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CARDIO & RESPIRATORY > 1b Respiratory Failure > Flashcards

1b Respiratory Failure Flashcards

1
Q

What is the broad definition of respiratory failure?

A

Syndrome of inadequate gas exchange due to dysfunction of one or more components of the respiratory system

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2
Q

Which parts of the nervous system are involved in the respiratory system?

A

CNS / Brainstem
Peripheral NS
Neuro-muscular junction

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3
Q

What respiratory muscles are involved in respiratory infections?

A

Diaphragm and thoracic muscles
Extra-thoracic Muscles

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4
Q

Where in the lung will there be more ventilation? and why?

A

At the base - the alveoli are smaller and more compliant

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5
Q

Describe the difference in transmural pressure gradient between the apex and the base of the lung?

A

Greater gradient at the apex of the lung, much smaller at the bottom as the Pleural Pressure is LESS NEGATIVE AT THE BOTTOM

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6
Q

What is meant by compliance?

A

Compliance is the tendency to distort under pressure (change in volume/ change in pressure)

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7
Q

In which part of the lung are the alveoli more compliant?

A

Base of the lung

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8
Q

Which part of the lung has a LOWER INTRAVASCULAR PRESSURE?

A

APEX

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9
Q

Which part of the lung has a higher intravascular pressure?

A

Base

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10
Q

What are the effects of the high intravascular pressure at the base of the lung?

A

More recruitment
less resistance
higher flow rate

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11
Q

What are the effects of a lower intravascular pressure at the apex of the lung?

A

Less recruitment
Greater resistance
Lower flow rate

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12
Q

What is the pulmonary transit time?

A

0.75s

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13
Q

What is the time taken for gas exchange to occur through?

A

0.25s

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14
Q

What is elastance?

A

The tendancy to recoil to its original volume

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15
Q

What is the formula to calculate compliance?

A

Change in Volume / Change in pressuer

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16
Q

What is the formula to calculate elastance?

A

Change in pressure / change in volume

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17
Q

What is the biggest risk factor for males with chronic respiratory failure?

A

Smoking

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18
Q

What is the biggest risk factor for women with chronic respiratory failure?

A

Household air pollution from solid fuels

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19
Q

What is an acute presentation of respiratory failure?

A

Acute Respiratory Distress Sydrome

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20
Q

How would you diagnose someone with ARDS based on timing?

A

Within 1 week of known clinical insult or new or worsening respiratory symptoms

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21
Q

What would be seen on chest imaging of someone with ARDS?

A

bilateral opacities, not fully explained by effusions, lung collapse, or nodules

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22
Q

What is the origin of oedema in a patient with ARDS?

A

Respiratory failure not fully explained by cardiac failure or fluid overload.

Need objective assessment (e.g. echocardiography) to exclude hydrostatic oedema if no risk factor present

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23
Q

What are acute on chronic types of respiratory failure?

A

Infective exacerbation of COPD, CF
Myasthenic crisis
Post operative

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24
Q

What is the tidal volume?

A

The amount of air breathed in and breathed out in a normal cycle of breathes

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25
Q

What is the inspiratory reserve volume?

A

The volume of air which can be inspired on top of the tidal volume to reach maximum inspiration capacity

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26
Q

What is the inspiratory capacity a sum of?

A

Tidal volume + Inspiratory reserve volume

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27
Q

What is functional residual capacity?

A

Expiratory reserve volume + residual volume

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28
Q

What is the residual volume?

A

The volume of air which is kept in the lungs in order for the pressure to be balanced in the lungs and prevent them from collapsing

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29
Q

What is the vital capacity?

A

Inspiratory reserve volume + Expiratory reserve volume + tidal volume

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30
Q

What is meant by minute ventilation?

A

The volume of gas which is entering and leaving the lungs per minute

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31
Q

How do you calculate minute ventilation?

A

Tidal Volume x breathing frequency

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32
Q

What is alveolar ventilation?

A

The gas entering and leaving the alveoli per minute

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33
Q

How is alveolar ventilation measured?

A

(Tidal volume - dead space) x breathing frequency

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34
Q

What is type 1 respiratory failure?

A

Failure of oxygen exchange (Hypoxemic)

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35
Q

What is the level of PaO2 for respiratory failure to be considered type 1?

A

PaO2 less than 60

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36
Q

what happens to the shunt fraction in type 1?

A

Increased due to alveolar flooding

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37
Q

What are the pulmonary causes of acute respiratory failure?

A

Infection

Aspiration - when something accidentally enters your lungs

Primary graft dysfunction (Lung Tx) - severe lung injury occurs within first 72 hours of lung transplantation

-

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38
Q

What would be the extra-pulmonary causes of acute respiratory failure?

A

Trauma

Pancreatitis - increased inflammatory chemicals secreted into the bloodstream

Sepsis

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39
Q

What are the neuromuscular causes of acute respiratory failure?

A

Myasthenia/ GBS - respiratory muscle weakness

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40
Q

What is meant by an increased shunt fraction?

A

Increased shunt fraction - percentage of blood put out by the heart that is not completely oxygenated (Q S)

Therefore less oxygenated blood in the body

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41
Q

What are the causes of Type 1 respiratory failure?

A

Collapse
Aspiration
Pulmonary Oedema
Fibrosis
Pulmonary Embolism
Pulmonary Hypertension

42
Q

What is type 2 respiratory failure?

A

Failure to exchange or remove carbon dioxide

43
Q

What is hypercapnic respiratory failure?

A

Type 2

44
Q

what is the physiology behind type 2 respiratory failure?

A

Decreased alveolar minute ventilation
Dead Space Ventilation

45
Q

What is type 3 respiratory failure?

A

Perioperative respiratory failure

46
Q

what is atelectasis?

A

Atelectasis is a complete or partial collapse of the entire lung or area (lobe) of the lung. It occurs when the tiny air sacs (alveoli) within the lung become deflated or possibly filled with alveolar fluid

47
Q

What is the main pathology behind perioperative respiratory failure?

A

Increased atelectasis due to low functional residual capacity with abnormal wall mechanics

Can be hypoxemic or hypercapnic

During surgery, there can be a reduction in the FRC -> this is due to anaesthetics and muscle relaxants

48
Q

How is type 3 respiratory failure prevented?

A

Anesthetic
Posture incentive spirometry
analgesia
attempts to lower the intra-abdominal pressure

49
Q

What is type 4 respiratory failure?

A

Shock - patients who are intubated and ventilated during a form of shock (septic / cardiogenic / neurologic)

50
Q

What is the basic pathophysiology of type 4 respiratory failure?

A

Poor perfusion of lung → gas doesn’t meet the blood and cannot transfer across alveolar capillary membrane

51
Q

What happens when the patient gets neurologic shock?

A

Patient becomes very vasoplegic (low systemic vascular resistance) so you get peripheral pooling of blood to get much central return of blood to the pulmonary vasculature.

This leads to significant drop in pulmonary perfusion gas exchange.

52
Q

When someone is in shock, they drop their conscious level, why does this mean they have to be intubated?

A

They no longer protect their airway

Intubation allows them to get positive pressure ventilation using a ventilator

-

53
Q

how does positive pressure affect the left ventricle?

A

Reduces afterload which is good for the LV as distress across the heart muscle wall is reduced because there is some pressure within the chest that is raised

54
Q

how does positive pressure affect the right ventricle?

A

Increased pressure in the thorax → much harder for right ventricle to fill with blood and its contractility is affected

55
Q

What are the risk factors of chronic respiratory failure?

A

COPD
Pollution
recurrent pneumonia
Cystic Fibrosis
Pulmonary FIbrosis

56
Q

What are the risk factors for acute respiratory failure?

A

Infection - Viral or bacterial
Aspiration
trauma
pancreatitis
Transfusion

57
Q

What are the origins of shortness of breath in acute respiratory failure?

A

Pulmonary vascular disease

Lower RTI

Aspiration

Trauma

Extrapulmonary: pancreatitis, new medications

58
Q

What are the two types of pulmonary vascular disease which result in shortness of breath?

A

Pulmonary Embolus
Haemoptysis

59
Q

What are the pulmonary causes of ARDS?

A

Aspiration
Trauma
Surgery
Drug Toxicity
Infection

60
Q

What are the extra-pulmonary causes of ARDS?

A

Trauma
pancreatitis
burns
Transfusion
Surgery
Drug Toxicity
Infection

61
Q

What is driving the response in acute lung injury in the image below?

A

When macrohpages are activated by an infection or inflammation, they will release further cytokines: IL-6, IL-8, TNF-alpha

Another TNF-alpha, IL-8 signalling pathway is mediated by TNFR-1

In response to inflammatory setup, there is alveolar fluid build-up or protein rich oedema forming within the lung

You can get degradation of surfactant, which means the lung is less efficient at expanding the alveoli which leads to a collapse of the alveoli

Due to inflammation, you get migration of neutrophils and leukocytes from capillary into interstitium where they can cause damage before they can get to their site of interest due to chemokines.

This damage increases oedema and this increases the distance between the alveolar and the capillary → gas exchange is less efficient.

62
Q

What cytokines are involved in the viral response and T-cell differentiation in the immune response in the lung?

A

IL-6, IL-8, TNF-alpha, IFN-gamma, IFN-beta

63
Q

What DAMP’s might be released in the lungs?

A

HMGB-1 and RAGE

64
Q

What apoptotic mediators cause cell death in the lungs?

A

Necrosis in lung biopsies
Apoptotic mediators ; FAS, FAS-1, BCl-2

65
Q

What happens to the leucocytes in acute lung injury?

A

Alveolar macrophage activation
Neutrophil Lung Migration

66
Q

What therapies have been tried in respiratory failure?

A

Steroids
Salbutamol
Surfactant
Statins
GM-CSL
Neutrophil esterase inhibitor
N-acetylcysteine

67
Q

What pharmacological interventions are being trialled?

A

Mesenchymal stem cells
Keratinocyte growth factor
Microvesicles
high dose vitamin C, thiamine and steroids

68
Q

Is there evidence to suggest that pulmonary vascular endothelial inflammatory response and angiogenesis is an underlying pathology in ARDS?

A

Yes

69
Q

What type of scan has allowed radiological evidence of poor perfusion?

A

CT

Shows widespread angiogenesis and poor perfusion due to microemboli

70
Q

What is measured in hypo inflammatory endotypes?

A

P/F Ration
plateau pressure
Tidal volume

71
Q

What is measured in hyper inflammatory endotypes?

A

Platelet
Biliruin
Creatinine
CRP
IL-6
sTNF

72
Q

What therapeutic intervention could be used to treat the underlying disease?

A

Inhaled therapies - bronchodilators and pulmonary vasodilators

Steroids
Anti-biotics
Antivirals
Drugs - Rituximab

73
Q

what therapeutic intervention could be used to provide respiratory support to those with ARDS?

A

Physiotherapy
High flow oxygen
Extra-corporeal support
Nebulisers
Oxygen
Mechanical ventilation
Non invasive ventilation

74
Q

What type of cardiovascular support could be given to someone with ARDS?

A

Fluids
Vasopressors
Inotropes
Pulmonary vasodilators

75
Q

What type of renal support could be given to someone with ARDS?

A

haemofiltration
haemodialysis

76
Q

What type of immune support could be given to someone with ARDS?

A

Plasma exchange
Convalescent plasma

77
Q

What are the sequelae of ARDS

A

Poor gas exchange - Inadequate oxygenation, poor perfusion, hypercapnoea

Infection - sepsis

Inflammation

Systemic Effects

78
Q

What are the four types of ventilation which could be used in ARDS?

A

Volume controlled
Pressure controlled
Assissted breathing modes
Advanced ventilatory modes

79
Q

What is compliance on the pressure volume loop?

A

The steepness of the line

80
Q

What is the UIP in a pressure volume loop?

A

Upper inflection point - above this pressure, additional alveolar recruitment requires a disproportionate increase in applied airway pressure

81
Q

what is the LIP?

A

Lower inflection point - can be thought of as the minimum baseline pressure needed for optimal alveolar recruitment

82
Q

How would you regulate pressure during ventilation to terminate exhalation?

A

You would increase the amount of pressure to allow flow of air back into the lungs and initiate inhalation

83
Q

When is alveolar recruitment at its highest?

A

At the Positive end expiratory pressure (PEEP)

84
Q

What is V/Q mismatch caused by?

A

Ventilation perfusion mismatch = when there is a mismatch between the amount of air which reaches the alveoli and the amount of blood which reaches the alveoli

85
Q

How can we reduce ventilator induced lung injury?

A

Maintaining driving pressure (difference between peak and what we call a plateau pressure, which is sort of static pressure within the lung after the initial inspiration)

86
Q

What effect does increasing the ventilation pressure too much have on lung recruitment?

A

It over distends the lungs and so more gas within the chest is trapped and ultimately this reduces the ability for perfusion and potentially causes right ventricular dysfunction as a result of that for a long time

Also increases the risk of damaging the lung with pressure or barotrauma

87
Q

What information can an ultrasound of the lungs provide?

A

Whether there is fluid in the lungs or not

88
Q

Would a CT or ultrasound be more useful when observing pathologies in lung injury?

A

CT

89
Q

What is the name of the scoring system used to guide escalation of Acute Respiratory Distress Syndrome?

A

Murray Score

90
Q

What is ECMO?

A

ECMO stands for extracorporeal membrane oxygenation. The ECMO machine is similar to the heart-lung by-pass machine used in open-heart surgery. It pumps and oxygenates a patient’s blood outside the body, allowing the heart and lungs to rest.

91
Q

At what Murray score will a patient be put on ECMO?

A

3

92
Q

What is the inclusion criteria for ECMO?

A

Severe respiratory failure with a non cardiac cause
Positive pressure ventilation is not appropriate

93
Q

What is the exclusion criteria for ECMO?

A

Contraindication to continuation of active treatment
Significant co-morbidity - when there would be a dependancy on ECMO, or co morbidity is life limiting

94
Q

What occurs in ECMO?

A

Pass canula up through the groin, usually up the femoral vein (in some cases jugular vein)

Withdraw blood through tubing that runs into a pump to run blood across an artificial membrane

Blood is pumped through the bottom section and gases flowed over the top layer to remove carbon dioxide from the blood and provide oxygen

This oxygenated blood is then carried back into the body

95
Q

What are the advantages of ECMO?

A

Improved oxygen delivery

Improved CO2 removal

Rest lung and prevent ventilator associated lung injury

Resolve respiratory acidosis

Reduce multiple organ dysfunction arising from hypoxaemia and hypercapnia

-

96
Q

What are the disadvantages of ECMO?

A

Time to access

Referral system - Geographical inequality

Consideration of referral

97
Q

What are the technical difficulties associated with ECMO?

A

Obtaining access - IJV, subclavian, femoral

Circuit

Haemodynamics

Clottting/ bleeding

98
Q

Is ARDS likely to lead to a prolonged disability?

A

No - it is a reversible disease process

99
Q

A patient admitted with bacterial pneumonia but despite antibiotics develops sepsis, and acute
respiratory distress syndrome. The clinical team have measured O2 saturation, positive end point
pressure and chest radiology. What else would they measure in order to accurately score the severity of
ARDS.

A

Lung Compliance

100
Q

What class of antibiotics should be given to a patient with severe pneumonia?

A

Penicillins and Macrolides

101
Q

What are the four parameters used in the Murray Score?

A

Positive End Expiratory Pressure
Chest X Ray
Lung Complicance
Partial Pressure of Oxygen / Oxygen Saturations

CARDIO & RESPIRATORY (26 decks)

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