Lung Physiology

Tidal volume

Inspiratory Reserve Volume

IRV

Residual volume

Anatomic and Physiologic

Anatomic dead space

Physiologic dead space

Physiologic

Lung diseases with V/Q defects

Vd= Vt X (PaC02 - PeC02)/ PaC02
PaC02 = alveolar gas = PC02 of arterial
PeC02 = PC02 of expired air

Minute ventilation

Alveolar ventilation

Inspiratory capacity

Functional Residual volume

FRC

Forced vital capacity

FVC

TLC

TLC

FRC and TLC

B/C it includes residual volume, so cannot be measured by spirometry

FEV1

80% of FVC

FEV1 is reduced more than FVC so

FEV1/FVC is DECDREASED

FEV1 and FVC are reduced so

FEV1/FVC are normal or increased

Asthma, can't get air out

Fibrosis, can't get air in

TLC= decreased
Residual volume = decreased
FEV1= decreased
FEV1/FVC = Normal to increased
Pa02 = Decreased
A-a gradient = Increased

TLC= increased
Residual volume = increased
FEV1= decreased
FEV1/FVC = decreased
Pa02 = Decreased
A-a gradient = Increased

Hypoxemia of pulmonary origin

Normal

Less likely to collapse b/c collapsing pressure is directly proportional to surface tension and inversely proportional to size

of increased pressure and tendency to collapse

Type II pneumocytes

DPPC, dipalmitoyl phosphatidycholine

Lecithin:sphingomyelin ratio > 2:1

the medium-sized bronchi

The smallest airways are connected in parallel

contraction or relaxation of bronchial smooth muscle

Parasympathetic stimulation
Irritants
Slow-reacting substance of anaphylaxis ASTHMA

Sympathetic stimulation
Sympathetic agonist

B2 receptor activation

dilates via B2 stimulation

Obstructive lung disease

Decreased FEV1
Decreased FVC
Decreased FEV1/FVC ratio

Air trapping, a barrel shaped chest
Increased FRC

Emphysema

They have mild hypoxemia with normal ventilation, normal pCO2
(normocapnia)

Bronchitis

B/c they have severe hypoxemia w/ Cyanosis
No alveolar ventilation, hypercapnia, increased pCO2
Right vent. Failure and systemic edema

A combination of bronchitis and emphysema

Obstructive lung disease with increased lung compliance and impaired expiration

It's increased

FE2+

Methemoglobin

α2β2

α2γ2

Tighter O2 affinity
Less 2,3 DPG affinity

Amount of O2 bound to hemoglobin

Total O2 in blood: bound to heme and dissolved O2

= (O2-binding capacity x %sat) + dissolved O2

X axis = PO2
Y axis = % sat.

40 mm Hg

50%, aka P50, 2 out 4 heme groups are saturated

Positive cooperativity, B/c of a change in affinity for hemoglobin with each O2 added.

Occur b/c of Decreased O2 affinity
Increase in pCO2
Decrease in pH
Increase in Temp
Increase in 2,3 DPG

P50 is increased; O2 unloading occurs

Decreasing the affinity for hemoglobin for O2 and facilitating the unloading of O2 in tissues

Rightward sift
By binding B-chains of deoxyhemoglobin and decreasing the affinity for heme O2

Increases synthesis of 2,3 DPG which binds hemoglobin and Facilitates O2 unlaoding

Left-ward shift, b/c 250-times binding affinity
CO decrease the O2 content by binding direct to O2 sites

A left-ward shift, Increase in pH

The P50 is decreased, unloading of O2 into tissues is difficult

Decreased in arterial pO2

Pao2-Pa2, difference between alveolar and arterial pO2

Can distinguish if hypoxemia is from the lungs or outside the lungs

<10mm Hg, b/c O2 equilibrates between alveolar gas and arterial gas

O2 is not equilibrating so;
Diffusion defect
V/Q defect
Right-to-left shunt

decreased O2 delivery to the tissues.

= Cardiac output X O2 content of blood

Hg concentration
O2-binding capacity
% saturation

Decrease CO
Decrease O2-binding capacity
Decreased arterial pO2

1) Hypoventilation

2)High altitude

Distinguish by high altitude b/c low air/ barometric pressure:

1.Lung tissue abnormalities: pulmonary fibrosis, silicosis, asbestosis, tuberculosis
2. Pluera problems: Pneumonthorax, Pleural Effusion
3. Neuromuscular: Polio, Myasthenia Gravis

1. Obstructed airway lumen; chronic bronchitis, edema, or food aspiration
2. Asthma, constricted of airway muscles
3. Outside of airway; emphysema = lung tissue destruction

Hypersensitivity reaction of the bronchioles; produces edema and bronchospasm

60 to 75 mm Hg

80 -100 mm Hg pCO2

60 to 75 mm Hg

80 -100 mm Hg pCO2

3 forms
1: Dissolved CO2, free in solution
2: Carbaminohemoglobin, CO2 bound to heme
3: HCO3-, major form ~ 90%

CO2 combines with H2O to form H2CO3-
H2CO3- dissociates into H+ + HCO3-

HCO3- is exchanged for CL- ion
HCO3- is then transferred in the blood, the major form of CO2

H+ is buffered by deoxyhemoglobin

HCO3- enters the RBC
Cl- is kicked out in exchange
H+ recombines to form H2CO3
H2CO3 decomposes to CO2 and H2O
CO2 is expired

Lower, eg pulmonary artery is 15mm Hg and aortic is 100mm hg

Much lower

Right ventricle

CO of the left ventricle

B/c the resistance in pulmonary circulation is low

the lowest

Alveolar>Arterial>venule

Zone 2
Arterial>Alveolar>Venule

Zone 3
Arterial pressure>Venula>Alveolar

By the difference in pressures between Arterial and Alveolar

By the difference in pressures between Arterial and Venous, like normal vascular beds.

Vasoconstriction, opposite of vascular beds, this redirects blood away from poorly ventilated areas

arterial PO2, b/c of mixture of venous blood

Have the pt breathe 100% O2 and measure the dilution of oxygenated to non-oxgenated

Left ot right b/c of higher pressures on the left

Congenital abnormalities eg patent ductus arteriousus
Traumatic Injury

Left to right shunts
PO2 will be elevated on the right b.c of mixture of blood

PO2 is Higher,
PCO2 is lower
more gas exchange in the upper

PO2 is lower
PCO2 is higher
less gas exchange

Zero, V/Q is zero, physiologic shunt

PO2 and PCO2 will approach their mixed values of blood, 40 mm Hg and 46 mm Hg respectively

It's increased

PE means no blood flow to the lung, V/Q is infinite, called dead space

PO2 and PCO2 will approach the values of inspired air
150 mm Hg and 0 mm Hg

Medullary respiratory center

Dorsal Medullary respiratory center

Reticular formation

Vagus and glossopharyngeal nerves

Relays peripheral chemoreceptors and mechanoreceptors in the lungs

The glossopharyngeal nerve relays peripheral information

Via phrenic to the diaphragm

EXPIRATION

During exercise, when expiration is an active process

PONS

Stimulates inspiration, produces a deep and prolonged inspiratory gasp

Located in the upper pons

Inhibits inspiration, regulates inspiratory volume and respiratory rate

Provides voluntary control; hyperventilate or hypoventilate

pH

Causes an increase in breathing rate

H+ ion acts directly

CO2 diffuses b/c it's lipid soluble
In the CSF, CO2 combines with H2O to produce H+ and HCO3-

Carotid and Aortic Bodies

at the bifurication of the common carotid

Below the aortic arch

1: A decrease in pO2
2:An increase in pCO2

Changes in H+ ions

Increased, hyperventilation

B/c of increase in arterial H+ ions and pH decrease

PO2 decrease to < 60mm Hg

in the smooth muscle of airways

Reflex decrease in breathing frequency

Reflexive decrease in breathing frequency when the lung stretch receptors are stimulated

In the alveolar walls, close to the capillaries

They cause rapid and shallow breathing, when pulmonary capillaries become engorged with blood, ie LHF

By matching the ventilation rate

No change in PO2 or PCO2 in moderate
Matching of ventilation rate

Venous PCO2 increases b/c of muscle CO2 production

PO2 is decreased so arterial PO2 is decreased in the high climate:
1:Hypoxemia stimulates the peripheral chemoreceptors
2:Hypoxemia stimulates EPO
3: 2,3 DPG concentrations are increased
4: Pulmonary vasoconstriction

Help in dumping O2 to the tissues

Causes a right shift, 2,3 DPG binds with greater affinity and facilitates O2 unloading

Increase RBC production, which increases Hg, increased O2 carrying capacity, increased O2 content

increase ventilation rate, hyperventilation
Which produces respiratory alkalosis

Acetasolamide

Right ventricle hypertrophy
B/c an increase in pulmonary arterial pressure causes an increased work load of right side