Pericardial Disease Flashcards

1
Q

how are most acute pericarditis cases diagnosed and treated (generally)?

A

acute pericarditis = 1-3 weeks duration

most cases considered idiopathic, but are presumed viral in origin (echovirus, coxsackievirus, adenovirus)

treated for symptoms of pericarditis, not root cause (usually doesn’t change management)

could also be bacterial, mycobaterium (MTB), HIV, fungal (histoplasmosis, coccidiomycosis)

can also be non-infectious (various causes)

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2
Q

how do patients with acute pericarditis present (2), and what are the clinical findings (3)?

A
  1. chest pain - pleuritic, relieved by leaning forward/worse lying down, radiates to trapezius ridge
  2. fever

findings:
1. pericardial friction rub - 3 components - ventricular systole, early diastolic filling, atrial contraction
2. widespread ST elevation - not fitting specific distribution of coronary artery (NOT ischemia)
3. PR segment depression

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3
Q

Pt is a 45yo M who recently underwent cardiac surgery, presenting with chest pain that is relieved by leaning forward, and worse while lying down, such as during the night. PE is remarkable for temperature of 101F and a friction rub. ECG reveals widespread ST elevation.

What is going on?

A

acute pericarditis: variety of causes (infectious and non-infectious), including post cardiac surgery

present with chest pain (as described), fever, pericardial friction rub, and widespread ST elevation + PR segment depression

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4
Q

hydralazine, isoniazid, and procainamide are similar in that they can also cause this acute heart condition, which presents with widespread ST elevation.

what is?

A

acute pericarditis: present with chest pain + fever, pericardial friction rub, widespread ST elevation + PR depression

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5
Q

how is acute pericarditis medically managed?

A

NSAIDs (1-2 weeks) and colchicine (3 months)

avoid steroids because they increase relapse/recurrence (unless you really need them)

also restrict physical activity

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6
Q

what is a possible complication of acute pericarditis due to scarring?

A

constrictive pericarditis - requires surgical intervention

*also note recurrent (relapsing) pericarditis is common

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7
Q

how will the clinical findings of acute pericarditis change if pericardial effusion develops?

A

[acute pericarditis - friction rub]

pericardial effusion - muffled heart sounds, reduced intensity of pericardial friction rub, Ewart sign (dullness over posterior L lung)

if severe: “water bottle” heart on CXR, electrical alternans (of QRS) on ECG

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8
Q

what is an Ewart sign in the evaluation of pericardial effusion?

A

dullness over posterior L lung

pericardial effusion presents with muffled heart sounds, Ewart sign, reduced intensity of pericardial friction rub, “water bottle” heart on CXR

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9
Q

what does electrical alternans represent on ECG, and what would this be caused by?

A

electrical alternans: alternating amplitude of QRS due to heart swinging back and forth in fluid due to pericardial effusion

not a common finding (would have to be severe pericardial effusion)

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10
Q

considering the pressure-volume relationship of the pericardium, when does cardiac tamponade start to develop when there is pericardial effusion?

A

pericardium is fibrous/acellular - has a limit of how far the collagen/elastin can stretch

once pressure reaches a threshold of what the pericardium can handle (dependent on volume, rate of fluid accumulation, and compliance of pericardium), pressure sky-rockets and cardiac tamponade develops (slope is straight up)

so you can imagine that if there is rapid effusion, cardiac tamponade will be reached sooner than if there is slower effusion, because the slope will be steeper

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11
Q

describe how high pericardial pressure affects the right and left sides of the heart, respectively

A

primary effect of high pericardial pressure is to impede the ability of the right side of the heart to fill

therefore, effects on the left side are largely due to under-filling

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12
Q

what are the clinical findings associated with cardiac tamponade? (2)

A

Beck’s Triad: hypotension, muffled heart sounds, elevated JVD

pulsus paradoxus: exaggerated drop in systemic BP during inspiration (more filling on inspiration, but increase in RV size in turn decreases LV size because the heart is being squeezed)

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13
Q

how does cardiac tamponade affect cavity pressures in the heart? why does this occur?

A

elevated and equal intracavitary pressure - the heart is being squeezed from all sides, so every cavity will hit the same limit of how much it is able to expand

—> low transmural filling pressure and low cardiac volumes, pulsus paradoxus (very low systemic BP on inspiration)

also causes RV collapse

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14
Q

Pt is a 77yo M in the ICU following an MI 3 days ago. During rounds, you notice they are showing signs of dyspnea and tachycardia. Upon examination, you note elevated JVP and pulsus paradoxus.

What is going on? Bonus if you can determine what caused this. Extra bonus if you know what should be done next.

A

cardiac tamponade, following rupture of LV (post-MI complication) - requires urgent pericardiocentesis

give-aways: dyspnea + elevated JVP (jugular venous pressure) + pulsus paradoxus

note the classic Beck’s Triad (hypotension, muffled heart sounds, elevated JVD) would also be a give-away

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15
Q

in the curve of atrial filling pressure, what does the a, c, x, v, and y wave present?

A

a wave = atrial systole

c wave = ventricle is starting to contract, moving tricuspid down, increasing RA pressure

x descent = decrease in pressure after atrial contraction

v wave = rapid filling of atrium when tricuspid is closed

y descent = AV valves open, blood rushes into ventricle

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16
Q

why does cardiac tamponade cause loss of the y descent in JVP/atrial pressure recordings?

A

y descent = AV valves open, blood rushes into ventricle

cardiac tamponade squeezes heart, so even as blood leaves atrium its pressure is high because of the physical restriction placed on it

17
Q

management of cardiac tamponade requires urgent pericardiocentesis, but what should be done if this procedure can’t be preformed right away?

A

give intravenous saline + isoproterenol to increase force of cardiac contraction (beta1/2 agonist)

18
Q

a patient is presenting with reduced CO (hypotension + reflex tachycardia), elevated systemic venous pressure (JVD + peripheral edema), pericardial knock (early diastolic sound at apex), Kussmaul sign (inspiratory increase in venous/RA pressure), and prominent x and y descents in atrial pressure wave - what does this collectively indicate?

A

constrictive pericarditis: end stage of pericarditis

pericardial knock = rapid filing of ventricle, due to y descent

x descent = decrease in pressure after atrial contraction
y descent = AV valves open, blood rushes into ventricle

all due to constriction/pressure of heart chambers

19
Q

contrast the nature of how cardiac tamponade vs constrictive pericarditis cause an increase in heart pressure - how do they each alter the atrial pressure recording?

A

cardiac tamponade: heart is being squeezed by pericardial fluid, more filling on inspiration causes increase in RV size that then takes up space, decreasing LV size —> pulsus paradoxus (big drop in BP on inspiration), loss of Y descent

constrictive pericarditis: inflammation of pericardium, can’t get more filling on inspiration because force cannot be transmitted —> Kussmaul sign (paradoxical rise in RA pressure during inspiration), steep x and y descent (M/W sign)

x descent = decrease in pressure after atrial contraction
y descent = AV valves open, blood rushes into ventricle

20
Q

why does a Kussmaul sign occur with constrictive pericarditis?

A

Kussmaul sign = paradoxical rise in RA pressure during inspiration

normally, inspiration increases venous return to heart and RA pressure goes down (due to compliance)

however with constrictive pericarditis, inflammation is preventing compliance of the heart chambers and force transmission - so RA pressure/venous pressure rises with inspiration

21
Q

how does cardiac tamponade alter ventricular pressure recordings?

A

ventricular pressure tracing shows “square root” or “dip and plateau” - due to rapid filling as soon as AV valves open

22
Q

how is pericardial constriction treated?

A

pericardial constriction can only be treated via pericardiectomy (removal of pericardium)

high mortality risk, MUST differentiate from restrictive cardiomyopathy (such as that caused by amyloids)

23
Q

cause of cardiac tamponade vs constrictive pericarditis

A

cardiac tamponade: accumulation of pericardial fluid under high pressure which compresses cardiac chambers (esp. RA and RV), often with resultant shock

constrictive pericarditis: late complication of pericarditis, resulting from thickening of pericardium which restricts filling of the heart