Chemical Control of Breahing (S5)

Question 1

Define Hypoxia
Types
Clinical features

Answer 1

Falls in pO2 (pO2 <8kPa= damage). O2 saturation below 94% but damage likely to occur below 90% 
Hypoxaemic: Air --> Airways --> Alveoli 
Anaemic: Pulmonary capillary 
Ischaemic: LH --> Regional arteries 
Histiocytic: Tissues 

Clinical features: Exercise intolerance, tachypnoea, confusion, central cyanosis
chronic: polycythaemia (abnormally high Hb due to increased erythropoetin activation)

Question 2

Define Hypercapnia (+Hypo)

Answer 2

Rise in pCO2 (fall in pCO2)

Question 3

Define Hyperventilation (+Hypo)

Answer 3

Removal of CO2 from the alveoli more rapid than its production (less rapid than its production- hypo)

Question 4

Describe the effects of hyperventilation on plasma pH

Answer 4

Alveolar CO2 falls, pH rises

Question 5

Describe the effects on plasma pH of hypoventilation

Answer 5

Alveolar CO2 rises, pH falls

Question 6

Describe the general effects of acute hypo- and hyper-ventilation.

Answer 6

Hypo: Alveolar CO2 rises, Dissolved [CO2] rises more than [HCO3-], fall in plasma pH –> Respiratory Acidosis
Hyper: alveolar CO2 falls, dissolved [CO2] falls more than [HCO3-], rise in plasma pH –> Respiratory Aklalosis

Question 7

Define Respiratory Acidosis

Answer 7

Increase in alveolar CO2, dissolved [CO2] rises more than [HCO3-] = fall in plasma pH
Hypoventilation

Question 8

Define Respiratory Alkalosis

Answer 8

Alveolar CO2 falls, dissolved [CO2] falls more than [HCO3-], rise in plasma pH
Hyperventilation

Question 9

Define Compensated Respiratory Acidosis

Answer 9

If Respiratory Acidosis persists, the kidney will respond to the low pH reducing excretion of HCO3- (and producing more) thus restoring the ratio of dissolved [CO2] to [HCO3-]

Question 10

Define Compensated Respiratory Alkalosis

Answer 10

If respiratory alkalosis persists the kindey will respond to the high pH by increasing excretion of HCO3-, so the ratio of dissolved [CO2]/ [HCO3-] returns to near normal

Question 11

Define Metabolic Acidosis

Answer 11

Acid produced by metabolising tissues reacts with HCO3- to produce CO2 which is blown off, any decrease in pH due to decrease in HCO3- is metabolic acidosis

Question 12

Define Metabolic Alkalosis

Answer 12

If plasma HCO3- rises there will be metabolic alkalosis

e.g. vomiting

Question 13

Define Compensated Metabolic Acidosis

Answer 13

Metabolic acidosis can be compensated for by increasing ventilation, blowing off excess CO2

Question 14

Define Compensated Metabolic Alkalosis

Why is there a problem is there is also volume depletion?

Answer 14

Can only be partially compensated for by decreasing ventilation
rise in pH in tubular cells (PCT) leads to decreased excretion of H+ ions and decreased HCO3- recovery
Problem: if volume depletion increased Na+ reabsorption favours H+ secretion

Question 15

Describe the acute affects upon ventilation of falling inspired pO2

Answer 15

The arterial pO2 is detected by peripheral chemoreceptors - carotid sinus and aortic sinus- stimulated by a decrease in O2 relative to their own oxygen usage which is small. A high rate of BF through these structures ensures that they do not normally change their response until pO2 is low.

Question 16

Describe the acute affects upon ventilation of increases in inspired pCO2

Answer 16

Chemoreceptors sensitive to raised pCO2: Peripheral chemoreceptors and central chemoreceptors- in the medulla

Question 17

What 3 affects can stimulation of the receptors have?

Answer 17

1. increase in tidal volume and rate of respiration (i.e increase breathing)
2. Changes in circulation directing more blood to brain and kidneys
3. Increased pumping of blood by heart (also detect changes in BP)

Question 18

Describe the location and function of central chemoreceptors and their role in the ventilatory respiratory changes in arterial pCO2 and the roles of the CSF, BBB and choroid plexus in that response

Answer 18

Located on the ventral surface of the medulla and exposed to CSF
Respond to a fall in CSF pH
The CSF is separated from the blood by the BBB which allows free passage of CO2 but not HCO3-
The pH of the CSF is determined by its own HCO3-/H2CO3 buffer system. It contains no Hb.
CSF HCO3- conc, is determined by the activity of choroid plexus cells which pump HCO3- into and out of the CSF and is largely dependent on plasma [HCO3-]
CSF dissolved [CO2] is determined by plasma pCO2 although rapid changes in plasma pCO2 can take time to influence the CSF.
CSF pH and thus stimulus to the central chemoreceptors determined by -Dissolved [CO2]/[HCO3-]
If arterial pCO2 changes then after a short delay the CSF pCO2 will follow =changes in CSF pH –> chemoreceptors =Changes in breathing which tend to restore the CSF pH, negative feedback.
If feedback does not occur (e.g additional stimulaus to ventilation-hypoxia) stimulation of choroid plexus ells to pump more/less HCO3- into CSF and change [HCO3-] to bring ratio back towards normal, CSF corrected much quicker than blood because of the reduced volume. RESET

Question 19

What cells is CSF produced by?

Answer 19

Choroid and ependymal cells
Total vol ranges 140-270ml, produced at a range of 500-600ml/day large amounts drain into the venous system and lymphatics
Major constituents; water, glucose (~2/3rd of blood con. ), NaCl and protein
Normal appearance: clear as almost devoid of cells

Question 20

What cells is CSF produced by?

Answer 20

Choroid and ependymal cells
Total vol ranges 140-270ml, produced at a range of 500-600ml/day large amounts drain into the venous system and lymphatics
Major constituents; water, glucose (~2/3rd of blood con. ), NaCl and protein
Normal appearance: clear as almost devoid of cells

Question 21

Discuss the permeability of the BBB

Answer 21

small lipid-soluble and unchaged molecules can pass BBB: H2o, CO2, O2, Ethanol, Nicotine
Can not cross: H+, HCO3-, Glycine, Catecholamines

Question 22

Define Type 1 respiratory Failures

Answer 22

pO2 <8kpa, O2 sat <90%, normal or low pCO2
V/Q mismatch (low PCO2)
Diffusion impairment (normal pCO2)

Question 23

Define Type 2 respiratory failures

Answer 23

pO2 <8kPa, O2 sat <90%, HIGH pCO2 > 6.7 kPa

Hypoventilation

Question 24

Describe how ventilation/perfusion mismatch and diffusion impairment result in type 1 respiratory failure

Answer 24

Ideally V/Q =1 
if V/Q <1 (pO2 decreased &amp; pCO2 increased) 
chemoreceptors stimulated = hyperventilation = decreased pCO2 and therefore causes Type 1 resp. failure. 
Diffusion Impairment (e.g. thickness of diffusion pathway increased in lung fribrosis or decreased SA in emphysema): O2 diff is affected, CO2 unaffected as its 20X more soluble. =Type 1 Resp failure

Question 25

Outline important cases of type 1 resp. failure

Answer 25

Reduced ventilation of part of lung: 
- pneumonia
- Actue asthma/COPD
- RDS of newborn 
Reduced perfusion of part of lung
- PE rest of lung receives increased Q, V/Q mismatch (<1)

Question 26

Describe how hyperventilation results in type 2 respiratory failure and outline important cases

Answer 26

Hypoventilation increased pCO2 and decreased pO2 —> stimulates central chemoreceptors= increase in ventilation
However due to disease unable to completely correct deficit, increase in CO2 = respiratory acidosis, acute presentation usually needs ventilation.
Causes:
Acute asthma/Late COPD
Respiratory Centre Depression- Opiates/head injury
Trauma @brain stem
Gullian Barre syndrome @nerves
Respiratory muscle weakness Myasthesia Gravis @neuromuscularis, Myopathy/MND @resp muscles
Severe obesity/kyphoscoliosis/Flaial segment @chest wall
Pneumothorax/pleural effusion @pleural cavity
RDS newborn/lung fibrosis @lung decreasing compliance
Laryngeal oedema/foreign body @URT obstruction

Treatment:
Acute: Ventilatory support & treat cause
Chronic: develops over time and allows for development of compensatory responses monitor for resp depression eventually require ventilatory support

Question 27

What is polycaethemia and why might it occur?

Answer 27

Increased Hb concentration in blood
Living at high altitude (also have increased 2,3 BPG and increased capillary density in tissues)
Chronic hypoxia increased erythropoetin

Question 28

Outline the distribution and composition of normal flora of the respiratory tract

Answer 28

Neisseria spp.
Anaerobes
Candidia sp
strep pneumonia
step pyogenes
Haem influenzae 
LRT: relatively bacteria free

Question 29

Outline the natural defences of the respiratory tract against infection

Answer 29

Nasal hairs, mucociliarly clearnece, cough/sneezing reflexes, lymphoid follicles of pharynx and tonsils, alveolar macrophages, local secretions igG and igA

Question 30

List the main infectious diseases of the URT and state the organisms commonly causing these infections

Answer 30

Rhinitis, pharyngitis, epiglottitis, laryngitis, tracheitis, sinusitis, otitis media
rhinovirus, influenza, RSV, parainfluenza, coranvirus
Bacterial super infection is common with sinusitis and otitis media can lead to mastoridits, meningitis and brain abscess

Question 31

Define the term pneumonia

Answer 31

General term denoting inflammation of the GE region of the lung, usually due to infection= cellular exudate in alveolar spaces
Presentation: Fever, cough, pleuritic chest pain, SOB, abnormal CXR

Question 32

Distinguish between lobar pneumonia, broncho pneumonia, interstitial pneumonia, aspiration pneumonia and chronic pneumonia

Answer 32

Lobar pneumonia: Localised to particular lobes of the lungs
bronchopneumonia: More diffuse and patchy, arising in bronchi/bronchioles
Interstitial pneumonia : Idiopathic, characterized by diffuse alveolar damage and subsequent fibrosis. Present with sudden onset dyspnea and rapid resp failure.
Aspiration pneumonia: Food/saliva/liquid/vomit inhaled and therefore bacteria inhaled leading to infection (common in stroke pts.)
Chronic pneumonia: Lasts at least 6 weeks and usually caused by slow growing organisms i.e fungi or mycobacteria

Question 33

Describe the infectious aetiology of acute community acquired and acute hospital acquired pneumonia

Answer 33

Community acquired:
~85% s.pneumoniae, H.influenzae, K.pneumonia, Staph aureus
~15% Legionella, mycoplsma
Hospital Acquired:
20-60% s.pneumoniae (also Gram -ve klebsiella, pseudomonas, E.coli etc), Staph aureaus