Resp 5 Flashcards

(73 cards)

1
Q

Define the term hyperventilation

What affect will this have on partial pressures of respiratory gases in the alveoli?

A

Ventilation increase with no change in metabolism

pCO2 falls

pO2 rises

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2
Q

Define hypoventilation

What affect will this have on alveolar gases partial pressure?

A

Ventilation decrease with no change in metabolism

pCO2 rises

pO2 falls

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3
Q

In what situations can changes in ventilation rate not correct imbalance in respiratory gases partial pressure?

A

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

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4
Q

What is hypoxia?

When does it become significant?

A

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

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5
Q

What is the link between pCO2 and plasma pH?

A

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

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6
Q

What are the effects of significantly increased or decreased plasma pH?

A

Plasma pH below 7.0:

Lethally denatured enzymes

Plasma pH above 7.6:

Free [Ca2+] increase

Tetany

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7
Q

Describe the effects of hyper/hypo-ventilation on plasma pH

A

Hyperventialtion:

pCO2 falls

pH rises

Causes respiratory alkalosis

Hypoventialtion:

Leads to rise in pCO2

pH falls

Causes repiratory acidosis

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8
Q

Describe the role of the kidneys in plasma pH control

A

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

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9
Q

Describe the involvement of other body tissues on the plasma pH

A

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)

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10
Q

What might cause rise in plasma HCO3-?

A

Vomiting

Stomach acid must be replaced

H20 + CO2 = HCO3- + H+

H+ enters stomach and HCO3- is expelled into blood

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11
Q

Describe Peripheral chemoreceptors

Hint: Functions and locations

A

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

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12
Q

What are the functions of central chemoreceptors?

Where are they found?

A

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

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13
Q

What structures control the pH of the CSF?

A

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

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14
Q

Describe short term control of CSF pH

A

[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

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15
Q

Describe longer term regulation of the CSF pH

A

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)

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16
Q

List the oxygen and CO2 transport chains

A

O2:

Air - Airways - Alveoli - Alveolar membrane - Arterial blood - Regional arteries - Capillary blood - Tissues

CO2:

Tissues - Regional veins - Venous blood - Alveolar membrane - Alveoli - Airways - Air

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17
Q

What are the typical pCO2 and pO2 in the:

    • Air*
    • Alveolar air*
    • Venous blood*
    • Arterial blood*
A

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

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18
Q

What is the ideal ventilation/perfusion ratio?

What is the V/P ratio at the lung apex and base?

A

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

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19
Q

What is the effect of fibrotic lung disease on alveolar exchange and hence the arterial blood?

A

Exchange surface is thickened

Arterial pO2 = Low

Arterial pCO2 = Normal (CO2 diffuses easier than O2)

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20
Q

What is the effect of Pulmonary Oedema on alveolar exchange and hence the arterial blood?

A

Exchange surface is normal but there is increased perfusion distance

Arterial pO2 = Lower

Arterial pCO2 = Normal (CO2 more soluble than O2)

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21
Q

What is the effect of Emphysema on alveolar exchange and hence the arterial blood?

A

Exchange surface area is decreased

Arterial pO2 = Low

Arterial pCO2 = Normal (Diffuses easier than O2)

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22
Q

What is the broad definition of respiratory failure?

A

Not enough oxygen enters the blood or not enough Co2 leaves the blood

Doesn’t necessarily occur together

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23
Q

What is type 1 resp failure?

A

Not enough O2 enters blood

CO2 removal not compromised

pO2 of arterial blood = Low

pCO2 of arterial blood = Normal of slightly low

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24
Q

What is type 2 resp failure?

A

Not enough O2 enters blood

Not enough CO2 leaves blood

Arterial pO2 = Low

Arterial pCO2 = High

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25
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%
26
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
27
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
28
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*
29
What are the common features of a patient with type 1 resp failure?
Breathlessness Exercise intolerance Central cyanosis
30
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
31
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**
32
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
33
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
34
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
35
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
36
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
37
Define Asthma
A chronic disorder characterised by: ## Footnote * - 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*
38
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
39
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
40
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
41
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*
42
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
43
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
44
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
45
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)
46
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
47
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
48
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
49
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)
50
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**
51
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
52
Describe an asthmatic cough
Often worse at night Exercise induced Dry (wet indicates infection/COPD etc)
53
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
54
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**
55
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
56
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
57
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
58
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
59
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
60
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*
61
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
62
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
63
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
64
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)
65
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
66
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)
67
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
68
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
69
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
70
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
71
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
72
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
73
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