myocarditis and pericardial disease Flashcards

1
Q

what is myocarditis

A

inflammation of the myocardium

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2
Q

what are the 2 main types of triggers for myocarditis

A

external - infections (usually viral e.g. Coxsackie B, COVID), drugs;
internal (immune mediated) - hypersensitivity reaction to vaccines, autoimmune disease

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3
Q

what is the pericardium and what are the components

A

two-layered sac that encircles the heart - tough outer fibrous layer (parietal pericardium); inner serosal layer (visceral pericardium - same as outer layer of the heart); there is a small fluid filled space between the layers to allow for reduced friction during beating

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4
Q

3 main roles of the pericardium

A
  1. anatomical - anchors the heart in the thorax, fixes the heart through its ligamentous function;
  2. barrier - acts as a barrier to infection and reduced external friction;
  3. mechanical - limits sudden dilation of the heart, maintains ventricular complicance, aids atrial filling
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5
Q

3 diseases of he pericardium and how to treat them

A
  1. effusion (fluid) - drain/diuretics;
  2. pericarditis (inflammation) - anti-inflammatory;
  3. constriction (fibrosis, thickened, scarred) - surgery
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6
Q

what is the usual cause of acute pericarditis

A

vrial/idiopathic

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7
Q

what is the treatment for acute pericarditis

A

NSAIDs and colchicine; usually self limiting; corticosteroids as 2nd line

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8
Q

ECG changes in acute pericarditis

A

widespread saddle shaped ST elevation

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9
Q

what is cardiac tamponade and what can cause it (4)

A

a medical emergency where effusion compresses the cardiac chambers and limits the filling of the heart; common causes - neoplastic, postviral, uraemic, traumatic

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10
Q

what is beck’s tirade

A
  1. low blood pressure (weak pulse or narrow pulse pressure)
  2. muffled heart sounds
  3. raised jugular venous pressure
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11
Q

what determines whether pericardial effusion will result in fatal effects (tamponade) or not

A

the rate at which fluid accumulates - if it accumulates slowly then the pericardium has time to adapt and can become stretchy and so it takes more fluid to constrict the heart, if it rises rapidly then it only takes a small amount to compress the heart

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12
Q

pericardial effusion QRS

A

QRS compleses may be short and vary in height form beat to beat (electrical activity insulated)

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13
Q

what is the tamponade quadrad

A
  1. hypotension - pericardial effusion interferes w filling of the heart -> decr preload -> decr SV -> hypotension;
  2. tachycardia - compensatory mechanism to hypotension, heart cannot tolerate normal venous return in tamponade due to increased pressure on the chambers;
  3. raised JVP - venous circulation pressure rises due to decr ability of heart chambers to accomodate;
  4. pulses paradox - a decr of BP by >10 during inspiration (occurs with a smaller change in healthy individuals)
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14
Q

normal pulses paradox mechanism

A

when breathing in, venous return incr to right heart causing the RV to bulge out and => the septum to bulge into LV, reducing its volume => filling decr -> decr SV -> systolic BP decr

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15
Q

why is pulses paradox exaggerated in tamponade

A

RV can’t bulge out so septum bulges even more => LV filling is even more impaired

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16
Q

how is tamponade treated

A

pericardiocentesis - aspirate with pericardial fluid

17
Q

what is constrictive pericarditis

A

thickened scarred paricardium forms a rigid shell around the heart -> inhibits normal filling of chambers

18
Q

what causes clinical features on constrictive pericarditis

A
  1. incr systemic venous pressure (incr JVP, distended neck veins, peripheral oedema etc.)
  2. low CO (fatigue, low BO)
18
Q

what is kussmaul’s sign

A

incr JVP on inspiration (opposite to normal); KEY differential for tamponade

19
Q

what is pericardial knock

A

an early diastolic sound due to ventricles filling v rapidly and stopping rapidly bc expanded to max

20
Q

treatment for constrictive pericarditis

A

surgical removal of pericardium

21
Q

what is dressler’s syndrome

A

an autoimmune form of pericarditis that occurs 2-3 weeks following MI (reaction to MI antigens)

22
Q

what is perimyocarditis

A

inflammation extending to the myocardium, can be fibrous or effusive w purulent, serous or haemorrhagic exudate

23
Q

what are the main causes of pericardial disease (9)

A

infectious: bacterial, TB, viral;
non-infectious: autoimmune, cancer, metabolic, trauma, radiation, drugs

24
Q

what are the 4 types of myocarditis

A

Giant cell myocarditis A: severe myocardial necrosis and fibrotic
replacement of the cardiomyocytes with granulation tissue and fibrosis in
anterolateral left ventricular wall
B: a sharp demarcating border between vital and necrotic myocardium,
confirmed by additional immunohistochemical staining for myoglobin
C: inflammatory border, cells consisting of prominent multi-nucleated
giant cells, macrophages, lymphocytes, and eosinophilic granulocytes
seen in close proximity to vital myocardium;
D: immunohistochemical staining for complement 4d is positive in all
vessels: complement cascade activation