Resp Week 6 Flashcards
1
Q
what are the two states of normal human sleep
A
REM
non-REM
2
Q
what is clinical sleep staging based on
A
EEG
EOG
EMG
3
Q
what are the subdivisions of NREM sleep
A
N1, N2, N3 (going from lighter to deeper sleep )
4
Q
describe EEG waves, percentage of time, and function during the different stages of sleep
A
stage W (awake but resting) = alpha waves, 5%, normal bodily activity
stage N1 = theta waves, 5%, cardiovascular rest
stage N2 = sleep spindles and K complexes, 50%, cardiovascular rest
stage N3 = delta waves, 15%, cardiovascular rest
stage REM = sawtooth waves, 25%, cardiovascular activation
5
Q
describe the normal changes in ventilation during sleep
A
drive to breathe is reduced during sleep
upper airway resistance increases during sleep, therefore reduced breathing capacity
metabolic rate decreases by 10-15% during sleep, decreasing breathing drive
PCO2 increases and PO2 decreases
as a result, hypoventilation occurs during sleep
6
Q
describe obstructive sleep apnoea
A
disordered breathing during sleep in which the airway is mechanically obstructed, leading to a cessation of airflow, resulting in intermittent hypoxia and fragmented sleep
has CV and cerebrovascular impacts
several risk factors e.g obesity, alcohol use, upper airway abnormalities
7
Q
what are 10 clinical features of OSA
A
daytime somnolence
nocturia
cognitive impairment
dry mouth
large neck
witnessed apnoeas
insomnia
morning headaches
high BMI
crowded oropharynx
8
Q
what is the mallampati score
A
clinical assessment tool used to evaluate the visibility of the oral structures and predict the difficulty of intubation
determined by having patient sit upright with their mouth open and tongue protruded
score is based on visualisation of oropharynx
a higher score indicates a higher likelihood of difficult intubation
9
Q
what are the 4 classes of the mallampati score and what can be seen in each
A
class 1 - full visibility of uvula, soft palate and fauces
class 2 - visibility of soft palate and part of uvula
class 3 - only soft palate seen
class 4 - only shows hard palate
10
Q
what are 3 diagnostic methods of OSA
A
polysomnography
blood O2
home sleep apnoea testing
11
Q
describe polysomnography
A
comprehensive overnight sleep study recording multiple physiological parameters
12
Q
what are 9 measurements taken during polysomnography
A
pulse ox - O2 in blood
EEG - brain electrical activity
EOG - tracks eye movement
EMG - monitors muscle activity
ECG - heart electrical activity
nasal pressure cannula - measure airflow through nostrils
thermocouple - measures airflow by detecting temp changes
microphone - records sounds like snoring during sleep
thoraco-abdominal bands - monitor chest/ab mvmt to assess breathing
13
Q
describe home sleep apnoea testing
A
portable assessment for detecting sleep-disordered breathing at home
14
Q
what is the difference between obstructive and central apnoea
A
obstructive apnoea is complete cessation of airflow due to upper airway resistance and obstruction, whereas central apnoea is complete cessation of airflow due to lack of control from brainstem respiratory centres
central apnoea is much less common than obstructive (10:1)
15
Q
what is mixed apnoea
A
combination of central and obstructive apnoea
16
Q
what is hypopnea
A
significant reduction in airflow, associated arousal during sleep, or oxygen desaturation
17
Q
what is the respiratory disturbance index (RDI)
A
number of apnoeas, hypopneas, and ‘unsures’ (reduction in airflow not reaching any of the criteria) per hour
this info forms basis of RDI
18
Q
what are 4 acute complications of sleep disorder breathing
A
excessive somnolence
inappropriate falling asleep
psychosocial consequences
snoring
19
Q
what are 4 chronic complications of sleep disordered breathing
A
pulmonary HTN
CVD
cerebrovascular accident
uncontrolled HTN
20
Q
what is the importance of early referral
A
indicated for individuals w cerebrovascular co-morbidities or risk factors, patients who are drowsy driving, and patients who operate heavy machinery
OSA must be reported to the DMV in all instances
21
Q
what are 5 Rx options for sleep apnoea
A
CPAP
mandibular splint
surgery
lifestyle modification
sleeping on side
22
Q
describe CPAP as a Rx for sleep apnoea
A
high efficacy
low risk
pressure is set based on body habitus
blows air into nose/mouth to splint open upper airway
provides major benefit
23
Q
describe mandibular splint as a Rx for sleep apnoea
A
moulded mouthpiece that pries open the airway
not effective for obese patients
24
Q
describe surgery as a Rx for sleep apnoea
A
variable results
generally, this is a second-line option due to invasiveness and associated costs
25
describe lifestyle modification as a Rx for sleep apnoea
reduced EtOH, sedatives, cigarettes, weight loss
has implications for other body systems e.g CV and GI
26
describe sleeping on side as a Rx for sleep apnoea
positional changes may be sufficient to provide symptomatic relief
easy method
27
what are 6 reasons for non-compliance with CPAP as a Rx for sleep apnoea
comfort - can be tight
xanthostoma - dry mouth due to airflow
aesthetic - may appear unattractive
claustrophobia - mask can be restricting in nature
cost - it is expensive
lack of symptomatic response - no immediate response, meaning less inclined to keep using
28
what is type 1 respiratory failure
lungs cannot move enough O2 into the blood, leading to hypoxaemia (PaO2 < 60mmHg)
29
what is type 2 respiratory failure
lungs cannot remove enough CO2 from the blood, leading to hypercapnia (PaCO2 > 45mmHg; often coexists w hypoxaemia)
30
compare and contrast pulse ox with ABG
pulse ox reflects tissue O2 supply by measuring the percentage of Hb saturated w O2 but does not measure blood CO2 or O2 level
whereas
arterial blood gas sample provides accurate assessment of hypoxaemia and hypercapnia, acid-base status, and extended parameters such as lactate
31
what are 2 key mechanisms of respiratory failure
failure of pulmonary ventilation
failure of pulmonary gas exchange
32
describe failure of pulmonary ventilation in regards to respiratory failure
| define, cause, impact
this is the failure to physically move air in and out of lungs, resulting in alveolar hypoventilation (smaller, slower breathing)
caused by extrapulmonary factors such as CNS depression and respiratory pump failure
this leads to hypercapnia and hypoxaemia
33
what are 3 things that can lead to CNS depression (extrapulmonary cause of failure of pulmonary ventilation)
drugs e.g opioids
structural abnormalities e.g stroke
raised ICP e.g tumour
34
what are 3 things that can lead to respiratory pump failure (extrapulmonary cause of failure of pulmonary ventilation)
phrenic nerve dysfunction e.g due to direct damage
neuromuscular weakness e.g diseases such as MND
chest cage restriction e.g kyphoscoliosis
35
describe failure of pulmonary gas exchange in regards to respiratory failure
| cause, impact
caused by pulmonary factors such as problems with the lungs or blood vessels
results in reduced O2 delivery from lung to blood
it does not usually cause CO2 retention except for in severe COPD where there is severely reduced lung reserve
36
what are 4 causes of pulmonary gas exchange failure and name one dominant mechanism for each with an example
diffusion limitation = thickened interstitium and alveolar-capillary membrane e.g interstitial lung disease
ventilatory defect (intrapulmonary shunt) = alveolar collapse e.g pneumothorax
perfusion defect (dead space) = pulmonary vascular narrowing or obstruction e.g PE
right to left anatomic shunt = de-O2 blood re-entering systemic circulation e.g intracardiac shunt
37
what are 4 major consequences of hypoxaemia
damage to vital organs and tissues via cellular hypoxia
increased sympathetic discharge, leading to tachycardia and HTN
lactic acidosis
chronic effects, such as impaired cough reflex and depressed asthma symptom perception
38
what are 4 major consequences of hypercapnia
cerebral autoregulation problems - there is an initial increase in inspiratory drive, but then due to an increase in cerebral blood flow there is increased ICP leading to headache, and decreased inspiratory drive, then there is CO2 narcosis and eventual seizure, coma or death
direct cardiorespiratory effects e.g arrthymia and cardioresp arrest
respiratory acidosis
physiologic responses e.g increase release of O2 to tissues
39
what are implications of O2 induced hypercapnia
increased alveolar dead space - normal compensatory mechanisms in chronic severe COPD act to redistribute pulmonary blood flow to better ventilated areas of the lung, but excessive O2 therapy will reverse this protective effect which leads to reduced CO2 clearance
haldane effect - excessive O2 will displace CO2 bound to Hb, thus raising blood CO2 retention
blunting of hypoxic ventilatory drive
40
what are 3 general principles for O2 therapy
always treat primary/reversible problems e.g pneumonia, HF
O2 therapy is vital for T1RF
O2 therapy can correct hypoxaemia in T2RF but does not correct hypercapnia, and may in fact make it worse
41
what are 5 treatment options for respiratory failure
high flow nasal O2 therapy (HFNOT)
continuous positive airway pressure (CPAP)
bi-level ventilation (BPAP)/non-invasive ventilation (NIV)
intubation and mechanical ventilation
extracorporeal membrane oxygenation (ECMO)
42
what are 2 acid-base consequences of respiratory failure
lactic acidosis in severe hypoxaemia
primary respiratory acidosis in hypercapnic respiratory failure (T2RF)
43
describe how lactic acidosis in severe hypoxaemia can occur due to respiratory failure
tissue hypoxia leads to an increased in anaerobic respiration, which produces lactic acid as a byproduct
this is compensated for by an increased respiratory drive in an attempt to blow off CO2 to normalise pH
44
describe how primary respiratory acidosis in hypercapnic respiratory failure can occur
an excess CO2 results in increased renal retention of bicarbonate ion to buffer in order to attempt to normalise pH
for metabolic compensation to occur to oppose this, you need to have normally functioning kidneys
45
what are 4 assessments that can be made by measuring ABG
pulmonary gas exchange
acid-base balance
lactate
co-oximetry
46
what is the normal range of PaO2
75-100mmHg, depending on age
47
what is normal range of pH
7.35-7.45
48
what is normal range of PaCO2
35-45mmHg
49
what is normal range of bicarbonate ion
22-28mmol/L
50
what is normal range of lactate
0.2-2.0mmol/L
51
what is the difference between hyperlactatemia and lactic acidosis
lactate >2mmol/L is hyperlactatemia
lactate >4mmol/L is lactic acidosis
52
what is type A lactic acidosis
severe tissue hypoxia or hypoperfusion eg hypovolemia or cardiac failure
53
what is type B lactic acidosis
impaired cellular metabolism or regional ischemia without severe hypoxia or hypoperfusion e.g high dose inhaled beta antagonists such as salbutamol
54
what are the four types of hypersensitivity reactions
type 1
type 2
type 3
type 4
55
outline type 1 hypersensitivity reaction
IgE mediated (Allergic) response e.g anaphylaxis
56
outline type 2 hypersensitivity reaction
antibody-dependent cellular cytotoxicity
57
outline type 3 hypersensitivity reaction
immune mediated responses involving IgG and IgM
58
outline type 4 hypersensitivity reaction
delayed or cell mediated response
59
define atopy
genetic predisposition to develop IgE mediated hypersensitivity reactions, manifesting as conditions such as asthma, allergic rhinitis, and atopic dermatitis (atopic triad)
often involves a heightened immune response to environmental allergens leading to chronic inflammation
60
define allergy
exaggerated immune response to specific antigens that typically involve the activation of mast cells and basophils, resulting in symptoms ranging from urticaria to anaphylaxis
clinical manifestations include respiratory, cutaneous, and GI symptoms
61
describe the pathophysiology of atopic disorders
exposure to allergens
leads to, antigen presenting cells activating naive t cells to differentiate into Th2 cells, which release cytokines e.g IL3, IL4, IL5
then, these promote IgE production by B cells and the recruitment of eosinophils causing chronic inflammation and tissue damage
62
what are 5 risk factors for atopic disorders
maternal exposures - pollutants, smoking, antibiotics etc
type of birth - C-section
skin epithelial dysfunction - pollutants, smoke exposure, vitamin D deficiency etc
lung epithelium dysfunction - bacterial pathogens, viral pathogens, genetic influence etc
gut epithelium - formula feeding, increased antibiotic use, food allergen etc
63
what are 5 causes of atopy
Th1/Th2 responses - responsible for immune responses by activating B cells and leading to the production of IgE
Th1/Th2 skewing - in western countries w smaller family sizes and good sanitation there is a skew in overactive Th2 whereas in developing countries w larger families and poor sanitation lead to a skew in Th1
dietary considerations - dietary profile changes likelihood of developing allergic responses due to the nutrients provided
genetic considerations - heritability is observed in atopic and allergic conditions
epigenetic considerations - biochemical changes to DNA that do not alter the gene sequence but instead modify expression / driven by environmental factors / e.g DNA methylation
64
outline allergic rhinitis
nasal congestion, sneezing and itching due to airborne allergens and asthma leading to recurrent episodes of wheezing and breathlessness
65
outline atopic dermatitis (eczema)
chronic, itchy, and inflamed skin lesions, often exacerbated by environmental triggers and skin barrier dysfunction
66
what are 5 Rx methods for management of atopy
corticosteroids - anti-inflammatory properties/suppress dendritic cells, t cells, b cells
anti-alarmin therapy - inhibits differentiation of naive t cells into Th2 cells
anti-Th2 therapy - blocks cytokine receptor signalling
immunosuppressants - same as corticosteroids
anti-IgE - binds to IgE and prevents IgE binding to mast cells
67
define anaphylaxis
any acute onset illness with typical skin features (e.g urticarial rash, erythema, flushing, angiodema) plus the involvement of respiratory and/or cardiovascular and/or severe GI symptoms
first line of Rx is intramuscular injection of adrenaline
68
what are 8 causes of IgE-mediated allergic reactions
food
meds
latex
cold temp
insects
airborne allergens
exercise
idiopathic
69
outline the pathophysiology of clinical allergic reaction
allergen contacts the integument
then, allergen detected by antigen presenting cell
then, allergen is processed
then, Th cells promote the activation of B cells
then, B cells produce IgE
then, IgE binds to mast cells
then, IgE cross linking on mast cells
then, release of chemical mediators
then, production of clinical signs
70
what are integumentary clinical signs of allergy
hives
swelling
71
what are GI clinical signs of allergy
emesis
abdominal pain
72
what are respiratory clinical signs of allergy
tongue swelling
cough
wheeze
dysarthria
73
what are CV clinical signs of allergy
hTN
pre-syncope
pale and floppy
74
what are neurological clinical signs of allergy
anxiety
headache
seizures
75
describe the pathophysiology of acute bronchoconstriction
release of mediators such as histamine, leukotrienes, prostaglandins from mast cells and other immune cells in response to allergens or irritants
then, these mediators bind to specific receptors on bronchial smooth muscle, initiating a cascade that increases intracellular calcium levels resulting in muscle contraction
then, parasympathetic NS activation via the vagus nerve can exacerbate bronchoconstriction by increasing acetylcholine release, which further stimulates muscarinic receptors on the smooth muscle within the bronchial wall
then, the reduced airway diameter impairs airflow leading to symptoms such as wheezing, shortness of breath and chest tightness
76
outline the role of airway inflammation in asthma
inflammatory cells release cytokines and other mediators that perpetuate inflammation and tissue damage, which leads to airway hyperresponsiveness where the bronchial smooth muscle reacts excessively to various stimuli resulting in bronchoconstriction
chronic inflammation also causes structural changes which further narrows airways
these give rise to recurrent symptoms
77
what are 5 characteristics of asthma
lung inflammation
airway hyper-responsiveness
airway remodelling
mucus hyper secretion
increased eosinophils and/or neutrophils in airway lumen
78
describe type 2 asthma
characterised by elevated levels of type 2 Th cell cytokines such as IL4, IL5, IL3 leading to eosinophilic inflammation and increased IgE production
commonly associated w atopy and allergic triggers and patients often respond well to corticosteroids and other anti-inflammatory treatments
79
describe non-type 2 asthma
associated w neutrophilic inflammation and lacks Th-2 driven inflammation
may not respond well to traditional corticosteroid Rx and is more commonly linked to environmental factors
80
what are 4 clinical features of asthma
wheezing
cough
dyspnoea
chest tightness
81
describe clinical features of COPD
persistent cough often accompanied by the production of thick, mucoid sputum
dyspnea that worsens w physical exertion
wheezing
chest tightness
potential cyanosis and peripheral oedema
82
compare and contrast clinical features of COPD and asthma
both have wheeze, chronic cough, dyspnea, chest tightness
COPD has chronic sputum production, whereas it is rarer in asthma
asthma worsens at night whereas COPD does not
acute exacerbations of COPD are triggered by infections or environmental pollutants whereas it is triggered by allergens or respiratory infections in asthma
COPD has cyanosis in advanced stage whereas there is no cyanosis in asthma
COPD has barrel chest whereas asthma doesn't
83
what would you find in a history in the diagnosis of COPD
dyspnea
chest tightness
cough
84
what would you find in examination in the diagnosis of COPD
barrel chest
expiratory wheeze
crackles
breath sounds adventitious
85
what would you find in a spirometry in the diagnosis of COPD
reduced FEV1/FVC ratio
present bronchodilator response to rule out asthma
86
what would you find in chest X-ray in the diagnosis of COPD
hyperinflation
other structural lung changes consistent w COPD ruling out alternative diagnoses
87
what would you find in bloods done in the diagnosis of COPD
assesses for polycythaemia or anaemia and screens for comorbid conditions such as infection or metabolic imbalances that may complicate COPD
88
describe the role of infection in acute exacerbation of COPD
increases airway inflammation and mucus production which leads to worsened airflow obstruction
89
what are some common organisms involved in the acute exacerbation of COPD
Haemophilus influenzae
Streptococcus pneumoniae
Moraxella catarrhalis
rhinoviruses
90
what is SABA, give example, what is is used for and how does it work
short acting beta agonist (e.g albuterol) which are used as rescue inhalers to provide quick relief from acute bronchospasm
stimulates beta-2 adrenergic receptors in the bronchial smooth muscle, leading to bronchodilation
91
what is LABA, give example, what is is used for and how does it work
long acting beta agonist (e.g salmeterol) which are used for sustained bronchodilation in asthma and COPD but are typically combined w inhaled corticosteroids for long term control
activates beta-2 adrenergic receptors in the bronchial smooth muscle for prolonged bronchodilation, typically lasting 12-24 hrs
92
what is LAMA, give example, what is is used for and how does it work
long acting muscarinic antagonists (e.g tiotropium) which are employed mainly in COPD to achieve long term bronchodilation and improve lung function
block muscarinic M3 receptors in the bronchial smooth muscle, providing extended bronchodilation and mucus reduction
93
what is SAMA, give example, what it is used for and how does it work
short acting muscarinic antagonist (e.g ipratropium) which are used a lot less frequently but can provide additional relief for acute symptoms and exacerbations of asthma
block muscarinic M3 receptors in the bronchial smooth muscle, reducing bronchorestriction and mucus secretion
94
how do inhaled corticosteroids work
reduce airway inflammation and oedema by inhibiting the release of inflammatory mediators and suppressing the activity of inflammatory cells
95
what are 6 non-pharmacological management methods of asthma
avoid known triggers
inhaler technique
breathing exercises
physical activity
adhere to medications
healthy diet
96
describe the role of the multidisciplinary team in the management of COPD as a model of chronic disease
key role in delivering comprehensive care
pulmonologists/resp physicians lead the clinical management, treatments etc.
resp therapists give education on inhaler techniques, breathing exercises and support w rehab
nurses offer ongoing patient education, symptom management, and coordinate care b/w specialists
dietitians and psychologists address nutritional needs and mental health
97
outline the concept of a preventer
e.g ICS are used daily to reduce airway inflammation and prevent asthma symptoms by decreasing the production of inflammatory mediators and suppressing inflammatory cells
they aim to control chronic inflammation and reduce the frequency of asthma exacerbations
98
outline the concept of relievers
e.g SABA provide rapid bronchodilation by stimulating beta-2 adrenergic receptors in the bronchial smooth muscle offering immediate relief of acute symptoms like wheezing and shortness of breath
99
describe oral glucocorticoids
steroids e.g ICS are used to manage asthma and COPD by reducing chronic airway inflammation and swelling
in asthma, decrease frequency and severity of exacerbations
in COPD, used during acute exacerbations to quickly reduce inflammation
100
describe mucolytics
used in asthma and COPD to reduce mucus viscosity and enhance mucus clearance from the airways
work by breaking down mucus, making it less sticky and easier to expel through coughing
in COPD< they have manage chronic productive cough
for asthma, less commonly used but may be prescribe to alleviate symptoms associated w excessive mucus production
101
describe the potential use of oxygen therapy amongst patients w COPD
manage chronic hypoxemia which can lead to complications such as pulmonary HTN and RHS-HF
supplemental O2 helps increase blood O2 level, alleviating symptoms like shortness of breath and improving exercise tolerance
recommended for patients w severe COPD who have resting hypoxemia
home O2 therapy requires them to quit smoking cos if you smoke near O2 therapy machine it may explode
102
outline the concept of self management in COPD
Pt taking active role in own care e.g monitoring symptoms, recognising early signs of exacerbation, adhering to prescribed Rx etc.
Pt encouraged to engage in regular physical activity, follow proper diet, avoid smoking etc.
103
outline the use of monoclonal antibodies for severe, chronic airway disease
in asthma, monoclonal antibodies (e.g omalizumab) inhibit IgE thereby reducing allergen-induced exacerbations / mepolizamub target IL5 to decrease eosinophilic inflammation
in COPD, benralizumab is used to target IL5 to manage eosinophilic COPD
monoclonal antibodies are typically for Pt that do not respond adequately to standard Rx
104
outline use of bronchial thermoplasty
uses controlled thermal energy to reduce airway smooth muscle mass and decrease excessive bronchoconstriction
