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The Patient Who Is Dicult to Ventilate

109



Ineffective effort–patient effort fails to trigger a breath.



Autotriggering–mechanical breath is delivered without any

spontaneous patient effort, sometimes seen with cardiac oscillations

or water droplets in flow sensor tubing.



Flow asynchrony–the delivered ow is insucient for the patient’s demands.



Termination asynchrony



Double triggering–a single patient effort results in two delivered

breaths without expiration in between.



Early cycling–the programmed breath is too short for the patient,

leading to spontaneous effort during ventilator expiration.



Delayed cycling–duration of the mechanical breath is longer than

the patient’s own spontaneous effort.

What is peak pressure and how is it different

from

plateau pressure?

Peak pressure is the pressure generated by the ventilator to overcome the total

airow resistance (upper airways and alveolar)

PQR

PEEP

(PIP= peak inspiratory pressure, Q = ow, R = resistance, V

= tidal volume,

C = compliance, PEEP = peak end- expiratory pressure).

It is measured during inspiration and sudden isolated increases may be due

to obstructed ventilator tubing, kinked endotracheal tube or bronchospasm,

for example.

Plateau pressure is more reective of smaller airways and pulmonary com-

pliance and should be measured during the inspiratory pause

plat

= plateau pressure, V

= tidal volume, C = compliance).

When both plateau and peak pressures are high, this is suggestive of low

pulmonary compliance due to, for example, atelectasis, pulmonary oedema,

acute respiratory distress syndrome (ARDS), pneumothorax, etc. See Case 24

for further discussion.

What are your options to combat Susan’s ventilator

dyssynchrony?



Change the mode of ventilation–in an unparalysed patient, particularly

one with a high CO

and light sedation, SIMV may be poorly tolerated,

even with pressure- augmented spontaneous breaths. The fact that her

respiratory rate is so much higher than the set rate, together with the

erratic ventilator curves, reveals that Susan is initiating many additional

breaths. Her tidal volumes are variable, ranging from 2 to 12 mL/kg. Ide-

ally, aim to achieve consistent low tidal volume ventilation for Susan,

approximately 340 mL,i.e. 6–8 mL/kg of IBW.

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Clinical Cases in Critical Care

110



Adjust ventilator settings–assess the ventilator ow curves and adjust

according to Susan’s individual requirements. This requires alteration

of advanced ventilator settings (e.g. pressure ramp time, trigger sensi-

tivities, etc.). When carefully considered, even small adjustments can

dramatically improve tolerance of mechanical ventilation.



Increase sedation –aiming to increase tolerance of mechanical

ventilation.



Consider neuromuscular blockade–if her drive to breathe cannot be

overcome with appropriate sedation, neuromuscular blockade may need

to be added.

If Susan’s condition were improving and she were in the process of weaning

from the ventilator, it may be appropriate to change her to a fully spontaneous

mode with pressure support set to achieve appropriate volumes. However, in

a deteriorating patient, it is usually more appropriate to increase the support

from the ventilator and facilitate tolerance of mechanical ventilation by

increasing sedation.

Susan has severe chest sepsis with associated multiple organ failure. You

decide to deepen her sedation to improve synchrony with the ventilator. You

increase her propofol infusion rate to 200

mg/h and her fentanyl infusion

rate to 200 mcg/h. Once she is well sedated, you give her a 50 mg bolus

of rocuronium and set the ventilator to a pressure- controlled, volume-

guaranteed mode with a PEEP of 10 cmH

One of the senior ICU nurses suggests that the chest radiograph taken

before admission shows ARDS (Figure8.2).

Figure 8.2: Chest radiograph demonstrating ARDS.

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The Patient Who Is Dicult to Ventilate

111

What is acute respiratory distress syndrome?

Acute respiratory distress syndrome is an acute diuse inammatory lung

injury, leading to increased vascular permeability, increased lung weight

and loss of aerated tissue (Ranieri etal., JAMA 2012). There is increased

physiological dead space and reduced lung compliance. Diagnosis, according

to the Berlin denition, requires hypoxaemia with bilateral inltrates on chest

radiograph (not explained by cardiac failure or uid overload) with a PEEP of

at least 5

cmH

O. There are three categories of severity:

Category PaO

:FiO

(P:F) ratio Mortality at 30 days

Mild 200–300

mmHg or 26.6–40 kPa 27%

Moderate 100–200

mmHg or 13.3–26.6 kPa 32%

Severe <100

mmHg or <13.3 kPa 45%

What is the Murray score?

The Lung Injury Severity Score (LISS or Murray score) was proposed by Mur-

ray etal. in 1988. This score is used to grade severity of lung injury and can

be used to aid decisions regarding whether patients with ARDS require extra-

corporeal membrane oxygenation (ECMO). It was not designed to prognosti-

cate outcomes.

This composite scoring system awards points for degree of derangement

within four parameters:



Extent of consolidation on chest radiograph



P:F ratio



PEEP level



Respiratory compliance

In those with a total score greater than 3, consider discussion with an

ECMO centre.

Is there evidence to support the use of

neuromuscular blockade in cases of ARDS?

The evidence is controversial. The ACURASYS trial in 2010 showed a 90-

day mortality benet with the use of a continuous infusion of cisatracurium

early in ARDS.

The ROSE Trial in 2019 (Re- evaluation Of Systemic Early neuromus-

cular blockade) challenged previous trial results and showed no evidence of

mortality benet.

As with all evidence- based medicine, these published studies can be criti-

cised, and overextrapolation is fraught with potential problems. Several other

studies report an association between increased asynchrony and worse out-

comes (e.g. Zhou etal., Sci Rep, 2021). A reasonable approach would seem to

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Clinical Cases in Critical Care

112

be to try and optimise all ventilator settings, sedation, analgesia, etc., and if

the patient remains dyssynchronous with potentially harmful pressures and

volumes, consider introducing a paralysing agent.

Why does Susan need so much noradrenaline

and

what can you do to improve her

cardiovascular status?

Susan is in septic shock. Although the pathophysiology of sepsis is not fully

elucidated, it is likely that bacterial infection induces release of proinamma-

tory cytokines like interleukins (IL) (particularly IL-

1 and IL- 6), and tumour

necrosis factor (TNF-

α) leading to a generalised inflammatory response.

Vascular dilation occurs and total peripheral resistance decreases. This is com-

pounded by capillary leakage. Her chest radiograph changes would be con-

sistent with excess interstitial uid. Susan’s reduced urine output may reect

reduced renal perfusion.

Susan will be prone to losing uid into third spaces, including the inter-

stitial areas of the lungs, yet she is probably intravascularly depleted. While

uid accumulation in the lungs (further impairing her gas exchange) should

be avoided, her circulating volume requires optimisation to reduce vasopressor

requirements and preserve end- organ perfusion.

Aim to augment the cardiac output element of the oxygen delivery equation

(Figure8.3).

Stroke volume depends upon preload, inotropy and afterload, so consider

uids, vasopressors and inotropic agents at this stage, depending upon the

clinical assessment of Susan’s needs. Ideally, clinical assessment and uid

management will incorporate bedside echocardiography (see Case 1).

Susan looks more settled after your interventions and she is easily

achieving tidal volumes of 340 mL with pressures consistently less than

cmH

O. Her HR has reduced to around 105 bpm, but her BP has also

fallen. Her

noradrenaline has risen to 0.65 mcg/kg/min aiming for a

MAP of 65

mmHg. Her temperature is 38.6 °C. In the 60 minutes that

you have been assessing and managing Susan's recent deterioration, she

has passed no urine.

HR × SV ((Hb × SpO

× 1.39) + (0.003 × PaO

))

= CO × CaO

× 10

Figure 8.3: Oxygen delivery equation. DO

, delivery of oxygen (mL/min); CO, cardiac

output (L/min); HR, heart rate; SV, stroke volume (mL); CaO

, oxygen- carrying capacity

of the blood (mL/dL; multiplication by 10 adjusts this to mL/L); Hb, haemoglobin (g/L);

SpO

, oxygen saturations (%); PaO

, partial pressure of oxygen (kPa); 1.39, oxygen-

binding capacity of Hb per gram; 0.003, amount of dissolved oxygen in the blood

(0.003 mL of oxygen gas is dissolved in 100 mL of blood).

Source: Theophilus Samuels.

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The Patient Who Is Dicult to Ventilate

113

Should you instigate renal replacement therapy?

What is the

evidence for ‘early’ vs ‘late’ renal

replacement therapy?

Susan has been in intensive care for a relatively short period of time. On arrival,

assuming her previous renal function was normal, there was blood panel evi-

dence of an acute kidney injury. She has now had decreased urine output for

the last few hours.

There is no strong evidence to support early renal replacement therapy

and no real consensus on what constitutes ‘early’ or ‘late’ in this context. The

AKIKI, ELAIN and IDEAL-

ICU trials gave conicting results. However, they

asked subtly dierent questions, with substantial dierences in study design

making meta-

analysis dicult. As with many clinical problems in critical care,

the best guidance remains to assess the individual patient and use clinical

judgement as to how to proceed.

What is the evidence for starting steroids?

In contrast to several earlier studies, one meta- analysis (Wu WF etal., Am

J Emerg Med, 2018) suggests that use of glucocorticoids in severe CAP may

reduce both the risk of in- hospital mortality and the length of hospital stay.

Steroids have also been used in critical care for a presumed positive impact

on haemodynamic instability, reducing dose and duration of vasopressor

requirement. However, steroids continue to be a contentious topic within

You decide to establish cardiac output monitoring. Standing at the bedside

and using a 50

mL syringe connected to the central venous catheter, you

administer a warmed 250

mL crystalloid uid bolus while observing the mon-

itors. Susan’s stroke volume variation (SVV) decreases from 24% to 18% and

her systolic blood pressure increases from 92 to 96

mmHg. You administer

three further uid boluses. The SVV is now 11% and you reduce the noradren-

aline to 0.47

mcg/kg/min. The next arterial blood gas shows gas exchange

is unchanged, but the metabolic acidosis is ongoing with a base decit of

−7.5

mmol/L (lactate 2.9 mmol/L). Her saturations are holding despite the

uid challenge, but you leave instructions to maintain a PEEP of at least

cmH

O until gas exchange has improved.

You decide to insert a VasCath™ now and review Susan's progress over the

next few hours. If her urine output remains poor despite optimising uids

and vasopressor support, you will commence continuous venovenous hae-

moltration tonight considering the likelihood that she will continue to

deteriorate. Signicant acidosis may impair cardiac contractility, shift the

oxyhaemoglobin dissociation curve, increase pulmonary vascular resis-

tance and impair enzyme function. Although her acidosis has a signicant

respiratory component, by correcting the metabolic component you will be

better able to tolerate hypercapnia and continue lung protective ventilation.

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Clinical Cases in Critical Care

114

critical care, with conicting evidence regarding their use in ARDS, sepsis

and in conjunction with high-

dose vasopressors. It also remains unclear as

to whether glucocorticoids should be given as bolus doses or as an infusion.

Surviving Sepsis guidelines (2021) suggest commencing treatment with

hydrocortisone in septic shock requiring noradrenaline 0.25 mcg/kg/min for

at least 4 hours.

In your department, steroids tend be used when there is refractory septic

shock. You prescribe 50

mg intravenous hydrocortisone QDS.

You return an hour later to review the eects of your interventions. The

arterial blood gas is as follows: pH

7.12, PaO

6.5 kPa, PaCO

10.5 kPa, base

excess −7.2

mmol/L, lactate 4.7 mmol/L.

What are the rescue methods for critical

hypoxaemia in severe ARDS?

In addition to manipulating the relevant ventilator settings to optimise oxy-

genation (i.e. PEEP, FiO

and inspiratory:expiratory ratio), and considering

neuromuscular blockade, the following techniques may be used:



Prone positioning– this technique has more supporting evidence than the

others listed below. Some of the trial data is conicting but the weight of

evidence is in favour of prone positioning being benecial in ARDS. Of

note, the PROSEVA Trial (Geurin etal., NEJM 2013) showed a signicant

mortality benet in severe ARDS.



Airway Pressure Release Ventilation (APRV) – APRV has some small sup-

porting trial evidence but is yet to be evaluated in a large multicentre trial.



Extracorporeal membrane oxygenation – there is some evidence to

support the use of ECMO in ARDS, but this is an extremely invasive

technique. The large intravascular cannulae and need for aggressive

anticoagulation can lead to complications. In addition, there is limited

availability of ECMO as it is only performed in a small number of cen-

tres throughout the UK.



High- frequency oscillatory ventilation (HFOV) – two trials examining

HFOV were published in the New England Journal of Medicine in 2013

(OSCAR and OSCILLATE). One showed no dierence in mortality and

one showed increased mortality. Since then, HFOV is less commonly

used in adult patients.



Inhaled pulmonary vasodilators– inhaled nitric oxide and aerosolised

prostacyclin are sometimes used in rescue therapy. Study data is limited

and equivocal.



Recruitment manoeuvres– various methods have been proposed (e.g.

staircase recruitment manoeuvre) to deliver this ‘open lung’ strategy.

There is no strong supporting evidence. In fact, the ART trial (2017)

found an increase in mortality associated with the use of recruitment

manoeuvres. Recruitment manoeuvres should be used with caution and

only performed in selected patients by experienced clinicians.

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The Patient Who Is Dicult to Ventilate

115

How do you achieve prone positioning?



Assemble the team –one airway trained doctor at the head and

six other trained members of staff to assist (depending upon local

protocol).



Staff should wear appropriate personal protective equipment (PPE)

including eye protection.



Ensure all lines and tubes are secured and gathered towards either Susan’s

head or her feet.



Ensure there is plenty of padding ready which will support and cushion

potential pressure areas and allow the abdomen to remain free.



Stop NG feed and aspirate the NG tube.



Give a bolus dose of paralysing agent and use the ‘Cornish pasty’ method

to prone Susan–a sheet beneath the patient and another over the top

are rolled tightly together to allow the patient to be turned prone in a

controlled manner. Multiple pillows are used to ensure the abdomen is

free and pressure points are protected.

How does prone positioning improve oxygenation?



Improved ventilation/perfusion matching with increased blood ow to

the dependant lung.



Increased functional residual capacity (FRC).



Reduced atelectasis.



More uniform distribution of plateau pressure.



Redistribution of transpulmonary pressure with a possible reduction of

right ventricle afterload.



Increased secretion drainage.

Once Susan is safely in the prone position, what

is your plan for

her ongoing management at this

stage (in addition to haemoltration)?



Prone position management should include setting ventilator parameters

and instructions on how long the patient should remain prone.



If patient is stable, remain prone for 16 hours.



Check ABG after 1 hour, looking for improvement in oxygenation.



Regular pressure point assessment and 4 hourly alternating movement

of arms and head in the ‘swimmer’s position’.



Regular suctioning.



Aim for lung protective ventilation with high PEEP. Use neuromus-

cular blockade if necessary. Consider using APRV in conjunction

with prone position.

You decide to place Susan in the prone position and ask the nurses to prepare

for haemoltration.

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Clinical Cases in Critical Care

116



Call the ICU consultant to discuss potential referral for ECMO.



Ensure critical care ‘housekeeping’ is maintained, e.g. consider NG tube

position and feed, thromboprophylaxis, glucose control and stress ulcer

prophylaxis.



Further imaging could include CT chest, but Susan is not stable enough.



Request a formal echocardiogram when she is in the supine position.



Call Susan’s family to update them regarding a change in her condition.

She is married with two small children and is very close to her

three siblings.

What is the likely outcome in this case?

Susan has a severe community- acquired pneumonia. Her CURB- 65 (Confu-

sion, Uraemia, Respiratory rate, Blood pressure and Age >65) score was 4 on

admission, placing her in the highest risk group with a 30- day mortality pre-

dicted risk of 27.8%. Her APACHE II score gives her an approximate mortality

of 40%. Her SOFA score gives her a mortality of 40–50%. Whichever scoring

system is used, Susan has a signicant chance of dying in critical care. This

should be communicated to the next of kin with support for the family and

safeguarding for the children oered if necessary.

Besides sepsis and multiorgan failure, what are

some possible complications of pneumonia?



Pleural eusion



Empyema



Lung abscess



Pulmonary brosis

Your consultant has just arrived in the hospital and performs bedside

cardiac and lung ultrasound (limited by position). The consultant calls the

regional ECMO referral centre who would like to take Susan but unfortu-

nately, they do not have any beds available right now. They will call you in

the morning but advise to keep Susan in the prone position in the mean-

time. The APACHE II score is 23 and the SOFA score is 10.

After 4days in your ICU, Susan starts to show signicant improvement.

She is extubated on her fth day of admission. She is discharged to a gen-

eral medical ward 2days later and goes home after 3weeks in hospital.

Her follow- up chest radiograph at 6weeks is clear and she plans to return

to work. She is invited for respiratory outpatient review and seen in the

ICU follow- up clinic.

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The Patient Who Is Dicult to Ventilate

117