pericardium Flashcards
what kinds of diseases can affect the pericardium?
pain- pericarditis
filled with fluid to a point where it impedes cardiac filling- tamponade
it can become an inelastic encasement (constriction)
pericarditis etiologies
pasically any microbe; TB; bacterial (rare but very aggressive). most are transient, resolve spontaneously, and are attributed to viral infections
also rhematoid disease, lupus
and uremia
metastatic disease, esp. from lung, breast, and lymphoma
or, inflammation of adjacent structures
basically always inflammed in acute MI and may become inflammed several weeks after MI as part of Dressler’s syndrome
symptoms of pericarditis
pain- similar to MI pain but often sharper. often pleuritic and position sensitive- worse supine. radiates like MI but may also go to the trapezius
signs of pericarditis
pathognomonic sign: pericardial rub. may be evanescent and position-dependent
widespread ST elevation and/or PR depression during first phase. usually downward convexity (downward convexity ST elevation also common among young African American men, but usually confined to precordial leads and without PR depression)
prognosis and treatment of idiopathic pericarditis
idiopathic and viral: good, though recurrences common
these kinds of pericarditis may be treated with NSAIDs and will run a self-limiting course
What determines severity of pericardial effusion?
largely determined by rate- slow effusions better tolerated than acute ones.
etiology of pericardial effusion
like pericarditis (TB, viral, bacterial, rheumatoid disease, mets), plus vol overload and CHF
some symptoms of pericardial effusion
tamponade
dysphagia, dyspnea or hoarseness form compression of adjacent structures, even in the absence of tamponade/hemodynamic probs
etiology of tamponade
any disease that can cause effusion can cause tamponade, though uncommon with myxedema (severe hypothyroid)
most effusions resolve without causing tamponade
malignancy is not the most common cause of effusion, but is the most freq cause of tamponade
pressure vol curves related to tamponade
pericardial sac has a slightly sub-atmospheric pressure until a critical vol is reached, and then the pressure rises rapidly. cardiac chamber pressures rise more gradually, but compliance curves become governed by pericardial sac pressures above a certain volume
pathophysiology of tamponade
as the pressures in the pericardial sac rise, the right ventricle (which has a thinner, more compressable wall) experiences higher right ventricular end-diastolic pressures. eventually, it will equal the left ventricular end-diastolic pressure. This is called tamponade and has a hemodynamic impact. There is an equalization of diastolic ventricular, atrial, and PCWP. Cardinal finding of tamponade.
What is the sequence of events once tamponade is present?
stroke volumes begin to fall off
sympathetic activation maintains cardiac output and bp. as tamponade worsens, RV and LV filling pressures rise, so stroke vol doesn’t increase.
what are the special physical findings of tamponade? explain JVP thing
attenuated y descent on JVP and pulsus paradoxus
this is a pan-diastolic compression of the heart, so filling the ventricles is impeded throughout diastole and must occur only when blood is leaving the heart. the y descent of the JVP is the fall in pressure that happens after systole is over and blood pours through the open tricuspid valve. this flow is impeded during tamponade, causing the disappearance of the y descent
explain pulsus paradoxus
exaggerated inspiratory fall of bp
basically, during normal inspiration, pleural pressures decrease, and air and blood rush into the thorax and right heart. somehow, this causes outward tug on left ventricle and increases afterload against which it must contract. so blood pressure normally falls by <10 mmHg during respiration.
if inspiration fall is greater than 10 mmHg, it is pulsus paradoxus. most commonly seen in people with obstructive lung disease (also raises afterlaod)
in tamponade, blood flows into right heart during inspiration. left heart has no place to got, so it becomes compressed. myofiber stretch decreases and LV contraction force goes down (Starling)
when isn’t pulsus paradoxus useful
A fib. extremely thick LV, weird cardiac outflow