Breathing Flashcards
what investigations should we use In assessing respiratory function?
NON-INVASIVE:
Peak flow, Pulse oximetry , Capnogrpahy, sputum sample
Spirometry - FEV1/FVC should be >80%
DLco = transfer factor = measures transfer of low carbon monoxide concentrations in inspired air to Hb Kco = DLco corrected for alveolar volume
CXR, CT, Echo
INVASIVE: ABG Bronchoscopy - rigid or flexi Lung biopsy Mediastinoscopy - if need tracheobronchial LNs PET scan
Applications of flexible bronchoscopy?
Diagnostic = biopsy via direct sampling or brushings, visualising obstruction
Therapeutic = Removing obstruction, argon coagulation therapy, difficult intubations, stenting
Advantage ov rigid brocnhosocpy over flexible?
Rigid bronchoscope permits simultaneous instrumentation, good if need to suction or remove foreign body
Outline the measurable lung volumes?
TV = volume of inspired air - 500ml OR 7ml/kg
ERV = volume that can be forcibly expired after quiet expiration
- 1.3L
IRV = volume that can be forcibly inspired above TV
- 3L
What lung volumes are there that are non measurable with spirometry?
Anything that involves residual volume.
Residual volume = Volume in lung after maximal expiration
- 1.2-1.5L
Total lung volume = VC + RV
Functional residual capacity = ERV + RV = volume left after quiet expiration
2.5-3L
Equation for FRC, normal range, and what can increase it or decrease it?
FRC = Functional residual capacity = ERV + RV
normal range = 2.5-3L
Increased in:
Obstructive disorders e.g. COPD / asthma
PEEP e.g CPAP
Decreased with: Age Obesity Pregnancy Factors limiting expansion = Effusions, abdo swelling, restrictive lung disease
Obstructive vs restrictive on spirometry?
Obstructive has reduced FEV1 = FEV1/FVC is low <0.8
Restrictive both are low but FVC is more low:
FEV1/FVC >0.8
What is atelectasis?
absence of gas from all or part of the lung
Plain CXR can be sub-segmental, segmental, lobar or pulmonary collapse
Causes of atelectasis?
Bronchial obstruction - sputum, FB or tumour
Alveolar hypoventilation leading to progressive airway collapse
Parenchymal compression due to oedema or effusions
Bronchial intubation collapses contralateral side
Why does airway obstruction cause atelectasis?
The gas trapped distally is absorbed as it has a higher partial pressure than the mixed venous blood = progressive collapse
Risk factors for post-op atelectasis?
Abdominal or thoracic surgery BMI > 27 Age >59 ASA >2 COPD IPPV > 1 day Smoking in the preceding 8 weeks
Management of post-op atelectasis?
Pre-op - breathing exercises
Intra-op:
Humidified air
Avoid unnecessarily high FiO2
Post-op: Upright position and breathing exercises Mobilise early Adequate analgesia CPAP Bronchoscopy for mucus plugs / secretions
What is CPAP and its effect on respiratory system?
Continuous positive airway pressure
Has a valve with set pressure.
On inspiration and expiration positive pressure cannot fall below this set pressure, if it does then pressure given.
Improves ventilation by: Opening of collapsed airways + prevention of collapsing on expiration Increases FRC Increases lung compliance Decreases work of breathing Increases V/Q ratio = improved perfusion
Disadvantages of CPAP?
Tight uncomfortable mask - pressure sores
Risk of barotrauma
Gastric dilation due to swallowed air
What is bronchiectasis?
The irreversible dilation of bronchi due to chronic inflammatory processes
name the types of bronchiectasis?
Follicular = loss of bronchial elastic tissue + multiple lymphoid follicles
Atelectatic = localised dilation of airways, associated with parenchymal collapse
Saccular / cystic = patchy dilation of airways, with loss of bronchial subdivisions
Aetiology of bronchiectasis?
Congenital:
Ciliary dyskinesia e.g. Kartageners
Cystic fibrosis
Ig deficiencies (will see recurrent infections in infancy)
Acquired: Post-infective bronchial damage e.g measles, pertussis, TB Bronchial obstruction - tumour, FB, LN's Immunodeficiency e.g. AIDS Autoimmune - RA, UC
What bacteria may colonise bronchiectasis?
Haem. Influenzae
Staph aureus
Strep pneumo
Complications of untreated bronchiectasis?
Early =
- haemoptysis
- infections > abscess and empyema
- metastatic infection e.g. cerebral abscesses
Late:
- Cor pulmonale
- Respiratory failure
- Secondary amyloidosis with protein A deposition
Mx of bronchiectasis?
Manage reversible airway obstruction with neb and steroids
Chest physio
Treat underlying cause and treat any infection
Surgery - lung transplant in CF
What is pneumonia?
Inflammatory process of lung characterised by consolidation due to exudate in alveolar space
Types of pneumonia?
Lobar - confined to one lobe, linear demarcation.
Exudate forms in bronchioles and alveoli and spills over to adjacent segments via pore of Kohn.
Bronchopneumonia = starts at bronchioles and extends into alveoli > numerous foci of consolidation
Interstitial = chronic alveolar inflammation, not necessarily infective in origin - may be immune based
Pathological classes of pneumonia?
1 = acute congestion, day 1-2
- lobe is heavy, dark and firm.
- inflame exudate and cellular infiltrate including erythrocytes
2 = red hepatisation, day 2-4
- lung is firm, red and consolidated
- neutrophils fibrin and extravasated erythrocytes
3 = grey hepatisation, day 4-8
- Heavy, consolidated and grey
- Extensive fibrin network and degenerating erythrocytes
4 = resolution > day 8
- Macrophage action liquefies exudate
- can take 3 weeks
Organsims involed in ICU pneumonias?
Ventilator related
Within 1-4 days of intubation = early onset:
- Strep. pneumonia, s. aureus and h influenza
Lates onset >4 days = gram negative
- Pseudomonas, enterobacter, aeruginosa
What are the normal respiratory defence mechanisms?
Nasal humidification of air Nascociliary action Intact cough reflex Alveolar macrophages Secretory IgA
RF’s for nosocomial pneumonia when intubated?
Breakdown of anatomical barriers Impaired cough reflex Re-intubation Colonisation of instruments Staff hygiene Aspiration of gastric contents Epithelial trauma due to airway / suction
What risk factors predispose the stomach to bacterial colonisation?
pH <4:
PPIs or H blockers
Continuous gastric feeding
Chronic atrophic gastritis = achlorydia
How can pneumonia be prevented?
Isolate high risk patients Staff hygiene Suctioning subglottic secretions Controlled ABx use = no resistance Use of sucralfate for prophylaxis of stress ulcers
Complications of bacterial pneumonia?
Respiratory failure - T1RF = hypoxaemic Effusions Empyema and abscess Metastatic abscess Sepsis
3 types of pneumothorax?
Simple = two way valve, no CVS compromise
Tension = closed valve system, quick CVS compromise
Open = sucking chest wound, must be greater than 2/3rds diameter trachea
Causes of pneumothorax?
Primary = idiopathic bursting of apical bled
Secondary:
Spontaneous = pre-existing lung disease
Traumatic - blunt and penetrating
iatrogenic - pleural aspiration, central line, barotrauma
How can pneumothorax be recognised in a ventilated patient?
Sudden increase In inflation pressure
Sudden hypoxia / hypotension
Raised JVP
Development of new cardiac arrhythmia
Management of pneumothorax?
Primary: <2cm not SOB = home with OPD >2cm with SOB > aspirate success = home failure = chest drain
Secondary:
> 2cm and SOB = chest drain
1-2cm = aspirate, if success and now <1cm = monitor, if failure = chest drain
<1cm = monitor for 24 hours
What is the definition of lung compliance?
Lung compliance is the volume change of lung per unit pressure applied i.e. the ease with which the lung inflates
What is surfactant and what purpose does it serve?
Surfactant is a phospholipid mixture, produce by type 2 pneumocytes
Acts to reduce surface tension of fluid lining alveoli = greater compliance:
- Reduces work of breathing
- Stabilises smaller alveoli preventing atelectasis
Definition of ARDS?
Diagnostic criteria?
Acute onset respiratory failure with persistent inflammatory change in the lungs.
- Acute onset <1week
- Bilateral pulmonary opacities
- Pa02:Fi02 <26.6kPa (200mmHg)
Also must have pulmonary artery capillary wedge pressure < 18mmHg = excluding. cardiac cause
How does ARDS relate to ALI and SIRS?
ARDS and ALI are on a spectrum. Acute Lung Injury is non-specific pathological changes in the lung due to a specific insult.
The changes are like ARDS but less severe
ARDS is the respiratory component of SIRS
Causes of ARDS?
Direct insult = pneumonia, aspiration, contusion, inhalation injury
Indirect = Sepsis, DIC, massive transfusion, pancreatitis
Describe the pathology of ARDS…
Initially during acute insult 3 things happen:
- Vasoactive mediators released
- Activation of neutrophils and macrophages
- Activation of complement and coag cascade
This then leads to other processes
Vasoactive mediators:
= pulmonary vasoconstriction = increase PVR = R heart strain
Activation complement and coag:
= Oedema:
- Vascular compression = increased PVR = RH strain
- V/Q mismatch = hypoxic = increased PVR = RH strain
- Increased secretion/retention = atelectasis / infection
Activation of neutrophils and macrophages:
= Free radicals, TNF, protease, collagenase:
- Oedema due to endothelial injury and capillary permeability
- Epithelial injury = reduced type 2 pneumocytes = reduced surfactant = atelectasis / infection
Management of ARDS?
ABCDE
Manage initial insult
Careful fluid resuscitation due to oedema
Mechanical ventilation:
- High PEEP to keep airways open
- small tidal volumes show improved outcome, leads to a hypercarbia but is usually well tolerated
- Increasing inspiratory phase
Inhaled NO = pulmonary vasodilation and increase oxygenation. Effect on survival is equivocal.
Prognosis of ARDS?
Poor - mortality 30-60%
If sepsis present mortality as high as 90%
How does NO work?
NO is a vasodilator. Works by acting upon cytoplasmic enzyme guanylyl cyclase.
This increases intracellular cyclic guanosine monophosphate cGMP which stimulate a protein kinase.
This leads to relaxation of vascular smooth muscle cells
What are the defining features of flail chest?
> 3 ribs broken, in > 2 places
Implications of flail chest?
Marker of severity - high impact force
Likely co-existing injuries
Early complications = respiratory failure, pneumo/haemothorax
Late complications = sepsis, atelectasis and pneumonia
Pathophysiological changes to the respiratory system in flail chest?
Reduced tidal volume:
- Flail segment exhibits paradoxical motion. On inspiration moves in, due to negative intrapleural pressure.
- Pain also reduces tidal volume
Retention of secretions due to reduced tidal volume and inefficient cough mechanism
Can lead to T1RF
Management of flail chest?
ATLS principles
Mx flail itself and any underlying injuries
Most will be managed conservatively with observation, humidified air and analgesia
If deterioration can intubate
What is a sucking chest wound?
Open pneumothorax
Wound size must be > 2/3rds diameter of the trachea for air to preferentially enter via open wound
PE - Risk factors?
Based around virchows triad:
Venous stasis
Hyper-coagulability
Vessel lumen
Stasis = AF, trauma, surgery (specifically neurosurgery due to controversy with anticoags), immobility.
Hyper coagulable = Pregnancy, cancer, OCP, Chemo, thrombophilias
Vessel lumen = Atherosclerotic disease
Where do DVTs commonly form?
Commonly form in deep venous system of calves or venous plexus in soleus
Specifically forms around valves.
Can form distally or more proximally, meaning higher risk of PE’s
Clinical signs of DVT?
Swollen painful calf
Phlegasmia alba Dolens = oedema, pain and white blanching skin
Phlegasmia cerulean Dolens = oedema, cyanotic and painful
Pathophysiology of PE?
Pulmonary artery obstruction as embolus is impacted past right ventricle outflow.
Activated platelets within the thrombus release vasoactive mediators = increase PVR = increased right ventricular afterload = RH strain and tachycardia
How may PE present?
Small = SOB, tachy, pleuritic pain
Large = Above +:
- Shock
- Severe central chest pain
- Signs of right ventricular strain = Wide splitting heart sound, tricuspid regurgitation, raised JVP, RV heave
Common ECG changes in PE?
Sinus Tachy
Tall p waves lead 2
RAD
RBBB
TWI anterior leads
Management of PE/DVT?
LMWH, the start them on DOAC
If unstable thrombolysis
If contraindications for thrombolysis = IR pulmonary catheterisation or surgical embolectomy
How can PE’s and DVTs be prevented?
TEDs / IPC
LMWH
Stop procoagulants 4 weeks pre-op e.g. OCP
Early mobilisation
What are normal ranges of Pa02 and PC02?
Pa02 = 10.6 - 13.3 kPA
PC02 = 4.7 - 6.0 kPa
What is best measure of ventilation?
Measuring CO2 is key using capnography
PaCO2 x alveolar ventilation = volume of CO2 exhaled in 1 minute
Definition of respiratory failure?
T1RF = Hypoxic <8kPa
T2RF = Hypoxic + PC02 >6.7
T1RF vs T2RF?
Causes of each?
Type 1 RF is hypoxic only, PO2 <8.
Due to a V/Q mismatch - typically problems that affect oxygenation:
- Shunt e.g. Congenital heart disease
- V/Q mismatch in PE as not enough blood to absorb oxygen
- Mismatch in parenchymal disease as oxygen cannot get to blood e.g. ARDS, pneumonia,
Type 2 RF is hypoxic, as well as PC02 >6.7 It is due to alveolar hypoventilation: - COPD, asthma - cerebral lesions - tumour, head injury - neuromuscular - MND, guillian barre - Thoracic cage - e.g. flail chest.
Mx of respiratory failure?
ABCDE approach
Adequate ventilation - may need high flow oxygen or NIV
Serial ABGs
Treat underlying cause
Purpose of a chest drain?
Diagnostic - Samples of pleural effusions - transudate or exudate
Therapeutic:
- effusions
- Pneumothorax
- Haemothroax
- Chylothroax
- Empyema
- Post op in thoracic, cardiac, oesophagectomy
Pre-procedure check prior to chest drain?
Lab:
PT
Platelets
CXR
Outline steps in chest drain insertion?
- position = supine, arm abducted and hand being head
- Marking - 5th ICS MAL
- Scrub, clean area, drape
- Local anaesthetic to make wheal, then insert 10-15ml to subcutaneous layers
- Incision - 2-3cm transverse incision with size 11 blade
- Blunt dissection suing Roberts clamp to open muscular layers to parietal pleura
- Confirm position by entering needle and aspirate air / fluid
- Secure incision with two 0 silk mattress sutures
- Insert chest drain. 24 for pneumothorax, 32 for Haemo
Clamp with Roberts forceps and insert and secure - Closed system drainage
Investigations post chest drain?
CXR
Chest drain complications?
Early = malpositioned, haemothorax ion hit bundle under rib, pulmonary trauma, abdominal injury
Late:
Blocked drain
Drain failure
Pneumothorax following removal
Indications for removal of chest drain?
Re-expansion successful
Drain no longer works
Air and fluid ceased to drain - no further swinging / bubbling
