Respiratory disease Lecture 16 & 18 Flashcards
Briefly describe the two types of respiratory failure
- Low PaO2 but normal/low PaCO2
- Low PaO2 but high PaCO2
What are causes of hypoxaemia?
Hypoventilation eg. Blocked airway
Low P(I)O2 eg. Altitude or asphyxia
Diffusion barrier eg. Fick’s law and fibrosis
ventilation-perfusion mismatch eg. Left-riught shunt
Describe type 2 respiratory failure
Low PaO2 with high PaCO2
Hypoventilation with reduced V(A)
Describe type 1 respiratory failure
Low PaO2 with normal/low PaCO2
Good and bad parts of lung average saturation to lower
Hypoxia stimulates increases ventilation but this only effects the good parts of the lung with little effect on the total saturation as normal lung function is already 100%
Extra CO2 blown off
The low O2 levels will stimulate chemoreceptors which will change the breathing pattern, but will only be able to affect the good part of the lung
What are the consequences of systemic hypoxia?
Central hypoxia- drowsiness and confusion, coma, death
Renal hypoxia- EPO production, increased O2 capacity
Pulmonary hypoxia- hypoxic pulmonary vasoconstriction (HPV), pulmonary hypertension
Hypercapnia- respiratory acidiosis
What is sleep apnoea?
A cessation of breathing during sleep
Absence if naso-oral airflow for more than 10s
Obstructive origin- respiratory efforts
Central origin- no respiratory efforts
Can be central or peripheral
What happens in sleep normally
Stages of sleep: Non-REM and REM (occur in 90 min cycles)
Slow wave sleep (Non-REM)(75-80%) - Stages 1-4 associated with the development of large slow delta waves. Arousal threshold increases with stage (the ability to wake up becomes harder). Within Non-REM, there is low blood supply to the brain asits inactive. Blood pressure and heart rate decrease with each stage of sleep. During Non-REM, CO2 provides the drive to breathe.
Rapid Eye movement (REM) - Paradoxical sleep similar to awake. Dream sate. High blood flow to brain as its active. Higher blood pressure and heart rate as more blood supply going to the brain.
Ventilation goes down in both types.
What happens in obstructive sleep apnoea?
Smooth muscle tone is lost and the airways close more easily- obesity is a risk factor and is associated with hypertension
Experimental modles often include:
Airway occlusion
Chronic intermittent hypoxia
What happens in central sleep apnoea?
Physiological causes:
Sleep-onset- removal of wakefulness exposes apneic threshold
Post-arousal/sigh- arousal has them return to wakefulness- hypercapnic response
Phasic REM sleep- pontogenicolo-occipal (PGO) waves bypass medullary centres and inhibit diaphragm
Hypocapnic CSA:
Low PaCO2 awake with increased CO2 sensitivity- falls below apneic threshold
Heart failure- no rise in PaCO2 in PaCO2 in sleep as no fall in ventilation
High altitude- by lost ventilation induces hypocapnia
Hypercapnia:
CSA Hypoventilation in wakefulness- worsenbs in sleep- arousal
CCHS
Brainstem disorders or opoiod use
What is CCHS?
Congenital central hypoventilation syndrome
During sleep the patient “forgets” to breath CO2 chemoreception?- CO2 provides the drive to breath
PHOX2B mutation- neuronal differentiation and maturation
Treatment- remove hypoventilation, mechanical ventilation, phrenic nerve pacing
Describe the work of breathing
To stretch elastic components of the respiratory system
To overome airway resistance
Diseases of the respiratory system increase the work of breathing by changing:
1) The compliance of the lungs, chest wall or total respiratory system
2) Airway resistance
So extra work is required to overcome airway resistance and move air
Describe asthma
Chronic airway inflammation- caused by alveolar wall infiltration by immune cells which cause swelling
Increased airway responsiveness (increased sensitivty to allergens)
Bronchoconstriction- effective diameter reduced and resistance increased
Airway obstruction (mucus plug)
Wheeze, cough and dyspnoea
Decreased alveolar ventilation- hypoventilation (decreased PAO2 and increased PACO2)
Decreased partial pressure gradients for diffusion of O2 and CO2 lead to hypoxia (decreased PaO2) and hypercapnia (PaCO2)
Reduced- FEV1 (volume of air expired out of lung in the first second maximal expiration), FEV:FVC (maximal air out of lungs in the first second), PEFR (peak expiratory flow rate - cant generate a high flow rate due to resistance)
Treatment-
Relievers: (act to reduce resistance)
Beta-2 agonists- salbutamol (short acting), salmeterol (long acting) (inhalers) Noradreneline/adreneline can bind to stimulating agenylate cyclase causing an increase in cAMP, activating PKA. which will phosphoylate and deactivate myosin light chain kinase causing bronchodilation
Theophyllines - Phosphodiesterase inhibitor- aminophylline Antimuscarinics- iprateropium bromide. Leads to increase in cAMP and causing bronchodilation
Preventers: (acts to cause chronic reduction in imflammaton and airway responsivness)
Steroids- beclometasone, pregnisolone. Counteract airway inflammation- keeps inflammatory cells in check so it reduces the molecules released that casue inflammartion
Leukotriene receptor antagonist- montelukast. Blocks the actions of bronchoconstricting and pro inflammatory leukotriens released from inflammatory cells
Describe chronic obstructive pulmonary disease
Emphysema- loss of elastic recoil and airway traction and reduced surface area for diffussion
Hyperinflation- air trapping
Decreased PEFR, FEV, FEV:FVC LOOK AT SLIDES FOR DIAGRAM
Management- smoking cessation
Bronchi dilators
Oxygen therapy
Reduce exacerbations- vaccinations and corticosteroids to reduce neutrophil infiltration
Describe fibrosis
Decreased lung compliance
Dyspnoea (breathlessness)
Dry cough, Lung crackles, Hypoxamia with hypocapnia
Increased fibroblast proliferation
Increased secretion of elastin and collagen
Fibro collegenous thickening of alveoli
Decreased lung compliance
Increased thickness of diffusion barrier (more difficult to get O2 into blood and CO2 out of blood)
Decreases TLC, VC but no change in FEV:FVC LOOK AT SLIDES FOR DIAGRAM
