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Chapter 20 The Heart 1 1
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Circulatory System: The Heart
cardiology – the scientific study of the heart and the treatment of its disorders cardiovascular system heart and blood vessels circulatory system heart, blood vessels, and the blood major divisions of circulatory system pulmonary circuit - right side of heart carries blood to lungs for gas exchange and back to heart systemic circuit - left side of heart supplies oxygenated blood to all tissues of the body and returns it to the heart
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Position, Size, and Shape
Heart lies in mediastinum (a central compartment of the thoracic cavity made of loose connective tissue) between lungs; 2/3 of its mass is to the left of the midline Size: equivalent to a person’s closed fist. Shape: cone-shaped, pointed apex inferior; flat base is superior. Heart protected on the anterior side by the sternum; on the posterior side by the vertebrae Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Aorta Pulmonary trunk Base of heart Apex of heart Diaphragm (c)
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SULCI - GROOVES on surface of heart containing blood vessels and fat
coronary sulcus Separates the atria from the ventricles anterior interventricular sulcus marks the boundary between ventricles anteriorly posterior interventricular sulcus marks the boundary between ventricles posteriorly
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Protective layers of the heart
Pericardium – 2 layered sac surrounds and protects the heart from external jerk or shock. Fibrous pericardium dense irregular connective tissue, protects and anchors the heart to diaphragm and mediastinum; prevents overstretching Serous pericardium Parietal pericardium Visceral pericardium (epicardium) covers the heart surface and becomes part of the heart wall Pericardial cavity lies between the parietal and visceral layers of the serous pericardium; filled with pericardial fluid that reduces friction between the two membranes. pericarditis. inflammation of the pericardium cardiac tamponade buildup of fluid in the pericardial cavity pericarditis: inflammation of the pericardium cardiac tamponade: buildup of fluid in the pericardial cavity- resulting in slow or rapid compression of the heart.
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Pericardium
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Heart Wall Epicardium (visceral pericardium)
visceral serous membrane covering heart; adipose in thick layer in some places Contain coronary blood vessels Myocardium cardiac muscle layer Endocardium covers the valve surfaces and continuous with endothelium of blood vessels
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Structure of CARDIAC MUSCLE
Cardiocytes – small, striated, short, thick, branched cells, one centrally located nucleus, involuntary control Abundant mitochondria, extensive blood supply intercalated discs - join cardiocytes end to end interdigitating folds –End of cells folded like the bottom of an egg carton. Produces interlocking and increased surface contact area. mechanical junctions tightly join cardiocytes to prevent heart cells from pulling apart during contraction fascia adherens –ribbon like structures that stabilizes non-epithelial tissue; actin of the thin myofilaments is anchored to the plasma membrane desmosomes – prevents cardiocytes from being pulled apart gap junctions allow ions to flow between cells –produces electrical stimulation to neighboring cells Propagate action potentials repair of damage of cardiac muscle is almost entirely by fibrosis (scarring)
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http://droualb. faculty. mjc
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4 CHAMBERS 2 upper atria 2 lower ventricles
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Right and Left Atrium Pectinate muscles internal ridges of myocardium in right atrium and right auricle. Increase force of contraction w/o increasing heart mass Interatrial septum separates right and left atrium Auricle flap like extension increases surface area. RIGHT ATRIUM Receives blood from 3 veins: superior / inferior vena cava, coronary sinus Blood flows through the right atrioventricular valve (AV valve) or the tricuspid valve) into the right ventricle. Each valve consists of 2-3 fibrous flaps of tissue called cusps. LEFT ATRIUM Forms MOST of the base (top) of the heart Receives blood FROM LUNGS via 4 pulmonary veins (2 right / 2 left) Remember blood always returns to the heart via veins Blood flows through the left atrioventricular valve (AV valve) or the bicuspid valve (has 2 cusps) into the left ventricle. This valve is also known as the mitral valve.
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Right auricle Left auricle Pectinate muscles internal ridges of myocardium in right atrium and both left and right auricles. Increase force of contraction w/o increasing heart mass
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Right and Left Ventricle
Inside ventricles are raised bundles of cardiac muscle called trabeculae carneae cone shaped traberculae carnae are called papillary muscles. Chordae tendineae cords connect cusps of the AV valves to the papillary muscles Interventricular septum: partitions the right and left ventricles RIGHT VENTRICLE Blood flows from the right ventricle into the pulmonary trunk (pulmonary artery) through the pulmonary semilunar valve. LEFT VENTRICLE The aortic semilunar valve allows the passage of blood from ventricle to the ascending aorta just above valve are openings to the coronary arteries Myocardium much thicker in the left ventricle - produces greater force for blood ejection to systemic tissues
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NOTE: difference in myocardium thickness between left and right ventricles
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Fibrous cardiac skeleton collagenous and elastic fiber provides
Heart Valves Fibrous cardiac skeleton collagenous and elastic fiber provides support structure attachment for cardiac muscle anchor for valve tissue electrically insulate ventricular cells from atrial cells Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Left AV (bicuspid) valve Right AV (tricuspid) valve Fibrous skeleton Openings to coronary arteries Aortic valve Pulmonary valve (a) 17
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Valve Action The heart valves open and close passively because of pressure differences on either side of the valve. When pressure is greater BEHIND the valve (Ex: as blood fills atria), the cusps are blown open and the blood flows through the valve; when pressure is greater in FRONT of the valve (ventricles are full and press against the AV valves), the cusps snap shut and blood flow is stopped (from atria). The motion of a heart valve is analogous to the motion of the front door of your house. The door, which only opens in one direction, opens and closes due to pressure on the door. Ventricle value action: Electrical stimulation signal from SA node in right atrium reaches papillary muscles on the floor of the ventricles before the myocardium muscle fibers. Causes tension that pulls the chordae tendinae and they tighten pulling the AV valves shut as blood in ventricles surges against valves closing them.
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Atrioventricular and Semilunar Valves
Values ensure a one-way flow of blood thru the heart; open and close in response to pressure changes as the heart contracts and relaxes. AV Valves When atria contract, the ventricular pressure is lower than atrial pressure cusps OPEN chordae tendineae slack; papillary muscles relaxed When ventricles initiate contraction: AV cusps CLOSED, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from slipping inside out AV valves close preventing backflow of blood into atria Semilunar Valves SL valves open with ventricular contraction allow blood to flow into pulmonary trunk and aorta. Pressure inside ventricles overpowers the pressure inside the aorta and pulmonary trunk. SL valves close with ventricular relaxation prevents blood from returning to ventricles. Pressure inside aorta and pulmonary trunk higher, closing the values.
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AV and SL Values
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Valve Disorders Stenosis - narrowing of a heart valve which restricts blood flow. Rheumatic Fever- inflammatory disease that occurs following a Streptococcus pyogenes infection (usually in the throat). The immune system stimulates antibodies to attack the infection. Inadvertently, the antibodies also attack the heart tissue damaging the heart valves. The damaged valves can lead to heart failure. Mitral valve prolapse- bulge too far into the left atrium during contraction A heart murmur is an abnormal sound that consists of a flow noise that is heard before, between, or after the lubb-dupp or that may mask the normal sounds entirely. Not all murmurs are abnormal or symptomatic, but most indicate a valve disorder. Sounds are thought to be produced by regurgitation through valves
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Heart Sounds The sound of a heartbeat comes primarily from the turbulence in blood flow caused by the closure of the valves. Listening to sounds within the body is called auscultation, usually done with a stethoscope. First heart sound S1 (lubb) created by blood turbulence associated with the closing of the ATRIOVENTRICULAR valves The second heart sound S2 (dupp) represents the closing of the SEMILUNAR valves close to the end of the ventricular systole.
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Blood Circulation Two closed circuits Systemic circulation
left side of heart pumps blood through body Receives oxygenated blood FROM the lungs and distributes it to body cells left ventricle aorta arteries arterioles capillaries gas and nutrient exchange venules veins right atrium Pulmonary circulation right side of heart pumps deoxygenated blood TO LUNGS for oxygenation. right ventricle pulmonary trunk pulmonary arteries lungs exchange of gases pulmonary veins left atrium
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Blood Circulation
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Blood Circulation Coronary Circulation
delivers oxygenated blood and nutrients to the heart and removes carbon dioxide and wastes from the myocardium. Left Coronary Artery blood to: left ventricle; left atrium; interventricular septum. Located above SL valve. Right Coronary Artery blood to: right atrium; portions of both ventricles; cells of sinoatrial (SA) and AV nodes. Located above SL value Route: Left Ventricle Aorta left and right coronary arteries supply blood to the atrium and the ventricles large coronary sinus right atrium. Sinus - large vein without smooth muscle layer Anastomoses provides alternate backup routes for blood to flow if one vessel is blocked or compromised.
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Blood Flow Right atrium pumps deoxygenated blood
Thru AV (tricuspid) Valve To right ventricle which pumps blood Thru pulmonary semilunar valve Into the pulmonary trunk Which divides into a right and left pulmonary artery Which carry deoxygenated blood to the lungs Gas exchange occurs Oxygenated blood returns via pulmonary veins (2 from left/2 from right Into the left atrium Thru the AV (bicuspid) valve Into the left ventricle pumps blood Thru the aortic semilunar valve Into the aorta In the ascending aorta which branches into 2 coronary arteries to heart Then the aorta arch with 3 branches to upper regions of the body Then to descending aorta with branches to lower regions of the body Where blood drops off oxygen and picks up carbon dioxide Returning the deoxygenated blood back to the atrium via Superior vena cava –upper body; inferior vena cava-lower; coronary sinus-heart = TAKES APPROXIMATELY ONE MINUTE!!!! Blood Flow
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Specialized Anatomy of Fetal Heart Circulation
Foramen ovale an opening through interatrial septum in the right atrium Connects the two atria Seals off at birth, forming fossa ovalis Fossa ovalis Ductus arteriosus – is a blood vessel CONNECTING the pulmonary artery (pulmonary trunk) to the proximal descending aorta. It allows most of the blood from the right ventricle to bypass the fetus's fluid-filled non-functioning lungs. O2 for the fetus is provided by the placenta. Closes at birth and becomes the nonfunctional ligamentum arteriosum.
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Clinical Problems CONGESTIVE HEART FAILURE (CHF)
results from the FAILURE of EITHER ventricle to eject blood effectively usually due to a heart weakened by myocardial infarction, chronic hypertension, valve insufficiency, or congenital defects in heart structure. left ventricular failure – blood backs up into the LUNGS causing pulmonary edema shortness of breath or sense of suffocation right ventricular failure – blood backs up in the VENA CAVA causing SYSTEMIC or generalized edema enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet eventually leads to total heart failure
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Figure 19.21
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Clinical Problems Coronary Artery Disease (CAD) - partial or complete blockage of coronary circulation Atherosclerosis -artery wall thickens as a result of the accumulation of fatty materials (plaque) producing a narrowing of vessels---results in artery spasm or clot first symptoms of CAD is commonly angina pectoris (chest pain due to obstruction or spasm of the coronary arteries) Angina pectoris – temporary ischemia (slow blood flow) obstructing 75% or more of the blood flow to cardiac muscle- produces lack of blood and oxygen When partially or fully blocked coronary artery constricts produces heaviness and pain. O2 deprived tissue shifts to anaerobic respiration resulting in lactic acid synthesis which stimulates pain receptors. The intermittent chest pain may radiate from the sternal area to the arms, back, and neck. Arteriosclerosis hardening/loss of elasticity of medium or large arteries Arteriolosclerosis hardening/loss of elasticity of arterioles
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Clinical Problems Myocardial infarction (MI) (heart attack)
sudden death of a area of myocardium due to long-term obstruction of coronary circulation interruption of blood supply due to a blood clot or fatty deposit- can result in death of cardiac cells within minutes protection from MI is provided by arterial anastomoses alternative route of blood flow (collateral circulation) within the myocardium MI responsible for about ½ of all deaths in the US 25% of MI patients die before obtaining medical assistance 65% of MI deaths under age 50 occur within an hour of infarction Diagnosis: 1) ECG (EKG) 2) damaged myocardial cells release ENZYMES measured by blood tests.
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Prevention and Treatment
> Medication –know for exam beta blockers [blocks sympathetic response that increases heart rate- Ex: inhibit receptors for norepinephrine and epinephrine; used for secondary heart attack, stroke and hypertension] ACE inhibitors [decrease BP; inhibit RAAS] Aspirin -thins blood – prevents platelet aggregation Heparin/Warfarin (Coumadin) blood thinners that interfere with chemical formation of clot Nitroglycerin [nitric oxide- dilates arteries offsets angina increasing blood flow] Calcium channel blockers [slows heart lowers electrical impulses, lowers BP] > Coronary Artery Bypass Graft (CABG) section of artery or vein (ex; great saphenous vein) used to create a detour around the obstructed portion of a coronary artery procedures named by number of vessels repaired-single, double, triple, or quadruple coronary bypasses > balloon angioplasty > laser angioplasty similar to balloon angioplasty uses laser tipped catheter instead of a balloon
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Electrical Conduction System of the Heart.
NODE special tissue acts like muscle and nervous tissue. A system of SPECIALIZED CARDIAC MUSCLE CELLS initiates and distributes electrical impulses that stimulate contraction. Automaticity - heart cells act as both nervous and muscle tissue. Cardiac muscle contracts automatically and generate spontaneous action potential that goes through ENTIRE heart muscle.
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The Beginning The human heart begins to beat and pump blood through the embryo around day 22 of gestation. The electric stimulus that triggers contractions in the myocardium arise spontaneously within the myocardium itself, and propagate from cell to cell. Input from the central nervous system can modify the heart rate (the frequency of heart beats), but it does not initiate beats. The ability of cardiac myocytes to beat is an intrinsic property of these cells. It has been found that myocytes removed from the early heart and grown in culture will beat sporadically, and if they become connected to each other, will then begin to beat rhythmically, in unison. As a functional organ, the heart begins to beat very early, even before it has assumed its final form. Interestingly, the heart begins to beat even before structures such as valves and septa (singular: septum; the muscular walls that divide the chambers) have formed! The initial contractions are peristaltic--that is, they proceed in a wave-like fashion along the length of the heart.
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Electrical Conduction System of Heart
SA (sinoatrial) node- pacemaker - cluster of cells in right atria wall When nodal tissue contracts it generates nervous impulses that travels to BOTH atria simultaneously, then to the AV node. Sets heart rhythm. Right atria contracts slightly before left as it receives signal from the SA node first. AV (atrioventricular) node- in atrial septum (alternative pacemaker) Slows the transmission of the action potential; transmits signal to bundle of His Fibrous skeleton helps to insulate and prevent currents from getting to the ventricles from other routes Bundle of His (AV Bundle) -connection between atria and ventricles; continues to slow the action potential allowing more time for ventricles to fill with blood for ejection. Right and Left Bundle Branches extend from the Bundle of His or AV bundle, and action potentials descend to the apex of the heart. Purkinje fibers in right and left ventricles carry action potentials from the bundle branches to trigger muscle fibers in ventricles to contract.
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Fibrous skeleton
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Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 SA node fires. 2 Excitation spreads through atrial myocardium. Right atrium 1 2 Sinoatrial node (pacemaker) Left atrium 3 AV node fires. 2 Purkinje fibers Atrioventricular node 3 4 Excitation spreads down AV bundle. Bundle branches Atrioventricular bundle 5 Purkinje fibers distribute excitation through ventricular myocardium. 4 5 GOOD ANIMATION Purkinje fibers
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Receives impulse from SA Node
Begins atrial activation Receives impulse from SA Node Delays impulse
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Conduction System of Heart
Heart contractions do not require nervous system intervention. Signals from the autonomic nervous system and hormones, such as epinephrine, MODIFY the heartbeat (rate and strength of contraction), but they do not ESTABLISH the fundamental rhythm. Cycle of events in heart SYSTOLE – “START” of atrial or ventricular CONTRACTION DIASTOLE – “DONE” with contraction atrial or ventricular = relaxation Sinus rhythm - normal heartbeat; SA node triggers; 60 – 100 bpm adult at rest is 70 to 80 bpm (vagal tone) Parasympathetic stimulation slows heart rate Ectopic focus – another area of heart fires BEFORE SA node Premature ventricular contraction (PVC) initiated by the Purkinje fibers–extra heartbeat can be caused by hypoxia (low oxygen), electrolyte imbalance, or caffeine, nicotine, and other drugs. Produces insufficient blood ejection from ventricles; may be perceived as a "skipped beat" or felt as palpitations in the chest. Nodal rhythm – if SA node is damaged, heart rate is set by AV node, 40 to 60 bpm (action potentials per minute) Intrinsic ventricular rhythm – if BOTH SA and AV nodes are not functioning, rate set at 20 to 40 bpm If occurs would require artificial pacemaker to sustain brain function
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REVIEW Muscle Physiology - Membrane Potential
Membrane potentials result from a separation of positive (+) and negative (-) charges (ions) across the membrane Voltage is a difference in electrical potential between the opposite sides of a plasma membrane. Voltage drives an electric current (the flow of electrons or electrical charge). Action potentials are generated by the movement of ions through membrane ion channels in muscle cells. This shift from a negative to a positive internal cellular environment allows for the transmission of electrical impulses
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REVIEW Muscle Physiology - Membrane Potential
When the muscle cell is not in a state of contracting it is said to be in a resting state, the INSIDE of the cell is more NEGATIVE than the OUTSIDE. Membrane is polarized. Each cell has an “at rest” potential to transmit an electrical current. This potential varies in different types of muscle cells. For a muscle cell to contract, the negative (-) value inside the cell must become more positive (+). This is called depolarization. Ion channels in the membrane open and positively charged ions move from the extracellular fluid into the interior of the cell Positively charge channels close to prevent release of positive ions. The change in electrical voltage generates electrical impulses that move along the surface of the membrane, alerting mechanisms inside the cell to produce a contraction. Following the contraction, the ion channels that opened or closed to increase the positive value inside the cell CLOSE and the cell begins to resume a more negative value. This is a state of repolarization or relaxing.
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The electrical current released during an action potential opens calcium channels that enable the binding of contractile proteins to produce contractions
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Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 SA node fires. 2 Excitation spreads through atrial myocardium. Right atrium 1 2 Sinoatrial node (pacemaker) Left atrium 3 AV node fires. 2 Purkinje fibers Atrioventricular node 3 4 Excitation spreads down AV bundle. Bundle branches Atrioventricular bundle 5 Purkinje fibers distribute excitation through ventricular myocardium. 4 5 Purkinje fibers
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Pacemaker Physiology – Atria Action Potential
The resting membrane potential of a SA node cardiac muscle CELL, is less constant than a skeletal muscle cell, due primarily to the increased permeability ("leakiness") of its cell membrane to Na+ and K+ ions; as a result: SA node cardiac muscle cells depolarize more easily. SA node CELLS’ resting potential start at -60 mV and drifts upward (to a more positive value) from a SLOW inflow of Na+ and no compensating outflow of K+ (K+ channels are closed) This gradual depolarization is called pacemaker potential When potential reaches threshold of -40 mV, voltage-gated FAST Ca2+ and Na+ channels open; Ca2+ and Na+ flow in rapidly depolarization occurs - peaking (maximum + value) at 0 mV At 0 mV “K+” channels open and K+ exits the cell triggering repolarization Each depolarization of the SA node produces one heartbeat at rest, fires every 0.8 seconds or 75 bpm Signal travels 1 m/sec thru atrial myocardium reaches AV node in approximately 50m/sec
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Graph Depiction of Atria Potentials
Animation: Atria
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Ventricular Filling from Atria
The ventricles RECEIVE blood from the atrium both PASSIVELY and as a result of ATRIAL CONTRACTIONS. The first one third (1/3) occurs quite rapidly (passive) The second one third (1/3) is somewhat slower (passive) The final third (1/3) completes the filling process and is the RESULT of atrial systole (contraction) Animation:
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Myocardium Conduction-AV Node
An impulse in a ventricular contractile muscle fiber is characterized by RAPID depolarization, plateau, and repolarization. AV node delays cardiac impulses from SA node to allow atria to contract and EMPTY Signal slows at AV node DUE to 1) less numbers of cardiocytes 2) less gap junctions 3) cardiocytes have a stable resting membrane potential 4) depolarize only when stimulated Depolarization Ventricular cardiac cell resting membrane potential is - 90mv Na+ channels open and depolarize the membrane. This triggers a positive feedback that initiates the opening of more Na+ channels resulting in a RAPID ALMOST VERTICAL RISING membrane voltage. Peaks at 30+ mV. Na+ channels then close.
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Cardiac Conduction System
Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. 1 SA node fires. 2 Excitation spreads through atrial myocardium. Right atrium 1 2 Sinoatrial node (pacemaker) Left atrium 3 AV node fires. 2 Purkinje fibers Atrioventricular node 3 4 Excitation spreads down AV bundle. Bundle branches Atrioventricular bundle 5 Purkinje fibers distribute excitation through ventricular myocardium. 4 5 Purkinje fibers
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Graph Depiction of Ventricular Action Potential
Na+ channels close Ca2+ channels open
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Myocardium Conduction-AV Node
Plateau phase – result of Ca2+ inflow Period of prolonged, sustained depolarization ( msec) allows for the greater ejection of blood from the ventricles Na+ channels close but slow Ca2+ channels open, Ca2+ enter from OUTSIDE the cell and binds to Ca2+ channels on sarcoplasmic reticulum releasing more Ca2+ ; cardiac muscle tissue very sensitive to extracellular calcium concentrations Ca2+ binds to troponin to allow for actin-myosin cross-bridge formation & muscle contraction. The plateau declines slightly due to leaky potassium (K+) channels but most K+ channels remain closed sustaining the depolarization. Repolarization Ca+2 channels CLOSE and K+ channels OPEN allowing K+ to rapidly LEAVE the cell restoring resting membrane potential -90mv. Refractory period the time interval when a second contraction cannot be triggered Prevents wave summation and tetanus which would stop the pumping actions of the heart and decrease amount of blood ejected from ventricles.
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Physiology of Contraction
Na+ gates open 2) Rapid depolarization Na+ gates close-cell depolarizes Slow Ca2+ channels open prolonging depolarization creates plateau 5) Ca2+ channels close, K+ channels open (repolarization) Plateau is the ST segment of the ECG –ventricle contraction and blood ejection.
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Electrocardiogram---ECG or EKG
A recording of the electrical changes (“ACTION POTENTIAL”) that accompany each cardiac cycle (heartbeat) Equipment detects and amplifies electrical changes on the skin when the heart muscle impulse is generated ECG helps to determine abnormal conduction pathway; if the heart is enlarged or has damaged regions
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Electrocardiogram---ECG or EKG
P wave atrial depolarization systole P to Q interval conduction time from SA node to AV node QRS complex Atrial repolarization diastole Ventricular depolarization ST plateau period of sustained contraction T wave ventricular repolarization ECG/EKG Good Animation (3.34 min)
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Normal Electrocardiogram (ECG)
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Atria contract Ventricles contract
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Fibrillation
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Cardiac Cycle A cardiac cycle includes all the events occurring in a SINGLE heart beat (0.8 sec) It consists of repetitive contraction (systole) and relaxation (diastole) of heart chambers In a cardiac cycle the atria then the ventricles contract and relax forcing blood from areas of high pressure to areas of lower pressure
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atrial depolarization begins
2) atrial depolarization complete (atria contracted) ventricles begin to depolarize at apex; atria repolarize (atria relaxed) ventricular depolarization complete (ventricles contracted) ventricles begin to repolarize at apex 6) ventricular repolarization complete (ventricles relaxed)
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Phases of Cardiac Cycle
Isovolumetric contraction Blood enters atria flows to the ventricles via the opened tricuspid and mitral valves. Atrial contraction follows As atria diastole ends, the ventricles BEGIN depolarizing- start contracting, the AV valves close, to prevent back flow to the atria; corresponds to the R peak or the QRS complex seen on an ECG Aortic and pulmonary valves are also closed; no overall change in volume as all four valves are closed. The isovolumetric contraction lasts about 0.03 sec, enough time to build sufficiently high pressure to overcome aortic and the pulmonary trunk semilunar valves (blood in ventricles) Relaxation period: isovolumetric relaxation Both atria and ventricles are relaxed. Pressure in the ventricles fall and the SL valves close. All four valves are closed (blood begins flowing into the atria). Pressure in the ventricles continues to fall, the AV valves open, and ventricular filling begins. It can be used as an indicator of diastolic dysfunction.
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Phases of Cardiac Cycle
Ventricular Filling and Ejection Pressure continues to rise as ventricle muscles decrease chamber volume size opening SL valves leading to ventricular ejection. In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in the right and/or left ventricle at end load or filling in (atrial diastole) or the amount of blood in the ventricles just before systole. The amount of blood REMAINING in a ventricle AFTER it has contracted is End Systolic Volume (ESV) Stroke volume (SV) is the volume of blood ejected by a ventricle with each heart beat. SV = EDV minus ESV Ejection fraction - % of blood at EDV ejected during SV (SV/EDV) A normal heart's ejection fraction may be between 55 and 70 Between 40 and 55 indicates damage, perhaps from a previous heart attack, but it may not indicate heart failure. Under 40 may be evidence of heart failure or cardiomyopathy. Examples: EDV = amount of blood available prior to ejection = 150 ESV = amount of blood left in ventricle following contraction = 50 Amount of blood ejected (SV) = 100ml (150-50) Ejection Factor: Divide SV by EDV EF= 100ml/150 ml= 67%
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CARDIAC OUTPUT Cardiac output (CO) is the volume of blood ejected from the ventricles into the aorta or pulmonary trunk in ONE MINUTE. Cardiac output equals the stroke volume (the volume of blood ejected by the ventricles with each contraction) multiplied by the heart rate (the number of beats per minute). CO = SV x HR 70 ml blood x 75 beats/min = 5250 ml divided by 1000 = 5.25 L/min Entire blood supply of the body passes through the circulatory system every minute. Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest. Average is 4-5 times the normal output (5.25 L/min x 4 = 21 L/min) Trained athlete’s cardiac reserve can be as much as 7-8 times the normal amount of blood sent through the circulatory system during intense exercise
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EDV= amount available that ESV = amount remaining
SV= 70ml EDV= amount available that ESV = amount remaining can be ejected after contraction
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Influences on Stroke Volume
PRELOAD – TENSION in heart muscle (affect of stretching) the more EACH muscle fiber sarcomere is stretched, greater the contraction force; STRETCH RESULT OF GREATER BLOOD VOLUME Ex: stretching a rubber band produces more tension Preload is affected by venous blood pressure and the rate of venous return to the heart. More blood volume in ventricles - greater tension; greater force of contraction -more blood ejected Higher volume = higher preload Frank Starling Law - stroke volume (SV) proportional to EDV Amount of blood ejected dependent on available blood in ventricles. CONTRACTILITY–strength/force of contraction (how hard) The more responsive cardiocytes are to stimulation the more force they can create; stimulation dependent on binding capacity of actin and myosin contractile proteins which is regulated by Ca Are all the fibers contracting together? Affected by: autonomic nerves (sympathetic, parasympathetic), hormones, pharmaceutical drugs, Ca2+ or K+ levels Positive inotropic agents increase force of contraction Ca2+ prolongs plateau increases actin/myosin coupling Negative inotropic agents decrease force of contraction Ca2+ reduces strength of myocardium action potential
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Influences on Stroke Volume
Afterload – Tension the ventricles produce to open the semilunar valves and eject blood If pressure increases, afterload also increases. It is the result of the pressure exerted in the aorta and pulmonary trunk. The pressure in the ventricles must be greater than the aortic and pulmonary pressure to open the aortic and pulmonic SL valves. As afterload increases, cardiac output DECREASES. The longer time it takes to open the valves the less time available for blood ejection during plateau; reducing blood output. Limits stroke volume (SV) [ventricle output] high BP creates high afterload decreasing ventricular ejection
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Regulation of Heart Rate
Intrinsic regulation: normal natural characteristics inside the heart - Gap junctions, SA rhythmic cells Chemoreceptors, proprioceptors, baroreceptors; Bainbridge reflex (causes increase in heart rate) Cations (Na+, K+, Ca+2) Cardiac centers of medulla oblongata control Parasympathetic stimulation (slow as bpm) Supplied by vagus nerve, DECREASES HEART RATE, acetylcholine is secreted and hyperpolarizes the heart Sympathetic stimulation (high as bpm) Cardiac nerves innervate the SA and AV nodes, coronary vessels and the atrial and ventricular myocardium. INCREASES HEART RATE and force of contraction. Epinephrine and norepinephrine released Nicotine, caffeine, medications, stress, emotional excitement Age, gender, physical fitness, temperature,
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Clinical Problems Congenital Heart Defect an abnormality or defect that exists AT or BEFORE birth. Arrhythmia (dysrhythmia) is an irregularity in heart rhythm resulting from a defect in the conduction system of the heart. Bradycardia- slow rate below 60 bpm resting-sleep, well-conditioned hearts Tachycardia – fast rate above 100 bpm stress, anxiety, drugs, heart disease Fibrillation – asynchronous contraction that can kill very easily- heart loses its rhythm- some parts of the atria and ventricle contract while others remain un-stimulated
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