Respiratory S5 (Done) Flashcards
Define the term hyperventilation
What affect will this have on partial pressures of respiratory gases in the alveoli?
Ventilation increase with no change in metabolism
pCO2 falls
pO2 rises
Define hypoventilation
What affect will this have on alveolar gases partial pressure?
Ventilation decrease with no change in metabolism
pCO2 rises
pO2 falls
In what situations can changes in ventilation rate not correct imbalance in respiratory gases partial pressure?
If pCO2 or pO2 change without an opposite reaction from the other gas such as in the case of hypo/hyper-ventilation then the system cannot be controlled by change in ventilation
In these cases one gases partial pressure is prioritised for control
E.g. If pO2 falls without change in pCO2 then increase in ventilation will correct hypoxia but produce hypocapnia
What is hypoxia?
When does it become significant?
Fall in pO2 in arterial blood below 8kPa
Fall of pO2 below 8kPa significantly reduces saturation of Hb
Further falls lead to large reduction in O2 transport
What is the link between pCO2 and plasma pH?
pCO2 affects plasma pH
pH = pK + Log10 ([HCO3-] / (pCO2 x 0.23))
At constant HCO3-
pCO2 fall leads to rise in pH and vise versa
Small changes in pCO2 lead to large changes in Plasma pH
Ratio of [HCO3-] and pCO2 determine plasma pH
What are the effects of significantly increased or decreased plasma pH?
Plasma pH below 7.0:
Lethally denatured enzymes
Plasma pH above 7.6:
Free [Ca2+] increase
Tetany
Describe the effects of hyper/hypo-ventilation on plasma pH
Hyperventialtion:
pCO2 falls
pH rises
Causes respiratory alkalosis
Hypoventialtion:
Leads to rise in pCO2
pH falls
Causes repiratory acidosis
Describe the role of the kidneys in plasma pH control
Changes in pCO2 can be compensated for by changes in [HCO3-] (which is controlled by the kidneys)
Respiratory alkalosis is compensated for by increase in [HCO3-]
Respiratory acidosis is compensated for by decrease in [HCO3-]
Takes 2-3 days
Describe the involvement of other body tissues on the plasma pH
Metabolic acidosis:
Tissue metabolism produces H+ and CO2
this reacts with HCO3- and increases CO2
Fall in pH results
Can be compensated for by increased ventilation (lowers pCO2)
Metabolic alkalosis:
Plasma HCO3- rise
Plasma pH rises
Can be compensated for by decreasing ventilation (to a degree)
What might cause rise in plasma HCO3-?
Vomiting
Stomach acid must be replaced
H20 + CO2 = HCO3- + H+
H+ enters stomach and HCO3- is expelled into blood
Describe Peripheral chemoreceptors
**Hint: **Functions and locations
Found in the carotid bodies and aortic bodies
Monitor arterial pO2:
Large falls in pO2 stimulate:
- increased ventialtion rate*
- changes in heart rate*
- diversion of blood flow to brain*
Hence they couteract and protect against the effects of hypoxia
Monitor arterial pCO2:
Detect changes in pCO2 but are very insensitive, this function is largely ignored
What are the functions of central chemoreceptors?
Where are they found?
Functions:
Detect small changes in pCO2 in the CSF
Will increase or decrease ventilation to compensate for changes in pCO2
Negative feedback control of breathing
Found:
Medulla
What structures control the pH of the CSF?
Blood brain barrier:
Allows free movement of CO2 therefore CSF pCO2 determined by arterial pCO2
Impermeable to HCO3-
Choroid plexus cells in blood brain barrier:
Control [HCO3-] in CSF
Describe short term control of CSF pH
[HCO3-] fixed in short term
Fall or rise in pCO2 of arterial blood and hence CSF leads to change in CSF pH
Change in pH detected by central chemoreceptors
Leads to change in vntialtion drive which in turn corrects pCO2
pH returns to normal and ventilation drive is changed accordingly
Describe longer term regulation of the CSF pH
Persistent change in pCO2 and hence CSF pH lead to change of [HCO3-] by the Choroid plexus cells
CSF [HCO3-] determines the pCO2 set points that are associated with ‘normal’ CSF pH
Change in the [HCO3-] leads to a change in these set points
E.g. Long term increase in pCO2 in CSF leads to a rise in [HCO3-] in CSF and therefore a rise in pH, this stops the response of the central chemoreceptors to the rise pCO2 by correcting/raising pH without correcting pCO2
As a result, the central chemoreceptors are reset to act around this new set point of pCO2 (which although is raised is now seen as normal by the central chemoreceptors)
List the oxygen and CO2 transport chains
O2:
Air - Airways - Alveoli - Alveolar membrane - Arterial blood - Regional arteries - Capillary blood - Tissues
CO2:
Tissues - Regional veins - Venous blood - Alveolar membrane - Alveoli - Airways - Air
What are the typical pCO2 and pO2 in the:
- Air*
- Alveolar air*
- Venous blood*
- Arterial blood*
Air:
p02 - 21kPa
pCO2 - 0.03kPa
Alveolar Air:
p02 - 13.3kPa
pCO2 - 5.3kPa
Venous Blood:
p02 - 5.3kPa
pCO2 - 6.1kPa
Arterial Blood:
p02 - 13.3kPa
pCO2 - 5.3kPa
What is the ideal ventilation/perfusion ratio?
What is the V/P ratio at the lung apex and base?
Ideal:
V/P = 1 (l/min)
Apex:
Alveolar ventilation - 0.24l/min
Blood flow - 0.07l/min
Ratio = 3.3
Base:
Alveolar ventilation - 0.82l/min
Blood flow - 1.29l/min
Ratio = 0.63
What is the effect of fibrotic lung disease on alveolar exchange and hence the arterial blood?
Exchange surface is thickened
Arterial pO2 = Low
Arterial pCO2 = Normal (CO2 diffuses easier than O2)
What is the effect of Pulmonary Oedema on alveolar exchange and hence the arterial blood?
Exchange surface is normal but there is increased perfusion distance
Arterial pO2 = Lower
Arterial pCO2 = Normal (CO2 more soluble than O2)
What is the effect of Emphysema on alveolar exchange and hence the arterial blood?
Exchange surface area is decreased
Arterial pO2 = Low
Arterial pCO2 = Normal (Diffuses easier than O2)
What is the broad definition of respiratory failure?
Not enough oxygen enters the blood or not enough Co2 leaves the blood
Doesn’t necessarily occur together
What is type 1 resp failure?
Not enough O2 enters blood
CO2 removal not compromised
pO2 of arterial blood = Low
pCO2 of arterial blood = Normal of slightly low
What is type 2 resp failure?
Not enough O2 enters blood
Not enough CO2 leaves blood
Arterial pO2 = Low
Arterial pCO2 = High
What is ‘Oxygen saturation’?
How is it measured?
What is the ideal measurement?
O2 saturation of Hb in arterial blood (SaO2)
Measured with a pulse oximeter and expressed as a %
Ideally >95%
What is arterial blood gas analysis?
Arterial blood obtained (usually from radial artery)
Blood is heparinised and put in cold water (prevents clotting)
Sample put through a blood gas analyser
Normally reads pCO2, pO2 and pH
What would be the results of an ABG, pulse oximetry and resp rate observation in a patient with type 1 resp failure?
Low pH
Hypoxic
Normal CO2
Low Hb saturation (<95%)
High resp rate
What are the 2 categories of Type 1 Resp failure?
Give examples of conditions in each category
Some alveoli poorly ventilated:
Pulmonary embolism
Pneumonia
Consolidation
Early stages of acute asthma
Most alveoli poorly ventilated:
Pulmonary Oedema
Fibrosis
- Fibrosing alveolitis*
- Extrinsic allergic alveolitis*
- Pneumoconiosis*
- Asbestosis*
What are the common features of a patient with type 1 resp failure?
Breathlessness
Exercise intolerance
Central cyanosis
What are the typical findings of an ABG, Pulse oximetry and observation of resp rate in a patient with type 2 resp failure?
Low pH
Hypoxia
Hypercapnia
<95% Hb saturation
High resp rate
Give some examples of causes of type 2 resp failure
Ineffective respiratory effort:
Poor resp effort
- Resp depression (narcotics)*
- Muscle weakness (upper or lower motor neurone disease)*
Chest wall problems
- Scoliosis/Kyphosis*
- Trauma*
- Pneumothorax*
Hard to ventilate lungs
- High airway resistance (bronchitis, asthma)
Emphysema
Describe the causes and effects of emphysema
Cause:
Alpha1 - antitrypsin deficiency (genetic or smoking)
Effects:
Increased lung compliance (Barrel chest)
Airway obstruction (bronchiole collapse during expiration)
V/P mismatch
Reduced O2 absorption
Type 1 failure initially
Progresses to type 2 as CO2 transport impaired
Describe how the body reacts to acute hypoxia
pO2 falls below 8kPa
Peripheral chemoreceptors sense this and increase respiratory drive
This leads to correction of hypoxia but causes hypocapnia
Leads to rise in CSF pH causing an attempted reduction in respiratory drive
How does the body react to acute hypoxia?
Increased ventilation causes hypocapnia
Renal correction of acid base balance in blood (decrease in HCO3- in blood corrects pH)
Increased ventilation persists due to continued action of peripheral chemoreceptors
What are the acute effects of type 2 resp failure?
pCO2 rises, pO2 falls
Central chemoreceptors increase respiratory drive
Breathlessness is felt and respiration rate increases
This provides some respiratory compensation
However poor ventilation (due to disease) prevents full compensation
What are the chonic effects of type 2 resp failure?
CO2 retention:
CSF rise in pCO2 corrected by choroid plexus
Central chemoreceptors are reset to higher CO2 level
Hypoxia persists
Reduction in respiratory drive (which is now driven by peripheral chemoreceptors (hypoxia)
Pulmonary circulation:
Hypoxia causes pulmonary hypertension
leads to right heart failure (cor pulmonale)
Hypoxia:
Increased Hb (polycythaemia)
2,3 BPG release
Increased respiratory effort:
Increased work required for breathing
Severely disabling
Define Asthma
A chronic disorder characterised by:
- Chronic inflammation leading to Airway wall remodelling*
- Reversible, variable airflow reduction*
- Increase in airway response to variety of stimuli (Airway hyper-responsiveness)*
- Susceptibility to infection*
Compare airway remodelling in Asthma with other weezing disorders
Asthma:
Increased acellular membrane thickness
Damaged epithelium
Thickened reticular basement membrane
Smokers or premature lungs:
As in asthma
+ Loss of alveolar septa
Describe the initial cellular reaction to allergen exposure in asthma
Th2 lymphocytes are activated by macrophages which have absorbed and processed the antigen
Th 2 cells release cytokines which attract and activate mast cells and eosinophils also B cells, which produce IgE
2 phase response results
Immediate response phase(0-20 minutes):
Interaction of allergen and specific IgE leads to mast cell degranulation and mediator release (Histamine, tryptase, prostaglandins and leukotriene)
This leads to bronchial smooth cell contraction/bronchoconstriction
Late phase response (3-12 hours later):
Complex array of inflammatory cells, mediators and cytokines that causes airway inflammation
Eosinophils release leukotriene C4 which causes shedding of epithelial cells
What cells/mediators are involved in airway remodelling in asthma?
What is the process called that leads to this airway remodelling?
Cellular:
Neutrophils
Eosinophils
Mast cells
Soluble mediators:
Cytokines (TNF-a)
Leukotrienes
Growth factor (involved in repair)
Process:
Chronic inflammation
In what ways do airway inflammation reduce airway diameter?
Mucosal oedema due to vascular leak
Thickening of bronchial walls due to infiltration of inflammatory cells
Mucus overproduction (thich, tenacious, slow moving, Doesnt come up in dry cough)
Smooth muscle contraction
Hyperresponsiveness of airways
Airway remodelling:
- Hypertrophy and hyperplasia of smooth muscle*
- Hypertrophy of mucus glands*
- Thickening of basement membrane*
What are the effects of airway narrowing in asthma?
Wheeze and other clincal features of asthma
Obstructive pattern on spirometry (decreased FEV1/FVC ratio and obstructive flow volume loop)
Air trapping increases residual volume
Describe the effects of asthma on the ventilation/perfusion ratio and the concequences of this
Airway narrowing leads to reduced ventilation
Hyperventilation cannot compensate for reduced O2 but can compensate for CO2 retention by increasing breathed out CO2
Mild to moderate attack:
Reduced pCO2 and pO2
Type 1 resp failure
Severe attacks:
More extensive airway involvement + exhaustion due to hyperventilation leads to further gas exchange impairment and the loss of CO2 compensation
Reduced pO2 and Increasing pCO2
Type 2 resp failure
Can be life threatening
Why do small smooth muscle contractions in the airway have such a large effect on breathing?
SM contraction lead to narrowing of airways
Flow is greatly impeded even by seemingly small contraction
There is also a large increase in the work required to breath
E.g. A 20% reduction in airway diameter leads to 60% reduced airflow and greatly increased work in breathing
What are some of the direct triggers to Airway smooth muscle (ASM) contractions?
Muscarinic antagonists (E.g. Ach)
Histamine
Cold air
Arachadonic acid metabolites (Prostaglandins, Leukotrienes)
What is airway hyper-responsiveness?
What is its relevance to asthma?
Where a larger % reduction in FEV1 is seen in response to increasing histamine levels than would be normally expected
AHR is a feature of asthma, however many non-asthmatics have AHR
You recieve the flow/volume loop of a patient showing airway obstruction, Suspected diagnoses based on other elements of the history are COPD or Asthma
How do you differentiate?
Airway obstruction in asthma is reversible:
>15% improvement spontaneously or on administration of bronchodilators or steroids
COPD airway obstruction is not:
<15% improvement with treatment
What are some of the causes of asthma?
Hereditary
Sensitisation to airborn allergens:
Air pollution
Tobacco smoke (pre/post-natal or direct)
Fungal spores (Damp housing)
Hygiene hypothesis:
Excess hygiene in childhood leads to derangement of normal immune development
Give examples of atopic and non-atopic asthma
Atopic (Type 1 hypersensitivity)
Allergic asthma
Viral induced wheeze (Classified as asthma in under 5s)
Non-atopic (not type 1 hypersensitivity associated):
Aspirin sensitive asthma
Occupational asthma (Farmers, Bakers, Welders)
How is an asthma diagnoses made?
Clinical diagnoses only, non standard definitions for type, severity, findings on investigation etc.
Includes 1 or more of these reccurent symptoms:
Wheeze
Breathlessness
Chest tightness
Cough
Variable airflow obstruction
AHR and airway inflammation assessment
Describe an asthmatic wheeze
Wheeze:
High pitched, expiratory, musical
Originates in airways which have been narrowed by compression or obstruction
In asthma:
Variable intensity and tone
Bilateral
Describe an asthmatic cough
Often worse at night
Exercise induced
Dry (wet indicates infection/COPD etc)
Describe the pattern of breathing difficulty experienced by asthma patients
Often with exercise
During acute exacerbations
Assessment might find:
- Tachypnoea*
- Intercostal Recession (negative pressures draw intercostal muscles inward)*
- Tracheal tug (movement of the trachea and thyroid cartilages downwards)*
A prolonged expiratory phase is with or without wheeze is a common marker of asthma
What are the features of a history in a patient with suspected asthma?
Onset and pattern of symptoms:
Symptoms
Disturbance to life
Precipitating factors
Past medical history:
Hayfever, eczema
Prenatal smoke exposure
Family history:
Asthma, smoking
Occupational history:
Farms, Woods, Coal fires
Non-asthma drug history
Pets
When performing an examination on a patient with suspected asthma what might you expect to find?
Inspection:
Chest:
- Scars or deformities*
- Hyperexpansion (barrel chest)*
General:
- Hayfever*
- Eczema*
- Lethargy*
- Can they talk?*
Room:
- Meds*
- Charts*
Percussion:
Hyperresonant
Ascultation:
Polyphonic wheeze
Give examples of common and uncommon chest wall deformities in asthma
Common:
Harrison’s Sulcus (indrawing of costal cartilages in children
Uncommon:
Sternal (pectus) deformities
How is PEFR measured?
With a peak flow meter:
Check flow meter is at zero, sit the patient upright
Hold device horizontal ask the patient to take a deep breath, firmly seal lips around the mouthpiece and exhale as hard as possible
What are PEFR reading taken with a peak flow meter used for?
What are the limitations?
Usage:
Better used for monitoring as opposed to diagnosis
Limitations:
Wide range of normal values
No correction for ethnicity
Less reproducible than FEV1
Effort dependent
How is spirometry performed?
Stand or sit patient in upright position
Incentivise patients that are children to put in maximum effort (visual cues or trained professional)
2-3 tidal breaths are taken with lips around spirometer
Deep breath taken to TLC and then blow out as hard as possible
Repeat 3 more times to achieve maximum of 5% variaion from largest FVC
Can then be repeated post bronchodilator to test obstructive reversibility
Describe the findings of spirometry that might indicate asthma
May be normal or show lower airway obstruction on a flow/volume graph
Normal or reduced FEV1 and FVC do not exclude asthma
Reversibility must be checked
Typical profile:
Low PEFR
Low FEV1/FVC ratio
Remember normal profile doesn’t exclude and to check reversibility
How is Airway hyperresponsiveness commonly tested?
Checking for exercise induced bronchoconstriction with an exercise stress test and spirometry
Spiro is done pre-exercise
6-8 mins of exercise monitoring SaO2 and HR
Perfore post-exercise spiro after 1, 5, 10 and 15 minutes
Repeat spiro post bronchodilator
What is an Exhaled NO test
How is it performed?
Exhaled NO testing (FeNO) is a test of exhaled levels of Nitric oxide, which is a biomarker for chronic inflammation and is found in higher levels with people with chronic inflammation of the airways, such as in asthma
Procedure:
Lungs are emptied as far as possible
Inhaled to Vital capacity through device filter
Ehale steadily into device
What are the limitations of FeNO and when is it performed?
Limitations:
Not specific to asthma
Normal result doesn’t exclude asthma
Uses:
In someone judged as intermediate risk of asthma after initial clinical examination can be tested (in conjuction with other tests) to aid diagnoses
Other than the tests described in previous cards, what are some investigations that could be performed in clinic to test or monitor asthma?
Skin prick allergy test
Blood IgE levels in response to specific allergens
Test for exercise induced asthma
Chest X-rays (exclude other disease such as pneumothorax in acute exacerbations)
When educating patients and professionals about asthma, what are the important topics?
Patients:
Correct recognition of symptoms
Timely use of medication
Appropriate use of health services
Personal asthma action plan
Professionals:
Appropriate medication
Concordance with treatment plans
List methods for primary prevention of asthma
Stop smoking
Remove wood/laminate flooring from house (Questionable)
Cleaning (Questionable)
Fresh air
Breast feeding
Exposure to allergen/triggers
Weight loss
Diet (Questionable)
What are the two main types of pharmacological treatment?
Give the drug types and examples of drugs for each
Reliever therapy:
B2 agonists
Muscarinic antagonists
Theophylline/Aminophylline
Preventer therapy:
Corticsteroids
Leukotriene receptor antagonist
What are the effects of Corticosteroids on someone with asthma?
Decrease secretion and number of eosinophils
Decrease cytokines released from T lymphocytes
Decrease mast cell numbers
Decrease macrophage numbers and cytokine secretion
Decrease epithelial cell cytokine release
Decrease mucos secretion from mucus glands
Decrease the leak of endothelial cells
What are the BTS treament guidelines for asthma?
Start treatment at step most appropriate to initial severity
Acheive early control
Maintain control by stepping up or down as necessary
Outline some of the key features of treatment for mild, modeate and severe asthma
Mild:
Inhaled short acting B2 agonist as needed
Moderate:
Add inhaled steroid daily
May add inhaled long action B2 agonists
Severe:
Consider increasing steroid dose and adding further drugs (E.g. theophylline)
Finally add daily steroid tablet
What are some of the clinical features of mild, moderate and severe acute asthma exacerbations?
Mild:
SaO2 >92% in air
HR <110
RR <25
Speech normal
Minimal wheeze
PEFR >75% predicted
Moderate:
As above however
Increased wheeze
PEFR 50-75% predicted
Severe:
SaO2 <92% in air
HR >110
RR >25
Cant complete sentences
No wheeze
PEFR 35-50% predicted
Outline the clinical features of life threatening asthma
SaO2 <92% in O2
Silent chest, Poor respiratory effort
Altered onciousness/hyper-aggressive
Exhaustion
PEFR <35% predicted
Rising or ‘normal’ pCO2
What is the treatment plan for acute severe asthma attacks?
GET HELP
A - Oxygen
B- Continuous salbutamol and iptatropium nebs
C - IV access (Salbutamol, Mg Sulphate, Aminophylline)
Intubate and ventilate
Short course of oral prednisilone may also be required
Increase through steps as required until symptoms resolve
