Human Physiology BIOL3205 Cardiovascular System PDF
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The University of Hong Kong
Prof. Chi Bun Chan
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These lecture notes cover the cardiovascular system, including the heart, blood vessels, and blood. The notes include diagrams and an outline of the lecture topics. The author is Prof. Chi Bun Chan from the School of Biological Sciences, at the University of Hong Kong.
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Human Physiology BIOL3205 Cardiovascular system - I Prof. Chi Bun Chan School of Biological Sciences 5N10 Kadoorie Biological Sciences Building [email protected] 39173823 Cardiovascular system Part I Heart Part II Blood vessel...
Human Physiology BIOL3205 Cardiovascular system - I Prof. Chi Bun Chan School of Biological Sciences 5N10 Kadoorie Biological Sciences Building [email protected] 39173823 Cardiovascular system Part I Heart Part II Blood vessel and pressure Lecture outline Basic anatomy of the heart Structure of the cardiomyocyte Cardiac cycle Autorhythmicity of pacemaker cells Generation of action potential in pacemaker cells and cardiomyocytes Control of cardiac output Heart failure What is the cardiovascular system? Cardio (Greek – heart) vascular (vessel) The cardiovascular system consists of three components Heart is the pump that imparts pressure to keep the continuous blood flow Blood vessels (vasculature) are the passageways Blood is the transport medium The system contributes to homeostasis by linking all the organ systems together providing a means of delivering nutrients (glucose, fatty acid, etc.), O2, hormones, and heat between all body parts. Removing organic wastes (CO2, ammonium, etc.) from the body Structure of the heart The first organ to become functional during fetus development Heart is the muscular organ consisting of mainly cardiac muscle To systemic circulation (upper body) (cardiomyocyte) Aorta Divided into right and left halves Superior vena cava Right and left (returns blood from (separated by septum), each consist of head, upper limbs) pulmonary arteries (to lungs) an atrium and a ventricle Right pulmonary Left pulmonary Right ventricular Left ventricular veins (return blood wall wall The atria and ventricles are separated from right lung) veins (return blood from left lung) by atrioventricular valves (AV valves) Pulmonary semilunar valve (shown open) Left atrium The vessels that return the blood to Right atrium Aortic semilunar valve (shown open) the heart are called veins; those that Right atrioventricular valve (shown open) Left atrioventricular carry blood away from the heart are Right ventricle valve (shown open) called arteries (semilunar valve) Inferior vena cava Left ventricle Septum Dual pump that right and left sides (returns blood from trunk, legs) KEY function as two separate pumps O2-rich blood To systemic circulation Asymmetric in muscle distribution (lower body) O2-poor blood Circulation Pulmonary The circulatory system consists of two divisions: the Lung pulmonary circuit and the systemic circuit Right Left Supplied blood by the different ventricle atrium sides of the heart Right Left Left – oxygenated blood atrium ventricle (bright red) Right – deoxygenated Tissues blood (dark red) Blood passes through the Systemic system in sequence i.e. unidirectional (http://notezonnursing.blogspot.hk/2011/05/circulation.html) Cardiac cycle Normal heartbeat: 60 to 100 beats/min To pump out blood effectively through the heart, the 2 cardiac muscle must contract in a highly synchronized manner, which is called the cardiac cycle. All the events associated with the flow of blood Heart sound through the heart during a single complete heartbeat. 1 The cycle can be divided into two major stages: Systole – contraction and emptying (0.3 s) Diastole – relaxation and filling (0.5 s) Heart 4 phases: sound 3 Ventricular filling Isovolumetric contraction Ventricular ejection 4 http://philschatz.com/anatomy-book/contents/m46661.html Isovolumetric relaxation Pacemaker cells and conduction fibers Cardiac muscle does not require commands from the central nervous system to contract Triggered by signals originating from within the Interatrial muscle itself pathway Sinoatrial (SA) Atrioventricular (AV) Autorhythmicity – the ability to generate its own node node signal that triggers its contractions on a periodic Right atrium Left atrium basis (i.e. own rhythm) Internodal Left branch of pathway bundle of His Pacemaker cells (SA node and AV node) initiate the action potential, which passes through the Right ventricle Left ventricle heart via conduction fibers (Bundle of His and Purkinje fibers). Right branch of bundle Purkinje fibers of His Action potential conduction is slower in AV node Heartbeats are highly coordinated work An action potential is initiated in the SA node Impulses travel from the right atrium to the left atrium like a wavefront (wave of excitation) As the wave spread, contraction of muscle follows Contraction of the atrium simultaneously (the atria and ventricles are separated by a layer of non-conductive fibrous tissue) Signal reaches AV node (the only point of contact between atrium and ventricles) The pulses are delayed (AV nodal delay) Signals travel bundle of His and Purkinje fibers Contraction of the ventricles Electrical activity in pacemaker cells Na+ Ext Pacemaker potential is an autorhythmic cell membrane’s slow drift to the threshold (-40 mV). Int Funny channel is named because it opens when the Na+ potential becomes more negative (hyperpolarized), which is different from a standard Na+ channel that opens when the membrane becomes less negative (depolarized) Three phases: 1 2 3 1. Pacemaker potential – sequential opening of funny and T-type Ca2+ channels → Na+ and Ca2+ move in 2. Depolarization phase - opening of L-type Ca2+ channel → Ca2+ moves in 3. Repolarizatrion phase - opening of K+ channel → K+ moves out Ion channels in pacemaker cells Ion channels are proteins that span the cell membrane to provide a highly selective passage of ions. 4 types of channels on cardiomyocyte membrane N+ channel (Funny channel, If) K+ channel Ca2+ channel (T-type) Ca2+ channel (L-type) Opening of channels causes ion movement across the membrane Funny channel - influx of Na+ K+ channel - outflux of K+ Ca2+ channel - influx of Ca2+ Marked changes in membrane permeability and ion movement lead to (Joaquim Fernández-Solà 2015 Nat Rev Cardiology) an action potential Generation of action potential in pacemaker cells F T L Funny channel T-type Ca2+ channel L-type Ca2+ channel K+ channel Na+ Na+ Ca2+ Ca2+ F T L F T L F T L F T L K+ - + - + - + + - +10 Membrane potential (mV) +10 +10 +10 -40 -40 -40 -40 -60 -60 -60 -60 Time Time Time Time Impulse transmission between cardiomyocytes and pacemaker cells Interconnected at a special structure called intercalated discs Two types of membrane junctions Desmosome: mechanically hold cells together Gap junction: allow electrical signals to spread from cell to cell Electrical activity in cardiomyocytes Once initiated in the SA node, the action potential spreads throughout the rest of the heart Caused by coordinated activities of various ion channels Different mechanism than the pacemaker Phrase 0 1 2 3 4 potential 30 Lasts for 250 ms (800 ms in pacemaker cells) Membrane potential (mV) Prolonged repolarization 0 It consists of 5 phases 0: Rising phase 1: Brief repolarization phase Threshold potential 2: Plateau phase 70 3: Repolarization phase 90 250 4: Resting phase Time (msec) Ion channels activities in cardiacT action potential K channel (transient) + K+ channel (ordinary) T L L Ca2+ Ca2+ channel (long-term) K+ T L Na+ channel Na+ T L T L (Brief repolarization phase) +3 K+ (Plateau phase) (Repolarization phase) T L 0 (Rising phase) Threshold T L (Resting phase) Cardiac Action Potential (https://youtu.be/v7Q9BrNfIpQ) Coupling of electrical signal and contraction Contraction of cardiac muscle is triggered by an increase in intracellular Ca2+ level Ca2+ binds to the troponin-tropomyosin complex Myosin crosses-bridge with actin and pulls thin myofilament inward Shorten the length of the sarcomere Myofibrils Electrical activity and contraction Cardiac muscle Skeletal muscle Cardiac muscle cannot be re-stimulated until the contraction is almost over No summation of contraction (tetanus) Protective mechanism to ensure complete filling and emptying of the heart chambers Caused by long closure of Na+ channels Refractory period and summation Ion balance and cardiac health Normal High K+ Threshold (Parham et al., Tex Heart Inst J. 2006 33: 40–47 https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/16572868/) Potassium gradient across the cell membrane is the most important factor in establishing the cardiomyocyte membrane potential When K+ levels in the blood rise (hyperkalemia), this reduces the electrical potential and can lead to potentially fatal abnormal heart rhythms (arrhythmia) Decreases resting membrane potential and myocardial conduction Mostly caused by kidney disease Cardiac defibrillation (http://electronicdesign.com/power/lightning-bolts-defibrillators-and-protection-circuitry-save-lives) (http://automaticdefibrillator.com/ automated-defibrillator/) Cardiac arrest Fibrillation is a random, uncoordinated excitation and contraction of cardiac cells Can be corrected by electrical defibrillation depolarizes all parts of the heart simultaneously, i.e. “reset” button Automated External Defibrillator (AED) Can heartbeats be controlled? (http://www.dailymail.co.uk/) (https://marcustamfitness.files.wordpress.com/2013/05/21.jpg) Cardiac output and its control Both heart rate (HR) and stroke strength [or stroke volume (SV)] can be modulated Cardiac output (CO) is the volume of blood pumped by each ventricle per min (not the total amount of blood pumped by the heart) CO is an important indicator of how efficiently the heart can meet the demands of the body Intrinsic control – end diastolic volume (EDV) Patient A has a heart beat of 70/min and each stroke Extrinsic control pumps out 70 mL of blood, his CO will be Parasympathetic nerves CO = HR X SV Sympathetic nerves = 70 beats/min x 70 ml/beats Hormones = 4900 ml/min (4.9L/min) Intrinsic control of cardiac output End-diastolic EDV = SV + ESV (SV = EDV – ESV) volume (EDV) EDV is the intrinsic factor that controls the stoke force Contraction varies in response to Stroke volume the stretch of the ventricle (venous (SV) return) when filled with blood Equalize the output between the right and left sides of the heart End-systolic Prevent accumulation of blood in the volume (ESV) heart (http://philschatz.com/anatomy-book/contents/m46661.html) Frank-Starling law of the heart Starling’s law states that when the rate at which blood flows into the heart from the veins (i.e. venous return) changes, the stretch on the ventricular myocardium changes, causing the ventricle to contract with greater or less force so that the stroke volume (output) matches the venous return (input) The Starling Curve (or cardiac function curve)- Length-tension curve of cardiac muscle Cardiac muscle is always operating at lengths less than optimum Extrinsic control of cardiac output Sympathetic nerves – the subdivision of the autonomic nervous system that dominates in an emergency or stressful situations and prepares the body for strenuous physical activity Parasympathetic nerves – the autonomic nervous system that dominates in quiet, relaxed situations and promotes body maintenance activities (e.g. digestion) Hormones (e.g. Epinephrine, thyroid hormones) Both heart rate and stroke volume can be modulated by the nervous system Sympathetic control of cardiac activity Thoracic nerve to the atrium (SA node, AV node) and ventricles Release norepinephrine at the neuromuscular junction Increases heart rate by speeding up the depolarization of SA node (increasing the Na+ and Ca2+ channels activities) → increases the frequency of action potential Ca2+-L Increases the contractile strength (prolonged opening of L-type Ca2+ channel) of both atrium and ventricle Ca2+ channel Funny channel (http://classes.midlandstech.edu/carterp/Courses/bio211/chap18/chap18.html) Parasympathetic control of cardiac activity Vagus nerve to the atrium (SA and VA nodes) Decrease heart rate by hyperpolarizing the SA node (increases the K+ channel) → decreases the frequency of action potential Reduces the contractile strength (shorten the plateau phase) of the atrium Release acetylcholine (ACh) at the neuromuscular junction (http://classes.midlandstech.edu/carterp/C ourses/bio211/chap18/chap18.html) Comparison of sympathetic and parasympathetic controls Parasympathetic Sympathetic Control area SA node/ AV node SA node/AV node /ventricles Heart rate ↓ ↑ Neurotransmitter Acetylcholine (Ach) Norepinephrine (NE) Ion channels Activates K+ channel Activates If, T-type Ca2+, L-Type Suppresses If, T-type Ca2+ Ca2+ channels Membrane potential ↓ (more negative) ↑ (more positive) Atrial muscle contraction Weaker and slower Stronger and faster What happen if we block all autonomous nerve to the heart? Integrative control of cardiac output Both heart rate and stroke volume can be changed simultaneously The control system is a complex network in that all control factors work together (balance of sympathetic and parasympathetic signals) Disruption of the system leads to heart failure Heart failure Heart failure (HF) is the inability of cardiac output to keep pace with the body’s demand for supplies and removal of wastes Systolic HF – inefficient blood pump out because of weakened cardiac muscle contractibility (http://www.md-health.com/) Also called congestive heart failure Dyspnea because of the congestion of blood in the venous system Commonly caused by (http://www.mayoclinic.org/) Damage of heart muscle (ischemia) Prolonged high blood pressure (http://www.rtmagazine.com/2015/08/ dyspnea-clinical-causes-therapy-options/) Complications – ventricle hypertrophy, dyspnea, edema After the lecture, you should be able to explain/describe Basic anatomy of the heart Structure of the cardiomyocyte Cardiac cycle Autorthymicity of pacemaker cells Generation of action potential in pacemaker cells and cardiomyocytes Electrocardiogram Control of cardiac output Heart failure