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Action potentials originate in the sinoatrial (SA) nodeand travel across the wall of the atrium (arrows) fromthe SA node to the atrioventricular (AV) node.
Action potentials pass through the AV node andalong the atrioventricular (AV) bundle, which extendsfrom the AV node, through the fibrous skeleton, intothe interventricular septum.
The AV bundle divides into right and left bundle branches,and action potentials descend to the apex of each ventriclealong the bundle branches.
Action potentials are carried by the Purkinje fibersfrom the bundle branches to the ventricular walls.
Contraction of the ventricles causespressure in the ventricles to increase.Almost immediately, the AV valvesclose (the first heart sound). Thepressure in the ventricles continuesto increase.
Continued ventricular contractioncauses the pressure in the ventriclesto exceed the pressure in the pulmonarytrunk and aorta. As a result, thesemilunar valves are forced open,and blood is ejected into thepulmonary trunk and aorta.
The atria contract and completeventricular filling.
The AV valves open, and blood flows intothe ventricles. The ventricles fillto approximately 70% of theirvolume.
At the beginning of ventriculardiastole, the ventricles relax, and thesemilunar valves close (the secondheart sound).
Sensory neurons (green) carryaction potentials from baroreceptorsto the cardioregulatory center.Chemoreceptors in the medullaoblongata influence thecardioregulatory center.
The cardioregulatory center controlsthe frequency of action potentials inthe parasympathetic neurons (red )extending to the heart. Theparasympathetic neurons decreasethe heart rate.
The cardioregulatory center controlsthe frequency of action potentials inthe sympathetic neurons (blue)extending to the heart. Thesympathetic neurons increase theheart rate and the stroke volume.
The cardioregulatory centerinfluences the frequency of actionpotentials in the sympatheticneurons (blue) extending to theadrenal medulla. The sympatheticneurons increase the secretion ofepinephrine and somenorepinephrine into the generalcirculation. Epinephrine andnorepinephrine increase the heartrate and stroke volume.
Adrenal medullaEpinephrine and norepinephrine
Circulation
Heart
SA node
Baroreceptorsin aorta
Carotid bodychemoreceptors
Baroreceptorsin wall of internalcarotid artery
Cardioregulatory center andchemoreceptors in medulla oblongata
The SA node and cardiac muscle (theeffectors) increase activity and heartrate and stroke volume increase.
The SA node and cardiac muscle (theeffectors) decrease activity and heartrate and stroke volume decrease.
Baroreceptors in the carotid arteries andaorta detect a decrease in blood pressure.
The cardioregulatory center in the brainincreases sympathetic stimulation of theheart and adrenal medulla and decreasesparasympathetic stimulation of the heart.
Baroreceptors in the carotid arteries andaorta detect an increase in blood pressure.
The cardioregulatory center in the braindecreases sympathetic stimulation of theheart and adrenal medulla and increasesparasympathetic stimulation of the heart.
The SA node and cardiacmuscle (the effectors) increaseactivity and heart rate and strokevolume increase, increasingblood flow to the lungs.
The SA node and cardiac muscle(the effectors) decrease activityand heart rate and stroke volumedecrease, reducing blood flow tothe lungs
Chemoreceptors in the medulla oblongata detect anincrease in blood pH (often caused by a decreasein blood CO2). Control centers in the brain decreasestimulation of the heart and adrenal medulla.
Chemoreceptors in the medulla oblongata detect adecrease in blood pH (often caused by an increasein blood CO2). Control centers in the brain increasestimulation of the heart and adrenal medulla.