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The Patient Who Deteriorates Post Intubation
179
you would conclude that even though most of the reported parameters t with
moderate AS, you cannot exclude severe AS at this point.
Howmightyouexplaintheinconsistenciesinthe
reported echocardiogram regarding the estimated
AVareaandpressuremeasurements?
The impaired LV systolic function decreases the gradient across the valve. This
is classied as a low-
gradient AS with impaired LV ejection fraction (LVEF).
This can lead to the clinical picture of non-
severe AS and potentially underes-
timates severity. Also, measurement error must be excluded, and this requires
the operator to recheck all measurements (e.g. LVOT diameter) and indices to
ensure the information is accurate.
Whatislow-gradientaorticstenosis?
Attempting to diagnose severe AS in critical care patients with low cardiac
output and a non- severe gradient across the valve can be challenging. Low-
gradient AS is divided into the following two possibilities:
Low-gradientASwithimpairedLVEF
This is dened as follows:
AVA <1.0 cm
2
AVAi <0.6 cm
2
/m
2
Mean gradient <35 mmHg
LVEF 40%
Measurement error must be excluded rst in these cases. As these patients
have reduced cardiac output, they can be distinguished from the other type of
low- gradient AS by examining the response of the left ventricle to low- dose
dobutamine. If LV systolic impairment can be improved using inotropes, then
the mean pressure gradient will exceed 40
mmHg in the presence of true severe
AS. Formal dobutamine stress echocardiography is not routinely performed
in critical care.
Low-gradientASwithLVEF>50%
This is dened as follows:
AVA <1.0 cm
2
AVAi <0.6 cm
2
/m
2
Mean gradient <40 mmHg
AV V
max
<4 m/s
LVEF 50%
Ensuring that accurate measurements have been taken is again an impor-
tant first step in preventing misdiagnosis. Additionally, examining the
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Clinical Cases in Critical Care
180
echocardiography report is essential. If the AV is not described as being both
heavily calcied and restricted, then signicant AS is unlikely. Calculating
an indexed stroke volume (SVi) is the next step. Patients with a ‘normal’ SVi
(
35 mL/m
2
) have a prognosis similar to conventional ‘moderate AS’ and usu-
ally only require observation. Patients with a ‘low’ SVi (<35
mL/m
2
) are very
challenging to dierentiate between truly severe AS and non-
severe AS and
this is beyond the scope of this book.
WhatistheprevalenceofASinthegeneralpopulation?
As the population continues to age, the prevalence of valvular heart disease
increases, with AS being the most common in developed countries. AS is pre-
sent in about 3% of patients over the age of 75
years. The increasing use of
echocardiography in critical care will continue to increase the detection of AS.
Whatarethemaincausesofaorticstenosis?
Acquired causes
Calcic AS– this is the most common cause of AS and should be consid-
ered an active and progressive disease process characterised by inam-
mation, brosis, lipid inltration and calcication. Predisposing factors
include male sex, age and hypercholesterolaemia.
Rheumatic heart disease– this remains the most common cause of val-
vular heart disease worldwide but is rarely the cause in Europe and
North America. Rheumatic AS most commonly coincides with mitral
valve disease.
Congenital causes
Bicuspid AV– as a congenital abnormality, there is a great deal more mechanical
stress placed on these structures and therefore the average age at presentation
of patients with bicuspid AV stenosis is signicantly lower than that seen in
the elderly population with normal AV morphology.
Whatisaorticsclerosis?
In aortic sclerosis, there is calcication and thickening of the aortic leaets but
without signicant outow obstruction (maximum velocity across the aortic
valve <2.5 m/s). In patients over age 65, aortic sclerosis is present in nearly 30%,
which increases to 50% by the age of 85. Aortic sclerosis suggests the presence
The measurements and indices from the formal echocardiogram are
rechecked and conrmed to be accurate. You discuss this with your critical
care lead for echocardiography. Given that the valve appears severely calci-
ed with severely reduced leaet motion and an estimated AVA of 0.8
cm
2
,
it is likely that this is a low-
gradient AS with impaired LVEF.
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The Patient Who Deteriorates Post Intubation
181
of vascular disease and, more importantly, coronary artery disease. Therefore,
the critical care clinician should be wary of vascular disease in any patient who
is reported to have aortic sclerosis.
Describe the morphological changes to the LV that
canoccurwithsevereaorticstenosis
In the presence of a xed outow obstruction causing pressure overload, the
left ventricle undergoes remodelling. This results in compensatory hypertrophy
in most cases. However, if the hypertrophic response is inadequate, the LV is
placed under extreme wall stress that can result in dilation and dysfunction
of the cavity.
WhatisthephysiologicalroleofLVhypertrophy?
According to the principle of LaPlace regarding wall tension, the left ventricle
wall stress (σ) is proportional to the pressure (P) multiplied by the radius (r)
of the cavity divided by the wall thickness (T)
Pr
T
Hence, as pressure increases, the heart attempts to keep wall stress constant
by increasing the wall thickness of the LV.
WhataretheproblemsthatcanarisewithLV
hypertrophy?
While the physiological response to increased pressure overload is hypertrophy,
this is associated with the following deleterious eects:
Increased myocardial oxygen demand– the increased muscle mass and
wall stress can potentially lead to a relative reduction in delivery of
oxygen and nutrients to cardiac myocytes.
Increased LV lling pressures– decrease in LV compliance, diastolic
dysfunction and increased diastolic lling pressures can impair suben-
docardial blood ow and give rise to ischaemia.
Whatdowemeanbytheterm‘preload’?
The force or load acting to stretch the cardiac myobril denes preload. It is
commonly estimated using the LV end- diastolic pressure, diameter or volume
(e.g. normal LV diastolic volume indexed to body surface area is between 35
and 75
mL/m
2
). The inherent stiness of cardiac muscle attempts to counteract
the stretching caused by preload, and therefore the actual degree to which the
myobril is stretched depends on this interaction. And note, since LV systolic
performance is related to this initial length (as demonstrated by the Frank–
Starling mechanism), it is also aected by preload.
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Clinical Cases in Critical Care
182
HowispreloadaffectedinAS?
As shown in Figure14.1, the pressure–volume loop in AS (red curve) demon-
strates an increased peak systolic pressure within the ventricle due to the high
outow resistance and large pressure gradient that occurs across the AV. This
increased afterload, when cardiac myobrils are exposed to greater stress during
systole, decreases SVi and increases end- systolic volume. As venous return occurs,
this increase in end- systolic volume leads to an increase in end- diastolic volume
with a resultant increase in preload. And as described, as preload increases so
does the stretch on the myobrils, which then through the Frank–Starling mech-
anism increases the force of contraction to overcome the outow resistance of AS.
Whatismeantbytheterm‘afterload’?
Afterload is the force or stress developed by the myocardium after the onset
of contraction and consequently varies with time. It can be measured at any
point during systole. It is important to note that while systemic vascular
resistance and LV systolic pressures can aect afterload, they should not be
considered equal to afterload, which is often a misconception.
Howisafterloadaffectedinthepresenceof
severeAS?
As the LV becomes hypertrophied in clinically signicant AS, this reduces wall
stress and therefore decreases the force exerted on each cardiac muscle unit
so that afterload remains near normal. As afterload is a key determinant of
ejection performance, this attempt at its normalisation is important in main-
taining normal ejection fraction and SVi.
0
100
200
LV pressure (mmHg)
LV volume (ml)
50 100 150 200
Figure 14.1: Left ventricle pressure–volume loop (blue line represents normal LV).
Source:TheophilusSamuels.
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The Patient Who Deteriorates Post Intubation
183
WhattreatmentoptionsareavailableforsevereAS?
Percutaneous interventions
Balloon valvuloplasty (BV)– as a temporising measure for those patients
who are haemodynamically unstable, BV can be considered. It should be
noted that this technique mainly exerts its eects by creating multiple
microscopic fracture lines in the calcied leaets and thereby tempo-
rarily improves leaet compliance. Hence, any haemodynamic benet
only lasts a few hours and within a few weeks to months, the AV returns
to its original calcied pre-
valvuloplasty state. The use of BV alone has
not been shown to improve long-
term outcomes. However, in a few
cases with severe haemodynamic compromise, it has been successfully
performed with haemodynamic support devices such as an intra-
aortic
balloon pump.
Transcatheter aortic valve replacement (TAVR)– being able to site a tissue
valve without the need for major surgery has dramatically altered the
management of AS in high-
risk patients. The Placement of Aortic Trans-
catheter valves study (PARTNER) demonstrated that the use of TAVR
in these types of patients produced results that were like surgical aortic
valve replacement (SAVR) at 2
years follow- up. TAVR is associated with
more vascular complications and stroke, whilst SAVR is associated with
more bleeding complications and atrial brillation. In addition, in a small
number of cases with pre- existing conduction disturbances (especially
right bundle branch block), the use of TAVR is associated with permanent
pacemaker placement. Patients are usually given 3
months of anticoagula-
tion due to supporting evidence of thrombus formation following TAVR.
Surgicalintervention
SAVR – this option remains the treatment of choice for the follow-
ing patients:
Symptomatic severe AS (valve area <1cm
2
) and low operative risk.
In addition, irrespective of symptoms, the following patients should
be considered for SAVR (class I recommendation):
Severe AS undergoing coronary artery bypass
Severe AS with LV dysfunction
Severe AS undergoing surgery for other heart valves or the aorta
What are the risk factors for increased surgical
mortality?
Renal failure
Age over 75 years
Reduced LV function
Congestive cardiac failure
Pulmonary hypertension
And like TAVR, these patients will require anticoagulation post surgery.
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Clinical Cases in Critical Care
184
Whatistheprognosisforpatientswithsymptomatic
severeAS?
Once patients with AS begin to develop symptoms (classically angina, dyspnoea
and syncopal episodes), prognosis is poor without valve replacement: 50%
mortality within the next 12–18
months.
Deneacuteheartfailure(AHF)
AHF ‘presents suddenly’ and results from any functional or structural impair-
ment of ventricular lling or ejection of blood, producing a complex clinical
syndrome. Heart failure may be classied as:
heart failure with reduced ejection fraction (HRrEF)– characterised by
reduced cardiac contractility, or
heart failure with preserved ejection fraction (HRpEF)– commonly the
result of diastolic dysfunction represented by impaired LV relaxation
and/or increased LV lling pressures.
WhatarethetreatmentprinciplesformanagingAHF?
Urgent treatment is designed to relieve symptoms, reverse acute haemody-
namic instability and preserve myocardial function as well as possible. The
main interventions include the following:
Intravenous diuretics– the loop diuretic furosemide is most used in
the acute setting and increases renal excretion of salt and water (other
loop diuretics include bumetanide and torsemide). The onset of action
is approximately 30 minutes, with a peak eect occurring at between
1and 2 hours, and a half- life of 6 hours. Loop diuretics also enhance
prostaglandin synthesis, which can lead to renal and venous dilation,
which may in turn reduce preload and relieve pulmonary congestion.
Michael's clinical condition improves, and his noradrenaline requirements
reduce with additional inotropic support and further IV uid boluses. His
blood pressure increases to 100/40
mmHg and his tachycardia reduces to
110
bpm. With ongoing treatment, Michael begins to improve over the next
72
hours. After a total of 10 days in your ICU, he is successfully extubated
with no further cardiac or respiratory support required. A repeat echocardio-
gram conrms that he does have severe AS now that his LV systolic function
has returned to normal.
On day 11, during your night shift, the nurse looking after Michael is
concerned that his breathing has become more laboured, his chest has wide-
spread crackles throughout, and his BP is approximately 170/110 mmHg.
You suspect that Michael has gone into acute heart failure (AHF). Focused
ultrasonography
demonstrates impaired LV systolic function and multiple
B- lines throughout.
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The Patient Who Deteriorates Post Intubation
185
Vasodilators– drugs such as glyceryl trinitrate (GTN) are often given in
combination with diuretic therapy. This eective systemic and coronary
vasodilator can be particularly useful in cases of coronary ischaemia. At
low doses, it is a venodilator and can also relieve symptoms of pulmonary
oedema. After 24
hours of continued use, GTN is subject to tachyphylaxis,
which is the rapid development of tolerance to its actions. Sodium nitroprus-
side is also used and is a potent vasodilator of both arterial and venous cir-
culations. It is the drug of choice in patients with severe heart failure due to
mitral regurgitation with associated hypertension and pulmonary oedema.
Caution should be exercised in patients with renal or hepatic impairment
as its toxic metabolites thiocyanate and cyanide may accumulate.
Inotropic drugs– dobutamine can be used in these patients to increase
contractility and cardiac output but may also cause tachyarrhythmias,
limiting its use. Of note, by exerting these inotropic eects, it should be
appreciated that myocardial oxygen demand increases and therefore it
can be detrimental in patients where the cause of the heart failure is
ischaemic in origin (e.g. following myocardial infarction). It should also
be noted that beta-
receptors are downregulated in patients with chronic
heart failure and therefore its eects may be attenuated. Another drug
that may be used is milrinone, which is a phosphodiesterase-
3inhibitor
that increases intracellular calcium levels and may be more ecacious
in patients on beta-
blockers. It increases cardiac output and SVi but
does also result in a decrease in systemic vascular resistance due to its
vasodilatory properties. While it acts as a coronary vasodilator, it does
not increase myocardial oxygen demand.
Vasopressors– noradrenaline is commonly used, and its main aim is to
restore systemic arterial pressure through peripheral vasoconstriction
with little eect on cardiac output. It is generally only used in those
patients who have severe hypotension and/or complicating conditions
such as sepsis.
Non- invasive ventilation– mortality and the need for endotracheal intu-
bation are reduced by the early use of non- invasive positive pressure
ventilation in those patients presenting with acute cardiogenic
pulmonary oedema.
HowmightyouadjustyourtreatmentforAHF
inMichaelgiventhathehassevereAS?
Your treatment would still follow the principles described for managing acute
cardiac failure, but you would need to be cautious in severe AS.
Diuretics and vasodilators– these drugs may cause refractory shock due
to their eect on reducing preload (especially if the LV cavity appears
small and hypertrophied as cardiac output in this setting is very much
preload dependent). However, nitroprusside can increase cardiac output
signicantly in patients with both severe LV dysfunction and severe AS
but who are not dependent on inotropes.
Inotropes– these may be required but patients may show little improve-
ment if their contractile reserve is limited.
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Clinical Cases in Critical Care
186
Furtherreading
Ring, L., Shah, B., Bhattacharyya, S. etal. (2021). Echocardiographic assessment
of aortic stenosis: a practical guideline from the British Society of Echocardiog-
raphy. Echo. Res. Pract. 8: G19. Detailed guideline regarding the echocardiographic
assessment of aortic stenosis, and includes haemodynamic considerations and other
useful information.
Anderson B. (2017). The Normal Examination and Echocardiographic Measure-
ments. Echotext Pty Ltd. Essential reading for anyone learning advanced echo-
cardiography.
Michael stabilises with your acute cardiac failure management. He is seen
the next day by the cardiothoracic team to assess for aortic valve replacement.
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Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
15
D
ebbie has been brought in by ambulance to the resuscitation area of the
ED. She is 45
years old. Her husband called emergency services after she
collapsed at home. She is normally very t, but this morning did not want to get
out of bed due to a headache. She vomited once then became unrousable. She
does not appear to have lost cardiac output at any point. She is tolerating the
oropharyngeal airway inserted by paramedics. BP162/94
mmHg, HR 86 bpm,
RR 10 per minute, pulse oximetry 98% on 15
L/min oxygen via non- rebreathe
mask. Glasgow Coma Scale (GCS) 8 (E1V2M5). Pupils equal and reactive to
light. Temperature 36.7
°C.
What could be the cause of Debbie’s low GCS?
Cerebrovascular event– haemorrhagic or thrombotic. This type of rapid
deterioration, associated with symptoms consistent with cerebral irri-
tation (i.e. headache and vomiting), could be compatible with a sudden
vascular event. There are more than 100 000 strokes in the UK each year
and stroke is a leading cause of death (NICE CKS 2022 Stroke and TIA).
Approximately 85% of strokes are ischaemic and 15% are haemorrhagic.
Space- occupying lesion– tumour, lymphoma, abscess. It is possible that
Debbie may have had a space- occupying lesion for some time which, due
to location and size, had not caused symptoms until now.
Tumours can be primary or secondary. Tumours commonly leading
to cerebral metastases include lung, breast, genitourinary, skin, colon
and osteosarcoma.
Tumours can be benign or malignant depending on growth rate
and likelihood of invasion into surrounding tissue. Malignant brain
tumours rarely spread beyond the central nervous system:
Common brain tumour types include the following:
Gliomas (>50%), which include astrocytomas (a type of glioma
originating in the cerebrum from astrocyte cells, can be any grade),
oligodendrogliomas and ependymomas.
The Patient
with
Reduced
Consciousness
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Clinical Cases in Critical Care
188
Meningiomas (approximately 25%)– arise from the meninges, usu-
ally benign and slow growing. Usually occur in those older than
70
years. Can be grades 1–3.
Intracranial abscesses are uncommon in developed countries and
in non-
immune suppressed populations (approximately 0.5–1in
100 000). Causes include bacteria, fungi, protozoa and helminths.
Look for systemic signs of sepsis, local sources of infection (e.g. dental
infection, mastoiditis, otitis media), and ascertain whether there is a
history of congenital cardiac disease, intravenous drug use or immune
suppression, such as HIV.
Meningitis or encephalitis – cerebral infection should be considered
in a previously well person presenting with low GCS and signs of
meningism.
Drugs – decreased GCS with a history of vomiting could be consistent
with paracetamol overdose, alcohol intoxication, opioid use, or misuse,
etc. So even though Debbie is apparently normally well, explore the pos-
sibility of drug side-
eects and overdose from prescription medication,
over-
the- counter drugs or recreational drug use. Obtain collateral history
from the GP, relatives and paramedics.
Sepsis– the clinical signs described here are non- specic. Sepsis can pre-
sent in a variety of ways but normally, a young t patient such as Debbie
would mount more of a physiological response with raised or lowered
temperature, hypotension, tachycardia and tachypnoea, etc. Consider
this as a possibility, but it is less likely than some other dierential diag-
noses on this list.
Metabolic– consider the possibility of hepatic or uraemic encephalop-
athy due to occult liver or renal disease. Acute liver failure and raised
ammonia can lead to cerebral oedema and a rapid, dangerous increase
in intracranial pressure (ICP).
Uraemic encephalopathy may develop when glomerular filtration rate
(GFR) falls to below 10–15mL/min. This would be a very unusual
primary presentation of renal failure. However, at this early stage,
consider the full range of possibilities.
Check electrolytes and never forget to test glucose (and sodium) in
patients with a low GCS.
Autoimmune– autoimmune encephalitis has an incidence of approx-
imately 0.5–2 per 100 000. Causes include acute disseminated
encephalomyelitis (ADEM), N- methyl D- aspartate (NMDA) receptor
encephalomyelitis, limbic and Hashimoto’ encephalitis (also, rarely, Ras-
mussen’s in children and young adults). Some cases occur following
infection but in many there is no identiable prodrome.
Haematological – thrombotic thrombocytopenic purpura classically pres-
ents with the pentad of fever, microangiopathic haemolytic anaemia,
thrombocytopenia, renal impairment and neurological symptoms
(including headache, confusion, seizures or focal neurological def-
icit). Autoantibodies against ADAMTS13 protease result in platelet
aggregation and clumping, accumulation of ultra- large von Willebrand
factor, and formation of microthrombi and microangiopathic haemolytic
anaemia (MAHA). This life- threatening condition can be triggered by
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