Cardiac Anatomy
The heart is located in the centre of the chest, posterior to the sternum. The base (superior part of the heart) is found at the level of the third rib, and approximately 1.2cm to the left side of the chest. The pointed end of the heart (apex) is located at the gap between the fifth and sixth ribs (the fifth intercostal space), and is approximately 7.5cm left of the midline. The heart has a slight tilt, and is rotated to the left, meaning that the most anterior surface is actually the right ventricle.
The superior and inferior vena cava enter the heart at the right atrium, and are found to the right of the sternum. The aorta, which originates from the left ventricle at the lower border of the third costal cartilage (behind the sternum), runs up to the second costal cartilage, before turning and heading inferiorly from the aortic arch.
Chambers
The heart is divided into four major chambers, with the atria superiorly and the ventricles inferiorly. These are then divided by the left and right sides.
The right atrium is the area where blood returns to the heart from both systemic and coronary circulation, via the superior vena cava, inferior vena cava and coronary sinus respectively. This is a low pressure chamber. From here, blood flows into the right ventricle, via the right atrioventricular valve (also known as the tricuspid valve). The right ventricle is muscular, and is responsible for pumping blood into the pulmonary circuit. The superior end of the ventricle tapers into the conus arteriosus, which directs blood flow through the pulmonary semi-lunar valve and into pulmonary circulation.
Upon returning from pulmonary circulation via the pulmonary veins (the only veins which carry oxygenated blood), blood enters the left atrium. Similarly to the right atrium, the left stores blood before allowing it into the left ventricle, via the bicuspid (mitral) valve.
The left ventricle is the powerhouse of the heart, as reflected by the greater amount of myocardial tissue. Although it stores the same volume as the right ventricle, it is responsible for propelling blood throughout the systemic circuit, and hence requires much greater pressure (this is reflected in systolic blood pressure). Blood entering the systemic circuit passes through the aortic semi-lunar valve, and then enters the aorta.
Major vessels
The two major veins in the body are the superior and inferior vena cava. They enter the heart at the right atrium, and provide blood return from the superior and inferior halves of the systemic circuit. They are large, low pressure, and hence thin walled vessels. As they are under only a low pressure (3 – 8mmHg) these vessels are unlikely to rupture. However, they are susceptible to being compressed, as is the case in tension pneumothorax.
As blood exits the right atrium, it is carried by the pulmonary trunk, which then separates into the left and right pulmonary arteries. These are the only arteries which carry deoxygenated blood, and they branch out repeatedly into smaller and smaller arterioles, until finally becoming pulmonary capillaries, the site of gas exchange.
After leaving the pulmonary capillaries, blood (which is now oxygen rich) enters the pulmonary venules, which combine to form the four pulmonary veins, two for each lung. These four veins then all exit into the left atrium.
Blood which is expelled from the left ventricle enters the ascending aorta. The aorta is the largest, highest pressure vessel in the body. The first vessels to branch off of the aorta are the left and right coronary arteries, found superior to the aortic semi-lunar valve, at the very beginning of systemic circulation. At the aorta’s point of curvature (the aortic arch), three major arteries branch off; the brachiocephalic (which supplies the right hand side of the body), the left common carotid and the left subclavian arteries.
Layers of the Heart Wall
Although the pericardium is not precisely a part of the heart wall, it is important to consider. The outer, fibrous layer of the pericardium, known as the parietal pericardium, is separated from the heart by the pericardial cavity, an area of space between the heart and the pericardial sac. This space is normally occupied by 15 – 50mL of pericardial fluid, which helps prevent friction during muscle contraction. The inner layer of the pericardium (the visceral pericardium) is also the outermost layer of the heart wall, known as the epicardium. The epicardium is a serous membrane composed of exposed mesothelium cells.
The middle layer of the heart wall is the myocardium. As the name suggests, this layer is muscular, and hence the thickest of the heart wall layers. It is also home to the blood vessels and nerves which supply the heart. The muscle fibres themselves form figure-eight patterns around the chambers of the heart, and are responsible for contraction of the atria and ventricles.
The innermost layer of the heart, the endocardium, is again a thin layer of simple squamous epithelium, which is a continuation of the inner layer of the great vessels. The endocardium also includes the heart valves.
Valves
The cardiac valves are separated into two pairs – the atrioventricular valves, and the semi-lunar valves.
The atrioventricular (AV) valves separate the atria from the ventricles on either side of the heart. The left AV valve has two flap-like cusps, and is hence called the bicuspid (or mitral) valve. The right AV valve has three, and is known as the tricuspid valve. These valves serve an important role in the direction of blood flow and the prevention of regurgitation. When the ventricles are relaxed, the valves are flaccid, allowing blood flow from the atrium to the ventricle. When the ventricle is contracting, the cordae tendonae (heart strings) become firm due to papillary muscle action, and the pressure in the ventricles forces the valve shut. The cordae tendonae are essential in that they prevent the valve from opening in the opposite direction. If either the cordae tendonae or the papillary muscles are damaged, regurgitation occurs.
The semi-lunar valves separate the right and left ventricles from the pulmonary trunk and aorta respectively. They are also essential for ensuring one way blood flow, but unlike the AV valves do not require muscular bracing as the arterial walls do not contract and the relative position of the cusps are stable.
Mechanics of Blood Flow
Venous blood flow enters the heart at the right atrium from the superior and inferior vena cavae, as well as the coronary sinus. Passive blood flow from the right atrium to the right ventricle occurs due to gravity, and on atrial systole (contraction) approximately 20 – 30% of ventricular volume is squirted into the ventricle. This is known as the ‘atrial kick’, and becomes more important when heart rate is rapid and ventricles lack sufficient time to fill passively. Right atrial pressure is the same as central venous pressure, as there are no valves between them. It averages 2 – 6mmHg at rest.
At rest (diastole), pressure in the right ventricle is as low as 0 – 5mmHg, due to the elasticity and compliance of the myocardium. When contracting, the right ventricular systolic pressure is usually between 20 – 30mmHg. This not only forces open the pulmonary semi-lunar valve (allowing blood to enter the pulmonary circuit), but also closes the tricuspid valve, preventing backflow into the atrium.
After travelling through the pulmonary circuit, blood enters the left atrium at approximately 4 – 12mmHg of pressure. This blood then passively enters the left ventricle via the bicuspid/mitral valve, and is assisted by an atrial kick, the same as the right atrium.
During left ventricular systole, pressure reaches 100 – 140mmHg (this is reflected by systolic blood pressure). The pressure of the left ventricle is much greater than the right, due to the extra distance blood must travel through the systemic circuit. During left ventricular systole, the bicuspid/mitral valve is closed, and once LV pressure exceeds aortic pressure, the aortic semi-lunar valve will open, allowing blood flow into the systemic circuit.
| R) atrium | R) ventricle | L) atrium | L) ventricle | ||
| 0 msec | Atrial systole | Contracts, providing ‘atrial kick’ | Fills with blood via the tricuspid valve | Contracts, providing ‘atrial kick’ | Fills with blood via the bicuspid/mitral valve |
| 100 msec | Atrial diastole Ventricular systole | Relaxes, passively filling (2-6mmHg) | Contracts, closing the tricuspid valve | Relaxes, passively filling (8-12mmHg) | Contracts, closing the bicuspid/ mitral valve |
| Pressure continues to build, all valves are shut (isovolumetric contraction) | Pressure continues to build, all valves are shut (isovolumetric contraction) | ||||
| Pressure exceeds that of the pulmonary trunk, pulmonary semi-lunar valve opens and blood is expelled. (20-30mmHg) | Pressure exceeds that of the aorta, aortic semi-lunar valve opens and blood is expelled. (100-140mmHg) | ||||
| 370 msec | Ventricular diastole | Relaxed, passively filling | Pressure drops, ventricle relaxes and pulmonary semi-lunar valve closes. Tricuspid valve remains closed due to high ventricular pressure, isometric relaxation occurs. | Relaxed, passively filling | Pressure drops, ventricle relaxes and aortic semi-lunar valve closes. Bicuspid/mitral valve remains closed due to high ventricular pressure, isometric relaxation occurs. |
| 800 msec | Relaxed, passively filling. Blood flows into the ventricles. | Pressure drops further, allowing the tricuspid valve to open and for blood to passively fill ventricle. (0-5mmHg) | Relaxed, passively filling. Blood flows into the ventricles. | Pressure drops further, allowing the bicuspid/mitral valve to open and for blood to passively fill ventricle. (4-12mmHg) |
Characteristics of cardiac cells
All cardiac cells have four qualities which are responsible for their unique behaviour. These are;
– Conductivity: the ability of myocardial cells to carry an action potential from one to the other, without the need for specialized nerve cells.
– Excitability: the ability of myocardial cells to produce their own action potential.
– Contractility: the ability of myocardial cells to contract in response to action potential, causing muscular contraction.
– Rhythmicity: the ability of myocardial cells to spontaneously depolarise after a set period of time, due to slow leak of ions.
Cardiac Action Potentials
Pacemaker Cells
Each heart beat requires a complex series of electrical changes, and associated muscular contraction. Before looking at the overall conduction system, it is important to understand that there are two types of cells in the myocardial tissue – pacemaker cells and contractile cells.
Pacemaker cells are a specialized group of cells which make up only 1% of cardiac muscle. They are structurally similar to neurons, but are in fact specialized cardiac muscle cells. They are unique in that, unlike other cells, they are stimulate rhythmic depolarisation by the slow ‘leak’ of potassium ions out and sodium ions into the cell. This movement of ions causes the pacemaker cells membrane potential to reach -40mV, which is known as threshold potential. Once threshold potential is reached, the pacemaker cell rapidly depolarises, stimulating an action potential which is then carried throughout the cardiac conduction system.
However, not all pacemaker cells ‘leak’ at the same rate. Those in the sinoatrial (SA) node rhythmically depolarise at a rate of 60-100 times per minute, whilst the AV node does 40-60 times per minute, and the Purkinje fibres at less than 40 times per minute.
Due to this, the SA node will always spontaneously depolarise first (in a healthy heart), with that action potential then depolarising the rest of the pacemaker cells, essentially resetting them. Because of this, the SA node is known as the dominant pacemaker in the heart. If the SA node were to become damaged or otherwise inoperable, then the AV node would depolarise spontaneous, providing a heart rate of 40-60 beats per minute, in what is termed a junctional escape rhythm. If both the SA and AV nodes fail, the Purkinje fibres will depolarise at less than 40 beats per minute, causing an idioventricular rhythm. This rhythm is unlikely to be sustainable due to the poor cardiac output associated with it.
Phase 4 “Pacemaker potential” (orange line):
The slow influx of sodium ions into the cell (known as the funny current), as well as a gradually decreasing outflow of potassium ions drives resting membrane potential (-60mV) to be more positive, until reaching about -40mV, which is threshold potential.
Phase 0 “Rapid depolarisation” (red line):
Once threshold potential is reached, voltage gated calcium channels open, allowing a rapid influx of calcium ions into the cell. An increase in the funny current (sodium influx) contributes to the increase in membrane potential, until it reaches +10-20mV.
Phase 3 “Repolarisation” (blue line):
At the peak membrane potential, potassium leak channels open, causing potassium ions to rapidly escape the cell, reducing membrane potential. Closure of calcium channels and decreased sodium permeability also contributes to this drop in membrane potential.
During repolarisation, specialized proteins in the cell membrane (sodium-calcium exchanger and the sodium-potassium-ATPase pumps) restore resting membrane potential by removing calcium and sodium from the cell, whilst pumping potassium in.
Myocardial Cells
The action potential produced by these pacemaker cells is then carried throughout the conduction system, and affects the cardiac muscle cells (which make up the other 99% of the myocardium). The cells also rely on depolarisation to both carry the action potential, as well as cause muscular contraction which is responsible to the heart’s pumping action.
Phase 0 “Depolarisation phase” (orange line):
Triggered when the cell reaches threshold potential, due to an action potential produced by a pacemaker cell. Voltage gated fast sodium channels open, allowing a rapid influx of sodium ions and increasing membrane potential. The cell is depolarising at this stage and beginning to contract.
Phase 1 “Early rapid repolarisation” (start of purple line):
Fast sodium channels shut, preventing further sodium ions from entering the cell. The rapid drop in membrane voltage is caused by the loss of potassium ions from within the cell.
Phase 2 “Plateau phase” (rest of purple line):
Slow calcium channels open, allowing calcium ions to enter the myocardial cells and causing increasing contraction as more calcium enters the cell. Membrane potential remains relatively stable (hence ‘plateau’) due to continuing loss of potassium from within the cell, and the slow influx of sodium ions.
Phase 3 “Terminal rapid repolarisation” (blue line):
Calcium channels close, preventing more from entering the cell and causing muscular relaxation. Potassium continues to leak out of the cell at an increasing rate as more potassium leak channels open, causing membrane potential to drop further until it reaches resting membrane potential.
Phase 4 “Resting membrane potential” (black line):
Once membrane potential returns to -90mV, sodium and potassium channels close. However, there is an excess of sodium ions inside the cell, whilst there are potassium ions outside the cell. This triggers the sodium-potassium-ATPase pumps to reverse this, restoring the cell to it’s resting state and ready for the next depolarisation.
Refractory Period
In the immediate moments after depolarisation, the myocardial cells are physically unable to conduct another action potential, as resting membrane potential has been lost and electrolytes have moved. This is known as the absolute refractory period, where no amount of stimulation will trigger another impulse. As outlined above, sodium and potassium are rapidly replaced, so that the heart can conduct another beat. There is a brief time between depolarisation and return to resting membrane potential where, although not completely repolarised, the myocardium is able to be depolarised by a stronger than normal stimulus. This is known as the relative refractory period, and corresponds with the second half of the T wave on an ECG. During this time, the heart is vulnerable to entering potentially lethal arrhythmias, as it is only partially repolarised. A strong blow to the chest, or an ectopic beat (R on T phenomena) is enough to trigger this. The risk of such an event increases in patients with abnormal conduction pathways (such as Wolf Parkinson White) or who have a prolonged QT interval, as seen in tricyclic anti-depressant overdose.
Cardiac Conduction System
The cardiac conduction system consists of several specialised structures designed to generate and propagate action potentials throughout the heart and stimulate contraction in a way which allows the effective ‘squirting’ of blood. The first part of the conduction system is the sinoatrial (SA) node. The SA node is located in the posterior wall of the right atrium, near the entrance of the superior vena cava. The SA node is known as the dominant pacemaker, as it depolarises at a rate of 60 – 100 beats per minute, as discussed previously. This intrinsic rate can be adjusted by external influence such a sympathetic or parasympathetic nervous action, hormone secretion and myocardial hypoxia. Cardiac rhythms which originate at the SA node are the sinus rhythms, and have a normal P-wave on ECG.
The action potential leaves the SA node, and travels through internodal pathways to the atrioventricular (AV) node, located in the floor of the right atrium. Impulses reach the left atrium via Bachmann’s bundle. It is important to note that in a normal heart, the AV node is the only means for transducing action potentials from the atria to the ventricles, as the cardiac skeleton separates the two.
The AV node is a specialised structure which actually serves to slow down conduction through the heart, with an impulse taking about 100msec to pass through. This is important as it allows the ventricles to receive atrial kick before contracting, hence ensuring a full stroke volume. This occurs due to the structure of the AV node, which consists of multiple nodal cells which are smaller in diameter and less efficient than other cells in the conducting system. The AV node can also serve as the dominant pacemaker, if the SA node is damaged or destroyed.
The action potential then exits the AV node, into the Bundle of His (AV bundle), which is the only normal connection between the atria and ventricles. It travels through the intraventricular septum before splitting into the right and left bundle branches, which innervate the right and left ventricles respectively. As the left ventricle is significantly more muscular, the left bundle branch then splits into the anterior and posterior fasicles. As the bundle branches further divide, they split off into Purkinje fibres, which directly innervate the myocardium. When stimulated, the bundle branches transfer action potential across the moderator band directly to the papillary muscles, which are attached the the cordae tendonae (heart strings). This causes them to tense up, and therefore secure the heart valves, just prior to ventricular contraction, protecting the valves from damage and preventing back flow. In addition, the layout of the bundle branches causes contraction to start at the apex (bottom) of the venticles, pushing upwards towards the base (top), resulting in a squirting action which forces blood into circulation.
