Afterload & Preload

Question 1

LV wall tension

Answer 1

T = pressure x radius

*as increased pressure exerts on outward force, the LV wall tension increases
*as radius increases, the LV wall tension increases

Question 2

LV wall stress

Answer 2

stress = (pressure x radius) / (2 x wall thickness)

*LV wall stress is INVERSELY related to LV wall thickness:
-as LV wall thickness increases, the LV wall stress decreases
-as LV wall thickness decreases, the LV wall stress increases
*ventricle is not a uniform sphere:
-the base experiences higher wall stress than the apex because the radius of the base is larger, which is why it is thicker

Question 3

preload - defined

Answer 3

*stretch on the LV wall at the end of DIASTOLE (LV filling) immediately before the LV starts to contract
*best described as end-diastolic LV wall stress
*clinically, universally taken to be the LEFT VENTRICULAR END-DIASTOLIC PRESSURE (i.e. the pressure inside the LV at which the mitral valve closes) or LV END-DIASTOLIC VOLUME (LV EDV)

Question 4

Frank-Starling Relationship

Answer 4

*an increase in LV filling results in an increase in cardiac output (by increasing stroke volume)

Question 5

effect of increased contractility on Frank-Starling Relationship

Answer 5

*an increase in LV contractility results in an increase in stroke volume with a small decrease in LV EDV (shifts the curve up)

Question 6

effect of decreased contractility on Frank-Starling Relationship

Answer 6

*a decrease in LV contractility results in a decrease in cardiac output (by reducing stroke volume) at a slightly larger LV EDV (shifts the curve down)
*frequently, in dilated hearts, they may reach a point where increasing preload results in less myosin-actin cross-bridging

Question 7

afterload - defined

Answer 7

*stretch on the LV wall through SYSTOLE (LV contracting)
*best described by the end-systole LV wall stress
*clinically, often represented by blood pressure, but better to think of it as the PRESSURE INSIDE THE LV DURING SYSTOLE
*high BP or aortic stenosis would result in increased afterload

Question 8

understanding afterload

Answer 8

*afterload reflects a combination of vascular, valvular, and ventricular resistance to propel blood forward
*under normal circumstances, the most important component is the arterial pressure, so AFTERLOAD ~ ARTERIAL PRESSURE (under normal circumstances)

Question 9

relationship between afterload and shortening velocity

Answer 9

*as afterload increases, the velocity of muscle/sarcomere shortening (contraction) decreases

Question 10

effect of increasing preload on the relationship between afterload and shortening velocity

Answer 10

*increasing preload shifts the curve such that, for a given afterload, the shortening velocity is increased (shifts the curve to the right)
*changes Fmax but not Vmax

Question 11

effects of increasing contractility on relationship between afterload and shortening velocity

Answer 11

*increasing contractility can shift the curve such that, for a given afterload, the shortening velocity is increased (shifts the curve to the right)
*changes Fmax AND Vmax

Question 12

effect of decreased afterload on Frank-Starling Relationship

Answer 12

*a decrease in afterload results in an increase in stroke volume with a small decrease in LV EDV

Question 13

effect of increased afterload on Frank-Starling Relationship

Answer 13

*an increase in afterload results in a decrease in cardiac output (by reducing stroke volume) at a slightly larger LV EDV

Question 14

effect of contractility on stroke volume (simple)

Answer 14

INCREASED contractility → INCREASED stroke volume (direct relationship)

Question 15

effect of preload on stroke volume (simple)

Answer 15

INCREASED preload → INCREASED stroke volume (direct relationship)

Question 16

effect of afterload on stroke volume (simple)

Answer 16

DECREASED afterload → INCREASED stroke volume (INVERSE relationship)

Question 17

relationship between heart rate and stroke volume

Answer 17

*as HR increases, there may be less filling of the LV, which results in decreased SV
*in spite of decreased SV at high rates, CARDIAC OUTPUT and OXYGEN CONSUMPTION continue to INCREASE

Question 18

left ventricular hypertrophy - overview

Answer 18

*LV hypertrophy means that there is an increase in myocardial muscle mass
*mass can be added in 2 different ways:
1. used to thicken the wall (concentric)
2. used to expand the LV cavity size (eccentric)

Question 19

CONCENTRIC left ventricular hypertrophy

Answer 19

*increase in WALL THICKNESS only, no change in chamber size
*response to chronic PRESSURE overload (HTN, aortic stenosis)
*wall thicker, but diameter unchanged → decreases wall stress and oxygen demand

Question 20

ECCENTRIC left ventricular hypertrophy

Answer 20

*increase in LV CHAMBER SIZE (chamber dilates)
*response to chronic VOLUME overload (mitral regurgitation, chronic anemia, chronic elevation of CO)
*results in an increase in wall stress and oxygen demand

Question 21

eccentric vs. concentric LV hypertrophy - sarcomere organization

Answer 21

*concentric: sarcomeres added in PARALLEL (allows greater force generation)

*eccentric: sarcomeres added in SERIES (allows more volume to be held)

Question 22

wall stress (wall thickness) in concentric LV hypertrophy

Answer 22

*certain factors produce chronic pressure overload (aortic stenosis, chronic HTN)
*not advantageous (pathological)
*adversely impacts diastolic relaxation, which may require higher LV EDP to fill the ventricle
*longer distance for blood vessels to travel to subendocardium

Question 23

3 major factors that affect myocardial oxygen demand

Answer 23

1. contractility: squeeze harder = more work = need more O2
2. heart rate: beat faster = more work = need more O2
3. ventricular wall stress: more wall stress = need more O2

Question 24

cardiac energy source

Answer 24

*preferred energy source: aerobic consumption of medium-chain fatty acids
*however, in presence of significant glucose load from diet, the heart can adapt

Question 25

ATP and the heart

Answer 25

*the average heart has 700 mg of ATP
*at a heart rate of 60 bpm, each beat takes 70 mg, which means our supply is exhausted in 10 seconds
*Kreb’s cycle is critical to maintaining supply of ATP → we NEED oxygen

Question 26

myoglobin

Answer 26

*has a single heme site to bind 1 oxygen molecule
*at high levels of activity with reduced oxygen levels, myoglobin can release its oxygen for the Kreb cycle to make more ATP
*oxygen supply from myoglobin lasts for several seconds

Question 27

creatine phosphate (phosphocreatine)

Answer 27

*in normal times (ATP in excess), creatine kinase generates phosphocreatine, which stays there like a “savings account” to provide an additional source of ATP
*used to regenerate ATP from ADP (facilitated by creatine kinase enzyme) in times of severe oxygen deficiency
*ATP generated lasts mere seconds
*creatine eventually broken down into creatinine
*essential, creatine phosphate PLUMMETS during ischemia to maintain ATP levels for a little bit

Question 28

only way to increase oxygen supply to heart muscle itself is…

Answer 28

to increase coronary artery blood flow