INTRODUCTION
Pericardologists were concerned almost exclusively with diastole (for good reasons of pericardial constriction and cardiac tamponade) before the late 1980s, when diastolic dysfunction (DD) started to attract widespread attention among other cardiologists. In many respects, acute and subacute constrictive pericarditis (CP) and cardiac tamponade epitomize DD, usually in the presence of normal systolic cardiac function. Indeed, both often have normal or high ejection fractions (EFs)—a consequence of ventricular underfilling with basically normal or compensatorily hyperfunctional myocardium. However, the normal pericardium also affects the cardiac filling dynamics of both normal and diseased hearts, although to a lesser degree.
PATHOPHYSIOLOGY
The normal pericardium becomes more important in dilated hearts and with increased central circulatory volume and less so with hypovolemia and normal responses to other influences that reduce cardiac size, like head-up tilt (HUT), lower body negative pressure (LBNP), and administration of such agents as nitroprusside and nitroglycerine. With the often low compliance of hearts with DD, the influence on filling of the normally stiff, low-compliance pericardium may be either less than normal or additive, but this relationship has not been investigated.
In the absence of formal, specifically targeted investigations of the influence of the pericardium on DD and diastolic heart failure (DHF), the current state of knowledge permits only reasonable extensions and hypothesis generation from what we know of pericardial function and behavior during normal cardiac function and to some extent during systolic cardiac impairments. Box 3-1 summarizes the macrophysiology of the normal pericardium, many elements of which—subject to investigation—may affect DD and DHF.
Mechanical Functions: Promotion of Cardiac Efficiency, Especially during Hemodynamic Overloads
- I.
Relatively inelastic cardiac envelope
- A.
Maintenance of normal ventricular compliance (volume-elasticity relation)
- B.
Defense of the integrity of any Starling curve: Starling mechanism operates uniformly at all intraventricular pressures because presence of pericardium
- 1.
Maintains ventricular function curves.
- 2.
Limits effect of increased left ventricular end diastolic pressure.
- 3.
Supports output responses to:
- a.
Venous inflow loads and atrioventricular valve regurgitation (particularly when acute)
- b.
Rate fluctuations
- a.
- 4.
Hydrostatic system (pericardium plus pericardial fluid) distributes hydrostatic forces over epicardial surfaces.
- a.
Favors equality of transmural end diastolic pressure throughout ventricle, therefore uniform stretch of muscle fibers (preload)
- b.
Constantly compensates for changes in gravitational and inertial forces, distributing them evenly around the heart
- a.
- 1.
- C.
Limitation of excessive acute dilation
- D.
Protection against excessive ventriculoatrial regurgitation (atrial support)
- E.
Ventricular interaction: relative pericardial stiffness
- 1.
Provides a mutually restrictive chamber favoring balanced output from right and left ventricles integrated over several cardiac cycles
- 2.
Permits either ventricle to generate greater isovolumic pressure from any volume
- 3.
Reduces ventricular compliance with increased pressure in the opposite ventricle (e.g., limits right ventricular stroke work during increased impedance to left ventricular outflow)
- 1.
- F.
Maintenance of functionally optimal cardiac (especially left ventricular) shape
- A.
- II.
Provision of closed chamber with slightly subatmospheric pressure in which:
- A.
The level of transmural cardiac pressures will be low, relative to even large increases in “filling pressures” referred to atmospheric pressure.
- B.
Pressure changes aid atrial filling via more negative pericardial pressure during ventricular ejection.
- C.
Diastolic suction can accelerate filling following systole.
- A.
- III.
“Feedback” cardiocirculatory regulation via pericardial servomechanisms
- A.
Neuroreceptors detect lung inflation and (via vagus): alter heart rate and blood pressure.
- B.
Mechanoreceptors: Lower blood pressure and contract spleen.
- A.
- IV.
Limitation of hypertrophy associated with chronic exercise
Membranous Functions
- I.
Reduction of external friction due to heart movements
- A.
Production of pericardial fluid
- B.
Generation of phospholipid surfactants
- A.
- II.
Buttressing of thinner portions of the myocardium: Myocardial thickness varies reciprocally with parietal pericardial thickness.
- A.
Atria
- B.
Right ventricle
- A.
- III.
Defensive immunologic constituents in pericardial fluid
- IV.
Fibrinolytic activity in mesothelial lining
- V.
Prostacyclin (PGE2, PG12 and eicosanoids) released into pericardial sac in response to stretch, hypoxia and increased myocardial loading/work
- VI.
Synthesis and release of endothelin, increased by angiotensin III stimulation
- VII.
Barrier to inflammation from contiguous structures
Ligamentous Function
- I.
Limits undue cardiac displacement
- II.
Modifies pericardial stress/strain by limiting directions of traction of its fibers
* Condensed from Spoclick DH: The pericardium: A comprehensive textbook. New York, Marcel Dekker, 1997.
Box 3-2 summarizes the many cardiac effects of pericardiectomy or sufficiently extensive pericardiotomy. Patients who have had pericardiectomy for any indication grossly appear to function quite well, although the subject has not been intensively studied in human patients and certainly not compared for individual patients acutely and especially chronically, which would permit a better estimate of the pericardium’s dispensability. In considering the many effects of pericardiectomy and pericardiotomy sufficiently widespread to remove pericardial mechanical influence (see Box 3-2 ), the apparent benignity of pericardiectomy/otomy is at least superficially surprising because it implies that there are either widespread and adequately compensatory adjustments or that the pericardium is really not indispensable. Nonindispensability would be especially surprising when one considers the items in Box 3-1 , as well as the very rich pericardial microphysiology (not a subject of this discussion). There is, however, broad and deep experience with experimental pericardiectomy and pericardiotomy (see Box 3-2 ) in hearts without cardiac disease, which, like the macro functions of the normal pericardium (see Box 3-1 ), should be considered in evaluating and further investigating DD and DHF.
A.
General Considerations
- 1.
Reduced or absent constraint of the cardiac chambers
- 2.
At matched LVEDV, pericardiectomy causes a fundamental alteration in RV but not LV filling.
- 3.
Pericardiectomy shifts LVEDP-V curve to the right.
- 4.
Pericardiectomy decreases RVEDP-V slope.
- 5.
Reduced atrioventricular and ventricular interaction (i.e., parallel interaction, due to pericardium); left ventricle dominates. (With an intact pericardium, the right ventricle dominates.)
- 6.
Decreased suction (less negative pressure) during ventricular systole
B.
Specific Effects
- 1.
Decreased:
- a.
RA mean pressure
- b.
RA filling rate
- c.
Pulmonary volume overload with intravascular volume loading
- d.
Excess intravascular volume redistribution from pulmonary systemic circulation
- e.
Decreased ventricular isovolumic pressure generation from any volume
- f.
Decreased base to apex intraventricular pressure gradient; filling velocity shifts toward the base
- g.
E/A and E′
- h.
Decreased LV mechanoreceptor activity
- a.
- 2.
Increased:
- a.
Cardiac chamber transmural pressures
- b.
RV size
- c.
LV stroke volume, SWI and CI due to Frank-Starling response to increased preload
- d.
LA compliance with greater increase in conduit than reservoir function
- e.
LV compliance
- f.
Peak dp/dt
- g.
Early LV filling velocity (A) and filling fraction
- h.
LV end diastolic diameter and volume
- i.
LV early filling rate
- j.
Ventricular series interactions (relative to direct interaction)
- k.
LV mechanoreceptor activity
- l.
Rate of myocardial protein synthesis producing increased LV mass
- m.
Exercise responses
- i.
Maximal O2 consumption
- ii.
Maximal stroke volume and cardiac output
- iii.
LA pressure and SV and LASV
- iv.
LV end diastolic pressure
- i.
- n.
Ventricular pressure-volume curves: Ventricular pressure begins its sharp rise later (at a higher cardiac volume) and increases more gradually thereafter.
- a.
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