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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3080_Библиотеки_им_академика_М_И_Перельмана
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The Patient with Chest Pain
129
Death–current evidence suggests that when patients with PE are com-
pared to matched controls, there is a threefold increase in mortality at
30
years. It is important to note that most of these deaths may be due
to other causes such as malignancy, sepsis, myocardial infarction, heart
failure and stroke.
Chronic thromboembolic pulmonary hypertension (CTEPH)–this unusual
complication presents with shortness of breath and reduced exercise tol-
erance within 2 years after the initial event. Additionally, patients may
present with symptoms of RV dysfunction such as peripheral oedema
or exertional chest pain.
Cardiovascular – there is an associated increase in subsequent
development of atrial brillation and cardiovascular events.
Further reading
Konstantinides, S., Meyer, G., Becattini, C. etal. (2020). 2019 ESC guidelines for the
diagnosis and management of acute pulmonary embolism developed in collabora-
tion with the European Respiratory Society (ERS). The task force for the diagnosis
and Management of Acute Pulmonary Embolism of the European Society of Car-
diology (ESC). Eur. Heart J. 41: 543–603. Comprehensive guideline on several key
aspects associated with managing patients with acute pulmonary embolism and
includes excellent descriptions of right ventricle pathology.
Grace is successfully extubated on day 5 and subsequently discharged to the
ward under the care of the respiratory team.
https://t.me/medicina_free
Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
10
The Out- of- Hospital
Cardiac Arrest Patient
Y
ou are called to the emergency department during your nightshift. You
nd the ED team preparing for the arrival of a 68-
year- old male patient
named Gary. He has suered an out-
of- hospital cardiac arrest (OHCA). Gary
was found collapsed on the toilet by his wife at approximately 01:00 am. She
managed to provide 10
minutes of basic life support whilst waiting for the
paramedic team to arrive. The paramedics have intubated his trachea and
have provided 30
minutes of continuous CPR prior to return of spontaneous
circulation (ROSC). The initial rhythm was shockable (ventricular brillation),
and Gary received 6 DC shocks. He is en route to the ED.
How can we dene cardiac arrest?
Cardiac arrest is dened as the sudden loss of cardiac function resulting in
the cessation of eective circulation (conrmed by an absent palpable pulse)
which may be reversible by rapid medical intervention. Delayed or inadequate
intervention signicantly lowers the chances of survival and increases the risk
of permanent neurological/psychological damage. The absence of medical
intervention will result in death.
What is the chain of survival?
The UK Resuscitation Council describes the chain of survival as a sequence
of events, or ‘links’, that when performed equally well maximises the chances
of survival for cardiac arrest patients:
Immediate recognition of cardiac arrest and calling for help (rst link).
Prompt initiation of eective CPR (second link).
Performing debrillation as early as possible (third link).
Optimising postresuscitation care (fourth link).
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The Out- of- Hospital Cardiac Arrest Patient
131
What are the approximate survival rates for OHCA
in the UK?
It is estimated that fewer than 1in 10 cases of OHCA in the UK survive to
return home. Neurological and functional recovery varies considerably amongst
survivors (e.g. ranging from being able to lead a normal life to permanent coma
or vegetative state).
How could you classify the causes of OHCA?
Classifying OHCA into cardiac and non- cardiac events (NCEs), one population-
based observational case series demonstrated that NCEs were the cause of 62.5%
of deaths. Causes could be categorised using the acronym OOHCAS as follows:
Obstructive– pulmonary embolism (PE), cardiac tamponade.
Oxygen (‘hypoxia’)– asthma, acute worsening of chronic obstructive
pulmonary disease (COPD), airway obstruction and submersion.
Hypovolaemia– major haemorrhage (trauma, gastrointestinal bleeding,
acute aortic dissection).
Cerebrovascular disease– stroke, acute intracranial haemorrhage.
Anaphylaxis (‘distributive’).
Sepsis.
For identifying and treating reversible causes during a cardiac arrest scenario,
the UK Resuscitation Council advises using the 4Hs and 4Ts aide-
mémoire:
Hypovolaemia
Hypoxia
Hypo/hyperthermia
Hypo/hyperkalaemia
Tension pneumothorax
Tamponade– cardiac
Thrombosis– cardiac or pulmonary
Toxins
What is the evidence surrounding thrombolysis
in cardiac arrest?
For thrombolysis
A meta- analysis in 2006, which examined one prospective and seven ret-
rospective cohort studies, found that thrombolysis during CPR can sig-
nicantly increase the chances of ROSC as it can improve/re- establish
blood ow in occluded coronary arteries. Seven of the studies used tissue
While you are waiting for the ambulance to arrive, the ED registrar suggests
you should prepare to thrombolyse the patient.
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Clinical Cases in Critical Care
132
plasminogen activator (tPA) and one used recombinant tPA, along with
either heparin, aspirin or heparin/aspirin for anticoagulation. As expected,
the risk of severe bleeding (dened as life-
threatening or bleeding that
requires transfusion) was higher in the thrombolysis group. However, there
was no clear evidence that a secondary bleed could result in death. The
risk of bleeding may also have been theoretically lower due to the inherent
survival bias in this cohort of patients (e.g. increased bleeding risk in those
receiving thrombolysis because of their increased survival rate).
Against thrombolysis
In the double- blind, multicentre Thrombolysis in Cardiac Arrest trial
(TROICA, 2008), the use of tenecteplase did not result in an improvement
in outcome when compared with placebo. The trial was prematurely ter-
minated for futility after enrolling 1050 patients and the incidence of
intracranial haemorrhage was higher in the treatment group. This trial
did not conclusively answer this question due to limitations regarding
its selection criteria and was criticised for the deliberate avoidance of
using aspirin and/or heparin for anticoagulation.
Should we perform immediate coronary
angiography in all patients after cardiac arrest?
Coronary angiography (CA) is recommended in survivors of OHCA with ST
segment elevation, with the potential for percutaneous coronary intervention.
However, the benet of CA in non-
ST segment elevation remains unclear. It is
important not to delay other postresuscitative modalities if these facilities are
not immediately available or will take an inappropriate time to put in place.
Describe how echocardiography can help in the
management of cardiac arrest
The 10- second pulse check provides an opportunity for focused echocardiog-
raphy to be performed by an experienced practitioner. It can help to determine
the following:
Ventricular brillation (VF)– ne VF can, on occasion, be mistaken
for asystole and can be detected by focused echocardiography. This can
potentially avoid delays in debrillation.
The paramedics hand over and state that Gary is an active and generally
t individual. His past medical history includes treated hypertension and
hypercholesterolaemia. He is intubated and being ventilated with a tidal
volume of 500 mL at a respiratory rate of 12 breaths per minute. He is mak-
ing no spontaneous respiratory eorts. Monitoring shows a HR of 100 bpm,
pulse oximetry 99% on 100% oxygen and a BP of 100/50 mmHg.
While you are examining Gary, the ECG trace and invasive blood pressure at-
line and the capnography trace falls to zero. You immediately perform a central
pulse check and declare he is in cardiac arrest. Your team commences standard
adult ALS measures according to the UK Resuscitation Council guidelines.
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The Out- of- Hospital Cardiac Arrest Patient
133
Hypovolaemia – generally, the presence of a small, underfilled left
ventricle with a totally collapsed inferior vena cava suggests the need
for aggressive uid resuscitation and a search for the cause.
Tamponade– demonstrating a pericardial eusion should lead to the
consideration of immediate drainage as the characteristic ndings of
tamponade may not be present during cardiac arrest. Current evidence
(class I) suggests that pericardiocentesis should be performed under
ultrasound guidance, as this signicantly reduces the risk of complica-
tions with experienced operators.
Pulmonary embolism– right ventricular dysfunction (in the absence of
left ventricular disease or known pulmonary disease) suggests PE is pos-
sible. On rare occasions, demonstrating thrombus in the right atrium
or ventricle, pulmonary arteries or both can conrm the diagnosis.
Can you use focused echocardiography
to
prognosticate in cardiac arrest?
The complete absence of cardiac activity, ‘cardiac standstill’, as demonstrated on
the focused subcostal echocardiography view, heralds an extremely poor prog-
nosis. M-
mode can be utilised in this instance to demonstrate zero movement
of the myocardium and will resemble a ‘barcode’ appearance.
How would you interpret the ABG result?
The ABG clearly demonstrates a severe mixed metabolic and respiratory acid-
aemia– a common nding in patients presenting with OHCA. With eective
mechanical ventilation, the initial severe hypercarbia associated with respiratory
arrest, the PaCO
2
, can be reduced (assuming adequate cardiac output). The
decreased bicarbonate and large base decit reect the physiological buer
present in the patient’s blood that aims to neutralise the increased hydrogen
ions (acid) being produced. The increased lactate is mostly due to the increased
anaerobic metabolism occurring in peripheral tissues. The high PaO
2
reects
hyperoxaemia, especially given the inspired oxygen fraction is 1.0.
What is the potential association between
hyperoxaemia and cardiac arrest?
One systematic review and meta- analysis in 2018 examined 16 observational
studies published between 2008 and 2017, which included a total of 40 573 adult
patients. Six of these studies included patients with OHCA only, eight studies
Gary achieves ROSC after a further three cycles and three shocks for VF. He
requires inotropic support to maintain his blood pressure. After a further
period of stability, you safely transfer Gary to your critical care unit to estab-
lish postresuscitation management. You successfully insert a central venous
catheter and arterial line. The arterial blood gas (FiO
2
1.0) demonstrates pH
6.9, PaO
2
55 kPa, PaCO
2
7.1 kPa, HCO
3
8 mmol/L, base excess −20 mmol/L
and lactate 15 mmol/L.
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Clinical Cases in Critical Care
134
included patients with both OHCA and in- hospital cardiac arrest (IHCA) and
the remaining two studies included IHCA patients only. The authors managed
to quantitatively analyse 10 of these studies and determined that:
Intra- arrest hyperoxaemia was associated with significantly
lower mortality
Postarrest hyperoxaemia was associated with a higher mortality.
Some of the studies in another systematic review on the eects of hyperox-
aemia in acutely ill patients suering cardiac arrest revealed no association bet-
ween poor outcome and hyperoxaemia during CPR or in the rst 24
hours after
cardiac arrest. However, they also found that severe hyperoxaemia (dened
as PaO
2
>39.9 kPa) appeared to be independently associated with increased
in-
hospital mortality.
Currently there is a low level of evidence describing the eect of hyper-
oxaemia on clinically relevant outcomes in OHCA. Hyperoxaemia during
postresuscitation care may be associated with lower survival rates and poorer
neurological outcomes.
Discuss the role of targeting hypothermia at 33 °C
in OHCA comatose survivors?
The Targeted Temperature Management 2 (TTM 2) trial investigated 1850
comatose OHCA survivors from any initial rhythm. In short, they found that
targeted hypothermia at 33
°C did not lead to a lower incidence of death com-
pared to targeted normothermia (preventing body temperature >37.7
°C)
at 6 months. The only intervention that is now recommended is the active
treatment of pyrexia (>37.7 °C) during the initial 72 hours in OHCA patients
who remain comatose.
What is the role of targeting MAP in OHCA
comatose survivors?
Part of the Carbon dioxide, Oxygen and Mean arterial pressure After Cardiac
Arrest and REsuscitation trial (COMACARE) looked at low- normal (65–
75 mmHg) and high- normal (80–100 mmHg) groups. Researchers used neuron-
specic enolase (NSE; discussed later) at 48 hours as the primary outcome.
Neurological outcome at 6 months was one of the secondary outcomes. Target-
ing a specied level of blood pressure was possible once admitted to the ICU.
They found that there was no dierence between the two groups in terms of
serum concentration of NSE or any of the secondary outcomes.
You decide to target a MAP of 75 mmHg for Gary. By day 3 of admission,
Gary has not demonstrated any neurological signs of recovery despite being
o sedation for over 24 hours. You meet with his wife and daughter to dis-
cuss his prognosis.
https://t.me/medicina_free
The Out- of- Hospital Cardiac Arrest Patient
135
Which tests can we use to predict poor neurological
outcome in OHCA survivors?
Prognostication should ideally be deferred until 72 hours after the arrest and
when the patient is sedation free, normothermic and other causes of coma or
paralysis have been corrected, where possible.
Pupillary light reex (PLR)– the absence of this reex at 72 hours
is a strong predictor of poor neurological outcome following cardiac
arrest. It has a high specicity but low sensitivity. However, this test
can be operator dependent and qualitative, which has led to some res-
ervation about its reproducibility in neuroprognostication. One novel
method using the PLR involves automated infrared pupillometry,
which provides a quantitative measure of pupil size, PLR and con-
striction velocity. Recent studies suggest that this technique has both
a higher specicity and sensitivity when compared to standard PLR
measurement by clinicians.
Corneal reex– when the corneal reex is bilaterally absent, this suggests
a probably poor neurological outcome. However, due to this reex being
more prone than PLR to the residual eects of sedatives and muscle
relaxants, it has a lower specicity and similarly low sensitivity.
Myoclonus– poor neurological outcome is almost invariably associated
with the development of status myoclonus (dened as continuous and
generalised myoclonus
>30 minutes) that occurs within the rst 48 hours
post cardiac arrest. Myoclonus should only be used in conjunction with
other indices, and it is a less robust predictor than PLR. When present,
it is recommended that an electroencephalogram (EEG) is performed to
exclude other more benign forms of postanoxic myoclonus (e.g. Lance-
Adams syndrome).
EEG– in comatose patients, the identication of burst suppression
and suppressed background (with or without periodic discharges) at a
median time of 77
hours after ROSC predicted poor neurological out-
come with 100% specicity and 50% sensitivity. Recent evidence sug-
gests that when continuous EEG is performed within the rst 24
hours
following cardiac arrest, the presence of isoelectric, low- voltage or
burst suppression with identical bursts can predict poor neurological
outcome at 6 months. However, the sensitivity of these ndings is
low. EEG will also aid in ruling out postanoxic seizure activity in the
comatose patient.
Bispectral index (BIS)– this form of automated EEG analysis is used
to monitor depth of anaesthesia. It has a maximum value of 100in an
awake patient to a minimal value of 0, which is equivalent to a at EEG
with no signal. It was recently demonstrated that if a total duration of
BIS 0was recorded for over 30 minutes, this predicted a poor neurolog-
ical outcome with 100% specicity and >60% sensitivity.
Short- latency somatosensory evoked potentials (SSEPs)– the bilateral
absence of N20 (negative peak at 20 ms) SSEPs is among the most
robust predictors to be tested at 72 hours post ROSC. It predicts poor
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Clinical Cases in Critical Care
136
neurological outcome with high accuracy and precision. Like the other
modalities, SSEPs suer from having a low sensitivity (rarely above 50%).
SSEPs are less aected by sedation than an EEG, but they are prone to
electrical interference.
Neuron specific enolase (NSE)– this is a cell- specific isozyme of the
glycolytic enzyme enolase and is highly specific for neurons and
peripheral neuroendocrine cells. There are three isozymes of eno-
lase, with enolase-
gamma being neuron specific. NSE has been shown
to provide quantitative measures of brain damage and/or improve
the diagnosis and outcome of OHCA comatose survivors. NSE is not
affected by hypothermia or sedation but is affected by haemolysis.
High levels are necessary (>97
ng/mL) to give a 100% positive predic-
tion value of poor outcome. This test is not routinely available, and it
should be used in conjunction with other tests that can predict poor
neurological outcome. Sampling at multiple time points (e.g. 24, 48
and 72
hours) is currently recommended to reduce the risk of a false-
positive result, which can occur in the presence of neuroendocrine
tumours and small cell carcinoma.
Neurolament light chain (NFL)– at 24 hours, this novel biomarker was
found to be a highly specic predictor of poor neurological outcome at
6
months. It has been shown to possess greater predictive value than
NSE, brain CT, SSEPs, EEG and clinical examination.
CT brain– attenuation of the grey/white matter interface on CT sug-
gests cerebral oedema and is one of the main findings for hypoxic-
ischaemic brain injury. The ratio of grey to white matter densities
(GWR) is used to prognosticate in these individuals. When performed
within 24
hours following the event, a GWR <1.22was found to pre-
dict in- hospital mortality with a 98% specificity but was not able to
differentiate survivors with poor versus good outcome. Currently,
there is no consensus on when to perform CT in survivors following
cardiac arrest for neuroprognostication. The presence of generalised
oedema without formal GWR measurement predicts poor neurolog-
ical outcome (CPC 3–5) with very high specificity and low sensi-
tivity within 24
hours from ROSC. Both the specificity and sensitivity
increase further if these findings are also present from 24 hours to
7 days following ROSC.
Magnetic resonance imaging (MRI)– current guidelines suggest that
MRI can be used for prognostication between 2 and 5 days after ROSC.
Modern evidence suggests that it can even predict neurological outcome
when performed within 3 hours after ROSC. However, the evidence for
using MRI is prone to selection bias in prognostic studies as its use is
limited in unstable patients post cardiac arrest. In addition, it is only
recommended in combination with other predictive measures and in
specialist centres.
It is important to remember that a multifaceted approach involving these
investigations and clinical ndings (e.g. organ failure) will allow for robust
neuroprognostication in these potentially challenging situations.
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The Out- of- Hospital Cardiac Arrest Patient
137
Which ndings, if any, might suggest a good
neurological outcome?
Despite most of the work done to identify markers of poor neurological out-
come, predictors of good neurological outcome have recently been recognised
(they have yet to be included in any international guidelines).
Presence of early EEG reactivity.
Improvement of auditory discrimination (through analysis of EEG
responses to auditory stimuli) from the rst to the second day after ROSC.
Absence of diusion weighted imaging abnormalities on MRI within
1
week of ROSC.
Describe the Cerebral Performance Category Scale
The Cerebral Performance Category (CPC) Scale is used to assess neurological
outcome in cardiac arrest survivors (Table10.1).
How does the CPC relate to long- term prognosis
following cardiac arrest?
A review of over 300 patients treated at Columbia University Medical bet-
ween 2008 and 2015 suggested that CPC at discharge was not predictive of
clinical outcome. Approximately 50% of patients with mild to no neurological
or psychological defect still had a poor outcome at 1 year.
Describe the modied Rankin Scale (mRS)
This aims to incorporate both quality of life and survival and is another widely
used tool in OHCA research. It uses a seven- point scale, with better recovery
associated with lower scores, and has been shown to have consistent inter- rater
reliability. A patient with no symptoms at all is given a score of 0 and those
who die a score of 6. A good outcome is generally considered to be between a
score of 0 and 3.
Table 10.1: Cerebral performance categories (CPC).
Category Comments
1 Good cerebral performance, is alert, able to work and lead a normal
life, but may have a mild psychological or neurological decit
2 Moderate cerebral disability but enough cerebral function for
independent activities of daily life (e.g. use public transport). May be
able to work in a sheltered environment
3 Severe cerebral disability, depends on others for daily support
and may range from being ambulatory to paralysed, usually in an
institution
4 Permanent coma or vegetative state
5 Certied brain dead or death
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Clinical Cases in Critical Care
138
What are the disadvantages of using measures
such as the CPC and mRS for classifying
outcomes following OHCA?
It is important to understand that these scores use strictly objective measures
to describe outcomes that are, in their very essence, completely subjective.
These reductionist measures clearly do not consider the state of neurodisability
perceived or experienced by the patient or their next of kin.
Further reading
Advanced Life Support, 8e. London: Resuscitation Council UK. Denitive guide to
resuscitation practices in the UK.
Sandroni, C., Nolan, J., Andersen, L. etal. (2022). ERC- ESICM guidelines on temperature
control after cardiac arrest in adults. Intensive Care Med. 48: 261–269. Informative
rapid practice guideline regarding temperature control.
On day 5, Gary begins to show signs of neurological recovery and is success-
fully extubated 8
days after the cardiac arrest and subsequently discharged
from your unit. At 6
months, he can function relatively independently from
others, but has mild problems with memory and recall.
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