Diseases of pericardium Flashcards
Etiology of constrictive pericarditis
1) Idiopathic
2) Any etiology of pericarditis (e.g. irradiation, post surgical)
How does dip and plateau in the right and left ventricular pressure correlate with jugular venous pressure (RAP)?
The dip and plateau corresponds to the marked y descent. The y descent indicates right atrial emptying, which occurs rapidly and then abruptly stops, which makes the marked y descent that goes back up quickly. The dip and plateau is occurs because at the onset of diastole when mitral and tricuspid valves open, the right atrium dumps its blood to the ventricle but suddenly stops, creating a sharp increase in ventricular pressure.
What are the two ways in which post MI causes pericaditis? Why have these become rarer in recently?
1) Early type (few days after MI)- transmural infarction leads to spread of inflammation from epicardial surface of injured myocardium to pericardium.
2) Dressler’s syndrome: develops 2 weeks- several months after acute MI. Inflammation of pericardium due to transmural infarction ledas to exposure of pericardial antigens to immune system. This produces an autoimmune response in which antibodies against pericardial antigens form, which attacks the pericardium, leading to pericarditis.
What are the different mechanisms of pathogenesis of pericarditis? (3)
1) Hematogenous seeding during bacteremia or fungemia
2) Direct extension from a contiguous focus of infection (e.g. pneumonia)
3) Immune mechanisms
What is pulsus paradoxus and what condition is it strongly associated with?
Pulsus paradoxus indicates cardiac tamponade. This is an exaggerated decrease in systolic BP (more than 10 mmHg) during normal inspiration. In normal physiology, systolic blood pressure drops a little during inspiration. This is because expansion of thorax during inspiration causes intrathoracic pressure to become negative, facilitating venous return to the right side of the heart and diminished LV filling (IV septum gets pushed towards left). This decreases LV SV and systolic blood pressure. However, in pulsus paradoxus, due to the fluids compressing on the ventricles, when more blood returns to the RV during inspiration, there will be significant pushing of interventricular septum toward the LV, having a greater effect on LV filling. Thus, there is a stronger decrease in CO, decreasing systolic pressure even more.
Difference in cardiac tamponade vs. constrictive pericarditis in regards to pulsus paradoxus and Kussmaul sign.
Constrictive pericarditis: A little bit of pulsus paradoxus and presence of Kussmaul sign.
Cardiac tamponade: Presence of pulsus paradoxus, absence of Kussmaul sign.
What condition is pericardial knock heard and why?
Pericardial knock is heard in constrictive pericarditis. The pericardial knock is heard at the time of when S3 would be heard (right after AV valves open/ early diastole), when blood rushes into the ventricle. The pericardial knock is due to when the blood rushes into the ventricle, the ventricle is compliant but hits the “brick wall”, making the sound of the knock.
What is the typical EKG finding of pericarditis? (2)
1) Diffuse ST segment elevations except in V1 and aVR
2) PR segment depression
What is the jugular venous pressure curve in constrictive pericarditis and why?
Prominent y descent on RAP tracing. This is because as soon as tricuspid valve opens, RA quickly empties into RV and the RAP falls rapidly during the very brief period before filling is arrested by the “concrete” pericardium.
What condition shows a “dip and plateau” (square root sign) configuration in RV and LV pressure tracings and why?
This pattern is seen in constrictive pericarditis during early diastole. This is because during early diastole just after mitral and tricuspid valves open, there is blood flow from the atria to the ventricles; however, due to the “concrete” pericardium surrounding the heart, there is a sudden stop of filling, rising the pressure a little bit and staying there. At this point at the plateau during diastole, the LV and RV pressures are equal.
What is the most common cause of pericarditis?
Idiopathic; probably viral (Coxsackie virus, echo virus)
Etiology of cardiac tamponade
1) Pericarditis progression to cardiac temponade (e.g. neoplastic, postviral, uremic, post MI)
2) Acute hemorrhage into pericardium (blunt of penetrating chest trauma, rupture of LV following MI, complication of aortic dissection)
What is constrictive pericarditis?
End stage of pericarditis in which the inflammatory processes result in fibrosis, often calcification, and adhesion of parietal and visceral pericardium. This results in impedence of filling of all of the heart chambers. (Think of it as concrete around the heart)
What are the 4 findings of constrictive pericarditis in cardiac catheterization?
1) Elevation and equalization of diastolic pressures in each of cardiac chamers
2) Early diastolic “dip and plateau” configuration in RV and LV tracings
3) Prominent y descent in RAP tracing
4) Rise in RV systolic pressure and decline in LV systolic pressure during inspiration: due to negative intrathoracic pressure → increased venous return to right side of the heart but decreased return to left side (movement of IV septum).
Is Kussmaul sign seen in cardiac tamponade? Why or why not?
Not seen because during inspiration, right side of heart is still filled more in cardiac tamponade (at the expense of moving the IV septum towards the left ventricle). As a result, there will be no venous back flow of blood and therefore during inspiration, jugular vein will not be distended.
Explain the pathophysiology of how both cardiac tamponade and constrictive pericarditis lead to the same sx of heart failure and tachycardia.
Both cardiac tamponade and constrictive pericarditis results in an impaired diastolic filling of ventricles which leads to #1) Elevated venous pressures (as compromised cardiac chambers cannot accomdate normal venous return) and #2) Decreased stroke volume. As a result of #1, there will be systemic venous congestion, leading to JVD, hepatomegaly + ascietes, and peripheral edema (right heart failure sx). There will also be pulmonary venous congestion, leading to pulmonary rales (left heart failure sx). As a result of #2, there will be decreased CO, leading to hypotension and subsequent reflex tachycardia.
What is the pressure- internal volume relationship of a normal pericardium vs. chronic accumulation of pericardial effusion?
In normal a normal pericardium, initial increases in internal volume leads to only a small rise in pressure. However, after a certain point, the parietal pericardium doesn’t want to stretch further and as a result, even small change in volume shoots the pressure up.
In slow accumulation of volume in the pericardium, the pericardium gradually stretches; as a result, the pressure-volume curve shifts to the right, allowing it to take in much more fluid without changes in pressure. Even in this case, however, after a certain point, the pressure begins to go up rapidly.
What is the relationship between intrapericardial pressure, intracardiac filling pressures, and CO in cardiac tamponade?
As intrapericardial pressure increases, both the right and left heart’s intracardial filling pressures increase. The right side of the heart is affected first because it operates at lower pressures to begin with. As all of these pressures increase, they all go toward each other, and the end result is that the diastolic (filling) pressure of all of the chambers is equal to the intrapericardial pressure. As soon as they equalize, the cardiac output decreases significantly due to less filling.
How does pericardial knock, y descent, and diastolic filling curve correspond to each other?
Pericardial knock is heard at the lowest point of y descent. This correlates when ventricle abruptly hits the brick wall of pericardium and cannot fill as fast anymore. Thus, the diastolic fililng volume stops increasing fast and “plateaus.”
