Week 6 Respiratory Flashcards
1
Q
What is normal sleep architecture
A
-normal human sleep comprises two states (REM and NREM sleep
-clinical sleep staging is based on EEG , EOG and submental (EMG criteria)
2
Q
what are the stages of NREM sleep
A
-N1,N2 and N3
3
Q
what are alpha waves representative of
BATD
A
awake but resting, eyes closed, not mentally concentrating on any one subject or task
4
Q
what are beta waves representative of
BATD
A
receiving sensory stimulation or engaged in concentrated mental activity
5
Q
what are theta waves representative of
BATD
A
drowsy or sleepy state in adults, common in children
6
Q
what are delta waves representative of
BATD
A
deep sleep
7
Q
what are the stages of sleep
A
W, N1,N2,N3,REM
8
Q
features of W stage of sleep
A
-alpha waves (8-13Hz)
*5% of sleep
-function=normal bodily activity
9
Q
features of N1 stage of sleep
A
-theta waves (4-7Hz)
*5% of sleep
-function=cardiovascular rest
10
Q
features of N2 stage of sleep
A
-sleep spindles and k complexes
*50% of sleep
-function=cardiovascular rest
11
Q
features of N3 sleep
A
-delta waves (0.5-2Hz)
*15% of sleep
-function=cardiovascular rest
12
Q
features of REM sleep
A
-sawtooth waves
*25% of sleep
-function=cardiovascular activation
13
Q
Discuss the normal changes in ventilation during sleep
A
-drive to breathe is reduced during sleep
-upper airway resistance increases during sleep , reducing breathing capacity
-metabolic rate drops by 10-15% during sleep
-PCO2 increases and PO2 decreases
-hypoventilation occurs in sleep
14
Q
Define obstructive sleep apnoea
A
disordered breathing during sleep in which the airway is mechanically obstructed, leading to cessation of airflow
15
Q
what are the clinical features of OSA
A
-daytime somnolence
-nocturia
-cognitive impairment
-dry mouth
-large neck (risk factor)
-witnessed apnoea
-insomnia
-morning headaches
-high BMI
-crowded oropharynx
16
Q
what is the mallampati score
A
-clinical assessment tool
-pt sits upright with mouth open and tongue protruded
-based to visualisation of uvula,softpalate,pillars
17
Q
Class I of mallampati score
A
complete visualisation of uvula, soft palate and fauces
18
Q
Class II of mallampati score
A
visibility of soft palate and part of uvula
19
Q
Class III of mallampati score
A
only see soft palate
20
Q
Class IV of mallampati score
A
only can see hard palate
21
Q
How is OSA diagnosed
A
polysomnography
blood oxygen
home sleep apnoea testing
22
Q
How is polysomnography used to diagnose OSA
A
comprehensive overnight sleep study recording multiple physiological parameters
23
Q
how is blood oxygen used to diagnose OSA
A
measurement of oxygen saturation levels in blood
24
Q
how is home sleep apnoea testing used to diagnose OSA
A
portable assessment for detecting sleep disordered breathing at home
25
what are the features of polysomnography
pulse oximetry
electroencephalogram
electrooculogram
electromyogram
ECG
nasal pressure canula
thermocouple
microphone
thoraco-abdominal bands
26
function of pulse oximetry in polysomnograph
measures oxygen levels in blood (attached to index finger)
27
function of EEG in polysomnograph
records brains electrical activity (attached to forehead)
28
function of EOG in polysomnograph
tracks eye movements during sleep (attached to next to eyes)
29
function of EMG in polysomnograph
monitors muscle activity (attached to neck)
30
function of ECG in polysomnograph
monitors hearts electrical activity (attached to chest)
31
function of nasal pressure canala in polysomnograph
measures airflow through the nostrils (attached to nose)
32
33
function of microphone in polysomnograph
records sounds like snoring during sleep (attached to above sternum)
34
function of thoraco-abdominal bands in polysomnograph
monitor chest and abdominal movements to assess breathing (attached around chest)
35
define apnoea
complete cessation of airflow
36
Contrast OSA and central apnoea
OSA = Complete cessation of airflow due to upper airway resistance and obstruction, characterised by effort to breathe against resistance
CA=Complete cessation of airflow due to lack of control from brainstem respiratory centres; caused by medications, cardiac failure, brainstem disease, or idiopathic in nature.
37
define mixed apnoea
combination of central and obstructive apnoea
38
define hypopnea
Significant reduction in airflow, associated arousal during sleep, or oxygen desaturation; definitions can vary.
39
define 'unsures'
Reduction in airflow, not reaching any of the above criteria.
40
what is respiratory disturbance index
-number of apnoeas and 'unsures' are measured per hour
41
identify the acute consequences of sleep disordered breathing
-excessive solomnence
-inappropriate falling asleep
-psychological consequences
-snoring
42
identify the chronic complications of sleep disorders breathing
-pulmonary HTN
-CVD
-CVA
-uncontrolled HTN
43
identify the treatments for OSA
CPAP
Mandibular splint
surgery
lifestyle modification
sleeping on side
44
describe the use of CPAP for OSA
high efficacy, low risk, pressure is set based on body habits, blows air into nose/mouth to splint open upper airway; provides major benefit
45
describe the use of mandibular splint for OSA
moulded mouthpiece that pries open the airway (not effective for obese patients)
46
describe the use of surgery for OSA
variable results, generally, this is a second line option due to invasiveness and associated costs
47
48
describe the use of sleeping on side for OSA
positional changes may be sufficient to provide symptomatic relief, easy method
49
what are some reasons why pt with OSA don't go on CPAP
-uncomfortable
-xanthostoma (dry mouth)
-aesthetic
-cost
-claustraphobia
-lack of symptomatic response
50
what is pulmonary ventilation
process of moving air into and out of the lungs, allowing for the continuous supply of oxygen and removal of carbon dioxide
51
what is pulmonary gas exchange
occurs in the alveoli, where oxygen from the inhaled air diffuses into the bloodstream and carbon dioxide from the blood diffuses into the alveoli to be exhaled
52
what is type 1 respiratory failure
failure of oxygenation with low PaO2 and normal/low CO2
53
what is type 2 respiratory failure
ventilatory failure with low PaO2 and elevated PaCO2
54
Examples of type 1 respiratory failure
impaired ability to exchange oxygen (pneumonia, pulmonary oedema)
55
Examples of type 2 respiratory failure
hypoxia (PaO2 <60mmHg) and hypercapnia (PaCO2 > 50mmHg)
-cant remove CO2 adequately
-COPD, obesity, neuromuscular disorders
56
identify the common causes of respiratory failure
pulmonary ventilation failure and gas exchange failure
57
Describe pulmonary ventilation failure
-lungs can not effectively move air in and out, leading to inadequate alveolar ventilation
-this leads to respiratory acidosis and tissue hypoxia
58
Describe gas exchange failure
-lungs are unable to effectively transfer oxygen from the alveoli to the blood due to issues in the alveolar compartment, ventilation, perfusion
-does not typically lead to CO2 retention
59
what is hypoxia
state where tissues and organs are deprived of adequate oxygen, affecting cellular function
60
what is hypoxaemia
low oxygen levels in the blood
61
what is hypercapnia
condition of elevated CO2 in blood, (due to inadequate ventilation)
62
identify the physiological consequences of hypoxemia and hypercapnia
cellular hypoxia
sympathetic discharge
lactic acidosis
chronic effects
cerebral autoregulation
cardiorespiratory effects
respiratory acidosis
physiologic changes
63
what is cellular hypoxia
inflammatory cascade and oxygen radical release, cases irreversible damage to the brain, lung,heart,liver,renal and GI cells
64
what is sympathetic discharge
can lead to uncontrolled tachycardia and hypertension
65
what is lactic acidosis
accumulation of lactic acid in the blood, leading to decreased blood pH
66
what are chronic effects of hypoxemia and hypercapnia
impaired cough reflex, depressed asthma symptom perception
67
what is cerebral auto regulation as a result of hypoxemia and hypercapnia
-cerebral autoregulation involves the vasodilation of cerebral arteries to increase blood flow and oxygen (o₂) delivery to the brain.
-this enhanced blood flow can help with the absorption and excretion of carbon dioxide (co₂) in the lungs.
-however, high co₂ levels in the brain can lead to headaches and confusion due to increased intracranial pressure.
-additionally, prolonged exposure to elevated co₂ can result in co₂ narcosis, which may cause cognitive impairment and other neurological effects.
68
what are the cardiorespiratory effects of hypoxemia and hypercapnia
decreases myocardial and diaphragmatic contractility, arrhythmia, cardiorespiratory arrest
69
what is respiratory acidosis
breathing causing accumulation of acidic products in the blood, with metabolic compensation if renal function intact
70
what are the physiologic effects of hypoxaemia and hypercapnia
stimulates Bohr effect on Hg-O2 dissociation curve
71
what are the implications on hypoxic drive in respiratory failure
-redistributed blood flow: the body naturally redirects blood to well-ventilated lung areas for effective co₂ clearance.
-high oxygen interference: excessive oxygen disrupts this redistribution, causing more blood to flow to poorly ventilated areas (alveolar deadspace) reducing co₂ elimination.
-haldane effect: high oxygen levels increase blood co₂ by displacing it from hemoglobin.
-blunted hypoxic drive: high oxygen reduces the breathing stimulus in COPD patients, worsening co₂ retention due to slower, shallower breathing.
72
how does hypoxemia impact acid-base levels
-lowered oxygen in cells and tissues
-increased anaerobic metabolism
-lactic acid produced
-causes lactic acidosis
73
how does hypercapnic (type 2 respiratory failure) impact acid base levels
-elevated CO2 levels lead to development of primary respiratory acidosis
-kidneys attempt to counteract this by increasing HCO3- retention (kidneys need to be functional)
74
changes to PaCO2,pH, HCO3- in T2RF
Acute T2RF:
PaCO2: Elevated
pH: Decreased significantly (severe acidosis)
HCO3-: Normal (no time for compensation)
Chronic T2RF:
PaCO2: Elevated
pH: Slightly decreased or near-normal (due to compensation)
HCO3-: Elevated (due to renal compensation)
75
when is oxygen therapy used for respiratory failure
-primary/reversible conditions should always be treated with oxygen therapy
-vital in T1RF; however, oxygen therapy can correct hypoxemia in T2RF but can worsen hypercapnia
76
list the main types of oxygen therapy
HFNOT
CPAP
BPAP
Intubation
ECMO
77
what does HFNOT stand for
high flow nasal oxygen therapy
78
describe use of HFNOT
provides high-flow, humidified oxygen through nasal prongs to improve oxygenation and breathing comfort
79
what does CPAP stand for
Continuous positive airway pressure
80
describe the use of CPAP
A device that delivers a steady flow of air through a mask to keep the airways open
during sleep
81
what does BPAP stand for
bi-level positive airway pressure
82
describe the use of BPAP/Bipap
offers two levels of pressure (inhalation and exhalation) to assist with breathing, often used fro patients with respiratory issues
83
describe the use of intubation
insertion of tube into airway to maintain an open airway and assist with ventilation
84
what does ECMO stand for
Extra-corporal Membrane Oxygenation
85
describe the use of ECMO
machine that provides long term support for patients with severe HF or lung failure by oxygenating blood outside the ovoid
86
how do ABG's work
-assesses pulmonary gas exchange by analysing partial pressures of oxygen and CO2, reflecting the efficiency of gas transfer in the lungs
-can also measure acid base balance and lactate + electrolytes
87
list the parameters measured in ABGs
PaO2
PaCO2
bicarbonate
pH
electrolytes
lactate
88
normal blood pH
7.35-7.45
89
normal PaCO2
45-35
90
normal HCO3-
22-26
91
acronym for hypersensitivity reactions
ACID
92
describe type 1 hypersensitivity reaction
(A)
IgE mediated (Allergic) responses eg anaphylaxis and atopic tetrad
93
describe type 2 hypersensitivity reactions
(C)
antibody dependent cellular cytoxicity
94
describe 3 hypersensitivity reaction
(I)
immune mediated responses involving IgG and IgM
95
describe type 4 hypersensitivity reaction
(D)
delayed or cell mediated responses
96
define atopy
describes genetic predisposition to develop IgE mediated hypersensitivity reactions, manifesting as things such as allergic rhinitis, asthma, atopic dermatitis
97
define allergy
exaggerated immune response to specific antigens that typically involve the activation of mast cells and basophils, symptoms range from urticaria to anaphylaxis
98
what is allergic rhinitis
inflammation of the nasal mucosa due to IgE-mediated response to airborne allergens, leading to symptoms such as sneezing, nasal congestion and itching
99
what is asthma
a chronic inflammatory disorder of airways with bronchial hyper-reactivity, leading to recurrent wheezing, SOB and cough
100
what is eczema
chronic skin condition marked by intense itching, erythema, dry, scaly patches often associated with FHx of atopy
101
what is a food allergy
immune mediated adverse reaction to specific food proteins, resulting in a spectrum of symptoms, ranging from mild urticaria to severe anaphylaxis
102
Outline a mechanism for atopic disorders
-Genetic and Environmental Triggers: Genetic predisposition and environmental allergens lead to an immune response.
-Th2 Cell Activation: Allergen exposure activates antigen-presenting cells, which stimulate naïve T cells to differentiate into Th2 cells.
-Cytokine Release: Th2 cells release cytokines (IL-4, IL-5, IL-13) that:
Promote IgE production by B cells.
Recruit and activate eosinophils.
-IgE and Mast Cell Activation: IgE binds to mast cells, which, upon re-exposure to the allergen, release histamine and other mediators.
-Chronic Inflammation: Eosinophils and other inflammatory cells cause ongoing inflammation and tissue damage.
103
what are the risk factors for atopic disorders
maternal exposures
C section birth
Skin epithelium dysfunction
Lung epithelium dysfunction
Gut epithelium dysfunction
104
what maternal exposures can make it a risk factor for atopic triad
pollutants, smoking, soaps/detergents, antibiotics, microplastics
105
function of Th1 cells
traditional immune responses to viral/bacterial pathogen
106
function of Th2 cells
immune responses to environmental allergens
107
function of T reg cells
regulate immune responses (remove responses to NONharmful antigens)
108
Outline Th1/Th2 skewing
-in western counties (small family size, affluent homes, high antibiotic use, good sanitation) skew direction of an overactive Th2 response
-In developing countries, large family sizes, rural homes, low antibiotic use, and poor sanitation lead to a skew
in the direction of an underactive Th2 response (Th1 skew)
109
how does diet influence atopy development
-diets high in sat fats, low fibre, less fresh food reduce efficacy of immunological response
-diet high in VD, folate and fish oils improve resistance to allergy
-probiotics and prebiotics support development of Treg cells
110
causes of allergic rhinitis
mostly driven by IgE
111
causes of eczema
epithelial danger signs
IgE mediation
allergic inflammation
112
causes of asthma
epithelial danger signs
IgE mediation
allergic inflammation
113
list the management of atopy
corticosteroids
anti-alarmin therapy
anti-Th2 therapy
immunosuppressants
anti-IgE
114
how does anti-alarmin therapy treat atopy
inhibits differentiation of naive T cells into th2 cells
115
how do corticosteroids treat atopy
anti-inflammatory properties, suppresses Dc, Tc,Bc
116
how do immunosuppressants treat atopy
anti-inflammatory properties, suppresses Dc, Tc,Bc
117
how does anti-Th2 therapy treat atopy
blocks cytokine receptor signalling
118
how does anti-IgE therapy treat atopy
binds to IgE, prevents IgE binding to mast cells
119
define anaphylaxis
any acute onset illness with typical skin features (urticarial/rash/erythema/flushing/angiodema) plus the involvement of respiratory and/or cardiovascular and/or severe GI symptoms
120
what are the causes of IgE allergic reactions
food
medications
latex
cold temperature
insects
airborne allergens
exercise
idiopathic
121
outline a clinical allergic reaction
-allergen contacts the integument
-allergen detected by APC
-antigen is processed
-Th cells promote the activation of B cells
-B cells produce IgE
-IgE binds to mast cell
-IgE cross-linking on mast cells
-release of chemical mediators
-production of clinical signs
122
what are the integument signs of allergy
hives, allergy
123
what are the GI signs of allergy
emesis, abdominal pain
124
what are the respiratory signs of allergy
tongue swelling, cough, wheeze, dysarthria
125
what are the CV signs of allergy
hypotension
pre syncope
pale and floppy appearance
126
what are the neurological signs of allergy
anxiety
headache
seizures
127
Describe the pathophysiology of acute bronchoconstriction
-Triggering Agents: Allergens or irritants cause mast cells and immune cells to release mediators like histamine, leukotrienes, and prostaglandins.
-Mediator Action: These mediators bind to receptors on bronchial smooth muscle.
Calcium Influx: This binding increases intracellular calcium levels.
-Smooth Muscle Contraction: Elevated calcium causes bronchial smooth muscle contraction, narrowing the airways.
-Parasympathetic Activation: The vagus nerve releases acetylcholine, which stimulates muscarinic receptors on the smooth muscle, worsening bronchoconstriction.
-Symptoms: Narrowed airways impair airflow, leading to wheezing, shortness of breath, and chest tightness.
128
identify the role of airway inflammation in asthma
- **Airway Hyperresponsiveness:** Inflammation increases bronchial smooth muscle sensitivity, leading to excessive airway constriction in response to stimuli.
- **Airway Remodeling:** Chronic inflammation causes structural changes like thickened airway walls and increased mucus production, resulting in persistent airway narrowing and obstructed airflow.
129
list the characteristics of asthma
-lung inflammation
-airway hyper-responsiveness
-airway remodelling
-mucous hypersecretion
-increased eosinophils and/or -neutrophils in airway lumen
130
describe lung inflammation as a characteristic of asthma
chronic inflammation of the airways in response to various triggers, leading to airway constriction and other asthma symptoms
131
describe airway hyper-responsiveness as a characteristic of asthma
exaggerated and excessive narrowing of the airways in response to irritants or allergens, a hallmark of asthma
132
describe airway remodelling as a characteristic of asthma
structural changes in the airways walls, including thickening and increased smooth muscle, which occur over time in asthma
133
describe mucous secretion as a characteristic of asthma
overproduction of mucous in the airways, leading to congestion and difficulty breathing
134
describe increased eosinophils and/or neutrophils in airway lumen
elevated levels of WBC's in the airways, which contribute to inflammation and airway obstruction in asthma
135
contrast type 2 asthma and non type 2 asthma
-T2=more common vs NT2=less common
-T2=more severe vs NT2=less severe
-T2=airways/systemic eosinophilia vs NT2=no airways/systemic eosinophilia
-T2=responsiveness to corticosteroids vs NT2=lack of responsiveness to corticosteroids
136
List the clinical features of asthma
wheezing
cough
dyspnoea
chest tightness
137
what is a wheeze
high pitched, whistling sound during breathing, especially on exhalation
138
what is a cough
persistent, often dry or mucous-producing, typically worsening at night or early morning
139
what is dyspnoea
shortness of breath or difficulty breathing, especially noticeable during exertion
140
what is chest tightness
a sensation of pressure or constriction in the chest, often described as feeling squeezed
141
define chronic bronchitis
chronic inflammation of the bronchi, resulting in mucous hyper secretion and goblet cell hypertrophy, chronic cough, and airway narrowing
142
define emphysema
destruction of alveolar walls, leading to loss of elastic recoil and impaired gas exchange
143
Outline a mechanism for the pathophysiology of COPD
-Exposure to Noxious Particles:
-Trigger: Long-term exposure to irritants, especially cigarette smoke.
-Chronic Inflammation:
Response: Inflammatory cells infiltrate the airways and lung tissue, releasing mediators that worsen inflammation.
-Oxidative Stress:
Damage: Increased reactive oxygen species (ROS) from smoke exacerbate inflammation and damage lung tissue.
-Airway Changes:
Chronic Bronchitis: Mucus hypersecretion and airway narrowing cause a persistent cough due to increased mast cell activty
-Emphysema: Destruction of alveolar walls leads to loss of elastic recoil due to release of proteolytic enzymes from inflammation
-Airflow Obstruction:
Mechanisms: Excessive mucus, airway narrowing, and loss of elastic recoil impair airflow.
-Impaired Gas Exchange:
Effect: Damaged alveoli reduce gas exchange efficiency, leading to low oxygen and high carbon dioxide levels.
-Exacerbation by Cigarette Smoke:
Impact: Increases oxidative stress and inflammation, worsening COPD symptoms.
144
list the clinical features of COPD
-persistent cough (with thick, mucoid sputum)
-wheezing
-chest tightness
145
contrast the clinical features of asthma and COPD
-chronic sputum production in COPD, rarer in asthma
-COPD worsens at morning time whereas asthma worsens in the night
-COPD exacerbated by infections of environment vs asthma is exacerbated by allergens or infections
-COPD has barrel chest and cyanosis whereas asthma doesn't
146
how is history used to diagnose COPD
pt presents with chest tightness, dyspnoea, cough
147
how is examination used to diagnose COPD
barrel chest, expiratory wheeze, crackles, breath sounds
148
how is spirometery used to diagnose COPD
confirms COPD by measuring airflow limitation, specifically a reduced FEV1/FVC ratio and bronchodilator to rule out asthma
149
how is chest x ray used to diagnose COPD
identifies hyperinflation and other structural lung changes consistent with COPD, ruling out alternative diagnoses
150
how are bloods used to diagnose COPD
assesses for polycythaemia or anaemia and screens for comorbid conditions
151
describe the role of infection in acute exacerbation of COPD
-infection increases airway inflammation and mucous production, leading to worsened airflow obstruction
-most common organisms include (H.influenzae, S.pneumoniae,M,catarrhalis)
152
identify pharmacoligical options for management of COPD
SABA
LABA
SAMA
LAMA
ICS
153
how do SABA work
stimulate beta-2-adrenergic receptors in the bronchial smooth muscle, leading to bronchodilator
154
how do LABA work
activate beta-2-adrenergic receptors in the bronchial smooth muscle for pre longed bronchodilator, typically lasting 12-24 hours
155
how do SAMA work
block muscarinic M3 receptors in the bronchial smooth muscle, reducing bronchoconstriction and mucous secretion
156
how do LAMA work
block muscarinic M3 receptors in the bronchial smooth muscle, providing extended bronchoconstriction and reduced mucous secretion
157
how do ICS work
reduce airway inflammation and oedema by inhibiting the release of inflammatory mediators and suppressing the activty of inflammatory cells
158
what are the non pharmacological management of asthma
avoid known triggers
inhaler technique
breathing exercises
physical active
adhere to medications
healthy diets
159
explain the concept of preventer vs reliever in terms of asthma
Preventers such as ICS are used daily to reduce airway inflammation and prevent asthma symptoms by
decreasing the production of inflammatory mediators and suppressing inflammatory cells.
Relievers, such
as (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.
160
principles of bronchodilator use
-Bronchodilators for asthma and COPD management can act via two principal mechanisms; agonising beta-2
receptors (SABA, LABA) or antagonising muscarinic-3 receptors (SAMA, LAMA).
-ICS is gold standard
161
describe use of mucolytics for asthma
-Mucolytics are used in asthma and COPD to reduce mucus viscosity and enhance mucus clearance from the
airways
-less common in asthma
162
Describe potential use of oxygen therapy amongst patients with COPD.
-Manages chronic hypoxemia, preventing complications like pulmonary hypertension and heart failure.
-Increases blood oxygen levels, reducing shortness of breath and improving exercise tolerance.
-Recommended for severe COPD with resting hypoxemia.
-Long-term use can improve survival and quality of life.
-Administered via nasal cannulas or masks, suitable for hospital or home use.
-Smoking cessation is crucial to avoid risks like explosions during home oxygen therapy.
163
Outline the use of monoclonal antibodies for severe, chronic airway disease
Target specific inflammatory pathways or cytokines to reduce chronic
inflammation and exacerbations in severe COPD.
164
Outline the use of bronchial thermoplasty for severe, chronic airway disease
Uses controlled thermal energy to reduce airway smooth muscle mass and
decrease excessive bronchoconstriction.
