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A. Pump Systems 1. Pulmonary: pumped blood to the lungs for oxygenation. 2. Systemic: Reese’s oxygenated blood from the lungs and pumps it out to the rest of the body. B. Location 1. Mediastinum: 2. Pericardial Cavity: function of the pericardium, which is a protective sack around the heart pericard...

A. Pump Systems 1. Pulmonary: pumped blood to the lungs for oxygenation. 2. Systemic: Reese’s oxygenated blood from the lungs and pumps it out to the rest of the body. B. Location 1. Mediastinum: 2. Pericardial Cavity: function of the pericardium, which is a protective sack around the heart pericardial uid, which is secreted by the pericardium helps to reduce the friction as the heartbeats C. Structure 1. External Structure a. Apex: point inferiorly toward left hip. b. Base: Posterior surface of the heart, that is about 9 cm wide and points toward the right shoulder 2. Chambers a. Atria (receiving chambers): the right atrium receives deoxygenated blood from the superior and inferior vena cavae and pumps it into the right ventricle, which sends that blood to the lungs for oxygenation. The left atrium received this oxygenated blood from the lungs via the pulmonary veins and pumps it into the left ventricle. b. Ventricles (discharging chambers): The left ventricle receives oxygenated blood from the left atrium and pump it into the aorta which distributes the blood to the rest of the body. This is the most thickest and most muscular of the chambers. The right ventricle receives deoxygenated blood from the right atrium and pumps it into the pulmonary trunk which carries the blood to the lungs 3. Valves (facilitators of ef cient pumping of blood): consist of the AV valves which prevent back ow into atria when the ventricles contract, and the SL valves, which prevent blood from returning to the ventricles after contraction. a. Bicuspid (Mitral Valve): L. AV valve b. Tricuspid: R. AV valve; 3 cusps c. Aortic Semilunar: insures that blood ows from left ventricle into aorta to prevent back ow, and to ventricle during diastole fl fl fi fl fl d. Pulmonary: right ventricle contracts, allowing blood to ow into pulmonary trunk. 4. Chordae tendinae (heart strings): tiny white collagen chords, which anchored the AV valves to papillary muscles to prevent them from protruding from ventricular walls 5 Papillary muscles: contract during ventricular systole to prevent AV valves from going into the aorta D. Coverings 1. Fibrous Pericardium: tough outer layer of the pericardium that protects the heart, anchors to heart to surrounding structures, and prevents over lling of the heart with blood. 2. Serous Pericardium: then slippery two layer membrane. a. Parietal layer: in membrane of the pericardial sac, that’s a serious uid, which is a lubricant to reduce friction between the parietal and visceral layer b. Visceral layer (Epicardium) E. Layers 1. Endocardium: innermost layer of the heart that consist of endothelial cells and covers the heart valves and lines chambers of the heart. 2. Myocardium: middle and thickest layer of the heart that is composed of cardiac muscle tissue. 3. Epicardium: outermost layer of the heart that acts as a thin protective layer. Functions of Blood Transportation! Gases (O2 and CO2) Nutrients/wastes Proteins (i.e. clotting) Communication Hormones Proteins fi Body Temperature II. Blood Flow A. Pulmonary: right side of the heart that is served by the right ventricle. Short, low pressure circulation allows blood to ow from the heart to the lungs. B. Systemic: left side of the heart that is served by the left ventricle. Longer pathway throughout the entire body. The systemic circulation encounters about ve times as much friction or resistance. Blood ows from heart to body. C. Coronary Circulation: functional blood supply of the heart; shortest circulation in the body. 1. Left coronary artery a. Anterior interventricular artery: supplies, blood to the septum and interior walls of both ventricles b. Circum ex artery: supplies blood to the left atrium, and the posterior wall of the left ventricle. 2. Right coronary artery a. Right marginal artery: serve the myocardium of the lateral right side of the heart b. Posterior interventricular artery: runs to the Apex of the heart and supplies the post ventricular walls 3. Coronary Veins a. Cardiac veins 1.) Great cardiac vein: anterior interventricular sulcus 2.) Middle cardiac vein: posterior interventricular sulcus 3.) Small cardiac vein: Heart inferior margin b. Coronary Sinus: empties blood into the right atrium. c. Anterior cardiac veins: empties blood into right atrium anteriorly 4 Angina pectoris: chest pain caused by the de ciency in blood delivery to myocardium. This may be caused by stress induce spasms. 5. Myocardial Infarction- Cardiac cells tend to die and they are replaced by non-contractile fi fl fl fl scar tissue III. Cardiac Muscle Cells A. Characteristics of cardiac myocytes 1. Branched: branched structure, allowing for ef cient communication and synchronization of contractions throughout the heart muscle. 2. Striated: Similar to skeletal muscle cells, cardiac myocytes exhibit a striated appearance due to the organized arrangement of contractile proteins, such as actin and myosin, within their cytoplasm. 3. Intercalated discs: Intercalated discs are specialized structures found at the junctions between cardiac muscle cells. These discs contain gap junctions and desmosomes, facilitating electrical and mechanical coupling between adjacent cells, which is essential for coordinated contraction of the heart. B. Physiology 1. Cardiac myocytes: Cardiac myocytes are primarily responsible for the contraction of the heart muscle, generating the force required to pump blood throughout the circulatory system 2. Pacemaker cells: known as autorhythmic cells, are specialized cardiac cells found in the sinoatrial (SA) and atrioventricular (AV) nodes a. Autorhythmicity: Pacemaker cells possess intrinsic electrical properties that enable them to spontaneously depolarize at regular intervals, initiating action potentials without external neural input. b. No Neural Input: Unlike skeletal muscle, which requires neural stimulation to contract, pacemaker cells generate rhythmic impulses independently, ensuring the heart maintains its intrinsic rhythm even in the absence of neural control. 3. Sarcoplasmic Reticulum (SR) a. Stores Calcium: The sarcoplasmic reticulum serves as the primary intracellular calcium store in cardiac muscle cells, holding a reservoir of calcium ions ready for release during muscle contraction. b. Extracellular Calcium Triggers SR Release: Upon stimulation, extracellular calcium in ux triggers the release of calcium from the sarcoplasmic reticulum into the cytoplasm, initiating the process of muscle contraction. c. Slow Calcium Channels Allow Entry: Slow calcium channels embedded in the cardiac cell membrane permit the entry of a small portion (10-20%) of extracellular calcium into the cell. fi fl This in ux contributes to the total calcium available for muscle contraction. d. SR Provides Majority of Calcium: The sarcoplasmic reticulum is responsible for releasing the majority (80-90%) of the calcium ions required for cardiac muscle contraction, highlighting its crucial role in regulating myocardial function. IV. Cardiac Rhythm A. Intrinsic Conduction System 1. Noncontractile Cardiac Cells a. Autorhythmic: Specialized cells within the heart, such as those found in the sinoatrial (SA) and atrioventricular (AV) nodes, exhibit autorhythmicity, spontaneously generating electrical impulses. b. About 1% of the Cardiac Fibers: While forming a small percentage of the cardiac muscle tissue, these autorhythmic cells play a crucial role in coordinating the heart's rhythmic contractions. c. Unstable Resting Potential: Unlike contractile cells, which have a stable resting membrane potential, autorhythmic cells display an unstable resting potential that gradually depolarizes, leading to the initiation of action potentials. 2. Action Potentials a. Pacemaker Potential: The gradual depolarization of autorhythmic cells, known as the pacemaker potential, eventually reaches a threshold, triggering an action potential. b. Depolarization: During the action potential, voltage-gated calcium channels open, allowing calcium ions to enter the cell, leading to depolarization. c. Repolarization: Following depolarization, potassium channels open, allowing potassium ions to exit the cell, leading to repolarization and restoration of the resting membrane potential. 3. Defects a. Arrhythmias: Irregularities in the heart's rhythm, known as arrhythmias, can result from abnormalities in the intrinsic conduction system, leading to inef cient cardiac function. b. Fibrillation: In severe cases, such as atrial or ventricular brillation, the heart's electrical signals become chaotic, impairing its ability to pump blood effectively and potentially leading to life-threatening complications. 4. Sequence of Excitation a. SA Node: The sinoatrial (SA) node, located in the right atrium, serves as the heart's natural pacemaker, initiating electrical impulses that trigger cardiac muscle contraction. b. AV Node: The atrioventricular (AV) node, located near the junction of the atria and ventricles, delays the electrical signal brie y to allow for complete atrial contraction before transmitting it to the ventricles. c. AV Bundle (Bundle of His): The AV bundle is a bundle of specialized bers that conducts the electrical impulse from the AV node down the interventricular septum. d. Right and Left Bundle Branches: After passing through the AV bundle, the electrical impulse travels down the right and left bundle branches, which extend along the septum toward the apex of the heart. e. Subendocardial Conducting Network (Purkinje Fibers): The nal stage of excitation involves the subendocardial conducting network, consisting of Purkinje bers, which rapidly distribute the electrical impulse throughout the ventricles, coordinating their contraction from the apex upward. B. Extrinsic Innervation of the Heart 1. Nerves of the Heart a. Medulla Oblongata: The medulla oblongata, part of the brainstem, plays a crucial role in regulating autonomic functions, including heart rate and rhythm. b. Cardioaccelerator Center: Within the medulla oblongata, the cardioaccelerator center controls sympathetic innervation of the heart, stimulating an increase in heart rate and contractility during times of stress or physical exertion. c. Cardioinhibitory Center: Also located within the medulla oblongata, the cardioinhibitory center regulates parasympathetic innervation of the heart via the vagus nerve, leading to a decrease in heart rate and contractility, promoting relaxation and conservation of energy. B. Extrinsic Innervation of the Heart 2. Action Potential of Contractile Cardiac Cells a. Depolarization: The initial phase of the cardiac action potential involves depolarization, triggered by the in ux of sodium ions through fast voltage-gated sodium channels. This rapid depolarization results in the rising phase of the action potential. b. Plateau Phase: Following depolarization, cardiac cells experience a prolonged plateau fl fl fl phase characterized by the in ux of calcium ions through slow voltage-gated calcium channels and ef ux of potassium ions. This plateau phase sustains the depolarized state, allowing for prolonged contraction and effective expulsion of blood from the ventricles. c. Repolarization: Subsequent to the plateau phase, repolarization occurs as potassium ions exit the cell, restoring the membrane potential to its resting state. This repolarization phase prepares the cell for subsequent depolarization and contraction. C. Cardiac Cycle 1. Systole: The phase of the cardiac cycle during which the heart contracts, ejecting blood into the circulation. 2. Diastole: The phase of the cardiac cycle during which the heart relaxes and lls with blood. 3. Phases of the Cardiac Cycle: a. Ventricular Filling: Occurs during early diastole when blood ows from the atria into the ventricles, lling them with blood. b. Isovolumetric Contraction: Following ventricular lling, the ventricles contract isometrically (without changing volume), closing the atrioventricular valves while ventricular pressure rises. c. Ventricular Ejection: Once ventricular pressure exceeds that of the aorta and pulmonary artery, the semilunar valves open, allowing blood to be ejected from the ventricles into the respective arteries. d. Isovolumetric Ventricular Relaxation: After ventricular ejection, both the atrioventricular and semilunar valves close, and the ventricles relax isometrically. This phase marks the beginning of diastole. In the Wiggers diagram, which represents the cardiac cycle, the terms “End Diastolic Volume (EDV),” “End Systolic Volume (ESV),” and “Stroke Volume (SV)” represent important parameters related to ventricular function. 1. End Diastolic Volume (EDV): This refers to the volume of blood in the ventricles at the end of diastole, just before ventricular contraction (systole) begins. It represents the maximum amount of blood that the ventricles can hold during the lling phase of the cardiac cycle. 2. End Systolic Volume (ESV): This indicates the volume of blood remaining in the ventricles at the end of systole, just after ventricular contraction. It represents the amount of blood left in the ventricles after they have ejected blood into the circulation during systole. fi fi fl fi 3. Stroke Volume (SV): This is the difference between the end diastolic volume (EDV) and end systolic volume (ESV). It represents the volume of blood ejected from the ventricles with each heartbeat. Mathematically, SV = EDV - ESV. These parameters are essential for assessing cardiac function and can provide valuable information about the ef ciency of the heart’s pumping action. Here’s a concept map for Cardiac Output: Cardiac Output | +--------+--------+ | | Determinants | Equation | +-----+-----+ | | | +-----+-----+ | Heart Rate Stroke Volume Explanation: Cardiac Output: Represents the total volume of blood pumped by the heart per unit time, typically measured in liters per minute (L/min). Determinants: Factors that in uence cardiac output, including heart rate and stroke volume. Heart Rate: The number of times the heart beats per minute (bpm). It is one of the primary determinants of cardiac output and can be in uenced by factors such as autonomic nervous system activity, hormonal regulation, and physical activity. Stroke Volume: The volume of blood ejected from the heart with each contraction (heartbeat), typically measured in milliliters per beat (mL/beat). Stroke volume is in uenced by factors such as preload, contractility, and afterload. Equation: Cardiac output is calculated by multiplying heart rate by stroke volume. Mathematically, Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV). This concept map provides a visual representation of the key components and relationships fl fl fi involved in determining cardiac output. Here’s a concept map for Heart Rate and its control mechanisms: Heart Rate | +-----------+------------+ | | Parasympathetic Control Sympathetic Control | | Acetylcholine Catecholamines (NE & Epi) K+ channels increase permeability β1-adrenergic receptors Increased permeability to Na+ and Ca2+ Ca2+ permeability decreases Explanation: Heart Rate: Represents the number of times the heart beats per minute (bpm). Parasympathetic Control: The parasympathetic nervous system, mediated by acetylcholine, decreases heart rate. Acetylcholine: Neurotransmitter released by parasympathetic neurons, which increases the permeability of potassium (K+) channels, leading to hyperpolarization of cardiac cells and a decrease in heart rate. Additionally, acetylcholine decreases calcium (Ca2+) permeability, further reducing heart rate. Sympathetic Control: The sympathetic nervous system, activated by catecholamines (norepinephrine and epinephrine), increases heart rate. Catecholamines (NE & Epi): Neurotransmitters released by sympathetic neurons and the adrenal glands, which bind to β1-adrenergic receptors on cardiac cells, leading to increased permeability to sodium (Na+) and calcium (Ca2+) ions, resulting in depolarization and an increase in heart rate. V. Embryology of the Heart A. Endocardial Tubes During early embryonic development, the heart begins as a pair of endocardial tubes, which form from the fusion of paired endothelial strands in the cardiogenic area of the embryo. B. Formation of Four Chambers 1. Sinus Venosus The sinus venosus is one of the early structures formed in the embryonic heart. It serves as a collecting chamber for deoxygenated blood returning from the body before it enters the developing heart. 2.Atrium As the embryonic heart continues to develop, the sinus venosus expands and gives rise to the atria. Initially, there is a single atrium, but eventually, it divides into the left and right atria. 3.Ventricle Concurrently, the primitive heart tube elongates and undergoes looping, resulting in the formation of the ventricles. Initially, there is a single ventricle, which later divides into the left and right ventricles. 4. Bulbis Cordis The bulbus cordis is a region of the embryonic heart tube that eventually contributes to the formation of the out ow tracts of the ventricles and the aorta and pulmonary arteries. It undergoes extensive remodeling and septation to give rise to these structures during embryonic development. C. Fetal Heart Adaptations 1. Umbilical Arteries and Vein During fetal development, the umbilical arteries and vein play a crucial role in the exchange of nutrients and oxygen between the fetus and the placenta. The umbilical arteries carry deoxygenated blood from the fetus to the placenta, where it picks up oxygen and nutrients, while the umbilical vein returns oxygenated blood from the placenta to the fetus. 2. Foramen Ovale The foramen ovale is a shunt between the right and left atria in the fetal heart. It allows a portion of the blood to bypass the non-functional fetal lungs and directly enter the systemic fl circulation. This adaptation helps maximize the oxygen-rich blood supply to vital organs, such as the brain, during fetal development. 3. Ductus Arteriosus The ductus arteriosus is a blood vessel that connects the pulmonary artery to the aorta in the fetal heart. It serves as a shunt that allows most of the blood from the right ventricle to bypass the fetal lungs and enter the systemic circulation. This adaptation helps divert blood away from the non-functional fetal lungs and directs it towards vital organs, ensuring adequate oxygen supply to support fetal growth and development. VI. Clinical Heart Problems A. Heart Rate 1. Tachycardia: A condition characterized by an abnormally rapid heart rate, typically exceeding 100 beats per minute in adults. Tachycardia may be caused by various factors, including physiological stress, fever, anxiety, certain medications, or underlying heart conditions. 2. Bradycardia: Bradycardia is the opposite of tachycardia and refers to a slower than normal heart rate, typically below 60 beats per minute in adults. It can be caused by conditions such as sinus node dysfunction, heart block, hypothyroidism, or the use of certain medications. B. Cardiac Output 1. Congestive Heart Failure: Congestive heart failure occurs when the heart is unable to pump blood effectively to meet the body’s demands. This can result from conditions such as coronary artery disease, hypertension, myocardial infarction, or cardiomyopathy, leading to symptoms such as shortness of breath, fatigue, and uid retention. 2. Coronary Atherosclerosis: Coronary atherosclerosis refers to the buildup of plaque in the coronary arteries, leading to reduced blood ow to the heart muscle. This condition can result in angina (chest pain), myocardial infarction (heart attack), or sudden cardiac death if a plaque ruptures and causes a complete blockage of blood ow to the heart. 3. High Blood Pressure (Hypertension): Hypertension is a common condition characterized by elevated blood pressure levels persistently exceeding 130/80 mmHg. Chronic hypertension can strain the heart, leading to hypertrophy (enlargement) of the left ventricle and an increased risk of heart failure, stroke, and other cardiovascular complications. 4. Multiple Myocardial Infarctions: Myocardial infarction, commonly known as a heart attack, occurs when blood ow to a part of the heart muscle is blocked, leading to tissue fl fl fl damage or death. Multiple myocardial infarctions can result in progressive damage to the heart muscle, impairing its ability to pump effectively and increasing the risk of heart failure. 5. Dilated Cardiomyopathy: Dilated cardiomyopathy is a condition characterized by the enlargement of the heart chambers and weakening of the heart muscle, leading to reduced cardiac function and heart failure. It can be caused by various factors, including genetic predisposition, viral infections, alcohol abuse, or certain medications. Symptoms may include fatigue, shortness of breath, and swelling of the ankles and legs. I. Structure and Function of Blood Vessels A. Categories 1. Arteries: Blood vessels that carry oxygenated blood away from the heart to various parts of the body. 2. Capillaries: Microscopic blood vessels where the exchange of gases, nutrients, and waste products occurs between the blood and tissues. 3. Veins: Blood vessels that carry deoxygenated blood from the body back to the heart. B. Structure – Layers 1. Lumen: The central hollow space within a blood vessel through which blood ows. 2. Tunica Intima: The innermost layer of blood vessels, consisting of endothelial cells that provide a smooth surface for blood ow. 3. Tunica Media: The middle layer of blood vessels, composed of smooth muscle cells and elastic bers responsible for regulating vessel diameter and blood pressure. 4. Tunica Externa: The outermost layer of blood vessels, primarily composed of connective tissue and collagen bers, providing structural support and protection. a. Collagen Fibers: Tough protein bers that provide strength and stability to blood vessel walls. b. Vasa Vasorum: Small blood vessels that supply blood to the walls of larger blood vessels, ensuring their nourishment and oxygenation. Vasoconstriction: The narrowing of blood vessels due to the contraction of smooth muscle cells in the vessel walls. Vasoconstriction reduces blood ow to a particular area or organ, increasing blood pressure and redirecting blood ow to areas where it is needed most, such as during times of stress or injury. Vasodilation: The widening or relaxation of blood vessels due to the relaxation of smooth muscle cells in the vessel walls. Vasodilation increases blood ow to a particular area or fl fl fl fi fi fi organ, lowering blood pressure and allowing for enhanced delivery of oxygen and nutrients to release of certain chemicals such as nitric oxide. C. Arteries 1. Elastic Arteries: Large arteries near the heart that contain abundant elastic bers in their tunica media, allowing them to stretch and recoil with each heartbeat to maintain continuous blood ow and smooth pressure uctuations. 2. Muscular Arteries: Medium-sized arteries that distribute blood to various parts of the body. They have a thick tunica media composed of smooth muscle cells that regulate blood ow by vasoconstriction and vasodilation in response to neural and hormonal signals. 3. Arterioles: Small arteries that regulate blood ow into capillary beds. They have a thin tunica media and are primarily responsible for controlling peripheral resistance and blood pressure by adjusting their diameter in response to local and systemic factors. D. Capillaries 1. Continuous Capillaries: The most common type of capillaries, characterized by an uninterrupted endothelial lining with tight junctions between cells. They allow for the exchange of small molecules and gases between the blood and tissues and are found in muscles, skin, and the central nervous system. 2. Fenestrated Capillaries: Capillaries with pores or fenestrations in their endothelial cells, allowing for increased permeability and the rapid exchange of larger molecules such as proteins and hormones. Fenestrated capillaries are found in organs with high rates of ltration and absorption, such as the kidneys, small intestine, and endocrine glands. 3- Sinusoid Capillaries: Highly permeable capillaries with irregularly shaped lumens and large gaps between endothelial cells. Sinusoid capillaries allow for the exchange of large molecules, cells, and even whole blood cells between the blood and tissues. They are found in organs with specialized functions, such as the liver, spleen, and bone marrow. Capillary Bed: A network of interconnected capillaries that supplies blood to a particular tissue or organ. Capillary beds are the sites of exchange between the blood and surrounding tissues, facilitating the diffusion of oxygen, nutrients, waste products, and hormones. Precapillary Sphincter: A band of smooth muscle bers located at the entrance of each capillary, where it branches off from an arteriole. Precapillary sphincters regulate blood ow into capillary beds by contracting or relaxing in response to local metabolic needs and neural signals. Constriction of precapillary sphincters reduces blood ow into fl fi fl capillaries, while relaxation allows for increased blood ow, ensuring that tissues receive fl fl fl tissues. It can occur in response to various stimuli, including relaxation, exercise, and the E. Venule: Small vessels collecting blood from capillaries, leading to larger veins. F. Veins 1. Valves: Flap-like structures within veins preventing back ow, aiding blood ow to the heart. 2. Venous Sinuses: Thin-walled veins serving as blood reservoirs or channels between organs. II. Circulation A. Blood Flow: The movement of blood through the blood vessels of the circulatory system, driven by the pumping action of the heart. B. Blood Pressure: The force exerted by the blood against the walls of the blood vessels. It is typically measured in millimeters of mercury (mmHg) and consists of two main components: 1. Systolic Pressure: The highest pressure exerted on the arterial walls during ventricular contraction (systole), when the heart is pumping blood into the arteries. 2. Diastolic Pressure: The lowest pressure exerted on the arterial walls during ventricular relaxation (diastole), when the heart is lling with blood between beats. C. Blood Viscosity: The thickness or stickiness of blood, determined by the concentration of red blood cells and proteins in the plasma. High blood viscosity can increase resistance to blood ow and contribute to hypertension and other cardiovascular disorders. D. Blood Vessel Diameter: The size of the lumen (inner space) of blood vessels, which can be regulated by the smooth muscle in their walls: 1-Vasoconstriction: The narrowing of blood vessels due to contraction of smooth muscle cells in the vessel walls. Vasoconstriction increases blood pressure by reducing the diameter of the vessels and restricting blood ow. 2- Vasodilation: The widening of blood vessels due to relaxation of smooth muscle cells in the vessel walls. Vasodilation decreases blood pressure by increasing the diameter of the vessels and promoting greater blood ow. E. Resistance: Opposition to blood ow in vessels, in uenced by factors like blood thickness and vessel size. Increased resistance, from factors like vasoconstriction, can strain the heart. 1. Blood Viscosity: Thickness of blood, which affects its ow resistance. Higher viscosity increases resistance. 2. Blood Vessel Length: Longer vessels offer more resistance to ow compared to shorter ones due to increased friction along the vessel walls. fl fl fi fi fl fl fl fl 3. Blood Vessel Radius: The most signi cant factor affecting resistance. Smaller vessel blood ow dynamics. TPR (Total Peripheral Resistance) is the overall resistance in the systemic circulation. Blood ow is directly related to the pressure difference (∆ ) and inversely related to TPR. Higher TPR means less blood ow, while lower TPR means more blood ow in the systemic circulation. F. Blood Pressure 1. Arterial Pressure: Higher in arteries due to muscular walls and proximity to the heart. 2. Factors Affecting Arterial BP: a. Compliance: Elastic arteries’ ability to stretch. b. Blood Volume: Amount of blood forced into arteries. c. Pulsatile Nature: BP uctuates with each heartbeat. 3. Pulse Pressure: Difference between systolic and diastolic BP. 4.Mean Arterial Pressure (MAP): Average pressure in arteries throughout the cardiac cycle, vital for organ perfusion. G. Venous Blood Pressure 1. Skeletal Muscle Pump: Contraction of skeletal muscles around veins squeezes blood toward the heart, aiding venous return. 2. Respiratory Pump: Changes in intrathoracic pressure during breathing facilitate venous return to the heart. 3.Sympathetic Venoconstriction: Activation of sympathetic nerves causes constriction of veins, increasing venous return and maintaining blood pressure. H. Control of Blood Pressure 1. Key Variables for Maintaining Blood Pressure: a. Cardiac Output: Volume of blood pumped by the heart per minute. b. Total Peripheral Resistance: Overall resistance to blood ow in the systemic circulation. c. Blood Volume: Total volume of blood in the circulatory system. The equation ∆ = × peripheral resistance ( represents the relationship between cardiac output ( ), total ), and the pressure difference (∆ ) required to maintain blood ow. 𝑃 𝑅 𝑃 𝑇 𝑅 𝑃 fl fl 𝑇 𝑂 𝐶 𝑃 This equation illustrates how changes in cardiac output or total peripheral resistance can affect blood pressure. fl fl radius increases resistance exponentially, while larger radius decreases resistance, affecting 2. Cardiovascular Center a. Cardioaccelerator Center: Part of the medulla oblongata that regulates sympathetic innervation to the heart, increasing heart rate and contractility. b. Cardioinhibitory Center: Also located in the medulla oblongata, it regulates parasympathetic innervation to the heart via the vagus nerve, decreasing heart rate and contractility. 3. Vasomotor Center: Located in the medulla oblongata, it regulates sympathetic innervation to blood vessels, controlling their diameter and thus peripheral resistance. 4. Baroreceptors: Specialized sensory receptors that detect changes in blood pressure and relay this information to the cardiovascular center. a. Carotid Sinuses: Baroreceptors located in the carotid arteries, near the bifurcation of the common carotid artery. b. Aortic Arch: Baroreceptors located in the wall of the aortic arch, near the heart. 5. Baroreceptor Re exes to Maintain Blood Pressure Homeostasis: a. Vasodilation: Results from decreased output from the vasomotor center, leading to relaxation of smooth muscle in blood vessel walls and widening of the vessel diameter. b. Arteriolar Vasodilation: Reduces peripheral resistance by widening arterioles, allowing for easier blood ow through the vascular system. c. Venodilation: Increases venous capacitance by relaxing smooth muscle in veins, reducing venous return to the heart and thus decreasing preload. d. Decrease in Cardiac Output: Results from decreased sympathetic stimulation to the heart and decreased heart rate and contractility, leading to reduced blood ow from the heart. I. Hormonal Controls – Short-term Regulation 1. Epinephrine and Norepinephrine: Released during stress, they increase heart rate and vasoconstriction. 2. Angiotensin II: Formed in response to low blood pressure, it promotes vasoconstriction and uid retention. 3. Atrial Natriuretic Peptide (ANP): Released due to increased atrial pressure, it promotes vasodilation and urinary sodium excretion. 4. Antidiuretic Hormone (ADH): Released in response to low blood volume, it conserves fl fl fl water and constricts blood vessels to raise blood pressure. J. Renal Mechanisms 1. Direct Renal Mechanism: Involves the regulation of blood volume and pressure through changes in renal blood ow and glomerular ltration rate (GFR). It directly in uences sodium and water excretion by the kidneys, thereby affecting blood volume and pressure. 2.Indirect Renal Mechanism: Involves the renin-angiotensin-aldosterone system (RAAS), which responds to changes in blood pressure and volume. Renin, released by the kidneys, catalyzes the conversion of angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II stimulates vasoconstriction, aldosterone release, and thirst, ultimately increasing blood pressure and volume. K. Imbalances in blood pressure 1. Hypertension a. Systolic pressure above 130mmHg, diastolic pressure above 80mmHg b. Primary (or essential) Hypertension 1.) Heredity 2.) Diet 3.) Obesity 4.) Age 5.) Diabetes mellitus 6.) Stress 7.) Smoking c. Secondary Hypertension 2. Hypotension a. Below 90/60mmHg b. Orthostatic hypotension c. Chronic Hypotension d. Acute Hypotension 3. Circulatory Shock: A life-threatening condition where blood ow to vital organs is inadequate to meet metabolic demands, leading to cellular dysfunction and organ failure. 4. Hypovolemic Shock: a. Results from signi cant blood or uid loss, such as from trauma, surgery, or severe fi fl fl fi dehydration. b. Symptoms include weak pulse and vasoconstriction in an attempt to maintain blood pressure. 5. Vascular Shock: a. Anaphylactic Shock: Results from a severe allergic reaction, causing widespread vasodilation and decreased blood pressure. b. Neurogenic Shock: Due to spinal cord injury or severe pain, leading to loss of sympathetic tone and vasodilation. c. Septic Shock: Caused by severe infection, leading to systemic in ammation and vasodilation, resulting in decreased blood pressure. 6. Cardiogenic Shock: Occurs when the heart is unable to pump suf cient blood to meet the body's needs, often due to myocardial infarction or severe heart failure. III. Capillary Exchange A. Movement of Molecules 1. Diffusion: a. Lipid-Soluble Substances: Easily pass through the lipid bilayer of capillary endothelial cells, such as oxygen and carbon dioxide. b. Insoluble Substances: Small water-soluble molecules, like glucose and electrolytes, diffuse through water- lled channels (pores) between endothelial cells. 2. Vesicular Transport: Larger molecules, such as proteins, are transported across endothelial cells via vesicles. 3. Bulk Flow: a. Filtration: Movement of uid and solutes out of the capillary into the interstitial space under pressure. b. Reabsorption: Movement of uid and solutes from the interstitial space back into the capillary, driven by osmotic pressure. B. Pressures 1. Hydrostatic Pressure: a. Capillary Hydrostatic Pressure: This is the pressure exerted by the blood against the walls of the capillary. It tends to push uid out of the capillary into the surrounding tissues, promoting ltration. b. Interstitial Fluid Hydrostatic Pressure: This is the pressure exerted by the uid in the interstitial space against the walls of the capillary. It opposes the movement of uid out of the fl fl fl fi fi capillary and into the tissues. a. Blood Colloid Osmotic Pressure: This is the pressure exerted by the proteins (primarily albumin) in the blood plasma. It tends to draw uid back into the capillary from the surrounding tissues, promoting reabsorption. b. Interstitial Fluid Osmotic Pressure: This is the pressure exerted by the proteins in the interstitial uid. It opposes the movement of uid back into the capillary. I. Anatomy of the Lymphatic System A. Functions 1. Draining Interstitial Fluid: Collects excess tissue uid (interstitial uid) from body tissues and returns it to the bloodstream. 2. Transporting Dietary Lipids: Absorbs dietary fats and fat-soluble vitamins from the digestive tract and transports them to the bloodstream. 3. Defense Against Viruses and Bacteria: Houses lymphocytes and other immune cells that help defend the body against pathogens. B. Lymphatic Capillaries 1. Blind-End Vessels: Have closed ends and are responsible for collecting interstitial uid. 2. Not Present in Bone: Lymphatic capillaries are absent in bone tissue. 3. Highly Permeable: Allow easy passage of tissue uid, proteins, and cellular debris into the lymphatic system. 4. Overlapping Endothelial Cells: Create ap-like valves that permit uid entry but prevent back ow. 5.Anchoring Filament: Help to keep endothelial cells open, ensuring uid entry into the lymphatic capillary. C. Collecting Lymphatic Vessels 1. Internal Valves: Present within lymphatic vessels to ensure one-way ow of lymph towards larger lymphatic vessels and ultimately back to the bloodstream. 2. Anastomose: Connect and merge with each other, forming a network that facilitates the transport of lymph throughout the body. D. Lymphatic Trunks 1. Lumbar Trunk: Drains lymph from the lower limbs, pelvis, and abdominal wall. 2. Intestinal Trunk: Collects lymph from the digestive organs, including the stomach, fl fl fl fl fl fl intestines, pancreas, and spleen. fl fl 2. Colloid Osmotic Pressure: 3. Subclavian Trunk: Drains lymph from the upper limbs, shoulder region, and thoracic wall. 4. Jugular Trunk: Collects lymph from the head and neck region. 5.Bronchomediastinal Trunk: Drains lymph from the thoracic viscera and thoracic wall. E. Lymphatic Ducts 1. Right Lymphatic Duct: Drains lymph from the right upper limb, right side of the head and neck, and the right thorax into the right subclavian vein. 2. Thoracic Duct: a. Cisterna Chyli: Dilated sac at the base of the thoracic duct where lymph from the lower body and intestines collects before entering the thoracic duct. b. Drains Most of the Body: Receives lymph from the left upper limb, left side of the head and neck, entire lower body, and the left thorax, ultimately emptying into the left subclavian vein. II. Lymph A. Formation 1.3L/day: Approximately 3 liters of lymph are formed daily from the ltration of interstitial uid. 2.Proteins: Lymph contains proteins, cellular debris, and other substances collected from the interstitial uid. B. Flow 1. Lymph Returns to Venous Blood: Lymphatic vessels transport lymph back to the bloodstream, where it re-enters circulation via the subclavian veins. 2. Skeletal Muscle Pump: Contraction of skeletal muscles surrounding lymphatic vessels helps propel lymph through the lymphatic system. 3.Respiratory Pump: Changes in thoracic pressure during breathing aid in the movement of lymph, particularly in the thoracic duct, enhancing lymph ow. III. Lymphatic Organs A. Primary Lymphatic Organs 1. Thymus Gland: a. Location: Located in the anterior mediastinum, superior to the heart and behind the sternum. b. 2 Lobes: Consists of two lobes connected by connective tissue. c. T Cells: The thymus is primarily responsible for the maturation and differentiation of T fl fl lymphocytes (T cells), crucial for cellular immunity. 2. Spleen a. Location: Located in the upper left abdomen, between the stomach and the diaphragm. b. Stores Blood: Acts as a reservoir for blood, especially in emergencies such as hemorrhage or shock. c. Removes Worn Out Blood Cells: Filters and removes old or damaged red blood cells and platelets from circulation. d. Site of Lymphocyte Proliferation: Supports the proliferation and differentiation of lymphocytes (white blood cells) involved in immune responses. e. White Pulp: Consists of lymphoid tissue rich in lymphocytes, where immune responses against pathogens occur. f. Red Pulp: Contains venous sinuses and splenic cords involved in ltering and removing old blood cells and storing blood. 3. Lymph Nodes a. Afferent Lymph Vessels: Lymph enters the lymph node through afferent lymphatic vessels, bringing in lymph from the surrounding tissues. b. Cortex: The outer region of the lymph node containing follicles with germinal centers, where B lymphocytes proliferate and differentiate. c. Medulla: The inner region of the lymph node containing medullary cords and sinuses, where lymphocytes, plasma cells, and macrophages are found. IV. MALT A. MALT – Mucosa-Associated Lymphoid Tissues: A network of lymphoid tissues located in mucosal linings, such as the gastrointestinal and respiratory tracts, contributing to immune defense at mucosal surfaces. B. Collections of MALT 1. Tonsils: Clusters of lymphoid tissue in the oral and nasal cavities, including the palatine, lingual, pharyngeal, and tubal tonsils, providing protection against pathogens entering through these routes. 2. Peyer’s Patches: Aggregated lymphoid nodules in the small intestine’s submucosa, involved in monitoring and responding to antigens in the intestinal lumen, supporting intestinal immunity. 3. Appendix: A small projection of lymphoid tissue at the junction of the small and large intestines, possibly playing a role in immune surveillance and supporting gut-associated lymphoid tissue.