Flashcards in Respiratory Deck (39):
What are the two types of respiratory epithelium lining the alveoli?
Type I - flat, large, basically the gas exchange cells
Type II - thick, less abundant than Type I and responsible for alveolar repair, as well as production of surfactant
What are the main immunological cells in the alveoli?
1. Pulmonary alveolar macrophages (PAMs) which directly phagocytose particles which manage to evade the mucociliary escalator.
3. Plasma cells
4. Mast cells
How much does movement of the diaphragm account for change intrathoracic volume?
Diaphragmatic movement accounts for 75% of the change in intrathoracic pressure.
What is eructation?
What are the parts of the diaphragm?
1. Crural - attached to the vertebral bodies
2. Costal - attached to the internal surface of the ribcage
3. Central tendon
What is the approximate volume of intrapleural fluid?
15-20mL only. Main function to serve as a lubricant between parietal and visceral pleura
How much air per normal breath?
500mL tidal volume = 6-8L per minute
How much dead space is there in the respiratory system?
150mL in the upper conducting zones of the airway
What is the average lung volume at rest?
What is the distinguishing feature between respiratory and terminal bronchioles?
Terminal bronchioles are the smallest of the conducting airways. They then transition into respiratory bronchioles which contain aveoli.
What is the average resting pressure in the pulmonary artery?
What are the main components of the respiratory membrane?
The alveolus has type I epithelium and these are essentially adjacent to capillary epithelium. In total this membrane is only around 0.3micrometres thick!
The capillary itself is only 10micrmetres wide, just enough for RBCs and that's it
How much surface area is available for gas exchange?
70 square metres or 50 square feet
What happens to the respiratory membrane when pulmonary pressure is too high?
The blood gas exchange barrier can be damaged and impair ventilation.
What are the phases of respiratory in regards to thoracic pressures?
1. Initially, diaphragmatic movement causes a negative intrapleural pressure to fall from -2mmHg to -8mmHg.
2. This is followed by expansion of the lung which causes intrapulmonary pressure to fall to around -2mmHg
3. Air flows in through a path of least resistance (usually the conducting airway system) until atmospheric and lung pressure is the same
4. Venous return also increases as a result of this negative intrathoracic pressure
How is the functional residual capacity calculated?
The FRC is a sum of the experiatory residual volume (the amount that normal sits in the lungs on passive respiration but can be pushed out if need be) plus the residual volume (the amount left in the airways even after expired residual volume is gone)
FRC = ERV + RV
What factors decrease the FRC?
1. Sitting in the supine position
2. Being pregnant - decreases the RV and ERV
3. Post-operative atelectasis obviously with lung collapse there is decrease ERV
4. Anything which impinges on lower airways such as chronic bronchitis with sputum retention
What is the best way to manage an acute drop in the FRC?
High flow oxygen delivered by mask
What pathologies can cause a restrictive lung disease pattern?
Anything which decreases the body capacity for expansion such as:
1. Fractured ribs
2. Splinting due to pain from upper abdominal surgery
3. Spinal cord pathology which impinges on intercostal function
Anything which directly compromises the capacity of the lung such as a lobar pneumonia will also reflect a restrictive lung disease pattern.
How long is capillary blood in contact with the respiratory membran in the resting state?
0.25 seconds in the active state
Where are the peripheral chemoreceptors involved in regulating respiration located?
1. Carotid bodies,
- The peripheral chemoreceptors are the only chemoreceptors in man which are capable of modifying the hypoxic respiratory response.
- These chemoreceptors are not affected by anaemia
- They are also minimally active until the Pa02 is down to 50-60mmHg
What is the Bohr effect?
The Bohr effect basically describes the effect of pH on oxygen affinity of haemoglobin.
In the exercising state where there is a large amount of CO2, an increased number of H+ ions are formed by virtue of buffer system in making CO2 more soluble.
With increased H+, haemoglobin becomes more likely to be bound by H+ and CO2, in exchange for dumping of oxygen.
How is CO2 transported from tissues back to the lung?
In BLOOD PLASMA:
2. Forms carbamino compounds with plasma proteins
3. Following buffering of H+ in the RBC, HCO3 lives in the plasma
2. Formation of carbamino-Hb
3. H+ buffered and 70% of the HCO3 produced enters the plasma in exchange for chloride ions
4. Overall there is increase in osmolality intracellularly so water also enters with chloride
What layers must gases traverse to enter RBCs?
2. respiratory epithelial cell *type I
4. Capillary endothelium
6. RBC membrane
How is oxygen carried in blood?
1. With Hb
2. Freely dissolved
What factors affect the affinity of haemoglobin for oxygen?
Hb will have higher affinity for oxygen in the following:
2. Low CO2
3. Low temperature
4. Low 2,3 DPG (biphosphoglyceric acid)
Hb has a lower affinity for oxygen in the inverse, think of peripheral tissues!
1. CO2, H+ and temperature are high in exercising muscle to haemoglobin has lower O2 affinity, therefore will more likely offload its oxygen which is good for tissue perfusion
How does carbon monoxide affect the haemoglobin-oxygen dissociation curve?
CO has 240x the affinity for Hb than oxygen. I therefore competitively antagonises the oxygen binding site on the Hb molecule.
Contrary to logic, CO actually INCREASES oxygen affinity on haemoglobin molecules. So when a single CO is bound, the remaining sites want for more O2 so the dissociation curve is actually shifted to the left initially.
Overall however, the dissociation curve will plateau out at an oxygen saturation much lower than normal, despite any changes in the PaO2
What are the features of CO poisoning?
Systemically reduced oxygen concentration in both arterial and venous blood.
O2 curve shifted to the left
Normal partial pressure of oxygen
What forms of CO2 exist in VENOUS blood? (i.e from tissues to the lungs)
60% is in the form of BICARBONATE
10% is dissolved
30% is formed with carbamino proteins
What forms of CO2 exist in ARTERIAL blood? from lung to tissues?
90% is in the form of BICARB (mostly in RBCs)
5% is dissolved
5% is as carbamino proteins
What is the Bohr EQUATION (not to be confused with Bohr Effect)?
The Bohr equation is basically a ratio that can be used to estimate the dead space with the understanding that only alveolar ventilation undergoes gas exchange. THEREFORE:
(PalveolarCO2 - PexpiredCO2) / PalveolarCO2 = Vd / Vt
where Vd = dead space.
How is respiration controlled in the body?
1. Affectors (sensors)
2. Central mediator (brain)
3. Effectors: cause change in ventilatory effort
What are the central mediators of respiration?
- medullary respiratory centre (below the 4th ventricle with two areas, dorsal for inspiration and ventral for expiration)
- Apneustic centre - lower part of pons which stimulates the dorsal inspiratory area
- Pneumotaxic centre - upper pons which can inhibit inspiration and thus regulates volume and RR
2. Cerebral cortex can override the medulla
Where are the central chemoreceptors located?
The are on the ventral surface of the medulla and are bathed in CSF with CO2 imbued. They mainly respond to changes in the pCO2. The chemoreceptors are mainly activated by the change in pH due to an increase in buffered CO2.
So with an increase in CO2 diffusing into the CSF, the pH drops relative to that of the blood.
Chronically, if the PCO2 is elevated, the pH is buffered eventually by movement of extra bicarbonate ions.
Therefore the most important controlled of medullary respiration in the action of pH on central chemoreceptors.
Where are the peripheral chemoreceptors located?
Only in carotid bodies.
They respond to changes in arterial blood, changes in PO2, pH and PCO2.
Normally the response to PO2 is pretty minimal, but response to PCO2 is much quicker, and even more rapid than that of central chemoreceptors.
What factors impact on the ventilatory control during exercise?
1, Afferent feedback from limb movement
2. Increase in body temperature
Additionally, increase in PCO2 and reduction in arterial pH causes more firing of arterial chemoreceptors whcih in turn leads to increases in activity of medullary respiratory centres - increased RR and ventilation volume.
What is the Hering Breuer reflex?
The Hering Breuer reflex is a nerual reflex in response to excessive stretching of pulmonary musculature indicating overinflation of the lungs.
It is mediated by pulmonary stretch receptors in airway smooth muscle. These send responses to the medulla and apneustic area of the pons via vagus.
This inhibits the dorsal inspiratory area of the medulla which in turn inhibits the apneustic area of the pons.
What effects on the ABG would be seen in a young healthy patient hyperventilating leading to the doubling of alveolar ventilation? (prior to activation of renal compensation)
1. Decreased PaCO2
2. Decrease in bicarbonate
3. Decreased ICP (low CO2 leads to vasoconstriction which leads to lowered ICP
4. Increase of PaO2