RESP Life Support

Question 1

Describe specific causes of acid-base disorders and how
they impact blood pH.

Answer 1

Acid Base Disturbances

1. RESP Acidosis
2. RESP alkalosis
3. Metabolic acidosis
4. Metabolic alkalosis

Broad Causes

1. Hypoventilation
2. Hyperventilation
3. Excessive acid production, HCO3 excretion
4. Basic substance consumption, excessive excretion of acid, deficient HCO3 GI absorption, excessive HCO3 reabsorption

Examples of Specific Conditions

1. COPD
2. anxiety and Altitude
3. Sepsis, Ketoacidosis, Renal Dysfunction
4. Antaacid abuse, Vomiting, Diarrhoea, Renal Dysfunction

Question 2

Describe the effects of respiratory acidosis/alkalosis,
including specific examples such as acidosis-induced hyperkalaemia and
alkalosis-induced cerebral vasoconstriction.

Answer 2

Acidosis-induced hyperkalaemia

Acidosis = ↑ blood [H+] = disrupted intra/extracellular H+ gradients = ↓H+/Na+ exchange =
↓Na+/K+ exchange = ↓ cellular K+ absorption = K+ accumulation in extracellular fluid and
blood = hyperkalaemia.

Alkalosis-induced cerebral vasoconstriction

Hyperventilation = ↓PaCO2 = ↓ CO2-induced vasodilation of cerebral arteries = ↑ cerebral 
vasoconstriction  =  ↓  cerebral  blood  flow  =  light-headedness,  headaches,  seizures,  loss  of consciousness, etc.

Question 3

Describe the normal processes involved in the initiation
and control of breathing, including the pathways and feedback mechanisms
involved.

Answer 3

Initiation of breathing:
1. Neuronal signal generated via activity within the central pattern generator within the
brainstem
2. Signal conducted from CNS to respiratory muscles via spinal cord and motor neurons
3. Respiratory muscle contraction and expansion/compression of the thoracic cavity and
lungs

Control of breathing:
Feedback mechanisms Activating stimuli
Central chemoreceptors (within medulla) ↑[H+] in CSF (linked to PaCO2)
Peripheral chemoreceptors (within aortic
and carotid bodies)
↑PaCO2, ↓PaO2 and ↓blood pH
Limbic system inputs Emotional stimuli (e.g. anxiety)
Stretch receptors Excessive physical stretch of lungs
(overexpansion)

Question 4

Describe the difference and differentiate between

obstructive and central sleep apnoea.

Answer 4

Obstructive sleep apnoea is caused by a temporary blockage of the upper respiratory tract.

Central sleep apnoeas are caused by dysfunction in the central nervous system processes that initiate breathing, causing cessation of the automated breathing during sleep (either temporarily or permanently) as the pathways involved in initiating breathing can no longer
function.

Obstructive and central sleep apnoeas can be differentiated during polysomnography by whether diaphragmatic contractions continue during the apnoea. Obstructive sleep apnoeas are associated with increasing diaphragmatic effort as it tries to overcome the upper respiratory blockade. In contrast, failure of the diaphragm to respond during periods of
apnoea is characteristic of central sleep apnoea (as there is a temporary cessation of the CNS- respiratory muscle pathway that initiates breathing).

Question 5

Describe the key pathophysiological changes associated

with asthma

Question 6

Define lung compliance and explain how and why it is
affected by respiratory diseases.

Answer 6

Lung compliance describes the relationship between changes in lung volume and
transpulmonary pressure (essentially, the level of force required to distend the lungs).
Lung compliance is determined by the structure of the lung tissue, e.g. the density of elastic
fibres such as elastin, collagen, and is reduced by the presence of pulmonary surfactant.
Lung compliance is increased in emphysema (due to degradation of elastin fibres) and
decreased in pulmonary fibrosis (due to fibrotic changes rendering the lung tissue stiffer).

Question 7

Describe the role of pulmonary surfactant in respiration
and pathology that occurs if insufficient quantities are produced.

Answer 7

Pulmonary surfactant reduces surface tension at the air-liquid interface – this surface tension is created by the presence of a bubble-like structure created within alveoli due to their
existing an air filled space lined by fluid.
By reducing surface tension, pulmonary surfactant increases lung compliance (less force is
required to inflate the lungs) and prevents alveolar collapse. It also counters the effect that

surface tension has on hydrostatic pressure, which would naturally draw water from
capillaries into the alveolar fluid. Surfactant thus also acts to preventing oedema.
If insufficient levels of pulmonary surfactant are present (as is the case in neonatal respiratory
distress syndrome), then lung function is negatively affected. Lung compliance decreases,
lungs become stiffer, alveoli are more likely to collapse, and pulmonary oedema can occur. If
untreated (via artificial surfactant supplementation), the net effect can be respiratory failure
and death.

surface tension has on hydrostatic pressure, which would naturally draw water from
capillaries into the alveolar fluid. Surfactant thus also acts to preventing oedema.
If insufficient levels of pulmonary surfactant are present (as is the case in neonatal respiratory
distress syndrome), then lung function is negatively affected. Lung compliance decreases,
lungs become stiffer, alveoli are more likely to collapse, and pulmonary oedema can occur. If
untreated (via artificial surfactant supplementation), the net effect can be respiratory failure
and death

Question 8

Define airway resistance and explain how and why it

affected by respiratory diseases

Answer 8

Airway resistance = the force generated by gas molecules colliding with the surfaces of the
airway, which opposes the flow of air.
The radius of the airway lumen radius is the primary determinant of airway resistance.
Pathological states which can decrease airway lumen radius include contraction of airway
smooth muscle (bronchoconstriction), mucus hypersecretion, airway oedema, and airway
collapse (loss of patency).

Question 9

Describe the factors that affect the rate of gas exchange in the lung, and how these change in specific disease states.

Answer 9

https://docs.google.com/document/d/1ghcZhxyyjNU1mzQ7Wy0JpDGHpBoqlmOWn5ypiVTY4xQ/edit

Question 10

List the factors that affect the oxygen-haemoglobin affinity and describe their effects.

Answer 10

https://docs.google.com/document/d/1JD-yxioUaey4ib9aZVDS-8f6yeLBFJ-tN2vxrsxnCCY/edit