Heart and Blood Flow

Electrical Impulses in the Heart and the Electrocardiogram (ECG)

Heart muscle cells transmit electrical impulses, which cause the heart muscle to contract and move blood out of the heart.

When the muscular walls of the heart contract, blood is ejected from the heart. During relaxation, the heart is filling with blood. As with skeletal muscle, the myocardial (heart muscle) cells contract once electrical impulses generated in the form of action potentials initiate a cascade of events that leads to force generation within the cell. Unlike skeletal muscle, the contraction of the heart needs to be highly coordinated. Therefore, the action potentials originate from specialized myocardial conducting cells and are then spread throughout the entire organ in a specific pathway that optimizes blood flow through the heart. The contraction of the heart is under both extrinsic (from an external source) and intrinsic (from an internal source) control. Without extrinsic neural and hormonal stimulation, the heart will continue to beat at a rate of ~100 beats/min. At a normal resting state, neural and chemical input decrease this value to a person's resting heart rate (75 beats/min on average). Heart rate can be altered to meet changing metabolic demands that can come from increased physical activity or stress.

A pacemaker is a group of noncontractile cells in the right atrium of the heart that regulates the depolarization of the myocardium. The plasma membrane that separates the inside and outside of pacemaker cells has specialized protein channels that allow sodium ions to slowly enter the cells, making the inside of the cell more positive. Once a threshold is reached, calcium channels open, and positively charged calcium ions rush into the cell, rapidly depolarizing the cell further. Potassium channels then open, and positively charged potassium ions flow out of the cells, leading to repolarization and the closing of the calcium channels. The slow influx of sodium then repeats, so the action potentials continue to fire automatically, which keeps the rhythmic contractions of the heart going.

Action Potentials in Pacemaker Cells

The pacemaker cells in the heart are specialized to allow for automatic depolarizations of the myocardium, the change in membrane potential of the heart muscle cells to make the inside more positive, which leads to heart contractions.
The action potentials in the contractile cells of the heart differ from those in the pacemaker cells. The depolarization is not automatic, as it is in pacemaker cells. Instead, the sodium channels open in response to a stimulus. Once the cell membrane is depolarized (becomes more positive) from sodium ion influx, calcium channels open, and positively charged calcium ions slowly enter the cell, creating a near plateau of the membrane potential. Repolarization occurs by closing the calcium channels and the opening of potassium channels. Because of the involvement of calcium, the contraction phase is longer, and the refractory period, the period of time after depolarization that the membrane does not respond to additional stimuli, is an order of magnitude greater than in skeletal muscle. This increased refractory period prevents the heart muscle from producing tetanic contractions, sustained force generation from rapid firing of action potentials. This is important to allow the heart to fill with blood during the relaxation phase between each contraction.

Action Potential in a Contractile Myocardial Cell

The action potential, or changes in membrane potential, in a contractile myocardial (heart) cell leads to force generation in the heart.
The intrinsic conduction system begins in the sinoatrial (SA) node, located within the wall of the right atrium near the superior vena cava. The SA node contains pacemaker cells and is responsible for initiating action potentials in the heart. Once the action potential is generated, the flow of ions continues through gap junctions (openings between cells), spreading the impulse from cell to cell. The signal spreads through both atria and reaches the atrioventricular (AV) node, located in the right atrium near the tricuspid valve. When the signal reaches the AV node, there is a brief delay to allow the atria to fully contract before ventricular contraction. The atrial cells are not connected to the ventricular cells by gap junctions, and the AV node is the only mechanism of communication between them. Once the AV node is triggered, the signal travels down the interventricular septum via the atrioventricular bundle (bundle of His) and bundle branches and then up the subendocardial conducting network (Purkinje fibers), located in the outer walls of the ventricles. The route of electrical transmission causes the bottom of the ventricles to contract first, and the wave of electrical impulses travels superiorly by gap junctions. This upward wave of contraction allows maximal blood ejection from the ventricles.

Heart Conduction

The conduction (electrical) pathway of the heart is coordinated to optimize the flow of blood through the heart.
The electrocardiogram (ECG or EKG) is a diagnostic tool used to measure electrical activity in the heart. An ECG is performed by attaching metal electrodes to specific locations on the arm, chest, and legs. A normal ECG reading has three main deflections (changes in electrical activity): a P wave, a QRS complex, and a T wave. The P wave is an upward deflection that occurs as a result of atrial depolarization, the QRS complex occurs during ventricular depolarization (and atrial repolarization), and the T wave is the result of ventricular repolarization. An ECG reading can be used to determine heart rate and various abnormalities in heart function.


An electrocardiogram measures the electrical activity of the heart. The three major activities are atrial depolarization (P wave), ventricular depolarization (QRS complex), and ventricular repolarization (T wave). Depolarization of the heart tissue leads to muscular contraction, and repolarization leads to relaxation. Atrial repolarization is masked by ventricular depolarization.