Afterload & Preload Flashcards
LV wall tension
T = pressure x radius
*as increased pressure exerts on outward force, the LV wall tension increases
*as radius increases, the LV wall tension increases
LV wall stress
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
preload - defined
*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)
Frank-Starling Relationship
*an increase in LV filling (preload, EDV) results in an increase in cardiac output (by increasing stroke volume)
effect of increased contractility on Frank-Starling Relationship
*an increase in LV contractility results in an increase in stroke volume with a small decrease in LV EDV (shifts the curve up)
effect of decreased contractility on Frank-Starling Relationship
*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
afterload - defined
*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
*approximated by mean arterial pressure (MAP)
understanding afterload
*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)
relationship between afterload and shortening velocity
*as afterload increases, the velocity of muscle/sarcomere shortening (contraction) decreases
effect of increasing preload on the relationship between afterload and shortening velocity
*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
effects of increasing contractility on relationship between afterload and shortening velocity
*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
effect of decreased afterload on Frank-Starling Relationship
*a decrease in afterload results in an increase in stroke volume with a small decrease in LV EDV
effect of increased afterload on Frank-Starling Relationship
*an increase in afterload results in a decrease in cardiac output (by reducing stroke volume) at a slightly larger LV EDV
effect of contractility on stroke volume (simple)
INCREASED contractility → INCREASED stroke volume (direct relationship)
effect of preload on stroke volume (simple)
INCREASED preload → INCREASED stroke volume (direct relationship)
effect of afterload on stroke volume (simple)
DECREASED afterload → INCREASED stroke volume (INVERSE relationship)
relationship between heart rate and stroke volume
*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
left ventricular hypertrophy - overview
*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)
CONCENTRIC left ventricular hypertrophy
*increase in WALL THICKNESS of LV 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
ECCENTRIC left ventricular hypertrophy
*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
eccentric vs. concentric LV hypertrophy - sarcomere organization
*concentric: sarcomeres added in PARALLEL (allows greater force generation)
*eccentric: sarcomeres added in SERIES (allows more volume to be held)
wall stress (wall thickness) in concentric LV hypertrophy
*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
3 major factors that affect myocardial oxygen demand
- contractility: squeeze harder = more work = need more O2
- heart rate: beat faster = more work = need more O2
- ventricular wall stress: more wall stress = need more O2
cardiac energy source
*preferred energy source: aerobic consumption of medium-chain fatty acids
*however, in presence of significant glucose load from diet, the heart can adapt
ATP and the heart
*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
myoglobin
*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
creatine phosphate (phosphocreatine)
*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
only way to increase oxygen supply to heart muscle itself is…
to increase coronary artery blood flow
