Flashcards in pericardium Deck (27):
what kinds of diseases can affect the pericardium?
filled with fluid to a point where it impedes cardiac filling- tamponade
it can become an inelastic encasement (constriction)
pasically any microbe; TB; bacterial (rare but very aggressive). most are transient, resolve spontaneously, and are attributed to viral infections
also rhematoid disease, lupus
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
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
Signs and symptoms of tamponade
syptoms related to hemodynamic consequences- dyspnea, cough from J receptors in lungs.
bedside: pulsus paradoxus, elvated JVP, attenuation of y descent.
basically ruled out when pulsus paradoxus and JVP are normal
lab eval for cardiac tamponade
usually nothing on EKG, though electrical alternans possible
clear lungs with incr. heart size
What is pericardial constriction
imprisonment of the heart by dense and inelastic tissue (fibrosis, tumor, calcification)
causes of cardiac constriction
TB, idiopathic, post infection radiation or surgery malignancy
pathophysiology of cardiac constriction
hard to distend in diastole; hard to contract in systole
when systole is comple, heart springs back to prefered dimention- filling pressure plummets and y descent is accentuated
also true for x descent
JVP - rapidly rising and falling waves
both ventriles face a common resistance to inflow- equal end-diastolic pressures. flow impeded for latter 2/3 of diastole
Is pulsus paradoxus a part of cardiac constriction?
not really- inelastic pericardium shields the heart from respiration-dependent fluctuations
constancy of JVP with inspiration is called Kussmaul's sign
What do you see in a right ventricle pressure catheter with cardiac constriction?
square root sign:
pressure in early diastole plummets as the ventricle springs back to preferred position
then, pressure rises rapidly and plateaus as the pericardial limit is reached
this is a disease of the latter 2/3 of diastole- most inflow occurs in first 1/3, so tachycardia is enough to sustain cardiac output
DDx for right >> left CHF symptoms
pericardial disease, restrictive cardiomyopathy, diseases of the lung or pulmonary vasculature
symptoms of pericardial constriction
equal PCWP and JVP. no edema in lungs (they have lots of lymphatics), but periphery does suffer due to lack of lymphatics. See edema, ascites, cardiac cirrhosis with portal HTN.
PE in cardiac constriction
accentuated y descent
cardiac exam has a loud sound in early diastole (pericardial knock) that represents the rapid deceleration of blood flow into the ventricles- like an S3 gallop but higher pitch
How do you distinguish between hepatic cirrhosis and pericardial constriction?
both can cause liver cirrhosis and portal HTN
pericardial constriction will also have greatly elevated venous pressures