 mmHg Decreasing V/Q ratio produces Lower PAO2 and Higher PACO2

Front 18

What happens with High V/Q?

Back 18

Over-ventilation relative to the level of perfusion.

PO2 increases (not sign-flat portion of curve)

PCO2 decreases (sign-linear curve)

pH increased

Front 19

What is physiologic dead space?

Back 19

Alveolar dead space+Anatomic dead space

Front 20

What happens with low V/Q?

Back 20

Area of the lung is under-ventilated relative to the amount of blood passing through the pulmonary capillaries.

Decreased PO2 (potentially lg, curve dependent)

Increased PCO2 (Large increase linear curve)

Decreased pH

Pulmonary Shunt (one type of)

Front 21

What are the two types of Pulmonary shunts?

Back 21

Anatomic-Portion of CO returns to heart without passing through pulmonary capillaries

Intrapulmonary-Blood that passes through pulmonary capillaries without obtaining normal PO2 or PCO2.

Front 22

What are normal and abnormal sources of anatomic shunts?

Back 22

Normal-Veins in the heart that drain straight into the ventricles and some veins in the lungs.

Abnormal-congenital defects

Will not be corrected by increasing FIO2

Front 23

What are the two types of intrapulmonary shunts?

Back 23

Shunt like-Low V/Q, alveoli with diffusion defect (increased diffusion distance)-unable to reach equilibrium due to not enough time(Increasing FIO2 would improve diffusion)

Absolute-Blood passes around alveoli that have are not ventilated (absolutely no gas exchange) like fluid filled or atelectasis(increasing FIO2 would not help)

Front 24

Back 24

Front 25

Are the lungs dependent on nerves and hormones to optimize the V/Q ratio?

Back 25

No-PCO2 and PO2 affect brochial and Vascular smooth muscles to affect V/Q ratio.

Front 26

What happens in a lung region with Low V/Q?

Back 26

Front 27

What happens in lung region with High V/Q?

Back 27

Front 28

What causes regional differences in V/Q ratio in healthy upright adults at resting Cardiac Output, and how does it happen?

Back 28

Gravity

Ventilation- Base better ventilated, Apex worse due to the effects of the compliance curve.

Perfusion-Bases best perfused, Apex least perfused related to gravity effect on low pressure/low resistance circuit.

Some of apex may not be perfused at all at rest.

Front 29

Does gravity have a greater effect on ventilation or perfusion?

Back 29

Affects Blood Flow Most

Front 30

Can regions of High V/Q compensate for regions of Low V/Q with respect to defending arterial O2 levels, what about CO2 levels?

Back 30

No- Not much extra O2 is picked up in High V/Q area related to the shape of disassociation curve.

Maybe-If relatively equal volumes of blood from low and high V/Q areas & if the difference in PCO2 levels were equal.