Myocarditis

Warning

Objectives

To outline the management of patients presenting to deployed medical facilities with symptoms consistent with myocarditis. 

Scope

This guideline intends to cover the initial investigations and management of patients presenting to the deployed medical treatment facilities with suspected and then confirmed acute myocarditis. It confirms the definition of myocarditis, typical presentation, management, and onward care. It does not include specific drug dosing which can be found in the formulary section of CGOs. Complications can include cardiogenic shock and this should therefore be read in conjunction with the “shock” guideline.  

Audience

This guideline is intended for use by registered healthcare professionals fulfilling a general role in a forward medical location or in an Emergency Department on deployed operations 

Initial Assessment & Management

Myocarditis: Inflammatory disease of the myocardium. In developed world most commonly due to viral infections*, occasionally due to autoimmune disorders or toxins e.g. cocaine or amphetamines. A spectrum ranging from mild chest pain with troponin elevation but no reduction in cardiac function, to fulminant myocarditis requiring mechanical circulatory support or transplantation.  

Myo-pericarditis: Pericarditis with associated myocardial inflammation and biomarker evidence of myocardial injury (raised troponin) – see pericarditis guideline 

*In developing countries, other infectious causes (most commonly tuberculosis) are more common than viruses. 

Diagnostic criteria

Multiple diagnostic criteria exist for myocarditis, but all hinge on imaging tests and tissue sampling (echocardiography, cardiac MRI, and endomyocardial biopsy - EMB) that are not available in the deployed setting.  Diagnosis is therefore pragmatic, and treatment supportive.  In the absence of such definitive tests in the deployed setting, in many cases it will not be possible to definitively distinguish between myocarditis, myopericarditis, and even NSTE-ACS. 

History is therefore of utmost importance in suggesting the diagnosis

History: 

Key historical features that raise suspicion for myocarditis include:

  • A recent viral illness or febrile episode within the preceding weeks, often accompanied by symptoms such as myalgia, fatigue, or upper respiratory tract infection.
  • Preceding gastrointestinal or systemic infections can point toward an infectious or immune-mediated aetiology.
  • Chest pain that is pleuritic or positional may suggest myopericarditis rather than isolated myocarditis, whereas pain resembling angina might suggest a coronary cause. 
  • Dyspnoea out of proportion to chest pain, particularly in a previously fit individual, should prompt consideration of myocardial involvement.
  • A history of palpitations or syncope may indicate arrhythmic complications, 
  • Absence of traditional cardiovascular risk factors (e.g., hypertension, diabetes, smoking) in a patient presenting with chest pain and troponin elevation should also raise suspicion for myocarditis over ACS.

In the deployed setting, these historical clues become critical in suggesting a diagnosis and considering treatments that may require definitive treatments rather than supportive ones. Management of myocarditis is supportive. 

Initial Presentation 

Clinical presentation highly variable, can include- 

  • Chest pain 
  • Features of heart failure  
  • Palpitations/arrhythmias 
  • Syncope 
  • Breathlessness 

 

Initial Investigations R1 – R3 

Routine observations: BP, pulse, O2 sats - may be tachycardic and hypotensive 

12 lead ECG: Non-specific changes which can include: 

  • ST elevation or depression, T wave inversion  
  • QRS prolongation 
  • Atrioventricular block 
  • Tachycardia 

 

Initial Management:  

Warning - High risk of haemodynamic instability and life-threatening arrhythmias.  

 

Management is supportive, treating complications 

  • All patients require continuous cardiac monitoring due to the risk of brady and tachyarrhythmias  
  • Observe for signs of low cardiac output state/cardiogenic shock: 

Clinical signs (bedside) 

Vital signs / simple investigations 

Altered mentation, agitation, reduced GCS 

MAP <65 mmHg, SBP <90 mmHg, Narrow pulse pressure (e.g. <25 mmHg); tachycardia >100 bpm  

Cool, mottled peripheries, central capillary refill >3 s, weak pulses, narrow pulse pressure with raised JVP 

Monitor urine output: oliguria <0.5 mL/Kg/hr

LV failure: Dyspnoea, tachypnoea, orthopnoea, new basal crackles 

ECG: ventricular arrhythmias, new high-grade AV block, diffuse ST-T changes 

Signs of RV failure (hepatomegaly, oedema) 

 

 

Chest pain, palpitations, syncope/presyncope 

 

 

fluid unresponsive hypotension 

 

 

 

  • Heart failure secondary to myocarditis should be managed as per standard acute heart failure treatment:  

Oxygenation: sats >92%

Perfusion:  Ensure euvolaemia with clinical assessment.  hypotension despite optimal management requires prioritisation of escalation to the next tier of care. 

Decongestion: Oral diuretics may help with early offload, but the mainstay would be evacuation for Role 2+ for intravenous Diuretic therapy.

Myopericarditis should be managed as per pericarditis – see separate guideline  

Patients should be urgently transferred to a role 2/3 setting to facilitate optimal supportive care. 

Advanced Assessment & Management

Investigations on arrival to R3:

Bloods: FBC, U+Es, LFTs, cardiac enzymes as available (Troponin - binary at role 2, quantitative iStat available in some modules: discuss with deployed biochemist), lactate 

CXR: assess for signs of heart failure, size of cardiac shadow 

POCUS: Bedside echo if available in clinical setting – reduced LVEF at presentation biggest predictor of outcome 

As at role 1, thorough clinical and biochemical evaluation should be repeated depending on available skillsets and biochemical tests: Tests expected to be newly available at a higher level of care highlighted in red. 

 

Clinical signs (bedside) 

Vital signs / biochemical / simple investigations 

Altered mentation, agitation, reduced GCS 

MAP <65 mmHg, SBP <90 mmHg, Narrow pulse pressure (e.g. <25 mmHg); tachycardia >100 bpm  

Cool, mottled peripheries, central capillary refill >3 s, weak pulses, narrow pulse pressure with raised JVP 

Monitor urine output: oliguria <0.5 mL/Kg/hr; rising creatinine 

LV failure: Dyspnoea, tachypnoea, orthopnoea, new basal crackles 

CXR (if available) with pulmonary oedema 

Signs of RV failure (hepatomegaly, oedema) 

 

ECG: ventricular arrhythmias, new high-grade AV block, diffuse ST-T changes 

Chest pain, palpitations, syncope/presyncope 

 

Positive / rising troponin (at role 2, tests are binary. some deployed modules also carry quantitative iStat capability; enquire to deployed biochemist), lactate ≥2 mmol/L (and/or rising), worsening acidosis; rising transaminases 

fluid unresponsive hypotension 

 

Echocardiography: if skillset is available, echocardiography may help exclude regional wall motion abnormalities consistent with coronary territory, supporting a more global or non-territorial dysfunction.

 

Management remains supportive:

Oxygenation: sats >92%, Hb >80g/L. If available, CPAP may effectively support blood pressure and improve oxygenation.  

Perfusion:  Ensure euvolaemia. If hypotensive despite optimal fluid management, discuss with critical care for consideration of vasopressors +/- inotropes. 

Decongestion:  IV furosemide 40-80mg IV, to target urine output of >0.5ml/kg/hr.  If anuric discuss with critical care. 

Patients should be urgently transferred to a role 2/3 setting to facilitate optimal supportive care. ALL cases will require evacuation to R4 to undertake specialist investigations including Coronary angiography and Cardiac MRI which will help to confirm the diagnosis.  

 

ALL cases will require evacuation to R4 to undertake specialist investigations including Coronary angiography and Cardiac MRI which will help to confirm the diagnosis.  

Prolonged Casualty Care

If the patient is clinically stable, perfusing, not congested or shocked, then the safest default is to continue supportive care. This includes strict exertion restriction, analgesia, rhythm surveillance, and prioritisation of evacuation for definitive investigations. 

If the patient has a convincing phenotype of heart failure: dyspnoea/orthopnoea, pulmonary congestion, then decongestion with diuretics is sensible.  Starting other heart failure pillar medication is best considered in conjunction with advice from cardiologists via reach back.

Service personnel with confirmed myocarditis should be referred to a service cardiologist to guide further investigations and determine safe return to exercise which will be a minimum of 3-6 months.  

Last reviewed: 16/02/2026

Next review date: 16/02/2027

References

 

Adler Y, et al. 2015 ESC Guidelines for the diagnosis and management of pericardial diseases: The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology 

Pelliccia A, et al. 2020 ESC Guidelines on sports cardiology and exercise in patients with cardiovascular disease: The Task Force on sports cardiology and exercise in patients with cardiovascular disease of the European Society of Cardiology 

Caforio ALP, et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. European Heart Journal. 2013; 34 (33): 2636–48 

Ammirati E, et al. Management of Acute Myocarditis and Chronic Inflammatory Cardiomyopathy: An Expert Consensus Document. Circulation: Heart Failure. 2020; 13 (11): e007405.