Victor Forge
The human heart is composed of cardiac muscle, also known as the myocardium. This muscle is responsible for pumping blood into circulation by generating sufficient force through coordinated contractions. These contractions are controlled by specialised cardiac muscle cells called pacemaker cells, which directly control heart rate. The pacemaker cells are self-excitable and able to depolarise and fire action potentials on their own, a feature called autorhythmicity. The action potential travels along the sarcolemma and into the t-tubules, causing the cell to contract. This process of excitation-contraction coupling (ECC) is fundamental to the functioning of the cardiac muscle.
| Characteristics | Values |
|---|---|
| Type of muscle | Cardiac muscle, also called the myocardium, is one of three major categories of muscles in the human body, the other two being smooth muscle and skeletal muscle. |
| Control | Unlike skeletal muscle, cardiac muscle is under involuntary control. |
| Composition | Cardiac muscle is made up of sarcomeres that allow for contractility. |
| Function | The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. |
| Contractions | The contractile functions of the heart require ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones. |
| Electrical activity | The cardiac conduction system is the network of nodes, cells, and signals that controls the heartbeat. Electrical signals move through the heart, causing it to beat and contract. |
| Action potential | The generation of a cardiac action potential is involuntary and occurs through excitation-contraction coupling (ECC). Action potentials travel along the sarcolemma and into the t-tubules, leading to depolarization of the membrane. |
| Calcium involvement | Calcium ions play a crucial role in cardiac excitation-contraction coupling. Calcium influx occurs through voltage-sensitive dihydropyridine (DHP) receptors and L-type calcium channels during the plateau phase of the action potential. This triggers the release of more calcium from the sarcoplasmic reticulum through the ryanodine receptor. |
| Contraction mechanism | The released calcium attaches to troponin C, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, leading to contraction. |
| Relaxation | Cardiac muscle cells undergo brief relaxation periods between contractions. This relaxation is essential for the heart to fill with blood for the next cycle. |
| Refractory periods | Cardiac cells have two refractory periods: the absolute refractory period, during which the cell cannot produce another action potential, and the relative refractory period, where a stronger stimulus is required to initiate another action potential. |
| Pacemaker cells | Pacemaker cells, or autorhythmic cells, are specialized cardiac muscle cells that directly control heart rate by generating and propagating electrical impulses throughout the heart. |
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What You'll Learn
The cardiac conduction system
The sinoatrial (SA) node is a collection of specialised cells (pacemaker cells) that can spontaneously generate electrical impulses. The SA node is located in the upper wall of the right atrium, at the junction where the superior vena cava enters. The wave of excitation created by the SA node spreads via gap junctions across both atria, resulting in atrial contraction. The rate at which the SA node generates impulses is influenced by the autonomic nervous system. The sympathetic nervous system increases the firing rate of the SA node, and thus the heart rate, while the parasympathetic nervous system decreases the firing rate and heart rate.
Upon reaching the atrioventricular (AV) node, the signal is delayed. It is then conducted into the bundle of His, down the interventricular septum. The bundle of His and the Purkinje fibres spread the wave impulses along the ventricles, causing them to contract and deliver blood out to the body.
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Electrical impulses
The cardiac conduction system is the heart's electrical system. This network of nodes, cells, and signals controls the heartbeat. Each heartbeat is the result of electrical signals travelling through the conduction pathway of the heart.
The process begins when the sinoatrial (SA) node creates an excitation signal. This electrical signal prompts the release of calcium ions from the sarcoplasmic reticulum, which is vital for the plateau phase of the action potential. This is known as calcium-induced calcium release. The increased intracellular calcium concentration triggers the sarcoplasmic reticulum to release more calcium through the ryanodine receptor.
The released calcium attaches to troponin C, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, and contraction occurs. Cross bridges last as long as calcium is attached to troponin. This process is known as excitation-contraction coupling (ECC).
The myocardial conducting cells form the conduction system of the heart. These cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart and triggers the contractions that propel blood. The action potential passes along the cell membrane, causing the cell to contract. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the next.
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Calcium and contraction
The human heart consists of over three billion heart muscle cells, which contract during each heartbeat, facilitating the pumping of blood. This process is known as excitation-contraction coupling (ECC). Calcium plays a crucial role in this mechanism.
Calcium particles carry an electrical charge and enter the heart muscle cells during each beat, contributing to the electrical signal that triggers contraction. These calcium particles initiate contraction by binding to specialised machinery within the cell. This machinery then starts to move, causing the cell to contract. The calcium particles bind to troponin, resulting in the sliding of thick and thin filaments, cell shortening, and the development of pressure within the ventricle, leading to the ejection of blood. The force of the contraction depends on the amount of calcium bound to troponin.
The sarcoplasmic reticulum, a large chamber inside the cell, stores most of the calcium required for heart contraction. Calcium enters the heart cell through the calcium ion channel, activating the ryanodine receptor to release sufficient calcium from the sarcoplasmic reticulum to initiate heart muscle contraction. This calcium release is known as calcium-induced calcium release. The calcium binds to troponin, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, and contraction occurs.
During relaxation, calcium must be detached from troponin and expelled from the cell or stored back inside the sarcoplasmic reticulum. This process allows the heart to refill with blood before the next heartbeat. Without calcium, the heart would stop beating immediately, as demonstrated experimentally by Dr Sydney Ringer in the early 1880s.
Impaired calcium release can lead to decreased muscle contraction (systolic dysfunction), while defective calcium removal can hinder relaxation (diastolic dysfunction). These calcium imbalances may contribute to heart failure and cardiac hypertrophy.
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Autorhythmicity
The heart is a muscular organ that maintains blood flow by contracting. Unlike skeletal muscle, cardiac muscle is under involuntary control. The heart's ability to contract without the need for an external stimulus is due to its autorhythmicity. Autorhythmicity is a property of the heart's autorhythmic cells, which include the cells of the SA node, AV node, and Purkinje fibres. These cells have the capacity for self-excitation and conduction of action potentials throughout the heart.
The increased intracellular calcium concentration triggers the release of more calcium from the sarcoplasmic reticulum through ryanodine receptors, a process known as calcium-induced calcium release. The released calcium attaches to troponin C, causing tropomyosin to detach from the myosin-binding sites on actin. Actin and myosin then form a cross-bridge, resulting in contraction. The contraction lasts as long as calcium remains attached to troponin.
Autorhythmic cells, also known as pacemaker cells, are self-excitable and can depolarize to the threshold required to fire action potentials on their own. These cells initiate and propagate the action potential that travels through the heart muscle. They contain sodium ion channels that allow a slow influx of sodium ions, causing the membrane potential to rise slowly. This movement of sodium ions creates a spontaneous depolarization that brings the cell to the threshold potential. At this point, voltage-gated calcium ion channels open, allowing calcium ions to enter the cell and further depolarize it, initiating the action potential.
The autorhythmicity of the heart ensures that it can contract and pump blood throughout the body without relying on external stimuli. This self-excitation property of autorhythmic cells is essential for maintaining the heart's function and regulating blood flow to meet the metabolic demands of the body.
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Cardiac output
The cardiac muscle is responsible for the heart's contractile functions, which require ATP. The contractile functions are controlled by electrical signals from the cardiac conduction system, which tell the heart when to beat and when to relax. The cardiac conduction system is a network of nodes, cells, and signals.
The body's demand for oxygen changes during exercise, and cardiac output is altered by modulating both heart rate and stroke volume. This is because blood delivers oxygen to the cells, and during exercise, the body requires more oxygen.
There are several methods to measure cardiac output, including the thermodilution method, which involves measuring the change in temperature of blood between a port in the catheter and a thermistor. Another method is transthoracic echocardiography to estimate stroke volume.
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Frequently asked questions
Cardiac muscle, also called the myocardium, is one of three major categories of muscles in the human body, the other two being smooth muscle and skeletal muscle. The heart is made up of three layers—the pericardium, myocardium, and endocardium.
The primary function of cardiac muscle is to pump blood into circulation by generating sufficient force. The mechanism behind each coordinated contraction involves the cardiac muscle and electrical impulses. These contractile functions of the heart require ATP, which can be obtained through various substrates, including fatty acids, carbohydrates, proteins, and ketones.
The cardiac conduction system is the network of nodes, cells, and signals that controls your heartbeat. Electrical signals move through your heart, making it beat. The sinoatrial (SA) node creates an excitation signal, which is like electricity travelling through wires to an appliance in your home.
Myocardial conducting cells initiate and propagate the action potential (the electrical impulse) that travels throughout the heart and triggers the contractions that propel the blood. All cardiac muscle cells are electrically linked to one another, by intercalated discs which allow the action potential to pass from one cell to the next.
