Physiology Flashcards
What is internal respiration
Intracellular mechanisms which consume oxygen and produce carbon dioxide
What is external respiration
Sequence of events leading to exchange of oxygen and carbon dioxide between external environment and cells of the body
Steps of external respiration
Ventilation - Gas exchange between atmosphere and alveoli in the lungs
Exchange O2 and CO2 between air in alveoli and blood coming into lungs
Transport O2 and CO2 in blood between lungs and tissues
Exchange O2 and CO2 between blood and tissues
What is ventilation
Mechanical process of moving air between atmosphere and alveolar sacs
How is lesser pressure in lungs compared to atmosphere achieved
During inspiration, lungs move outwards, increasing volume. This leads to a decrease in pressure exerted by the gas.
What forces hold thoracic wall and lungs close
Intrapleural fluid cohesiveness - Water molecules in intrapleural fluid are attracted to each other and resist being pulled apart. Hence, pleural membrane stick
Negative intrapleural pressure - Subatmospheric intrapleural pressure creates a transmural pressure gradient across lung wall and chest wall
What happens to diaphragm during inspiration
It flattens out, increasing volume of thorax vertically
Contraction of which muscles help in inspiration
External intercoastal muscles, contraction lifts rib cage
Which is an active process, in or exspiration
Inspiration
What is Pneumothorax
Air in pleural cavity, abolishes pressure gradient
Pneumothorax symptoms
Chest pain, shortness of breath (dyspnoea)
Hyperresonant percussion note, decreased or absent breath sounds
Normal pressure gradients in the lung
Intraalveolar/Intrapulmonary - 760 mm Hg
Intrapleural/Intrathoracic - 756 mm Hg
What causes lungs to recoil during expiration
Elastic connective tissue in lungs and alveolar surface tension
Which alveoli have a higher tendency to collapse
Smaller alveoli due to LaPlace law
What is pulmonary surfactant
Pulmonary surfactant is a mixture of proteins and lipids secreted by type II alveolar cells
Function of pulmonary surfactant
Pulmonary surfactant is interspersed between water molecules lining the alveoli and helps lower surface tension. This prevents collapse of alveoli
What is respiratory distress syndrome of new born
New borns may not have enough pulmonary surfactant lining the alveoli. The baby has to make very strenuous inspiratory efforts in an attempt to overcome high surface tension and inflate the lungs
Another factor for keeping the alveoli open
Alveolar interdependence
What is alveolar interdependance
Mutual supporting structures, termed interdependence, combine with surfactants tension lowering property provide physical stability. If an alveolus starts to collapse, the surrounding alveoli are stretched and then recoil, exerting expanding forces in the collapsing alveolus to open it.
Major inspiratory muscles
Diaphragm and external intercoastal muscles
Muscles during forceful inspiration
Sternocleiodomastoid, scalenus, pectoral
Muscles of active expiration
Abdominal and internal intercoastal muscles
What is tidal volume (TV)
Volume of air entering or leaving the lungs during a single breath (0.5L)
What is inspiratory reserve volume (IRV)
Extra volume of air that can be inspired over the typical resting tidal volume (3 L)
What is expiratory reserve volume (ERV)
Extra volume of air that can be expired beyond the normal volume of air after resting tidal volume (1 L)
What is residual volume (RV)
Minimum volume of air in the lungs after maximal expiration (1.2 L)
What are the 4 lung volumes
Tidal volume, inspiratory reserve volume, expiratory reserve volume and residual volume
What is inspiratory capacity (IC)
Maximum volume of air that can be inspired at the end of a normal quiet expiration (3.5 L)
IC = IRV + TV
What is functional residual capacity (FRC)
Volume of air in lungs at end of normal passive expiration (2.2 L)
FRC = ERV + RV
What is vital capacity (VC)
Maximum volume of air that can be moved out during a single breath following a maximal inspiration (4.5 L)
VC = TV + IRV + ERV
What is total lung capacity (TLC)
Total volume of air lungs can hold (5.7 L)
TLC = VC + RV
When does residual volume increase
When elastic recoil of lungs is lost, e.g. emphysema
What do volume time curves help determine
FVC - Forced vital capacity which is the maximum volume that can be forcibly expelled from lungs following a maximum inspiration
FEV1 - Forced expiratory volume in 1 s which is volume of air that can be expired in the first second of expiration
Normal FEV1/FVC ratio
FEV1/FVC > 70% is normal
What are dynamic lung volumes
Lung volumes that depend on rate of air flow
FEV1/FVC ratio in obstructive vs restrictive lung disease
Obstructive lung disease, FEV1/FVC < 70%
Restrictive lung disease, FEV1/FVC > 70%, FVC is reduced
What is reduced in restrictive lung disease, FEV1 or FVC
FVC and FEV1 hence ratio of FEV1/FVC is unchanged
However they are both reduced
What part of ANS causes bronchodilation
Sympathetic stimulation
Which is harder, expiration or inspiration when diseased
Expiration
What happens to intrapleural pressure during in and expiration
Intrapleural pressure follows intralveolar pressure
Intrapleural pressure falls during inspiration and rises during expiration
What is dynamic airway compression
Rising pleural pressure during expiration compresses the alveoli and airway. This causes the wheezing sound heard in patients with obstructive disease
When is peak flow useful
To assess obstructive lung disease: Asthma and COPD
What pattern does decreased pulmonary compliance cause in spirometry
Restrictive pattern of lung volume
What can cause increased pulmonary compliance
Is elastic recoil is lost: emphysema. Patients have to work harder to get air out of lungs
Relation between compliance and age
Compliance increases with age
When does work of breathing increase?
Pulmonary compliance is decreased, airway resistance increased, elastic recoil decreased or need to increase ventilation
Formula for pulmonary ventilation
Pulmonary ventilation = Tidal volume * Respiratory rate (
0.5 L * 12 breaths/min = 6 L
What is alveolar ventilation
(Tidal volume - dead space) * Respiratory rate
(0.5 - 0.15) * 12 = 4.2 L
Why is it better to increase depth of breathing than RR
Due to presence of anatomical dead space
What does transfer of gases between body and atmosphere depend on
Ventilation - Rate at which air passes the lungs
Perfusion - Rate at which blood passes the lungs
Which part of lung has maximum blood flow and ventilation
Bottom lung has maximum blood flow whereas top lung has maximum ventilation
What is alveolar dead space
Ventilated alveoli not adequately perfused with blood
What is physiological dead space
Anatomical dead space - Alveolar dead space
Ventilation perfusion match in the lungs
Increase in CO2 due to increased perfusion decreases airway resistance leading to increase airflow
Increase in 02 due to increased ventilation causes pulmonary vasodilation which increases blood flow
Effect of O2 on arterioles
O2 vasodilates pulmonary arterioles whereas it vasoconstricts systemic arterioles
What affects rate of gas exchange across alveolar membrane
Partial pressure gradient of O2 and CO2
Diffusion coefficient for O2 and CO2
Surface area of alveolar membrane
Thickness of alveolar membrane
What is the respiratory exchange ratio (RER)
Ratio between amount of CO2 produced in metabolism and O2 used. RER = 0.8
Equation for partial pressure of oxygen in alveolar air
Alveolar gas equation -
PAO2 = PiO2 - (PaCO2/0.8)
Which gas is more soluble in membranes
CO2 is more soluble than O2. Solubility of gas in membranes is diffusion coefficient. The diffusion coefficient of CO2 is 20 times that of O2.
What does a big gradient between arterial (PaO2) and alveolar oxygen indicate (PAO2)
Problem with gas exchange or left-right shunt in heart
Ficks’s law of diffusion
Amount of gas that moves across a sheet of tissue in unit time is proportional to the area of the sheet but inversely proportional to to it’s thickness
What do walls of alveoli contain
Flattened type 1 alveolar cells. Space inside contains alveolar macrophage whereas type 2 alveolar cells secrete pulmonary surfactant
Major influence on the rate of gas transfer
Partial pressure gradient of O2 and CO2
What is Henry’s law
Amount of gas dissolved in a liquid is proportional to the partial pressure of the gas in equilibrium with the liquid
How is most oxygen transported in the body
Bound to heamoglobin and dissolved oxygen in blood
Oxygen binding to haemoglobin
Each haemoglobin has 4 haem groups. One haem group can bind to one O2 molecule.
What determines oxygen delivery to tissues
Oxygen content of arterial blood and cardiac output
What is oxygen delivery index
DO2I = CaO2 * Cl DO2I = Oxygen content of arterial blood * Cardiac index
What determines oxygen content of blood
CaO2 = 1.34 * Hb * SaO2 CaO2 = 1.34 * Haemoglobin concentration * %Hb saturation with O2
Convert kPa to mmHg
Multiply by 7.5
Binding of one O2 to Hb increase affinity for more?
True, sigmoid shape curve
Significance of steep lower part of sigmoid curve in % Hb saturation vs blood PO2
Peripheral tissues get a lot of oxygen for a small drop in capillary PO2 as easier for O2 to dissociate
What is the Bohr effect
Bohr effect states that Hb O2 binding affinitiy is inversely related to acidity and concentration of CO2. Since more CO2 is released from metabolically active tissue, there is a fall in pH leading to release O2 from Hb
By what effect do metabolically active tissues get more O2
Bohr effect, oxygen dissociation curve shifts right
How is foetal haemoglobin (Hb) different from adult heamoglobin
Foetal hemoglobin has 2 alpha and 2 gamma subunits. This interacts less with 2,3 - bisphosphoglycerate in red blood cells. Hence, HBf has higher affinity for O2 than Hb and O2-Hb dissociation curve shifts to the left
Significance of foetal haemoglobin
Foetal haemoglobin allows O2 transfer from mother to foetus even if PO2 is low
Where is myoglobin present
In skeletal and cardiac muscle
Myoglobin-PO2 dissociation curve
Hyperbolic curve, releases O2 at very low PO2
Presence of myoglobin in blood indicates?
Muscle damage and can damage kidneys eventually
Function of Myoglobin
Provides short term storage of O2 for anaerobic conditions
How is CO2 transported in blood
Dissolved (10), bicarbonate (60) and carbamino (30)
How is bicarbonate formed in blood
CO2 + H2O = H2CO3 = H+ + HCO3-
This is mediated by Carbonic Anhydrase in RBC
What is choride shift
HCO3- forms from CO2 in RBCs. Thus, rise in intracellular bicarbonate leads to bicarbonate export and chloride intake using anion exchanger protein. This ensures the reaction proceeds from CO2 to HCO3- and not the other way round
Haemoglobin has a higher affinity for?
CO2 to form carbamino-haemoglobin
What is the Haldane effect
Removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+
What effects work in synchrony to facilitate O2 liberation and CO2 and CO2 generated H+ at tissues
Bohr effect and Haldane effect
Haldane effect shifts CO2 dissociation curve to?
The right
Haldane effect at lungs
Blood picks up O2 at the lungs, decreasing affinity for CO2 and CO2 generated H+
How do red blood cells exchange CO2 for O2 in alveoli
Closer to the lungs, CO2 concentration falls. This leads to dissociation of H+ from Hb shifting the concentration towards CO2 formation. The decrease in bicarbonate (HCO3_) levels reverses chloride shift with HCO3- moving into RBC. This leads to more formation of CO2 via carbonic anhydrase which is exchanged for O2 due to concentration gradient.
FVC is reserved in Asthma or COPD
Asthma
What is peak expiratory flow rate (PEFR)
Person’s maximum speed of expiration as measured by peak flow meter
PEFR in obstructive vs restrictive
Less in obstructive, unchanged in restrictive
FEV1 in obstructive vs restrictive
Less in obstructive and restrictive
FVC in obstructive vs restrictive
Normal in asthma, reduced in COPD and restrictive
FEV1/FVC in obstructive vs restrictive
< 75% in obstructive, >75% in restrictive
FEV1 response to B2-agonist in obstructive vs restrictive
> 15% in Asthma, <15% in COPD, no response in restrictive
What is bronchial challenge testing
Patient is adminstered methacholine/histamine/mannitol. These are markers of airway hyper-responsiveness and cause bronchoconstriction. A fall of 20% in FEV1 is calculated and compared to healthy individuals
What is bronchial challenge testing used for
To assess allergic or occupational asthma
How can exercise induced asthma be tested for
Exercise testing. Decrease in FEV1 or PEF post exercise is indicative.
Use of full cardiopulmonary exercise test (CPET)
Differentiate cardiac vs respiratory dyspnoea
It monitors heart rate vs oxygen uptake vs ventilatory rate
TCL in emphysema
Increase
TLC in restrictive lung disease
Decreases
What is transfer factor for carbon monoxide (TLCO)
Also called diffusing capacity of lungs for carbon monoxide (DLCO). It measures ability of the lungs to transfer gas from inhaled air to RBC in pulmonary capillaries.
DLCO manoeuvre advantage
Easier for elderly patients to perform the ten second breath holding in DLCO that forced exhalation in spirometry
How can airway resistance be measured
Plethysmography or impulse oscillometry
More sensitive method than spirometry in differentiating small and large airway obstruction
Impulse oscillometry; sound waves are superimposed on normal tidal breathing and disturbances to flow and pressure by external waves are used to calculate resistance to airflow
Exhaled breath nitric oxide (FeNO)
Non-invasive marker of eosinophilic airway inflammation in asthma. Not useful in smokers with COPD as nitric oxide is suppressed by smoking
What do high levels of nitric oxide in asthmatics show
(> 35ppb) Uncontrolled asthmatic inflammation. Used as as adjunct to bronchial challenge
Major respiratory rhythm generator
Medulla oblongata by network of neurons called Pre-Botzinger complex. They display pacemaker activity near the upper end of medulla respiratory control centre
Neural activity leading to inspiration
Rhythm is generated by Pre-Botzinger complex. This excites dorsal respiratory group neurones (inspiratory) which fire in bursts. This firing causes contraction of inspiratory muscles - inspiration. Cessation of firing causes passive expiration
How does active expiration occur
Increase firing of dorsal neruones excites ventral neurones. These activate internal intercoastal muscles, abdominals etc to cause forceful expiration.
Parts of pons respiratory centre
Pneumotaxic center and apneustic center
How is inspiration terminated
Firing of dorsal neurones causes stimulation of the pneumotaxic center. This terminates inspiration.
What is apneusis
Breathing with prolonged inspiratory gasps and brief expiration due to absence of pneumotaxic center in pons.
Function of apneustic center in pons
Apneustic neurones stimulates inspiratory area of medulla prolonging inspiration.
Respiratory rhythm control in the brain
Rhythm is generated in medulla: Pre-Botzinger complex (generates rhythm), dorsal neurones (contraction and inspiration) and ventral neurones (forceful expiration). Rhythm is controlled in the pons: pneumotaxic center (terminates inspiration) and apneustic center (prolongs inspiration)
Respiratory centers are influenced by?
Higher brain centres - cerebral cortex, hypothalamus
Stretch receptors - Hering-Breuer reflex guards against hyperinflation of lungs
Juxtapulmonary (J) receptors - Stimulated by pulmonary capillary congestion and pulmonary oedema; also pulmonary emboli causes rapid, shallow breathing
Joint receptors - Joint movement
Baroreceptors - Decrease blood pressure, increase respiratory rate
Pulmonary stretch receptors are also known as
Hering-Breuer reflex
What contributes to increased ventilation during exercise
Joint receptors that increase breathing due to movement at joints
Factors increasing ventilation during exercise
Reflexes originating from body movement
Adrenaline release, impulse from cerebral cortex, increase in body temperature, accumulation of CO2 and H+ by active muscles
Where is the cough reflex centre
Medulla
Steps in cough reflex
Short intake of breath, closure of larynx, contraction of abdominal muscles (increase intra-alveolar pressure) and opening of larynx and expulsion of air
Chemical control of respiration is by
Blood gas tension especially CO2
Peripheral chemoreceptors that sense tension of O2, CO2 and H+ in the body are situated at
Carotid body (Hering's nerve part of glossopharyngeal) Aortic body (Vagus nerve)
Central chemoreceptors that response to H+ of CSF are
Surface of medulla of brainstem
Only CO2, not H+ or HCO3-, can diffuse across blood-brain barrier. What can this cause?
CO2 and diffuse across the barrier and react with H20 leading to the formation of HCO3- and H+. This increases acidity of blood. This activates central chemoreceptors leading to an increase in depth and rate of inspiration.
What causes hypoxia at high altitudes
Decrease partial pressure of inspired oxygen (PiO2)
Acute response to hypoxia
Hyperventilation and increased cardiac output
Symptoms of acute mountain sickness
Nausea, headache, fatigue, tachycardia, dizziness, sleep disturbance, exhaustion, SOB, unconsciousness
Chronic adaptation to high altitudes hypoxia
Increased RBC production, 2,3-BPG produced within RBC (O2 offloaded more easily into tissues), number of capillaries, number of mitochondria, kidneys conserve acid to decrease arterial pH
Hypoxic drive is via what receptors
Peripheral chemoreceptors
H+ drive of respiration
Via peripheral chemoreceptors. Increase in non-carbonic acid H+ (eg: lactic acid during exercise, diabetic ketoacidosis) leads to hyperventilation in an attempt to remove CO2 from the body. This is imporant in acid-base balance in body
When does arterial oxygen level become important
If PO2 < 8 kPa
Type 1 vs type 2 respiratory failure
Type 1 - Hypoxia
Type 2 - Hypoxia + Hypercarbia
What percentage do we try and keep the percent saturation at
90% sO2 which corresponds to oxygen partial pressure pO2 of 60mmHg
What is percent saturation of oxygen
The amount of haemoglobin bound by oxygen
What can very high oxygen levels cause
High CO2 levels leading to acidosis
Do all COPD patients retain oxygen
No, only 1 in
What chemoreceptors does the body generally use
CO2 chemoreceptors. Normal respiration is driven by amount of CO2 in arteries. Increase in CO2 leads to an increase in respiration
What is the hypoxic drive
A form of respiration in which the body uses oxygen chemoreceptors instead of CO2 chemoreceptors to regulate respiratory cycle
Where do you get low inspired oxygen
High altitudes with low barometric pressure
What is Ondine’s curse
Central hypoventillary synrome (CHS) is a respiratory disorder that results in respiratory arrest during sleep
Shunting and dead space
Perfusion without ventilation is shunting
Ventilation without perfusion is dead space
Is oxygen the therapy for breathlessness
No but it can help maximise potential, target the cause of breathlessness while eliminating hypoxaemia
Oxygen target for type 2 respiratory failure
88 - 92 %
Oxygen target for type 1 respiratory failure
94 - 98 %
Risk factors for type 2 hypercapnic respiratory failure
Moderate or severe COPD, kyphoscoliosis, severe obesity, neuromuscular disease, cystic fibrosis, brochiectasis.
What flow can nasal cannulae be used till
1 to 4 l/min
Variable performance mask flow limit
5 - 15 l/min
Venturi mask flow limit
Upto 250 l/min
