Lecture 9 Flashcards
factors that affect stroke volume and the force of ventricular contraction
1- Preload 2-inotropism 3- Autonomic NS 4- Intracellular calcium levels 5- Afterload
Preload
o Preload is the “load” or “stretch” on the ventricular cardiac muscle before it contracts
o Preload is directly influenced by EDV
o The effects of preload are confirmed by the Frank-Starling Law of the Heart –within physiological limits, the more the ventricles are filled during diastole, the more blood they will eject during systole (i.e. – the greater the preload, the greater the force of contraction)
o This type of control of SV is referred to as heterometric regulation
Cardiac Contractility (Inotropism)
o An increase in cardiac contractility is an increase in contractile strength that is independent of Starling’s Law
o The SNS has a positive inotropic effect on the heart, meaning it causes an increase in SV at a constant preload
o Enhanced contractility results in more complete ejection of blood from the heart, hence a lower ESV & greater SV
o This type of regulation is referred to as homometric regulation
o Sympathetic stimulation via b1 receptors [POSITIVE INOTROPIC EFFECT]
o This increases the force of contraction by 2 mechanisms (short version):
• NEP increases the inward Ca+2 current during the plateau of each cardiac action potential
• NEP increases the activity of the SERCA pumps; as a result, more Ca+2 is accumulated by the SR and thus more Ca+2 is available for release in subsequent beats
After load
o The “load” the heart must overcome after (and while) it contracts
o Afterload is essentially the back pressure exerted on the aortic & pulmonary semilunar valves by arterial blood in the aorta and pulmonary trunk respectively
o ↑ afterload:
• The ventricle must pump blood against a higher pressure, resulting in a ↓ in stroke volume
o ↓ afterload:
• The ventricle pumps blood against a lower pressure, resulting in an ↑ in stroke volume
o Examples of increased afterload:
• Vasoconstriction (increased systemic vascular resistance)
• Increased blood volume or viscosity
o Vasodilators are often used to decrease afterload
• decreases myocardial oxygen demand
cardiac output or performance is enhanced by
o ↑ Preload
o ↑ Inotropy (SNS)
o ↑ Heart rate
o ↓ Afterload
cardiac output or performance is depressed by
o ↓ Preload
o ↓ Inotropy (SNS)
o ↓ Heart rate
o ↑ Afterload
Heterometric regulation of stroke volume
different volumes (EDV)
o stretching out the ventricles with different volumes of EDV causes a response to different forces of contraction.
• The more the ventricles are filled during diastole, the more blood they will eject during systole. (CO increases)
Homometric regulation of stroke volume
same volume (EDV) o The SNS can increase the force of contractility independent of EDV. (CO increases) • CO can decrease if HR increases too much and ventricles do not have time to fill.
Frank-Starling law of the heart
- Based on the length-tension relationship in the ventricle; increases in EDV cause an increase in ventricular fiber length, which produces an increase in developed tension
- Additionally, stretch of the myocardium by greater ventricular filling may enhance the affinity of troponin C for Ca+2 and also may increase Ca+2 uptake and release from the SR; hence, these two effects increase developed force and thereby contribute to the increase in force when the cardiac muscle fiber length increases
effects of nitrates on afterload
- Vasodilators are often used to decrease afterload
* decreases myocardial oxygen demand
entricular pressure-volume loops and the effects that preload, inotropism and afterload on these loops
• 4 → 1 is left ventricular filling
• 1 → 2 is isovolumetric ventricular contraction
o @ 2, we start to eject blood into the aorta.
• @ 3, the aortic SL valve closes
• 3 → 4 is isovolumetric ventricular relaxation
o @4 the mitral valve opens
- A = Increase in preload, you see an increase in volume and an increase in ejected blood.
- B = Increased afterload, you see an increase in required ventricular pressure during contraction and a decrease in ejected blood.
- C = Decreased afterload, you see an increase in contractility and more blood is ejected