Respiratory system Flashcards
Flow equation equation using SA
Flow is proportional to the change in pressure x surface area
Organisation of the respiratory system
Nasal cavity
Pharynx/Larynx
Trachea
Bronchi
Bronchioles
Terminal bronchioles
Respiratory bronchioles
Alveolar ducts
Alveolar sacs
Conduction space =
dead space
Respiratory zone
gas exchange
How is diffusion distance minimized?
By proximity and density of capillaries to the air in the alveolus
Static mechanics of breathing
Generate flow by creating a pressure gradient
Inspiration mechanics
Chest cavity expands in size
Contracting diaphragm, pulls down and flattens out
External intercostal hinge the ribs up and out
Muscles of inspiration
Diaphragm
External intercostal
Accessory muscles:
Scalenes
Sternocleidomastoids
Neck and back muscles
Upper respiratory tract muscles
Expiration mechanics
Normally passive (elastic recoil)
Active expiration
Abdominal muscles - force diaphragm up
Internal intercostals - pull ribs in and down
Neck and back muscles
Pleural membranes
Double layered sac
Allows the lungs to move
Filled with thin layer of fluid (-20um)
Forms connection between lungs and chest wall
Elastic recoil of lungs
Inwards
Elastic recoil of chest wall
Outwards
Intrapleural pressure
Pressure in the pleural cavity
Sub-atmospheric to keep airways open
Will not expand when greater negative pressure is generated
Intra-alveolar pressure
Pressure in the alveolar of the lungs
What happens to intrapulmonary pressure during inspiration?
During inspiration, intrapulmonary (alveolar) pressure decreases as the lung volume increases, causing the pressure to drop below atmospheric pressure (approximately -1 mmHg relative to atmospheric pressure), allowing air to flow into the lungs.
What happens to intrapulmonary pressure during expiration?
During expiration, intrapulmonary (alveolar) pressure increases as the lung volume decreases, causing the pressure to rise above atmospheric pressure (approximately +1 mmHg relative to atmospheric pressure), pushing air out of the lungs.
What changes occur to intrapleural pressure during inspiration?
Intrapleural pressure becomes more negative during inspiration (e.g., from -4 mmHg to -6 mmHg) due to the thoracic cavity expanding more than the lungs do, which helps expand the lungs as the vacuum effect pulls them outward.
What happens to intrapleural pressure during expiration?
Intrapleural pressure becomes less negative during expiration (e.g., from -6 mmHg back to -4 mmHg) as the thoracic cavity decreases in volume, allowing the lungs to recoil and air to be expelled.
What is transpulmonary pressure and how does it change during inspiration?
Transpulmonary pressure is the difference between alveolar pressure and intrapleural pressure (P_tp = P_alv - P_pl). It increases during inspiration as the alveolar pressure decreases more slowly than the intrapleural pressure, facilitating lung expansion.
How does the diaphragm affect pressures in the lungs during inspiration?
During inspiration, the diaphragm contracts and moves downward, increasing thoracic cavity volume, decreasing intrapleural and intrapulmonary pressures, and allowing air to flow into the lungs.
What role does elastic recoil play during expiration?
Elastic recoil of the lungs is primarily responsible for increasing intrapulmonary pressure during passive expiration by reducing lung volume, which helps to push air out of the lungs.
Compliance
How easily the lung expands = change in V/change in P
What happens to lung volume when the pleura is punctured?
When the pleura is punctured, air can enter the pleural space, leading to a pneumothorax. This causes the intrapleural pressure to become less negative or even positive relative to atmospheric pressure, disrupting the vacuum that holds the lung expanded. As a result, the lung on the affected side typically collapses partially or completely, reducing lung volume and compromising respiratory function.
Pressure at function residual capacity
Pressure in the airways is equal to barometric pressure
Minute ventilation
Volume of air shifted in & out of the lungs per minute
Alveolar ventilation
Only the volume of air per minute contact with the respiratory surfaces of the lungs
Breathing mechanics
Movement of air into and out of the lungs occurs when a pressure gradient is created
Airway resistance definition
Change in transpulmonary pressure needed to produce a unit of flow of gas through the airways of the lung
Factors influencing airway resistance
Airflow velocity, the diameter of the airway and lung volume
Total airflow resistance
The sum of all resistances
How does airflow resistance arise?
Friction between gas molecules, & between gas molecules and airway walls
Airway resistance»_space;» viscous tissue resistance
Poiseuille’s Law
Relationship for laminar flow in a cylindrical tube
Rate of flow is due to pressure differences
Resistance is proportional to 1/r^4 viscosity and length
Facts of airway resistance
Doubling the length of an airway doubles the airway resistance
Halving the radius increases the resistance sixteen-fold
Total airway resistance trends
Intermediate sized airways contribute most of the total resistance
Total cross-sectional area increases towards the periphery, whereas total airflow is constant
Flow is more laminar in small airways
Anatomic deadspace
Conducting portion of airways
Physiological deadspace
Deadspace in respiratory zone
Saline-filled lungs
Lungs inflated with saline have a much larger compliance
Air-filled lungs
Show the effects of elastic elements and surface tension
Require larger pressures during inflation (hysteresis)
Law of La Place
Transmural pressure is directly proportional to surface tension & inversely proportional to radius
Therefore deflating pressure are greater in smaller sphere
Type 1 cells
Gas exchange
Type II pneumocytes
Secrete surfactant
Many elastic fibres
Many capillaries
Surfactant
In the liquid lining alveoli reduces its surface tension along the flat and curved surfaces, reducing, resistance to inflation
Forces that promote lung collapse
Natural elasticity of lungs
Lung surface tension
Pleural pressure (from the weight of the lung)
Forces that favour lung expansion
Natural elasticity of the chest wall
Surfactant produced by type 2 pneumocytes
Transpulmonary pressure (the difference between the intrapulmonary and intrapleural pressures)
Flow Volume curves - flow and effort at different lung volumes
Flow is effort dependent at high lung volumes
Effort independent at low lung volumes
Work
Proportional to change in P x change in V
Inspiration works against…
- Compliance, or elastic work that required to expand the lung against elastic forces (recoil)
- Tissue resistance work, i.e that required to overcome the viscosity of the lung and chest wall structures.
- Airway resistance work, ie that required to move air through the airways into the lungs
Work of breathing has 2 components: Elastic and frictional
0AECDO - Insp work done overcoming elastic works
ABCEA - Insp. work done overcoming airway + tissue resistance
AECFA - Work done on expiration to overcome airway +tissue resistance
Rapid shallow breathing
decreases elastic work but increases frictional (viscous) work
Slow deep breathing
decreases frictional work but increases elastic work
Respiratory control is an example of what?
Negative feedback system
Control of breathing
Influences from higher centres influence cycle of expiration & inspiration
Reflexes from lungs,airways, CV system, muscles & joints, skin, arterial and central chemoreceptors affect this which affects the muscles of breathing
Exercise ventilatory response
Increases Vt, Fr, Ve
Whereas PaO2 remains normal unit very high exercise level
Partial pressure definition
Measure of the concentration of the individual components in a mixture of gases
Dalton’s Law of Partial Pressure
Total pressure of a gas is simply the sum of the individual partial pressures (Pi) of each constituent gas
Air we breathe %
Inhale
O2 - 20.71
CO2 - 0.04
H2O - 1.25
Exhaled
O2 - 14.6%
CO2 - 4.0%
H2O - 5.9%
O2 cascade pathway
- Oxygen exchange at alveolar-capillary interface
- Oxygen transport
- Oxygen exchange at cells
- CO2 exchange at cells
- CO2 transport
- CO2 exchange at alveolar-capillary interface
Why does the partial pressure of O2 decrease from inspired air to mixed venous blood?
Inspired air mixes with dead space air decreasing pressure and O2 is consumed with CO2 pressure increasing as its produced
Why are we interested in alveolar gas composition
Inspired air contains virtually no CO2. Therefore, the CO2 contained in the alveoli must come from metabolism
However, VCO2 depends not only on how fast O2 is utilized, but also on the kind of fuel metabolised.
Metabolism of carbohydrates
Produces 1 molecule of CO2 for every O2 consumed
Respiratory exchange ratio
VCO2/VO2
In steady state R = Respiratory Quotient (RQ)
RQ is measured at the tissue/blood compartment
If Ve is equal to Vi
If R is equal to 1 during exercise (i.e carbohydrate)
Typical R
R is more typically 0.8 i.e. 10 molecules of O2 consumed for 8 molecules of CO2 produced
Oxygen uptake
Oxygen consumption per kilogram of body weight
Most relevant measure of the cardiorespiratory system
Maximal oxygen uptake is the…
Maximal aerobic capacity, is the maximum rate of oxygen consumption possible by an individual
Fick Principle
Oxygen consumption is (arterial oxygen content - venous oxygen content) x cardiac output
What does the hatched area represent at rest?
Hatched area represents the amount of O2 transported in the blood and used in cellular metabolims
Perfect lung
PAO2 would totally equilibrate to the oxygen in the pulmonary veins and be equal to the PaO2
Initial drop in partial pressure
Inspired air & air in the upper airway is due to humidification
Smaller drop in PO2 occurs between alveoli & arterial blood
Well ventilated lung
PACO2 is approximately PaCO2
Rest changes in alveolar gas is…
Small since VT/FRC is small
Changes during hyper and hypoventilation
PACO2 decreases in hyperventilation so does PaCO2
PACO2 increases in hypoventilation so does PaCO2
Ventilation/Perfusion inequalities from alveoli to arteries
Alveoli, capillary and arteries experiences a further decrease between PAO2 and PaO2
Ventilation & Perfusion
Ventilation in alveoli is matched to perfusion through pulmonary capillaries
Ventilation-perfusion ratio
V/Q ration takes in account regional variations in VA and capillary perfusion
Blood Flow (perfusion) standing
When standing, gravitational effects mean that blood flow decreases from the base to the apex of lungs.
Blood flow at apex
Low arterial pressure in the pulmonary circulation tends to collapse the smaller vessels. Increase in resistance and decreased blood vessels
Blood flow at base
At base of lungs, higher pressure distends. Lower resistance and increased blood flow
Ventilation standing
When standing gravitation effects mean that ventilation decreases from the base to the apex of the lung, but to a much lesser extent than the affect on blood flow
Pulmonary hypoxic vasoconstriction
Decreased tissue PO2 around under ventilated alveoli constricts their arterioles, diverting blood to better ventilated alveoli.
Hypoxemia
Abnormally low levels of oxygen (partial pressure, content or % saturation) in arterial blood
Diagnosed by large A-a difference in PO2
Forms of O2 carried in the blood
As a gas in simple solution in the plasma i.e physically dissolved
- 3mL L-1
As oxy-haemoglobin in erythrocytes (RBCs)
-1.34mL O2 g-1 Hb
Haemoglobin hugely increase O2 carrying capacity of blood
Which form contributes to PaO2
Physically dissolved O2
Oxygen is chemically bound to haemoglobin (& therefore no longer physically dissolved) so exerts no partial pressure, however, the partial pressure of oxygen determines the oxygen that is bound to Hb (% saturation)
Henrys Law
The amount dissolved is proportional to the partial pressure of the gas, and its solubility
c =ōP
Haemoglobin
Respiratory pigments increase the O2-carrying capacity of the blood
Increase the O2-carrying capacity of the blood 65-70x
Molecule made up of 2a &2b globin subunits each with 1 haem at the centre. Haem contains iron atom that combines with O2
Hb carries up to 200mL O2 Lblood-1
Oxyhaemoglobin
O2 bound due to inc. PO2 and dec PCO2 and is relaxed binding structure
Deoxyhaemoglobin
2,3-DPG to haemoglobin and is caused by increase PCO2, inc 2,3-DPG and dec PO2. It is a tight binding structure and is increased in blood by hypoxia
Oxygen content of blood
O2 content is the sum of the O2 combined with Hb plus the O2 that is physically dissolved
Increased affinity for HbO2
Decreased temp
Decrease PCO2
Decreased 2,3-DPG
Increased pH
Decreased affinity for HbO2
Increased temp
Increased PCO2
Increased 2,3-DPG
Decreased pH
Haldane effect: Lungs
Binding of Hb with O2 tends to displace CO2 from the blood
Bohr effect: Tissues
Increase in CO2 causes O2 to be displaced from Hb
CO2 excretion
From the blood:
CO2 in the lungs
HCO3- in the kidneys
From the body:
Exhalation
Micturition (urine production)
Relationship between CO2 and H2O
Converted into H2CO3 by carbonic anhydrase which is highly concentrated within RBCs and into H+ + HCO3-. These reactions are reversible and obey the laws of mass action
Transport of CO2 in blood
7% dissolved CO2 in simple solution
23% protein-bound as HbCO2
70% chemically-modified as HCO3-
Total CO2 stored in the body
Blood contains only a small part of total CO2 stored in the body - 5L
Much of it is dissolved in fat or stored in bone which total CO2 stored - 100L
O2 stores
Minute
1.5L in blood + alveoli + myoglobin
Control of breathing by autonomic NS
Parasympathetic slows breathing rate
Sympathetic increases breathing rate
Chemoreceptors
Peripheral - located in carotid and aortic bodies. Primarily detect low arterial O2 levels, but can also respond to increased CO2 and H+.
Central - sense pH changes in CNS caused by alteration in PaCO2
What is the chief determinant of respiratory drive under normal conditions
PaCO2
Physiological stresses with immersion of water
Body experiences:
increased pressure or hyperbarism, pressure increases 1 atm for every 10m depth
Effects air-filled cavities of the body (Boyle’s Law)
Reduced gravitational effects. Central shift in blood volume. Increased diuresis, Na+ and K+ excretion
Reduced ambient temperature - hypothermia
Immersion up to the neck (Respiratory)
Positive pressured by surrounding water on the chest wall
Decrease in FRV
Decrease ERV
Slight decrease in VC
IRV increases
Small decrease in RV
Pressure gradient from top to lung base
Increase in work of breathing (60%)
Immersion up to Neck: Cardiovascular & Renal
Increased venous return, RA pressure, SV & CO
- Increased abdominal pressure
- Decreased peripheral pooling of blood due to decrease gravitational effects
- Vasoconstriction due to reduced temperature
Increased intra-thoracic blood volume
- ADH suppression
- Increased ANP release
Boyles Law
P1V1 = P2V2
Breath-hold diving (voluntary)
Limited by oxygen stores
Full inspiration yields - 1L O2 in lungs
Hypoxia alone does not trigger ventilation
Changes associated with the “dive reflex”
Changes in alveolar gas exchange during ascent and descent
Breath-hold diving up to 10m - ascent and descent
During descent - compression of abdomen. PAO2 maintained, although VO2 decreases
Transfer of CO2 from the blood into the alveoli is compromised during descent, resulting in significant retention of CO2 in the blood
During ascent, theres expansion of abdomen & reversal of pressure. The transfer of O2 from the alveoli to the blood will then be compromised as PAO2 decreased.
Free diving adaptations with training
Bradycardia
Vasoconstriction of peripheral vessels
Splenic contraction ^ RBC
Plasma accumulates in pulmonary circulation, reducing VR & preventing collapse of lungs at > 30m
Shallow water blackout (Latent hypoxia)
Loss of consciousness at shallow depth
Occurs within 5m of surface where expanding lungs literally suck oxygen from the divers blood
Blackout occurs quickly, victims die without any idea of their impending death
Pre dive hyperventilation
Increases risk of SWB by increases PaCO2 level at the start of the dive
Barotrauma
Rapid ascent from a dive may cause barotrauma
Most serious is pulmonary barotrauma
If a lung/alveoli is obstructed during ascent, then expansion can cause pneumothorax
Rapid ascent can lead to gas bubbles in the joints
Decompression sickness
During descent increased partial pressure of inert gases causes greater uptake of dissolved gases by the tissues
Diver needs to ascend slowly to allow gases dissolved in tissues to pass back into the lungs (Arterial gas embolism)
Nitrogen narcosis
Nitrogen is poorly soluble in water and blood, but much more soluble in lipids, and hence cell membranes, and importantly, neurological tissues.
At depth, N2 acts as an anesthetic
Hypobaric exposure
Decrease in air around you
Changes in PB
As altitude increases, barometric pressure (PB) decreases
Fewer molecules of O2 per unit volume of inspired air
A fall in PAO2 is therefore predicted by the alveolar gas equation
Compensatory responses to altitude hypoxia - chemoreceptors
Ventilation is stimulated by peripheral chemoreceptors sensitive to PaO2
Result of increased volume of alveolar gas is to decrease PACO2, allowing an increase in PAO2
However, the decline in PaCO2 reduces stimulation of central chemoreceptors, counteracting the initial hypoxic response
Changes in PO2 along the pulmonary capillary at rest (high altitude)
At high altitude, change in PO2 between alveolar and mixed venous is less, therefore reducing the pressure gradient for diffusion.
Acute response to very high altitude
Physiological responses
Hyperventilation and consequent lowering of PaCO2
Increased heart rate
Increased plasma urinary catecholamines
Increased cardiac output
Effects on cerebral function (loss of consciousness with severe hypoxia)
Alterations to regional blood flow in lungs due to selective hypoxic vasoconstriction.
Time course of altitude effects: Initial
Hyperventilation & hypocapnia followed by reflex inhibition of ventilation
Time course of altitude effects: Acclimatization
Achieved through reduced HCO3- reabsorption & conserving H+
Result is compensated respiratory alkalosis
High altitude adaptation/acclimatisation
Primary disturbance
Decrease PaO2
Environmental hypoxia
Leads to increased pulmonary ventilation
Leads in increased PaO2 and decreased PaCO2
Causes secondary disturbance increasing blood pH
Increased renal excretion of bicarbonate lowering blood pH
Hypoxia leads to…
Increased pulmonary ventilation leading to increased PaO2, increasing organ oxygen delivery
Increased CO - increased blood flow increasing organ oxygen delivery
Increased blood vessel density - increased blood flow increasing organ oxygen delivery
Increased renal sodium and water excretion - increased RBC increasing organ oxygen delivery
How do we increase body’s oxygen level (organ changes)
Lungs - increase breathing
Heart - Increased cardiac output
At the organs - Increase blood flow, increase capillary density
Blood - Red blood cells count
Increased cerebral blood flow
May contribute to headache and AMS
What improves arterial blood O2, oxygen delivery, aerobic exercise performance?
Increasing:
Erythropoiesis
Muscle capillary density
Haemoglobin
Haemoconcentration
High altitude adaptations of blood, muscles, respiratory system
Blood: Increased haemoglobin-oxygen affinity and plasma volume
Muscles: Decreased mitochondrial volume density and muscle cross sectional area. Increased muscle capillary density and increase myoglobin concentration and decreased oxygen consumption during exercise
Respiratory : Increased ventilation efficiency and lung size
Acute mountain sickness
Depends on:
Speed of ascent
Altitude reached
Physical exertion
Individual factors
Can develop into life-threatening high altitude cerebral edema and high altitude pulmonary edema
High altitude cerebral edema
Excessive increase in brain blood flow
Hypoxic exposure - pathology
Causes the blood vessels inside the lungs to constrict which leads to pulmonary hypertension
Too much pressure inside the lungs leads to fluid build up, which further exacerbates hypoxemia.
Treatment of acute mountain sickness
Acetazolamide (Diamox)
Increases diuretic effects, CO2 retention and ventilation
Dexamethasone
Decreases AMS severity
Calcium channel blockers
Decreases pulmonary vasoconstriction
Chronic mountain syndrome symptoms
Deep purplish color of lips and gums
Clubbing of the fingers
Marked cyanosis in nail beds and palms of the hands
Vein dilatation of lower limb
Chronic mountain sickness - hypoventilation
Hypoventilation decreases SaO2. Leads to chronic hypoxia - induces pulmonary hypertension then right heart then left heart failure
Development of acute mountain sickness can lead to
Can develop into life-threatening high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE)
Cerebral edema
High altitude cerebral edema is due to excessive increase in brain blood flow
Chronic high-altitude maladaptation
Increased red blood cell count - excessive erythrocytosis
Severe hypoxemia
Alveolar ventilation equation
Alveolar Ventilation=(Tidal Volume−Dead Space Volume)×Respiratory Rate
Result of high altitude acclimatization is called?
Respiratory alkalosis
