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EncouragingRetinalite4868

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Universiti Putra Malaysia

Nur Fariesha Md Hashim

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heart physiology human anatomy nutrition cardiovascular system

Summary

This lecture notes details the impact of diet and nutrition on heart physiology, including normal and pathological conditions. It covers factors like sodium, potassium, omega-3 fatty acids, saturated and trans fats, fiber, antioxidants, refined sugars, and magnesium. The lecture explores the mechanisms of action for each factor in both healthy and disease states.

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PKK3004: The Cardiovascular System (Heart) Human Anatomy & Physiology Associate Professor Dr. Nur Fariesha Md Hashim Department of Biomedical Science, FMHS, UPM Role in Impact on Diet/ Heart Heart Mechanism of Action Nutrition...

PKK3004: The Cardiovascular System (Heart) Human Anatomy & Physiology Associate Professor Dr. Nur Fariesha Md Hashim Department of Biomedical Science, FMHS, UPM Role in Impact on Diet/ Heart Heart Mechanism of Action Nutrition Physiology Physiology in Pathological Factor (Normal (Pathological Condition Condition) Condition) Maintains fluid High sodium intake balance, is linked to affecting blood High sodium increases water hypertension, which pressure retention, raising blood volume increases strain on regulation. and thus blood pressure. the heart, Increased pressure triggers Sodium High sodium intake triggers contributing to left ventricular vasoconstriction and stimulates the kidneys to the renin-angiotensin-aldosterone hypertrophy, heart retain water, system (RAAS), leading to vascular failure, and increasing blood and cardiac remodeling. increased risk of volume and stroke. cardiac output. Low potassium Counters the levels can lead to Potassium helps balance sodium effects of sodium arrhythmias and levels. on blood weaken heart Low potassium disrupts electrolyte Potassi pressure and supports normal muscle contraction. Adequate intake is balance, affecting cellular excitability and heart muscle um muscle contraction, essential for lowering blood contraction strength, leading to arrhythmias and increased Impact on Role in Heart Mechanism of Diet/ Heart Physiology Action in Nutrition Physiology (Normal Pathological Factor (Pathological Condition) Condition Reduces inflammation, improves endothelial Condition) Deficiency may contribute Omega-3s reduce inflammation by modulating Omega-3 function, and supports to higher blood triglycerides, arrhythmias, eicosanoid pathways, lower stable heart rhythms. triglycerides, and stabilize Fatty Found in fish, nuts, and and chronic inflammation, which increases risk of heart cell membranes, which seeds, omega-3s help supports regular heart Acids maintain lower triglyceride atherosclerosis and myocardial infarction. rhythms and reduces levels. endothelial dysfunction. Excessive intake leads to Saturated and trans fats atherosclerosis due to LDL Increases low-density increase LDL cholesterol and buildup in arterial walls, Saturated lipoprotein (LDL) cholesterol, potentially increasing the risk of decrease HDL, promoting lipid accumulation in the arterial coronary artery disease and Trans causing fatty deposits in arteries. Moderate intake and heart attacks. High walls and plaque formation. This causes endothelial injury trans fat intake is Fats is crucial for balanced cholesterol levels. particularly linked to and initiates an inflammatory response, leading to inflammation and atherosclerosis. endothelial dysfunction. Fiber binds to bile acids and Helps lower cholesterol Low fiber intake is cholesterol in the intestine, levels by binding to associated with higher reducing LDL absorption. Low cholesterol in the cholesterol, elevated blood fiber diets lead to higher LDL Fiber digestive tract, supports healthy blood pressure, sugar levels, and an increased risk for levels and blood glucose spikes, contributing to and reduces risk of hypertension and endothelial damage and obesity. cardiovascular disease. inflammatory responses in blood vessels. Impact on Role in Heart Mechanism of Diet/ Heart Physiology Action in Nutrition Physiology (Normal Pathological Factor (Pathological Condition) Protects heart Low antioxidant intake Condition tissue from Condition) can lead to increased Antioxidants neutralize free radicals, reducing oxidative Antioxidan oxidative damage oxidative stress, stress and preventing damage ts and maintains endothelial damaging blood vessels and to endothelial cells. Low antioxidant levels allow (Vitamins function. contributing to free radicals to damage Found in fruits, hypertension, vascular walls, promoting C, E) vegetables, and atherosclerosis, and inflammation and whole grains. heart failure. atherogenesis. Excess sugar Excess sugar causes insulin intake raises High sugar intake is spikes, leading to insulin insulin, which may linked to obesity, resistance over time. increase blood insulin resistance, and Refined pressure and type 2 diabetes, all of This promotes hyperglycemia and inflammation, which triglyceride levels which increase risks for Sugars Moderation helps hypertension, coronary damages blood vessels, increasing the risk for maintain a healthy artery disease, and atherosclerosis and weight, reducing metabolic syndrome. hypertension. strain on the heart. Low magnesium levels Supports proper Magnesium regulates ion can cause arrhythmias muscle and nerve channels, especially calcium and increase blood function, channels. pressure. stabilizing heart Low magnesium disrupts Magnesium rhythms. Magnesium deficiency calcium influx, affecting is linked to higher risk Found in nuts, vascular tone and heart rhythm, of coronary artery seeds, and leafy increasing arrhythmogenic risk Impact on Heart Role in Heart Diet/Nutrition Physiology Mechanism of Action in Physiology (Normal Factor (Pathological Pathological Condition Condition) Condition) Deficiency is associated Vitamin D regulates calcium Contributes to vascular with hypertension, metabolism and vascular smooth increased arterial stiffness, health and helps muscle function. and a higher risk of heart modulate blood pressure. Deficiency increases parathyroid Vitamin D Adequate levels help disease. hormone levels, causing vascular Chronic low vitamin D maintain overall calcification, arterial stiffness, and levels are linked to heart cardiovascular function. impaired blood pressure failure and cardiovascular regulation. events. Excessive cholesterol leads to LDL Necessary for hormone High dietary cholesterol, oxidation, causing endothelial cell synthesis and cell especially in combination injury. membrane structure, but with high saturated fat Dietary the body typically intake, can raise blood This triggers an inflammatory response, promoting foam cell Cholesterol regulates cholesterol cholesterol levels, leading formation and plaque buildup, production to avoid to atherosclerosis and which narrows arteries and excess. coronary artery disease. increases risk for ischemic events. Excessive alcohol intake Alcohol disrupts lipid metabolism, Moderate consumption increases blood pressure, increasing triglycerides, and can may raise high-density weakens heart muscle damage myocardial cells, lipoprotein (HDL) (cardiomyopathy), and Alcohol cholesterol and support raises triglyceride levels, impairing heart muscle function. It also activates the sympathetic vascular health, but heightening risks for nervous system, increasing heart effects vary. hypertension, arrhythmias, rate and blood pressure over time. and heart failure. The Cardiovascular System A closed system of the heart and blood vessels – The heart pumps blood – Blood vessels allow blood to circulate to all parts of the body The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide and other waste products The structure of the heart Heart Anatomy Approximately the size of your fist Location – Superior surface of diaphragm – Left of the midline – Anterior to the vertebral column, posterior to the sternum 9 Heart Anatomy 10 Coverings of the Heart: Anatomy Pericardium – a double-walled sac around the heart composed of: 1. A superficial fibrous pericardium 2. A deep two-layer serous pericardium a. The parietal layer lines the internal surface of the fibrous pericardium b. The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity 11 Coverings of the Heart: Physiology The Function of the Pericardium: – Protects and anchors the heart – Prevents overfilling of the heart with blood – Allows for the heart to work in a relatively friction-free environment Chapter 18, Cardiovascular System 12 Pericardial Layers of the Heart 13 Heart Wall Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue Endocardium – endothelial layer of the inner myocardial surface 14 External Heart: Major Vessels of the Heart (Anterior View) Vessels returning blood to the heart include: 1. Superior and inferior venae cavae 2. Right and left pulmonary veins Vessels conveying blood away from the heart include: 1. Pulmonary trunk, which splits into right and left pulmonary arteries 2. Ascending aorta (three branches) – a. Brachiocephalic b. Left common carotid c. Subclavian arteries External Heart: Vessels that Supply/Drain the Heart (Anterior View) Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries Veins – small cardiac, anterior cardiac, and great cardiac veins External Heart: Anterior View External Heart: Major Vessels of the Heart (Posterior View) Vessels returning blood to the heart include: 1. Right and left pulmonary veins 2. Superior and inferior venae cavae Vessels conveying blood away from the heart include: 1. Aorta 2. Right and left pulmonary arteries External Heart: Vessels that Supply/Drain the Heart (Posterior View) Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove) Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein External Heart: Posterior View Gross Anatomy of Heart: Frontal Section Atria of the Heart Atria are the receiving chambers of the heart Each atrium has a protruding auricle Pectinate muscles mark atrial walls Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins Ventricles of the Heart Ventricles are the discharging chambers of the heart Papillary muscles and trabeculae carneae muscles mark ventricular walls Right ventricle pumps blood into the pulmonary trunk Left ventricle pumps blood into the aorta Heart Function to Circulate Human Blood Myocardial Thickness and Function Thickness of myocardium varies according to the function of the chamber Atria are thin walled, deliver blood to adjacent ventricles Ventricle walls are much thicker and stronger – right ventricle supplies blood to the lungs (little flow resistance) – left ventricle wall is the thickest to supply systemic circulation Thickness of Cardiac Walls Myocardium of left ventricle is much thicker than the right. Atrial Septal Defect Ventricular Septal Defect Pathway of Blood Through the Heart and Lungs Right atrium  tricuspid valve  right ventricle Right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs Lungs  pulmonary veins  left atrium Left atrium  bicuspid valve  left ventricle Left ventricle  aortic semilunar valve  aorta Aorta  systemic circulation Pathway of Blood Through the Heart and Lungs Coronary Circulation Coronary circulation is the functional blood supply to the heart muscle itself Collateral routes ensure blood delivery to heart even if major vessels are occluded Coronary Circulation: Arterial Supply Coronary Circulation: Venous Supply Heart Valves Heart valves ensure unidirectional blood flow through the heart Atrioventricular (AV) valves lie between the atria and the ventricles – AV valves prevent backflow into the atria when ventricles contract Chordae tendineae anchor AV valves to papillary muscles Heart Valves Semilunar valves prevent backflow of blood into the ventricles Aortic semilunar valve lies between the left ventricle and the aorta Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk Heart Valves Heart Valves Atrioventricular Valve Function Semilunar Valve Function Mitral Valve Prolapse How the heart pumps blood? Microscopic Anatomy of Heart Muscle Cardiac muscle is striated, short, fat, branched, and interconnected The connective tissue endomysium acts as both tendon and insertion Intercalated discs anchor cardiac cells together and allow free passage of ions Heart muscle behaves as a functional syncytium Microscopic Anatomy of Heart Muscle Chapter 18, Cardiovascular System 43 Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology Cardiac Cycle Cardiac Output Controls & Blood Pressure Cardiovascular System Function Functional components of the cardiovascular system: – Heart – Blood Vessels – Blood General functions these components provide: – Transportation Everything transported by the blood – Regulation Of the cardiovascular system – Intrinsic v extrinsic – Protection Against blood loss – Production/Synthesis Cardiovascular System Function To create the “pump” we have to examine the functional anatomy of the: – Cardiac muscle – Chambers – Valves – Intrinsic Conduction System More about our Pumping hearts Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology Cardiac Cycle Cardiac Output Controls & Blood Pressure Functional Anatomy of the Heart Cardiac Muscle Characteristic s – Striated – Short branched cells – Uninucleate – Intercalated discs – T-tubules larger and over z-discs Functional Anatomy of the Heart Chambers 4 chambers – 2 Atria – 2 Ventricles 2 systems – Pulmonary – Systemic Functional Anatomy of the Heart Valves Function is to prevent backflow – Atrioventricular Valves (AV) Prevent backflow to the atria Prolapse is prevented by the chordae tendinae – Tensioned by the papillary muscles – Semilunar Valves Prevent backflow into ventricles Functional Anatomy of the Heart Intrinsic Conduction System Consists of “pacemaker” cells and conduction pathways – Coordinate the contraction of the atria and ventricles How does the heart work? Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology – Autorhythmic Cells (Pacemaker cells) – Contractile cells Cardiac Cycle Cardiac Output Controls & Blood Pressure Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells – Smaller than contractile cells – Don’t contain conduction myofibers many myofibrils normal contractile – No organized myocardial cell sarcomere structure do not contribute to the contractile SA node cell AV node cells force of the heart Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells – Unstable membrane potential “bottoms out” at -60mV “drifts upward” to -40mV, forming a pacemaker potential – Myogenic The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself This is due to 1. Slow leakage of K+ out & faster leakage of Na+ in 2. Ca2+ channels open as membrane approaches threshold 3. Slow K+ channels open as membrane depolarizes causing an efflux of K+ and a repolarization of membrane Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Characteristics of Pacemaker Cells Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Altering Activity of Pacemaker Cells – Sympathetic activity NE and E increase If channel activity Myocardial Physiology Autorhythmic Cells (Pacemaker Cells) Altering Activity of Pacemaker Cells – Parasympathetic activity ACh binds to muscarinic receptors – Increases K+ permeability and decreases Ca2+ permeability = hyperpolarizing the membrane » Longer time to threshold = slower rate of action potentials Myocardial Physiology Contractile Cells Special aspects – Intercalated discs Highly convoluted and interdigitated junctions – Joint adjacent cells with » Desmosomes & fascia adherens – Allow for synticial activity » With gap junctions – More mitochondria than skeletal muscle – Less sarcoplasmic reticulum Ca2+ also influxes from ECF reducing storage need – Larger t-tubules Internally branching – Myocardial contractions are graded Myocardial Physiology Contractile Cells Special aspects – The action potential of a contractile cell Ca2+ plays a major role again Action potential is longer in duration than a “normal” action potential due to Ca2+ entry Phases 4 – resting membrane potential @ -90mV 0 – depolarization » Due to gap junctions or conduction fiber action » Voltage gated Na+ channels open… close at 20mV 1 – temporary repolarization » Open K+ channels allow some K+ to leave the cell 2 – plateau phase » Voltage gated Ca2+ channels are fully open (started during initial depolarization) 3 – repolarization » Ca2+ channels close and K+ permeability increases as slower activated K+ channels open, causing a quick repolarization – What is the significance of the plateau phase? Myocardial Physiology Contractile Cells Skeletal Action Potential vs Contractile Myocardial Action Potential Myocardial Physiology Contractile Cells Plateau phase prevents summation due to the elongated refractory period No summation capacity = no tetanus – Which would be fatal » Tetanus =a sustained muscle contraction evoked when the motor nerve that innervates a skeletal muscle emits action potentials at a very high rate. Summary of Action Potentials Skeletal Muscle vs Cardiac Muscle Lecture Outline Cardiovascular System Function Functional Anatomy of the Heart Myocardial Physiology – Autorhythmic Cells (Pacemaker cells) – Contractile cells Cardiac Cycle Cardiac Output Controls & Blood Pressure The Cardiac Conduction System Cardiac Cycle Coordinating the activity Cardiac cycle is the sequence of events as blood enters the atria, leaves the ventricles and then starts over Synchronizing this is the Intrinsic Electrical Conduction System Influencing the rate (chronotropy & dromotropy) is done by the sympathetic and parasympathetic divisions of the ANS Cardiac Cycle Coordinating the activity Electrical Conduction Pathway – Initiated by the Sino-Atrial node (SA node) which is myogenic at 70-80 action potentials/minute – Depolarization is spread through the atria via gap junctions and internodal pathways to the Atrio-Ventricular node (AV node) The fibrous connective tissue matrix of the heart prevents further spread of APs to the ventricles A slight delay at the AV node occurs – Due to slower formation of action potentials – Allows further emptying of the atria – Action potentials travel down the Atrioventricular bundle (Bundle of His) which splits into left and right atrioventricular bundles (bundle branches) and then into the conduction myofibers (Purkinje cells) Purkinje cells are larger in diameter & conduct impulse very rapidly – Causes the cells at the apex to contract nearly simultaneously » Good for ventricular ejection Cardiac Cycle Coordinating the activity Electrical Conductio n Pathway Cardiac Cycle Coordinating the activity The electrical system gives rise to electrical changes (depolarization/repolarization) that is transmitted through isotonic body fluids and is recordable – The ECG! A recording of electrical activity Can be mapped to the cardiac cycle Cardiac Cycle Phases Systole = period of contraction Diastole = period of relaxation Cardiac Cycle is alternating periods of systole and diastole Phases of the cardiac cycle 1. Rest Both atria and ventricles in diastole Blood is filling both atria and ventricles due to low pressure conditions 2. Atrial Systole Completes ventricular filling 3. Isovolumetric Ventricular Contraction Increased pressure in the ventricles causes the AV valves to close… why? – Creates the first heart sound (lub) Atria go back to diastole No blood flow as semilunar valves are closed as well Cardiac Cycle Phases Phases of the cardiac cycle 4. Ventricular Ejection Intraventricular pressure overcomes aortic pressure – Semilunar valves open – Blood is ejected 5. Isovolumetric Ventricular Relaxation Intraventricular pressure drops below aortic pressure – Semilunar valves close = second heart sound (dup) Pressure still hasn’t dropped enough to open AV valves so volume remains the same (isovolumetric) Back to Atrial & Ventricular Diastole The Cardiac Cycle Cardiac Cycle Phases Cardiac Cycle Blood Volumes & Pressure Cardiac Cycle Putting it all together! A Quick revision Cardiac Muscle Contraction Heart muscle: – Is stimulated by nerves and is self- excitable (automaticity) – Contracts as a unit – Has a long (250 ms) absolute refractory period Cardiac muscle contraction is similar to skeletal muscle contraction Heart Physiology: Intrinsic Conduction System Autorhythmic cells: – Initiate action potentials – Have unstable resting potentials called pacemaker potentials – Use calcium influx (rather than sodium) for rising phase of the action potential Pacemaker and Action Potentials of the Heart Heart Physiology: Sequence of Excitation Sinoatrial (SA) node generates impulses about 75 times/minute Atrioventricular (AV) node delays the impulse approximately 0.1 second Heart Physiology: Sequence of Excitation Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His) – AV bundle splits into two pathways in the interventricular septum (bundle branches) 1. Bundle branches carry the impulse towards the apex of the heart 2. Purkinje fibers carry the impulse to the heart apex and ventricular walls Heart Physiology: Sequence of Excitation Heart Excitation Related to ECG ECG Extrinsic Innervation of the Heart The heart is stimulated by the sympathetic cardio-acceleratory center Heart is inhibited by the parasympathetic cardio-inhibitory center 87 Electrocardiography Electrical activity is recorded by electrocardiogram (ECG) P wave corresponds to depolarization of SA node QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex Electrocardiography Heart Sounds Heart sounds (lub-dup) are associated with closing of heart valves – First sound occurs as AV valves close and signifies beginning of systole (contraction) – Second sound occurs when SemiLunar valves close at the beginning of ventricular diastole (relaxation) Heartbeat and Pulse Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart – Systole – contraction of heart muscle – Diastole – relaxation of heart muscle Phases of the Cardiac Cycle Ventricular filling – mid-to-late diastole – Heart blood pressure is low as blood enters atria (passively) and flows into ventricles – AV valves are open, then atrial systole occurs Phases of the Cardiac Cycle Ventricular systole (contraction) – Atria relax – Rising ventricular pressure results in closing of AV valves – Isovolumetric contraction phase – Ventricular ejection phase opens semilunar valves Phases of the Cardiac Cycle Isovolumetric relaxation – early diastole – Ventricles relax – Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves Phases of the Cardiac Cycle Chapter 18, Cardiovascular System 96 Figure 18.20 Cardiac Output (CO) and Reserve Cardiac Output is the amount of blood pumped by each ventricle in one minute – CO is the product of heart rate (HR) and stroke volume (SV) HR is the number of heart beats per minute SV is the amount of blood pumped out by a ventricle with each beat Cardiac reserve is the difference between resting and maximal CO Cardiac Output: Example CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) CO = 5250 ml/min (5.25 L/min) Regulation of Stroke Volume SV = end diastolic volume (EDV) minus end systolic volume (ESV) – EDV = amount of blood collected in a ventricle during diastole – ESV = amount of blood remaining in a ventricle after contraction Factors Affecting Stroke Volume Preload – amount ventricles are stretched by contained blood Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume Slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV Preload and Afterload Extrinsic Factors Influencing Stroke Volume Contractility is the increase in contractile strength, independent of stretch and EDV Increase in contractility comes from: – Increased sympathetic stimuli – Certain hormones – Ca2+ and some drugs Extrinsic Factors Influencing Stroke Volume Agents/factors that decrease contractility include: – Acidosis – Increased extracellular K+ – Calcium channel blockers Contractility and Norepinephrine Sympathetic stimulation releases norepinephrin e and initiates a cyclic AMP second- messenger system 107 Regulation of Heart Rate Positive chronotropic factors increase heart rate – Caffeine Negative chronotropic factors decrease heart rate – Sedatives Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS – PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone If the Vagus Nerve was cut, the heart would lose its tone. Thus, increasing the heart rate by 25 beats per minute. Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria – Causes stimulation of the SA node – Stimulates baroreceptors in the atria, causing increased SNS stimulation Damming= obstruction Chemical Regulation of the Heart The hormones epinephrine and thyroxine increase heart rate Intra- and extracellular ion concentrations must be maintained for normal heart function Factors Involved in Regulation of Cardiac Output Congestive Heart Failure (CHF) Congestive heart failure (CHF) is caused by: – Coronary atherosclerosis – Persistent high blood pressure – Multiple myocardial infarcts – Dilated cardiomyopathy (DCM) – main pumping chambers of the heart are dilated and contract poorly Heart Disease Developmental Aspects of the Heart Developmental Aspects of the Heart Fetal heart structures that bypass pulmonary circulation – Foramen ovale connects the two atria – Ductus arteriosus connects pulmonary trunk and the aorta Examples of Congenital Heart Defects Age-Related Changes Affecting the Heart Sclerosis and thickening of valve flaps Decline in cardiac reserve Fibrosis of cardiac muscle Atherosclerosis Congestive Heart Failure Causes of CHF – coronary artery disease, hypertension, MI, valve disorders, congenital defects Left side heart failure – less effective pump so more blood remains in ventricle – heart is overstretched & even more blood remains – blood backs up into lungs as pulmonary edema – suffocation & lack of oxygen to the tissues Right side failure – fluid builds up in tissues as peripheral edema Congenital Heart Conditions Coronary Artery Disease Heart muscle receiving insufficient blood supply – narrowing of vessels--- atherosclerosis, artery spasm or clot – atherosclerosis-- smooth muscle & fatty deposits in walls of arteries Treatment – drugs, bypass graft, angioplasty, stent Clinical Problems MI = myocardial infarction – death of area of heart muscle from lack of O2 – replaced with scar tissue – results depend on size & location of damage Blood clot – use clot dissolving drugs streptokinase or t-PA & heparin – balloon angioplasty Angina pectoris – heart pain from ischemia (lack of blood flow and oxygen ) of cardiac muscle What happens during a heart attack? By-pass Graft Percutaneous Transluminal Coronary Angioplasty Artificial Heart Revision again….. The Heart Location – Thorax between the lungs – Pointed apex directed toward left hip About the size of your fist The Heart: Coverings Pericardium – a double serous membrane – Visceral pericardium - Next to heart – Parietal pericardium - Outside layer Serous fluid fills the space between the layers of pericardium The Heart Wall: 3 layers Epicardium Outside layer This layer is the parietal pericardium Connective tissue layer Myocardium Middle layer Mostly cardiac muscle Endocardium Inner layer Endothelium External Heart Anatomy The Heart: Chambers Right and left side act as separate pumps Four chambers – Atria Receiving chambers – Right atrium – Left atrium – Ventricles Discharging chambers – Right ventricle – Left ventricle Blood Circulatio n The Heart: Valves Allow blood to flow in only one direction Four (4) valves – Atrioventricular valves – between atria and ventricles Bicuspid valve (left) Also Called Mitral Valve Tricuspid valve (right) – Semilunar valves between ventricle and artery Pulmonary semilunar valve Aortic semilunar valve The Heart: Valves Valves open as blood is pumped through Held in place by chordae tendineae (“heart strings”) Close to prevent backflow Operation of Heart Valves The Heart: Associated Great Vessels Aorta - leaves left ventricle Pulmonary arteries - leave right ventricle Vena cava - enters right atrium Pulmonary veins (four) - enter left atrium Coronary Circulation Blood in the heart chambers does not nourish the myocardium The heart has its own nourishing circulatory system – Coronary arteries – Cardiac veins – Blood empties into the right atrium via the coronary sinus The Heart: Conduction System Intrinsic conduction system (nodal system) – Heart muscle cells contract, without nerve impulses, in a regular, continuous way Special tissue sets the pace Sinoatrial node (SA) - Pacemaker Atrioventricular node (AV) Atrioventricular bundle Bundle branches Purkinje fibers The Heart’s Cardiac Cycle Atria contract simultaneously Atria relax, then ventricles contract Systole = contraction Diastole = relaxation Heart Contractions Contraction is initiated by the sinoatrial node Sequential stimulation occurs at other autorhythmic cells Filling of Heart Chambers – the Cardiac Cycle The Heart: Cardiac Cycle Cardiac cycle – events of one complete heart beat – Mid-to-late diastole – blood flows into ventricles – Ventricular systole – blood pressure builds before ventricle contracts, pushing out blood – Early diastole – atria finish re-filling, ventricular pressure is low The Heart: Cardiac Output Cardiac output (CO) – Amount of blood pumped by each side of the heart in one minute – CO = (heart rate [HR]) x (stroke volume [SV]) Stroke volume – Volume of blood pumped by each ventricle in one contraction Cardiac Output Regulation Regulation of Heart Rate Stroke volume usually remains relatively constant – Starling’s law of the heart – the more that the cardiac muscle is stretched, the stronger the contraction Changing heart rate is the most common way to change cardiac output Regulation of Heart Rate Increased heart rate – Sympathetic nervous system Activated in a Crisis Low blood pressure – Hormones Epinephrine Thyroxine – Exercise – Decreased blood volume Regulation of Heart Rate Decreased heart rate – Parasympathetic nervous system – High blood pressure or blood volume – Decreased venous return Blood Vessels: The Vascular System Taking blood to the tissues and back – Arteries – Arterioles – Capillaries – Venules – Veins The Vascular System Blood Vessels: Anatomy Three layers (tunics) – Tunic intima: Endothelium – Tunic media Smooth muscle Controlled by sympathetic nervous system – Tunic externa Mostly fibrous connective tissue Differences Between Blood Vessel Types Walls of arteries are the thickest and their smooth muscle helps move blood Lumens of veins are larger because walls are thinner Larger veins have valves to prevent backflow Skeletal muscle “milks” blood in veins toward the heart Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue Movement of Blood Through Vessels Most arterial blood is pumped by the heart Veins use the milking action of muscles to help move blood Capillary Beds Capillary beds consist of two types of vessels – Vascular shunt – directly connects an arteriole to a venule Capillary Beds True capillaries – exchange vessels Oxygen and nutrients cross to cells Carbon dioxide and metabolic waste products cross into blood Diffusion at Capillary Beds Major Arteries of Systemic Circulation Major Veins of Systemic Circulation Arterial Supply of the Brain Hepatic Portal Circulation Circulation to the Fetus Pulse Pulse – pressure wave of blood Monitored at “pressure points” where pulse is easily palpated Blood Pressure Measurements by health professionals are made on the pressure in large arteries – Systolic – pressure at the peak of ventricular contraction – Diastolic – pressure when ventricles relax Pressure in blood vessels decreases as the distance away from the heart increases Understanding Blood Pressure Measuring Arterial Blood Pressure Blood Pressure: Effects of Factors Neural factors – Autonomic nervous system adjustments (sympathetic division) Renal factors – Regulation by altering blood volume – Renin – hormonal control Blood Pressure: Effects of Factors Temperature – Heat has a vasodilation effect – Cold has a vasoconstricting effect Chemicals – Various substances can cause increases or decreases Diet Variations in Blood Pressure Human normal range is variable – Normal 140–110 mm Hg systolic 80–75 mm Hg diastolic – Hypotension Low systolic (below 110 mm HG) Often associated with illness – Hypertension High systolic (above 140 mm HG) Can be dangerous if it is chronic Capillary Exchange Substances exchanged due to concentration gradients – Oxygen and nutrients leave the blood – Carbon dioxide and other wastes leave the cells Capillary Exchange: Mechanisms Direct diffusion across plasma membranes Endocytosis or exocytosis Some capillaries have gaps (intercellular clefts) – Plasma membrane not joined by tight junctions Fenestrations of some capillaries – Fenestrations = pores Developmental Aspects of the Cardiovascular System A simple “tube heart” develops in the embryo and pumps by the fourth week The heart becomes a four-chambered organ by the end of seven weeks Few structural changes occur after the seventh week The Heart This organ is what pumps oxygen rich blood, nutrients, Pulmonary Artery hormones, and the other things (Superior Vena Cava) From the (Aortic Artery) To the your body needs to maintain Body body Pulmonary Veins your health, to your organs and tissues. Valves: (tricuspid valve semilunar The pulmonary veins you see on (pulmonary) valve, bicuspid (mitral) valve, and the semilunar (aortic) valve the right side of the diagram come from your lungs, where the blood cells collect oxygen. It’s then pumped out to the rest of the body through the Aorta (Top). All of the blue sections show blood cells carrying waste, (C02) moving back to the lungs (where (Inferior Vena the C02 will be replaced by Cava) From the oxygen) through the Pulmonary Body Artery (Top, blue) By The Way… Whenever the blood is pumped from one section of the heart another valve closes behind it preventing the blood from moving backwards. Blood Flow through the Heart Blood from the body travels into the right atrium, moves into the right ventricle, and is finally pushed into lungs in the pulmonary arteries The blood then picks up oxygen and travels back to the heart into the left atrium through the pulmonary veins The blood then travels through the Left Ventricle and Left Atrium exits to the body through the Right Atrium Aorta… Blood Flow to Arms Oxygen rich blood leaves the heart and travels through arteries In the capillaries the oxygen and food/nutrients is given to the body’s cells The blood finally travels back through veins to the heart to pick up oxygen ARTERIES- FROM HEART CAPILLARIES VEINS- TO HEART Path to the Exchange Pulmonary Vein Aorta A red blood cell then travels Brachial Artery from the heart through arteries that eventually Renal Artery branch into the body’s vast Redial Artery system of capillaries (microscopic Ulnar Artery blood vessels which connect Iliac Artery arteries and veins), they eventually lead to… The Exchange TRANSACT Sub-Title When the itty bitty teeny tiny red blood cells pass the desired tissue they………………………………. Oxy-Rich Blood Cell Tissue The oxygen the blood cells are carrying is given to the body’s tissue. And the CO2 Tissue (waste) from Oxy-Poor Blood Cell the tissue is given to the same blood Technically the Hemoglobin in the blood (a substance full of iron) attracts cell to be oxygen from the lungs. The red blood cell then carries it to the desired exhaled. tissue. Because this tissue has a high CO 2 count the hemoglobin lets go of its oxygen and collects the carbon dioxide. You see the hemoglobin has an How It Works… affinity for whichever gas has a greater count. Because the tissue has a large amount of built up waste (CO2) the hemoglobin attracts it and then replaces it with oxygen, and vise versa in the lungs. Now lets travel to the legs!!! Blood Flow to Legs !FUN FACT! 500 ml of Approximately blood moves from the heart and lungs down to the legs when a person stands up after lying down The oxygen rich blood cells then travel through the capillaries where yet another… Gas Exchange Occurs, The oxygen and CO2 are exchanged…in the cells Oxygen Rich Tissue Don’t forget that the Hemoglobin in the blood cells let go of Oxygen Poor the cell’s oxygen because of the large CO2 (waste) count in the tissue. Oxygen Rich Oxygen Poor Now lets go back to the heart!!! Circulation back to Heart To upper body From upper Capillaries carry the blood body to… To lung To lung Venules that connect to From From lung veins and the… lung Veins (wide blood vessels) Right Atrium Left carries the oxygen-poor Atrium blood back to the heart. Right Left Ventricle Ventricle From lower To lower body body Conclusion As you have learned (Hopefully) the Circulatory and cardiovascular System is one of the most important systems in the human body… It is the only reason you’re still alive and you can today… attribute the cooling down, feeding of and protection of your body to it. So the next time you bust open your leg skateboarding you can thank your Circulatory System for patching you up. Terima Kasih

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