M
Mary
Oh, boy! Do I have questions for you!
What kind of fluid balance are you aiming for? The cardio I saw yesterday said that my problem had been made worse -- I'm wondering if it was even caused by -- the diuretics and fluid restrictions prescribed by my surgeon to deal with the fluid around my lung. I think I forgot to tell everyone that one of the reasons I was in the ER for hours was that they were pumping me full of fluids. Even after three days of re-hydrating (prescribed by the cardio I saw Tuesday) I was still dehydrated.
If your doctor has you restricting fluids, maybe we don't have the same thing.
What is a "somewhat normal" life?
Also, I was told something totally different about pericardium removal than you -- that it's not as dangerous as something like valve replacement.
I've copied this from Cleveland Clinic. It's a different source than ones I've used before, but it covers most of the areas you asked about. Please note the mortality quoted; that is higher than the figures given for valve replacement.
I had the Kussmaul's sign and pericardial knock at diagnosis, but the knock is less noticeable on recent echos.
If you look at the section on Therapy, I think you will see how I'm being treated.
I am dealing with symptoms of heart failure/pulmonary hypertension/ascites.
I am able to exercise to a moderate extent, but two nights ago, after 25 minutes on the elliptical my HR was 120; 35 minutes on the elliptical brought my HR up to 160, and an additional 5 minutes pushed me to 185.
Once my heart starts to stress, I can get into trouble quickly. I suppose that's what I mean by "some what normal." Maybe it's not normal for others, but it's normal for me!
PERICARDIAL CONSTRICTION
DEFINITION
Constrictive pericarditis refers to an abnormal thickening of the pericardium, resulting in impaired ventricular filling and decreased cardiac output.
ETIOLOGY
Most cases are idiopathic, although a history of acute or chronic pericarditis may occasionally be elicited.
PATHOPHYSIOLOGY
The initiating event causes a chronic inflammatory pericardial process, resulting in fibrinous thickening, calcification of the pericardium (Figures 2, 3 (CXR), and 13 (CT)), and limitation of intrapericardial volume. This leads to impaired ventricular filling and decreased cardiac output. Ultimately, right and then left ventricular heart failure develop.
SIGNS AND SYMPTOMS
Clinical Symptoms
Symptoms are often vague and their onset is insidious, and include malaise, fatigue, and decreased exercise tolerance. With progression of constriction, symptoms of right-sided heart failure (peripheral edema, nausea, abdominal discomfort, ascites) become apparent and usually precede signs of left-sided failure (exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea).
Physical Examination
Increased ventricular filling pressures cause jugular venous distention and Kussmaul's sign, (absent inspiratory decline of jugular venous distention), which is sensitive but nonspecific for constriction.29 Auscultation reveals muffled heart sounds and occasionally a characteristic pericardial knock (60-200 msec after the second heart sound), caused by sudden termination of ventricular inflow by the encasing pericardium.
Constrictive-Effusive Pericarditis
This entity consists of a tense pericardial effusion in the presence of pericardial constriction, and both tamponade and constrictive signs and symptoms are present. Therapy includes pericardiocentesis initially, followed by pericardiectomy for long-term management.30
DIAGNOSIS
Electrocardiograph
ECG does not show specific findings, but low voltage may be seen.
Chest Radiograph
Pericardial calcifications (Figures 2 and 3), pleural effusions, and bi-atrial enlargement may be noted on chest radiograph.
Echocardiography
This is the best imaging modality for assessing hemodynamic parameters noninvasively. M-mode echocardiography is useful to look for flattening of the left ventricular free wall. Two-dimensional echocardiography shows septal bounce and inferior vena cava plethora with absent inspiratory collapse. Doppler-echocardiographic findings have the highest sensitivity and specificity for detecting constrictive physiology. Excessive respiratory variations in transmitral, transtricuspid, pulmonary venous, and hepatic vein flow are characteristic.31,32
Right Heart Catheterization
Direct pressure measurements are performed if there is doubt about the diagnosis. M- or W-shaped atrial pressure waveforms and "square root" or "dip-and-plateau" right ventricular pressure waveforms reflect impaired ventricular filling. Because of the fixed and limited space within the thickened and stiff pericardium, end-diastolic pressure equalization (typically within 5 mm Hg) occurs between these cardiac chambers.
Magnetic Resonance Imaging
and Computed Tomography
MRI is the imaging modality of choice to evaluate the pericardium, being slightly superior to CT in spatial resolution. Pericardial calcifications may easily be identified on CT (Figure 13).
THERAPY
Medical treatment is difficult and does not affect natural progression or prognosis of the disease. Diuretics and a low-sodium diet may be tried for patients with mild to moderate (NYHA class I-II) symptoms or contraindications to surgery.33 For most patients, pericardiectomy is advised, with 80-90% of patients experiencing improvement and 50% complete relief of symptoms. Thirty-day perioperative mortality averages 5-10%.34,35
OUTCOMES
Recurrence following surgery is caused mainly by incomplete resection. Without surgical treatment, biventricular heart failure develops.