Adaptation to short-term changes is provided by the Frank-Starling mechanism. Long-term changes in cardiac activity are regulated by the autonomic nervous system.
1. Frank-Starling mechanism:
a law that describes the relationship between end-diastolic volume and cardiac stroke volume Cardiac contractility is directly related to the wall tension of the myocardium.
- An increase in end-diastolic volume (preload) will cause the myocardium to stretch (↑ end diastolic length of cardiac muscle fibers), which increases contractility (↑ force of contraction) and results in increased stroke volume in order to maintain cardiac output.
This relationship between end-diastolic volume and stroke volume is shown in the Frank-Starling and stroke volume is shown in the Frank-Starling curve. and stroke volume is shown in the Frank-Starling
Maintain CO by modulating contractility and SV Stroke volume of both ventricles should remain the same.
Autonomic innervation : The autonomic nervous system is able to regulate heart rate, excitability, conductivity, relaxation, and contractility.
- Sympathetic fibers
innervate both the atria and ventricles.
only innervate the atria.
modulation of cardiac action by sympathetic and/or parasympathetic nerve fibers
long-term regulation of cardiac action
Chronotropy: any influence on the heart rate
Dromotropy: any influence on the conductivity of myocardium
Inotropy: any influence on the force of myocardial contraction
Lusitropy: any influence on the rate of relaxation of the myocardium
Bathmotropy: any influence on the excitability ofof the myocardium
Bathmotropy: any influence on the excitability of the myocardium.
A. Sympathetic effect :
a. Atria and ventricles : Fibers from the sympathetic cervical trunk (superior, middle, and
inferior cardiac nerve).
It increase the heart rate, conduction, contractility and relaxation.
The mechanism :
Activation of beta1 adrenergic receptors (Gs protein-coupled) of the heart by epinephrine and
norepinephrine → ↑ activity of adenylyl cyclase → ↑ intracellular cAMP concentration in SA node
cardiomyocytes, which then:
1. Increases the conductance of funny sodium channels and L-type calcium channels → ↑ influx
of cations during spontaneous depolarization → faster attainment of the threshold potential
during phase 4 of pacemaker action potential for initiating the rhythmic cardiac action potential →
↑ heart rate (positive chronotropic)
2 . Activates protein kinase A , which leads to two effects:
- Phosphorylation of L-type Ca2+ channels in AV node → increased Ca2+ entry → increased Ca2+-induced Ca2+ release during action potential → increased contraction and conduction (positive dromotropic and inotropic)
- Phosphorylation of phospholamban → activation of sarcoplasmic reticulum Ca2+- ATPase (SERCA) → increased transport of Ca2+ back into sarcoplasmic reticulum after a contraction → faster relaxation (positive lusitropic).
B. Parasympathetic effect :
Atria : Branches of the vagus nerve
- Cervical cardiac branches
- Thoracic cardiac branches
It decrease the heart rate and atrial contractility.
The Mechanism :
- Exerts its action on the heart through parasympathetic muscarinic ACh receptors
- Exerts its action on the heart through parasympathetic muscarinic ACh receptors (subtype M2) on SA and AV node cardiomyocytes.
- Activation of M2 receptors on SA node (negative chronotropic).
- Reduces the conductance of funny sodium channels via adenylyl cyclase, decreasing cAMP → ↓ pacemaker current (lengthens the rate of depolarization in the slow depolarization phase).
- Increases conductance of the slow potassium channels → hyperpolarization of the resting membrane potential (harder to overcome).
- Vagal fibers innervate the AV node (negative dromotropic): slows cardiac action potential propagation (can result in complete AV block).