Fcm - Cardiac Mechanics

Front 1

Preload

Back 1

The force (load) acting to stretch resting muscle fiber; it can be defined in the intact ventricle as the end diastolic wall stress (the force at the maximal resting length of the sarcomere.

As preload increases, ventricular performance is improved, and stroke volume increases.

A ventricle with depressed contractile function will dilate, increasing preload, in an attempt to increase contraction and maintain stroke volume and cardiac output, as in dilated cardiomyopathies.

Front 2

How do you measure preload?

Back 2

Due to difficulty measuring wall stress in vivo, end diastolic pressure or end diastolic volume are often used as easily obtainable approximations of ventricular preload.

Front 3

Afterload

Back 3

Force applied to myocardium in systole which must be overcome in order for shortening to occur.

It is the resistance against which the myocardium contracts, and influences extent of shortening.

Front 4

Contractility

Back 4

Intrinsic myocardial contractility, or inotropic state, determines the force and rate of contraction independently of preload and afterload.

Contractile state is directly related to degree of interaction between calcium ions and contractile proteins; it is modulated by neurohumoral factors, and is affected by the adrenergic nervous system.

An increase in contractility results in an increase in the force and rate of myocardial contraction and shortening.

Front 5

Systole

Back 5

Phase of the cardiac cycle where the myocardium is contracting in a coordinated manner in response to an endogenous electrical stimulus, and pressure is being generated within the chambers of the heart driving blood flow.

Front 6

What are the stages of diastole?

Back 6

Isovolumic Relaxation - active, energy requiring process

Early (rapid) diastolic filling - approximately 70% of normal cardiac output enters ventricle during rapid filling phase

Diastasis - slow ventricular filling phase

Atrial systole - follows atrial contraction, late in diastole

Front 7

Does heart rate have a greater impact on diastole or systole? Why?

Back 7

Diastole

Increased heart rate reduces diastolic filling time.

Front 8

Starling's law

Back 8

Force of contraction, or extent of shortening, is dependent on initial length of muscle.

As resting myocardial length increases, extent of contraction increases in direct relation to initial sarcomere length and extent of overlap between actin and myosin filaments.

In cardiac muscle, the optimal overlap of filaments occurs in sarcomeres between 2.0 and 2.2 microns.

Front 9

What happens when filament overlap in sarcomeres is below 2.0 microns?

Back 9

Tension development is reduced - "double" overlap of filaments impeding cross bridge formation (descending limb of Starling curve).

Front 10

Wall stress

Back 10

The force normalized to the cross-sectional area to which the force is applied; wall stress is the solid-phase analog of pressure.

The larger the ventricular cavity, the greater the wall stress. For a given chamber size, the greater the pressure developed in the chamber, the greater the wall stress.

Front 11

What is the law of LaPlace?

Back 11

Stress = (Pressure x Radius) / (2 x Wall thickness)

Front 12

What is the ventricle's response to chronic pressure overload?

Back 12

In an effort to normalize wall stress the muscle hypertrophies, increasing wall thickness, and maintaining wall stress within a narrow range.

Front 13

How does ventricular compliance affect a diastolic pressure-volume curve?

Back 13

The slope of a tangent to the ventricular pressure reflects the compliance of the ventricular chamber.

A stiffer ventricle fills along a curve that is shifted to the left and upward. In this setting, any change in volume will result in a greater change in pressure than in the normal ventricle.

Front 14

Abnormal relaxation

Back 14

Can result in delay of ventricular filling, or incomplete relaxation, resulting in an increase in diastolic pressure.

Patients with left ventricular hypertrophy, such as from hypertension or aortic stenosis, or with myocardial ischemia manifest abnormal relaxation.

Front 15

Atrial contraction

Back 15

As atrial and ventricular pressure equalize, ventricular filling slows (diastasis); with atrial systole (atrial contraction) pressure gradient from atrium to ventricle increases and ventricular filling increases, raising ventricular pressure above atrial pressure, and mitral valve then closes.

Front 16

Concentric hypertrophy

Back 16

Parallel replication of myofibrils. Wall thickness increases, cavity radius may decrease, and systolic wall stress normalizes.

Due to pressure overload and increased systolic wall stress, such as in hypertension or aortic stenosis.

Front 17

Eccentric hypertrophy

Back 17

Replication of myofibrils in series. Myocytes elongate and ventricular cavity dilatation occurs. Systolic wall stress increases mildly, triggering wall thickening, and return of systolic wall stress toward normal to maintain contractile performance. With chronic volume overload ventricular geometry is altered as the ventricle becomes more spherical in shape.

Due to volume overload, as in mitral or aortic regurgitation or fluid overload states, which increase diastolic wall stress.

Front 18

Ventricular remodeling

Back 18

The myocardium responds to an increased hemodynamic load associated with pathological states in order to maintain ventricular contractile performance. Can be concentric or eccentric hypertrophy.

Front 19

Diastolic dysfunction

Back 19

Characterized by increased diastolic filling pressure, and will be exacerbated by rapid heart rates, in which shortened filling times result in even greater diastolic pressure.

Increased diastolic pressure is manifested clinically by dyspnea.

Commonly seen in disorders with significant ventricular hypertrophy.