Myocarditis & Pericarditis Flashcards

1
Q

Name infective organisms that can cause myocarditis from the following classifications [2]

Viral [5]
Bacterial [4]
Spirochaete [1]

A

viral:
- HIV
- Coxsackie B
- Influenza A
- Herpes virus 6
- Parvovirus B-19

Bacterial:
- Diptheria
- Streptoccous A (rheumatic fever)
- Clostridia
- TB

Spirochaete:
- Lyme disease

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2
Q

Which protozoa can cause myocarditis? [2]

A

Chagas’ disease
toxoplasmosis

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3
Q

Which chemotherapeutic drugs may cause myocarditis? [2]

A
  • Doxorubicin
  • Trastuzumab (also known as Herceptin)
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4
Q

Describe the pathophysiology for:

  • Viral myocarditis [2]
A

In the case of viral myocarditis, the mechanisms proposed are:
* Direct cellular injury resulting from viral infection
* Immune response arising from the viral proteins intracellularly

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5
Q

Describe the process of radiation causing myocarditis and potential further complications [3]

A

Radiotherapy:
- Causes inflammation that progresses to myocardial or pericardial fibrosis; fibrosis related CAD and/or valve abnormalities

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6
Q

Which is the most common cause of myocarditis

Viral
Bacterial
Spirochaete
Protozoa

A

Which is the most common cause of myocarditis

Viral
Bacterial
Spirochaete
Protozoa

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7
Q

Describe the clinical presentation of a patient with myocarditis

A
  • Chest pain
  • Systemic features (fatigue, fevers)
  • SOB
  • Reduced exercise tolerance
  • Palpitations (could be triggered by arrythmias)
  • Collapse (arrhythmias leading to low output cardiac state)
  • Sudden death

The is often a history of a recent preceding viral infection, which may be upper respiratory or gastrointestinal.

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8
Q

What sign might indicate myocarditis on ascultation of heart? (if they have concurrent pericarditis) [1]

A

On auscultation of the heart, a pericardial friction rub may be heard in patients with concurrent pericarditis and a pansystolic murmur may be present in patients with functional mitral regurgitation

A pericardial friction rub is a grating, to-and-fro sound produced by friction of the heart against the pericardium. This sounds similar to sandpaper rubbed on wood.

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9
Q

What blood results would indicate myocarditis? [3]

A

↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP

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10
Q

Which autoimmune diseases (and tests used) would you conduct to rule out autoimmune disesaes when investigating myocarditis? [4]

A

Anti-nuclear antibodies (if positive, may suggest an underlying autoimmune aetiology)
Rheumatoid factor (if positive, may suggest rheumatoid arthritis)
Serum ACE (if positive, may suggest sarcoidosis)
Ds-DNA (if positive, may suggest systemic lupus erythematosus )

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11
Q

What would an ECHO help determine in a patient with myocarditis? [1]

A

Confirm whether there is any evidence of pericardial effusion and if present, whether this is causing any degree of cardiac tamponade, which may suggest the effusion should be drained.

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12
Q

What ECG changes would indicate myocarditis [3]

A
  • tachycardia
  • Prolonged QRS
  • QT prolongation
  • Diffuse T wave inversion

Can trigger arrhythmias

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13
Q

What are the potential complications of myocarditis? [2]

A

Complications
* heart failure
* arrhythmia; frequent premature ventricular complexes, irregular and polymorphic VT, or ventricular fibrillation possibly leading to sudden death
* dilated cardiomyopathy: usually a late complication

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14
Q

What are differential diagnoses for myocarditis? [5]

A

Myocardial ischaemia secondary to vasospasm or infarction

Aortic dissection

Sudden cardiac death of another cause e.g. long QT syndrome

Pericarditis

Takotsubo cardiomyopathy

Cardiomyopathy

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15
Q

How would you differentiate between myocarditis to the following:

Aortic dissection

Pericarditis

A

Aortic dissection:
- tearing chest pain radiating to the back (as opposed to the more generalised pain typically described in myopericarditis)

Pericarditis
- usually presents with chest pain, typically described as dull, central and relieved by sitting forwards
- Pericarditis patients should NOT exhibit the raised cardiac enzymes found in myocarditis patients
- Echocardiogram should demonstrate clear differentiation between pericarditis and myocarditis with associated pericarditis.

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16
Q

How would you treat myocarditis? [6]

A

Maintsay is supportive managment:

  • Oxygen where required.
  • Monitoring for and control of any underlying arrhythmias.
  • Fluid balance management.
  • Treat underlying cause if any identified.
  • Early escalation to specialist intensive care physicians
  • Organ support as required.
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17
Q

What treatment is given to patients with suspected giant cell myocarditis? [1]

A

In patients with suspected giant cell myocarditis, steroids are recommended and have been shown to improve survival

E.g. methylprednisolone

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18
Q

Define pericardial effusion [1]

Define pericardial tamponade [3]

A

Pericardial effusion is when the potential space of the pericardial cavity fills with fluid. This creates an inward pressure on the heart, making it more difficult to expand during diastole (filling of the heart).

Pericardial tamponade
* Pericardial effusion is large enough to raise the intra-pericardial pressure.
* This increased pressure squeezes the heart and affects its ability to function: it reduces heart filling during diastole, decreasing cardiac output during systole.
* This is an emergency and requires prompt drainage of the pericardial effusion to relieve the pressure.

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19
Q

Explain the effect of cardiac tamponade on chamber pressures [2]

A
  • Because the pericardial sac isn’t very compliant, when it becomes full of liquid it doesn’t expand much
  • Therefore the pressures inside the heart chambers equalise as the ventricles have less room to fill during diastole
  • Therefore EDV, SV & BP decrease
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20
Q

Define pulsus paradoxus [1]
Explain what is meant by pulsus paradoxus in cardiac tamponade [4]

A

Pulsus paradoxus:
* Auscultation of heart sounds in the inspiration associated with a drop in systolic blood pressure of > 10 mmHg

Pathophysiology:
* During inspiration, get decrease in intrathoracic pressure
* However, in cardiac tamponade you have an increased return to RA (due to equalised chamber pressures)
* This means that increase in RV filling
* Causes expansion into septal side & into the LV
* Thereby reducing stroke volume and blood pressure.

21
Q

What are the triad (Beck’s) assocaited with cardiac tamponade? [3]

A

Classical features - Beck’s triad:
* Hypotension
* Raised JVP
* Muffled heart sounds

Other features:
* Dyspnoea
* Tachycardia
* An absent Y descent on the JVP - this is due to the limited right ventricular filling
* Pulsus paradoxus - an abnormally large drop in BP during inspiration
* Kussmaul’s sign - much debate about this
* ECG: electrical alternans

22
Q

What are key differences between constrictive pericarditis and cardiac tamponade with regards to: [4]

  • JVP
  • Pulsus paradoxus
  • Kussmauls sign
  • Features on CXR
A
23
Q

Define acute pericarditis [1]

A

Acute pericarditis is a condition referring to inflammation of the pericardial sac, lasting for less than 4-6 weeks.

24
Q

Describe the major clinical feature of acute pericarditis

A

Retrosternal chest pain (85-90%)
* Usually sharp and pleuritic in nature
* Improved by sitting up and leaning forward
* Radiation to the trapezius ridge

Pericardial friction rub (≤33%)
* Superficial, scratchy or squeaky quality on auscultation, best heard using the diaphragm of the stethoscope
* Usually best heard at the left lower sternal border

25
Q

Describe the chest pain associated with acute pericarditis [5]

A

The chest pain is:

  • Sharp
  • Central/anterior
  • Worse with inspiration (pleuritic)
  • Worse on lying down
  • Better on sitting forward
  • Radiates to trapezius bridge
26
Q

What sign is thought to be is considered to be specific for pericarditis? [1]

A
  • Pain that has radiation to the trapezius ridge
27
Q

How can you differentiate between pericardial friction rub and retrosternal chest pain? [11]

A
  • pericardial friction rub can be differentiated from pleural rub by asking patient to hold their breath
  • Superficial, scratchy or squeaky quality on auscultation
28
Q

What are the ECG changes associated with acute pericarditis? [3]

A
  • Widespread concave / saddle shaped ST-elevations with PR-segment depression
  • PR-segment depression is 85% specific for acute pericarditis, but not sensitive
  • T-wave changes may last for weeks after resolution of symptoms but are of no clinical significance
29
Q

Describe the blood changes seen in acute pericarditis [3]

A

C-reactive protein, ESR, FBC
* Elevated inflammatory markers have a 90% sensitivity and may support the diagnosis of acute pericarditis
* Can also be used to monitor progress

Serum troponins
* Elevation suggests myocardial involvement (‘myopericarditis’) and indicates a poorer prognosis

Urea
* Elevation suggests uraemic aetiology of the pericarditis

30
Q

Mild [] seen in 60% of patients when performing an ECHO of a patient with acute pericariditis [1]

A

Mild pericardial effusion seen in 60% of patients

31
Q

When is pericardiocentesis indicated in pericarditis? [2]

A

Pericardiocentesis is only indicated where there is suspicion of a bacterial or neoplastic aetiology.

It may also be done as a therapeutic intervention for a large pericardial effusion.

32
Q

What are the differential diagnoses for pericarditis? [3]

A
  • Myocarditis
  • Acute coronary syndromes
  • Pulmonary embolism
33
Q

Describe how you would differentiate between these pathologies and pericarditis [3]

  • Myocarditis [2]
  • Acute coronary syndromes [2]
  • Pulmonary embolism
A

Myocarditis:
* patients will myocarditis alone will not exhibit ST-elevation on ECG

Acute coronary syndromes
* pleuritic chest pain is typically described differently, with exacerbation on inspiration and lying supine (for pericarditis)
* ECG is critical for diagnosis

Pulmonary embolism
* risk factors for PE (recent travel, immobility, surgery) are typically different from those of pericarditis.

34
Q

How would you diagnose myopericarditis? [1]

A

If patients have elevated cardiac enzyme biomarkers with widespread ST-elevation on ECG, this is a diagnosis of myopericarditis

35
Q

FYI

A

Elevated cardiac biomarkers indicate myocarditis

36
Q

Describe the managment of pericarditis [3]

A
  1. NSAIDs are the mainstay of treatment (e.g., aspirin or ibuprofen)
    AND Colchicine (taken longer-term, e.g., 3 months, to reduce the risk of recurrence)
  2. Steroids may be used second-line, in recurrent cases or associated with inflammatory conditions (e.g., rheumatoid arthritis)

strenuous physical activity should be avoided until symptom resolution and normalisation of inflammatory markers

37
Q

The main consequence of chronic pericarditis is development of [].

A

The main consequence of chronic inflammation of the pericardium is development of constrictive pericarditis.

38
Q

Describe the pathophysiology of constrictive pericarditis

A

Chronic inflammation leads to scarring and loss of the normal fibroelastic pericardial tissue. This can impede normal cardiac filling leading to features of right heart failure (raised JVP, peripheral oedema, tender hepatomegaly, exercise intolerance).

39
Q

Patients with constrictive pericarditis typically present with symptoms related to what? [1]

A

Patients characteristically present with features of right heart failure.

Symptoms
* Shortness of breath
* Leg swelling
* Abdominal swelling
* Exercise intolerance

Signs
* Raised jugular venous pressure
* Peripheral oedema
* Ascites
* Hepatomegaly

40
Q

What is the most common mechanism resulting in heart failure in patients with myocarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

A

What is the most common mechanism resulting in heart failure in patients with myocarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

41
Q

What is the most common mechanism resulting in heart failure in patients with constrictive pericarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

A

What is the most common mechanism resulting in heart failure in patients with constrictive pericarditis?

High-output heart failure
Low-output heart failure
Systolic dysfunction
Diastolic dysfunction

42
Q

A patient presents with

Recent viral illness, pleuritic chest relieved by sitting forwards, PR depression, ST elevation

What is the most likely diagnosis? [1]

A

Acute pericarditis

43
Q

A 60-year-old man with a history of tuberculosis presents with dyspnoea and fatigue. On examination the JVP is elevated, there is a loud S3 and Kussmaul’s sign is positive. Hepatomegaly is also noted is a stereotypical history of? [1]

A

Constrictive pericarditis

44
Q

Which heart sound is likely heard in constrictive pericarditis

S1
S2
S3
S4

A

Which heart sound is likely heard in constrictive pericarditis

S1
S2
S3
S4

45
Q

What is Kussmaul’s sign? [1]

A

Increased jugular venous pressure with inspiration

46
Q

Name the ECG alteration shown [1]
What pathology is it pathognomic for? [1]

A

Electrical alternans
- Alternating loud and soft QRS complexes during to variation in fluid around the heart in each beat

  • is suggestive of cardiac tamponade
47
Q

What is the difference between Kussmaul’s sign and pulsus paradoxus? [2]

Which pathologies do they relate to? [2]

A

Kussmaul’s sign is typical of constrictive pericarditis, and is a raised JVP with inspiration

Pulsus paradoxus, which is an abnormally large drop in blood pressure (and stroke volume) caused by inspiration, and is typical of cardiac tamponade.

48
Q

What size pericardial effussion is classified as small, moderate and large? [3]

A

Small: < 1cm
Moderate: 1-2cm
Large: > 2cm