Control of Breathing Flashcards
wwhy is the air from the atmosphere different from the air in alveoli
Air entering the alveoli is different from atmospheric air due to two main reasons:
Moist Airways:
- Water Vapor Presence: Airways are moist, contributing water vapor to the air. Moisten and warmed at different temp by nasal cavity
==> moistens to not irritate airflow and improve transport (CO2 transports better in solution) - Effect on Partial Pressure: Water vapor exerts a partial pressure of 47 mmHg, diluting inhaled gases.
- Resulting PO2: This lowers the partial pressure of oxygen (PO2) to 150 mmHg.
Mixing with “Old” Air:
- Dead Space: Inspired air mixes with “old” air left in the respiratory system from the previous exhalation.
- Further Lowering PO2: This mixing further lowers the PO2 to around 100 mmHg within the alveoli.
- Nasal Cavity’s Role: The nasal cavity acts as a first line of defense, warming, humidifying the air, and trapping debris and irritants.
partial pressurem
essentially the concentration of something in the blood e.g. increase in PCO2 means higher concentration of CO2 in blood
Blood coming to the lungs is lower in partial
pressure than the alveoli
* Allows exchange to occur
PO2 decreases from arterial blood to venous blood
==> Oxygenation: The blood leaving the lungs through the pulmonary veins has a higher PO2 (oxygenated blood) ready to be delivered to the tissues.
PCO2 increases from arterial blood to venous blood
==> Blood returning to the lungs via the pulmonary arteries is deoxygenated and has picked up carbon dioxide (CO2) from the body tissues where cellular respiration occurs.
Factors that influence gas transfer
Diffusion rates are also dependent on three additional factors
* Surface area = High SA to increase gas exchange
* Thickness of the membrane = thicker will decrease gas exchange
* Gas diffusion constant = how diffusable/ soluble it is in H2O (CO2 greater diffusing rate than O2, both can diffuse )
* All of these are relatively constant under normal conditions
conditions
emphesyma : destruction of alveoli// low SA, same thickness, same diffusion distance, same resistance => less gas exchange (lower PO2 or normal)
fibrotic lung disease : thicked alveolar membrane/loss of lung compliance// same SA, same diffusion distance, same resistance (lower PO2 or normal) => less gas exchange
pulmonary edema : fluid in interstitual space// increases diffusion distance, (normal PO2,) surface area normal, => less gas exchange
asthma : bronchioles constricte // same SA, same thickness, same diffusion distance, decrease airway resistance, (low PO2)
haemoglobin and PO2
PO2 is not the total O2 content ==> amount of O2 in the blood is prortional to PO2
amount bound to Hb is not accounted for to its partial pressure
the PO2 in the alveoli should be slightly higher than in the blood arriving at the lungs, but not excessively high
a) when there is no Hb: the PO2 in alveoli and plasma is the same = no pressure gradient // no gas exchange [PO2 is all O2 in plasma]
b) with HB, pressure gradient, O2 can move through
c) Hb full, same O2, no pressure gradient, no exchange
A moderate PO2 ensures that hemoglobin can release oxygen efficiently in tissues with lower PO2.
Haemoglobin saturation
As Hb can carry 4 O2 molecules, when all sites are bound, this is
considered fully saturated
* % saturation can vary between 0-100%
If PO2 is high, it promotes the binding of oxygen to hemoglobin, resulting in the formation of oxyhemoglobin (Hb + O2 ⇌ HbO2). This is a reversible reaction, meaning that oxygen can bind to hemoglobin in the lungs (where PO2 is high) and be released in the tissues (where PO2 is lower).
Relationship is Not Linear: Oxygen-Hemoglobin Dissociation Curve:
==> The relationship between PO2 and hemoglobin saturation is represented by the oxygen-hemoglobin dissociation curve, which is sigmoidal (S-shaped) rather than linear. This curve illustrates that:
At low PO2: Small increases in PO2 result in large increases in hemoglobin saturation. This is seen in the steep portion of the curve.
At high PO2: Large increases in PO2 result in small increases in hemoglobin saturation. This is seen in the plateau portion of the curve.
carbon monoxide and Hb
Odourless, colourless, tasteless and non-irritating gas
- CO and O2 compete for the same binding sites on Hb
- Stronger affinity for CO
Hb can no longer carry O2, reduce bloods capacity to carry o2
co can affect structure of Hb, so it wont let go of o2
==> o2 can’t be released to tissues and organs
Carbon dioxide transport
- Transported in the blood by three different mechanisms:
- Dissolved in plasma
- Bound to Hb
- ## As bicarbonate (HCO3)
- Dissolved
- Higher % dissolved in blood as CO2 is more soluble than O2
- Bound to Hb == carbaminohemoglobin
* ~25% is transported this way
* Binds to globin portion, not heme (doesn’t compete with O2 like CO)
* Offloading of O2 facilitates CO2 uptake from tissues/organs
- Bicarbonate ion (HCO3-)
- Most important, catalysed by carbonic anhydrase
- ~70% transported this way
- CO2 + H2O ⇆ H2CO3 (skips this product in syllabus) ⇆ H+ + HCO3-
HCO3- leaves RBC enters in the plasma and Cl- enters RBC inside instead (chloride shift : one anion in, one anion out)
=> reversible reaction, can take the HCO3- back into the RBC and converting it back into co2 to the lungs
Abnormal blood-gas levels
Abnormalities in arterial PO2
* Hypoxia (low)
* Hyperoxia (high)
* Oxygen toxicity = reactive oxygen species (ROS)
–> oxidative stress
- Abnormalities in arterial PCO2
- Hypercapnia (increase CO2) == Caused by hypoventilation
- Hypocapnia (decrease CO2) == Caused by hyperventilation
- Abnormal CO2 levels alter acid-base balance
in the body
Control of respiration
- Breathing pattern must be regular and continuous
- Accomplished automatically (some conscious)
- Controlled by CNS
- Contraction of diaphragm and other muscles controlled by
neurons in the brain stem - Spontaneous firing is additionally influenced by sensory input
- Chemoreceptors
- Quite contentious still (still unknown)
Question: What are the primary components of the neural control of breathing?
- Neurons in the medulla control inspiratory and expiratory muscles.
- Neurons in the pons integrate sensory inputs and influence medullary neurons to alter ventilation.
- Rhythmic pattern of breathing arises from a neural network in the brainstem with spontaneous firing of neurons.
- Ventilation is also altered by chemoreceptor and mechanoreceptor reflex pathways and higher brain centers.
any change in CO2 levels, medullary chemoreceptors detects and sends signals to medulla oblongata + pons
=> muscle to either breathe more or less
Question: What chemical factors influence ventilation and how are they monitored?
Ventilation matches metabolic levels
* Medullary respiratory centre receives input on body’s need for gas
exchange
* Adjusts rate and depth of breathing
Carbon Dioxide (CO2): Monitored by central and peripheral chemoreceptors.
Oxygen (O2): Monitored by peripheral chemoreceptors in the carotid and aortic bodies.
Plasma pH: Monitored by chemoreceptors.
- Monitored by chemoreceptors
- Located in arterial circulation and medulla
Question: What do peripheral chemoreceptors monitor and where are they located?
Answer: Peripheral chemoreceptors monitor arterial PO2, PCO2, and pH. They are located in the carotid bodies (peripheral chemoreceptors) and aortic bodies (chemoreceptors).
Located in medulla (central chemoreceptors)
- Not overly sensitive to small
reductions in PO2 - Must fall below 60 mmHg
- Predominantly an emergency
mechanism - H+ strongly stimulates
Question: How does an increase in PCO2 regulate ventilation?
Answer: An increase in PCO2 causes CO2 to cross the blood-brain barrier to active medullary chemoreceptors, which triggers alterations in respiratory centers to increase ventilation.
Central chemoreceptors in the medulla respond to the pH of cerebrospinal fluid (CSF), not directly to CO2 levels.
increase in PO2 causes CO2 moves down gradient into CSF, CO2 is catalysed by carbonic anhydrase and H+ is produced
only H+ produced in CSF can active central chemoreceptor, not H+ in capillary
=> H+ in the plasma has little influence on central chemoreceptors
