Lung (3) Flashcards
O2 consumption
240 - 280 ml/min
Co2 Production
190 - 220 ml/min
Overall water loss per day from breathing
250 ml/day
Layers of Mucous
- Inner Sol layer (Cilia)
- Outer gel layer
Clearance of particles
- Impaction: Nasal cavity
- Sedimentation: lower airways
- Diffusion: alveoli (macrophage clearance)
Lung metabolic function
- Renin: Angiotensinogen to Ang1
- ACE: Ang1 to Ang 2
- ACE2: Ang2 to Ang 1-7
(viruses use ACE2 to enter)
Dichotomic divisions
- Conducting zone (1-16) : Dead space
- Respiratory zone (17-23) : alveolar space
Physiological Dead space
Sum of anatomical dead space (150ml) and Functional/Alveolar dead space (negligible)
Functional Dead space
Space of the ventilated alveoli that does not participate in gas exchange
Alveolar cells
- Type-1: Squamous for gas exchange
- Type-2: Smaller, produce surfactant
Alveolar Ventilation
4900 ml/min
Dynamic lung volumes
Related to rate at which air flows in/out of lungs
Static lung volumes
Not affected by the rate of air in/out of lungs
Tidal Volume (TV)
500 ml
Amount of air entering/leaving the lungs without extra effort
Inspiratory Reserve Volume (IRV)
3100 ml (1900 ml F)
Max inspiration above tidal volume
Expiratory Reserve Volume (ERV)
1200 ml (800 ml F)
Volume exhaled above tidal volume
Residual Volume (RV)
1200 ml (1000 ml F)
Air remaining in the lungs after complete exhalation
Inspiratory Capacity (IC)
3600ml (2400 ml F)
Largest amount that can be inhaled
(TV+IRV)
Functional Residual Capacity (FRC)
2400 ml (1800 ml F)
Volume after normal expiration
Vital Capacity (VC)
4800 ml (3200 ml F)
Entire volume that can be maximally inhaled and exhaled
Total Lung capacity (TLC)
6000 ml (4200 ml F)
All of the lung volume
(VC + RV)
How do we determine FRC
- Helium Dilution method
- Plethysmography
- Spiroscope
- Clinical spirogram
Helium Dilution method
Closed circuit with spirometer and patient asked to breathe until helium is equilibrated
c1 * v1 = c2 * (v1+v2)
v2 = FRC
Plethysmography
Air tight cabin with shutter, after expiration patient is asked to do a forceful inspiration while shutter is closed. Chest extends and pressure is measured.
Spiroscope
Measures gas flow
V = Q * T
Clinical Spirogram
To measure forced expiratory volume in 1 second
- Ask patient for max inh & ex. (VC)
- Tiffeneau-index: FEV / VC
How much of the VC can be exhaled in 1 second, should be 80% normally
How to determine Dead space
- O2 inh & N2 exh.
- pCO2 measurement
Dead space, O2 inh & N2 exh.
1) Patient inhales pure oxygen
2) During exhalation N2 conc is detected
3) As long as person is exhaling from dead space no N2 is detected
4) If volume where N2 appears is known, V of dead space can be calculated
Relationship bw Alveolar ventilation and pCO2
Inverse hyperbolic
PaCO2
40 mmHg
Effects of ventilation on PaCO2
- Hyperventilation: PaCO2 < 40 mmHg (hypocapnia)
- Hypoventilation: PaCO2 > 40 mmHg (hypercapnia)
What keeps alveoli open in resting position?
Negative pressure of intrapleural space counteracts retraction tendency
Ppl = - 5 cmH2O
Transmural Pressure (Ptm)
Pressure difference bw Pa and Ppl
Ptm = Pa - Ppl
= 0 - (-5) = + 5 cmH2O
Surfactant
- Composed of lipids and proteins
- Reduces surface tension
- Reduces cohesion force of H2O
Surfactant and Work of breathing
Reduced work
- W = P * V
- Surfactant lowers retraction tendency
- Less work needed
Surfactant and Alveoli collapse
- Smaller radius, higher pressure (Laplace law)
- More surfactant in smaller alveoli to reduce pressure by surface tension
Surfactant and Pulmonary Edema
- Retraction tend. in alveoli creates suction force on capillaries causing fluid movement from cap to interstitium. (Pulmonary edema)
- Surfactant reduces retraction tend., less suction force, no edema
Hysteresis
- Difference in curves of expiration and inspiration
- Caused by surfactant, less compliance on inspiration since more surface tension due to smaller alveoli
Compliance
How volume changes as a result of pressure change
C = V / P
- Compliance of the lung is high
Compliance of Lung
Ptm = Pa - Ppl
0.2 L/cmH2O
What other pressure can be measured to tell us Ppl
Pesophegeal
Due to sphincters
Fibrosis
- Less elastic fibers
- Less lung compliance
- Difficult breathing
Emphysema
- Walls of lung more flexible
- Increased lung compliance
- Exhaling will require more effort due to less retraction tendency
Compliance of the Chest
Ptm = Ppl - Pb
= 0.2 L/mmH2O
Compliance of Respiratory system (Lungs + Chest)
Ptm = Pa - Pb
= 0.1 L/mmH2O
Equal Pressure Point (EPP)
When Pa = Ppl
Respiratory membrane layers
1 um thick
1) Surfactant layer
2) Alveolar epithelium
3) Epithelial basement mem.
4) Interstital space
5) Capillary basement layer
6) Capillary endothelium
pO2 Alveolus, Venous, Arterial
- Alveolus: 100 mmHg
- Capillary: 40 mmHg
- Arterial: 95 mmHg
pCO2 Alveolus, Venous, Arterial
- Alveolus: 40 mmHg
- Capillary: 46 mmHg
- Arterial: 40 mmHg
Why is arterial PO2 not 100mmHg but only 95mmHg?
- Mixing with blood from the bronchial system (lung b.s)
- Ventilation-perfusion mismatch due to gravitation
Why does Oxygen have a 10x larger pressure gradient than CO2
O2 has a lower diffusion capacity meaning it needs a very larger pressure gradient to drive the diffusion
2 types of gas exchange
- Diffusion limited gas exchange
- Perfusion limited gas exchange
What law describes solubility of a gas?
Henry’s Law
Total blood volume in Pulmonary circulation
500 ml
(10% of total)
Right ventricle pressure
25 mmHg
Pulmonary Artery pressure
25 / 9
= 14 mmHg
Pulmonary Capillary pressure
10 mmHg
Pulmonary Vein pressure
9 mmHg
Ppl at apex of Lung
More negative compared to base
Apex of Lung R, P, Q
- High resistance
- Low pressure
- Low flow
Base of Lung R, P, Q
- Low resistance
- High pressure
- High flow
Ventilation / Blood flow ratio
- Higher: More ventilation vs flow (apex)
- Lower: More flow vs ventilation (base)
Due to Shunt and Dead space
Physically dissolved O2
3 mlo2/L of blood (100mmHg)
Body uses 250 ml/min
O2 binding capacity of hemoglobin
2.3 mmol/L
How much O2 in hemoglobin at 100% O2 saturation
206 ml O2/L
Effect of CO2 on Hb affinity
- Increase in H+
- Lower O2 affinity
- Right-shift
Effect of Temperature on Hb affinity
- Higher temp denatures bond bw Hb and O2
- Lower O2 affinity
- Right-shift
CO2 tension
24 ml/L (40 mmHg)
(= carbamino form)
Total CO2 in blood
480 ml/L
O2 conc. in Blood Arteries & Veins
- Artery: 200 ml/L
- Vein: 150 ml/L
High HCO3- effect on RBC
RBC swell due to Cl-/HCO3- exchanger
Bohr effect
Effect of CO2 on affinity of Hb to O2
Haldane effect
Effect of O2 on the affinity of Hb for CO2
Types of Hypoxia
- Hypoxic Hypoxia
- Anemic Hypoxia
- Circulatory Hypoxia
- Histotoxic Hypoxia
Hypoxic Hypoxia
Due to low O2 levels
Anemic Hypoxia
Due to less functional Hb
Circulatory Hypoxia
Due to Low perfusion (Q)
(blockage)
Histotoxic Hypoxia
Tissue is unable to use O2
(cyanide poisons)
Upright position
- 0.5 - 1 L of blood acc. in lower
- Decreased venous return
- Decreased CO (heterometric)
- Drop in MABP
Mechanisms to restore BP in upright position
- Decreased Vagal tone
- Increased release of Sympathetic agonists
pO2 and pCO2 in Exercise
DO NOT CHANGE
Effects during Exersise
- Rise in venous pCO2
- Increased blood flow
- AVDO2 increases
- Lower oxygen affinity
- Lower TPR (vasodilation)
Anaerobic Threshold
The level of exercise at which sustained metabolic lactic acidosis begins
What is Max CO?
30 L/min
(can not increase further)
Where is phrenic nerve exit from spinal cord
C4
What controls breathing (4)?
- Respiratory control centers
- Central chemoreceptors
- Peripheral chemoreceptors
- Mechanoreceptors
Respiratory Control Centers + Place + Nuclei
- In medulla
- Ventilatory pattern generator
- Integrator
- Dorsal, Ventral, Pontine Resp. groups
Dorsal respiratory group (DRG)
- Cells in NTS
- Dorsomedial
- Afferent input from CN IX, X
Ventral respiratory group (VRG)
- Ventrolateral
- Nucleus Retrofecialis (exh)
- Nucleus Retroambiguous (inh)
- Nucleus Para-ambiguous (both)
What controls basic rhythm of breathing
VRG
Botzinger and Pre-Botzinger complexes
3 Respiratory centers of brainstem
- Medullary center (V/D/P RG)
- Apneustic center (pontine)
- Pneumotaxic center (pontine)
Apneustic center
Stimulation of prolonged inspiration
Pneumotaxic center
Turns off inspiration to prevent over inflation
(can live without this center)
Pacemaker Theory
Cells of Botzinger complex in VRG
Central Chemoreceptors
- In CSF behind BBB
- Sensitive to pCO2 changes
- CO2 can pass BBB
Peripheral Chemoreceptors
- In Carotid and Aortic bodies
- Sensitive to pO2 drop, pCO2 rise, pH drop, K+ rise
Why does K+ effect any of this?
Higher E.C K+ causes H+ to enter cells to compensate for the loss of positive charge
= Acidic environment inside cells
= Acidosis
Mechanoreceptors in Lungs
- Stretch receptors
- Irritant receptors
- Juxtacapillary receptors
Hering-Breuer Reflex
Initiation of expiration when the Lungs are stretched