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MRCS Critical care > Critical care: respiratory > Flashcards

Critical care: respiratory Flashcards

1
Q

What is ARDS?

A

-Syndrome of respiratory failure
-Formation of non-cardiogenic oedema–> reduced lung compliance and hypoxaemia refractory to oxygen therapy

Berlin definition:
-Bilateral diffuse pulmonary infiltrates on CXR/CT
-Acute onset within 7 days
-PaO2:FiO2 ratio <300mmhg with PEEP or CPAP >5cmH2O
-Alveolar oedema not explained by fluid overload or cardiogenic causes

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2
Q

Pulmonary wedge pressure:

A

-Pressure measured by wedging a pulmonary artery catheter with an inflated balloon into a small pulmonary arterial branch

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3
Q

PaO2:FiO2 ratio

A

PaO2/FiO2 ratio is the ratio of arterial oxygen partial pressure (PaO2 in mmHg) to fractional inspired oxygen

Ie how much inspired oxygen gets into the blood stream

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4
Q

How would you classify ARDS causes

A

Direct lung injury
Indirect lung injury

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5
Q

ARDS direct lung injury causes

A

-Pneumonia
-Aspiration of gastric contents
-Fat emboli
-Smoke inhalation injury

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6
Q

ARDS indirect lung injury causes

A

-Sepsis
-Severe trauma
-Major burns
-Acute pancreatitis
-Multiple blood transfusion

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7
Q

Describe phases of ARDS pathophysiology

A

Exudative phase
Proliferative phase
Fibrotic phase

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8
Q

Describe exudative phase ARDS pathophysiology

A

-Alveolar damage initiated from the initial tissue injury
-Cytokines and inflammatory mediators–> alveolar and endothelial injury.

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9
Q

Describe proliferative phase ARDS pathophysiology

A

-Restoration of alveolar-capillary membrane integrity, by the fibroblasts and type-2 pneumocytes
-New surfactant is produced

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10
Q

Describe fibrotic phase of ARDS

A

-fibrin deposition leading to ‘scarring’ of the lung tissue.
-can lead to long-term oxygen or even ventilation dependency.

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11
Q

What is CPAP and how does it work?

A

-Form of invasive or non-invasive ventilation
-continuous pressure is given throughout respiratory cycle to increase functional residual volume and improve hypoxia
-This decreases work of breathing and prevents alveolar collapse

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12
Q

What type of respiratory failure is CPAP applicable for?

A

Type 1

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13
Q

Define respiratory failure

A

Type 1 (hypoxaemic)
-PaO2 <8 kpa
-Normal or reduced PaCO2

Type 2
-PaO2 <8 kPa
-PaCO2 is >6.7kPa

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14
Q

What are the indications for a tracheostomy

A

Maintain airway in:
-Congenital pathologies (tracheal stenosis)
-Following surgical procedures e.g. laryngectomy
-Emergency setting e.g. laryngeal trauma/oedema, inhalation injury
-If prolonged intubation expected

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15
Q

What are the two methods of performing a tracheostomy?

A

-Percutaneous
-Surgical

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16
Q

Name the types of tracheostomy tubes

A

-Metal or plastic
-Cuffed or uncuffed
-Fenestrated or unfenestrated

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17
Q

What are the advantages of tracheostomies?

A

-Expedites extubation and weaning
-Decreases work of breathing
-Avoids continued vocal cord injury
-Improves bronchopulmonary hygeine
-Improves ability of pt to communicate

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18
Q

What are the disadvantages of tracheostomies?

A

-Long-term risk of tracheal stenosis
-Blockage of tracheostomy tube leading to airway compromise
-Dislodged tracheostomy tube

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19
Q

Name some complications related to performing a tracheostomy

A

-Bleeding
-Pneumothorax
-Vascular injury
-Oesophageal trauma
-Death

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20
Q

When would you consider extubation?

A

-Resolution/stabilisation of disease process
-Intact cough/gag reflex - protected airway
-Spontaneous respirations
-FiO2 <40%
-PEEP <8
-PaO2 >10kPa (if no pre-existing lung disease)
-pH >7.35
-Good muscle strength
-Neurologically intact

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21
Q

Indications for intubation

A

-Acute respiratory failure
-Acute ventilatory failure
-Surgery
-Raised ICP to avoid hypoxia/hypercarbia
-Trauma (chest injury and lung contusion)
-Severe LVF with pulmonary oedema
-GCS <8
-ARDS
-Prophylactic establishment of airway e.g. smoke inhalation
-Raised ICP to avoid hypoxia/hypercarbia

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22
Q

What is IPPV

A

-Lungs are intermittently inflated with positive pressure
-Intubation is required to facilitate IPPV

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23
Q

Pulmonary embolus definition

A

-A pulmonary embolism (PE) refers to a blockage of the pulmonary artery by a substance that has travelled there in the bloodstream.
-Most commonly an embolus from DVT in leg
-Other causes include AF, right mural thrombus post MI, neoplastic cells or fat cells e.g. from tibial fracture

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24
Q

What ECG changes would you expect in pe?

A

-Often no changes
-Sinus tachycardia

RV strain: TWI V1-V4 and/or avf + 3
S1Q3T3
-Large S wave V1
-Large Q wave in V3
-T wave inversion lead 3

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25
Q

What are the risk factors for developing PE?

A

Wells score is useful predictor of PE/DVT assessing:
-Symptoms of DVT
-Advanced age
-Immobilisation >: 3 days
-Recent surgery
-Previous history DVT/PE
-Malignancy

Other risk factors include pelvic or leg trauma, pregnency, genetic predisposition

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26
Q

Describe mechanism of action of heparin

A

Binds to anti-thrombin 3 which inhibits factors IX, X, XI and XII and prevents conversion of fibrinogen to fibrin

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27
Q

Describe mechanism of warfarin

A

Competitive inhibitor vitamin K, which is co-factor for production of factor 2, 7, 9, 10

28
Q

When would thrombolysis be indicated for PE?

A

May be indicated in PE with haemodynamic compromise: however, would require input from respiratory/ITU teams

29
Q

Absolute contraindications for thrombolysis

A

-Active internal bleeding
-Recent spontaneous intracranial bleeding

30
Q

Relative contraindications for thrombolysis

A

-Major surgery within 10 days
-Ischaemic stroke within 2 months
-GI bleed within 10 days
-Major trauma within 15 days
-Recent CPR
-Platelet count <100
-Severe uncontrolled hypertension

31
Q

Explain O2 dissociation curve

A

-greater affinity hb for o2 after binding first molecule
-left shift: greater affinity
-right shift: lesser affinity

-Demonstrates relationship between pO2 and blood oxygen concentration
-Shape of curve reflects increasing ability of hb to take up o2 following binding of first molecule
-Left shift increases o2 affinity and so o2 is less readily available for use in tissues
-Right shift of curve decreases o2 affinity so it is more readily available for use in tissues

32
Q

What are the causes of left shift in oxygen dissociation curve?

A

-Decrease in temperature
-Decrease in 2,3 diphosphoglycerate
-Alkalosis
-carbon monoxide poisoning

33
Q

What is 2,3 diphosphoglycerate?

A

-Present in RBCs
-Binds with greater affinity to deoxygenated haemoglobin (ie haemoglobin in respiring tissues)
-Decreases affinity for oxygen and promotes release of remaining molecules

34
Q

How does dissociation curve in foetal hb differ from adult?

A

-Curve is shifted to left and therefore has greater affinity to o2
-Readily takes up o2 from maternal adult hb

35
Q

How is cO2 transported in body?

A

-As bicarb ions
-Dissolved in plasma
-Bound to hb as carbamino-compounds

36
Q

How would you classify pneumothorax?

A

-Traumatic
-Spontaneous
-Tension

37
Q

Describe traumatic pneumothorax causes

A

Results from penetrating or blunt injury to chest

Iatrogenic - complications of invasive medical procedures such as:
–Central line placement
–Thoracocentesis
–Lung biopsy

Accidental

38
Q

Describe and classify sponteneous pneumothorax

A

Occurs without preceding trauma or precipitating event
-Primary: No obvious lung disease
-Secondary: complication of lung disease

39
Q

Describe tension pneumothorax

A

-air is trapped in the pleural space under positive pressure
-Mediastinal structures are displaced
-cardiopulmonary function is compromised

40
Q

How would you classify causes of tension pneumothorax

A

Iatrogenic
Non iatrogenic

41
Q

What are the iatrogenic causes of tension pneumothorax

A

-Central line
-Mechanical ventilation
-Incorrect chest drain insertion
-CPR
-Needle lung biopsy
-Liver biopsy/surgery
-Neck surgery

42
Q

Non-iatrogenic causes tension pneumothorax

A

-Blunt and penetrating trauma
-Asthma
-COPD
-Pneumonia
-Pertussis
-TB
-Lung abscess
-CF

43
Q

What are clinical features of tension pneumothorax?

A

-Respiratory distress
-Raised JVP
-Tracheal deviation
-Reduced breath sounds
-hyper-resonance
-shock
-distended neck veins

44
Q

Describe immediate management for tension pneumothorax

A

-100% O2
-Needle thoracocentesis: large bore cannula inserted into 5th intercostal space mid axillary line

45
Q

What procedure would you perform for tension pneumothorax after needle thoracocentesis?

A

Chest drain

46
Q

What are the indications for inserting chest drain?

A

-Pneumothorax
-Haemothorax
-Chylothorax
-Drain pleural fluid or empyema
-Peri-operative procedure e.g. thoracotomy, oesophageal surgery, cardiothoracic surgery

47
Q

Name some complications following chest drain insertion

A

-Bleeding from an injured intercostal artery
-Accidental injury to the heart, arteries, lung, liver on right, spleen on left
- infection
-Air leaks in tube
-Dislodged tube
-Incorrect positioning of tube
-Insertion of chest tube can cause open or tension pneumothorax

48
Q

Label spirometry graph

A
  1. Tidal volume
  2. Inspiratory reserve volume
  3. Inspiratory capacity
  4. Functional residual capacity
  5. Vital capacity
  6. Functional residual capacity
  7. Total lung capacity
49
Q

Define tidal volume

A

The amount of air that moves in or out of the lungs with each respiratory cycle

50
Q

Define inspiratory reserve volume

A

The amount of air a person can inhale forcefully after normal tidal volume inspiration

51
Q

Define expiratory reserve volume

A

Expiratory reserve volume is the amount of air a person can exhale forcefully after a normal exhalation

52
Q

Define functional residual capacity

A

the volume remaining in the lungs after a normal, passive exhalation

53
Q

Define vital capacity

A

total amount of air exhaled after maximal inhalation

54
Q

Define residual volume

A

the amount of air that remains in a person’s lungs after fully exhaling

55
Q

Total lung capacity

A

the maximal volume of gas in the lungs after a maximal inhalation

56
Q

How would you differentiate obstructive from restrictive lung disease on lung function test?

A

-Normal FEV1:FVC ratio around 80%
-In restrictive lung disease FEV1:FVC ratio >79%
-in obstructive lung disease <80%

57
Q

Define FEV1:FVC ratio

A

-The ratio of the forced expiratory volume in the first one second vs forced vital capacity of the lungs.
-The normal value for this ratio is above 0.75-85, though this is age dependent.

58
Q

Define inspiratory capacity

A

The maximum volume of air that can be inspired after reaching the end of a normal expiration

59
Q

What are the different systems that regulate acid-base balance?

A

Respiratory
Kidney
Blood
Bone
Liver

60
Q

How does respiratory system control acid/base balance?

A

-PCO2 controlled by alteraltions in alveolar ventilation
-CO2 crosses blood-brain barrier and dissoves in CSF forming H+ ions
-This stimulates central chemoreceptors in ventrolateral surface of medulla oblongata

61
Q

How does kidney control acid/base balance?

A

-Controls bicarbonate ion which is important for long-term control and compensation of acid-base disturbances

62
Q

How would you manage pt with post operative pneumonia?

A

-Resuscitate as per ccrisp protocols
-Oxygen
-Antibiotics
-Chest physio
-Discuss with critical care team

63
Q

What are the defence mechanisms of the respiratory system?

A

-Airway mucus secretion
-Muco-ciliary action of upper respiratory tract
-Alveolar macrophages

64
Q

What are the indications for intubation?

A

GCS <8
-Traumatic chest injury + pulmonary contusion
-Respiratory/ventilatory failure
-Prophylactic establishment of airway e.g. smoke inhalation

-Decreased level of consciousness/coma
-Upper airway obstruction
-Traumatic chest injury
-ALI/ARDS
-Respiratory failure
-Apnoea
-Neuromuscular disease
-Prophylactic establishment of an airway – eg smoke inhalational injuries, angioedema, drug overdose

65
Q

If post op pneumonia pt does not improve, what type of respiratory support could be considered?

A

Non invasive ventilation (IPAP/EPAP)
Invasive ventilation

66
Q

Describe negative feedback pathway that acts within respiratory centre of the brain

A

-High pO2, low pcO2: less ventilation
-Low pO2, more pCO2: more ventilation
-Arterial pCO2 detected by peripheral chemoreceptors in carotid and aortic bodies
-Send signals to medullary respiratory centre to alter rate of respiration

-Raised pO2, decreased pCO2 and drop in hydrogen ions discourage ventilation to retain more CO2 and restore normal CO2 levels
-Fall in pO2, increased pCO2 and rise in hydrogen ions encourage ventilation to blow off more CO2 and, therefore, restore normal CO2 levels
-These actions are a result of altered arterial pCO2 being sensed by peripheral chemoreceptors in carotid and aortic bodies
-These send signals to medullary respiratory centre to alter rate of respiration

MRCS Critical care (11 decks)

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