ECG Cases 46 ECG in Fever and Infectious Disease

In this ECG Cases blog we look at 10 patients who presented with fever and/or infectious disease and ECG changes. Can you make the diagnosis?

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. October 2023

10 patients presented with fever or infectious symptoms. What does the ECG show and how would you manage the patient?

Case 1: 70yo history AF with fever and cough. Febrile, tachycardic and hypoxic

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Case 2: 50yo with fever, cough diarrhea and weakness.

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Case 3: 55 year old one week fever/chills, dry cough and loss of taste, and 6 hours of chest pressure. Old and new

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Case 4: 60yo with 3 days fever, nausea and chest pain. Tachycardic and hypotensive

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Case 5: 65 year old recent URTI with exertional chest pain

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Case 6: 65 year old with a few days of fever and shortness of breath. Tachycardic but other vitals normal. Old then new ECG:

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Case 7: 35 year old previously healthy with palpitations, a month after having a rash after hiking. Normal vitals

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Case 8: 40 year old with 2 months of weight loss, chills and leg swelling, then sudden shortness of breath and flash pulmonary edema

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Case 9: 60yo, no cardiac/pulmonary history, with two days of shortness of breath without fever or cough, sent to ED for ‘pneumonia’ based on infiltrate on chest x-ray

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Case 10: 60 year old with one day of chest pain, fever and cough

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The ECG in fever and infectious disease

There are many ways in which fever or infectious disease can affect the heart.

1. Sepsis and demand ischemia

Just as septic patients can get tachycardic, septic patients with atrial fibrillation can develop rapid ventricular response. So the first step in patients with atrial fibrillation and rapid ventricular response is to identify and treat secondary causes including sepsis, rather than starting with rate/rhythm control. Similarly, sepsis is a common cause of demand ischemia[1], and is on the differential for diffuse ST depression with reciprocal ST elevation in aVR, a nonspecific sign of subendocardial ischemia.

2. Peri/myocarditis, diagnosis of exclusion

Pericarditis can follow viral infections, but it is a diagnosis of exclusion – first to exclude more dangerous causes of chest pain like Occlusion MI, second to exclude complications of pericarditis like myocarditis or tamponade, and finally to consider excluding the diagnosis altogether if the ECG simply represents normal variant ST elevation. We might assume that myocardial injury in the context of infectious disease is from demand ischemia (type 2 MI) or myocarditis. But infectious disease can also cause acute coronary occlusion (type 1 MI). As a recent review article explained, “the prothombotic, procoagulant state that is associated with acute infection further increases the risk of coronary thrombosis at sites of plaque disruption.”[2] This has also been seen with the COVID-19 pandemic. Patients with myocarditis can present with the same symptoms, ECG changes and troponin elevations of acute coronary occlusion, making myocarditis a post-angiographic diagnosis.[3,4]

3. Infectious AV block: endocarditis and lyme carditis

There are cardiac infections that are often initially missed because they present with nonspecific symptoms and ECG findings. These diseases and their risk factors are important to consider especially in the setting of AV block, where the treatment may be antibiotics or surgery rather than pacemaker. Infective endocarditis often presents with subacute constitutional symptoms, but can have sudden decompensation from acute valve failure. ECG may reveal new AV block from aortic abscess, but this is not sensitive.[5]

On the other hand, high-degree AV block is the most common presentation of Lyme Carditis, and resolves with antibiotics. Combining ECG interpretation with risk factor evaluation (eg outdoor activities, constitutional symptoms, tick bite, rash) is essential for an accurate diagnosis that can facilitate correct treatment and prevent unnecessary pacemaker.[6]

4. Non-infectious fever
   

Not all fever is from infectious disease: PE, malignancy, autoimmune conditions, hyperthyroidism, heat stroke, stimulants, and alcohol withdrawal are examples of other causes of low grade fever. These can also be associated with ECG changes, for example acute RV strain from PE.

5. Fever unmasking Brugada

Finally, fever can unmask the temperature-sensitive sodium channelopathy of Brugada syndrome. The resulting ST elevation in V1-2 might be mistaken as false positive STEMI, but pattern recognition and clinical correlation can help. Brugada pattern in the context of fever is important for diagnosis, treatment and prognosis. As the expert review explains, “Fever is a triggering factor for ventricular arrhythmias in BrS patients are increased temperature may unmask a BrS ECG pattern…Fever should be treated promptly…An important stratification is a fever-induced type 1 ECG, because patients exhibiting this feature show an intermediate risk for sudden death.”[7]

Back to the cases

10 patients presented with fever or infectious symptoms. What does the ECG show and how would you manage the patient?

Case 1: 70yo history AF with fever and cough. Febrile, tachycardic and hypoxic – with rapid ventricular response secondary to pneumonia/sepsis.

• Heart rate/rhythm: atrial fibrillation with rapid ventricular response and a PVC
• Electrical conduction: otherwise normal conduction
• Axis: normal axis
• R-wave progression: normal R wave progression
• Tall/small voltages: normal voltages
• ST/T changes: no significant ST/T changes

Impression: Atrial fibrillation with rapid ventricular response in the context of hypoxia and sepsis. Treated with fluids, oxygen, antibiotics – with resolution of tachycardia:

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Case 2: 50yo with fever, cough diarrhea and weakness – with diffuse ST depression and reciprocal ST elevation in AVR secondary to demand ischemia and hypokalemia.

• H: sinus borderline tachycardia
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: diffuse ST depression and flat T waves, with reciprocal ST elevation in aVR

Impression: subendocardial ischemia vs hypokalemia, in context of sepsis and diarrhea. Lactate was 8, potassium 2.9 and Magnesium 0.3, trop 3,000 ng/L (normal <26 in males and <16 in females) from demand ischemia. Next day ECG after fluid resuscitation and electrolyte replacement showed resolution of subendocardial ischemia:

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Case 3: 55 year old one week fever/chills, dry cough and loss of taste, and 6 hours of chest pressure – with LAD occlusion in the context of COVID.

• H: sinus tach
• E: normal conduction
• A: physiologic left axis
• R: loss of anterior R waves with new Q waves V2-5
• T: normal voltages
• S: ST elevation and hyperacute T waves V2-5. Baseline saddle back ST segment in V2

Impression: mid LAD occlusion with Q waves that could be acute or subacute but ongoing hyperacute T waves. Cath lab activated: 100% mid LAD occlusion (beyond first diagonal, so no lateral changes or inferior reciprocal changes). First trop only 1000 (so Q waves acute) and peak 90,000 ng/L. Tested positive for COVID. Echo mid to apical septum and apex severe hypokinesis. Discharge ECG showed ongoing loss of anterior R waves, and reperfusion T wave inversion:

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Case 4: 60yo with 3 days fever, nausea and chest pain. Tachycardic and hypotensive – from myocarditis diagnosed after angiography

• H: borderline sinus tach
• E: RBBB
• A: normal axis
• R: early R wave from RBBB
• T: normal voltages
• S: ST elevation and hyperacute T waves anterolateral and around apex to II, with mild reciprocal ST depression III

Impression: proximal LAD occlusion pattern in patient with fever and hypotension, with myocarditis as angiographic diagnosis of exclusion. Cath lab activated: normal coronaries. First troponin 40,000 and peak 250,000 ng/L. Diagnosed with fulminant myocarditis and cardiogenic shock, refractory to treatment, and died.

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Case 5: 65 year old recent URTI with exertional chest pain – from pericarditis provoking non-occlusive MI from triple vessel disease

• H: normal sinus rhythm
• E: normal conduction
• A: normal axis
• R: normal R wave
• T: normal voltages
• S: mild inferolateral concave ST elevation with reciprocal ST depression in avR only

Impression: ECG could be normal variant or pericarditis, but patient is 65 year old with exertional chest pain. First troponin was 100 but myocarditis is still diagnosis of exclusion. Angiogram revealed triple vessel disease, received multiple stents. Peak troponin 2,000 and echo showed pericardial effusion without regional wall motion abnormality. Discharge ECG had resolution of mild ST elevation:

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Case 6: 65 year old with a few days of fever and shortness of breath. Tachycardic but other vitals normal – with pericardial effusion and tamponade

• H: sinus tachycardia
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: new low voltage
• S: mild inferolateral T wave inversion

Impression: URTI/SOB with tachycardia and low voltage. This was not initially appreciated. Patient first had CXR showing bilateral pleural effusion, then CTPA that excluded PE but revealed large pericardial effusion. Cardiology consulted and found early tamponade. Admitted for pericardiocentesis and colchicine/aspirin for viral pericarditis, troponin normal. Discharge ECG showed normalization of heart rate and voltages:

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Case 7: 35 year old previously healthy with palpitations, a month after having a rash after hiking – with high grade AV block from lyme carditis

• H: sinus rhythm with 2^nd degree AV type 2, only QRS #3/6/9 are narrow complex and conduct from atria, the remaining are wide complex ventricular escape
• E: long PR for the conducted beats, and variable PR for the rest
• A: can’t tell axis because only escape beats at time of recording lead I
• R: normal R wave progression
• T: normal voltages
• S: T wave inversion V2-4, and secondary changes during ventricular escapes

Impression: high grade AV block with history of hiking and rash. Diagnosed as lyme carditis and treated with antibiotics, did not require pacemaker

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Case 8: 40 year old with 2 months of weight loss, chills and leg swelling, then sudden shortness of breath and flash pulmonary edema – from endocarditis with nonspecific ECG

• H: sinus tach
• E: normal conduction
• A: normal axis but S1
• R: normal R wave
• T: normal voltages
• ST: no ST/T changes

Impression: sinus tach in patient with flash pulmonary edema preceded by constitutional symptoms. Found to have severe mitral regurgitation and flail leaflet, and a vegetation from endocarditis. Treated with mitral valve replacement and antibiotics

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Case 9: 60yo, no cardiac/pulmonary history, with two days of shortness of breath without fever or cough, sent to ED for ‘pneumonia’ based on infiltrate on chest x-ray – with acute RV strain ECG changes from PE

• H: normal sinus
• E: normal conduction
• A: LAFB + dominant S in I
• R: delayed R wave progression
• T: normal voltage
• S: primary T wave inversion anterior (in V2 could be from high lead placement) + inferior

Impression: signs of RV strain. CT chest revealed PE, no pneumonia

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Case 10: 60 year old with one day of chest pain, fever and cough – with false positive STEMI from Brugada unmasked by fever

• H: sinus tach
• E: normal conduction
• A: normal axis
• R: normal R wave
• T: normal voltages
• S: coved ST elevation V1-V2

Impression: fever and Brugada pattern on ECG. Cath lab was activated for “STEMI” but there were no culprit lesions, and troponin was normal. Diagnosed with pneumonia and Brugada. Discharge ECG showed Brugad pattern type 2 (saddle back ST elevation with wide angle) in V2:

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Take home points for ECG in fever and infection disease

1. Sepsis is a common cause of rapid Afib and diffuse ST depression with reciprocal ST elevation in aVR
2. Myo/pericarditis is a diagnosis of exclusion
3. Endocarditis or lyme carditis can cause AV block
4. PE can cause low grade fever and ECG signs of acute RV strain
5. Fever can unmask Brugada syndrome

References for ECG Cases 46 – ECG in fever and infectious disease

1. Sandoval Y and Jaffe A. Type 2 myocardial infarction: JACC review topic of the week. JACC 2019 Apr 16;72(14):1846-1860
2. Musher DM, Abers MS, Corrales-Medina VF. Acute infection and myocardial infarction. NEJM 2019 Jan 10;380(2):171-176
3. Ammrati E, Friegerio M, Adler ED, et al. Management of acute myocarditis and chronic inflammatory cardiomyopathy: an expert consensus document. Circ Heart Fail 2020 Nov;13(11):e007405
4. Adler Y, Charron P, Imazio M, 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 (ESC) endorsed by: the European Association for Cardio-Thoracic Surgery (EACTS). Eur Heart J 2015 Nov 7;36(42):2921-2964
5. Baddour LM, Wilson WR, Bayer AS, et al. Infective endocarditis in adults: diagnosis, antimicrobial therapy, and management of complications. A scientific statement for healthcare professionals from the American Heart Association. Circulation 2015;132:1435-1486
6. Yeung C and Baranchuk A. Diagnosis and treatment of lyme carditis: JACC review topic of the week. J Am Coll Cardiol 2019 Feb 19;73(6):717-726
7. Brugada J, Campuzano O, Arbelo E, et al. Present status of Brugada syndrome: JACC state-of-the-art review. J Am Coll Cardiol 2018 Aug 28;72(9):1046-1059