Lec 1 Heart Review(1) cardio F 24 PDF

FIRST A few reminders Lecture quizzes ( NOT QUIZLET) included in EXAMS = PTS= Attendance Answer keys posted after class- scantrons returned EXAMS scantrons (lec or lab) NOT returned Office hrs: good for going over any exam Syllabus is a CO...

FIRST A few reminders Lecture quizzes ( NOT QUIZLET) included in EXAMS = PTS= Attendance Answer keys posted after class- scantrons returned EXAMS scantrons (lec or lab) NOT returned Office hrs: good for going over any exam Syllabus is a CONTRACT so read it No make up BLACKBOARD has GUIDELINES & a lot of material Check FOLDERS SEC recommended - no pts PENCIL and a GOOD ERASER needed for scantrons: no grade change due to erasure Grab and save a few blank scantrons  Advanced AP = Pathophysiology Applying A & P learned or memorized to CASE studies, critical thinking questions or problems, clinical scenarios Requiring UNDERSTANDING and APPLYING that understanding to CLINICAL SITUATIONS Integrating all or many systems of the Human Body FIRST A REVIEW OF HEART STRUCTURES AND FUNCTION which is TO PUMP BLOOD TO MAKE “ BLOOD CIRCULATE”  Functions of the Circulatory System/blood moving Main function is transport. – Delivers oxygen and nutrients to the tissues – Carries waste products from cellular metabolism to the kidneys and other excretory organs – Circulates electrolytes and hormones – Transports various immune substances that contribute to the body’s defense mechanisms Helps to regulate body temperature LOCATION OF THE HEART Figure 18.1  Dextrocardia, congenital birth defect HEART POSITION TOWARD THE RIGHT , NOT THE LEFT  Functional Anatomy of the Heart #1 Pericardium – Forms a fibrous covering around the heart holding it in a fixed position and providing physical protection and a barrier to infection Myocardium – Muscular portion; forms the wall of the atria and ventricles Endocardium – Thin, three-layered membrane lining the heart Heart wall: Pericardium Fused  Heart wall: Pericardium Fibrous pericardium – dense irregular CT – protects and anchors the heart, prevents overstretching Serous pericardium – thin delicate membrane parietal layer-outer layer pericardial cavity with pericardial fluid Functions of Pericardium: visceral layer Prevents displacement of heart (epicardium) Provides physical barrier against infection & inflame. Has pain and mechanoreceptors to elicit reflex changes in BP and heart rate  Heart Wall- MYOCARDIUM MYOCARDIUM: Branching, intercalated discs with gap junctions, involuntary, striated, single central nucleus per cell. Electrically, cardiac muscle behaves as single unit. Contraction depends on calcium derived from extracellular fluid. Microscopic Anatomy of cardiac Muscle or Myocardium Chapter 18, Cardiovascular System 13 Figure 18.11  Heart Wall-ENDOCARDIUM ENDOCARDIUM: A thin, 3 layered membrane – inner layer consist of smooth endothelial cells (continuous with the lining of blood vessels) on top of a layer of connective tissue and outer layer consists of irregularly arranged connective tissue cells. continuous with the 4 VALVES  Endocardium Innermost layer Composed of: – Simple squamous epithelium (endothelium) – Connective Tissue – Subendocardium: in contact with cardiac muscle and contains small vessels, nerves, and Purkinje Fibers.  Now take a look and locate the 4 heart VALVES Left common carotid artery Left subclavian artery Frontal plane Brachiocephalic trunk Ascending Arch of aorta aorta Ligamentum arteriosum Superior vena cava Left pulmonary artery Right pulmonary artery Pulmonary trunk PULMONARY VALVE Left pulmonary veins Right pulmonary veins LEFT ATRIUM Opening of superior vena AORTIC VALVE cava Fossa ovalis BICUSPID (MITRAL) VALVE RIGHT ATRIUM CHORDAE TENDINEAE Opening of coronary sinus LEFT VENTRICLE Opening of inferior vena INTERVENTRICULAR cava SEPTUM TRICUSPID VALVE PAPILLARY MUSCLE RIGHT VENTRICLE TRABECULAE CARNEAE Inferior vena cava Descending aorta (a) Anterior view of frontal section showing internal anatomy Copyright © 2014 John Wiley & Sons, Inc. All rights reserved. IF VALVES ARE OPENING AND CLOSING PROPERLY- blood moves in the proper direction 4. In pulmonary capillaries, blood loses CO2 and gains O2 3. Pulmonary trunk 5. Pulmonary veins and pulmonary (oxygenated blood) arteries Pulmonary valve 2. 6. Right ventricle Left atrium Tricuspid valve Bicuspid valve 1. Right atrium 7. Left ventricle (deoxygenated blood) Aortic valve 10. Superior Inferior Coronar 8. Aorta and vena vena cava y systemic arteries cava sinus 9. In systemic capillaries, blood loses O2 and gains CO2 (b) Path of blood flow through systemic and pulmonary circulations Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  Figure 18.9 The heart is a double pump, each side supplying its own circuit. Slide 12 Both sides of the heart pump at the same time, but let’s Oxygen-poor blood follow one spurt of blood all the way through the system. Oxygen-rich blood Pulmonary Tricuspid Semilunar Superior vena cava (SVC) Right valve Right valve Pulmonary Inferior vena cava (IVC) Coronary sinus atrium ventricle trunk Pulmonary Tricuspid arteries SVC Coronary valve Pulmonary sinus trunk Right atrium Pulmonary Right semilunar IVC ventricle valve Oxygen-poor blood is carried Oxygen-poor blood To heart in two pulmonary arteries to To lungs returns from the body tissues back to the heart. the lungs (pulmonary circuit) to be oxygenated. Systemic Pulmonary capillaries capillaries Oxygen-rich blood is Oxygen-rich blood returns To body delivered to the body to the heart via the four To heart tissues (systemic circuit). pulmonary veins. Aorta Pulmonary veins Mitral Left Aortic semilunar valve atrium valve Left ventricle Aortic Semilunar Mitral © 2013 Pearson Aorta valve Left valve Left Four pulmonary ventricle atrium Education, Inc. veins Characteristics of the Pulmonary and Systemic Circulations Both have a pump, an arterial system, capillaries, and a venous system. – Arteries and arterioles function as a distribution system to move blood to the tissues. – Capillaries serve as an exchange system where transfer of gases, nutrients, and wastes takes place. – Venules and veins serve as collection and storage vessels that return blood to the heart.  Circulatory System Pressure The circulatory system is a closed system in which the heart consists of two pumps in series. Blood pressure – Arterial Higher pressure, 90–100 mm Hg Propel blood to all other tissues of the body (i.e., systemic circulation) – Venous Lower pressure, 12 mm Hg Propel blood through the lungs (i.e., pulmonary circulation) LEFT VENTRICLE IS MORE MUSCULAR THAN THE RIGHT VENTRICLE-take a look at the size of the wall Figure 18.6 Another view of the size difference in the WALL of right ventricle vs the left ventricle – look how WIDE and MUSCULAR the wall isANTERIOR on the LEFT Right ventricle Left ventricle Lumen Lumen Interventricular septum Transverse plane View POSTERIOR (c) Inferior view of transverse section showing differences in thickness of ventricular walls Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  Hypoplastic left heart syndrome Rare heart defect present at birth (congenital). left side of the heart is extremely underdeveloped. the left side of the heart can't pump blood well. the right side of the heart must pump blood to the lungs and to the rest of the body. Treatment of hypoplastic left heart syndrome requires medication to prevent Physiological hypertrophy Functional Anatomy of the Heart #2 One-way valves – Atrioventricular valves and semilunar valves are pressure valves that ensure one-way flow. Fibrous skeleton – Provides structural support and isolating force for electrical impulse AV & Semilunar Valves THE 4 VALVES KEEP THE MUSCLE BUNDLES ANCHORED= FROM UNWINDING AND HELP SHAPE THE HEART TOO Figure 18.3  Heart Valves -A Ensure unidirectional blood flow through heart Open and close in response to pressure changes Two atrioventricular (AV) valves – Prevent backflow into atria when ventricles contract – Tricuspid valve (right AV valve) – Mitral valve (left AV valve, bicuspid valve) – Chordae tendineae anchor cusps to papillary muscles- ( special muscles derived from Blood vessel wall )prevent valves from everting up or into atria Hold valve flaps in closed position © 2013 Pearson Education, Inc. Atrioventricular valves= AV valves Left BICUSPID VALVE CUSPS atrium Open Closed CHORDAE TENDINEAE Left Slack Taut ventricle PAPILLARY MUSCLES Relaxed Contracted (a) Bicuspid valve open (b) Bicuspid valve closed Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  CUSP OF TRICUSPID VALVE CHORDAE TENDINEAE PAPILLARY MUSCLE (c) Tricuspid valve open Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  Figure 18.7 The atrioventricular (AV) valves. 1 Blood returning to the heart fills atria, pressing against the AV valves. Direction of The increased pressure forces AV blood flow valves open. Atrium Cusp of 2 As ventricles fill, AV valve flaps atrioventricular hang limply into ventricles. valve (open) Chordae 3 Atria contract, forcing additional tendineae blood into ventricles. Papillary Ventricle muscle AV valves open; atrial pressure greater than ventricular pressure Atrium Cusps of 1 Ventricles contract, forcing atrioventricular blood against AV valve cusps. valve (closed) 2 AV valves close. Blood in ventricle 3 Papillary muscles contract and chordae tendineae tighten, preventing valve flaps from everting into atria. AV valves closed; atrial pressure less than ventricular pressure © 2013 Pearson Education, Inc.  Heart Valves –B Two semilunar (SL) valves – Prevent backflow into ventricles when ventricles relax – Open and close in response to pressure changes – Aortic semilunar valve – Pulmonary semilunar valve – No chordae tendinae needed © 2013 Pearson Education, Inc.  Figure 18.21 Summary of events during the cardiac cycle. (2 of 2) Recall : VENTRICLE MUST FILL UP - AV VALVES open ( early to mid) then ATRIA CONTRACT to get all blood in Ventricles ( 30% more)= END DIASTOLIC VOLUME = about 130 ml Atrioventricular valves Open Closed Open Aortic and pulmonary valves Closed Open Closed Phase 1 2a 2b 3 1 Left atrium Right atrium Left ventricle Right ventricle Ventricular Atrial Isovolumetric Ventricular Isovolumetric Ventricular filling contraction contraction phase ejection phase relaxation filling 1 2a 2b 3 Ventricular filling Ventricular systole Early diastole (mid-to-late diastole) (atria in diastole) © 2013 Pearson Education, Inc.  Operation of Cardiac Valves Opening and closing of heart valves is /are pressure driven LA LV Aorta Mitral Valve Aortic Valve  Question #1 Blood flow is not based on which of the following properties? A. Pressure B. Vessel compliance C. Volume D. Contraction of the heart E. Distensibility of vessels F. All the above  Answer to Question #1 F. All the above Rationale: All the above are contributing factors to the flow of blood.  The Cardiac Cycle The events taking place within a single beat During a cardiac cycle each heart chamber goes through systole (contraction) and diastole (relaxation). With increased BPM – which phase gets shortened the MOST? Importance of exercise and hypertension in this?  Figure 18.9 The heart is a double pump, each side supplying its own circuit. Slide 12 Both sides of the heart pump at the same time, but let’s Oxygen-poor blood follow one spurt of blood all the way through the system. Oxygen-rich blood Pulmonary Tricuspid Semilunar Superior vena cava (SVC) Right valve Right valve Pulmonary Inferior vena cava (IVC) Coronary sinus atrium ventricle trunk Pulmonary Tricuspid arteries SVC Coronary valve Pulmonary sinus trunk Right atrium Pulmonary Right semilunar IVC ventricle valve Oxygen-poor blood is carried Oxygen-poor blood To heart in two pulmonary arteries to To lungs returns from the body tissues back to the heart. the lungs (pulmonary circuit) to be oxygenated. Systemic Pulmonary capillaries capillaries Oxygen-rich blood is Oxygen-rich blood returns To body delivered to the body to the heart via the four To heart tissues (systemic circuit). pulmonary veins. Aorta Pulmonary veins Mitral Left Aortic semilunar valve atrium valve Left ventricle Aortic Semilunar Mitral © 2013 Pearson Aorta valve Left valve Left Four pulmonary ventricle atrium Education, Inc. veins Heart as a Pump (Atria act as primer pump- see notes on Atrial systole /diastole) P wave PR interval QRS wave ST segment T wave  R T (a) ECG P 1 Q 8 4 S 0.1 sec 0.3 sec 0.4 sec Atrial Ventricular Relaxation systol systole period e 9 Aortic valve 120 closes Aortic pressure 100 Dicrotic wave (b) Pressure 80 Left (mmHg) 5 ventricular 60 Bicuspid 6 Aortic pressure valve valve closes opens 40 10 Bicuspid Left atrial valve opens pressure 20 2 0 (c) Heart sounds S1 S2 S3 S4 Copyright © 2014 John Wiley & Sons, Inc. All rights reserved. (c) Heart sounds S1 S2 S3 S4 End-diastolic volume 3 130 Stroke volume 60 (d) Volume in ventricle (mL) 7 End-systolic volume 0 (e) Phases of the cardiac cycle Atrial Isovolumetric Ventricular Isovolumetric Ventricular Atrial contraction contraction ejection relaxation filling contraction Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  Cardiac Cycle Used to describe the rhythmic pumping action of the heart Divided into two parts – Systole: the period during which the ventricles are contracting and emptying – Diastole: the period during which the ventricles are relaxed and filling with blood  Main Atrial Pressure Waves Occurring During the Cardiac Cycle- see image next a wave – Caused by atrial contraction c wave – Occurs as the ventricles begin to contract, and their increased pressure causes the AV valves to bulge into the atria v wave – Results from a slow buildup of blood in the atria toward the end of systole when the AV valves are still closed  Four Phases of Cardiac Cycle- in terms of ventricle action Filling Phase (LA à LV) Diastole Isovolumic Contraction (LV Volume Constant) Systole Ejection Phase (LV à Aorta) Isovolumic Relaxation (LV Volume Constant) Diastole 1. Filling Phase: Diastole Early and Mid diastole: AV valves open and blood fills the ventricle - Period of rapid filling which occurs during first 1/3 of diastole. During middle 1/3rd, small amount of blood flows. Late diastole (last 1/3 of diastole) : Atria contract (c wave) and another 30% blood drops. This function becomes important during periods of increased activity when the diastolic filling time is decreased (eg; exercise or an increase in heart rate or heart disease). Atrial contraction can contribute as much as 30% to cardiac reserve during periods of increased need, while having little or no effect on cardiac output during rest. (healthy heart healthy diastole) 2. Systole Period of Isovolumic contraction (Early Systole): All the valves are closed(S1). Ventricle contracting but there is no emptying and volume of blood remains the same. Isometric contraction - (pressure rising b/c valves are closed and muscles are contracting) Period of ejection (Late systole): Left ventricular pressure rises > 80 mm Hg (higher than pressure in great vessels), semilunar valves open and blood flows in aorta. - 70% of blood flows during first 1/3rd of systole - period of rapid ejection - remaining 30% during next 2/3rd - period of slow ejection Diastole begins again Period of isovolumic relaxation: All the valves are closed and ventricle start relaxing – part of diastole. 130 mls = EDV ( end diastolic v) 70mls = ESV ( end systolic V  Cardiac Cycle Green – aorta pressure Blue- ventricle pressure Purple – atrial pressure A - Semilunar valves open B - Semilunar valves close C - AV valves close D - AV valves open E - EDV - 135 ml F - ESV - 65 ml Stroke volume or SV = EDV-ESV Cardiac Cycle Pressure Changes during Cardiac Cycle Questions to consider and answer 1. What are the differences between cardiac and skeletal muscle in terms of histology and physiology? 2. What maintains movement of blood in atria? 3. Which factors regulate right atrial pressure? Please list all of them. (see lecture notes posted : page 4/ 5 )  CONTROL OF HEART ACTION Function of heart: to discharge volume of blood sufficient for metabolic needs of the body. Therefore The BODY controls CARDIAC OUTPUT ( CO) Factors Determining the Workload of the Heart Preload – Volume of blood it pumps out Afterload – The pressure it must generate to pump the blood out of the heart  Cardiac Output (CO) Amount of blood the heart pumps each minute Determined by – CO = SV x HR Stroke volume: the amount of blood pumped with each beat Heart rate: the number of times the heart beats each minute – Venous return and contractility  Question #2 Cardiac output is a direct reflection of how well blood is flowing through the arteries and veins. True or False?  Answer to Question #2 False Rationale: CO is a measure of blood flow out of the heart, but does not reflect the flow through the circuit as there are many factors affecting the flow once BLOOD gets out of the heart. If Cardiac output not appropriate what are the consequences? Circulatory SHOCK Hemorraghic SHOCK SHOCK= ISCHEMIA ,INFARCTION Cardiac output  CO= CARDIAC OUTPOUT volume of blood ejected from ventricles/minute Formula: CO= Heart Rate ( HR) x Stroke Volume ( SV) HR= # beats/minute SV= ml or cc of blood/beat SV= ml or cc of blood/contraction (systolic ejection= contractility)  Recall from AP 1 : VENTRICLE MUST FILL UP – COMPLETELY AV VALVES open ( early to mid) then ATRIA CONTRACT to get all blood in Ventricles ( 30% more)= END DIASTOLIC VOLUME = about 130 ml – to make sure this happen that way, that is why the Action PotentiaL( FROM SA node) which is causing Contraction had to be DELAYED by AV NODE to allow time for atria to empty their blood completely into the Ventricles ( end Diastolic volume) so that ventricles could PUMP out the MOST blood during VENTRICULAR SYSTOLE Stroke volume= ml /stroke = ml/contraction  Cardiac Output CO = HR X SV Range of normal at rest is 3.5 – 8 L.min Maximum CO is in range of 20 – 35 L/ min, depending on level of activity, size, age, heredity, and conditioning. Cardiac index- a better indicator of cardiac function Cardiac index = Cardiac output (CO) L/min. Body surface area (m2)* Cardiac reserve = maximum CO CO at rest  Ejection volume = SV = 120/130-60= 70ml blood ESV (end-systolic volume) Ejection fraction = SV/EDV which is usually 55 to 75% (left ventricular function) as determined by echocardiography CO can be held constant despite alterations in one variable by making adjustments in other. Highly trained athletes have low heart rate, high stroke volume and low peripheral resistance.  What is cardiac index = it is determined by dividing CO by body surface area BSA Why is it a better indicator ? = The clinical significance of cardiac index comes from the fact that it is a measure of cardiac function that can be normalized for the patient's body habitus, which means that the clinician can gain critical insight into the patient's heart function given the variations in body type. In metric terms" the body surface area = the square root of product of the weight in kg times the height in cm divided by 3600. 3 main factors affect stroke volume specifically a. Preload – the amount of stretch of ventricular muscle caused by filling of the ventricles before contraction. b. Contractility – represents the forcefulness of ventricular muscle contraction. c. Afterload – represents the pressure in the arteries that must be overcome before the ventricles can eject blood. Factors Affecting Stoke Volume 1. Preload: 2. Contractility: 3. Afterload:  1. Preload  Preload is dependent upon EDV & two factors determine EDV. 1. Venous return or venous pressure: Increase in venous return increases preload = increases SV- which in turn depends on the Duration of diastole: faster HR = less time in diastole Remember: (When heart rate increases, diastole period decreases. People who have slow heart rate have long diastolic period). 2. stretching of the cardiomyocytes  According to Frank Starling’s Law, increase in EDV increases stretching (Preload) which increases stroke volume.  FRANK-STARTING LAW The more “ stretched” the myocardium/myocytes is/are, the GREATER the contraction or SV Or: The GREATER venous return -> the more STRETCHED THE VENTRICULAR MUSCLE is the GREATER THE CONTRACTION or SV. The more Stretched the myocardium is in the VENTRICLES, the GREATER the CONTRACTION of the VENTRICLES Figure 18.21 Frank-Starling and Cardiac Reserve Frank-Starling Mechanism: the greater the volume of blood in the heart before contraction, the greater the volume of blood ejected from the heart – Increased contractility from EDV stretch Cardiac reserve: maximum percentage of increase in cardiac output achieved above normal resting level Factors Influencing Stroke Volume (Ventricular Function Curve- importance of stretch ) Figure 14-29: Length-force relationships in the intact heart  The size of Sarcomere determines the force contraction (CO) Actin 2 Myosin 1 3 Max. force is achieved when venous return incrs preload to stretch fibers to 2/3 of resting length Frank Starling’s Ventricular Function curve: explained : A CO and AORTIC pressure B Summary: Factors Affecting Cardiac Output - Preload Figure 20.20 2. Afterload (Ventricular Wall Tension) La Place Equation: Wall Tension = Intraventricular pressure x Radius Ventricular wall thickness Increase in AORTIC pressure increases resistance to ventricular ejection. Increase in chamber size (radius) means ventricles must generate more tension during systole to generate a given pressure. Increase in thickness at first improves SV and hence cardiac function = hypertrophy 3. Contractility Sympathetic stimulation (Nor epinephrine – NE, epinephrine -E) increases heart rate & contractility Calcium also increases force of contraction by heart. Parasympathetic N.S. (vagal stimulation decreases heart rate) Activation of beta receptors by Sympathetic N.S. INCREASED import of Ca+ into cells  Ventricular Function Curve & Myocardial Contractility Positive and Negative Inotropic (affecting muscle contraction) Agents Positive Sympathetic Stimulation Epinephrine, digitalis, caffeine normal curve Negative hypoxia, acidosis, hypercapnia, CHF barbiturates Hypercapnia = excess CO2 in blood Hyperkalemia = excess K+ Action of Digitalis Leads to INC intracellular Ca+ = INC force contraction = INC SV Summary of the Factors Affecting Cardiac Output (Preload, Myocardial contractility & Afterload) Figure 20.24  Local Control of Blood Flow by Tissues (Short Term regulation) Local control – In most tissues, blood flow is proportional to metabolic needs of tissues and each tissue can control its own blood flow - autoregulation Blood flow can increase 7-8 times as a result of vasodilation due to increased rate of metabolism Know the following terms: Hyperemia: Functional hyperemia Reactive hyperemia Erythema can be a symptom of hyperaemia  DEFINITIONS Hyperemia = an excess of blood in vessels (vasodilation ) supplying organ /tissue Functional hyperemia – during exercise – inc. blood flow Reactive hyperemia- the transient inc. blood flow to organ occurring after brief ischemia Erythema can be a symptom of hyperaemia Normal arteriolar tone Vasodilation (hyperemia) Vasoconstriction Vasodilation Caused by: (decreased contraction of  Myogenic activity circular smooth muscle in the  Oxygen (O2) Caused by: arteriolar wall, which leads to  Myogenic activity  Carbon dioxide (CO2) decreased resistance and  Oxygen (O2) increased flow through the  Nitric oxide  Sympathetic stimulation  Carbon dioxide (CO2) vessel)  Histamine release and other metabolites Vasoconstriction  Heat  Sympathetic stimulation (increased contraction of circular  Lactic acid, H+ ion  Cold smooth muscle in the arteriolar  K+ wall, which leads to increased resistance and decreased flow through the vessel)  Tissue Factors controlling Blood Flow short term regulators Vasodilators – histamine (mast cells, basophils), bradykinin (blood cells and body fluids) and prostaglandins called prostacyclin (many tissues) Vasoconstrictor – serotonin (play role in migraine prostaglandins called Thromboxane (many tissues) Endothelial control of blood flow EDRF ( EDRF = endothelium derived RELAXIGN factor = endogenous vasodilator ) also known as nitric oxide (NO) (vasodilator) Prostaglandins : prostacyclin as vasodilators Angiotensin II, endothelins ; vasoconstrictors (also endostatin)  Production of nitric oxide can be stimulated by acetylcholine, bradykinin, histamine, and thrombin. NO inhibits platelet aggregation and secretion of platelet contents, many of which cause vasoconstriction. NO protects against both thrombosis and vasoconstriction.  Collateral Circulation Most organs receive blood from more than one arterial branch - Arterial anastomosis - where arteries supplying the same area join. Coronary collateral arteries may prevent myocardial ischemia in healthy subjects and in patients with CHD. Exercise produces strong heart muscle and promotes collateral circulation.  Coronary arteries Small ( collateral ) and large ( Rt, Lf , circumflex etc) Collateral arteries may prevent MI But if a major coronary A. ( such as circumflex) is blocked/occluded the small ones unable to restore blood flow  Collateral routes= side or extra routes Collateral circulation is a network of tiny blood vessels, and, under normal conditions, not open. When the coronary arteries narrow to the point that blood flow to the heart muscle is limited (coronary artery disease), collateral vessels may enlarge FROM THAT BLOCKED ARTER Y and become active. Blood vessels interconnect or form SHUNTS and help supply blood to an area if one blood vessel is unable to. (ex: clot obstructing blood flow)  Heart rate Sympathetic Parasympathetic activity activity (and epinephrine) - Connected to vagus nerves – “fight or flight” response - Slows down heart rate (no – Speeds up heart rate and SV effect on contractility) – Sympathetic tone can increase - Parasympathetic tone 40 bpm heart rate upto 180-200 bpm - Under resting conditions, – Increases force of contraction parasympathetic N.S. – People with heart disease, sym. predominates. N.S. predominates.  NERVOUS CONTROL OF BP- the MEDULLA INPUT TO CARDIOVASCULAR CENTER (nerve impulses) From higher brain centers: cerebral cortex, limbic system, and hypothalamus From proprioceptors: monitor joint movements From baroreceptors: monitor blood pressure From chemoreceptors: monitor blood acidity (H+), CO2, and O2 OUTPUT TO EFFECTORS Vagus nerves (increased frequency of nerve impulses) Heart: decreased rate (parasympathetic) Cardiac accelerator Heart: increased rate and contractility nerves (sympathetic) Vasomotor nerves Cardiovascular (sympathetic) Blood vessels: vasoconstriction (CV) center Copyright © 2014 John Wiley & Sons, Inc. All rights reserved. Nervous System Control of the Heart Copyright 2009, John Wiley & Sons, Inc.  Factors affecting Heart Rate Autonomic Innervation of the Heart & Hormone (Epinephrine) Digitalis (plant)=digoxin Helps with CHF, Afib Figure 19.8 HOW BLOOD FLOW CHANGES from REST to Tennis for example ( physical activity) just dilating different blood vessels and constricting others for BLOOD TO GO WHERE NEEDED THE MOST at that time. -BRAIN and HEART muscle always need a lot but SKELETAL MUSCLES need the greatest INCREASE in blood flow (compared to Resting skeletal muscles) Figure 19.12  NERVOUS CONTROL OF BP- again the MEDULLA INPUT TO CARDIOVASCULAR CENTER (nerve impulses) From higher brain centers: cerebral cortex, limbic system, and hypothalamus From proprioceptors: monitor joint movements From baroreceptors: monitor blood pressure From chemoreceptors: monitor blood acidity (H+), CO2, and O2 OUTPUT TO EFFECTORS Vagus nerves (increased frequency of nerve impulses) Heart: decreased rate (parasympathetic) Cardiac accelerator Heart: increased rate and contractility nerves (sympathetic) Vasomotor nerves Cardiovascular (sympathetic) Blood vessels: vasoconstriction (CV) center Copyright © 2014 John Wiley & Sons, Inc. All rights reserved.  A FEW KEY TERMS FROM GENERAL AP /applications Heart Murmurs (causes: Valvular, endocarditis, HBP, anemia,congenital, cardiomyopathy, other) Aneurysm Aortic aneurysm Thoracic aneurysm( blood may back up in upper body, edema ) Jugular vein ( distention , issues in right side of heart ) Auscultation (pressure pulsation heard with stethoscope while taking BP)  Definitions Ischemia is a condition in which blood flow (and thus oxygen) is restricted or reduced in a part of the body. Cardiac ischemia is decreased blood flow and oxygen to the heart Hypoxia is a state in which oxygen is not available in sufficient amounts at the tissue level to maintain adequate homeostasis; this can result from inadequate oxygen delivery to the tissues either due to low blood supply