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Cardiovascular System – The Heart (Lecture Unit #2, BIOL 2222, Ch. 19)
Overview of the Cardiovascular System
Anatomy: The cardiovascular system is made of the heart and all the blood vessels that carry blood throughout your body.
Heart: This is a powerful, four-chambered muscular organ that acts like a double pump, pushing blood to two separate circuits.
Vessels: These are the tubes that carry blood:
Arteries: Carry o2 blood away from the heart.
Veins: Carry non o2 blood toward the heart. (Other then pulmonary vein)
Capillaries: Tiny, thin-walled vessels where oxygen, nutrients, and waste products are exchanged between blood and tissues.
Key function: The main job of the cardiovascular system is to transport blood constantly, which helps maintain a stable internal environment (homeostasis).
It delivers essential oxygen (O2O2) and nutrients to every cell in the body.
Simultaneously, it removes waste products like carbon dioxide (CO2CO2) and other metabolic byproducts.
Adequate perfusion: This term refers to the condition in which sufficient blood (measured in millilitres per minute per gram of tissue, mL/min/g) reaches all cells to maintain their viability and proper function.
Requirements for proper perfusion:
The heart must pump continuously without interruption.
The blood vessels must remain open, flexible, and healthy to allow blood to flow freely.
Blood Vessels & Circulatory Circuits
Blood Composition: In most cases, arteries carry oxygen-rich (oxygenated) blood, while veins carry oxygen-poor (deoxygenated) blood.
Capillaries: These are the smallest and most numerous blood vessels, forming networks within tissues. Their walls are extremely thin, allowing for efficient exchange of gases, nutrients, and wastes.
Pulmonary circuit: This circuit specifically moves blood between the heart and the lungs.
Path: Deoxygenated blood from the right side of the heart goes to the lungs, picks up oxygen, and then returns oxygenated blood to the left side of the heart.
Unique feature: Unlike the systemic circuit, in the pulmonary circuit, the pulmonary arteries carry deoxygenated blood away from the heart to the lungs, and the pulmonary veins carry oxygenated blood back to the heart from the lungs. This is the opposite of how systemic arteries and veins typically carry blood (systemic arteries carry oxygenated, systemic veins carry deoxygenated).
Systemic circuit: This circuit moves oxygenated blood from the heart to all the body tissues and returns deoxygenated blood from the tissues back to the heart.
Basic blood flow pattern (the full loop):
Right heart→Lungs (pulmonary circuit)→Left heart→Systemic tissues (systemic circuit)→Right heartRight heart→Lungs (pulmonary circuit)→Left heart→Systemic tissues (systemic circuit)→Right heart
Heart Anatomy: Chambers & Great Vessels
The Heart as a "Double Pump"
The heart is called a "double pump" because it effectively functions as two separate pumps working in parallel to circulate blood through two distinct circuits: the pulmonary circuit and the systemic circuit. The right side of the heart pumps deoxygenated blood to the lungs (pulmonary circuit), and the left side of the heart pumps oxygenated blood to the rest of the body (systemic circuit).
While described as a double pump, the atria and ventricles of each side actually work as functional units:
The two atria (right and left) contract together to push blood into their respective ventricles.
The two ventricles (right and left) then contract together to pump blood into the pulmonary artery and aorta, ensuring blood is simultaneously sent to the lungs and the rest of the body.
Four Chambers (Receiving and Pumping Areas)
Atria (the receiving chambers, located superiorly):
Right atrium (RA): Receives oxygen-poor blood from the body through three large veins: the superior vena cava (SVC), inferior vena cava (IVC), and the coronary sinus.
Left atrium (LA): Receives oxygen-rich blood from the lungs via four pulmonary veins (two from each lung).
Ventricles (the pumping chambers, located inferiorly):
Right ventricle (RV): Pumps oxygen-poor blood into the pulmonary trunk, which then splits into the right and left pulmonary arteries to go to the lungs.
Left ventricle (LV): Pumps oxygen-rich blood into the aorta, the body's largest artery, to be distributed to the entire systemic circuit.
Septa (internal walls dividing the chambers):
Interatrial septum: The wall separating the right and left atria. It has an indentation called the fossa ovalis, a remnant of a fetal opening (foramen ovale).
Interventricular septum: The thick muscular wall separating the right and left ventricles.
Five Great Vessels (Largest Blood Vessels Connected to the Heart)
Veins (bringing blood to the heart):
Superior vena cava (SVC) & Inferior vena cava (IVC): These large veins bring deoxygenated blood from the upper and lower body, respectively, into the Right Atrium (RA).
Pulmonary veins: Four veins (two from each lung) that bring oxygenated blood from the lungs into the Left Atrium (LA).
Arteries (carrying blood away from the heart):
Pulmonary trunk: A large artery that emerges from the Right Ventricle (RV) and quickly divides into the right and left pulmonary arteries, carrying deoxygenated blood to the lungs.
Aorta: The largest artery in the body, emerging from the Left Ventricle (LV) and distributing oxygenated blood to the entire systemic circulation.
Heart Valves (Ensuring One-Way Flow)
Purpose: Heart valves act like one-way gates. They open and close in response to pressure changes within the heart chambers, ensuring blood flows in a single, correct direction and doesn't flow backward (regurgitate).
Atrioventricular (AV) valves: Located between the atria and ventricles.
Right AV valve (tricuspid valve): Has three flaps (cusps) and allows blood flow from the Right Atrium (RA) to the Right Ventricle (RV).
Left AV valve (mitral valve or bicuspid valve): Has two flaps and allows blood flow from the Left Atrium (LA) to the Left Ventricle (LV).
Chordae tendineae and papillary muscles: String-like tendons (chordae tendineae) attach the cusps of the AV valves to small muscular projections (papillary muscles) in the ventricles. These structures prevent the valve flaps from inverting or prolapsing into the atria when the ventricles contract, ensuring the blood pumps forward rather than backward.
Semilunar (SL) valves: Located at the base of the great arteries leaving the ventricles.
Pulmonary SL valve: Located between the Right Ventricle (RV) and the pulmonary trunk.
Aortic SL valve: Located between the Left Ventricle (LV) and the aorta.
Structure: Each semilunar valve has three cup-shaped (half-moon) cusps that fill with blood when pressure drops, effectively closing the valve.
Gross Anatomy Diagram (Description of Structures to Sketch and Label)
Imagine a diagram of the heart with the following elements clearly marked:
Four Chambers:
Right Atrium (RA): Superior chamber on the right, receiving blood.
Right Ventricle (RV): Inferior chamber on the right, pumping blood to lungs.
Left Atrium (LA): Superior chamber on the left, receiving blood.
Left Ventricle (LV): Inferior chamber on the left, pumping blood to body.
Four Valves:
Tricuspid Valve: Between RA and RV.
Pulmonary Semilunar Valve: Between RV and Pulmonary Trunk.
Mitral (Bicuspid) Valve: Between LA and LV.
Aortic Semilunar Valve: Between LV and Aorta.
Five Great Vessels:
Superior Vena Cava (SVC): Entering RA from superior aspect.
Inferior Vena Cava (IVC): Entering RA from inferior aspect.
Pulmonary Trunk (and its branches, Pulmonary Arteries): Exiting RV towards lungs.
Pulmonary Veins: Entering LA from lungs (typically four).
Aorta: Exiting LV, arching over pulmonary trunk.
Septa:
Interatrial Septum: Vertical wall between RA and LA.
Interventricular Septum: Thick, vertical muscular wall between RV and LV.
Grooves (Sulci):
Coronary Sulcus (Atrioventricular Groove): Horizontal groove circling the heart, separating the atria from the ventricles; often holds the coronary arteries.
Anterior Interventricular Sulcus: Vertical groove on the front surface of the heart, separating the right and left ventricles.
Posterior Interventricular Sulcus: Vertical groove on the back surface of the heart, also separating the right and left ventricles.
Pectinate Muscles: Ridges of muscle within the walls of the atria, especially prominent in the right atrium.
Chordae Tendineae: String-like tendons connecting the AV valve cusps to the papillary muscles within the ventricles.
Trabeculae Carneae: Irregular ridges and folds of muscle found on the inner surfaces of the ventricular walls.
Papillary Muscles: Cone-shaped muscle projections within the ventricles, from which the chordae tendineae arise, controlling valve tension.
Path of Blood Flow Through the Heart and Lungs (Label on Diagram)
Starting from the systemic circuit, blood flows as follows:
Deoxygenated blood from the body enters the Right Atrium via the SVC and IVC.
From the Right Atrium, blood passes through the Tricuspid Valve into the Right Ventricle.
The Right Ventricle pumps blood through the Pulmonary Semilunar Valve into the Pulmonary Trunk.
The Pulmonary Trunk divides into the Pulmonary Arteries, which carry deoxygenated blood to the lungs.
In the lungs, blood releases CO2CO2 and picks up O2O2 at the capillaries (gas exchange).
Oxygenated blood returns from the lungs to the Left Atrium via the Pulmonary Veins.
From the Left Atrium, blood passes through the Mitral (Bicuspid) Valve into the Left Ventricle.
The Left Ventricle pumps blood through the Aortic Semilunar Valve into the Aorta.
The Aorta then distributes oxygenated blood to the rest of the body tissues.
Deoxygenated blood returns to the Right Atrium, completing the cycle.
Heart Wall & Coverings
Pericardium (Protective Layers Surrounding the Heart)
Imagine layers like an onion around the heart:
Fibrous pericardium: This is the outermost layer, a tough, dense connective tissue sac. Its purpose is to anchor the heart to surrounding structures (like the diaphragm and great vessels), prevent overfilling of the heart with blood, and provide protection.
Serous pericardium: This is a thinner, two-layered membrane inside the fibrous pericardium.
Parietal serous layer: This layer lines the inside surface of the fibrous pericardium.
Visceral serous layer (Epicardium): This layer adheres directly to the surface of the heart muscle itself.
Pericardial cavity: This is a narrow space located between the parietal and visceral serous layers. It contains a small amount of serous fluid, which acts as a lubricant, allowing the heart to beat with minimal friction. This fluid helps the two serous layers glide smoothly past each other with each heartbeat.
Pericarditis: This condition is an inflammation of the pericardium. It can cause painful friction between the layers (a characteristic "friction rub" sound) and, in severe cases, lead to cardiac tamponade (excess fluid buildup in the pericardial cavity, compressing the heart and hindering its pumping ability).
Remaining Two Tissue Layers of the Heart Wall
In addition to the epicardium (visceral serous layer of the pericardium), the heart wall has two more layers:
Myocardium: This is the thickest, middle layer of the heart wall and is composed almost entirely of cardiac muscle cells. These muscle cells are arranged in complex spiral and circular bundles. The myocardium is primarily responsible for the heart's pumping action (contraction). The thickness of this layer varies between chambers; it's thickest in the Left Ventricle (LV), followed by the Right Ventricle (RV), and thinnest in the atria, reflecting their pumping power requirements.
Endocardium: This is the innermost layer that lines the heart chambers and covers the heart valves. It is a smooth, thin layer made of endothelium (simple squamous epithelium) overlaying a thin layer of areolar connective tissue. This layer is continuous with the inner lining (endothelium) of all blood vessels, ensuring a smooth, friction-reducing surface for blood flow and preventing blood clotting within the heart.
Surface Anatomy & Coronary Circulation
Sulci (Grooves on the Heart's Surface that House Vessels)
Coronary sulcus: This is a prominent groove that encircles the heart, marking the boundary between the atria and the ventricles. It contains the main coronary arteries and veins.
Anterior and posterior interventricular sulci: These grooves run vertically on the front and back surfaces of the heart, respectively, indicating the division between the left and right ventricles. They also contain major coronary vessels.
Coronary Arteries (Blood Supply to the Heart Muscle Itself)
The heart muscle (myocardium) needs its own rich blood supply to function. This is provided by the coronary arteries, which are considered "functional end arteries" because even though they have some small connections, a blockage in one can severely impact the area it supplies.
Right coronary artery (RCA): Originates from the aorta and typically branches into the right marginal artery (supplying the right side of the heart) and the posterior interventricular artery (supplying the posterior walls of both ventricles a.k.a. RaMP).
Left coronary artery (LCA): Also originates from the aorta and quickly branches into two major arteries:
Circumflex artery: Follows the coronary sulcus to supply the left atrium and posterior left ventricle.
Anterior interventricular artery (LAD - Left Anterior Descending): Runs down the anterior interventricular sulcus and supplies the anterior parts of both ventricles. This artery is often called the "widow-maker" because blockages in its proximal (upper) part are particularly dangerous and can lead to massive heart attacks.
Coronary Veins (Collecting Deoxygenated Blood from the Heart Muscle)
After blood has supplied the myocardium, it is collected by several cardiac veins: the great cardiac vein, middle cardiac vein, and small cardiac vein. These veins eventually drain into a large vein on the posterior side of the heart called the coronary sinus.
The coronary sinus then empties this deoxygenated blood directly into the Right Atrium (RA).
Blood Flow Timing: Blood flow through the coronary arteries mainly occurs during diastole (when the heart muscle is relaxed). This is because during systole (contraction), the contracting myocardium compresses the coronary vessels, reducing blood flow. When the heart relaxes, the vessels open up, allowing blood to flow in and deliver oxygen and nutrients to the muscle.
Medical Significance of Coronary Circulation (CC)
Disruptions in coronary circulation are a major cause of heart disease:
Ischemia: This is a condition where localized tissue experiences an insufficient blood supply (and thus inadequate oxygen). In the heart, myocardial ischemia occurs when a coronary artery is narrowed, often by atherosclerosis (plaque buildup), reducing blood flow to parts of the heart muscle.
Angina pectoris: Severe chest pain that occurs when the heart muscle is deprived of oxygen (ischemia) but the cells have not yet died. It's often triggered by physical exertion or stress and relieved by rest or medication that dilates coronary arteries.
Myocardial infarction (MI): Commonly known as a heart attack, an MI occurs when blood flow to a section of the heart muscle is completely blocked (e.g., by a blood clot in a narrowed coronary artery), leading to the death (necrosis) of that heart tissue (tissue death). The dead tissue is replaced by non-contractile scar tissue, impacting the heart's pumping ability. Prompt treatment is crucial to save myocardium.
Heart Wall & Fibrous Skeleton
Layers: The heart wall is anatomically detailed as follows:
Epicardium: This is the outermost layer of the heart wall, also known as the visceral layer of the serous pericardium. It provides a smooth, protective outer surface.
Myocardium: The muscular middle layer, responsible for contracting and pumping blood. Cardiac muscle cells here are arranged in complex spiral and circular patterns, enabling efficient wringing motion during contraction. The LV has the thickest myocardium, reflecting its role in pumping blood to the entire body.
Endocardium: The smooth, innermost layer lining the heart chambers and valves. It is continuous with the endothelium of the great vessels, ensuring unimpeded blood flow and preventing clotting.
Fibrous skeleton (Dense Irregular Connective Tissue Framework)
This is a framework of dense, irregular connective tissue within the heart, primarily located around the valves and at the junction between the atria and ventricles.
It serves several crucial functions:
Provides strong support for the heart valves, preventing them from overstretching.
Acts as a point of attachment for the cardiac muscle fibers, allowing them to exert force effectively.
Crucially, it acts as an electrical insulator between the atria and the ventricles. This insulation prevents the electrical impulses (action potentials) from spreading directly from the atria to the ventricles. Instead, the impulses must pass through specialized conduction pathways (like the AV node), ensuring that the atria contract first, followed by the ventricles in a coordinated manner. This prevents simultaneous atrial and ventricular depolarization, which would impair efficient pumping.
Microscopic Structure of Cardiac Muscle
Cells: Cardiac muscle cells (cardiomyocytes) are unique:
They are short, branched, and typically have one or two nuclei.
Like skeletal muscle, they are striated, meaning they have a striped appearance due to the organized arrangement of contractile proteins.
They are packed with many mitochondria (making up 25–35% of their volume) to produce the large amounts of energy (ATP) needed for continuous pumping.
Intercalated discs: These are specialized junctions between adjacent cardiac muscle cells. They are vital for the heart's coordinated function:
Desmosomes: These are strong anchoring junctions that mechanically hold the cardiac muscle cells together, preventing them from pulling apart during vigorous contractions.
Gap junctions: These are channels that allow ions (and thus electrical currents) to pass directly from one cardiac muscle cell to another. This electrical coupling allows the entire myocardium to act as a single, coordinated unit, often called a "functional syncytium." When one cell is stimulated, the impulse quickly spreads to all connected cells, causing them to contract almost simultaneously.
Sarcolemma forms T-tubules: The cell membrane (sarcolemma) of cardiac muscle cells forms invaginations called T-tubules that penetrate deep into the cell, allowing the action potential to rapidly reach all parts of the muscle fiber.
Sarcoplasmic Reticulum (SR) stores extCa2+extCa2+: The specialized endoplasmic reticulum in muscle cells, the SR, stores calcium ions (Ca2+Ca2+), which are essential for muscle contraction.
Metabolism: Cardiac muscle relies almost exclusively on aerobic respiration (requires oxygen) to produce ATP. This makes it highly dependent on a continuous oxygen supply. It has high myoglobin content (to store oxygen) and creatine kinase (an enzyme involved in energy transfer). It's very flexible in its fuel source, readily using fatty acids (its primary fuel), glucose, lactate, amino acids, and even ketones for energy. This high oxygen demand and reliance on aerobic metabolism mean the heart is very susceptible to ischemia (lack of oxygen).
Electrical Activity: Conduction System
Autorhythmic (pacemaker) cells: Unlike most body cells, certain specialized cardiac cells (pacemaker cells) do not need nervous system stimulation to generate action potentials (APs). They spontaneously generate their own electrical impulses (autorhythmicity). These impulses then spread via gap junctions to the contractile (working) heart muscle cells, causing them to contract.
Pathway of electrical conduction (the normal sequence, taking approximately $0.22 s$0.22s for the impulse to travel):
Sinoatrial (SA) node: Located in the superior wall of the Right Atrium (RA), it is the heart's natural pacemaker. It has the fastest intrinsic rate of depolarization (about 75 beats per minute, bpm, intrinsically, but can be influenced). It initiates each heartbeat.
Atrioventricular (AV) node: Located in the interatrial septum, near the junction of the atria and ventricles. The electrical impulse from the SA node reaches the AV node, where it is delayed for approximately 0.1 s0.1s. This crucial delay allows the atria to fully contract and empty their blood into the ventricles before the ventricles begin to contract.
Atrioventricular (AV) bundle (Bundle of His): This is the only electrical connection between the atria and ventricles, piercing through the fibrous skeleton. Without it, impulses couldn't reach the ventricles directly.
Right and Left Bundle Branches: The AV bundle quickly splits into these two branches, which run down either side of the interventricular septum towards the apex of the heart.
Purkinje fibers: These fibers extend from the bundle branches into the ventricular walls and papillary muscles. They rapidly conduct the electrical impulse throughout the ventricular musculature, ensuring a nearly simultaneous contraction of both ventricles. They also reach the papillary muscles, causing them to contract just before the main ventricular walls, thus tightening the chordae tendineae and preventing valvular prolapse.
Innervation (Nervous System Control, Modifying Intrinsic Rate)
Parasympathetic nervous system (PNS): Via the vagus nerve (Cranial Nerve X) and the cardioinhibitory center in the brainstem. It releases acetylcholine (ACh) which slows down the heart rate (↓HR↓HR).
Sympathetic nervous system (SNS): Via nerves from the T1–T5 spinal segments and the cardioacceleratory center in the brainstem. It releases norepinephrine (NE) which increases heart rate (↑HR↑HR) and contractility (force of contraction), and also causes dilation of the coronary arteries to increase blood flow to the heart muscle.
Pacemaker (SA Node) Action Potential
The unique electrical activity of pacemaker cells (like those in the SA node) is what drives the heart's rhythm:
Pacemaker potential (or prepotential): This is a slow, spontaneous depolarization. Unlike other cells, pacemaker cells don't have a stable resting membrane potential. Instead, specialized "funny" channels (IfIf channels) slowly open, allowing a slow, continuous influx of sodium ions (Na+Na+) into the cell. This causes the membrane potential (VmVm) to gradually drift from approximately −60 mV−60mV towards the threshold (−40 mV−40mV).
Depolarization: Once the threshold is reached (−40 mV−40mV), fast voltage-gated calcium channels (Ca2+Ca2+ channels) open, allowing a rapid influx of calcium ions (Ca2+Ca2+) into the cell. This rapid Ca2+Ca2+ influx causes the membrane potential to quickly rise to about 0 mV0mV.
Repolarization: Shortly after depolarization, calcium channels inactivate, and voltage-gated potassium channels (K+K+ channels) open, allowing potassium ions (K+K+) to flow out of the cell. This efflux of positive charges causes the membrane potential to fall back to −60 mV−60mV. The potassium channels then close, and the slow Na+Na+ influx begins again, restarting the cycle.
No stable RMP: Pacemaker cells do not have a stable resting membrane potential; they are constantly depolarizing, which is why they exhibit autorhythmicity (automatic rhythmic activity).
Contractile Cell Action Potential (What Causes the Heart to Contract)
These are the action potentials of the actual working heart muscle cells, initiated by the pacemaker cells:
Rapid depolarization: When an electrical impulse from a neighboring cell reaches a contractile cell, voltage-gated fast sodium channels (Na+Na+ channels) open. A rapid influx of sodium ions (Na+Na+) causes the membrane potential to quickly rise from a resting value of about −90 mV−90mV to +30 mV+30mV.
Plateau phase (about 200 ms200ms long): This is a unique feature of cardiac contractile cells. Immediately after the initial rapid depolarization, some potassium channels (K+K+ channels) close, and slow voltage-gated calcium channels (Ca2+Ca2+ channels) open. This causes a slow, sustained influx of calcium ions (Ca2+Ca2+) into the cell, which roughly balances the efflux of potassium ions (K+K+). This balance maintains the membrane potential in a plateau phase close to 0 mV0mV for an extended period. The plateau is crucial because it ensures a prolonged refractory period, preventing the heart muscle cells from being stimulated again too quickly. This prevents tetany (sustained, uncontrolled contraction) in the heart, allowing it to fill with blood between beats.
Repolarization: After the plateau, the calcium channels close, and more potassium channels (K+K+ channels) open. This massive efflux of potassium ions (K+K+) from the cell rapidly restores the membrane potential back to its resting value of −90 mV−90mV. The cell then prepares for the next action potential.
Contrast to Neuron Action Potentials: Unlike neuron action potentials, which are very brief (only a few milliseconds) and primarily involve sodium and potassium ion movements, cardiac contractile cell action potentials are significantly longer (about 200 ms200ms). This extended duration is due to the plateau phase caused by the sustained extCa2+extCa2+ influx. This long plateau and the resulting long absolute refractory period in cardiac muscle prevent sum
mation of contractions and tetany, which would be fatal for the heart. Neuron action potentials are primarily for rapid signal transmission, while cardiac action potentials are designed for a sustained contraction.
Electrocardiogram (ECG)
An Electrocardiogram (ECG or EKG) is a graphic recording of the composite (sum) of all the electrical activity (action potentials) generated by the cardiac muscle cells throughout the entire heart, as detected from the surface of the body. It does not measure a single action potential.
Waves & Intervals (Key Features on a Typical ECG Pattern)
P wave: This small, upward deflection represents atrial depolarization (the electrical impulse spreading through the atria, causing them to contract). The atria contract shortly after the P wave begins.
QRS complex: This large, spiked deflection represents ventricular depolarization (the electrical impulse spreading rapidly through the ventricles, causing them to contract). The ventricles begin to contract during the R wave. The QRS complex is typically much larger than the P wave due to the greater muscle mass of the ventricles. Notably, atrial repolarization (relaxation) also occurs during the QRS complex but is typically masked by the much larger electrical signal of ventricular depolarization.
T wave: This rounded, upward deflection represents ventricular repolarization (the electrical recovery of the ventricles, as they prepare for the next beat). The ventricles relax just after the T wave ends.
P–R interval (or P–Q interval): This interval measures the time from the beginning of atrial excitation (start of the P wave) to the beginning of ventricular excitation (start of the QRS complex). It represents the time taken for the impulse to travel from the SA node through the atria and the AV node delay, and then to the ventricles. A longer than normal P-R interval can indicate an AV block.
Q–T interval: This interval measures the total time from the beginning of ventricular depolarization (start of QRS) through ventricular repolarization (end of T wave). It represents the entire electrical activity of the ventricles (depolarization and repolarization). A prolonged Q–T interval can indicate certain repolarization abnormalities that increase the risk of arrhythmias.
P–Q segment (or P–R segment): This is the flat line between the end of the P wave and the start of the QRS complex. It represents the atrial plateau (when atrial muscle cells are depolarized) and the pause at the AV node. During this segment, the atria are fully contracted and systole is occurring.
S–T segment: This is the flat line between the end of the S wave and the beginning of the T wave. It represents the ventricular plateau phase, where the entire ventricular myocardium is depolarized and undergoing contraction. It should be isoelectric (flat). Elevation or depression of the S-T segment is a critical indicator of myocardial ischemia or infarction.
Clinical interpretations (What an ECG Can Tell Us):
Enlarged R wave: Often suggests ventricular hypertrophy (enlargement of the ventricular muscle).
S–T elevation or depression: A key indicator of myocardial ischemia (S-T depression or T-wave inversion) or acute myocardial infarction (S-T elevation).
Prolonged Q–T interval: Can indicate issues with ventricular repolarization, increasing the risk of dangerous arrhythmias.
An ECG can also reveal various heart rhythm abnormalities (arrhythmias) like blocks in the conduction system, fibrillation (chaotic electrical activity), and ectopic foci (abnormal sites of impulse generation).
Cardiac Cycle & Hemodynamics
Cardiac cycle: This refers to all the events associated with one complete heartbeat, including both the electrical and mechanical events. It encompasses the period from the start of one heartbeat to the start of the next.
It involves coordinated sequences of atrial systole (contraction) and atrial diastole (relaxation), followed by ventricular systole and ventricular diastole.
Pressures drive valve status: Blood flow is always from an area of higher pressure to an area of lower pressure. The opening and closing of heart valves are entirely determined by these pressure differences between the chambers and great vessels.
Blood flows high ightarrowightarrow low P: This fundamental principle governs all blood movement within the cardiovascular system.
Phases (using the left heart as an example; the same sequence occurs in the right heart, but at significantly lower pressures):
Ventricular Filling: Atrial Contraction & Early Diastole:
This phase begins with the ventricles relaxed (diastole) and the AV valves open.
Blood flows passively from the atria into the ventricles (filling about 80% of the ventricular volume).
The P wave on the ECG occurs.
Then, the atria contract (atrial systole, initiated by the P wave), pushing the remaining 20% of blood into the ventricles. Atrial pressure (PextatriumPextatrium) is greater than ventricular pressure (PextventriclePextventricle).
At the end of this phase, the ventricles contain their maximum volume of blood, called the end diastolic volume (EDV), which is approximately 120 mL120mL.
Isovolumetric Contraction (Ventricular Systole Begins):
The ventricles begin to contract (ventricular systole, initiated by the QRS complex), causing ventricular pressure (PextventriclePextventricle) to rise sharply.
As soon as ventricular pressure exceeds atrial pressure (Pextventricle>PextatriumPextventricle>Pextatrium), the AV valves close suddenly. This closure produces the first heart sound (S₁) or "lub".
For a brief moment, all four heart valves are closed (both AV and semilunar valves).
During this phase, ventricular volume remains constant (isovolumetric) as the pressure rapidly builds up, but no blood is ejected yet.
Ventricular Ejection (Blood Pumping Out):
As ventricular contraction continues, ventricular pressure (PextventriclePextventricle) eventually exceeds the pressure in the great arteries (aorta and pulmonary trunk), i.e., Pextventricle>PextarteryPextventricle>Pextartery.
This forces the semilunar (SL) valves open, and blood is rapidly ejected from the ventricles into the aorta (from the LV) and pulmonary trunk (from the RV).
The force of ventricular contraction determines the stroke volume (SV), the amount of blood ejected per beat (approximately 70 mL70mL at rest).
Aortic pressure peaks around 120 mmHg120mmHg during this phase.
Isovolumetric Relaxation (Ventricular Diastole Begins):
The ventricles begin to relax (ventricular diastole, marked by the T wave on the ECG).
As they relax, ventricular pressure (PextventriclePextventricle) drops rapidly.
When ventricular pressure falls below the pressure in the aorta/pulmonary trunk (Pextventricle<PextarteryPextventricle<Pextartery), blood in the arteries tries to flow back into the ventricles.
This backflow causes the semilunar (SL) valves to snap shut, producing the second heart sound (S₂) or "dup".
Again, for a brief moment, all four heart valves are closed (isovolumetric), and ventricular volume remains constant as the muscle continues to relax.
The amount of blood remaining in the ventricles at the end of this phase is the end systolic volume (ESV), which is approximately 50 mL50mL.
Atrial & Ventricular Diastole (Passive Filling):
As the ventricles continue to relax, their pressure drops even further, eventually falling below atrial pressure (Pextventricle<PextatriumPextventricle<Pextatrium).
This difference in pressure causes the AV valves to open, and blood stored in the atria (which have been filling during ventricular systole) quickly flows passively into the ventricles, accounting for about 80% of the subsequent EDV. This phase marks the rapid filling of the ventricles.
The cycle then repeats with the next P wave and atrial contraction.
Heart sounds:
S₁ ("lub"): The first heart sound is caused by the closing of the atrioventricular (AV) valves (tricuspid and mitral valves) at the beginning of ventricular systole (isovolumetric contraction phase). It signifies the start of ventricular contraction and prevents backflow into the atria.
S₂ ("dup"): The second heart sound is caused by the closing of the semilunar (SL) valves (aortic and pulmonary valves) at the beginning of ventricular diastole (isovolumetric relaxation phase). It signifies the start of ventricular relaxation and prevents backflow from the great arteries into the ventricles.
Extra heart sounds (S₃, S₄): While S₁ and S₂ are normal, sometimes additional sounds can be heard, often indicating pathology. S₃ can be heard during rapid ventricular filling in some conditions; S₄ may indicate stiff ventricles (poor compliance).
ECG Deflections and Cardiac Cycle Relationships
P wave: Signifies atrial depolarization, which immediately precedes atrial systole (contraction). The P-wave initiates the atrial contraction phase of the cardiac cycle.
QRS complex: Signifies ventricular depolarization, which immediately precedes ventricular systole (contraction). The QRS complex marks the beginning of isovolumetric contraction and then ventricular ejection. Atrial repolarization also occurs during the QRS complex, but its electrical signal is small and hidden by the large QRS deflection.
T wave: Signifies ventricular repolarization, indicating the start of ventricular diastole (relaxation). The T-wave occurs during the isovolumetric relaxation phase, and relaxation continues as the ventricles fill.
Where does atrial diastole occur? Atrial diastole (relaxation) occurs during the QRS complex and continues throughout the S-T segment and T wave. This means the atria are repolarizing and relaxing (and refilling) while the ventricles are contracting and ejecting blood.
Explain the P-R interval: The P-R interval (or P-Q interval) represents the time from the beginning of atrial excitation (start of the P wave) to the beginning of ventricular excitation (start of the QRS complex). It reflects the time taken for the electrical impulse to travel from the SA node, spread through the atria, pass through the AV node (where the critical delay occurs), and then enter the ventricular conduction system.
Explain the S-T segment: The S-T segment is the flat (isoelectric) line between the end of the S wave and the beginning of the T wave. It represents the period when the entire ventricular myocardium is depolarized and is undergoing sustained contraction (the plateau phase of the ventricular action potential). Blood is being ejected from the ventricles during this phase. An elevated or depressed S-T segment is a significant clinical indicator of problems like myocardial ischemia or infarction.
Clinical Definitions: Arrhythmias and Murmurs
Arrhythmia: An arrhythmia (or dysrhythmia) is any abnormality in the heart's rhythm or rate. This means the heart beats too fast, too slow, or irregularly. Arrhythmias result from problems with the heart's intrinsic conduction system (e.g., SA node failure, blockages in the pathway) or from unusual electrical activity (ectopic foci).
Examples of Arrhythmias:
SA node failure: If the SA node fails, another part of the conduction system may take over as the pacemaker, leading to a slower rhythm (e.g., "junctional rhythm" at 40-50 bpm if the AV node takes over).
AV block (1st, 2nd, 3rd degree): Impaired conduction between the atria and ventricles, meaning the impulse does not get from the atria to the ventricles efficiently. In a 3rd-degree (complete) AV block, atrial and ventricular contractions become completely uncoordinated, often requiring an artificial pacemaker.
Premature Ventricular Contractions (PVCs): Extra, abnormal heartbeats that begin in the ventricles, often felt as a "skipped beat." Usually harmless but can indicate underlying issues.
Atrial Fibrillation (AFib): Rapid, irregular, and ineffective contractions of the atria, leading to disorganized P waves and an irregularly irregular pulse. Increases stroke risk.
Ventricular Fibrillation (VFib): A severe and often fatal arrhythmia where the ventricles quiver uselessly instead of pumping blood. Requires immediate defibrillation (an electrical shock) to reset the heart's rhythm.
Murmur: A heart murmur is an unusual "whooshing" or "swishing" sound heard during the cardiac cycle, distinct from the normal "lub-dup." Murmurs indicate turbulent (non-smooth) blood flow through the heart. They are typically caused by problems with the heart valves (valve disorders).
Examples of Valve Disorders causing Murmurs:
Incompetent (insufficient) valve: A valve that does not close completely, allowing blood to flow backward when it should be closed (regurgitation). This creates a swishing sound as blood leaks through the partially open valve. For example, a mitral regurgitation murmur is heard during ventricular systole as blood flows back into the left atrium.
Stenosis: A valve that has a narrowed opening, making it difficult for blood to flow forward. This causes the heart to work harder to push blood through the constricted opening and produces a harsh, distinct sound as blood is forced through. For example, aortic stenosis produces a systolic murmur as blood is ejected through a narrow aortic valve.
Both incompetent valves and stenosis increase the heart's workload and can lead to heart failure over time.
Replacement options: Damaged valves can sometimes be repaired or replaced with mechanical valves (durable but require lifelong anticoagulation due to clot risk) or biologic valves (from animals or cadavers, less durable but less need for anticoagulants).
Cardiac Output (CO)
Formula: Cardiac Output (CO) is the total volume of blood pumped by one ventricle (typically the left ventricle) per minute. It is calculated by multiplying the heart rate (HR) by the stroke volume (SV).
CO=HR×SVCO=HR×SV
Where:CO is in Liters per minute (L min⁻¹)
HR is in beats per minute (bpm)
SV is in milliliters per beat (mL) or Liters per beat (L)
Normal resting values:
Typical resting heart rate (HR) is around 75 bpm75bpm.
Typical resting stroke volume (SV) is around 70 mL70mL (or 0.07 L0.07L).
Therefore, normal resting cardiac output (CO) = 75 bpm×70 mL/beat=5250 mL/min75bpm×70mL/beat=5250mL/min or 5.25 Lmin−15.25Lmin−1.
Cardiac reserve: This is the difference between the maximum cardiac output an individual can achieve and their resting cardiac output. A healthy individual can typically increase their CO by 4–5 times the resting rate during intense exercise, and highly trained athletes can increase it by up to 7 times.
Regulation of Stroke Volume (Amount of Blood Ejected per Beat)
Stroke volume can be altered by three main factors:
Preload (Frank-Starling Law of the Heart):
Preload refers to the degree to which the ventricular muscle cells are stretched just before they contract. It's largely determined by the end diastolic volume (EDV) – how much blood fills the ventricles during diastole.
Frank-Starling Law of the Heart: This law states that, within physiological limits, the greater the stretch of the cardiac muscle fibers (due to increased preload), the greater the force of contraction, and consequently, the greater the stroke volume (SV).
Mechanism: Increased venous return (more blood flowing back to the heart) leads to a higher EDV, which stretches the ventricular walls more. This optimal stretch allows the actin and myosin filaments in the muscle cells to overlap more efficiently, leading to a more forceful contraction and a larger amount of blood ejected (increased SV).
Contractility (Inotropic State):
Contractility refers to the intrinsic strength and force of contraction of the heart muscle, independent of muscle stretch or preload. It reflects how forcefully the heart pumps blood for a given preload.
Positive inotropic agents (Increase contractility): These agents increase the force of contraction by typically increasing the amount of calcium available to the cardiac muscle cells or their sensitivity to calcium.
Sympathetic nervous system (SNS) stimulation (via norepinephrine released by nerves or epinephrine/norepinephrine hormones from the adrenal medulla).
Hormones like epinephrine (EpiEpi), thyroxine (thyroid hormone).
Increased extracellular calcium ions (Ca2+Ca2+).
Certain drugs like digitalis.
These agents decrease the ESV (more blood ejected) and thus increase SV.
Negative inotropic agents (Decrease contractility): These agents weaken the heart's contraction.
Acidosis (low blood pH).
Hyperkalemia (high blood potassium, extK+extK+).
Calcium-channel blockers (drugs that reduce calcium influx).
These agents increase the ESV (less blood ejected) and thus decrease SV.
Afterload:
Afterload is the pressure that the ventricles must overcome to eject blood into the great arteries (aorta and pulmonary trunk). It's essentially the resistance to ejection from the heart.
In the systemic circuit, normal afterload is approximately 80 mmHg80mmHg (aortic diastolic pressure).
In the pulmonary circuit, normal afterload is much lower, only about 10 mmHg10mmHg (pulmonary trunk diastolic pressure).
Effect on SV: Increased afterload makes it harder for the ventricles to eject blood. This leads to a higher End Systolic Volume (ESV) because more blood is left behind in the ventricles after contraction, which in turn decreases stroke volume (SV).
Conditions like hypertension (high blood pressure) and atherosclerosis (hardening and narrowing of arteries due to plaque buildup) increase afterload, making the heart work harder and potentially reducing CO over time if not compensated.
Factors Affecting Venous Return to the Heart
Venous return is the amount of blood flowing back to the heart from the systemic circulation, directly influencing preload.
Muscle pump: Contraction of skeletal muscles, particularly in the legs, compresses deep veins, pushing blood toward the heart. One-way valves prevent backflow.
Respiratory pump: During inhalation, diaphragm descent increases abdominal pressure and decreases thoracic pressure, squeezing abdominal veins and expanding thoracic veins, promoting blood flow to the heart.
Venoconstriction: Sympathetic nervous system stimulation causes veins to constrict, reducing the volume of blood in the veins and pushing more blood toward the heart.
Blood volume: Higher total blood volume directly increases venous return and preload.
Regulation of Heart Rate (HR)
Heart rate is how many times the heart beats per minute. It is primarily controlled by chronotropic agents.
Chronotropic agents: These are factors that influence the heart rate.
Positive chronotropic agents (Increase HR):
Sympathetic nervous system (SNS) stimulation: Releases norepinephrine (NE) which binds to beta-1 (β1β1) adrenergic receptors on SA and AV node cells, increasing their rate of depolarization and thus heart rate.
Hormones: Epinephrine (Epi) and thyroid hormone.
Chemicals: Caffeine, nicotine, cocaine.
Bainbridge reflex (atrial reflex): Increased venous return (more blood returning to the atria) stretches the atrial walls, triggering receptors that send signals to the cardiovascular center, increasing HR. This helps prevent blood pooling in the atria.
Fever: Increases metabolic rate, thus increasing HR.
Negative chronotropic agents (Decrease HR):
Parasympathetic nervous system (PSNS) stimulation: Via the vagus nerve (Cranial Nerve X). It releases acetylcholine (ACh) which slows the depolarization rate of the SA and AV nodes, decreasing heart rate.
Beta-blockers: Drugs that block the effects of beta-adrenergic stimulation, thus reducing HR.
Hypothermia: Low body temperature slows metabolic processes, including heart rate.
Vagal tone: The parasympathetic nervous system (PNS), specifically the vagus nerve, exerts a constant inhibitory effect on the SA node. This "vagal tone" is what keeps the adult resting heart rate at approximately 75 bpm75bpm, which is significantly lower than the intrinsic (natural) firing rate of the SA node (around 100 bpm100bpm).
Regulation of Heart Function: Blood Volume and Blood Pressure Receptors
The heart's function is constantly monitored and adjusted by the nervous system, primarily through feedback loops involving baroreceptors and chemoreceptors. These sensory receptors send information to the Medulla Cardiac Center in the brainstem.
Baroreceptors: These are mechanoreceptors located in the walls of large arteries (e.g., carotid sinuses, aortic arch) that detect changes in blood pressure.
Role in cardiac feedback: If blood pressure suddenly increases (e.g., due to increased blood volume), baroreceptors are stretched and send more frequent signals to the cardioinhibitory center (CIC) in the medulla via glossopharyngeal (CN IX) and vagus (CN X) nerves. The CIC activates the parasympathetic nervous system to decrease heart rate and contractility, thereby lowering cardiac output and normalizing blood pressure.
Conversely, if blood pressure drops, baroreceptors send fewer signals, activating the cardioacceleratory center (CAC). This increases sympathetic activity to the heart, raising heart rate and contractility to increase cardiac output and restore blood pressure.
Chemoreceptors: These receptors are found in the carotid bodies and aortic arch (alongside baroreceptors) and in the medulla oblongata. They are sensitive to changes in blood chemistry, specifically levels of O2O2, CO2CO2, and blood pH.
Role in cardiac feedback: If blood O2O2 levels decrease significantly, or if CO2CO2 levels increase, or blood pH decreases (becomes more acidic), chemoreceptors are stimulated. They send signals to the medulla, which then activates the sympathetic nervous system to increase heart rate and contractility. This response aims to increase cardiac output to deliver more oxygen to tissues and remove excess CO2CO2. They are primarily important in regulating respiration but also have secondary effects on cardiac activity.
Nervous & Chemical Influence Summary (Medulla Cardiac Center)
The Medulla Cardiac Center in the brainstem is the primary control center for heart rate and contractility.
Cardioacceleratory (CAC) center: Activates the sympathetic nervous system. It sends impulses via sympathetic cardiac nerves (originating from T1–T5 spinal segments) to the SA node, AV node, and ventricular myocardium, leading to an increase in HR and contractility.
Cardioinhibitory (CIC) center: Activates the parasympathetic nervous system. It sends impulses via the vagus nerves (Cranial Nerve X) to the SA node and AV node (and less so to the ventricles), leading to a decrease in HR.
Sensory input: Both centers receive crucial sensory information from:
Baroreceptors: Monitor blood pressure.
Chemoreceptors: Monitor blood oxygen, carbon dioxide, and pH levels.
These inputs allow for continuous fine-tuning of cardiac output to maintain homeostasis.
Effects of Aerobic Exercise on the Heart
Regular aerobic exercise leads to several beneficial adaptations in the heart:
Increased Cardiac Reserve: Aerobic training significantly increases the heart's ability to increase its cardiac output when needed, often by 4-5 times at rest, and up to 7 times in highly trained athletes. This means the heart can pump more blood to meet the demands of physical activity.
Increased Stroke Volume: Over time, exercise strengthens the myocardium, especially the left ventricle. This leads to a larger chamber volume and more forceful contractions, increasing the resting stroke volume. A larger SV means the heart can pump more blood with each beat.
Lower Resting Heart Rate (Bradycardia): Because the stroke volume increases, the heart can pump the same amount of blood at rest with fewer beats. This leads to a lower resting heart rate (more efficient pumping), a phenomenon known as physiological bradycardia.
Improved Myocardial Efficiency and Coronary Circulation: Exercise can lead to the growth of new capillaries in the myocardium (angiogenesis) and improved blood flow through existing coronary arteries, enhancing oxygen delivery to the heart muscle itself. The heart becomes more efficient at using oxygen.
Reduced Afterload: Regular exercise often leads to lower resting blood pressure and improved flexibility of blood vessels, which reduces the afterload (resistance) the heart has to pump against. This makes it easier for the heart to eject blood and reduces its workload.
Clinical Correlations & Pathology
Congestive Heart Failure (CHF): A progressive condition where the heart is unable to pump enough blood to meet the body's metabolic needs, resulting in inadequate tissue perfusion. The heart becomes inefficient as a pump.
Causes: Common causes include chronic high blood pressure (persistent hypertension), multiple myocardial infarctions (which damage heart muscle), coronary artery disease (leading to reduced blood supply), and dilated cardiomyopathy (enlargement and weakening of the ventricles).
Left-sided heart failure: If the left ventricle fails, blood backs up into the lungs, leading to pulmonary edema (fluid accumulation in the lungs), causing shortness of breath and coughing.
Right-sided heart failure: If the right ventricle fails, blood backs up into the systemic circulation, leading to systemic edema (swelling) in the extremities (ankles, legs) and organs like the liver.
Cardiomegaly & hypertrophic cardiomyopathy: Cardiomegaly is a general term for an enlarged heart. Hypertrophic cardiomyopathy is a specific condition where the heart muscle (myocardium), particularly the ventricular walls, thickens abnormally. This thickening reduces the volume of the chambers and can obstruct blood flow, leading to decreased cardiac output and an increased risk of sudden death, especially during exertion.
Congenital remnants: These are structures from fetal circulation that normally close or regress after birth but can sometimes persist.
Foramen ovale: A fetal opening between the right and left atria, which normally closes at birth to become the fossa ovalis.
Ductus arteriosus: A fetal blood vessel connecting the pulmonary trunk to the aorta, which normally closes at birth to become the ligamentum arteriosum.
Pericarditis: Inflammation of the pericardium.
Cardiac tamponade: A life-threatening condition where excessive fluid accumulates in the pericardial cavity, compressing the heart and severely restricting its ability to pump blood.
Valve disorders: As discussed, include regurgitation (incompetent valves) and stenosis (narrowed valves).
"Widow-maker" lesions: Refers to blockages in the proximal Left Anterior Descending (LAD) artery or the left main coronary artery due to their critical role in supplying a large portion of the left ventricle; occlusion here can cause massive myocardial infarction.
Bradycardia ( These refer to abnormally slow or fast heart rates, respectively. They can be physiological (e.g., bradycardia in athletes, tachycardia during exercise) or pathological (due to underlying disease, e.g., sick sinus syndrome for bradycardia, atrial fibrillation for tachycardia).
Developmental Aspects
Fetal shunts bypass lungs: During fetal development, the lungs are not functional, so blood largely bypasses them via specialized shunts:
Foramen ovale: An opening in the interatrial septum that allows blood to flow directly from the right atrium to the left atrium, bypassing the pulmonary circulation entirely. This opening normally closes at birth, forming the fossa ovalis.
Ductus arteriosus: A short vessel connecting the pulmonary trunk to the aorta, allowing most of the blood from the right ventricle to bypass the non-functional lungs and flow directly into the systemic circulation. This vessel normally closes shortly after birth, forming the ligamentum arteriosum.
Changes That Occur in the Heart with Age
As individuals age, several changes can occur in the heart, making it less efficient and more susceptible to disease:
Sclerosis and Thickening of Valve Flaps: Heart valves, especially the mitral valve, tend to stiffen and become thicker due to fat and collagen deposits. This can make them less efficient, potentially leading to mild stenosis or regurgitation.
Decline in Cardiac Reserve: The ability of the heart to increase its output in response to stress or exercise decreases. Maximum heart rate (HRmaxHRmax) declines with age (estimated as 220−age220−age in years), and the contractility of the myocardium may also lessen.
Fibrosis of Cardiac Muscle: Some cardiac muscle cells may die and be replaced by non-contractile fibrous (scar) tissue. This reduces the number of functional muscle cells, decreasing the force of contraction and potentially altering the heart's electrical conduction.
Thickening of the Myocardium: The left ventricular wall may thicken (hypertrophy) due to increased afterload from age-related arterial stiffening (arteriosclerosis) or chronic hypertension. While initially compensatory, this can reduce the size of the ventricular chamber and make it harder for the ventricle to fill properly.
Decreased Elasticity of Arteries (Arteriosclerosis): The major arteries become less elastic and stiffer with age. This increases peripheral resistance, raising afterload and consequently increasing blood pressure, which places a greater workload on the heart.
Decline in Conduction System Function: The SA node may lose some pacemaker cells, and the efficiency of the conduction system may decrease, leading to an increased incidence of arrhythmias and heart blocks in older adults.
Key Equations & Values
Cardiac Output (CO): CO=HR×SVCO=HR×SV
Stroke Volume (SV): SV=EDV−ESVSV=EDV−ESV
Normal pressures:
Aortic systolic pressure (during ejection) ≈120 mmHg≈120mmHg
Aortic diastolic pressure (during relaxation) ≈80 mmHg≈80mmHg (this contributes to systemic afterload)
Pulmonary trunk systolic pressure ≈25 mmHg≈25mmHg
Pulmonary trunk diastolic pressure ≈10 mmHg≈10mmHg (this contributes to pulmonary afterload)
Normal volumes (at rest):
End Diastolic Volume (EDV): Maximum volume in ventricle after filling ≈120 mL≈120mL
End Systolic Volume (ESV): Volume remaining in ventricle after ejection ≈50 mL≈50mL
Stroke Volume (SV): Volume ejected per beat ≈70 mL≈70mL
Practical & Ethical Considerations
Maintaining cardiovascular health (through a healthy diet, regular exercise, and avoiding smoking) is crucial. These lifestyle choices help reduce afterload, prevent plaque formation in arteries (atherosclerosis), and maintain the overall efficiency of the cardiovascular system.
Prompt treatment of a myocardial infarction (heart attack) with interventions like reperfusion therapy (e.g., angioplasty) is an ethical imperative as it can save significant amounts of heart muscle (myocardium) from irreversible damage.
The widespread availability and proper training in the use of Automated External Defibrillators (AEDs) in public places are vital for improving survival rates for sudden cardiac arrest caused by ventricular fibrillation.
When considering valve replacements, surgeons and patients must balance the durability and long-term effectiveness of mechanical valves (which require lifelong anticoagulation therapy to prevent blood clots) against the advantages and disadvantages of biologic valves (animal or cadaveric tissue grafts, which are less durable but carry a lower risk of clot formation and generally do not require lifelong anticoagulation).