Ventricular action potential

The action potential of a ventricular myocyte

In electrocardiography, the ventricular cardiomyocyte membrane potential is about −90 mV at rest, which is close to the potassium reversal potential. When an action potential is generated, the membrane potential rises above this level in four distinct phases.

The beginning of the action potential, phase 0, specialized membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell. This causes the membrane potential to rise at a rate of about 300 V/s. As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation.

The Na⁺ channel opening is followed by inactivation. Na⁺ inactivation comes with slowly activating Ca²⁺ channels at the same time as a few fast K⁺ channels open. There is a balance between the outward flow of K⁺ and the inward flow of Ca²⁺ causing a plateau of length in variables. The delayed opening of more Ca²⁺-activated K⁺ channels, which are activated by build-up of Ca²⁺ in the sarcoplasm, while the Ca²⁺ channels close, ends the plateau. This leads to repolarisation.

The depolarization of the membrane allows calcium channels to open as well. As sodium channels close calcium provides current to maintain the potential around 20 mV. The plateau lasts on the order of 100 ms. At the time that calcium channels are getting activated, channels that mediate the transient outward potassium current open as well. This outward potassium current causes a small dip in membrane potential shortly after depolarization. This current is observed in human and dog action potentials, but not in guinea pig action potentials.

Repolarization is accomplished by channels that open slowly and are mostly activated at the end of the action potential (slow delayed-rectifier channels), and channels that open quickly but are inactivated until the end of the action potential (rapid delayed rectifier channels). Fast delayed rectifier channels open quickly but are shut by inactivation at high membrane potentials. As the membrane voltage begins to drop the channels recover from inactivation and carry current.

Cardiac output	Cardiac cycle Cardiac output Heart rate Stroke volume Stroke volume End-diastolic volume End-systolic volume Afterload Preload Frank–Starling law Cardiac function curve Venous return curve Wiggers diagram Pressure volume diagram

Ultrasound	Fractional shortening = (End-diastolic dimension End-systolic dimension) / End-diastolic dimension Aortic valve area calculation Ejection fraction Cardiac index

Heart rate	Cardiac pacemaker Chronotropic (Heart rate) Dromotropic (Conduction velocity) Inotropic (Contractility) Bathmotropic (Excitability) Lusitropic (Relaxation)

Conduction	Conduction system Cardiac electrophysiology Action potential cardiac atrial ventricular Effective refractory period Pacemaker potential Electrocardiography P wave PR interval QRS complex QT interval ST segment T wave U wave Hexaxial reference system

Chamber pressure	Central venous Right atrial ventricular pulmonary artery wedge Left atrial ventricular Aortic

Other	Ventricular remodeling

Vascular system/
Hemodynamics

Blood flow	Compliance Vascular resistance Pulse Perfusion

Blood pressure	Pulse pressure Systolic Diastolic Mean arterial pressure Jugular venous pressure Portal venous pressure

Regulation of BP	Baroreflex Kinin–kallikrein system Renin–angiotensin system Vasoconstrictors Vasodilators Autoregulation Myogenic mechanism Tubuloglomerular feedback Cerebral autoregulation Paraganglia Aortic body Carotid body Glomus cell

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Ventricular action potential

See also