Clinical
Non traumatic chest pain –
pericarditis
Andrew Mootham, Emergency Nurse Practitioner, Care UK.
E-mail for correspondence: andrew.mootham@hotmail.com
Abstract
Pericarditis is an inflammation of the two layers of the thin, sac-like membrane
that surrounds the heart. This membrane is called the pericardium, so the term
pericarditis means inflammation of the pericardium. The causes of pericarditis
are thought to be viral, fungal or bacterial in nature. Pericarditis may also
present as a result of a myocardial infarction (MI). The presenting signs and
symptoms of pericarditis are described as a chest pain which may radiate to the
arm and jaw, a pericardial friction rub (a scratching or creaking sound produced
by the layers of the pericardium rubbing over one another) on auscultation of
heart sounds. The diagnosis of straight forward pericarditis may be within the
scope of practice of the Emergency Care Practitioner (ECP). It would be possible
for the ECP to reach a working diagnosis and even to initiate a treatment
regime, which would predominantly consist of providing analgesia to make the
patient more comfortable.
Key words
l Pericarditis l Pre-hospital setting l Analgesia l Emergency care
Accepted for publication 25 March 2017
T his article will look at the pathophysiology,
signs and symptoms/presentation and
management of pericarditis.
It will examine the evidence relating to the
management of the condition and discuss the issues
surrounding the need for hospital admission versus
management within the community/primary care
setting.
'Pericarditis is an inflammation of the two
layers of the thin, sac-like membrane that
surrounds the heart. This membrane is called
the pericardium, so the term pericarditis
means inflammation of the pericardium.'
(Unknown 2013)
Knudson (2011, p504) describes the pericardium
as surrounding the cardiac muscle. Consisting of
two layers of tissue, encapsulating part of the aorta
and vena cava.
172
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032_JPAR_2017_9_4_172_176.indd 172
The pericardium as well as protecting and
restraining the heart it also determines cardiac
filling by preventing over stretching of the
myocardium. (Asher, Klein and Loughton, 2004
p718).
Derrickson and Tortora (2009 p720) describe
pericarditis as falling into two categories; Acute
Pericarditis (which begins suddenly and has no
known cause (although may be linked to viral
infection) and chronic pericarditis (begins gradually
and symptoms are long lasting with an associated
build up of pericardial fluid).
Evidence from the United States suggests that
pericarditis is relatively rare, resulting in less than
one percent of hospital admissions. Pericarditis is
most common in men age twenty to fifty, although
it does occur in woman as well. ( Jacob and Grimm
2013).
The causes of pericarditis are thought to be
viral, fungal or bacterial in nature. Pericarditis may
also present as a result of a myocardial infarction
(MI). Davidson, Foulkes, Longmore, Mafi and
Wilkinson (2010 p148) suggest that the cause may
be idiopathic (of unknown cause) or secondary
to; viruses (e.g. Coxsackie or influenza), bacterial
(e.g, pneumonia), fungal, post MI or caused by
medication or other complex complaints such as
uraemia in renal failure.
Both Davidson Et al (2010 p148) and Clancy,
Graham, Illingworth, Robertson and Wyatt (2008
p80) identify “Dressler’s Syndrome” as a cause of
pericarditis.
Unknown-2 (2013) identifies Dressler’s syndrome
as inflammation of the pericardial sack which
occurs after trauma to the pericardium for example
post MI or after surgery.
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The presenting signs and symptoms of
pericarditis are described by Derrickson and
Tortora (2009, p720) as a chest pain which may
radiate to the arm and jaw, a pericardial friction rub
(a scratching or creaking sound produced by the
layers of the pericardium rubbing over one another)
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07/04/2017 12:16
 Clinical
on auscultation of heart sounds. Clancy et al (2008
p80) suggest that auscultation of heart sounds may
be unreliable due to the pericardial rub often being
intermittent, position and elusive.
Clancy et al (2008, p80) further describe the
symptoms as a left sided or retrosternal chest pain
made worse by deep inspiration, changing position,
exercise and swallowing.
Camm (1999 p727) suggests that the pain from
pericarditis may be relieved by sitting forward and
aggravated by lying prone or supine.
Jacob and Grimm (2013) state that the patient
may describe symptoms such as back/neck pain,
a dry cough and anxiety or fatigue as well as the
classical chest pain. Knudson (2011 p504) identifies
shortness of breath on exertion in addition to the
symptoms identified by Camm (1999) and Jacob
and Grimm (2013).
Rahman and Liu (2011 p791) suggest that during
examination and assessment of patients presenting
with query pericarditis will present symptoms
such as a raised jugular vein pressure and pulsus
paradoxus (a decrease in systolic blood pressure
during inspiration) in addition to the symptoms
identified above. Rahman et al (2011 p 791) also
suggests that the chest pain may be pleuritic in
nature.
Imazio, Parrini, Giuggia, Cecchi, Gaschimo,
Demarie, Ghiso and Trinchero (2004 p1042)
that pyrexia over 38°C, subacute onset,
immunodepression, trauma, oral anticoagulant
therapy, myopericarditis, severe pericardial
effusion, cardiac tampanade are all poor prognostic
indicators and could highlight more serious disease.
There is evidence to suggest that pericarditis can
lead to a number of ECG changes. Camm (1999
p728) suggests that in the first week the ECG will
display ST segment elevation with a concave shape
to the ST segment. This change is seen within the
anterior, inferior and lateral leads.
Rahman et al (2011 p792) identifies the ECG
changes which may be evident in pericarditis as;
diffuse ST segment changes; ST elevation with a
saddle/concave shape or ST segment depression.
The ECG will often lack any reciprocal changes
between leads III and AVL. Changes will usually
involve more than one cardiac territory.
Pericarditis can become complicated. These
complications are pericardial effusion which
Dudzinski, Hung and Mak (2012 p81) describe as
an accumulation of fluid within the pericardial sac.
© 2017 MA Healthcare Ltd
© 2017 MA Healthcare Ltd
The fluid can come from several aetiologies;
Hydopericardium – usually a non infective
collection of fluid occurring from similar situations
as pleura effusion or ascites e.g. Heart or Liver
Failure.
Clyclopericardium – a collection of white fluid,
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032_JPAR_2017_9_4_172_176.indd 173
usually results from chest trauma, malignancy or
tuberculosis.
Hemopericardium – a collection of blood
resulting from trauma to the heart or aorta
(Dudzinski, Hung and Mak 2012 p81-82).
Pericardial effusion may have significant
homodynamic consequences as it leads to reduced
filling of the heart and may produce a cardiac
tampanade. (Dudsinki et al 2012 p83).
Shabatai (2004 p255) describes the
heamodynamic effects of pericardial effusion as
being a spectrum from mild to life threatening,
supporting the statement of Dudsinki et al (2012
p83) who also suggest a link between pericardial
effusion and cardiac tampanade.
Cardiac Tampanade is a collection of fluid within
the pericardium which compresses the heart and
prevents adequate cardiac filling thus reducing
cardiac output. This is a medical emergency (March
and schub 2013)
Cardiac Tampanade can be suspected during a
clinical examination of the patient, Clancy Et al
(2006 p340) describes “Becks Triad” which is a
raised JVP, hypotension and muffled heart sounds.
Imazio et al (2004 p 1042) have identified cardiac
tampanade as being a poor prognostic indicator in
patients suffering pericarditis.
Constrictive Pericarditis is a long-term (chronic)
inflammation of the pericardium with thickening,
scarring, and muscle tightening/contracture (Zeive
2012).
Dato, Coluzzi. Al-Mohanni, Della Bona, Piro,
Natale, Luciani, Biasucci, and Crea (2008 p79)
describe constrictive pericarditis as a progressive
fibrotic change in the pericardium which constricts
the myocardium impairing ventricular filling.
Zeive (2012) goes on to identify the difficulty
in reaching a diagnosis of constrictive pericarditis
as the signs and symptoms are similar to those of
cardiac tampanade and restrictive cardiomyopathy.
Dato, Coluzzi, AlMohanni, Della-Bona, Piro,
Natale, Luciani, Biasucci and Crea (2008 p 79)
support the argument that it is difficult to reach
the correct diagnosis due to restrictive pericarditis
having a similar presentation to restrictive
cardiomyopathy.
Their work highlights the importance of a correct
diagnosis due to their being surgical intervention
available for the long term management of
constrictive pericarditis.
The diagnosis of constrictive pericarditis can
therefore not be made purely using clinical skills
such as observation and auscultation of heart
sounds, patients who have a working diagnosis
of pericarditis should undergo imaging such as
plain xray and computed tomography/magnetic
resonance imaging scans to confirm the diagnosis.
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07/04/2017 12:16
 Clinical
Young, Glockner, Williamson, Morris, Araoz,
Julsrud, Schaff, Edwards, Oh and Breen (2012
p1099)
Once the working diagnosis of pericarditis
is reached the practitioner should formulate a
treatment plan and consider the need for referral
for expert opinion.
Whilst considering the treatment/management
of pericarditis it is important to differentiate
between uncomplicated pericarditis and constrictive
pericarditis as there are differences in the way in
which the conditions are management.
Imazio et al (2004 p1042) suggest that pericarditis
should have “a brief and benign” course following
treatment with oral non steroidal anti-inflammatory
drugs (NSAIDS)
Clancy et al (2006) support the use of NSAIDS
in the treatment of the symptoms (chest pain).
Additionally Clancy et al recommend bed rest and
a referral to the cardiology team for review/advice
regards the treatment of the patient. This infers the
need for the patient to be admitted to hospital.
Gianni and Solbiati (2012) identify the risk
of recurrence of pericarditis and suggest that
up to 50% of patients may have a recurrence
of the condition. To avoid this recurrence
they recommend the use of colchicine to treat
pericarditis. The British Pharmaceutical Society
(2012) identify colchicine as a drug normally used
in the treatment of gout. They identify that it is
safe for patients who cannot take NSAIDS and also
those on anticoagulant therapy, there is also less
risk of fluid retention than NSAIDS.
The evidence regards analgesia for patients
suffering with pericarditis points to the use of
NSAIDs there is no specific research or evidence to
suggest the use of additional analgesia using opiate
based medications such as codeine or morphine
sulphate preparations.
Brown, Cooke and Fisher (2013) advocates the
use of morphine for the management of cardiac
chest pain, specifically recommending the use
the intravenous morphine to reduce the pain and
anxiety suffered by the patient and also reduce the
pre-load on the heart.
Herlitz, Bang, Omerovic and Wireklint-Sundström
(2011) support the statements made by Brown
et al (2013) however their research is specific to
acute coronary syndrome and does not support or
suggest the use of morphine as an analgesic option
for pericarditis.
Wedro, Kulick and Sheil (2013) specifically
name ibuprofen as the NSAID of choice for the
management of pericarditis, highlighting the action
of the drug stating that ibuprofen reduces the
inflammation of the pericardium and reduces fluid
accumulated within the pericardium.
174
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032_JPAR_2017_9_4_172_176.indd 174
Ibuprofen works by acting upon prostaglandins.
The prostoglandins are involved in the
inflammatory response. Ibuprofen inhibits the
synthesis of prostaglandin therefore reducing the
inflammatory response. Ibuprofen does this by
interfering with the action of an enzyme (cyclo-
oxygenase) which catalyses the conversion of
arachidonic acid into prostaglandic . (Neupert,
Brugger, Euchenhofer, Brune and Geisslinger 1997
p490). This is not specific to ibuprofen, all NSAIDs
work in this manner.
Wedro et al (2013) also support the short
term use of narcotic analgesia such as codeine
and morphine for the management of the pain
associated to pericarditis.
Research undertake by Imazio et al (2004 p
1043) suggests that low risk patients who do not
present with any poor prognostic indicators (who
are therefore low risk) can be safely managed out
of hospital. Their research considered the cases of
254 low risk patients and found that 87% of these
patients were successfully managed at home the
other 13% of patients suffered complications and
required hospital admission. It should be noted
that patients within this trial received a clinical
examination, blood tests and appropriate imaging
study’s to support the diagnosis prior to the
formulation of a treatment plan and discharge from
a day case hospital.
A statement by Black and Thompson (2012)
does not support the care of chest pain patients at
home, suggesting all patients with non traumatic or
suspected cardiac chest pain need to be reviewed
in hospital. Due to the differential diagnosis for
non traumatic chest pain having potentially life
threatening consequences. Thompson and black
identify the differential diagnosis for chest pain
as being acute MI, acute coronary syndrome and
pulmonary embolism.
The suggestion of avoiding hospital admission
made by Imazio et al (2004) is based on research
from an American study where the patients
attended a day hospital for their examinations
and assessments and were discharged home on
completion for treatment within the community;
the UK based evidence is suggestive that patients
would need to be assessed by cardiology specialist
doctors. This cardiology assessment will require a
visit to the emergency department as a minimum,
but in the experience of the author most patients
will require admission to the medical assessment
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unit or cardiology ward to allow for assessment
and treatment of their condition. Whilst the UK
based evidence does not specifically state that a
patient would require admission to hospital the
tests required to confirm the diagnosis infer that a
hospital visit would be necessary.
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 Clinical
Wedro et al (2013) identify that the patient would
require a chest x-ray, blood tests, an ECG and an
echocardiogram.
The evidence presented by Wedro et al (2013)
positively supports referring the patient to hospital.
Where appropriate and the pathway is in place the
practitioner should be considering a referral direct
to cardiology.
There is evidence to suggest that pericarditis
can be an acute or chronic in nature. The acute
presentation has already been discussed at length
above. The chronic presentation of pericarditis
is linked to the slow build up of fluid within the
pericardial sac (Derrickson and Tortora (2009
p720).
This slow build up of fluid is a pericardial
effusion.
The evidence presented above identifies the
fact that pericarditis can become complicated
by a pericardial effusion or by developing into
constrictive pericarditis.
The management of constrictive pericarditis is
discussed by Lin, Zhou, Xiao, Wang and Wang
(2012) their statement identifies the need for
surgical intervention for the definitive treatment
of constrictive pericarditis. This work identifies
the need for rapid identification of the presenting
features of constrictive pericarditis, whilst the ECP
would not be able to provide a definitive treatment
they would be able to recognise it as a differential
diagnosis.
Pericardial effusion whilst it is not something
which can be managed by the ECP. The ECP has
the skills to be able to recognise it as a possible
differential diagnosis based on findings from a
cardiac assessment. Salami, Adeoye, Adegboye and
Adebo (2012 p407) describe symptoms of Becks
Triad with shortness of breath as the key features in
the presentation of pericardial effusion.
Salami et al (2012 p408) also describe the
management of this condition as requiring a
pericardial drain.
In the cases of both a pericardial effusion and
constricive pericarditis is it the role of the ECP to
consider these as a possible differential diagnosis
in young patients presenting with chest pain of a
non traumatic nature and refer the patient to an
appropriate care centre.
Conclusion
The diagnosis of straight forward pericarditis may
© 2017 MA Healthcare Ltd
© 2017 MA Healthcare Ltd
be within the scope of practice of the Emergency
Care Practitioner (ECP). It would be possible
for the ECP to reach a working diagnosis and
even to initiate a treatment regime, which would
predominantly consist of providing analgesia to
make the patient more comfortable.
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032_JPAR_2017_9_4_172_176.indd 175
Key points
llPericarditis is an inflammation of the two layers of the thin, sac-like
membrane that surrounds the heart.
llThis membrane is called the pericardium, so the term pericarditis means
inflammation of the pericardium. The causes of pericarditis are thought to be
viral, fungal or bacterial in nature. Pericarditis may also present as a result of a
myocardial infarction (MI).
llThe presenting signs and symptoms of pericarditis are described as a chest
pain which may radiate to the arm and jaw, a pericardial friction rub (a
scratching or creaking sound produced by the layers of the pericardium
rubbing over one another) on auscultation of heart sounds.
llThe diagnosis of straight forward pericarditis may be within the scope of
practice of the Emergency Care Practitioner (ECP).
llIt would be possible for the ECP to reach a working diagnosis and even to
initiate a treatment regime, which would predominantly consist of providing
analgesia to make the patient more comfortable.
The evidence presented makes it clear
that the drug of choice is ibuprofen based
upon the actions of NSAIDs being to reduce
inflammation by the inhibition of the synthesis of
prostoglandins. However there is also evidence
to support the use of opiate based drugs such as
codeine in addition to ibuprofen.
Considering constrictive pericarditis there are
difficulties in reaching the correct diagnosis
as the condition mimics other conditions e.g.
restrictive cardiomyopathy. Without detailed
and comprehensive imaging it would be near
impossible for the ECP working within the
community to be able to reach the correct
diagnosis.
There is also evidence which suggests that
the differentiation between pericarditis and MI
can be difficult due to both conditions having
only subtle differences in presentation and also
the risk of pericardial effusion and or cardiac
tampanade as a result of pericarditis I believe
the evidence shows that it would unsafe for
patients to be treated within the community and
not reviewed and monitored within a hospital
environment.
The evidence is clear that the ECP should refer
patients who they suspect to have pericarditis
to an appropriate secondary care facility. In
line with local guidelines and agreements this
referral may be via acute medicine or direct to
cardiology. JPP
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07/04/2017 12:16
 Clinical
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