Respiratory Flashcards
Respiration definition
The metabolic respiration of oxygen by cells and the process by which gaseous exchange occurs between an organism and its environment
Upper airway ends at…
larynx
Lower airway starts at….
trachea
Structures of the chest wall in to out
lung, visceral pleura, pleural cavity, parietal pleura, chest wall
What is the pleural cavity filled with?
Intrapleural fluid
What lines the surface of the lung?
visceral pleura
What does the visceral pleura line?
lung
What lines the surface of the chest wall?
parietal pleura
What does the parietal pleura line?
chest wall
What does the high branching of bronchi cause?
Large surface area for gas exchange and therefore greater rate of diffusion and huge number of alveoli respirating
Is the chest wall recoil tendency inwards or outwards?
Outwards
Is the lung elastic recoil tendency inwards or outwards?
Inwards (collapse)
What is “negative pressure”
A suction pressure due to chest wall expansion, increase in pressure of intrapleural fluid and therefore suctions the visceral pleura to expand the lungs
What is “negative pressure”
A suction pressure due to opposite recoil forces causing adherence between the two pleura
Pip
Intrapleural pressure (relative to Patm) = -4mmHg
Patm
Atmospheric pressure at 760mmHg or 1013Pa
Palv
Alveolar pressure (relative to Patm) = 0 (same as atmospheric)
Ptp
Transpulmonary pressure: pressure difference between alveoli and the pleural cavity (force acting to expand the lungs)
Transpulmonary pressure
Force required to expand the lung, determined by the difference between alveolar pressure and elastic recoil of the chest wall
4mmHg (Palv - Pip)
Elastic recoil of chest wall
-4mmHg (Pip - Patm)
Alveolar Dead Space
Some alveoli are insufficiently perfused and don’t contribute to gas exchange
Physiological Dead Space
= anatomical dead space + alveolar dead space
Minute ventilation
total tidal volume into the lungs per minute (Tidal volume x frequency of breathing)
What is the approx volume of dead space?
150mL
What is the approx tidal volume?
500mL
What is the approx volume of alveolar ventilation?
350mL
Alveolar ventilation equation
(tidal volume - dead space) x frequency of breathing
(500mL - 150mL) x 12/min = 4200mL/min
Alveolar ventilation and dead space when breathing deeply
Increased tidal volume and decreased breathing frequency results in increased alveolar ventilation
Alveolar ventilation and dead space when taking short shallow breaths
tidal volume only as much as the dead space, so no matter how many breaths are taken nothing reaches the alveoli
Alveolar ventilation and dead space when breathing through a snorkel
Dead space increases but tidal volume increases to maintain alveolar ventilation
High compliance
Easy to breathe in, hard to breathe out
What happens to breathing if our lungs have low compliance?
Hard to breathe in, easy to breathe out
Emphysema
destruction of alveoli = decreased elastic recoil and increased compliance, hard to breathe out
Pulmonary fibrosis
Restrictive lung disease, stiff alveolar walls = low compliance, hard to breathe in, shallow rapid breaths
Lung compliance and elastic recoil depend on:
Elasticity and surface tension at alveoli
Elastic fibres account for ….% of the elastic recoil
25%
Resistance to stretching
Surface tension accounts for ….% of the elastic recoil
75%
Alveoli want to collapse, but surfactant reduces this surface tension
Surfactant is produced by what type of cells?
Type II pneumocytes
Does surfactant increase or decrease lung compliance?
Increase: allows easy inspiration by not letting alveoli walls stick together
Respiratory distress syndrome
Premature babies cannot synthesise surfactant causing lung collapse and death
Airways resistance is due to:
Friction
- Viscosity of air
- Length of pathway (fixed)
- Diametre/radius (varies)
Resistivity proportional to radius?
r is proportional to 1/r^4
Therefore:
R = 4r
2R = 16r
lateral/radial traction
elastic tissues outside airways linking to surrounding tissue, increasing transpulmonary pressure which pull airways open
chemical factors effecting bronchi radii
blockages by mucus or inflammation
Local inflammators like histamine and leukotrienes causing smooth muscle to contract (bronchoconstriction)
neural factors effecting bronchi radii
stimulation of parasympathetic nerves to airways
Determinants of airway radius
Physical (lateral traction and elastic recoil)
Chemical (inflammation and mucus)
Neural (effecting amount of constriction)
Volume of O2 breathed per minute assuming:
tidal volume = 500mL,
breathing frequency = 8 breaths/min
21% of air is O2
840mL entering the alveoli per minute
concentration of O2 in the arteries
200ml/L
1000mL total in the 5L of blood
amount of O2 passing into capillaries from alveoli
per minute
250mL
840mL into alveoli - 250mL going into blood = 590mL leaving capillaries
(per minute and of the 4000mL breathed in that minute)
could also say 50ml/L
amount of O2 passing from capillaries into tissues
per minute
250mL
1000mL of O2 in arteries, 750mL in veins as 250mL of O2 is put into tissues
could also say 50ml/L
Amount of CO2 breathed out per minute
200mL
conc of CO2 in the arteries
2600mL
520ml/L
conc of CO2 in the veins
2800mL
540ml/L
conc of O2 in the veins
750mL
150ml/L
Respiratory quotient equation and definition
VCO2/VO2
Volume of CO2 breathed out compared to O2 breathed in
Respiratory quotient depends on:
Depends on the food consumed and metabolised, what macronutrient is being broken down
Normal respiratory quotient for a normal mixed diet
RQ
= 200mL of CO2 / 250mL of O2
= 0.8
Respiratory quotient for carbs
0.8
6O2 -> 6CO2
Respiratory quotient for fat
0.7
Boyles Law
Increase in volume = decrease in pressure
P1V1 = P2V2
Daltons Law
Partial pressure of gases
Each individual gas will have its own partial pressure in a space (PO2, PCO2)
Sum of partial pressures of gases
Two partial pressures will add to a total pressure
PO2 in air
Partial pressure of O2 in the atmospheric air is 160mmHg (21% of total 760mmHg)
Partial pressure equation
P = fractional concentration x total pressure
percent of the gas in the total
PAO2 (partial pressure of O2 in the alveoli)
105mmHg
PACO2 (partial pressure of CO2 in the alveoli)
40mmHg
Factors affecting PAO2 (partial pressure of O2 in the alveoli)
Pio2 - How much O2 inspired from the atmosphere
VA - Volume of fresh air getting to alveoli
Vo2 - how much O2 is being used by the body
Factors affecting PACO2 (partial pressure of CO2 in the alveoli)
Pio2 - almost always 0
VA - Volume of fresh air getting to alveoli
Vo2 - how much CO2 is being produced by the body
Henry’s Law
The number of O2 molecules entering the liquid is proportional to the Po2 in the gas
Diffusion of gases in a liquid (Henrys Law explained)
A gas will diffuse into a liquid until an equilibrium is reached
- Rate of diffusion is proportional to the partial pressure
PvO2
40mmHg
PvCO2
46mmHg
PaO2
100mmHg
PaCO2
40mmHg
Factors effecting diffusion
Thickness of alveolar walls
Conc/pressure gradient
Surface area
Diffusion coefficient for the gas
Fick’s Law of diffusion
Rate of diffusion =
(Diffusion constant of gas x surface area x partial pressure of gas) / thickness
Pulmonary Oedema
Fluid leaks out of the pulmonary capillaries into the interstitial space, reducing the rate of O2 diffusion
Interstitial Fibrosis
Thickening of the alveolar wall reducing the rate of O2 diffusion
Emphysema
Destruction of alveolar walls reducing the surface area for diffusion and number of pulmonary capillaries
Ventilation/perfusion mismatching
- lung diseases
- gravity
Emphysema causes blood to go to alveoli that cant undergo gas exchange and bronchitis/asthma causes mucus to block airflow to particular areas of the lung
Gravity causes lower portions of the lung to receive more blood supply
Ventilation/perfusion mismatching
- lung diseases
- gravity
Emphysema causes blood to go to alveoli that cant undergo gas exchange and bronchitis/asthma causes mucus to block airflow to particular areas of the lung
Gravity causes lower portions of the lung to receive more blood supply
Minimising ventilation/perfusion mismatching
(constriction)
Diverts blood and airflow to healthy areas of the lung
Vasoconstriction of blood vessels to portions of the lung that don’t receive airflow
Bronchoconstriction of bronchioles to decrease airflow to areas not receiving blood
Hb dissolves ….mL of O2 for every L of blood
197mL by Hb
3mL dissolved into plasma for 200mL total
Hb conc in blood
150g/L
How to find the O2 content (mL of O2/L of blood) =mL/L
[Hb] x 1.34 x (%saturated/100)
Max amount of O2+Hb in the blood
1.34 x [Hb]
1.34 x 150mL O2/L
= 201mL O2/L of blood
Each gram of Hb can carry …mL of O2
1.34mL
Percent O2 saturation
= the amount of O2 bound to Hb / maximal capacity of Hb to bind O2
= 98%
= percent saturation of arterial blood
Venous blood O2 saturation percent
75%
Advantage of Steepness of the O2-Hb dissociation curve
Large quantities of O2 can be offloaded from Hb with only a small decrease in PO2
Advantages of the plateau of the O2-Hb dissociation curve
It allows Hb to keep a good O2 saturation even if atmospheric pressure (then Palv and Parterial) fell to 60mmHg (still about 90% saturated) like at a high altitude or if you had a lung disease
P50
The affinity of Hb for O2 at which Hb is 50% saturated
Increased affinity of Hb for O2
reduced P50
left shift
Reduced P50
Increased affinity of Hb for O2
left shift
facilitates loading of O2 on to Hb
Decreased affinity of Hb for O2
Increased P50
right shift
Increased P50
Decreased affinity of Hb for O2
right shift
facilitates release of O2 from Hb
Bohr Effect
Increased release of O2 at high CO2/low pH
Increased P50
Rightwards shift
Bohr Effect in lungs vs Haldane in working tissues
When we take O2 into the blood, Hb is supposed to carry O2 and very little CO2, therefore low in H+ and blood has a left shift and can bind O2 stronger
When blood reaches working tissue, it has produced CO2 and H+ and caused the curve to shift to the right, meaning Hb doesn’t bind O2 as strongly /less affinity/ lose saturation and will offload the O2 to the working tissue
Shifting of the curve fits intended purpose for where we need O2 offloading
Movement of O2 from lungs capillaries
O2 moving from atmosphere into alveoli due to the partial pressure gradient between blood and air
O2 dissolves into plasma and Hb soaks up O2 out of solution driving more O2 to dissolve into the plasma
This occurs until the Hb is 98% saturated
Get highest amount of O2 possible in the blood
Movement of O2 from capillaries to working tissue
The blood transports O2 to the working tissue
PP gradient between tissue and blood drives the offloading of O2 from Hb into the plasma then into the tissue
This is facilitated by the lower binding affinity due to environment - low pH high CO2
At the same time Hb is picking up CO2 from tissues
Carbamino haemoglobin (HbCO2)
30% of CO2 bound as HbCO2
Binds to the globin in the RBC
Bicarbonate (HCO3-)
60% of CO2 bound as HCO3-
Conversion of CO2 to HCO3-
Once in RBC (contains carbonic anhydrase) - the CO2 can be converted into bicarbonate and H+
Reaction between CO2 and water creates 2 osmotically active particles (bicarbonate and H+ ions)
H+ is buffered quickly
HCO3- is osmotically active and carries a negative charge
A build up causes the bicarbonate to move out (down conc gradient) into the plasma, and therefore to maintain electroneutrality and osmolarity, a CL- moves into the RBC and pulls water in with it
As blood cell travels around, we would see it swell as it enters the venous circulation and shrink (lost water) in the arterial circulation
Movement of CO2 from blood to lungs
When the CO2 comes back to the alveoli, the processes reverse
CO2 comes out of plasma to alveoli down partial pressure difference drive
Drives the dissociation of CO2 off the globin into the plasma then out of capillary
Also reverses the Cl- shift, bicarbonate HCO3- goes back into the RBC, Cl- and water move out and the bicarbonate is converted back to CO2 and then comes back out of RBC and out of plasma to lungs to be breathed out
CO2 - blood dissociation curve
relationship between the PCO2 of blood and the amount of CO2 in the blood (in all 3 forms)
Haldane Effect
The effect presence of O2 has on CO2 and H+ (opposite of Bohr)
Blood buffers (3)
H+ binding to hemoglobin in RBC
Carbonic acid- bicarbonate buffer
H+ binding to other plasma proteins
DeoxyHb and blood buffering
binds H+ - buffers acid
Respiratory acidosis
Caused by reduced ventilation (not breathing out CO2 and H+) and increased production of H+
Respiratory alkalosis
Caused by increased ventilation (breathing out too much CO2 and H+) and decreased production of H+
How to fix respiratory acidosis
Breathe more
What detects respiratory acidosis and alkalosis
Chemoreceptors
How to fix respiratory alkalosis
Breathe deeper/slower into a paper bad to breathe in more CO2 and bring levels back to normal
Generation of rhythmic breathing (involuntary control) - where in brain?
Medulla oblongata
Neurons in the inspiratory centre also spontaneously discharge to induce muscle contraction to breathe in
Inspiratory and Expiratory neurons are R… I…. to stop firing at the same time
reciprocally inhibitive
both send inhibitory signals to the opposite centres
Forced breathing (voluntary control) - controlled by where in brain? and acts on where?
Cerebral cortex - sends inhibitory signals directly to respiratory muscle’s motor neurons in the spinal cord (bypassing the respiratory centres (in medulla oblongata) that act on the expiratory muscles, inspiratory muscles, and diaphragm
Cerebral cortex takes over for medulla oblongata
Sensory input in involuntary control of breathing (2 receptors)
Mechanoreceptors and chemoreceptors to cause reflex readjustment in response to exercise, irritants and environmental changes
Chemo/Mechanoreceptors communicate to the medulla oblongata via the……
NTS
Nucleus of Tractus Solitarius
Located in periphery
Protective reflexes
Sneezing is caused by irritation of the nasal mucosa and stimulates mechanoreceptors
Coughing is caused by irritation of the larynx and stimulates mechanoreceptors
Peripheral chemoreceptors
Vagus nerve and glossopharyngeal nerve
Hypoxia
decrease in arterial PO2
Hypercapnia
increase in arterial PCO2
Hypoxia, hypercapnia and acidosis all cause an …
increase in ventilation
Peripheral chemoreceptors are stimulated by (3):
Hypoxia
Hypercapnia
Acidosis
Central chemoreceptors are sensitive to:
CO2
The concentration of H+ in the brain ECF
- source of H+ is CO2, which can pass the blood-brain barrier and is then converted into H+ and HCO3- and the H+ is then detected and ventilation increases
Ventilation is not stimulated until you reach an arterial PO2 of …..mmHg
60mmHg
A small increase in arterial PCO2 leads to a large increase in ventilation T/F?
TRUE
Metabolic Alkalosis (increased pH) is caused by:
loss of H+
can be caused by sustained vomiting
