Respiratory Physiology 5 Flashcards
Explain how respiratory motor movements are affected by the central nervous system.
Ventilatory control:
- requires stimulation of the (skeletal) muscles of inspiration. This occurs via the phrenic (to diaphrgam) and intercostal nerves (to external intercostal muscles).
- At rest, expiration is passive so no neural input is required.
- resides within ill defined centres located in the pons and medulla (Respiratory Centres)
- is normally subconscious
- can be subject to voluntary modulation
- entirely dependent on signalling from the brain (sever spinal cord above origin of phrenic nerve (C3-5) breathing ceases)
Respiratory Centres have their rhythm modulated by:
1. Emotion (via limbic system in the brain)
2. Voluntary over-ride (via higher centres in the brain)
3. Mechano-sensory input from the thorax (e.g. stretch reflex).
4. Chemical composition of the blood (PCO2, PO2 and pH) – detected by chemoreceptors.
Describe the location of the two classes of chemoreceptors and identify the stimuli which activate them.
Central Chemoreceptors:
Location:
- medulla
- respond directly to H+ (directly reflects PCO2)
- primary ventilatory drive
Peripheral Chemoreceptors:
Location:
- carotid and aortic bodies
- respond primarily to PO2 and plasma [H+] (less so to PCO2)
- secondary ventilatory drive
List the factors involved in changing ‘respiratory drive’ i.e. the rate and depth of breathing.
Central Chemoreceptors in the medulla
Detect changes in [H+] in CSF around brain
Cause reflex stimulation of ventilation following rise in [H+] (driven by raised PCO2 = Hypercapnea)
Ventilation is reflexly inhibited by a decrease in arterial PCO2 (reduces CSF [H+])
(hyperventilation)
Explain how the central chemoreceptors serve to regulate arterial PCO2 by monitoring the pH of CSF.
When arterial PCO2 increases carbon dioxide crosses the blood-brain barrier not H+
Central chemoreceptors monitor the PCO2 indirectly in the cerebrospinal fluid.
Bicarbonate and H+ are formed and the receptors respond to the H+
Feedback via the Respiratory Centres increases ventilation in response to increased arterial PCO2 .
Decreased arterial PCO2 slows ventilation rate
Explain how the peripheral chemoreceptors become important during hypoxia and acid-base disturbances
Carotid and aortic bodies
Detect changes in arterial PO2 and [H+]
Cause reflex stimulation of ventilation following significant fall in arterial PO2 (<60mmHg - consider haemoglobin dissociation curve)
Respond to arterial PO2 not oxygen content (plasma not haemoglobin).
Describe sedation/anaesthesia and ventilatory control.
Most gaseous anaesthetic agents increase RR but decrease TV so decrease AV.
Barbiturates and opioids depress respiratory centres – overdose often results in death as a result of respiratory failure. Decreased sensitivity to pH and therefore response to PCO2 . Also decreased peripheral chemoreceptor response to decreased PO2.
Nitrous oxide, a common sedative/light anaesthetic agent, blunts peripheral chemoreceptor response to falling PaO2. Very safe in most individuals, problematic in chronic lung disease cases where individual often on “hypoxic drive”. Administering O2 to these patients aggravates situation.
Explain how the peripheral chemoreceptors become important during hypoxia and acid-base imbalance.
The peripheral chemoreceptors also respond to increasing plasma [H+]
Often, but not always, the H+ originates from CO2.
Changes in plasma pH will alter ventilation via the peripheral chemoreceptor pathways.
If plasma pH falls ([H+] increases) ventilation will be stimulated (acidosis)
If plasma pH increases ([H+] falls) e.g.vomiting (alkalosis), ventilation will be inhibited
Explain how CO2 affects acid-base balance
CO2 is capable of changing ECF pH because:
CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+
Normally pH is stable because all the CO2 produced is eliminated in expired air.
However hypo/hyperventilation will alter plasma PCO2 and plasma [H+] will vary accordingly.
Outline how the respiratory system can both create, and compensate for, acid-base disturbances.
Hypoventilation, causing CO2 retention, leads to increased [H+] bringing about respiratory acidosis.
Hyperventilation, blowing off more CO2, lead to decreased [H+] bringing about respiratory alkalosis