Restrictive ventricular physiology


A restrictive ventricle is one that fills to a significantly lower end diastolic volume (indexed to BSA) compared to a normal ventricle at the same atrial pressure. Said another way, the end diastolic pressure-volume relationship is a steep one, such that EDV is limited in its ability to increase without prohibitive elevations in EDP. This physiology is similar to that which occurs in patients with diastolic dysfunction in whom the pressure-volume relationship is abnormally steep. Clinical Examples

•Pathologic myocardium, whether due to ischemia or postoperative edema, primary or acquired restrictive myopathy

•Anatomically small ventricle (e.g. following repair of unbalanced CAVC defect or TOF with a muscle-bound RV)

•Large, inelastic component of the ventricle due to patch material (e.g. TOF repair with large ventriculotomy or TOF/CAVC repair)

•Endocardial fibroelastosis Treatment considerations Patients with restrictive physiology have a limited ability to recruit stroke work (i.e. the ability to increase stroke volume or ventricular pulse pressure) through the administration of volume. Unfortunately, though, they are also less tolerant of volume loss (e.g. hypovolemia). Stroke volume can be assessed by palpation of pulse strength, pulse pressure on arterial waveform, and signal strength of the pulse oximeter (though these can all be falsely reassuring in patients with runoff lesions).

•Patients with inadequate cardiac output may be helped by increasing heart rate (if low-normal) and inotropic support (inotropes are the best lusitropes acutely). Administration of volume should be done in small aliquots (e.g. 5 mL/kg), ideally with monitoring of atrial and arterial pressure changes.

•Patients with restrictive physiology who experience intravascular volume losses (e.g. bleeding, diuresis) have a more pronounced decrease in atrial pressure –> end diastolic volume –> stroke volume (leading to hypotension) when compared with a normal heart.

•Patients with restrictive physiology may become hypotensive when vasodilated (e.g. with fever or medications), as this lowers atrial pressure and pools preload in systemic veins. Vasoconstrictor agents (e.g. norepinephrine) are often helpful in such circumstances.

•The presence of an atrial level ‘popoff’ is particularly helpful in the treatment of isolated restrictive RV physiology, as it allows blood to bypass the restrictive RV and pass directly to the LV. This preserves cardiac output at the cost of cyanosis. In restrictive LV physiology, an ASD creates a volume load on the LA which may or may not decrease LAP.

Restrictive ventricular physiology and diastolic dysfunction can be conceptualized as follows. The ventricle is like a balloon that is filled during diastole by an atrial pressure head (this is of course an oversimplification in order to focus on ventricular dynamics). A normal ventricle is compliant, a term which indicates how a ventricle responds to an increase in volume. If additional volume is added to a compliant ventricle (e.g. a fluid bolus is administered), the additional fluid flows into the ventricle as shown to the right of the arrow. As the added volume enters the ventricle, the end diastolic volume increases and stroke volume (and stroke work) increase. (Recall Frank Starling’s law: the heart pumps the volume it receives.) Note that because the fluid enters the ventricle, the atrial pressure head does not significantly increase. Thus, it is a marker of health for the end diastolic pressure volume relationship to be nearly flat except at extremes. Said another way, the administration of volume to a healthy heart should increase stroke volume (and therefore pulse pressure) to a much greater extent than it does atrial pressure.

A non-compliant (or restrictive) ventricle behaves very differently; it is stiff and is less able to respond dynamically. As volume is added to the circulation, the ventricle is unable to relax to accomodate it, and the atrial pressure head increases as a result. Because end diastolic volume does not increase, stroke volume does not either. Clinically, patients with restrictive physiology may manifest a significant change in atrial pressure for a small administration of volume with a proportionately lower change in pulse pressure than a healthy heart. Similarly, a restrictive ventricle may also have a more dramatic decrease in atrial pressure for a given loss of volume (e.g. during bleeding) and may be less able to maintain stroke work in that circumstance for the same reason.

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