Cardiac Performance

Grading the Force

syncytium—depolarization propagates through gap junctions at intercalated discs (1.6-2.0 um)

each layer of cells in different orient (for smooth contraction), best conduction along parallel cells

can’t recruit more cells, so force proportional to overlap; myosin 1.6 um, actin 1.0 um, Z-line 0.05 um

no force if sarcomere more than 3.65 um (no contact) or less than 1.65 um (myosin hits Z-lines)
ideal overlap occurs at 2-2.50 um, from 1.65 to 2.00 (or 3.65 to 2.50) produces progressively more force
cardiac sarcomeres are at about 1.80 um, thus on the "ascending limb," and stretching will increase force

this stretch, proportional to the force, and is called preload

determined by left ventricular end diastolic volume (LVEDV)
estimated from LVED pressure, pulmonary cap wedge pressure PCWP, pulmonary artery end diastolic press (PAD), or central venous pressure (CVP)

force is also affected by calcium concentration, perhaps due to binding of Tn-C

Contractility (= Power = Force x Velocity)

max. force is isometric (no motion), so optimal contraction maximizes power (at about 1/3 Vmax)

velocity is determined by afterload (force contracted against = peripheral vascular resististance)

force vs. velocity curve indicates that bigger afterload = smaller velocity

positive inotropic effect (beta agonist) increases power, negative (Ca⁺⁺channel blockers) decreases

Analyzing the Cardiac Cycle

measure left ventricular pressure over time to determine timing of contraction

maximum positive rate of pressure change (dP/dt) is the systolic contractility

pressure tracing can show chronotrophy (change in heart rate) and lusitrophy (ability of heart to relax)

measure pressure in atrium, ventricle, and aorta to determine timing of valve opening and closing

aortic valve—open only when more pressure in ventricle than in aorta (open during contraction)
mitral valve—open only when more pressure in atrium than ventricle (closed during contraction)

ejection fraction (index of contractility) = (LV end diastolic volume – LV end syst) / LV end diast

percentage of volume of blood in ventricle pushed out during contraction (normal 50-60%)

Mapping the Cardiac Cycle: The Pressure-Volume Relationship

PV graph of end systolic pressure = heart’s ability to contract (develop force)—best measure of contractility

PV graph of end diastolic pressure = properties when heart relaxed (compliance/stiffness—lusitrophy—ischemia/heart failure makes steeper relationship, so more pressure to change volume)

map path of pressure and volume in ventricle

end systolic volume on left, end diastolic on right, stroke volume is difference
top is systole (rapid and slow), bottom is diastole

changing preload, afterload, and contractility (power) changes this relationship (Fig. 14)

increase preload: greater end diastolic volume (right leg to right) SV
increase afterload: increase end systolic volume and systolic pressure (left leg to right, top up) ¯ SV
increase contractility: decrease end systolic volume, increase systolic pressure (left leg left, top up) SV

Heart Failure—net effect is up and to the right

loss of contractility = lower end systolic pressure (top falls and left moves right)

diastolic pressure increases (less lusitrophy, heart cannot relax)

end diastolic volume increases to increase preload (compensate for loss of force)

end systolic volume increases even more than end diastolic, so smaller stroke volume

Mechanisms to Regulate Stroke Volume

change preload (Frank Starling mechanism)

increase rate (force increases if rate increases—staircase or Treppe phenomenon)

increase Ca⁺⁺more depol=more action potentials, also more Ca flux per action potential

post extrasystolic potentiation—beat after extra beat will be very strong due to pause between beats

more Ca⁺⁺ into SR and longer filling (increased preload)