High Yield Medical Physiology

LaPlace's Law for the Heart

(from Hurst's, The Heart)

The impedance to ejection of blood by the ventricles includes blood viscosity, vascular resistance, vascular distensibility, and myocardial wall tension. The afterload is the total load that the heart must work against during contraction. Much of the afterload is made up of ventricular myocardial wall tension. In the ventricle, the tension on the walls increases as ventricular chamber volume increases even if intraventricular pressure remains constant. As the ventricle empties, tension is reduced, even as pressure increases. Calculations of myocardial wall tension are defined by the Laplace equation and are expressed in terms of tension, T, per unit of cross-sectional area (dynes per centimeter [dyn/cm]).

Within a cylinder, the law of Laplace states that wall tension is equal to the pressure within the cylinder times the radius of curvature of the wall:

T = P R

where T is wall tension (dyn/cm), P is pressure (dyn/cm2), and R is the radius (cm). Basically, wall tension is proportional to the radius. Because the heart has thick ventricular walls, wall tension is distributed over a large number of muscle fibers, thereby reducing tension on each. The equation for a thick-walled cylinder such as the heart is:

T = (P x R)/h

where h is wall thickness. 

Because the geometry of the ventricles is more complex than that of a cylinder, ventricular wall tension cannot be measured with precision. Wall stress, the force distributed across an area, is actually more correct but is seldom measured.

Two fundamental principles stem from the relationship between the geometry of the ventricular cavity and the tension on its muscular walls:

1. Dilatation of the ventricles leads directly to an increase in tension on each muscle fiber.
2. An increase in wall thickness reduces the tension on any individual muscle fiber. Therefore, ventricular hypertrophy reduces afterload by distributing tension among more muscle fibers.

Dilatation of the heart decreases cardiac efficiency unless hypertrophy is sufficient to normalize wall stress. In heart failure, wall tension (or stress) is high, and thus afterload is increased. The energetic consequences of the law of Laplace can have some role in progressive deterioration of energy-starved cardiac myocytes in the failing heart.

Ventricular dilatation, although initially adaptive as an attempt to sustain SV, eventually becomes a substantial disadvantage and contributes importantly to impaired myocardial performance. As the left and right ventricles dilate, functional mitral and tricuspid regurgitation can occur, adding to circulatory congestion. Stretched myocardial cells can induce programmed cell death (apoptosis), thereby contributing to further disease progression.31 Any treatment that slows progressive dilatation of the heart, such as angiotensin-converting enzyme (ACE) inhibitors or β−adrenergic blockers, will likely have a powerful role in the treatment of heart failure. The plasticity of progressive dilatation is now more apparent, with remarkable reversal of dilatation observed in response to ACE inhibitors and β−adrenergic blockers, cessation of alcohol use in patients with alcoholic cardiomyopathy, and spontaneous improvement in patients with inflammatory myocarditis.

EKG Memory Tools & Mean Electrical Axis

Leads I II & III

Count the "L's"
I = RA LA  = 1 L
II = RA LL = 2 Ls
III = LA LL = 3 Ls

Normal electrical axis 
Leads I & II both positive
Mean electrical axis = -30 to + 90

2nd degree Mobitz type 1 (Wenckebach) = "going, going, gone"

Why is the T wave positive if it is repolarization of the ventricles?

because the repolarization is going in the opposite direction.  A is negative charges going towards positive electrode.  B is positive charges going towards positive electrode.  C is positive charges going away from positive electrode (what happens in the ventricles).