Pericardial Disease Flashcards
how are most acute pericarditis cases diagnosed and treated (generally)?
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)
how do patients with acute pericarditis present (2), and what are the clinical findings (3)?
- chest pain - pleuritic, relieved by leaning forward/worse lying down, radiates to trapezius ridge
- 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
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?
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
hydralazine, isoniazid, and procainamide are similar in that they can also cause this acute heart condition, which presents with widespread ST elevation.
what is?
acute pericarditis: present with chest pain + fever, pericardial friction rub, widespread ST elevation + PR depression
how is acute pericarditis medically managed?
NSAIDs (1-2 weeks) and colchicine (3 months)
avoid steroids because they increase relapse/recurrence (unless you really need them)
also restrict physical activity
what is a possible complication of acute pericarditis due to scarring?
constrictive pericarditis - requires surgical intervention
*also note recurrent (relapsing) pericarditis is common
how will the clinical findings of acute pericarditis change if pericardial effusion develops?
[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
what is an Ewart sign in the evaluation of pericardial effusion?
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
what does electrical alternans represent on ECG, and what would this be caused by?
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)
considering the pressure-volume relationship of the pericardium, when does cardiac tamponade start to develop when there is pericardial effusion?
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
describe how high pericardial pressure affects the right and left sides of the heart, respectively
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
what are the clinical findings associated with cardiac tamponade? (2)
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)
how does cardiac tamponade affect cavity pressures in the heart? why does this occur?
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
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.
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
in the curve of atrial filling pressure, what does the a, c, x, v, and y wave present?
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