Respiratory physiology Flashcards
Surface tension issues
- Causes collapsing of alveoli
- Creates unequal ventilation
- If alveoli collapse it pulls water into alveoli that are collapsing, resulting pulmonary oedema
Surfactant composition
90% phospholipid
10% protein
Explain phospholipids, what is their composition?
2 dipalmitoyl tails- hydrophobic
1 phosphatidylcholine head- hydrophilic
Proteins that make up surfactant
Albumin
IgA
Apoproteins: SpA, SpB, SpC, SpD
What is the name of CO2 when its bound to certain amino acids in the haemoglobin
Carbaminohaemoglobin (20%)
Deoxyhaemoglobin is said to be in the
T state
What is deoxygenated oxygen bound to?
Little 02
A lot of CO2
H+
2,3BPG (Helps stabilise deoxy HB)
Describe affinity for deoxy Hb
low O2 affinity
high CO2 affinity
high H+ affinity
stabilised by 2,3BPG
What is the chloride shift?
HCO3- is coming into/out of red blood cells, and Cl- is coming out/in
It depends if it’s inspired/expired respiration
Necessary so there isn’t a build-up of charge in red blood cell
How is carbonic acid made in red blood cells?
Due to chloride shift HCO3- is entering red blood cells. The oxygen bound Hb doesn’t want the H+protons and therefore the positive and negative charged ions attract and form carbonic acid.
What happens to the carbonic acid in the red blood cells during expired respiration?
It dissociates into H20 + CO2.
CO2 then diffuses out of blood cells -> capillary-> alveoli
Carbaminohaemoglobin what happens when O2 binds to Haemoglobin
Diffuses out into alveoli (High CO2 conc -> Low CO2 conc)
Where is carbonic anhydrase found? What is the effect of this on expired respiration
Red blood cells
This means that red blood cells would produce more CO2 which is leaving the cell and diffusing to alveoli in comparison to the blood plasma which is doing it at a much slower rate due to the absence of this enzyme
What is the Haldane effect?
red blood cell has:
Low affinity for CO2, H+, temp and 2,3 BGP
High affinity for O2
decrease in O2 disassociation
What structures contribute to the respiratory pump during normal quiet breathing?
Bones (ribs and sternum), muscles (diaphragm and intercostals), pleura, and nerves.
What structures make up the conducting airways?
Nose, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles.
What is the function of the conducting airways?
To filter, warm, humidify and conduct air to the lungs.
What is respiratory epithelium?
Pseudo-stratified, columnar, ciliated, interspersed with goblet cells.
Where is the resistance greatest in the airway?
In the trachea - the trachea is longer (length adds resistance), and there is only one of it (the combined cross-sectional area is the least, which increases resistance).
What equation can be used to demonstrate resistance of an airway?
Poiseuille’s law: R = 8ƞl / πr^4.
ƞ = viscosity, l = length
Briefly describe quiet inspiration.
Inspiration is an active process.
- The external intercostal muscles and diaphragm contract (By phrenic nerve and intercostal nerves).
- The volume of the thoracic cavity increases
- Decrease in PPUL and PIP
- Increase in Tp Decrease in TTP + TRP
What is the ‘pump handle’ representing?
The movement of the sternum. In inspiration, the sternum moves anteriorly and superiorly increasing thoracic cavity volume
The movement of the rib cage. In inspiration the rib cage moves upwards and outwards.
This happens when the external intercostals contract
What muscles are involved in forced inspiration
Scalene
Sternocleidomastoid
Pectoralis minor in some cases
Briefly describe expiration
Expiration is usually passive.
The ribs move down and in, and the diaphragm relaxes.
The intra-thoracic volume decreases and the pressure increases.
Air is forced out.
What is quiet expiration dependent on?
Elasticity of lungs
What muscles are involved during forced expiration
Internal intercostals
Abdominal wall muscles:
External & Internal oblique
Transversus Abdominis
Recta abdominis
What is V/Q mismatch?
When the perfusion of blood in capillaries isn’t matching the ventilation of the alveoli.
This is due to the fact that alveoli higher up would have better ventilation but worse perfusion due to gravity working against it and vice versa for alveoli near the bottom of the lung. This means that V and Q can never be fully equal
What is it called when you have a high V/Q ratio?
High ventilation low perfusion. Dead space
What is a cause of a high V/Q ratio (dead space)?
Pulmonary embolism.
What is it called when you have a low V/Q ratio?
Shunt. Lots of perfusion but no ventilation.
What is a cause of a low V/Q ratio (shunt)?
Pulmonary oedema.
What is perfusion of pulmonary capillaries dependent on?
- Pulmonary artery pressure.
- Pulmonary venous pressure.
- Alveolar pressure.
Does the apex of the lung have a high or a low V/Q? Why?
High - effect of gravity, far more perfusion at the base of the lung.
What are the 7 layers for gas exchange?
- Alveolar epithelium.
- Interstitial fluid.
- Capillary endothelium.
- Plasma layer.
- RBC membrane.
- RBC cytoplasm.
- Hb binding sites.
Name 4 causes of hypoxia.
- Hypoventilation.
- V/Q mismatch.
- Diffusion abnormality.
- Reduced PiO2.
DR. HV
Name 4 causes of hypercapnia.
- Increased dead space ventilation; rapid, shallow breathing.
- V/Q mismatch.
- Increased CO2 production.
- Reduced minute ventilation.
What is the alveolar gas equation?
PAO2 = PiO2 - (PaCO2/R)
Daltons law
In a mixture of non reacting gases Ptotal = Pa + Pb. (P total is the sum of the pressures of individual gases).
What is Boyle’s law?
Pressure and Volume are inversely proportional:
P1V1 = P2V2.
What is Henry’s law?
The solubility of a gas is proportional to the partial pressure of the gas when it’s in equilibrium. S1/P1 = S2/P2.
What is the acid/base dissociation equation?
CO2 + H2O = H2CO3 = HCO3- + H+
What enzyme catalyses the formation of bicarbonate and hydrogen ions from CO2 and H2O?
Carbonic anhydrase.
What is the henderson hasselbalch equation?
pH = pKa + log [A-]/[HA]
What is Laplace’s law?
P = 2T/R.
Where is surfactant produced?
Lamellar bodies of type 2 pneumonocytes in the alveoli
When is surfactant produced?
It starts being produced from 24 weeks gestation and production increases rapidly around week 34 week. The increase production of surfactant is due to cortisol which is secreted by mother.
List 4 functions of surfactant.
- Prevents alveoli collapse.
- Allows homogenous aeration.
- Reduces surface tension.
- Maintains functional residual capacity.
Premature babies may have surfactant deficiency. What are the consequences of this?
- Respiratory distress syndrome.
- Non-compliant lungs.
- Unequal aeration.
- Reduced lung volume.
How can you treat surfactant deficiency?
Ensure the patient is warm and is receiving O2 and fluids. Begin surfactant replacement.
Briefly describe the controller-effector-sensor loop.
The sensor detects a change (hypoxia), sends signals along the afferent pathway to the controller. The controller then sends signals along the efferent pathway to the effector. The effector responds.
What does the pneumotaxic area do and where is it located?
It switches off inspiratory neurones and so allows expiration. It is located in the upper pons.
What does the apneustic centre do and where is it located?
It inhibits expiration by activation inspiratory neurones. It is located in the lower pons.
Where are SASR (slow adapting stretch receptors) located?
Found in smooth muscle around airways.
What activates SASR?
Lung distension.
How do SASR respond to activation?
They inhibit inspiration and so promote expiration.
Where are RASR (rapidly adapting stretch receptors) located?
Between airway epithelial cells.
What activates RASR?
Lung distension and irritants.
How do RASR respond to activation?
Bronchoconstriction.
What activates C fibres J receptors?
Increased interstitial fluid volume.
How do C fibres J receptors respond to activation?
They cause rapid, shallowing breathing. Bronchoconstriction and cardiovascular depression.
Where are central chemoreceptors located?
Medulla oblangata.
What stimulates central chemoreceptors?
An increase in H+ concentration in the ECF.
Where are peripheral chemoreceptors located?
Carotid and aortic bodies.
What stimulates peripheral chemoreceptors?
increase PaCO2.
Decrease in O2
Change in pH due to metabolic acids
What is the respiratory drive more sensitive to, CO2 or O2?
O2 is a bigger drive once it drops below 60mmHg otherwise its CO2
Oxygen dissociation curve: what causes the curve to shift to the right?
BOHR EFFECT. An increase in temperature and a decrease in pH.
Oxygen dissociation curve: what does it mean when the curve shifts to the right?
Hb affinity decreases
Oxygen dissociation curve: what causes the curve to shift to the left?
A decrease in temperature and an increase in pH.
What is a cause of respiratory acidosis?
Inadequate ventilation; could be due to obstruction e.g. COPD.
What is the renal compensation mechanism for respiratory acidosis?
Increased ammonia formation. H+ secretion increases and there is increased HCO3- reabsorption.
What can cause respiratory alkalosis?
Hyperventilation in response to hypoxia.
What is the renal compensation mechanism for respiratory alkalosis?
H+ secretion decreases; more H+ is retained. HCO3- secretion.
What is a cause of metabolic acidosis?
Renal failure; loss of HCO3-, excess H+ production.
What is the respiratory compensation mechanism for metabolic acidosis?
Chemoreceptors stimulated, enhancing respiration, PaCO2 decreases.
What is the respiratory compensation mechanism for metabolic alkalosis?
Chemoreceptors are inhibited, reduced respiration, PaCO2 increases.
What is the cause of metabolic alkalosis?
-
What is the cause of metabolic alkalosis?
FAST!
What is type 1 respiratory failure and what are its causes?
Hypoxemia.
Causes: V/Q mismatch due to alveolar hypoventilation, high altitude, shunt, diffusion problem.
What is type 2 respiratory failure and what are its causes?
Hypoxemia and hypercapnia.
Causes: inadequate alveolar ventilation due to reduced breathing effort, decreased SA, neuromuscular problems.
What is forced vital capacity?
Volume of air that can be forcibly exhaled after maximum inhalation.
How could you diagnose a patient with having an obstructive lung disease?
The FEV1/FVC ratio would be less than 70% predicted value.
How could you diagnose a patient with having an restrictive lung disease?
The FEV1/FVC ratio would be normal but their FVC value would be very low.
How can you work out total lung capacity?
Add vital capacity to residual volume.
What is tidal volume?
The volume of air moved into or out of the lungs during normal, quiet breathing.
What changes are seen in an aging lung?
Decreased compliance, muscle strength, elastic recoil, immune function. Decreased response to hypoxia and hypercapnia. Impaired gaseous exchange.
What happens to the FEV1 and FVC in an elderly person?
They both decrease and the residual volume increases.
What effect does hypoxia have on pulmonary vessels?
It vasoconstricts the vessels and so redirects blood to O2 rich alveoli.
What is hypersensitivity?
The undesirable reaction produced by the immune system.
Hypersensitivity: What is the mechanism of a type 1 reaction?
Antigens interact with IgE bound to mast cells. Histamine is released. This can cause hayfever, asthma, acute anaphylaxis etc. (Antihistamines are often given as treatment).
What is the parasympathetic neurotransmitter in the lungs?
Acetylcholine.
What is the sympathetic neurotransmitter in the lungs?
Noradrenaline.
What is the effect of Ach on the pulmonary vessels?
Bronchoconstriction and vasodilation.
What is the effect of noradrenaline on the pulmonary vessels?
Bronchodilation and vasoconstriction
Name 2 receptors for Ach.
Muscarinic (G protein coupled) and Nicotinic (ligand gated ion channels).
Host defense: What is innate immunity?
Immunity that doesn’t require prior exposure. It usually involves phagocytosis and inflammation.
Briefly describe the mechanism of inflammation.
Vasodilation results in the exudation of plasma. Neutrophils and monocytes migrate into tissues.
What are alveolar macrophages derived from?
Monocytes. They are the resident phagocyte in the lungs and they coordinate inflammatory response.