7

Question 1

What is the difference between hypoxia and hypoxaemia?

Answer 1

• hypoxia: O2 deficiency at TISSUE level

- hypoxaemia: low pO2 in blood

Question 2

In regards to hypoxia and hypoxaemia, define anaemia

Answer 2

-when pt. Is hypoxic but not hypoxaemic

Question 3

What is hypoxaemia caused by?

Answer 3

• low inspired pO2: at high altitudes
• hypoventilation: respiratory pump failure
• ventilation/perfusion mismatch
• diffusion defect: problems of the alveolar capillary membrane
• intra-lung shunt: acute respiratory distress syndrome (ARDS)
• right to left shunt (cyanotic heart disease): extrapulmonary, no ventilation but still perfusion

Question 4

What are the effects of hypoxaemia?

Answer 4

• impaired CNS function, confusion, irritability, agitation
• cardiac arrhythmias and cardiac ischaemia
• hypoxic vasoconstriction of pulmonary vessels
• cyanosis

Question 5

What are the compensatory mechanisms for chronic hypoxaemia?

Answer 5

• increased EPO secreted by kidney to raise Hb (Polycythemia)
• increased 2,3 BPG which shifts Hb saturation curve to right so O2 is released more freely

Question 6

What results due to chronic hypoxic vasoconstriction of pulmonary vessels?

Answer 6

• pulmonary hypertension
• right heart failure aka cor pulmonale
• Hypertrophy occurs which leads to arrhythmia and eventually right heart failure

Question 7

What is respiratory failure? Describe the two types

Answer 7

-impairment in gas exchange causing hypoxaemia with or without hypercapnia

Type 1

• low pO2 < 8kPa or O2 saturation <90% breathing room air at sea level
• pCO2 normal or low
• gas exchange is impaired at the level of alveoli-capillary membrane
• hypoxaemic, O2 problem only

Type 2

• low pO2 and high pCO2 (>6.5 kPa) breathing room air at sea level
• respiratory pump failure
• hypoxaemic and hypercapnic

Question 8

What is hypoventilation?

Answer 8

• inability to normally ventilate the lung
• insufficient air moved in and out of lungs leading to low pO2 and high pCO2
• alveolar ventilating is reduced
• pO2 decreases in alveoli so it decreases in arteries leading to hypoxaemia
• alveolar pCO2 rises leading to rise in arteries resulting in hypercapnia
• type 2 resp failure

Question 9

Can hypoventilation be solved with oxygen?

Answer 9

No because it will only correct the hypoxaemia but not the hypercapnia

Question 10

What are the causes of hypoventilation?

Answer 10

Acute

• opiate overdose
• head injury
• severe acute asthma

Chronic

• severe COPD
• LRT infection
• end stage lung fibrosis
• scoliosis/kyphosis/both
• rib fractures
• obesity
• stabbing
• neuromuscular disorders such as polio

Question 11

How does scoliosis and kyphosis cause hypoventilation?

Answer 11

• scoliosis: sideways curvature of spine
• kyphosis: spinal disorder in which results in abnormal rounding of upper back
• kyphoscoliosis: both
• have impaired ability to expand chest due to bony deformities

Question 12

What are the effects of hypercapnia and the chronic version?

Answer 12

• resp acidosis
• impaired CNS function: drowsiness, confusion
• peripheral vasodilation: warm hands, bounding pulse
• cerebral vasodilation: headache

Chronic

• respi acidosis compensated by retention of HCO3 by kidney
• acclimatation to CNS effects
• vasodilation mild but may still be present: “pink” puffers

Question 13

What is chronic CO2 retention and what is its effect on central chemoreceptors?

Answer 13

• CO2 diffuses into CSF, so CSF pH drops which stimulates central chemoreceptors
• persistently CSF acidity is harmful to neurons
• low CSF pH corrected by choroid plexus cells which secrete [HCO3] in to CSF
• CSF pH returns to normal; central chemoreceptors no longer stimulated
• pCO2 in blood is still high but central chemoreceptors now unresponsive to this pCO2 (i.e. chemoreceptors have “reset” to a new higher CO2 level)
• therefore persistent hypoxia stimulates peripheral chemoreceptors
• respiratory drive is now driven by hypoxia (via peripheral chemoreceptors)
• peripheral chemoreceptors are sensitive to O2 in blood, so even if CNS doesn’t work, the peripheral chemoreceptors will sense drop in O2

Question 14

Why can treatment of hypoxia worse hypercapnia in chromic type 2 resp failure?

Answer 14

1. Treatment of O2 will improve O2 levels but remove stimulus for hypoxic resp drive
   - resp rate will reduce, alveolar ventilation drops which will worsen hypercapnia
2. Correction of hypoxia removes pulmonary hypoxic vasoconstriction
   - leads to increased perfusion of poorly ventilated alveoli
   - blood will be diverted away from better ventilated alveoli

Question 15

How can we treat chronic type 2 resp failure without worsening the hypercapnia?

Answer 15

• watch out for rising blood HCO3
• give controlled oxygen therapy with target saturation of 88-92%
• if oxygen therapy causes rise in pCO2, you need ventilatory support

Question 16

What is the ventilation/perfusion mismatch?

Answer 16

-mismatch of the V/Q ratio
V/Q ratio is usually 1 and V/q matching happens at alveolar level
-when V/Q ratio is <1 the alveolar pO2 falls and pCO2 rises
-when V/Q ratio is >1 the (eg. Hyperventilation due to anxiety) pO2 rises and pCO2 falls

Question 17

In what instances will v/q be less than 1?

Answer 17

• occurs in disorders where some alveoli are being poorly ventilated
• eg. Asthma, pneumonia
• alveolar pO2 falls and pCO2 rises
• hypoxic vasoconstriction occurs which diverts SOME blood to better ventilated areas
• mixed blood in left atrium will have low arterial pO2 and high arterial pCO2
• central and peripheral chemoreceptors are stimulated which causes hyperventilation
• minimal compensation
• see lecture 7.1 slide 11

Question 18

In hyperventilation, what happens to the V/Q of unaffected segments?

Answer 18

• would have increased ventilation, V/Q>1
• pO2 rises and pCO2 falls
• leads to small increase in dissolved O2
• but Hb is fully saturated when pO2 is above 10 kPa
• further increase in pO2 will not affect Hb
• increase is insufficient to compensate for low pO2 from segments with v/Q <1
• results in type 1 resp failure
• see lecture 7.1 slide 12

Question 19

What are some causes of V/Q mismatch?

Answer 19

• occurs in disorders where some alveoli are being poorly ventilated
• ex: asthma, pneumonia, RDS in newborn, pulmonary oedema, pulmonary embolism
• these conditions respond to O2 so patients can improve

Question 20

What happens in a pulmonary embolism regarding V/q?

Answer 20

• embolus results in redistribution of pulmonary blood flow
• blood is diverted to unaffected areas of pulmonary circulation
• leads to V/Q ratio <1 if hyperventilation cannot match the increased perfusion
• causes hypoxaemia
• hyperventilation sufficient to get rid of CO2

Question 21

How can diffusion be impaired?

Answer 21

• barrier is thicker, as in lung fibrosis; slows gas exchange
• pulmonary edema, fluid in interstitial space will increase diffusion distance, occurs in emphysema

Question 22

What condition involves a “shunt” in the respiratory system?

Answer 22

Acute Respiratory Distress Syndrome

Question 23

What is Acute Respiratory Distress Syndrome?

Answer 23

• end result of acute alveolar injury
• caused by damage to alveolar capillary unit
• injury produces increased vascular permeability, edema, heavy and red lungs showing congestion, alveoli containing fluid
• intra-pulmonary shunt
• diffuse loss of surfactant resulting in alveolar atelectasis
• lungs become stiff and less compliant
• very hard to manage on a ventilator since O2 may not correct hypoxaemia, always need to add positive pressure

Question 24

What is asthma?

Answer 24

• chronic inflammatory airways disease characterized by intermittent airway obstruction and hyper-reactivity
• disease of small airways with variable expiratory airflow limitation
• inflammation is usually reversible

Question 25

How common and severe is asthma? Why is it important to get the right diagnosis?

Answer 25

- very common - scan be extremely severe as people can die - important to diagnose since people can die from acute severe asthma

Question 26

What is the difference between asthma and COPD?

Answer 26

- asthma is reversible with bronchodilators, dry cough, wheeze, history of atopy, typically in youngins - COPD is not fully reversible with bronchodilators, productive cough, wheeze, history of smoking, typically older adults

Question 27

What is the pathophysiology of asthma?

Answer 27

- initially a type 1 hypersensitivity reaction - driven by Th2 cells - macrophage present antigens to T lymphocytes which then activates T cells (i.e TH2) - TH2 cells release cytokines which activate mast cells and eosinophils and B cells - B cells produce IgE Immediate response - interaction of allergen and IgE - leads to mast cell degranulation and release of histamine and leukotrienes causing bronchial smooth muscle contraction Late phase response - type 4 hypersensitivity - inflammatory cells release mediators and cytokines which cause airway inflammation See asthma lecture slide 7-8

Question 28

What will an asthmatic patient present with

Answer 28

History of: - cough: worse at night or first thing in the morning due to parasympathetics - wheeze - breathlessness: when you feel more aware of the fact that you’re breathing - chest tightness - atopy: when you get asthma, hay fever and eczema

Question 29

What are the precipitating factors of asthma?

Answer 29

- allergens: pollen, pets - dust - cigarette smoke - cold weather - exercise - infection - aerosols

Question 30

How is asthma diagnosed?

Answer 30

- do peakflow and spirometry test | - see asthma lecture slides 13-16

Question 31

How is chronic asthma damaged?

Answer 31

Primary prevention - evidence is lacking - avoidance of potential triggers during pregnancy/childhood Secondary prevention - remove triggers if possible: pets, dust, smoke, occupation, vaccination - pharmacological: antimuscuranics, B2 agonist, inhaled corticosteroids -look at asthma lecture slide 21-22

Question 32

How is asthma managed using puffers?

Answer 32

-have stepwise management for adults and children separately Different puffers - Reliever: salbutamol - preventer: inhaled corticosteroid - preventer inhaler + symptom controller: seretide or fostair (combination of steroid and long-acting beta agonist) -see asthma lecture slide 25-26

Question 33

How do you distinguish and recognize between acute severe asthma and life threatening asthma

Answer 33

-should do A to E assessment (airways, breathing, circulation, disability, exposure) Acute severe - RR _> 25 - O2 _> 92% (ideally for normal people it is _> 96%) - PEF 33-50% decreasing - HR _>115 - wheezing - cyanosis - cant speak, incomplete sentences Life threatening - RR decreasing less than 25 - O2 < 92% - PEF < 33% - BPis low - altered consciousness (drowsy) - silent chest sounds - cyanosis - cant speak, incomplete sentences

Question 34

How does gas exchange differ in mild/moderate asthma and severe asthma?

Answer 34

- mild/moderate: type 1 resp failure, decrease in both pCO2 and pO2 - severe: type 2 resp failure, increase in pCO2 and decrease in pO2