The heart is made of two main types of myocardial cells: contractile and conductive cardiomyocytes.
The conductive cells generate the electrical impulse that drives cardiac activity, and transmit this signal throughout the heart. These make up structures such as the SA node, AV node, internodal tracts, Bachmann’s bundle, bundle of His, and the Purkinje fibres.
The contractile cells are activated by the conductive cells. When activated, they cause heart muscle contraction.
Note some important differences between contractile and conductive myocardium:
Electrical conduction is much faster in conduction cells than contractile cells
Most of the myocardium in the heart is contractile; only a small proportion, mass-wise, is conductive.
The cardiac muscle cells combine to form a functional syncytium, in which the several individual cells are interconnected such that they function as one unit. There are gap junctions between cells that are permeable to ions, allowing action potentials to permeate from one cell to the next. Due to this, an action potential at one point in the heart tends to propagate through the entirety of the myocardium.
Note that, anatomically, there are fibrous tissues, particularly those around the mitral and tricuspid valves, which interrupt the syncytium by insulating the atrial myocardium from the ventricular myocardium. This is so that, physiologically, the only path through which the atria and ventricles can communicate is the AV node.
Cardiac Action Potentials
The normal cardiac cell has a slightly negative resting membrane potential of -70 mV. This is maintained by differing concentrations of various organic and inorganic ions across the cell membrane, but mainly sodium and potassium. At rest, the cell has a much greater concentration of potassium inside the cell (~150 mEq) compared to outside (~5 mEq), whereas it has a much greater concentration of sodium outside the cell (~150 mEq) compared to inside (~15 mEq). The difference in ionic concentrations across the membrane leads to the development of a potential difference.
Despite the drastically different ionic potentials across the cell membrane, the concentration gradient is maintained by ion channels that don't permit ion diffusion across the membrane.
Below are the action potentials for conductive cells and contractile cells:
Conductive Cardiomyocytes
In conductive cardiomyocytes, there are three main phases of the action potential:
Phase 4: the "pre-potential" phase, in which there is a leaky inward Na+ current into the cell, causing slow depolarization. This is also known as spontaneous diastolic depolarization.
Phase 0: the depolarization phase, which occurs after the leaky Na+ current manages to increase the membrane potential to the threshold voltage. Ca++ channels open and allow a rapid influx of calcium ions that depolarize the cell.
Phase 3: the repolarization phase, during which K+ channels open and allow outward flow of potassium.
During all the phases of the action potential, the Na/K-ATPase pump is working to restore ionic gradients by pumping 3 Na+ ions outside the cell, and 2 K+ ions into the cell. There is net charge movement outside the cell, and so the Na/K-ATPase pump tends to drop the membrane potential, in what is called a "hyperpolarizing current".
Contractile Cardiomyocytes
The contractile cardiomyocytes have a different and longer action potential than conductive cardiomyocytes. In contractile cardiomyocytes, there are five main phases of the action potential:
Phase 4: resting membrane potential, with no leaky inward currents. Without an external stimulus, threshold voltage for depolarization will not be reached.
Phase 0: rapid depolarization due to inward Na+ current. For this to happen, an external stimulus (i.e. depolarization of an adjacent cell) causes partial depolarization, enough to pass the threshold voltage and initiate rapid depolarization.
Phase 1: efflux of K+ causes partial repolarization.
Phase 2: Continued K+ efflux combined with Ca++ influx. The opposing movement of cations causes a balance of membrane potential which appears as a plateau on the action potential. The Ca++ is necessary for myocardial contraction.
Phase 3: Ca++ influx stops, followed by rapid repolarization secondary to faster K+ efflux.
Again, the Na/K-ATPase pump works in the background during all these phases, resetting the ionic gradients across the cell and creating a hyperpolarizing current all the while.
There is also another membrane protein known as the sodium-calcium exchanger (NCX) that restores the intracellular calcium concentration following the Phase 2 calcium influx. This antiporter moves one Ca++ ion out for 3 Na+ ions in, thus creating a net depolarizing current as there are more positive charges moving into the cell.
There's also an important concept known as the refractory period, which is subdivided into the absolute and relative refractory period. During the absolute refractory period, additional action potentials cannot trigger a new impulse. During the relative refractory period, a strong enough impulse can overcome repolarization and trigger a new impulse, which is an important mechanism of abnormal heart rhythms.
Physiologic Regulation of the Heart Rate
Heart rate (HR) is slower at rest and faster with exertion to meet the metabolic demands of the body.
The physiologic variation in HR is caused by the autonomic effects on the sinus node, the pacemaker of the heart.
Sympathetic stimulation (SNS) speeds up the HR
Parasympathetic stimulation (PSNS) slows the HR
How does the autonomic system regulate heart rate?
SNS stimulation increases the permeability of Na+ channels, which increases automaticity of the pacemaker cells (as shown below).
PSNS stimulation increases the permeability of potassium ion channels, which causes excess efflux of K+ from pacemaker cells, leading to hyperpolarization. Therefore, the cells become less excitable.
Excitation-Contraction Coupling
Excitation-contraction coupling (ECC) refers to the process wherein an action potential triggers a myocyte to contract. ECC is an important concept that helps us understand the states of inotropy (the speed and strength of muscle contraction) and lusitropy (the ability of the heart to relax).
The action potential, as discussed above, travels along the sarcolemma and down the T-tubule, causing depolarization of the cell membrane. Receptors within the membrane of the T tubule open, causing calcium influx into the sarcoplasmic reticulum (SR) of the cell during phase 2 of the action potential. This influx triggers a release of existing calcium ions from the SR into the sarcoplasm. Free calcium binds to troponin-C (TN-C), causing a conformational change that exposes a site on the actin molecule that allows myosin heads to bind to actin. This binding results in ATP hydrolysis which provides the energy required for the myosin and actin filaments to slide past each other, decreasing the sarcomere length, and effectively, causing contraction. This will occur for as long as the sarcoplasmic calcium remains elevated.
At the end of phase 2, calcium influx slows and free calcium is re-sequestered back into the SR. Calcium is thereby removed from TN-C causing a conformation change again and the myosin-binding site on actin is no longer exposed. The original sarcomere length is restored and the muscle fibre relaxes.
As you have hopefully realized, sarcoplasmic free calcium determines the contraction and relaxation of the muscle fibre. Mechanisms that increase sarcoplasmic calcium increases the amount of ATP hydrolyzed which enhances the force generated by the myosin-actin interaction and the speed of sarcomere shortening. Essentially, this causes positive inotropy. Beta-adrenergic stimulation caused by the sympathetic nervous system acts to increase the conductance of calcium channels on the SR. That causes increase influx of calcium into the sarcoplasm and also enhances uptake of calcium back into the SR. There, beta-adrenergic stimulation increases inotropy and lusitropy, which ultimately results in increased stroke volume.
