Respiratory System Flashcards
What is the function of respiration?
Gas exchange
*CO2 produced through oxidative processes in body and exhaled by lungs
Supply of O2 to the cells
What is the respiratory tract?
Order and functions
mouth and nose –> lungs
1. nasal septum + nasal turbinates: clean air of big dust particles, moistens and warms up air
2. Pharynx: comon for air and food
3. Larynx (vocal cords)
Periphery of lungs (share chest cavity with heart, great vessels and esophagus):
4. Trachea
5. 2 main bronchi
6. Each divides into lobar and segmental bronchi (2x2):
Right main bronchus»_space; 3 lobar bronchi (right lung has 3 lobes)
Left main bronchus»_space; 2 lobar bronchi (left lung only has 2 lobes)
7. Divides into smaller branches until terminal bronchioles (smallest airway without alveoli)
What are the 2 sections of the respiration airways?
Conducting zone (Mouth/nose –> Trachea, Bronchi, Bronchioles, terminal bronchioles)
Functions:
- Defense against bactriral infections/foreigh particles
- Warm and moisten inhaled air
- Sound/speech w/ vocal cords
- Regulation of air flow (smooth muscles contract to increase resistance, not desired, seen in asthma)
- Don’t contribute to gas exchange so contribute to ANATOMICAL DEAD SPACE
Respiratory zone (respiratory bonchioles (have alveoli opening in their lumen), Alveolar ducts, Alveolar sacs)
Functions:
- Gas exchange (approx. 300 millions alveoli, each associated with 1000 capillaries)
What is the pleura and the pleural space?
Pleural = thin sheet, parietal pleural attached to thoracic cage and visceral pleura attached to lungs surface, for 2 pleural sacs (1/lung)
Pressure in pleural space always negative bc 2 sides pulling to extend it
(positive pressure is when push to compress)
What is the difference between bronchi and bronchioles?
Bronchi have cartilage around them
What is an acinus?
What is lobule?
The smallest physiological unit of the lungs:
one bunch of repspiratory bronchioles and their alveolar ducts and sacs
Lobule = group of acinus attached to one terminal bronchiole
Blood Supply to the lungs?
(2 circulations)
Pulmonary circulation:
comes from right ventricle by pulmonary artery (deoxygenated blood) and gas is exchanged via capillaries, then leaves via pulmonary veins
Bronchial circulation:
Part of systemic circulation, oxygenated blood comes via bonchial arteries from aorata supply air walls with O2. (very small amount), leaves via pulmonary veins with oxygenated blood, makes no big difference bc so little
What are the Alveolar cell types?
Epithalial type 1 and 2 cells:
form epithelial layer sealed together by tight junction, type 1 = regular, type 2 produce pulmonary surfactant (decreases surface tension of alveoli)
Endothelial cells:
constitute walls of pulmonary capillaries (very thin for better diffusion)
Alveolar macrophages:
remove foreign particles in alveoli that may have escaped mucociliary defense system
*Between alveoli and capillaries, a bit of intersitial fluid (Interstitium)
What is surface tension? (formula)
What are the roles of pulmonary surfactant?
Pressure inside alveoli like in soap bubble makes alveoli want to collapse
(more impotant in smaller alveoli)
P = 4T/r
Surfactant produced by endothelial cells of type 2 reduces it bc if not, smaller alveoli would empty to bigger and bigger and we couldn’t breathe
Functions of pulmonary surfactant:
- Equilibrates pressure (prevents pressure in small alveoli to exceed pressure in larger alveoli by reducing surface pressure more in smaller alveoli)
- Reduce overall surface tension
What are the inspiratory respiratory muscles?
Principals:
- External intercostals (when contract, elevate the ribs)
- Parasternal intercartilageous muscles (elevate ribs)
- Diaphragm (domes descend to increase volume, increase longitudinal dimension of chest + elevates lower ribs)
**Diaphragm splits thorax from abdominal section
Diaphragm innervated by nerves from cervical segments 3, 4, 5
Neck muscles may assist (accessory)
- Sternocleidomastoid (elevate sternum)
- Scalenus (anterior, middle, posterior) (elevate and fix upper ribs)
*Innervation of these muscles also appears is asthma and other disorders
What the expiratory respiratory muscles?
Quiet breathing:
- Expiration results from passive recoil of lungs (brain tells respiratory muscles to relax)
Active breathing (exercise, higher level of ventilation)
- Intercostal extercostal, except parasternal intercartilageous (depress ribs)
Abdominal muscles (depress lower ribs, compress abdominal content, pull diaphragm up):
- Rectus abdominis
- External oblique
- Transversus abdominis
*Forcing would lead to decrease of cardiac output bc bc increase in pressure in thoracic cage
*Important in coughing, singing, talking, vomiting
What is a Spirometry?
What is a Spirometer used to measure?
Measuring lung volume
*Cannot measure functional residual capacity (air left in lungs forced expiration), total lung capacity (max air the lungs can contain) and residual volume (air left after forced expiration)
What are the following definitions?
Tidal volume (TV)
Inspiratory reserve volume (IRV)
Epiratory reserve volume (ERV)
Residual volume (RV)
Vital capacity (VC)
Inspiratory capacity (IC)
Function residual capacity (FRC)
Total lung capacity (TLC)
Tidal volume (TV) = volume of quiet breathing - 500 mL
Inspiratory reserve volume (IRV) = volume of air inpired more than TV with forced inspiration - 3000mL
Epiratory reserve volume (ERV) = volume of air exhaled more than TV with forced expiration - 1200mL
Residual volume (RV) = volume remaining in lungs after max expiration (mixes with fresh air w/ next inspiration) - 1200mL
Vital capacity (VC) = Amount of air exhaled with max effort after max inspiration (strength of thoracic cage) - 4700mL
Inspiratory capacity (IC) = max amount of air inhaled starting from normal (TV + IRV) - 3500mL
Function residual capacity (FRC) = Amount air in lungs after tidal respiation (RV + ERV) - 2400mL
Total lung capacity (TLC) = Max amount of air lungs can contain (RV + VC) - 5900mL
How can FRC be measured ?
FRC = functional residual capacity = Amount air in lungs after tidal respiation
Not by spirometer bc this air is in the lungs
put He in air inhaled and measure concentration
C1V1 = C2(V1 + FRC)
What is minute ventilation vc Alveolar ventilation ?
Ve (minute ventilation) = Vt(tidal volume) x f = mL/min
But not all air inhaled into lungs participates in gas exchange, some aire remains in anatomical dead space –> 150 mL(/respiration) in adult
Va (alveolar ventilation = amount of air participating in gas exchange/minute) = (Ve - 150mL) x f
What is the alveolar dead space?
Some alveoli get reduced or blocked blood flow so no gas exchange
Pathological dead space = Physiological dead space + Alveolar dead space
What are the normal pressure in Normal Alveolar Ventilation?
Partial pressures in air
Partial pressures in alveoli
In different section of circulation
VA keeps PaCO2 at cste level
Air: PO2 = 160 mmHg, PCO2 = 0.3 mmHg
Alveoli: PO2 = 105 mmHg, PCO2 = 40 mmHg (coming from circulation)
Pulmonary Arteries: PO2 = 40 mmHg, PCO2 = 46 mmHg
Pulmonary veins: PO2 = 100 mmHg, PCO2 = 40 mmHg
Systemic arteries PO2 = 100 mmHg, PCO2 = 40 mmHg
Systemic veins = PO2 = 40 mmHg, PCO2 = 46 mmHg
O2 oxy = 100 mmHg, O2 deoxy = 40 mmHg
CO2 oxy = 40 mmHg, CO2 deoxy = 46mmHg
*bigger change is O2 than CO2!!!
What is Alveolar hyperventilation?
What is Alveolar hypoventilation?
Hyperventilation
When + O2 supplied and + CO2 removed than metabolic consumption
Result: PAO2 ↑ PACO2↓
*Does not consider exercise bc in exercise, metabolic rate increases also
Hypoventilation
Result: PAO2 ↓ PACO2↑
*Can occur w/ disorders ex: chronic obstructive lung disease, damage to respiratory muscles, CNS depressed, pneumothorax
*If breathe air with low PO2 (high altitude) → decrease in PO2, but no change in PCO2 bc not more production
*If change in metabolic rate, both affected
What is the diffusion rate proportional to?
How does EDEMA affect diffusion rate?
- Surface of exchange
- 1/Thickness
- partial pressure gradient
*For gas to diffuse, has to be soluble with liquid, CO2 20x more soluble than O2 so diffuses 20x faster
As blood goes through capillaries, diffusion rate decreases bc gradient decreases bc some diffusion has already been made
- Since O2 has way bigger gradient, diffuses faster but CO2 = more soluble so takes approx same time to diffuse O2 and CO2
EDEMA increase thickness in intersitial space, thicker membrane = less efficient diffusion
How long is the transit time through the pulmonary capillaries?
transit time = 0.75 sec
In normal lungs, diffusion is completed within 1/3 fo the red blood cell transit time
Someone with EDEMA would still have time to diffuse but is it deos exercise and blood flow increases, may not have time
How is vascular resistance different in systemic circulation than in pulmonary circulation?
Flow = pressure/resistance
pressure drop in pulmonary ciruclation = 10 mm Hg
pressure drop in systemic ciruclation = 100 mm Hg
So pulmonary resistance = 1/10 of systemic (to have same flow)
+ high complicance (too offer less resistance) of pulmonary system to accept cardiac output
What is accommodation of pulmonary blood?
Drugs, Nitric Oxide, reflex vasoconstriction
Pulmonary circulation has capacity to accomodate 2, 3 fold increase in cardiac output with little of pulmonary arterial pressure: Increase cross sectional area!!
Recruitment (cardiac vessels may open)
Distension (blood vessels already perfused increase their caliber)
Drugs causing contraction of smooth muscles → increase resistance of pulmonary arteries (Serotonin, histamine, norepinephrine)
Drugs causing smooth muscles to relax → decrease pulmonary vascular resistance (acetylcholine, isoproteranol)
Reflex vasoconstriction in regions of poor oxygenation
Nitric oxide produced by endothelial cells relax smooth muscles → vasodilatation
What are the effects of gravity on pulmonary blood?
Pulmonary blood flow differs with body posture and is affected by gravity
Uneven distribution of blood flow from top to bottom of the lungs
Top:
Alveolar pressure > Pulmonary arterial pressure so capillaries are compressed when low arterial pressure or positive ventilation
*for young healthy subjects, doesn’t happen bc arterial pressure in high enough
Middle:
Pulmonary arterial pressure > alveolar pressure > venous pressure so flow depends on difference between arterial and alveolar pressure, bc if not enough pressure lung will collapse shortly later
Bottom:
pulmonary arterial pressure > venous pressure > alveolar pressure, flow depends on artery-venous difference
*Measure with radioactive xenon
How does gravity affect the distribution of ventilation?
For upright, at rest subject
SLINKY
alveoli at the top of the lungs are more open than bottom ones at rest so during breathing, bottom ones can have more new air so preferrential ventilation for bottom part of lungs
*measured with inhaled radioactive Xenon (instead of infused in blood)
What is ventilation-prefusion ratio?
It’s the ratio between ventilation and perfusion of blood in capillaries depending on hydrostatic pressure/gravity effects
Ventilation increases slowly from top to bottom
blood flow increases rapidly so ventilation-perfusion ratio abnormally high at the top and much lower at bottom
*Normal lung not perfect!
If there was no gravity, we would have a much better ventilation-perfusion ratio
*For subject lying vs standing it is top to bottom in the other sens
How do we calculate O2 consumption/minute?
VO2
It’s O2 taken up by blood in the lungs in 1 minute.
CaO2 = O2 entering the lungs (from artery)
CvO2 = O2 leaving the lungs via the veins (measured w/ catheter)
VO2 = Q(CaO2 - CvO2)
Q = pulmonary blood flow = VO2/(CaO2-CvO2)
What does Henry’s Law state?
gas molecules dissolved in liquid proportional to partial pressure of the gas above the liquid.
Amount of Gas carried by blood directly proportional to the partial pressure of the gas
O2 relatively insoluble in H2O → 0.3 volume % when equilibrated with PO2 of 100 mmHg
BUT consumption much greater → at rest = 300mL O2/min
How are the O2 needs fufilled as O2 is not soluble in H2O?
O2 bound to Hemoglobin
Hb = 1/3 weight of RBC (147g O2/L blood)
Hb = 4 subunits, each has Heme (w/ F++ ion) bound to a globin, every Heme can bind 1 O2 (4/molecule)
cooperative binding → binding of O2 to first subunit increases affinity for second, etc.
O2 bound to Hb = 19.5 volume %
+ 0.3 vol.% dissloved → O2 in arterial blood 20 vol.%
O2 bound to Hb does NOT contribute to PO2 of blood, but PO2 of plasma determiens amount of O2 that combines with Hb
Hb + O2 → HbO2 is REVERSIBLE
O2 dissociation curve
Determines amount of O2 bound to Hb for given partial pressure:
- flat at high alveolar levels of PO2
- steep at low peripheral tissue levels of PO2, bc at low levels, Hb desaturates to let O2 get used
So PO2 has to drop to 60 mmHg for HbO2 drops significantly
Important bc in peripheral tissues, if minor drop in PO2, a lot of Hb desaturates: HbO2 → Hb + O2
*If O2 needed, Hb desaturates, if not, transports it other place where needed
*Peripheral tissues can only use dissolved O2 so needs to desaturate
At rest, Hb still 75% saturated at end of tissue capillaries, protective measure bc when need more, its there (ex: exercise)
So total amount of O2 in blood determined by Hb concentration (ex: anemia)
What is the role of myoglobin in the muscles?
intracellular carrier to facilitate diffusion of oxygen throughout muscle cell (similar to Hb)
Ressembles Hb but only binds 1 O2 at the time Follows hyperbolic shape, only release O2 at very low PO2 in the msucles
What is the Bohr Effect?
Shift of HbO2 dissociation curve to the RIGHT when blood CO2, Temperature of blood pH decreases
ex: when exercice (produce acid, generate heat, increase CO2) → additional amount of O2 released for higher PO2 to prevent from going down to much
Little effect on amount over 80 mm Hg still
Same effect seen when 2, 3-DPG (end product of RBC metabolism) increases → chronic hypoxia
*↓ T˚, ↓ CO2, ↑ acid have opposit effect 9shift to left)
