Flashcards in Pericardial Disease Deck (20):
1. Describe the typical presentation, ECG and significant thoughts in diagnosis of pericarditis.
pleuritic pain (aggravated by inspiration and coughing and relieved by sitting forward)
evanescent pericardial rub (three phases: ventricular contraction, ventricular relaxation and atrial contraction)
diffuse ST elevation, depression of PR segment (lead 2)
additional tests include echocardiograph, TB test, serologic test for connective tissue disease and careful search for malignancy (pericardiocentesis only in those with large effusions)
3. Identify the most common and most serious cases of cardiac tamponade and when drainage of the pericardium is necessary.
cardiac tamponade, where pericardial fluid accumulates under high pressure, compresses the cardiac chambers and severely limits filling of the heart causes a decrease in ventricular stroke volume and cardiac out
the most common causes for acute pericarditis to progress to cardiac tamponade are neoplastic, post viral and uremic percarditis, also acute hemorrhage (trauma)
4. Discuss the pathophysiology of both cardiac tamponade.
as a result of the tense pericardial fluid, the heart is compressed and the diastolic pressure within each chamber becomes elevated and equal to the pericardial pressure and equalization of diastolic pressures (RA=LA=PCWP=LVEDP=RVEDP)
venous return to the heart is reduced and systemic and pulmonary venous pressures rise resulting in JVD and congestion and ultimately leading to inadequate organ perfusion as systolic SV and CO declines
drop in arterial pressure can trigger reflex tachycardia
Name the three apparent functions of the pericardium.
1. fixes heart with in mediastinum
2. prevents extreme dilation of heart during sudden rises of intracardiac volume
3. function as a barrier to limit spread of infection from adjacent lungs
however patients with absent pericardium are generally asypmtomatic
Discuss the possible infectious causes of pericarditis.
viral infection (echovirus or Coxsackie virus group B are the most common, others include flu, varicella, mumps, Hep B and infectious mono, and associated with HIV)
associated with TB in imunosuppressed, due to reactivation of TB organism in mediastinal lymph nodes, spreading into the lymph nodes
non-TB bacterial infection (pneumococcus and staphylococci frequently
Discuss the non-infectious causes of pericarditis
1. pericarditis following MI due to acute inflammation or Dressler's syndrome (autoimmune?)
2. uremic pericarditis as a complication of renal failure
3. neoplastic pericarditis (usually with hemorrhagic tamponade)
4. radiation-induced (esp +4,000 rads) due to local inflammatory response
5. connective tissue disease ie. SLE, rheumatoid arthritis and progressive systemic sclerosis
6. drug-induced (ie. procainamide or hydralazine, methyldopa, isoniazid, phenytoin)
2. Discuss the different types of pericarditis (4) and their basic characteristics.
serous pericarditis: exudate is thin fluid secreted by mesothelial cells
serofibronous pericarditis: exudate with plasma proteins, including fibrinogen (thickened and fused)
suppurative pericarditis: intense inflammatory response, erythematous and coated with purulent exudate
hemorrhagic pericarditis: bloody, most often from TB or malignancy
Discuss the treatment(s) for acute pericarditis.
idiopathic or viral pericarditis is self limited and runs its course in 1-3 weeks (rest and pain relief with NSAIDs; oral corticosteroids only in complicated cases)
MI related pericarditis: rest and aspirin
Purulent pericarditis requires aggressive tx. including catheter drainage and intensive antibiotic therapy
uremia requires intensive dialysis and neoplastic care is often just palliative
In addition to the setting of acute pericarditis, serous effusion may result from which conditions (3).
increased capillary permeability (severe hypothyroidism)
increased capillary hydrostatic pressure (congestive heart failure
decreased plasma oncotic pressure (cirrhosis or nephrotic syndrome
chylous effusions with lymphatic obstruction of pericardium ie. neoplasm or TB
List the 3 factors that determine whether a pericardial effusion remains clinically silent or whether symptoms of cardiac compression ensue.
volume of fluid
rate at which fluid accumulates
compliance of the pericardium
even more serious with pericardium is pathologically noncompliant and stiff
Describe the presentation of pericardial effusion along with the clinical features of a large pericardial effusion.
asymtomatic or complain of dull constant ache in left chest; accompanying symptoms: dysphagia, dyspnea, hoarseness (recurrent laryngeal) or hiccups (phrenic nerve)
muffled heart sounds, reduced intensity of friction rub, Ewart's sign (dullness over posterior left lung)
possible globular heart on CXR
EKG reduced voltage or electrical alternans
best test is electrocardiogram (volume, ventricular filling and pericardiocentesis needle
What are the standard routes of treatment for pericardial effusion?
therapy directed toward the underlying disorder, without knowledge of cause, clinical state of patient determines whether pericardiocentesis is necessary
Discuss the pathophysiology of constrictive pericarditis.
following episode of acute pericarditis, effusion undergoes organization with subsequent fusion of pericardial layers followed by fibrous scar formation (calcification is possible)
this condition effects diastole and inhibits normal filling of the cardiac chambers which leads to increased filling pressure for both RV and LV and congestion leading up to those chambers
What are the key clinical findings for cardiac tamponade?
jugular venous distention
"small, quiet heart", due to insulating effects of effusion (Beck's triad)
sinus tachycardia and pulses paradoxes (decrease of systolic blood pressure during normal inspiration)
if effusion develops slowly, fatigue and peripheral edema may be the presenting symptoms
What is pulses paradoxus and how is it important in relation to cardiac tamponade?
cyclical decrease of systolic blood pressure during normal inspiration
the transient increase in RV cause by negative intrathoracic pressure on inspiration causes a shift in the inter ventricular septum, which slightly diminishes LV, this is exaggerated in cardiac tamponade because both ventricles share a reduced, fixed volume due to external compression leading to a more dramatic reduction in stroke volume
What are the diagnostic and treatment approaches for possible cardiac tamponade?
echo is most useful to detect compression of early RV diastole collapse and RA early systolic collapse, differentiating tamponade from ventricular contractile dysfunction (ventricular interdependence) or respiratory variation in mitral and tricuspid inflow velocities
definitive diagnosis is by catherterization with measurement of intracardiac and intrapericaridial pressure; note y decent of the atrial wave form is normally blunted due to pressure of tamponade because RV does not fill rapidly
removal of high-pressure pericardial fluid is the only intervention that reverses the life threatening physiology (usually done in cath lab but can also be done blind on the floor)
What is restrictive pericarditis sometimes confused with based not eh elevated systemic venous pressure that can cause hepatomegaly, peripheral edema and ascites?
insidious development of hepatomegaly and asites is often mistaken for hepatic cirrhosis or intra-abdominal tumor
can by differentiate by inspection of jugular veins; cardiac exam may reveal an early diastolic "knock" following S2 in patients with sever calcifications
How can cardiac tamponade be differentiated from pericardial constriction?
in pericardial constriction, inspiratory augmentation of right ventricle does not occur, no pulses paradoxus, instead the venous return cannot be accommodated and accumulates int eh intrathoracic systemic tens, causing jugular vein to become more distended during inspiration (Kussmaul's sign)
What diagnostic testing could confirm constrictive pericarditis?
CXR- may show calcifications
EKG shows nonspecific ST and T wave abnormalities, atrial arrhythmias are common
Echo pericardium may be thickened, ventricular cavities are small and contract vigorously and diastolic ventricular fill ing terminates abruptly in early diastole; CT or MRI can also show pericardial thickening
dx. confirmed by cardiac catherterization with 3 features:
1. elevation and equalization of diastolic pressures in each of the cardiac chambers
2. R and LV tracings show and early diastolic dip and plateau (sq root sign)
3. right atrial pressure tracing shows prominent y descent
endomyocardial biopsy may be necessary to distinguish from restrictive cardiomyopathy