Frank Starling Mechanism Flashcards
Frank-starling mechanism
-the relationship between length and tension at the level of the cardiac muscle fiber and the left ventricle
Sarcomere
- contractile unit of the cardiomyocyte
- when you increase stretch then force of contraction also increases
**there is an optimal length to produce maximal force (too much or too little stretch decrease force production)
Operating point
-the point in which the length and force of contraction are at during cardiac muscle contraction
Diastole
-filling of ventricle
Left ventricle during diastole
-fills during diastole (preload)
-an increase in venous return will increase the preload (filling), which increases the stretch, and therefore the stroke volume
Way to increase venous return
exercise
Ways to decrease venous return
-hemorrhage
Left ventricle end diastolic pressure (LVEDP)
-can be a surrogate for filling meaning it is the pressure/fill of the left ventricle during diastole (before systole)
Afterloads effect on LVEDP
-afterload is the amount of pressure that the heart needs to exert to eject blood during ventricular contraction
-if increased, then a decrease in stroke volume will occur, and therefore an increase in LVEDP
-if decreased, then an increase in stroke volume, and decrease in LVEDP
Inotropys effect on LVEDP
-Inotropy is the force/strength of muscular contractions
-if increased then an increase in stroke volume will occur, and therefore a decrease in LVEDP
-if decreased then a decrease in stroke volume will occur, and an increase in LVEDP
Left ventricle pressure and volume
Phase A: diastole, LV filling
- increasing/high volume, low pressure
- mitral valve closes at end of this phase
Phase B: Systole, isovolumetric contraction
- High volume, increasing/high pressure
- aortic valve opens at end of this phase
Phase C: Systole, Ejection period
- low volume, high pressure
- aortic valve closes at end of this phase
Phase D: diastole, isovolumetric relaxation
- decreasing/low pressure, low volume
- mitral valve opens at end of this phase
Stroke volume equation
End diastolic volume (EDV)-end systolic volume (ESV) = stroke volume
Effects of increase preload
-increase preload (venous return/filling prior to contraction)
-results in increased end diastolic volume, increased stroke volume and increased contractility
Effects of decreased preload
-decreased preload (venous return/filling prior to contraction)
-results in decreased end diastolic volume, stroke volume and contractility
Effects of removed pericardium
-pericardium restricts ventricular filling (preload)
-when removed, dogs had better cardiac outputs during exercise because the ventricles are able to fill more
Modulators of preload
-blood volume
-ventricular filling
Modulators of blood volume
-RAAS
-blood loss
-fluid therapy
-muscle/respiratory pump
-venous compliance
-venous resistance
-right atrial pressure
Modulators of ventricular filling
-tricuspid valve
-pulmonary valve/circulation
-pericardium (tamponade)
Effects of increased afterload
-increased afterload (pressure LV must overcome to pump blood)
-results in increased end systolic volume (blood left after contraction), decreased stroke volume.
Effects of decreased afterload
-decreased afterload (pressure LF must overcome to pump blood)
-results in decreased end systolic volume (ESV) and an increased stroke volume
Modulators of afterload
-blood pressure
-ventricular ejection
Ways that blood pressure is effected
CO X SVR
-affected by blood volume and sympathetic activity
- constriction/dilation of arteries (affected by sympathetic activation or deactivation, RAAS, local dilation vs hypertension)
Ways that ventricular ejection is affected
-aortic or pulmonic valves
Remodelling of heart and the next beat
-next beat will be higher or lower depending on the previous beat.
-an increase in afterload will result in an increased preload on the next beat = Self-correcting
Effects of increased inotropy
- increased inotropy (contractility)
- results in decreased end systolic volume, and increased stroke volume
Effects of decreased inotropy
-decreased inotropy (contractility)
-results in increased end systolic volume, and decreased stroke volume
Modulators of inotropy
-state of arousal
-sympathetic activity (local norepinephrine, circulating factors epinephrine)
-parasympathetic activity (local acetylcholine)
-Calcium handling
-drug targets
