LEARNING OUTCOMES
After completing this module, the paramedic will be able to:
This article will look at the pathophysiology, signs and symptoms/presentation and management of pericarditis. It will also examine the evidence and discuss the issues surrounding the need for hospital admission versus management within the community or primary care setting.
‘Pericarditis is inflammation of the pericardium, the protective sac that surrounds your heart. The pericardium has two layers (inner and outer) and can become inflamed if blood or fluid leaks between these two layers.’
The pericardium surrounds the cardiac muscle. It consists of two layers of tissue, encapsulating part of the aorta and vena cava (Knudson, 2011: 504). As well as protecting and restraining the heart, it determines cardiac filling by preventing the myocardium from becoming overstretched (Troughton et al, 2004: 718).
Pericarditis falls into two categories:
Evidence from the United States suggests that pericarditis is relatively rare, accounting for <1% of hospital admissions. It is most common in men aged 20–50 years, although it also occurs in women (Phelan et al, 2015).
Acute/uncomplicated pericarditis
The causes of pericarditis are thought to be viral, fungal or bacterial in nature; it may also present as a result of a myocardial infarction (MI). Longmore et al (2010: 148) suggest that the cause may be: idiopathic; secondary to viral (e.g. Coxsackie or influenza), bacterial (e.g. pneumonia) or fungal infection; following an MI; medication; or secondary to complex complaints such as uraemia in renal failure.
Both Longmore et al (2010: 148) and Wyatt et al (2008: 80) identify Dressler's syndrome as a cause of pericarditis. Dressler's syndrome is inflammation of the pericardial sac that occurs after trauma to the pericardium, for example after an MI or after surgery (Mayo Clinic, 2020).
The presenting signs and symptoms of pericarditis are chest pain, which may radiate to the arm and jaw, and a pericardial friction rub (a scratching or creaking sound produced by the layers of the pericardium rubbing over one another), heard on auscultation (Derrickson and Tortora, 2009: 720). However, auscultation of heart sounds may be unreliable because the pericardial rub is often being intermittent and elusive (Wyatt et al, 2008: 80).
Wyatt et al (2008: 80) further describe the symptoms as a left-sided or retrosternal chest pain made worse by deep inspiration, changing position, exercise and swallowing. Camm (1999: 727) suggests that the pain from pericarditis may be relieved by sitting forward and aggravated by lying prone or supine.
The patient may describe symptoms such as back and/or neck pain, a dry cough and anxiety or fatigue, as well as the classical chest pain (Phelan et al, 2015). Knudson (2011: 504) identifies shortness of breath on exertion in addition to the symptoms identified by Camm (1999) and Phelan et al (2015).
Patients with suspected pericarditis will present with 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. The chest pain may be pleuritic in nature (Rahman and Liu, 2011: 791).
Pyrexia above 38°C, subacute onset of symptoms, immunodepression, trauma, myopericarditis, severe pericardial effusion, cardiac tamponade and use of oral anticoagulant therapy, are all poor prognostic indicators and could be sign of more serious disease (Imazio et al, 2004: 1042).
There is evidence to suggest that pericarditis can lead to a number of electrocardiogram (ECG) changes. Camm (1999: 728) notes that, in the first week, the ECG will typically display ST segment elevation with a concave shape to the ST segment. This change is seen in readings from the anterior, inferior and lateral leads.
Rahman and Liu (2011: 792) identify the ECG changes that 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 the aVL. Changes will usually involve more than one cardiac territory.
Complicated pericarditis
Pericarditis can become complicated. One complication is pericardial effusion, which Dudzinski et al (2012: 81) describe as an accumulation of fluid within the pericardial sac.
This can have several aetiologies:
Pericardial effusion may have significant haemodynamic consequences as it reduces filling of the heart and may lead to cardiac tamponade (Dudsinki et al 2012: 83).
Cardiac tamponade occurs when blood or fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock. This is considered a medical emergency (Stashko and Meer, 2019.)
Shabetai (2004: 255) describes the haemodynamic effects of pericardial effusion as being in a spectrum from mild to life-threatening, which is supported by Dudzinski et al (2012: 83), who also suggest a link between pericardial effusion and cardiac tamponade.
Cardiac tamponade can be suspected during a clinical examination of the patient. Wyatt et al (2008: 340) describe Beck's triad, three medical signs associated with cardiac tamponade: raised jugular venous pressure, hypotension and muffled heart sounds. Imazio et al (2004: 1042) note that cardiac tamponade is a poor prognostic indicator in patients with pericarditis.
Constrictive pericarditis
Constrictive pericarditis is long-term (chronic) inflammation of the pericardium with thickening, scarring and muscle tightening/contracture (Yadav and Siddique, 2019). It involves a progressive fibrotic change in the pericardium that constricts the myocardium and impairs ventricular filling (Dato et al, 2008: 79).
Dato et al (2008: 79) also say it is difficult to reach the correct diagnosis because constrictive pericarditis has a similar presentation to restrictive cardiomyopathy.
Constrictive pericarditis cannot be diagnosed purely using clinical skills such as observation and auscultation of heart sounds; patients with a working diagnosis of pericarditis should undergo imaging such as X-ray and computed tomography (CT) or magnetic resonance imaging (MRI) scans to confirm the diagnosis (Young et al, 2012: 1099).
Management
Once the working diagnosis of pericarditis has been reached, the practitioner should formulate a treatment plan and consider the need for referral for expert opinion.
While considering the treatment and 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 managed.
Imazio et al (2004: 1042) suggest that uncomplicated pericarditis should have ‘a brief and benign’ course following treatment with oral non-steroidal anti-inflammatory drugs (NSAIDs).
Wyatt et al (2008) support the use of NSAIDs to treat chest pain. They also recommend bed rest and a referral to the cardiology team for review and advice regarding treatment. This implies that the patient should be admitted to hospital.
Gianni and Solbiati (2012) identify that up to 50% of patients are at risk of pericarditis recurrence. To prevent this, they recommend the use of colchicine. Colchicine, a drug normally used in the treatment of gout, is safe for patients who cannot take NSAIDs, as well as those on anticoagulant therapy, and has a lower risk of fluid retention than NSAIDs (National Institute for Health and Care Excellence (NICE), 2020).
The evidence regarding analgesia for patients with pericarditis refers to the use of NSAIDs. No specific research or evidence suggests the use of additional analgesia using opiate-based medications such as codeine or morphine sulphate preparations.
The Joint Royal Colleges Ambulance Liaison Committee (JRCALC) clinical guidelines (Association of Ambulance Chief Executives (AACE), 2019) advocate the use of morphine for the management of cardiac chest pain, specifically recommending the use the intravenous morphine to reduce pain and anxiety, as well as to lower the preload on the heart.
This is supported by Herlitz et al (2011); 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 et al (2019) name ibuprofen as the NSAID of choice for the management of pericarditis, as the drug decreases inflammation and reduces fluid accumulated in the pericardium. Ibuprofen works by acting on prostaglandins, which are involved in the inflammatory response. Ibuprofen inhibits the synthesis of prostaglandins, reducing the inflammatory response. Ibuprofen does this by interfering with the action of cyclooxygenase, an enzyme that catalyses the conversion of arachidonic acid into prostaglandic acid (Neupert et al, 1997: 490). This action is not specific to ibuprofen; all NSAIDs work in this manner.
Wedro et al (2019) also support the short-term use of narcotic analgesics such as codeine and morphine for the management of pain associated with pericarditis.
Research by Imazio et al (2004: 1043) suggests that patients who do not present with any poor prognostic indicators (and are therefore at low risk) can be safely managed out of hospital. Their research considered the cases of 254 low-risk patients and found that 87% of them were successfully managed at home; the other 13% of patients experienced complications and required hospital admission. The patients within this trial received a clinical examination, blood tests and imaging studies to support the diagnosis before a treatment plan was formulated and prior to discharge from a hospital as a day case.
A clinical directive by Black and Thompson for South Central Ambulance Service NHS Trust (2012) does not support caring for patients with chest pain at home, noting that all patients with non-traumatic or suspected cardiac chest pain should be reviewed in hospital; the differential diagnoses for non-traumatic chest pain mean that not doing this can have life-threatening consequences.
The suggestion of avoiding hospital admission made by Imazio et al (2004) is based on research from a United States study where the patients attended a day hospital for examination and assessment, and were discharged home for completion of treatment in the community. The UK-based evidence suggests that patients need to be assessed by specialist cardiology doctors. This cardiology assessment will require a visit to the emergency department at a minimum; in the author's experience, most patients will require admission to the medical assessment unit or cardiology ward for assessment and treatment. While the UK evidence does not state that a patient requires admission to hospital for tests to confirm the diagnosis, it implies a hospital visit is necessary.
For example, Wedro et al (2019) 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 patients to hospital. Practitioners should consider a referral direct to cardiology.
Chronic pericarditis and pericardial effusion
Pericarditis can be acute or chronic. The chronic presentation of pericarditis is linked to the slow build-up of fluid within the pericardial sac (Derrickson and Tortora (2009: 720). This slow build-up of fluid is called a pericardial effusion.
Pericarditis can become complicated by a pericardial effusion or by developing into constrictive pericarditis.
The management of constrictive pericarditis is discussed by Lin et al (2012), who note that surgical intervention is the definitive treatment for constrictive pericarditis. This work identifies that it is necessary to identify constrictive pericarditis quickly. While an emergency care practitioner (ECP) would not be able to provide a treatment, they could recognise it as a differential diagnosis.
While pericardial effusion cannot be managed by the ECP, they have the skills to be able to recognise it as a possible differential diagnosis based on findings from a cardiac assessment. The symptoms of Beck's triad and shortness of breath are the key features in the presentation of pericardial effusion (Salami et al, 2012: 407). Salami et al (2012: 408) note that the management of this condition requires a pericardial drain.
The ECP should consider pericardial effusion and constrictive pericarditis as possible differential diagnoses in young patients presenting with chest pain of a non-traumatic nature and refer the patient to an appropriate care centre.
Conclusion
A diagnosis of straightforward pericarditis may be within an ECP's scope of practice. It would be possible for an ECP to reach a working diagnosis and even to initiate treatment, which would predominantly consist of providing analgesia to make the patient more comfortable.
The evidence makes it clear that the drug of choice is ibuprofen, based on the actions of NSAIDs to reduce inflammation through the inhibition of the synthesis of prostaglandins. 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 such as restrictive cardiomyopathy. Without detailed and comprehensive imaging, it would be near impossible for the ECP working in the community to reach the correct diagnosis.
Differentiating between pericarditis and MI can be difficult as the differences in presentation are subtle. Given the risk of pericardial effusion and cardiac tamponade as a result of pericarditis, it would be unsafe for patients to be treated in the community and not reviewed and monitored in a hospital.
The evidence is clear that ECPs should refer patients who they suspect to have pericarditis to secondary care. In line with local guidelines and agreements, this referral may be via acute medicine or directly to cardiology. JPP