Ventilation quiz question

Q
• Which of the following
features of an asthma attack
are classified as ‘life-
threatening’ in the 2011 BTS
asthma guideline?
a. Inability to complete sentences
in one breath.
b. PaO2 of >8kPa.
c. Silent chest.
d. PaCO2 >6kPa.
e. Peak expiratory flow rate
(PEFR) <50% of predicted.
F, F, T, F, F
A raised PaCO2 is a sign of a
‘near-fatal’ asthma attack. A
peak expiratory flow rate
(PEFR) <33% predicted is
associated with a life-
threatening acute
exacerbation. A PaO2 of <8kPa
is a life-threatening sign
according to the guideline as is
a silent chest and arrhythmias.
An inability to complete
sentences in one breath is a
sign of acute severe asthma.

Q
The following statements are true regarding
the management of acute severe asthma:
a. PEFR <33% is a criterion diagnosis.
b. Aminophylline should be given as a first-line
intravenous bronchodilator.
c. The use of IV magnesium sulphate to reduce
mortality is supported by level I evidence.
d. Ketamine 5mg/kg is the preferred induction
agent if rapid sequence intubation is
required.
e. A restrictive fluid regime should be used in
patients at risk of intubation.
F, F, F, F, F
A peak expiratory flow rate (PEFR) of <33%
defines life-threatening asthma. There is
limited evidence to support the use of
aminophylline and British Thoracic Society
guidelines suggest consideration only. The
3MG trial showed only a minor reduction in
patient-reported breathlessness with the use
of IV magnesium, with no effect on morbidity
or need for invasive ventilation. Ketamine
should be dosed at 1-2mg/kg. It has
bronchodilator properties that make it an
attractive induction agent for asthmatic
patients. Fluid administration should be
generous due to the common reduction in
preload, as a result of gas trapping and raised
intrathoracic pressure often limiting venous
return.

Regarding the mechanics of positive pressure ventilation:
a.Setting an extrinsic positive end-expiratory pressure (PEEP) less than
intrinsic PEEP will reduce elastic work of the respiratory system.
b. One risk of applying PEEP is a reduction in oxygen delivery (DO2).
c. A decelerating flow pattern is seen in volume-controlled ventilation.
d. The difference between peak and plateau pressures is greater with volume-
controlled ventilation than pressure-controlled ventilation.
e. Dynamic compliance equals the tidal volume divided by (peak pressure
minus total positive end-expiratory pressure).

ANSWER
Regarding the mechanics of positive pressure ventilation:
a.Setting an extrinsic positive end-expiratory pressure (PEEP) less than
intrinsic PEEP will reduce elastic work of the respiratory system. T
b. One risk of applying PEEP is a reduction in oxygen delivery (DO2). T
c. A decelerating flow pattern is seen in volume-controlled ventilation. F
d. The difference between peak and plateau pressures is greater with volume-
controlled ventilation than pressure-controlled ventilation. T
e. Dynamic compliance equals the tidal volume divided by (peak pressure
minus total positive end-expiratory pressure). T

• Total positive end-expiratory pressure (PEEP) is an
increase in the endexpiratory pressure. It is made up of
intrinsic PEEP (PEEPi, an increase in the static recoil
pressure of the respiratory system, usually due to
airflow obstruction) and extrinsic PEEP (PEEPe, positive
pressure applied to the expiratory limb of the circuit).
During spontaneous ventilation, work must be done to
overcome PEEPi before airflow can occur. Applying
PEEPe less than the PEEPi will reduce this elastic work
required to initiate airflow. PEEP maintains recruitment
of collapsed lung, increases functional residual capacity
and minimises intra-pulmonary shunt, thus improving
oxygenation. PEEP reduces venous return and
therefore cardiac output;oxygen delivery may
therefore fall despite an improvement in oxygenation.

• PEEP must be titrated to achieve a balance between oxygenation andhaemodynamic optimisation.
Volume-controlled ventilation (VCV) delivers a constant flow and pressure increases linearly until a
peak pressure is achieved. Pressure-controlledventilation (PCV) produces a decelerating flow
pattern and a constant pressure is delivered. The peak pressure (Ppk) achieved during VCV is
dependent on the elastic and resistive properties of the respiratory system. When an end-
inspiratory pause is added, airways and tissue resistance dissipate and the pressure falls to reach a
plateau pressure (Pplat). In PCV this resistance dissipates during inspiration so that Ppk and Pplat
are equal, and thus an end-inspiratory pause is not usually required to measure Pplat. Compliance
is the change in volume per unit change in pressure and elastance is the inverse of compliance.
Static compliance is measured when there is no airflow and dynamic where airflow is present.
• Static compliance Vt/(Pplat-PEEPtotal)
• Dynamic compliance Vt/(Ppk-PEEPtotal)
• Static elastance (Pplat-PEEPtotal)/Vt
• Dynamic elastance (Ppk-PEEPtotal)/Vt
Bersten AD, Soni N. Oh’s Intensive Care Manual, 6th ed. Philadelphia, USA:
Butterworth Heinemann, Elsevier, 2009

The 2012 Berlin definition of ARDS includes the
following components:
a. Continuous positive airway pressure (CPAP) or
positive endexpiratory pressure (PEEP) >5cm
H2O.
b. Murray score >2.
c. Pulmonary artery occlusion pressure <15cm H2O.
d. pH <7.3.
e. Evidence of a direct precipitant occurring within
the preceding week.

ANSWER
The 2012 Berlin definition of ARDS includes the
following components:
a. Continuous positive airway pressure (CPAP) or positive
endexpiratory pressure (PEEP) >5cm H2O. T
b. Murray score >2. F
c. Pulmonary artery occlusion pressure <15cm H2O. F
d. pH <7.3. F
e. Evidence of a direct precipitant occurring within the
preceding week. T

The previous American and European Consensus Conference definition ARDS was
updated to the modern Berlin definition in 2012. This new definition addressed
several suggested failings of the previous; namely issues of reliability and validity
relating to limited clarity of timeframe/onset, interpretation of chest radiograph
criteria and issues with identifying hydrostatic oedema.
The new definition incorporates four specific aspects to diagnosis. These aspects focus
specifically on timing of onset, supporting chest imaging, the origin of pulmonary
oedema and oxygenation. When calculating P/F gradient the new definition
mandates positive endexpiratory pressure (PEEP) or continuous positive airway
pressure (CPAP) of at least 5cmH2O. The Murray score is a grading system for
severity of ARDS and plays a limited role in initial diagnosis. Respiratory failure
must be unexplained by cardiac failure/fluid overload in the new definition, but
specific pulmonary artery occlusion pressure measurements are discounted in light
of the move away from PA catheter placement in recent years. pH plays no role
and acute precipitant is now a specific diagnostic aspect as above. Additional
advantages to the new diagnosis include more robust diagnostic criteria for
inclusion in research studies and the added value of clearly defining hypoxia
despite PEEP.

When considering the diagnosis of ventilatorassociated pneumonia
(VAP) in a mechanically ventilated patient:
a. A CPIS score >6 has poor specificity for the diagnosis of VAP.
b. A VAP is defined as a hospital-acquired pneumonia occurring at any
time point in a mechanically ventilated patient.
c. Ventilator care bundles may include the use of a low-volume
lowpressure tapered cuff.
d. Use of endotracheal tubes with subglottic suction have level I
evidence showing a reduced incidence of VAP.
e. Late VAP (>5 days) is most commonly caused by streptococcal or
staphylococcal organisms.

ANSWER
When considering the diagnosis of ventilatorassociated pneumonia
(VAP) in a mechanically ventilated patient:
a. A CPIS score >6 has poor specificity for the diagnosis of VAP. T
b. A VAP is defined as a hospital-acquired pneumonia occurring at any
time point in a mechanically ventilated patient. F
c. Ventilator care bundles may include the use of a low-volume
lowpressure tapered cuff. F
d. Use of endotracheal tubes with subglottic suction have level I
evidence showing a reduced incidence of VAP. T
e. Late VAP (>5 days) is most commonly caused by streptococcal or
staphylococcal organisms. F

Ventilator-associated pneumonia (VAP) is the most common hospitalacquired infection
in patients receiving mechanical ventilation, with aconsiderable morbidity burden. The
diagnosis is challenging. Both the Clinical Pulmonary Infection Score (CPIS) and Hospital in
Europe Link for Infection Control through Surveillance (HELICS) scoring systems have been
developed as decision tools, but are limited in their sensitivity and specificity.
A VAP is defined as a hospital-acquired pneumonia occurring after 48 hours of mechanical
ventilation. There has been justifiable criticism of this definition and the current trend
appears to be moving in favour of a tiered approach, recognising various ventilator-
associated events as a ventilatorassociated condition (VAC), an infection-related ventilator-
associated condition (IVAC) and probable/possible VAP. Ventilator care bundles include a
series of measures attempting to reduce
the incidence of VAP. These measures often include tapered high-volume low-pressure cuffs,
head elevation, subglottic suction, mouthcare and occasionally selective oral and digestive
tract decontamination. Of all these, subglottic suction appears to have the best evidence
base for reduction in events. Early VAP is usually caused by oropharyngeal flora, including
streptococcal and staphylococcal organisms. Late VAP is usually a result of infection by Gram-
negative enteric organisms.

Q
A 77-year-old man is admitted to the intensive care unit following
emergency repair of a ruptured abdominal aortic aneurysm. During
the operation he received a 10-unit blood transfusion and was
transferred to ICU intubated and ventilated, initially with minimal
oxygen requirements. Twenty-four hours later his oxygen
requirement has begun to increase. His P:F ratio is 28.3kPa and his
chest X-ray shows new bibasal interstitial shadowing.
echocardiogram demonstrates good right and left ventricular
function with an ejection fraction of 55%. His stroke volume
variation is 14%. The most likely diagnosis is:
a. Acute lung injury (ALI).
b. Acute respiratory distress syndrome (ARDS).
c. Ventilator-associated pneumonia.
d. Transfusion-related acute lung injury.
e. Cardiogenic pulmonary oedema.

B
The Berlin definition (2013) of ARDS no longer
differentiates between ARDS and acute lung
injury (ALI). ARDS is categorised as being mild
(PaO2/FiO2)(6.6-39.9kPa), moderate
PaO2/FiO2 13.3-26.6kPa) or severe
(<13.3kPa). The definition has four key
components.

Berlin definition
1. Acute — onset over 1 week or less
2. Bilateral opacities consistent with pulmonary
oedema on CXR or CT
3. PaO2/FiO2 <300mmHg (40kPa) with a
minimum PEEP of 5cm H2O
4. Not fully explained by cardiac failure or fluid
overload

Transfusion-related acute lung injury is defined as
new-onset acute lung injury that occurs during or
within 6 hours of transfusion, not explained by
another acute lung injury risk factor. Ventilator-
associated pneumonia is, by definition, only
diagnosed after the patient has been ventilated
for more than 48 hours. The good cardiac
function as demonstrated by echocardiography
suggests that cardiogenic pulmonary oedema is
unlikely and the stroke volume variation of 14%
(assuming full mechanical ventilation) suggests
that the patient is still fluid-responsive.

A 32-year-old male asthmatic is admitted to the emergency
department with a 2-day history of increasing wheeze and
shortness of breath. His HR is 115bpm, blood pressure is
120/60mmHg, respiratory rate is 28 breaths per minute
with saturations of 92% on room air. He has a widespread
expiratory wheeze refractory to his normal inhalers. The
most appropriate next step in his management is:
a. Intubation and ventilation.
b. Intravenous magnesium 2g.
c. Urgent chest X-ray.
d. Back to back bronchodilator nebuliser therapy.
e. Intravenous hydrocortisone.

D
As per the British Thoracic Society (BTS) guidance in
2011, asthmatics with acute severe signs as this
patient, nebulised bronchodilator therapy should be
used as first line. Steroids may follow and can be either
intravenous or orally administered. Intravenous
magnesium should be given to patients with acute
severe asthma not responding to initial therapy or with
life-threatening features. Antibiotics are not always
warranted in such cases. A chest X-ray will be required
urgently to exclude other causes of shortness of
breath, but this should not delay the administration of
nebulised bronchodilators.

Q
A 60-year-old man with chronic obstructive pulmonary disease (COPD)
presents with sudden onset shortness of breath to the emergency
department. He has a respiratory rate of 24 breaths per minute. His
saturations are 92% on room air. A 4cm right-sided pneumothorax
is diagnosed on a plain chest X-ray. The most appropriate course of
action is:
a. Simple needle aspiration of the pneumothorax with a 16G or 18G
cannula.
b. Insertion of an intercostal chest drain on the right side.
c.High-flow oxygen therapy and close observation in a monitored area.
d. Emergency needle decompression on the right side.
e. Discharge home if there is no deterioration over a 4-hour period
with return next day with repeat chest X-ray.

B
BTS guidance suggests in patients with pre-existing
chest disease and greater than 50 years, a
pneumothorax should be treated as secondary. If they
are breathless and/or have a pneumothorax greater
than 2cm, then this should be treated with a chest
drain. If the pneumothorax is small (1- 2cm), then this
could be aspirated with a 16G or 18G cannula. If
successful, then the patient should be observed for 24
hours. If unsuccessful, then this should be followed by
chest drain insertion. If the pneumothorax is less than
1cm on admission then they should be observed with
high-flow oxygen unless oxygen-sensitive.

Q
You are called to see a patient with a percutaneous tracheostomy in
situ who has become distressed. He has desaturated to 85% and the
nursing staff have placed him on a Water’s circuit with an FiO2 of
1.0 and removed the inner tube. The bag is barely shifting. The
capnography trace is poor with no obvious waveform. He is sweaty
and agitated. High-flow oxygen has been applied to the mouth and
stoma. What is the most appropriate first step?
a. Attempt to place a suction catheter down the tracheostomy.
b. Bronchoscopy down the tracheostomy to assess position.
c. Apply PEEP 5-10cm H2O using the Water’s circuit.
d. Deflate the cuff of the tracheostomy tube.
e. Remove the tracheostomy and attempt oral intubation.

A
A blocked tracheostomy requires a timely response and stepwise
intervention. Whilst all the above options are reasonable, the lack of
movement in the Mapleson C circuit and absent capnograph trace implies
near complete obstruction. The most important next step is to focus on
identification of whether this is due to distal tracheobronchial occlusion or
misplacement of the tracheostomy itself. To this end, the National
Tracheostomy Safety Project algorithim suggests the passage of a suction
catheter as the first step to discriminate. If this passes freely, then
aspiration of a sputum plug may resolve the issue. Although bronchoscopy
would be equally reasonable, the urgency in this situation would render
set up and use inappropriate. Following an inability to pass a suction
catheter, deflating the cuff is the final step in an attempt to render the
tracheostomy patent. If this achieves no benefit, the tracheostomy should
be removed and the patient oxygenated via the mouth with an occluded
stoma, or via the mouth and stoma prior to attempts at resiting a
definitive airway. This could be via oral endotracheal intubation (with the
tube sited distal to the stoma) or intubation of the stoma itself.

An 82-year-old female has been intubated and ventilated on the ICU for
the past 6 days following emergency surgery for a ruptured abdominal
aortic aneurysm. Her oxygen requirements increase and she becomes
tachypnoeic. She develops an increased load of non-purulent secretions.
She develops a tachycardia and spikes a temperature of 39.1°C. On
auscultation there is decreased air entry and some crackles bibasally with
dullness to percussion at the right base. Bloods show an FiO2/PaO2 of
34kPa and serum white cell count 13 x 109/L with 55% band forms. Chest
X-ray shows new shadowing in the lower zones with loss of the right hemi-
diaphragm. What is the most appropriate diagnosis?
a. Pulmonary embolism.
b. Pleural effusion.
c. Ventilator-associated pneumonia.
d. Acute respiratory distress syndrome.
e. Pulmonary oedema.

C
Ventilator-associated pneumonia (VAP) is pneumonia in a patient who has been
intubated for at least 48 hours. If a VAP is suspected every effort must be made to
exclude other sources of infection. There is a lack of consensus ‘gold standard’
definition to test the diagnostic accuracy of potential criteria; therefore, there are
multiple potential criteria to diagnose VAP, including microbiological and clinical,
which lack sensitivity and specificity. The Clinical Pulmonary Infection Score (CPIS)
is a diagnostic scoring 0-12, based on six variables: body temperature; leucocyte
count; volume and character of tracheal secretions; arterial oxygenation; chest
radiograph findings, and results of microbiological analysis. A CPIS >6 is a
reasonable indicator of the presence or absence of pulmonary infection, as
signified by bacterial culture. Using the CPIS this patient has a score of 7 and VAP
can be diagnosed. Sputum samples should be sent in an attempt to identify a
causative organism. While she also meets the criteria for acute respiratory distress
syndrome (new bilateral infiltrates and an FiO2/PaO2 34kPa), the increase in
temperature and leucocyte count suggest infection is the more likely diagnosis.
Loss of the right hemidiaphragm suggests there is a pulmonary effusion present, in
this case, likely parapneumonic.

During a respiratory wean, the following numerical
indices suggest a spontaneous breathing trial is
likely to be followed by successful extubation:
a. Rapid Shallow Breathing Index (RSBI) <105.
b. Respiratory rate <35/min.
c. Vital capacity >5ml/kg.
d. PO2 >10kPa.
e. ETCO2 <5kPa.

ANSWER
During a respiratory wean, the following numerical
indices suggest a spontaneous breathing trial is
likely to be followed by successful extubation:
a. Rapid Shallow Breathing Index (RSBI) <105.T
b. Respiratory rate <35/min.T
c. Vital capacity >5ml/kg. F
d. PO2 >10kPa. F
e. ETCO2 <5kPa. F

Weaning from mechanical ventilation is the stepwise process of reducing
respiratory support with the ultimate aim of extubation and satisfactory
spontaneous breathing. Many critically ill patients will tolerate this process
rapidly following improvement from their acute event. Some patients will
need a more gradual approach. General features associated with
successful weaning include improvement in the underlying condition,
optimisation of general physiology and identification of potentially
deleterious airway or breathing issues. Following this, numerical indices
are a fairly reliable way of predicting the likelihood of success with a
spontaneous breathing trial and have been consistently shown to
outperform clinical judgement when used systematically. Numerical
indices in current use include the Rapid Shallow Breathing Index <105
(respiratory rate divided by tidal volume measured in litres), respiratory
rate in isolation (<35/min), vital capacity >10ml/kg and PaO2/FiO2 >26kPa.
However, there remain concerns regarding the sensitivity and specificity of
chosen cut-offs and they must be used as part of a rational decision-
making process, rather than as standalone targets. Isolated measurements
of PO2 or CO2 have a limited role.

The application of continuous positive airway
pressure (CPAP) or positive end-expiratory
pressure (PEEP) typically leads to:
a. Increased functional residual capacity.
b. A reduction in preload in patients with acute
cardiogenic pulmonary oedema.
c. Redistribution of extravascular lung water.
d. Increased cardiac output.
e. Decreased intracranial pressure.

ANSWER
The application of continuous positive airway
pressure (CPAP) or positive end-expiratory
pressure (PEEP) typically leads to:
a. Increased functional residual capacity. T
b. A reduction in preload in patients with acute
cardiogenic pulmonary oedema. T
c. Redistribution of extravascular lung water. T
d. Increased cardiac output. F
e. Decreased intracranial pressure . F

Continuous positive airway pressure has multiple physiological ramifications within the intensive
care unit. While it may be a very familiar treatment, understanding of these effects will lead to best
use in clinical practice.
Functional residual capacity (FRC) will impact on gas transfer due to an impact on alveolar surface
area available for exchange. Positive endexpiratory pressure (PEEP) can reduce atelectasis and
maintain recruitment of collapsed alveoli, thus increasing the FRC and subsequently increasing
surface area for the transfer of oxygen to the bloodstream.
PEEP can also have important cardiovascular effects such as a reduction in preload, redistribution of
extravascular lung water (secondary to increased hydrostatic pressure within the alveoli) and
decreased left ventricular afterload. This latter feature has led some authors to suggest that PEEP
can increase cardiac output, although the general consensus at present suggests that the impact of
decreased preload and consequent decreased left ventricular filling cause little positive effect on
cardiac output. In a small cohort of patients with a failing myocardium and hypervolaemia
(congestive cardiac failure), PEEP may result in improved cardiac output due to the decrease in
afterload providing greater overall benefit. There is trial evidence to support CPAP in this situation
to reduce symptoms and work of breathing.
PEEP will invariably increase intracranial pressure by impairing venous drainage to the thorax,
resulting in a degree of intracranial venous congestion and resultant pressure increase alongside
volume expansion.

You are asked to review a 45-year-old man on the ICU with refractory
hypoxia. He was admitted several days ago with acute pancreatitis and has
subsequently developed severe acute respiratory distress syndrome. His
PEEP and FiO2 have been escalated over the course of the day. He is now
saturating at 85% on FiO2 0.65 with PEEP at 15cm H2O and plateau
pressures of 29cm H2O. There is little to remove on tracheal suction. He is
sedated and paralysed and the I:E ratio is currently 1:1. Which of the
following options would be the most effective next step?
a. Commencing inhaled nitric oxide.
b. Adjusting the PEEP to 20cm H2O in line with the ARDSnet high
PEEP ladder.
c. Placing the patient in the prone position.
d. Inverting the I:E ratio.
e. Commencing high-frequency oscillatory ventilation.

C
Use of the prone position for refractory hypoxaemia in acute respiratory distress
syndrome (ARDS) has gained favour in recent years. Previous data demonstrated
physiological improvement via surrogate endpoints, but limited impact on hard
outcomes. In 2013, the well-conducted PROSEVA (Proning Severe ARDS patients)
trial managed to demonstrate a statistically significant reduction in death at both
28 and 90 days with 16- hour sessions in the prone position for patients with
severe ARDS. As such, use of the prone position is rapidly becoming a standard of
care for those patients with a P/F ratio of <20kPa (<150mmHg). Intensivists should
be well aware of the complications and risk/benefit analysis. A supplementary
appendix for the PROSEVA trial provides data on many complications. Interestingly,
there was no difference in the rate of mainstem bronchus intubations, although
the rate of endotracheal tube obstruction doubled in the prone group. There was
no difference in the rates of cardiac arrest between groups. A further paper has
gone on to analyse the rate of pressure sores in patients turned prone, which are
significantly increased when compared to those nursed in the supine position. This
risk is likely to be outweighed by the significant mortality benefit and as such
should be an expected complication, although vigilance and reflection to
continually minimise harm should be frequent. None of the other interventions
listed has been shown to improve mortality in randomised controlled trials.

A 27-year-old man is bought into the emergency department
by ambulance complaining of shortness of breath. He has a
history of asthma and takes salbutamol and beclometasone
inhalers regularly. Which of the following examination
findings would be the most worrying clinical sign?
a. Heart rate of 125/minute.
b. Speaking in short sentences due to breathlessness.
c. Respiratory rate of 28/minute.
d. Peak expiratory flow rate of 40% predicted.
e. Blood pressure of 80/60mmHg.

C
Hypotension is a feature of life-threatening asthma, as
opposed to merely acute severe asthma as defined in
the British Thoracic Society guidelines, reflecting
obstruction to venous return in the thoracic
compartment due to gas trapping. The parameters for
diagnosing an acute severe asthma attack are:
• Peak expiratory flow rate of between 30% and 50% of
expected.
• Respiratory rate greater than 25 breaths/minute.
• Tachycardia: heart rate >110 beats per minute.
• Inability to complete sentences with one breath.

The parameters of life-threatening asthma are:
• Peak expiratory flow rate of <33% of best or predicted.
• Silent chest or poor respiratory effort.
• Exhaustion.
• Hypotension or arrhythmia.
• Bradycardia.
• Cyanosis or SpO2 <92%.
• ‘Normal’ PaCO2 (4.6-6kPa).
Near-fatal asthma is signified by a patient with a rising
PaCO2 requiring mechanical ventilation with raised
inflation pressures.

Regarding non-invasive ventilation (NIV) in criticaly ill patients:
a. It has a clear mortality benefit in patients with Type I respiratory
failure due to chronic obstructive pulmonary disease (COPD)
compared with standard medical therapy.
b. It is contraindicated in patients with thoracic wall deformities.
c. It is an effective treatment for severe community-acquired
pneumonia.
d. It should be first-line therapy for asthmatic patients with worsening
respiratory acidosis.
e. It is effective rescue therapy following failed extubation.

ANSWER
Regarding non-invasive ventilation (NIV) in criticalLy ill patients:
a. It has a clear mortality benefit in patients with Type I respiratory
failure due to chronic obstructive pulmonary disease (COPD)
compared with standard medical therapy. F
b. It is contraindicated in patients with thoracic wall deformities. F
c. It is an effective treatment for severe community-acquired
pneumonia. F
d. It should be first-line therapy for asthmatic patients with worsening
respiratory acidosis. F
e. It is effective rescue therapy following failed extubation. F

Non-invasive ventilation (NIV) has been the subject of many randomised
controlled trials in various patient groups. The strongest evidence for its
use is in patients with Type II respiratory failure secondary to exacerbation
of chronic obstructive pulmonary disease (COPD) where there is a large
mortality benefit compared with usual medical care. Its role in asthma is
not well established, and is not recommended in consensus guidelines for
patients with a worsening respiratory acidosis who should be intubated.
There is no good quality evidence to suggest a benefit in pneumonia,
especially where there is a high secretion burden, although NIV may have
a role in selected patients who would not be for escalation to mechanical
ventilation. While planned extubation directly onto NIV is a reasonable
weaning strategy, the use of NIV as a rescue therapy in cases of failed
intubation has been shown not to be effective. NIV is not contraindicated
in thoracic wall deformities and may be a valuable strategy to avoid the
need for intubation in selected patients.

Evidence-based rescue strategies shown to
reduce mortality in severe acute
respiratorydistress syndrome (ARDS) include the
following:
a. Paralysis using non-depolarising muscle relaxants.
b. Therapeutic hypothermia.
c. High-frequency oscillatory ventilation.
d. Airway pressure release ventilation.
e. Inhaled nitric oxide.

ANSWERS
Evidence-based rescue strategies shown to
reduce mortality in severe acute
respiratorydistress syndrome (ARDS) include the
following:
a. Paralysis using non-depolarising muscle relaxants.
T
b. Therapeutic hypothermia. F
c. High-frequency oscillatory ventilation. F
d. Airway pressure release ventilation. F
e. Inhaled nitric oxide. F

There has been much focus on rescue therapies for severe hypoxaemia
in acute respiratory distress syndrome (ARDS) over the last 20
years. An emerging evidence base is developing and continues to
guide best practice.
Early neuromuscular blockade to support invasive ventilation and
decrease metabolic requirement has recently been shown to
reduce mortality and the duration of mechanical ventilation in
patients with severe ARDS. Therapeutic hypothermia has no
evidence base to support its use in this condition. High-frequency
oscillatory ventilation (HFOV) has recently been the subject of two
large randomised controlled trials (RCTs) and found to offer no
benefit to conventional mechanical ventilation. Airway pressure
release ventilation (APRV) and inhaled nitric oxide have both been
purported as rescue measures for severe disease. However, the
current evidence has not demonstrated any evidence of benefit and
their role in management remains limited.

In a patient with a percutaneous tracheostomy that is
potentially blocked:
a. Oxygen should be applied to the face and tracheostomy
immediately. T
b. Inner tubes should be left in to facilitate connection to a breathing
circuit. F
c. The cuff should be deflated prior to attempting to pass a suction
catheter. F
d. The tracheostomy tube should not be removed if difficult
endotracheal intubation is predicted. F
e. A paediatric face mask applied to the stoma can be used as a
primary emergency oxygenation strategy. T

Adult tracheostomy emergencies are uncommon, but carry a high risk of morbidity
and mortality. Patients on the intensive care unit are particularly vulnerable to
complications and often managed in an arena where specific surgical expertise is
lacking. Much work has been undertaken recently on the management of, and
complications with, tracheostomies on the intensive care unit, including a national
report, multidisciplinary project initiative and consensus guideline.
The UK National Tracheostomy Safety Project contains readily accessible guidelines for
a stepwise approach to the management of a tracheostomy critical incident. An
ABCDE approach is supported, with particular emphasis on look, listen and feel at
both the mouth and stoma for evidence of airflow and explicit use of waveform
capnography. Oxygen should be applied early as stated. Most inner tubes are best
removed early to exclude physical obstruction unless there is a specific dependent
connection. Following these measures, attempts to pass a suction catheter should
be instigated, with the cuff only deflated if first attempts fail. The trachestomy
should be removed early and oral intubation attempted (where feasible) if the
catheter cannot be passed or if the patient continues to deteriorate despite
attempted intervention. A paediatric facemask/LMA applied to the stoma or
standard oral airway manoeuvres with the stoma occluded are recommended as
primary emergency oxygenation strategies.

Regarding the physiology of the lungs during
mechanical ventilation:
a. Normal static lung compliance is 50-100ml/cmH2O.
b. Plateau pressure = Pcompliance - Presistance.
c.Volume-controlled ventilation produces a square
inspiratory flow pattern.
d. CO2 elimination is proportional to minute volume.
e.Ventilation is greater at the lung bases in healthy
spontaneously breathing individuals.

Regarding the physiology of the lungs during
mechanical ventilation:
a. Normal static lung compliance is 50-100ml/cmH2O. T
b. Plateau pressure = Pcompliance - Presistance. F
c.Volume-controlled ventilation produces a square
inspiratory flow pattern. T
d. CO2 elimination is proportional to minute volume. F
e.Ventilation is greater at the lung bases in healthy
spontaneously breathing individuals. T

Plateau pressure is a measure of compliance with the
resistive element
negated by an inspiratory hold manoeuvre.
Plateau pressure therefore = Ppeak - Presistance.
CO2 elimination is proportional to alveolar minute
volume, but total minute volume includes anatomical
dead space. Hence, a low rate, deep breath strategy
will eliminate more CO2 than a high rate with lower
tidal volumes. E is true as alveoli are less distended in
the lung bases and therefore on a steeper part of the
compliance curve.

A 49-year-old patient with an infective exacerbation of chronic
obstructive pulmonary disease (COPD) presents to the emergency
department with increased shortness of breath. Controlled oxygen,
nebulised salbutamol and ipratropium, prednisolone and antibiotics
are administered. After 1 hour of treatment he remains
tachypnoeic, with a respiratory rate of 28, SpO2 88% and GCS 15.
An arterial blood gas (ABG) is performed which shows: pH 7.24,
pCO2 9.4kPa, pO2 7.6kPa. He has not received any intravenous
bronchodilators. The best treatment plan is:
a. Repeat nebulised salbutamol and ipratropium until clinical response.
b. Trial of non-invasive ventilation (NIV) in a critical care area.
c. Low-dose ketamine infusion.
d. Intravenous aminophylline loading.
e. Doxapram infusion.

C
NICE guidelines state that non-invasive ventilation (NIV) should be considered
for all COPD patients with a persisting respiratory acidosis after 1 hour of
standard medical therapy. Standard medical therapy should include
controlled oxygen to maintain SaO2 88-92%, nebulised salbutamol,
nebulised ipratropium, prednisolone and an antibiotic if indicated.
Patients with a pH <7.26 may benefit from NIV but they have a higher risk
of treatment failure and should be managed in a high dependency or ICU
setting. As this patient has a persisting respiratory acidosis with a pH of
7.24 after an hour of optimal management, he should be transferred to a
critical care area for a trial of NIV. A management plan should be put in
place should he fail to improve with this therapy. There is currently
minimal evidence for the use of aminophylline in the management of an
exacerbation of COPD. This, along with its high incidence of side effects,
means that it is only recommended in cases where all other management
has failed. Ketamine has a role in intractable asthma but is not used in the
management of exacerbations of COPD. The evidence base supporting the
use of doxapram is very limited.

Ventilation quiz question

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Ventilation quiz question