Physiology Lectures 23 - Circ. + Resp. Integrated

Front 1

What is the Fick Principle?

Back 1

Pulmonary Blood Flow equals Cardiac Output which equals the O2 Consumed divided by the difference between Arterial and Venous O2 content:
CO = VO2/(CaO2-CvO2)

Front 2

What factors constrict pulmonary vessels but dilate peripheral blood vessels?

Back 2

Hypoxia - the most important!!
Hypercapnia (CO2)
Anaphyllaxis
Histamine

Front 3

What factors can cause pulmonary hypertension?

Back 3

Hypoxemia causes pulmonary vasoconstriction (Rx: low flow O2, inhaled NO)
Loss of alveolar capillaries (emphysema)
Elevated left atrial pressure (mitral stenosis, left heart failure)
Pulmonary emboli

Front 4

What affect does gravity, inspiration, and expiration have on pulmonary blood flow?

Back 4

When standing, some parts of the lung are above the heart, making the top lobes barely perfused by the heart. Upon inspiration, blood flow through the pulmonary capillaries experiences increased resistance due to the expanding alveoli. This resistance is lowered during expiration.

Front 5

Describe Zone 1 perfusion.

Back 5

Pa <PA >Pv
The arterial pressure is less than the alveolar pressure so that the alveoli are not perfused.
This is only seen in patients with low pulmonary perfusion pressures (e.g. shock, or in patients being ventilated with PEEP)

Front 6

Describe Zone 2 perfusion

Back 6

Pa > PA > Pv
Arterial pressure exceeds the alveolar pressure, but the alveolar pressure is still greater than the venous pressure. Here blood flow will be intermittent as alveoli pressure fluctuates during inspiration (higher PA) and expiration (lower PA).
This is present in the normal lung.

Front 7

Describe Zone 3 perfusion

Back 7

Pa > PA < PV
Arterial pressure is greater than the alveolar pressure and the alveolar pressure is less than venous pressure. Here now alveoli are always perfused.This is present in the normal lung.

Front 8

How does gravity affect ventilation in the lung?

Back 8

Although gravity does not affect air pressure in the airways and alveoli, it does affect the flow of air, because the weight of the lungs compresses the airways and compresses the lower airways more than the upper ones. Thus, when you breathe in starting from residual volume more of the air flows into the upper lobes. However, when you breathe in starting from FRC--as one normally does-- most of this air goes to the lower lobes. As a consquence, the lower lobes are better ventilated than the upper lobes during normal breathing.

Front 9

How to measure Ventilation/Perfusion ratios?

Back 9

Inject radioactive Xenon w/ saline into the blood, use Geiger counter to measure perfusion of lungs in different lobes.
Similarly, ventilation can be measured by inhaling radioactive Xenon gas and measuring its distribution in the lobes using a Geiger counter.

Front 10

What would the PO2, PCO2, and pH be in blood collected from pulmonary veins draining the upper and lower lung lobes?

Back 10

Upper lobe: pH high, PCO2 low, PO2 high

Lower lobe: pH low, PCO2 high, PO2 low

This is because in the upper lobes, Va/Qc >1, but in the lower lobes, Va/Qc < 1

Front 11

What happens the ventilation/perfusion ratio if the left bronchus is obstructed by a mucus plug? How does the lung compensate, and by what mechanism?

Back 11

Ventilation/perfusion ratio will be close to 0 --> right-to-left shunting (i.e. same effect as right ventricle deoxy blood --> left ventricle).

Compensation: low O2 --> local arteriolar constriction to divert venous blood to ventilated units. This occurs by the following mechanism: Low PAO2 -> K+channel closes in arteriolar smooth muscle -> depolarization -> Volt.Gated Ca2+ channels open -> Ca2+ influx, arteriolar constriction

Front 12

What happens to the ventilation/perfusion ratio if the rifht pulmonary artery is obstructed by a thrombus?

Back 12

Va/Qc ratio will be >>>1, close to infinity. This increases physiological dead space.
To compensate, the alveolar duct muscle constricts and diverts air towards healthy units. The alveolar duct constriction is mediated by the lower PACO2 as well as the release of histamine.

Front 13

What is the Bohr Equation, and what does it tell you?

Back 13

Vd/Vt = (PaCO2 - PeCO2)/PaCO2
This tells you the fraction of the tidal volume that is dead space. PeCO2 = expired CO2, which if is equal to the PaCO2 (i.e. not diluted by dead air volume), means there is no dead space.

Front 14

How do you measure physiological dead space?

Back 14

Via the Bohr Equation!
Vd/Vt = (PaCO2 - PeCO2)/ PaCO2

Front 15

What is the distribution of alveoli with high or low Va/Qc's in a normal person, a person with a bronchial obstruction, a person with a PE, or a person with COPD?

Back 15

Normal: Most alveoli have a Va/Qc close to 1.
Bronchial obstruction: The alveoli of the obstructed lung have a low Va/Qc, whereas those in the unobstructed lung have a slightly higher Va/Qc.
PE: Alveoli have a Va/Qc higher than 1 in the obstructed lung, but alveoli in the unobstructed lung have a Va/Qc lower than 1.
COPD: Alveoli are widely distributed with an average Va/Qc of 1.

Front 16

What are some sign of hypoxemia?

Back 16

Nervous, irritable, forgetful
Cyanosis
tachycardia
Increase BP
30-40 Breaths/min

Front 17

What are some signs of Hypercapnia?

Back 17

Drowsy, yawning
Flushed skin

Front 18

What neural dysfunctions can cause Ventilatory Failure?

Back 18

Stroke, heroin OD, Ondine's curse, crib death

Front 19

What chest wall dysfunctions can cause ventilatory failure?

Back 19

Kyphoscoliosis, Obesity

Front 20

What neuromuscular dysfunction can cause ventilatory failure?

Back 20

Polio, Guillain-Barre, Curare, Myasthenia gravis, Exhaustion

Front 21

What upper airway obstruction can cause Ventilatory failure?

Back 21

Laryngospasm, Diphteria, Foreign Body

Front 22

How to get use airflow/ventilation to get PACO2? How to get PAO2?

Back 22

The PACO2 will be inversely proportional to the airflow, so that if an obstruction reduces the flow by a half, the PACO2 will double, etc.

PAO2 requires the alveolar gas equation.

Front 23

How to estimate the PaO2 of mixed blood when given two values of the CaO2?

Back 23

Use Hb-O2 binding curve: Take the average of the CaO2s, and look at the corresponding PaO2 on the Hb Saturation curve.

Front 24

What is the Haldane effect?

Back 24

The effect of oxygen displacing CO2 from the RBC's when venous blood travels through the lungs to become oxygenated.

Front 25

What is the distribution of CO2 in the body?

Back 25

90% of the CO2 produced by cells enters RBC's in the capillaries, and the remaining 10% is transported to the lungs in plasma. One-half of the plasma-CO2 is in physical combination with the plasma, the other half is bound to plasma proteins by forming caramino compounds.

Front 26

What happens to CO2 as it enters the RBCs?

Back 26

Of the CO2 enter RBC's, 2/3rds is rapidly hydrated via carbonic anhydrase to carbonic acid, which dissociates into bicarbonate and hydrogen ions. The bicarbonate ions exchange with Cl ions via a Band III membrane protein. Thus 2/3 of the CO2 is carried as bicarbonate ions in plasma to the lungs. The extra H+ ions are buffered by the imidazole groups of histidine in the hemoglobin molecule-- H+ binding decreases Hb-O2 affinity (Bohr effect).
25% of the CO2 entering RBCs forms carbamino groups with hemoglobin.

Front 27

Why is the hematocrit of venous blood a little greater than the hematocrit of arterial blood?

Back 27

During CO2 uptake, RBC's swell as water moves in, because the number of osmotically active particles have increased as a result of chloride entry. For this reason, the hematocrit of venous blood is a little greater than the hematocrit of arterial blood.

Front 28

What is the Henderson-Hasselbach Equation?

Back 28

pH = pK + log[HCO3-]/PaCO2*0.03
Normally [HCO3]=24, PaCO2=40, thus pH = 7.4

Front 29

What is a PaCO2 40 Isobar?

Back 29

It is the graph of [HCO3] vs pH while the PaCO2 is kept constant at 40mmHg. Bicarbonate and pH decline when blood is infused with acid; and bicarb and pH rise when blood is infused with base.

Front 30

What happens to the pH and [HCO3] when you increase the PaCO2 isobar (e.g. from 40 to 60mmHg)?

Back 30

Bicarbonate increases, pH decreases

Front 31

Describe the normal buffer lines on a [HCO3] vs pH plot

Back 31

When altering the PaCO2 concentrations, all the points will fall on a line-- the so-called normal buffer line. The slope of this line is related to the buffering capacity of blood, that is, the ability of the imidazole groups of the histidine residues of Hgb to accept H+ ions. This depends on [Hb] and [O2].
NOTE: Slope of buffer line steeper above pH 7.4

Front 32

What is the normal range of ABG's for pH, PaCO2, and HCO3?

Back 32

pH 7.36 - 7.44
PaCO2 36-77 mmHg
HCO3 22-26 meq/L

Front 33

Describe how the [HCO3] vs pH graph changes with the introduction of a fixed acid into the circulation.

Back 33

Initially, the pH will lower along a isobar line. Then, the body will compensate by breathing off CO2, so that the isobar will change to one with a lower PaCO2, lower [HCO3], and higher (almost normal) pH.

Front 34

What change is expected with a decrease in HCO3 concentration by 1meq/L?

Back 34

A corresponding decrease in PaCO2 by 1.2mmHg.

I.e. 24 --> 14meq/L
will change PaCO2 40 --> 28mmHg

Front 35

What change is expected with an increase in HCO3 concentration by 1 meq/L?

Back 35

A corresponding increase in PaCO2 by 0.7 mmHg.

24 --> 34 meq/L will change PaCO2 = 40 --> 47 mmHg

Front 36

What happens to the blood gases of a person who is vomiting?

Back 36

Metabolic Acidosis. Excess bicarbonate enters the circulation. ABGs will move up the PaCO2 isobar (of 40 initially). At this elevated pH and HCO3 state, the body will respond by diminishing ventilation so that ABGs move along buffer line to higher isobar (lower pH)

Front 37

What happens to the ABG's of a person who begins hypoventilating because of emphysema?

Back 37

Respiratory Acidosis. Hypoventilation leads to increase in PaCO2 --> increase isobar along normal buffer line. This results in a low pH, high bicarb ABG. This is acute respiratory acidosis. To compensate, the body retains bicarb, moving the ABGs up along the PaCO2 buffer line to a higher pH. This is chronic respiratory acidosis.

Front 38

What changes in ABG's are expected for an increase in PaCO2 by 10mmHg in an acute vs chronic resp. acidosis patient?

Back 38

Acute: ^ PaCO2 by 10mmHg --> ^ HCO3 by 1meq/L.

Chronic: ^ PaCO2 by 10mmHg --> ^ HCO3 by 3.5meq/L

Front 39

What changes in ABG's are expected if a person hyperventilates because of an altitude change?

Back 39

ABGs will change by moving down the normal buffer line to a lower PaCO2 isobar. This the point her PaCO2 will be les and her pH will be high. She will be in acute respiratory alkalosis. Now her kidneys, being perfused with blood low in CO2, retain and make less bicarbonate than usual and as a result, her ABGs gradually move down the low PaCO2 isobar towards a normal pH, but low HCO3-- this is chronic respiratory alkalosis.

Front 40

What changes in HCO3 is expected in a decreased in PaCO2 of 10mmHg?

Back 40

Acute Respiratory Alkalosis:
Decrease of HCO3 by 2meq/L

Chronic Respiratory Alkalosis:
Decrease of 4meq/L