Respiratory System: Integrated Ventilation Control Flashcards
Low pH accompanied by hypercapnia is…
Low pH accompanied by high PaC02 (hypercapnia) is respiratory acidosis.
Hypoventilation is responsible for the increase in CO2 levels and decreased pH
High pH accompanied by hypocapnia is…
High pH accompanied by low PaCO2 is respiratory alkalosis.
Hyperventilation is responsible for the decrease in CO2 levels and increased pH
Low pH accompanied by low [HCO3-] is…
Low pH accompanied by low [HCO3-] is metabolic acidosis.
Excessive metabolic acid production and/or increased excretion of HCO3- is responsible for the decreased pH
High pH accompanied by high [HCO3-] is…
High pH accompanied by high [HCO3-] is metabolic alkalosis
Reduced metabolic acid production or reduced excretion of HCO3- is responsible for the increased pH
How does the body react to acidosis?
Acidosis has increased [H+] within the blood, causing increased activation of respiratory chemoreceptors and resp activity (compensatory hyperventilation).
The resulting increase in CO2 removal from the blood/body increases pH until normal level is re-established.
How does the body react to alkalosis?
Alkalosis has less [H+] w/in the blood, causing decreased activation of respiratory chemoreceptors and decreased resp activity (compensatory hypoventilation).
The resulting C02 accumulation in the blood/body decreases pH until normal level is re-established via negative feedback.
What is the difference between respiratory and metabolic acidosis and what they’re associated with?
Respiratory acidosis: associated w chronic resp failure, hypoventilation, and accumulation of CO2, e.g. COPD.
Metabolic acidosis: associated w excessive acid production (sepsis, ketoacidosis) or excessive excretion of HCO3 (renal failure)
What is the difference between respiratory and metabolic alkalosis?
Respiratory alkalosis: associated w hyperventilation and excessive C02 removal e.g. anxiety or altitude-induced hyperventilation.
Metabolic alkalosis: associated w excessive consumption of basic substances (antacid abuse), excessive acid excretion from the body (vomiting), deficient absorption of HCO3 from the GI tract (chronic diarrhoea), or excessive reabsorption of HCO3 (renal dysfunction).
Describe potassium homeostasis
Potassium homeostasis w/in blood is dependent on pH.
One mechanism is via H+ efflux, Na+ influx.
This mechanism is followed by Na/K exchange (sodium efflux, potassium influx).
So K+ enter the cell in exchange for H+ ions leaving
How does acidosis affect potassium homeostasis to cause hyperkalaemia?
Remember, before H+ diffusion out the cell in exchange for Na+, H+ conc inside the cell> outside the cell!!
In acidosis, this process breaks down as pH falls, [H+] increases.
Overall uptake of K+ by cells is reduced, leading to K+ accumulation within the ECF in blood.
K+ affect membrane potential and muscle function, so arrhythmia and muscle weakness is seen in hyperkalaemic patients.
Describe alkalosis induced vasoconstriction
Contractility of vsm is sensitive to changes in pH, esp cerebral arteries.
C02 (via conversion to H+) acts as vasodilator, relaxing smooth muscle and increasing blood flow.
In hyperventilation-induced alkalosis, reductions in PaCO2 and H+ (↑pH) induce vasoconstriction of cerebral arteries, reducing blood flow to the brain.
Symptoms: headache, light-headedness, seizures or loss of consciousness.
What is compensation in acid base disorders?
Metabolic acidosis and alkalosis can be compensated by respiratory alkalosis and acidosis and vv:
Increased PaCO2 in the presence of high pH, or decreased PaCO2 in the presence of low pH = respiratory compensation.
Increased [HCO3-] in the presence of low pH, or decreased [HCO3-] in the presence of high pH = metabolic compensation
Respiratory and metabolic disfunction can occur simultaneously, this mixed acidosis or mixed alkalosis
What is the difference between full and partial compensation?
If the level of compensation has restored pH to its normal range (7.35 - 7.45), then it is full compensation.
If pH is still abnormal then it is partial compensation.
How can ABG samples be used to diagnose acid base disorders?
Which muscles are used in different types of breathing?
Describe the neural pathway involved in the initiation and control of breathing
All skeletal respiratory muscles need nervous stimulation to contract. Contractile signals are initiated within the brain and descend via spinal tracts.
These spinal tracts synapse w the lower motor neurons that innervate the respiratory muscle tissue.
VRG/DRG= Ventral/dorsal resp group
Draw a flow chart to represent pathways involved in the initiation and control of breathing.
The CPG receives inputs from central and peripheral chemoreceptors.
Describe peripheral chemoreceptors
Peripheral chemoreceptors: type-I glomus cells which have carotid and aortic bodies:
What other inputs does the CPG receive to modulate ventilation?
The CPG also integrates info from other inputs like stretch receptors within the lungs to prevent damaging over-inflation, or irritant receptors within airways that initiate cough:
How can Obstructive and central sleep apnoeas can be differentiated during polysomnography?
Obstructive sleep apnoea has increased respiratory effort to overcome the obstruction in response to rising PaCO2 levels (due to hypoventilation).
Rising PaCO2 levels also occur in central sleep apnoea, but temporary cessation of the CNS-respiratory muscle pathway that initiates breathing means the diaphragm doesn’t respond.
Draw a diagram to show the breathing patterns that characterise Cheyne-Stokes respiration
Altitude, CR disfunction or heart failure causes hypercapnia/hypoxaemia which induces hyperventilation. This causes hypocapnia and alkalosis. The body has to compensate in the opp direction. This keeps happening in an alternating pattern:
