Respiratory conditions Flashcards
How is asthma diagnosed?
A combination of:
- Decrease in lung function/expiratory airflow on spirometry (difficult to perform <5 years old)
AND
- Respiratory symptoms (wheeze, SOB, cough, chest tightness)
What does untreated asthma cause to the pt
- Chronic inflammation
- airway hyperresponsiveness
- Intermittent airway narrowing
Define atopic and non atopic asthma
Atopic/extrinsic
- Triggered by the environment
- Inflammation due to systemic IgA production
(smoke, animals, medications, mould etc)
Non-Atopic/intrinsic:
- Not caused by exposure to an allergen
- Inflammation due to local IgA production
(exercise, URTI, emotions, comorbid medical diseases)
Why is asthma not diagnosed <12 months?
Wheezing is usually due to bronchiolitis or small, floppy airways
Define early and late phases of asthma
Early:
- Initial allergen response within 10-20minutes
- Production of IgE-mast cell complex - release histamine and inflammatory mediators which causes smooth muscle constriction, increased cap permeability and oedema in the bronchioles.
Late phase:
- 4-8 hours after exposure
- Inflammation and airway responsiveness prolongs asthma attack
- Reaches max after a few hours-weeks
- Responsiveness to cholinergic medications as often increased
Define severe asthma
- Persistent symptoms despite treatment
- Increased risk of fatal/near fatal attacks
- Death usually due to asphyxia and associated cardiac dysrhythmias
Define uncontrolled asthma
- Poor symptom control
- Frequent exacerbations
- Serious exacerbations (ICU/hospitalization/mechanical ventilation)
- controlled asthma worsening on tapering off corticosteroids
Define a flair up/exacerbation of asthma
- Symptoms commence or become worse than usual
- Symptoms do not spontaneously resolve and require treatment
- Rapid onset or can occur over hours/days
Pathophysiology of the early stage of asthma
Dendritic cells engulf the allergen - activate - release chemokins that attract specific T-helper 2 cells.
T-helper 2 cells produce interleukins that: stimulate plasma cells to produce more IgE antibodies, binds to mast cells creating IgE-mast cell complex - releases prostiglandins, histamines and leukotrines.
This stimulates smooth muscle to bronchoconstrict, increased cap permeability, vasodilate, increase blood flow to the area.
Interleukins also stimulates bone marrow to produce eosinophils.
Pathophysiology of the late response of asthma
- Latent release of inflammatory mediators from lymphocytes, eosinophils, neutrophils
- Synthesis of leukotrines (inflammatory mediators produces by leukocytes) contributes to smooth muscle contraction
- Eosinophils cause direct injury and fibroblast proliferation
- Toxic neuropeptides increase bronchial hyperresponsiveness
- Impaired mucocilliary function (mucus trapping and removing pathogens from the airways)
- Accumulation of cellular debris forms plugs
- Increased nitric oxide causes oxidative injury and chronic inflammation
- Airway remodelling occurs (increased goblet cells and eosinophils in the tissue and mucous, thickening of basement membrane, more mast cells in the lamina propria, hypertrophy of smooth muscle cells, subepithelial fibrosis)
What does in increased airway resistance in asthma cause?
- Impaired expiration and gas trapping
- Hyperinflation distal to obstruction
- Increased WOB
- V/Q mismatch in different areas of the lungs
- hyperventilation and hypoxaemia without co2 retention - respiratory alkalosis (EARLY STAGE)
- Hyper-extension of lungs
- Thorax and respiratory muscle dysfunction
- Decreased Vt and respiratory acidosis (T2 resp failure)
- Decreased LV filling time and decreased CO due to severe hyperinflation
- Cardiorespiratory arrest
Clinical manifestations of asthma
Early:
- Chest tightness
- Expiratory wheeze
- SOB
- Dry cough
- Prolonged expiration
- Tachycardia/tachypnoea
- Increased WOB
- Wheeze during inspiration and expiration
- Pulsus paradoxus
- Hypoxaemia
Status asthmaticus:
- Not reversed by normal measures
- Effective ventilation decreases
- Respiratory acidosis
Life threatening:
- Silent chest
- PaO2 >70mmHg
Chronic asthma management
SABA (short acting beta-agonist) PRN
–>
Low dose regular preventer ICS (inhaled corticosteroid) + SABA PRN
–>
Low dose combination ICS plus LABA (long acting beta agonist) + ‘reliever’ PRN
–>
High dose ICS/LABA + ‘reliever’ PRN
Acute asthma management in adults
Mild-moderate:
4-12puffs salbutamol via MDI
Severe: 12 puffs salbutamol MDI 8 puffs ipratropium MDI (or combined in neb) O2 therapy
Life threatening:
2 x 5mg salbutamol plus ipratropium neb
O2 therapy
? ventilate
- reassess*
- give systemic corticosteroids within 1/24
Mild/moderate:
Hour of power
Severe:
Continuous nebs until symptoms resolve, then MDI
poor response?
Add IV magnesium 10mmol over 20min
Acute asthma management in paediatrics
Mild-moderate:
1- 5 years: 2-6 puffs salbutamol MDI
>6 years: 4-12puffs salbutamol via MDI
Severe:
1-5years: 6 puffs salbutamol, 4 puffs ipratropium MDI
>6years: 12 puffs salbutamol, 8 puffs ipratropium MDI
(or combined in neb 1-5 years: 2.5mg, >6years: 5mg)
O2 therapy
Life threatening:
2 x dose of salbutamol plus ipratropium neb
O2 therapy
? ventilate
- reassess*
- give systemic corticosteroids within 1/24
Mild/moderate:
Hour of power
Severe:
Continuous nebs until symptoms resolve, then MDI
poor response?
Add IV magnesium 0.1-0.2mmol/kg over 20min
What is an obstructive airway disease?
More force or time is required to exhale a volume of gas and emptying is slowed. It is associated with increased airway resistance and gas trapping.
Eg: asthma.
Clinical manifestations: Dyspnoea Decreased FEV1 V/Q mismatch Increased WOB
What is a restrictive airway disease?
The lungs are restricted from fully expanding.
Most often results from a condition causing stiffness in the lungs themselves. In other cases, stiffness of the chest wall, weak muscles, or damaged nerves may cause the restriction in lung expansion.
Eg: pulmonary fibrosis, obesity, sarcoidosis.
Define COPD
A progressive obstructive airway disease associated with abnormal inflammatory response to noxious particles or gas.
Chronic bronchitis - hypersecretion of mucous and chronic productive cough for 3 months of the year for 2 consecutive years. Frequent infective excassebations.
Emphysema -
Abnormal permanently enlarged acini accompanied by destruction of alviolar walls without obvious fibrosis. Usually due to ttoxic smoke or alpha 1 antitrypsin disorder.
Chronic Asthma -
Risk factors for COPD
- Tobacco smoke
- Occupational dusts and chemicals
- Air pollution
- factors affecting lung development during gestation and childhood
Diagnosis of COPD
FEV2/FVC ratio <0.7
and
FEV1 <80% predicted
Pathophysiology of COPD
Progressive pulmonary changes due to inflammatory response of the large central airways, small peripheral airways and lung parenchyma. Mainly:
- Chronic bronchitis
- Emphysema
Pathophysiology of chronic bronchitis
Continual bronchial inflammation causing increased mucocillary dysfunction and goblet cell production. Therefore excessive mucous production and decreased clearance (chronic cough). Bronchoconstriction/oedema causes wheeze.
This causes alviolar hypoxia and a V/Q missmatch, decreased O2 causes polycythemia (increased Hb) and increased CO2 causes respiratory acidosis, both causing cyanosis.
Alviolar hypoxia causes vasoconstriction in order to shunt blood flow to healthier alvioli. Therefore, there is an increase in resistance, backflow to RV and increased JVP.
Also pulmonary hypertension causes decreased LV filling, decreased CO, activation if the RAAS and fluid retention.
Airway obstruction due to mucous and hypertrophies smooth wall muscle, airway collapse occurs early in expiration causing gas trapping.
Pathophysiology of Emphysema
Inflammatory response causes elastic fibre breakdown and destruction of alviolar wall integrity causing air trapping.
Alviolar macrophages are activated by a toxin, causing secretion of protease and cytokines.
-Protease destructs the alviolar wall (decreases ventilation) and capillary bed (decreases perfusion)..
- Cytokines attract neutrophills which release elastase - this decreases elastic recoil (decreases ventilation).
Decreased elasticity causes air trapping and increased end expiratory volume (causing barrel chest). There is therefore a matches V/Q deficit.
Airflow loss and gas trapping due to decreased elastic recoil and alviolar collapse causing inadequate expiration.
Clinical manifestations of chronic bronchitis
‘blue bloater’
- Wheeze
- Productive cough
- SOB
- Decreased FEV1
- Frequent pulmonary infections
- Decreased FVC and residual volume
- Increased PaCO2
- Hypoxaemia
- Polycythemia
- Cyanosis
- Pulmonary hypertension
- Cor Pulmonale (r sided heart failure)
Clinical manifestations of emphysema
- Weight loss
- Muscle weakness
- Increased susceptibility to comorbidities
- Barrel chest
- Increased WOB
- Little coughing with little sputum
- Prolonged FEV1
- Hyper resonant sound on percussion
- Pursed lip breathing, tripid position
On CXR: large airspaces in the lungs (bullae) and adjacent to the pleura (blebs).
Management of COPD
Long term:
Risk reduction - stop smoking, flu vax
Optimise function - exercise, nutrition
Consider comorbidities - ?pulmonary rehab
Short acting reliever medication - LAMA, LABA
Exacerbation prevention - LABA/ICS combination therapy
Exacerbations: Bronchodilators - inhaled _ antimuscarinic Corticosteroids pred 30-50mh for 5/7 Antibiotics - amoxicillin or doxycycline Controlled O2 (88-92% RA) NIPPV if PaCO2 >45mmHg and pH <7.35
What are the two types of pneumonia?
Community acquired:
Onset in the community or within 48 hours of admission
or
Hospital acquired:
Occurs within 48 hours or more of hospital admission.
(inc chemo and aged care)
Pathophysiology of pneumonia
Alteration in bacterial lung resistance of the host - defence mechanisms overwhelmed
CONGESTION STAGE
accumulation of fluid in the alvioli, organism multiplies in the fluid
–>
endotoxins cause inflammation
–>
proliferation of organism throughout the lobe
–>
RED HEPATISATION PHASE
massive vasodialation of capillaries
–>
alvioli become leaky and fill with organisms, neutrophils, RBC and fibrin
GREY HEPATISATION PHASE
decreased RBC, increased neutrophils
RESOLUTION
Exudate is lysed by macrophages. Lung tissue and function is restored
Management of pneumonia
- Infection control
- Adequate fluid intake/IVT
- O2 therapy
- Minimise risk of aspiration
- Positioning
- Nutrition
- Deep breathing and coughing/physio
- ABx - amoxycillin
- Antipyuretic
- Analgesia
What is a thrombus made of?
A collection of RBC’s and platelets. Thrombin converts fibrinogen into fibrin, which clumps RBC and platelets together in the vein.
What is Virchows triad?
Factors causing thrombus formation:
- Abnormal blood flow
- Hypercoaguability (eg. thrombophillia)
Altered vessel wall
Pathophysiology of PE
A thrombus is formed in a vein (usually DVT) and breaks off –> inferior vena carva –> RA –> RV –> pulmonary trunk –> pulmonary arteries (L or R).
This leads to increased pulmonary pressure and backflow of blood to the RV, causing increasing RV pressure, dilation and R heart failure. Decreased SV causes decreased CO –> stimulates SNS causing tachycardia and vasoconstriction to nil effect on BP.
An obstruction in the pulmonary capillary causes a VQ missmatch and inflammation –> bronchoconstriction –>hyperventilation –> hypocapnia –> RESPIRATORY ALKALOSIS.
Clinical manifestations of PE
- Tachycardia
- Tachypnoea
- SOB
- Pleuritic CP
- Assess for DVT
- Unexplained anxiety
Nursing management of PE
DRSABCD
O2 therapy
Haemodynamic stabilization with fluids +/- inotropes
Anticoagulation (heparin)
Fibrinolytic agent - eg streptokinase
Emergency percutaneous or surgical embolectomy
ECMO
best management is prevention!
- ID at risk pts
- early ambulation
- prophylactic anticoagulation
- Compression stockings
-
Investigations for PE
CXR - usually normal, to rule out pnemonia/pneumothorax
ABG - hypoxaemia
ECG - usually to rule out MI and pericarditis. Can show R heart strain (inverted t wave in v1-v4)
CTPA *gold standard
?D dimer
Pathophysiology of a simple pneumothorax
Air in the pleural space disrupts the negative pressure between the visceral pleura and lung, causing separation and lung collapse.
No apparent trauma/event.
Causes of simple pneumothorax
- Rupture of bleb/bullae
- Mechanical ventilation
- Nosocomial (lung biopsy, subclavicular catheter)
- Perforated oesophagus
- Fractured ribs
Primary spontaneous pneumpthorax = tall, thin males at rest.
Secondary spontaneous pneumpthorax = secondary to primary lung disease
Clinical manifestations of simple pneumothorax
- SOB
- Decreased breath sounds on the affected side
- Asymmetry of chest wall
- Evidence on XRAY
- Tachycardia
- Pleuritic CP
- Cough
- Heamoptysis
Investigations for simple pneumothorax
- History
- Physical assessment
- CXR
Management of simple pneumothorax
- Assess tracheal position
- o2 therapy, ECG, vitals etc
- Analgesia
- Aspiration (ICC, needle 14-16g, flutter valve)
- Surgical (pleurectomy, stapling, pleurodesis)
Classifications of severity of COPD
Mild:
- 60-80% predicted
- recurrent chest infections
- breathleSsness on moderate exertion
- little to no effect on daily living
Moderate:
- 40-59% predicted
- cough and sputum production
- exacerbations requiring SABA and corticosteroids
- breathlessness walking on level ground
- increased limitation on daily living
Severe:
- <40% predicted
- chronic cough and sputum production
- daily activities severely limited
- Daily activities severely curtailed
Define good, partial and poor symptom control of asthma
GOOD:
- Daytime Sx <2 days/week
- need SABA <2 days/week
- No limitations of activities
- No Sx during the night or on walking
PARTIAL: 1-2 of :
POOR: 3 or more of:
- Daytime Sx >2 day/week
- Need SABA >2 days/week
- Any limitation of activities
- Any Sx during the night or on walking
