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The Patient Who is Hypotensive
169
How does sepsis lead to hypotension?
There are several factors that can lead to hypotension in sepsis, and it remains
one of the most challenging tasks for clinicians to manage.
Hypovolaemia and decreased cardiac lling–endothelial cell surface
integrity becomes compromised by the release of proinammatory medi-
ators. This results in severe capillary leak and extravasation of uid into
the tissues along with reduced venous return due to venodilation. This
redistribution of blood volume leads to the inability to maintain vascular
wall tension, mean systemic lling pressure, venous return, cardiac
lling, cardiac output and arterial blood pressure. Hypovolaemia may
continue to be dicult to manage despite adequate uid resuscitation
due to the ongoing capillary leak that occurs.
Vasodilation–peripheral maldistribution of blood can persist despite a
normal or high cardiac output and is referred to as ‘distributive shock’.
Both the micro-
and macrocirculation are aected. For example, blood
is shunted away from the splanchnic circulation to preserve blood ow
to the myocardium, brain and skeletal muscles.
Myocardial dysfunction–biventricular function can be depressed with
a decrease in ejection fraction. Potential causes include disruption
to myocardial bioenergetics, circulating inammatory cytokines and
altered cardiac adrenergic signalling. Despite this, if adequate volume
resuscitation is achieved, the resulting tachycardia, arteriolar dilation
and biventricular dilation (which increases stroke volume through the
Frank–Starling Law) can still produce a high cardiac output.
What is the ‘hour- 1 bundle’?
In 2018 the Surviving Sepsis Campaign (SSC) published the initial resuscita-
tion for sepsis and septic shock bundle that should be completed within the
rst hour (the ‘hour-
1 bundle’). In addition to ongoing resuscitation:
Measure lactate level
Obtain blood cultures before administering antibiotics
Administer broad- spectrum antibiotics (according to your local
guidelines)
Begin rapid administration of 30 mL/kg crystalloid for hypotension or
lactate 4 mmol/L
Commence vasopressors if hypotensive during or after uid resuscitation
to maintain a MAP 65 mmHg.
Joan's urine dip on admission was positive for leucocytes and nitrites
(aspecimen was sent to the laboratory, results are outstanding) and she
has received four doses of intravenous co-
amoxiclav. There are no previous
urine samples in the lab. Over the past 24 hours, her WBC and CRP have
increased from 16 to 32 × 10
9
/L and 35 to 186 respectively. Her NEWS2
remains elevated at 15.
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Clinical Cases in Critical Care
170
Even though these goals are highly desirable, in real- world practice this
timeframe is not always met, especially if the diagnosis of sepsis is not consid-
ered at the time of initial presentation.
What is the signicance behind developing
the
‘hour- 1 bundle’?
Sepsis and septic shock, just like an AMI or acute stroke, should be considered
a medical emergency. It has been shown extensively that rapid assessment and
treatment lead to improved patient outcomes. Even though more than 1
hour
may be needed to complete resuscitation eorts, it is of paramount impor-
tance that the resuscitation and treatment measures, as outlined in the ‘hour-
1
bundle’, begin immediately.
Which antibiotics would you start?
Joan has developed septic shock despite already receiving four doses of co-
amoxiclav (amoxicillin and clavulanic acid). Therefore, depending on your local
guidelines and advice from your microbiologist, following blood cultures, one
option would be to change this to another beta-
lactam beta- lactamase inhibitor
combination (e.g. piperacillin- tazobactam [Tazocin®]) with an aminoglycoside
(e.g. gentamicin) for synergistic activity.
How can focused echocardiography help
in differentiating the causes of shock?
Hypovolaemic or distributive shock–when imaging the inferior vena cava
(IVC) using a subcostal approach, a small (<1 cm) and collapsing IVC
may suggest that uid administration might be benecial (for further
details see Case 1). In addition, a hyperdynamic left ventricle (LV) with
near total or complete eacement of the papillary muscles seen on a
parasternal short-
axis view also may suggest uid responsiveness.
Cardiogenic shock –assessment of LV systolic function can be rap-
idly achieved via parasternal and apical windows. Attention should be
directed to how well the ventricular walls contract and move inwards
towards the centre of the chamber. Recognising a signicantly impaired
LV strongly suggests cardiogenic shock, especially if it is a new nding.
RV function can also be assessed well using the apical view, with its
chamber size visually compared to the LV chamber (RV is considered
dilated if > two- thirds the width of the LV).
You arrange for Joan to be transferred to your ICU. As you are informed
that this will take at least an hour due to lack of an immediate bed space,
you decide to perform point-
of- care echocardiography whilst resuscitative
measures and preparations for her transfer are ongoing.
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The Patient Who is Hypotensive
171
Obstructive shock–pericardial eusion with compression of the RA
and RV during diastole would suggest cardiac tamponade. Conversely, a
dilated RV with or without poor contraction of the free wall and absence
of hypertrophy might indicate a massive pulmonary embolism.
For the dierent types of shock, focused echocardiography can provide
valuable information that should be used in conjunction with other clinical
ndings to aid in diagnosis and ongoing management. But remember that
ultrasonography is no substitute for a thorough history and physical exami-
nation. This amalgamation of all the available evidence is much more useful
than making an inference from a single nding. For example, a patient with
known malignancy developing signicant hypotension with a normally func-
tioning RV on echocardiography makes the probability of a massive pulmonary
embolism extremely low.
How do you proceed at this point?
Increase the ow of oxygen from 10 to 15 L/min.
Site an arterial catheter for invasive blood pressure monitoring and
repeat lactate measurement.
Ideally, site a central venous catheter (CVC) and commence an infusion
of noradrenaline aiming for a MAP of at least 65 mmHg or higher if the
patient is a known hypertensive. However, if it is impractical to site a
CVC, then starting vasopressors peripherally to restore MAP is increas-
ingly accepted practice. But only for a short period of time (consult your
local guidelines).
Insert a urinary catheter and monitor hourly urine output.
Perform a complete septic screen.
Liaise with your microbiologist to discuss your antibiotic choice,
taking into consideration the most likely pathogens and local resis-
tance patterns.
Continue to bolus IV uid up to the recommended limit of 30 mL/kg.
Liaise with your consultant regarding admission to ICU.
Which vasopressors are recommended in sepsis?
Noradrenaline (NA) is the preferred rst- line vasopressor in sepsis. It should be
borne in mind that at high doses, NA can cause intense vasoconstriction, which
may result in reduced tissue perfusion despite maintaining blood pressure. For
second- line agents to maintain a MAP >65 mmHg, instead of escalating the
You have given Joan a litre of uid intravenously in 250 mL boluses while
still on the medical ward. With the last bolus of uid, her blood pressure
did not improve. Her BP is now 89/45, MAP60
mmHg, HR 134 bpm sinus
rhythm, RR 28 breaths per minute. Her lactate on the arterial blood gas is
4.6
mmol/L.
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Clinical Cases in Critical Care
172
dose of NA, vasopressin should be commenced (usually when NA dose is in
the range of 0.25–0.5
mcg/kg/min). If both NA and vasopressin fail to reach
the target MAP, then adrenaline can be added.
Describe how these vasopressors work
Noradrenaline is an endogenous catecholamine that exerts its eects
via alpha-
1and beta- 1 adrenergic receptors (it has little eect on beta- 2
receptors) and is the initial agent of choice for sepsis. Alpha-
1receptor
activation is cyclic adenosine 3,5-
monophosphate (cAMP) independent
and beta-
1 adrenergic receptor activation is cAMP dependent. Like
other natural and synthetic catecholamines, NA increases the amount
of intracellular calcium, which leads to shortening of the contractile
apparatus. NA has a short half- life between 1 and 2 minutes and achieves
a steady-
state plasma concentration within 5–10 minutes following a
constant infusion. NA results in increased stroke volume (beta-
1 adren-
ergic eect), mean arterial pressure and left ventricular afterload. More
importantly, by constricting the venous circulation which contains most
of the intravascular volume, this also increases preload and cardiac lling
pressures with minimal eect on heart rate. NA enhances coronary blood
ow due to coronary vasodilation secondary to improved cardiac metab-
olism and increases in diastolic blood pressure.
Vasopressin is an endogenous hormone secreted from the neurohypoph-
ysis in response to arterial hypotension and hypovolaemia. Vasopressin
acts on specic vasopressinergic receptors (V
1
, V
2
) located within the
sympathetic nervous system. Interestingly, vasopressin levels are low in
patients with septic shock, and exogenous administration of vasopressin,
or its analogues, quickly restores MAP and vascular tone, and reduces
noradrenaline requirements. However, the Vasopressin And Septic Shock
(VASST) study demonstrated no signicant dierence in mortality when
low-
dose vasopressin was compared to noradrenaline.
Adrenaline is a potent beta- 1 adrenergic agonist with moderate beta- 2
and alpha- 1 adrenergic receptor activity. It increases both the cardiac
index and MAP by vasoconstriction. Adrenaline is very eective at raising
arterial pressure, but potentially at the cost of signicantly impairing
splanchnic circulation.
What role do corticosteroids have in the
management of sepsis?
When at least 4 hours of noradrenaline or adrenaline at a dose 0.25 mcg/kg/
min have been required to maintain the target MAP, intravenous hydrocorti-
sone should be given in a divided dose of 200 mg per day.
Increased vigilance may be required to prevent associated hypernatraemia
and hyperglycaemia. Interestingly, even though the evidence consistently dem-
onstrates that steroid therapy leads to a faster resolution of shock, there appears
to be minimal or no eect on mortality.
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The Patient Who is Hypotensive
173
What do you think has happened based on her
clinical ndings?
Cardiogenic pulmonary oedema (CPO)–this is the most likely cause
of her current breathing problems. Either the volume, infusion rate or
both can lead to CPO in these situations, especially if there is underlying
cardiac disease.
Iatrogenic pneumothorax– pneumothorax is a known complication of
central line insertion into the internal jugular veins and should be ruled
out. However, given her clinical ndings, the probability of this having
occurred remains relatively low.
How can lung ultrasonography help you differentiate
between these two potential causes?
As already stated, history and clinical examination are essential to fully inter-
pret ultrasonographic ndings. Nevertheless, lung ultrasonography can help
distinguish between these two clinical entities as follows:
A- or B- line patterns–when the predominant ndings change from an
A- line to a B- line pattern, this suggests that the patient has developed
new- onset interstitial oedema alongside uid resuscitation. If ultraso-
nography is only performed following aggressive uid administration
and bilateral B-
lines are found, then it is possible this could represent
pre- existing CPO. However, other causes should also be considered such
as chronic lung disease and infection.
Lung point/lung sliding–see Case 5.
When you and Joan arrive in intensive care, you administer two further
boluses of 250mL intravenous uid and site the CVC into the right internal
jugular vein. Around 20
minutes after you have completed the procedure,
Joan complains that her breathing is becoming more dicult. On auscul-
tation of her chest, you nd bilateral widespread crepitations. She denies
chest pain. Her BP is unchanged, her HR is 135 bpm sinus rhythm, her RR
is now 35 breaths per minute and her saturations are 88% on 8
L/min oxygen
via a Hudson mask.
You request a chest radiograph and perform lung ultrasound (US). Both
conrm that this is CPO. After successfully treating the CPO, Joan begins
feeling better. Her blood pressure has increased to 124/53 (MAP77) mmHg
with noradrenaline. The ECG remains unchanged, and bedside focused
echocardiography shows a hyperdynamic LV. Her HR is now 112 bpm and
RR 19 breaths per minute. Microbiology informs you the following morning
that blood cultures taken on admission have grown gram- negative bacilli.
She currently requires 0.25 mcg/kg/min noradrenaline.
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Clinical Cases in Critical Care
174
What is the signicance of gram- negative bacilli
in a blood culture?
The presence of gram- negative bacilli is always a signicant nding that needs
to be acted upon. Discussing the likely pathogen, possible sources and any
previous/current antimicrobial therapy with a microbiologist is of paramount
importance. Your microbiology laboratory will hopefully be able to identify
the pathogen within 24
hours of receiving the sample, which will enable you
to target your antimicrobial therapy.
Which organisms are most likely to be responsible
for gram- negative sepsis in this case?
There are many gram- negative bacilli that can cause bacteraemia. However, in
this case the most common organisms include Escherichia coli, Proteus spp.,
Enterococcus spp. and Klebsiella spp.
Briey describe the differences between gram-
positive and gram- negative bacteria
In gram- positive bacteria, the cell membrane is covered by a thick (20–
80 nm) protective cell wall made from peptidoglycan. This wall forms the
external surface of the cell and disrupting its integrity constitutes one of
the targets for antimicrobial therapies (e.g. beta-
lactam antibiotics). How-
ever, in gram- negative bacteria the peptidoglycan layer is thin (5–10 nm)
and there is an additional outer layer rich in lipopolysaccharides (LPS) and
lipoproteins. This extra layer oers protection against antibiotics and the
host’s immune system. LPS in the membrane has both antigenic properties
(e.g. carbohydrate chain O antigens) and toxic properties (e.g. lipid A com-
ponent endotoxin).
To which class of antibiotics does meropenem
belong and what is its general spectrum
of activity?
Meropenem (along with ertapenem and imipenem) is classed as a car-
bapenem. These carbapenem drugs belong to the much larger family of
beta-
lactam bactericidal compounds (i.e. they all contain the beta- lactam
ring). Carbapenems are active against both gram- positive and gram-
negative bacteria.
The microbiologist calls back to say that they have isolated E. coli from the
urine culture and that it is sensitive to meropenem only.
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The Patient Who is Hypotensive
175
Briey describe the other beta- lactam antibiotics
and how they work
Beta- lactam antibiotics are dierentiated according to the structure of the
chemical ring that is attached to the beta-
lactam ring. They bind to and inhibit
the enzymes responsible for the nal stages of cross-
linking of the bacterial
peptidoglycan cell wall subunits once they have been transported across the
cell membrane. Apart from the carbapenems, the other beta-
lactam drugs are
as follows:
Penicillins–these include naturally occurring compounds such as pen-
icillin V or G, and semisynthetic compounds such as amoxicillin, ampi-
cillin and piperacillin. Eective mainly against gram-
positive bacteria,
some of the semisynthetic penicillins have been developed for their
activity against gram-
negative rods (e.g. piperacillin).
Cephalosporins–currently, there are ve generations of cephalosporins
that can be used. The rst three generations (that contain cephalexin,
cefuroxime and ceftriaxone) are eective against gram-
positive bacteria.
However, fourth- and fth- generation cephalosporins (such as cefepime
and ceftrolozane) have improved activity against gram-
negative bacteria,
with the fth generation also being eective against methicillin- resistant
Staphylococcus aureus (MRSA).
Monobactams–aztreonam is generally eective against gram- negative
bacteria including Haemophilus inuenzae and Pseudomonas aeruginosa.
Cephamycins–these drugs are often classied as second- generation
cephalosporins. However, both cefotetan and cefotixin are effective
against gram-
positive bacteria as well as Bacillus fragilis.
What does the term extended- spectrum beta-
lactamase (ESBL) mean?
Ongoing mutations in the beta- lactamase genes confer resistance against the
beta- lactams in gram- negative bacteria. Enterobacteriaceae (e.g. E. coli and
Klebsiella spp.) are the most often identied bacteria that produce ESBLs. The
ESBLs that E. coli produces most often are called CTX-
M enzymes, which
inevitably make these infections much harder to treat. With ever increasing
resistance to beta-
lactam beta- lactamase inhibitor combinations, there remain
few options in our arsenal to tackle these challenges. Carbapenem- resistant
ESBL- producing Enterobacteriaceae are a major and constant health problem
worldwide.
By day 6 on critical care, Joan has been over 48 hours without the need for
noradrenaline and she is only requiring nasal oxygen therapy. As she no
longer requires any organ support, she is transferred back to the ward, and
you're informed when she is successfully discharged home the following day.
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Clinical Cases in Critical Care
176
Further reading
Singer, M., Deutschman, C., Seymour, C. etal. (2016). The third international con-
sensus denitions for sepsis and septic shock (sepsis- 3). JAMA 315: 801–810. World
leading experts dene sepsis.
Evans, L., Rhodes, A., Alhazzani, W. etal. (2021). Surviving sepsis campaign: inter-
national guidelines for management of sepsis and septic shock 2021. Intensive
Care Med 47: 1181–1247. Important updates to sepsis and its management by the
ESICM and SCCM.
Goering, R., Dockrell, H., Zuckerman, M. etal. (2019). MIMS’ Medical Microbi-
ology and Immunology. St Louis: Elsevier. Invaluable textbook when dealing with
infectious diseases.
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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.
14
Y
ou are asked to review Michael, a 75- year- old man who has just been
admitted to your ICU with shortness of breath, a productive cough, oliguria
and pyrexia. The presenting ECG demonstrates left ventricular hypertrophy
and a chest radiograph demonstrates bilateral consolidation. On examination,
a late peaking systolic ejection murmur is detected, but accurate assessment
of heart sounds is not possible. Following initial uid resuscitation, lactate
is 2.4
mmol/L and urine output improved to >0.5 mL/kg/h. He requires nor-
adrenaline at a dose of 0.05 mcg/kg/min. However, due to his deteriorating
respiratory function, Michael is intubated and mechanically ventilated with
propofol/fentanyl sedation. Within 20
minutes, the noradrenaline requirement
has increased to 0.6
mcg/kg/min to maintain a MAP >65 mmHg, and despite
this increase he remains haemodynamically unstable: BP78/58 mmHg, HR
130 bpm sinus rhythm.
What could be the causes of his persistent
hypotension despite increases in noradrenaline
andadequateuidresuscitation?
Acute coronary syndrome
Acute heart failure (AHF)
Pulmonary embolism
Tension pneumothorax
Severe aortic stenosis
Septic shock
Artefact (e.g. equipment failure or user error)
Eects of anaesthetic agents used for intubation
The Patient Who
Deteriorates Post
Intubation
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Clinical Cases in Critical Care
178
What is the normal range for aortic valve area
andpeak
transvalvularow?
The normal area is considered to be between 3 and 4 cm
2
and under normal
circumstances, the ow velocity through the aortic valve (transvalvular ow)
should be less than 2
m/s.
What are the echocardiographic criteria for diagnosing
severe
aorticstenosis?
The British Society of Echocardiography defines severe aortic stenosis
(Table14.1) as follows:
Aortic valve area (AVA) <1.0 cm
2
Aortic valve area indexed (AVAi) <0.6 cm
2
/m
2
Peak velocity (Vmax) between 4.0 and 4.9 m/s
Mean pressure gradient 40–59 mmHg
Dimensionless Index (DI) is obtained from the ratio of left ventricle
outflow tract (LVOT)/AV velocities, and a ratio <0.25 is consistent
with severe AS
Howwouldyouinterpretthereported
echocardiogram?
The estimated aortic valve area suggests severe aortic stenosis (AS). However,
the mean pressure gradient and peak velocity through the valve do not meet
the denition of severe AS. Considering that the report states:
‘severely calcied’
‘severely reduced leaet motion’
‘left ventricle appears hypertrophied’
Table 14.1: Grading aortic stenosis severity.
Aortic
sclerosis
Mild Moderate Severe Very severe
AV V
max
(m/s) <2.5 2.5–2.9 3.0–3.9 4.0–4.9 5.0
Mean gradient
(mmHg)
– <20 20–39 40–59 ≥60
AVA (cm
2
) – >1.5 1–1.5 <1 ≤0.6
The focused echocardiogram demonstrates LV impairment. A subsequent
formal echocardiogram is performed that demonstrates moderate left
ventricular hypertrophy with a small cavity, a peak velocity through the
AV of 3.5
m/s, mean pressure gradient of 33 mmHg but with an estimated
AV area of 0.8
cm
2
. The report also states that the valve appears severely
calcied with severely reduced leaet motion. Ejection fraction is estimated
to be 40%, indicating impaired LV systolic function.
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