Chemical Control of Breahing (S5) Flashcards
Define Hypoxia
Types
Clinical features
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)
Define Hypercapnia (+Hypo)
Rise in pCO2 (fall in pCO2)
Define Hyperventilation (+Hypo)
Removal of CO2 from the alveoli more rapid than its production (less rapid than its production- hypo)
Describe the effects of hyperventilation on plasma pH
Alveolar CO2 falls, pH rises
Describe the effects on plasma pH of hypoventilation
Alveolar CO2 rises, pH falls
Describe the general effects of acute hypo- and hyper-ventilation.
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
Define Respiratory Acidosis
Increase in alveolar CO2, dissolved [CO2] rises more than [HCO3-] = fall in plasma pH
Hypoventilation
Define Respiratory Alkalosis
Alveolar CO2 falls, dissolved [CO2] falls more than [HCO3-], rise in plasma pH
Hyperventilation
Define Compensated Respiratory Acidosis
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-]
Define Compensated Respiratory Alkalosis
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
Define Metabolic Acidosis
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
Define Metabolic Alkalosis
If plasma HCO3- rises there will be metabolic alkalosis
e.g. vomiting
Define Compensated Metabolic Acidosis
Metabolic acidosis can be compensated for by increasing ventilation, blowing off excess CO2
Define Compensated Metabolic Alkalosis
Why is there a problem is there is also volume depletion?
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
Describe the acute affects upon ventilation of falling inspired pO2
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.
Describe the acute affects upon ventilation of increases in inspired pCO2
Chemoreceptors sensitive to raised pCO2: Peripheral chemoreceptors and central chemoreceptors- in the medulla
What 3 affects can stimulation of the receptors have?
- increase in tidal volume and rate of respiration (i.e increase breathing)
- Changes in circulation directing more blood to brain and kidneys
- Increased pumping of blood by heart (also detect changes in BP)
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
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
What cells is CSF produced by?
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
What cells is CSF produced by?
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
Discuss the permeability of the BBB
small lipid-soluble and unchaged molecules can pass BBB: H2o, CO2, O2, Ethanol, Nicotine
Can not cross: H+, HCO3-, Glycine, Catecholamines
Define Type 1 respiratory Failures
pO2 <8kpa, O2 sat <90%, normal or low pCO2
V/Q mismatch (low PCO2)
Diffusion impairment (normal pCO2)
Define Type 2 respiratory failures
pO2 <8kPa, O2 sat <90%, HIGH pCO2 > 6.7 kPa
Hypoventilation
Describe how ventilation/perfusion mismatch and diffusion impairment result in type 1 respiratory failure
Ideally V/Q =1 if V/Q <1 (pO2 decreased & 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
Outline important cases of type 1 resp. failure
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)
Describe how hyperventilation results in type 2 respiratory failure and outline important cases
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
What is polycaethemia and why might it occur?
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
Outline the distribution and composition of normal flora of the respiratory tract
Neisseria spp. Anaerobes Candidia sp strep pneumonia step pyogenes Haem influenzae LRT: relatively bacteria free
Outline the natural defences of the respiratory tract against infection
Nasal hairs, mucociliarly clearnece, cough/sneezing reflexes, lymphoid follicles of pharynx and tonsils, alveolar macrophages, local secretions igG and igA
List the main infectious diseases of the URT and state the organisms commonly causing these infections
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
Define the term pneumonia
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
Distinguish between lobar pneumonia, broncho pneumonia, interstitial pneumonia, aspiration pneumonia and chronic pneumonia
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
Describe the infectious aetiology of acute community acquired and acute hospital acquired pneumonia
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
