Physiology Flashcards
Internal Respiration
intracellular process which consumes oxygen and produces carbon dioxide
External Respiration
Sequence of events leading to the exchange of oxygen and carbon dioxide between the atmosphere and the cells of the body
4 steps of external respiration
- Ventilation - Moving gas in and out of the lungs. Gas exchange between atmosphere and alveoli (air sacs).
- Gas exchange - between the air in the alveoli and the blood
- Gas transport - in the blood
- Gas exchange - between the blood and the tissues
Boyle’s Law
As the volume of a gas increases, the pressure exerted by the gas decreases.
Inversely proportional
Eg:
Before inspiration - intra-alveolar pressure is equivalent to the atmospheric pressure
During inspiration - Thorax and lungs expand (volume increases) causing the intra-alveolar pressure to become less than the atmospheric pressure (pressure decreases).
Intra-pleural pressure
The pressure within the pleural sac. The pressure exerted outside the lungs within the thoracic cavity.
Falls during inspiration.
Rises during expiration.
Linkage of lungs to thorax
Negative intra-pleural pressure - the below-atmospheric intra-pleural pressure creates a transmural pressure gradient across the lung wall and chest wall. Causes lungs to expand outwards while chest squeezes inwards.
Intra-pleural fluid cohesiveness - water molecules in intra-pleural fluid are attracted to each other and resist being pulled apart. Pleural membranes therefore stick together.
Inspiratory muscles
Diaphragm - major inspiratory muscle. Contraction (flattening) of the diaphragm lowers the diaphragm and thus increases the volume of the thorax vertically, increasing the vertical diameter of the chest.
External Intercostal Muscle - contraction elevates rib cage and causes the sternum to move upwards and outwards. This increases the AP diameter of the chest
Expiratory muscles
Diaphragm - Relaxes (moves up to original position).
External Intercostal Muscles - relaxation causes rib cage to get smaller and return to original position
Chest wall and stretched lungs recoil (volume decreases) causing intra-alveolar pressure to rise (pressure increases) as air is now contained in a smaller volume. Air then leaves the lungs until intra-alveolar pressure = atmospheric pressure
Recoiling of lungs during expiration
Elastic connective tissue - everything bounces back into place
(If elastic properties are lost, air is trapped in the lungs (hyperinflation) as it can’t be pushed out causing difficulties in expiration).
Alveolar surface tension - attraction of water molecules at liquid air interface which produces a force which resists the stretching of lungs. Makes the lungs recoil or collapse
Pulmonary Surfactant
Reduces alveolar surface tension. Smaller alveoli have a higher tendency to collapse and pulmonary surfactant helps to prevent this from happening.
Secreted by type II alveoli and lowers alveolar surface tension by interspersing between the water molecules lining the alveoli.
Premature babies may not have enough and this can result in respiratory distress syndrome
Alveolar Interdependence
Helps to keep the alveoli open.
If an alveolus starts to collapse the surrounding alveoli will stretch then recoil which exerts expanding forces on the collapsing alveoli and forces it to open
Inspiration
Active process, depends on contraction of inspiratory muscles.
Expiration
Passive process, relaxation of inspiratory muscles.
Forces promoting alveoli opening (3)
Pulmonary surfactant
Alveolar interdependence
Transmural pressure gradient (negative intra-pleural pressure)
Forces promoting alveolar closure (2)
Elastic connective tissue
Alveolar surface tension
Major muscles of inspiration
Diaphragm
External Intercostal Muscles
Sternum
Ribcage
Accessory muscles of inspiration
Sternocleidomastoid
Scalenus
Muscles of active expiration
Internal Intercostal Muscles
Abdominal Muscles
Tidal Volume (TV)
Volume of air entering of leaving the lungs in a single breath
Inspiratory Reserve Volume (IRV)
Extra volume of air maximally inspired beyond the tidal volume
Inspiratory Capacity (IC)
Maximum volume of air inspired after a normal quiet expiration (IC=TV+IRV)
Expiratory Reserve Volume (ERV)
Extra volume of air maximally expired beyond the tidal volume
Residual Volume (RV)
Volume of air left in the lungs after a maximal expiration
Functional Residual Capacity (FRC)
Volume of air remaining in the lungs after a normal passive expiration
Vital Capacity (VC)
The maximum volume exhaled after a maximal inspiration. (VC=TV+IRV+ERV)
Total Lung Capacity (TLC)
The maximum volume the lungs can hold (TLC=VC+RV)
Forced Vital Capacity (FVC)
The maximum volume of air forcibly expelled from the lungs following a maximal inspiration
Forced Expiratory Volume in 1 second (FEV1)
The volume of air expelled during the first second of expiration in an FVC determination.
FEV1/FVC ratio
The proportion of FVC that can be expired in one second.
Useful in diagnosis of obstructive and restrictive lung diseases
Obstructive lung disease (FEV1/FVC)
FEV1/FVC ratio = low (<70%)
FEV1 = low
FVC = normal/low
Restrictive lung diseases (FEV1/FVC)
FEV1/FVC ratio = normal (>70%)
FEV1 = low
FVC = low
Airway Resistance
Primary determinant is the radius of the conducting airway. The smaller the radius, the higher the resistance, the lower the air flow.
ie: as resistance increases, air flow decreases.
As resistance increases, there is an increase in airway pressure upstream which helps open the airways by increasing the driving pressure between the alveolus and airway
Dynamic Airway Compression (normal)
Rising intra-pleural pressure during expiration compresses the airway and alveoli.
Pressure applied to alveoli - helps push air out of lungs
Pressure applied to airways - compresses airway
Dynamic Airway Compression (obstructive)
Decreased airway pressure along the airway downstream resulting in airway compression by the rising intra-pleural pressure during active expiration. Airway is more likely to collapse.
Peak Flow Meter
Assesses airway function - estimates speed at which someone can get air out of lungs.
Useful for obstructive lung diseases
Pulmonary Compliance
Measure of effort that goes in to stretching or distending the lungs
Decreased Pulmonary Compliance
More work required to inflate the lungs, lungs are stiffer.
Can cause a restrictive spirometry pattern
eg: pulmonary fibrosis, pulmonary oedema, pneumonia, lung collapse
Increased Pulmonary Compliance
Where elastic recoil of lung is lost.
Patients work harder to get air out of lungs
eg: emphysema, increasing age
Anatomical Dead Space
Inspired air which remains in the airways
Not available for gas exchange.
Pulmonary Ventilation
Volume of air breathed in and out per minute.
PV=RRxTV
Alveolar Ventilation
Volume of air exchanged between atmosphere and alveoli per minute.
Represents the air available for gas exchange with blood.
AV=(TV-ADS)xRR
Ventilation Perfusion (V/Q)
Rate at which gas is passing through the lungs (V) vs the rate at which blood is passing through the lungs (Q)
Low V/Q ratio at the bottom of the lungs - decreased ventilation, increased perfusion
High V/Q ratio at the top of the lungs - increased ventilation, decreased perfusion
Can be a slight variation in normal people
Significant difference in disease
Alveolar Dead Space
Ventilated alveoli which are not adequately perfused.
Decreased O2 causes pulmonary arteries to _____ and systemic arteries to _____ (vice versa)
Vasoconstrict
Vasodilate
Factors influencing the rate of gas exchange across alveolar membrane (4)
Partial pressure gradient
Diffusion coeficient
Surface area
Thickness
Partial Pressure Gradient
Gases move from high to low partial pressure.
Favours the movement of O2 as the partial pressure gradient for CO2 is much smaller.
Most important factor.
Diffusion Coefficient
Solubility.
CO2 diffuses more readily than O2 as CO2 is 20 times more soluble than O2
Surface Area
As the surface area increases, the rate of gas exchange also increases
Thickness of the membrane
The thicker the membrane, the lower the rate of gas exchange.
Inverse proportion
Henry’s Law
As we increase the partial pressure of a gas, the more gas will dissolve in the liquid
O2 transport in the blood (2)
Bound to haemoglobin (majority)
In a dissolved form
Hb structure
2 alpha chains, 2 beta chains
4 haem groups - each haem group reversibly binds one O2 molecule
If all 4 haem groups are bound with O2 then we say the Hb is saturated
Saturation
Depends on PO2. If the PO2 is normal then the Hb will be saturated.
O2 Hb dissociation curve
Sigmoidal shaped curve.
Relationship between the PO2 in the blood and the % of Hb saturation with O2 (SpO2).
If one O2 molecule binds to Hb then this increases the affinity of Hb for O2 (co-operativity).
Oxygen delivery to tissues
Heart - cardiac output delivers blood to the tissues
O2 content of arterial blood - determined by the Hb concentration and the saturation of Hb with O2.
Bohr Effect
Shifts the O2 Hb sigmoid curve to the right.
Increased release of O2 at tissues in the presence of the following conditions:
- Increased PCO2 - aids delivery of O2 to tissues as this decreases the affinity of Hb for O2
- Increased H+ ions - aids delivery of O2 to tissues as Hb affinity to bind to O2 decreases thus giving the O2 up to the tissues
- Increased temperature
Foetal Hb
2 alpha chains, 2 gamma chains
Higher affinity for O2 compared to normal adult Hb.
Thus the O2 Hb sigmoid curve shifts to the left.
Myoglobin (Mb)
Present in skeletal and cardiac muscles.
Produces a hyperbolic curve.
One haem group per Mb molecule thus there is no co-operative binding of O2.
Presence of Mb in the blood represents muscle damage.
CO2 transport in the blood (3)
As bicarbonate (majority)
Dissolved form
As carbamino compounds
CO2 transport in blood - As bicarbonate
CO2 diffuses down it’s partial pressure gradient from the tissue into the blood (RBC’s). In RBC’s:
CO2 reacts with H2O in the presence of CA to from H2CO3.
From H2CO3, HCO3- (bicarbonate) and H+ ions are formed. These products are constantly removed from the process to ensure that the reaction continues to proceed.
CO2 transport in blood - In dissolved form
CO2 is 20 times more soluble than O2.
By Henry’s Law: the higher the partial pressure, the greater the amount of soluble CO2 will be present.
CO2 transport in blood - As carbamino compounds
Formed by combo of CO2 with terminal amine groups in blood proteins.
Deoxygenated Hb can bind more CO2 than oxygenated Hb
Haldane Effect
Removing O2 from tissues (Bohr effect) increases the affinity for CO2 to bind to Hb and increases the affinity of CO2 generated H+.
CO2 dissociation curve
Linear curve.
More CO2 content in the tissues than at arterial blood.
What is the major rhythm generator
The Medulla Oblongata
Pre-Botzinger complex and inspiration
Generates the breathing rhythm
This excites dorsal respiratory group neurones (inspiratory)
Contraction of inspiratory muscles
When firing stops, passive expiration occurs
Pons respiratory centres
Modify the breathing rhythm
- pneumotaxic centre (terminates inspiration)
- apneustic centre (prolongs inspiration)
Active expiration
Ventral respiratory group neurones are excited
This excites muscles of active expiration
Leads to active expiration
CO2 and H+ diffusing across BBB
CO2 diffuses well
H+ doesn’t diffuse well
