Resp Session 5 Flashcards
What are changes in blood pH called before HCO3- becomes involved?
Alkalaemia/acidaemia
What happens in to pO2 and pCO2 in exercise?
Metabolism increases –> decreased pO2 and increased pCO2 –> breathing alters to restore partial pressures
What happens to pO2 and pCO2 in hyperventilation?
Ventilation increases but metabolism stays constant so pO2 increases and pCO2 decreases
What happens to pO2 and pCO2 in hypoventilation?
Ventilation decreases but metabolism stays constant –> decreased pO2 and increased pCO2
What happens if pO2 decreases without a change in pCO2?
Correction of decreased pO2 by increasing RR leads to hypocapnia
Why do small pCO2 changes cause big pH changes?
Logarithmic function in the relationship
What happens in respiratory acidosis?
Hypoventilation –> increased pCO2 –> hypercapnia –> decreased pH
How is respiratory acidosis compensated?
Kidneys increase [HCO3-] by reducing excretion over 2-3 days
What happens in metabolic acidosis?
Tissues produce acid –> acid reacts with HCO3- –> decreased [HCO3-] and increased CO2 –> decreased pH
How is metabolic acidosis compensated?
Increase ventilation to decreased pCO2
What happens in respiratory alkalosis?
Hyperventilation –> decreased pCO2 –> hypocapnia –> increased pH
How is respiratory alkalosis compensated?
Kidneys decrease [HCO3-] by increasing excretion over 2-3 days
What happens in metabolic alkalosis?
Loss of H+ –> decreased HCO3- –> increased pH
How is metabolis alkalosis compensated?
Decreasing ventilation but this is limited by hypoxia risk
What sensors have inputs into the respiratory control sensors?
Central chemoreceptors
Peripheral chemoreceptors
Pulmonary receptors
Joint and muscle receptors
What do central chemoreceptors detect?
H+
What do peripheral chemoreceptors detect?
O2, CO2, H+
What do pulmonary receptors detect?
Stretch
What do joint and muscle receptors detect to send signals to the respiratory control centre?
Stretch and tension
What are the effectors of the respiratory control centre?
Diaphragm
Inspiration: external intercostals and accessory muscles
Expiration: internal intercostals and abdominal muscles
What partial pressure can pO2 decrease down to before sats markedly affected as shown by the plateau on the Hb dissociation curve?
8 kPa
Where are peripheral chemoreceptors located?
Carotid and aortic bodies
How do peripheral chemoreceptors signal respiratory changes?
Have highest bloodflow of any tissue so signal large decrease in pO2 when their metabolic demands are not met
Why are peripheral chemoreceptors relatively insensitive to pO2 changes?
Have low metabolic demands
What might cause peripheral chemoreceptors to respond to normal pO2?
Circulatory problems impacting bloodflow
What do peripheral chemoreceptors stimulates?
Increased breathing
Change in heart rate
Change in bloodflow distribution to protect more vulnerable tissues
Are peripheral chemoreceptors sensitive to pCO2?
No, relatively insensitive
Where are central chemoreceptors found?
Ventral surface of brainstem in the medulla very close to effector neurones
What do central chemoreceptors respond to changes in?
[H+] in CSF
What causes changes in [H+] in the CSF?
Production from CO2 moving across blood-brain barrier and undergoing carbonic anhydrase activity in the CSF
What do small variations in pCO2 detected by central chemoreceptors stimulate?
Increase –> increased ventilation
Decrease –> decreases ventilation
What controls CSF composition?
Choroid plexus cells
What is the result of the blood-brain barrier being impermeable to HCO3-?
Changes in pCO2 controlled by changes in ventilation cause changes in CSF pH
What can choroid plexus cells do to tolerate a persistent change in pCO2?
Selectively add H+ or HCO3- to alter CSF composition
What is the response of choroid plexus cells to persisting hypoxia as seen in early lung disease?
Hypoxia detected by peripheral chemoreceptors –> increased ventilation –> pCO2 decreases –> CSF changes composition to accept new pCO2 as normal
What is the action of choroid plexus cells in persisting hypercapnia as seen in progression of lung disease?
Hypoxia and hypercapnia –> respiratory acidosis –> decreased pH of CSF –> peripheral and central chemoreceptors increase breathing –> acidic pH bad for neurones -> choroid plexus add HCO3- to CSF to accept high pCO2
Give the stages in transport of oxygen from the air to tissues.
Air -> airways -> alveoli -> diffusion across alveolar capillary membrane -> binds to Hb in pulmonary capillary -> pulmonary veins -> L atrium -> L ventricle -> CO -> aorta -> regional arteries -> capillary blood -> tissues
What are the four types of hypoxia?
Hypoxaemic/respiratory
Anaemic
Stagnanct/circulatory
Cytotoxic
What’s is stagnant/circulatory hypoxia?
Reduced delivery of oxygen due to poor perfusion which can be global (shock) or local (peripheral vascular disease)
What is cytotoxic hypoxia?
Where tissues can’t utilise delivered oxygen e.g. cyanide poisoning
What is respiratory failure?
Not enough oxygen enters the blood +/- not enough CO2 leaves
What is type I respiratory failure?
Decreased oxygen entry but CO2 is not compromised
O2 sats
What causes type I respiratory failure?
Diffusion defects such as fibrotic lung disease, pulmonary oedema or emphysema which affect oxygen exchange more due to its lower solubility
V/Q mismatch
Why is pCO2 normal or low in type I respiratory failure?
Hypoxia stimulates hyperventilation
What is type II respiratory failure?
Decreased oxygen entry and decreased CO2 exit causing pO2
What causes type II respiratory failure?
Ventilatory failure which can be due to suppression of the respiratory centre, muscle weakness, chest wall problems, very severe fibrosis or increased airway resistance
Why is TB usually seen at the apex of lungs?
Higher pO2 for mycobacteria
How does the V/Q vary across the lung?
Apex: V/Q>1
Most of lung = 1
Base: V/Q
How is respiratory failure managed?
Test cause
Type I: O2 therapy to improve gradient for diffusion and O2 uptake in V/Q mismatch
Type II: hypercapnia may need assisted ventilation
What are some clinical fractures of hypoxia which are common to both type I and II respiratory failure?
Exercise intolerance
Tachypnoea
Confusion
Central cyanosis
What visible changes occur in a pt with sats
Central cyanosis with concomitant peripheral cyanosis due to arrival of already desaturated blood to peripheries
How does the body respond to the gradual development of chronic hypoxia in COPD?
Increased EPO increases Hb levels by causing polycythaemia
2,3-DPG increased to aid tissue oxygenation
What leads to cor pulmonale in chronic hypoxia?
Hypoxic vasoconstriction of pulmonary arterioles eventually –> pulmonary hypertension –> RH failure
Is chronic hypoxia seen in type I or II respiratory failure?
Can be either
What is the commonest cause of chronic type II respiratory failure?
COPD
What happens in chronic type II respiratory failure?
CO2 retention in some pts –> central chemoreceptors reset -> increased tolerance of high pCO2 acts on CNS –> warm hands and flapping tremors
What drives respiration in chronic type II respiratory failure?
Hypoxia via peripheral chemoreceptors
How is chronic type II respiratory failure treated?
Titrated O2 therapy which needs close monitoring
Why does O2 therapy need to be closely monitored when treating COPD pts with chronic type II respiratory failure?
Can worsen hypercapnia by reducing respiratory drive and shunting hypoxic vasoconstriction in place to improve V/Q mismatch
What environmental cause can lead to chronic hypoxia?
High altitude
What is asthma characterised by?
Reversible airflow obstruction
Airway wall inflammation and remodelling
Increased airway responsiveness
What is the function of airways smooth muscle in utero and in the adult?
In utero: airway persistalsis to create a mechanical stimulus for growth
In adult: no function - have no resting tone
What differences are seen in the structure of the asthmatic airway wall?
Increased airway smooth muscle thickness
Damaged epithelium
Thickened basement membrane
Same number of alveolar attachments
What mediates airway wall remodelling in development of asthma?
Cells and soluble mediators of chronic inflammation - cytokines, neutrophils, mast cells and growth factor
What can trigger airway smooth muscle contraction?
Muscarinic agonists
Histamine
Cold air
Arachadonic acid metabolites e.g. prostaglandins
What effect does a 10% decrease of effective radius in the airways have on flow?
Decreases by 35%
What effect does a 20% decrease of effective radius in the airways have on flow?
Decreases by 50%
How can triggers of airway smooth muscle contraction be used to assess FEV1 in asthma diagnosis?
Most healthy people can tolerate toxic doses of these without any contraction but asthma pts will experience contraction (airway hyper-responsiveness)
Describe the aetiology of asthma.
FHx due to genetics Sensitisation to airborne allergens Pre/post natal/active exposure to tobacco smoke Aspirin sensitive asthma Occupational Viral induced wheeze
What is aspirin sensitive asthma?
Over production of pro-inflammatory leukotrienes due to anomaly in arachidonic acid metabolism seen only in adults
Are asthma symptoms experienced outside of the working environment in occupational asthma?
No
How does viral-induced wheeze compare to asthma?
Children
What is the immediate response in allergic asthma?
Allergen and specific IgE antibodies –> mast cell degranulation –> mediator release –> bronchoconstriction
What is the immediate response in allergic asthma an example of?
Type I hypersensitivity
How long after exposure to an allergen does the immediate response peak in allergic asthma?
~20 mins
What happens in the late phase response of allergic asthma?
Full spectrum of inflammatory cells infiltrate and thicken bronchial walls
Release of mediators and cytokines –> oedema in mucosa due to vascular leak
Abnormal mucus over-production
ASM contraction
Shedding of epithelium due to toxic cytokines
What is the late phase response in allergic asthma am example of?
Type IV hypersensitivity
How long after exposure to an allergen is the late phase response seen in allergic asthma?
3-12 hrs
What features lead to a clinical diagnosis of asthma?
Recurrent wheeze Recurrent breathlessness Recurrent chest tightness Recurrent cough which is non productive with diurnal pattern Variable airflow obstruction
What is a wheeze?
Variable intensity and tonicity expiratory sound originating from vocal cords
What lung function tests can be used in asthma diagnosis?
PEFR - often shows diurnal pattern Spirometry Exercise induced bronchoconstriction Exhaled NO Allergy testing CXR
How is asthma managed?
Education: recognise symptoms, how to use medication
Primary prevention: stop smoking, exposure to allergens, fresh air
Pharmacology: airway relaxants to provide relief e.g. beta agonists, antimuscarinics, anti inflammatory agents for prevention e.g. corticosteroids, leukotriene receptor antagonists
Why do preventer pharmacological interventions used in asthma have poor compliance?
Have no visible effects
What is the classification of mild acute asthma?
> 92% sats in air
HR75% predicted
What is the classification of moderate acute asthma?
Same as mild but with PEFR 75-50% predicted
What is the classification of severe acute asthma?
110 RR>25 Can't complete sentences No wheeze due to lack of air PEFR 35-50% of predicted
What type of respiratory failure do mild/moderate acute asthma pts experience?
Type I
What type of respiratory failure do severe acute asthma pts experience?
Type II
