Ch18: Heart

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27 Terms

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Pulmonary circuit

  • The right side of the heart receives oxygen-poor blood from body tissues and then pumps this blood to the lungs to pick up oxygen and dispel carbon dioxide

  • The blood vessels that carry blood to and from the lungs from the pulmonary circuit

  • Left atrium receives blood returning from pulmonary circuit

  • Right ventricle pumps blood into the pulmonary circuit

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System Circuit

  • Left side of heart receives oxygenated blood returning from lungs and pumps blood throughout body to supply oxygen and nutrients to body tissues

  • Blood vessels that carry blood to and from body tissues form systemic circuit

  • Right atrium receives blood from systemic circuit

  • Left ventricle pumps blood into systemic circuit

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Blood floor

  • Deoxygenated blood from extremities and body go to the superior and inferior vena cava and coronary sinus

  • Blood goes to right atrium

  • Blood passes through the tricuspid valve into the right ventricle

  • Deoxygenated blood passes through the pulmonary semilunar valve into the pulmonary trunk

  • Pulmonary arteries brings blood to lungs to be oxygenated

  • Blood enters back from lungs through 4 pulmonary veins into left atrium

  • Bicuspid valve opens for blood to enter left ventricle

  • Blood leaves through aortic semicircular valve into aorta to go to body

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Size and location

  • Heart is about the size of a fist, is hollow and cone-shaped

  • Mass of 250-350 grams

  • Enclosed within the mediastinum or medial cavity of thorax

  • Heart extends obliquely for 12 to 14 cm from the 2nd rib to the 5th intercostal space

  • Rests on superior surface of diaphragm and lies anterior to the vertebral column and posterior to the sternum

  • ⅔ of mass lies left of midsternal line and balance projects to the right

  • The flat base, or posterior surface is about 9 cm wide and directed toward right shoulder

  • Its apex pointed inferiorly toward left hip

  • Apical impulse: caused by beating heart’s apex where it touches chest vali

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Coverings

  • Heart is enclosed in pericardium(double walled sac)

  • Fibrous pericardium (outermost)

    • Tough, dense connective tissue layer

    • Protects heart

    • Anchors heart

    • Prevents overfilling

  • Serous pericardium

    • Forms closed sac around heart

    • Parietal layer: lines internal fibrous pericardium

    • Visceral layer (epicardium): is integral part of heart wall

    • Pericardial cavity: contains serous fluid for lubrication

  • Pericarditis

    • Inflammation of pericardium

    • Roughens serous membrane surface

    • Heart rubs against pericardial sac

    • Pain beneath sternum

    • Impedes function

    • Cardiac tamponade

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3 Layers

  • Epicardium: visceral layer of the serous pericardium

    • Often infiltrated with fat

  • Myocardium: the middle layer is composed mainly of cardiac muscle and forms the bulk of the heart. This is the layer that contracts

    • Branching cardiac muscle cells are tethered to one another by criss crossing connective tissue fibers and arranged in spiral or circular bundles. interlacing bundles link all parts of the heart together.

    • Connective tissue fibers form a dense network, the fibrous cardiac skeleton reinforces the myocardium internally and anchors the cardiac muscle fibers

      • Cardiac skeleton allows action potentials to spread only via specific pathways in the heart

  • Endocardium: 3rd layer of the heart wall is a glistening white sheet of endothelium resting on a thin connective tissue layer. Located on the inner myocardial surface, it lines the heart chambers and covers the fibrous skeleton of the valves

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Atria: Receiving Chambers


  • Auricles: small, wrinkled appendages which increase atrial volume

  • Internally, the right atrium has two basic parts 

    • smooth-walled posterior part

    • anterior portion in which bundles of muscle tissue form ridges in the walls

      • (bundles are pectinate muscles)

  • The left atrium is mostly smooth and pectinate muscles are found only in the auricle.

  • Function: the atria are receiving chambers for blood returning to the heart from the circulation

  • Interatrial septum: where it separates the atria

  • Interventricular septum: where it separates the ventricles

  • Blood enters right atrium

    • The superior vena cava returns blood from body regions superior to the diaphragm. 

    • The inferior vena cava returns blood from body areas below the diaphragm. 

    • The coronary sinus collects blood draining from the myocardium.

  • Blood enters left atrium

    • 4 pulmonary veins: transport blood from the lungs back to heart

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Ventricle: Discharging Chambers


  • Make up most volume of the heart

  • irregular ridges of muscle called trabeculae carneae ("crossbars of flesh") mark the internal walls of the ventricular chambers. 

  • Other muscle bundles, the papillary muscles, which play a role in valve function, project into the ventricular cavity

  • Right ventricle: pumps blood into the pulmonary trunk, which routes the blood to the lungs where gas exchange occurs. 

  • Left ventricle: ejects blood into the aorta, the largest artery in the body.

  • Interventricular septum: where it separates the ventricles

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Valves


  • 2 atrioventricular valves. One located at each atrial-ventricular junction

    • Prevents backflow into the atria when ventricles contract

    • Tricuspid valve: right AV valve that has 3 flexible cusps

    • Mitral valve: left AV valve that has 2 cusps, also called bicuspid valve

  • Each AV valve flap has a white collagen cord attached called Chordae tendineae

    • Anchors the cusps to papillary muscles protruding from the vascular walls

  • Semilunar valves are made up by the aortic and pulmonary valves

    • Guard the bases of large arteries from the ventricles

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Coronary circulation


  • Coronary arteries provide an arterial supply of the coronary circulation

  • Left C.A. = runs toward left side of the heart and then divides into 2 major branches

    • Anterior interventricular artery: follows anterior ventricular sulcus and supplies blood to the interventricular septum and interior walls of both ventricles 

    • The circumflex artery: Supplies left atrium and posterior walls left ventricle

  • Right coronary artery courses right side of the heart, where it gives rise to 2 branches:

    • Right marginal artery serves the myocardium of the lateral right side of the heart

    • Posterior interventricular artery runs to the heart apex and supplies the posterior ventricular walls. Merges anastomoses with the anterior interventricular artery

  • Branches of right coronary artery supply right atrium and nearly all right ventricle

  • Arterial supply of the heart varies for everyone

  • Right side blockage shows pitting edema in limbs and jugular vein distention where left side blockage causes respiratory emergencies (loss breath, cyanosis)

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Skeletal vs Cardiac muscle


  • Skeletal

    • Striated, long, cylindrical, multinucleate

    • No gap junctions

    • No motor units, must be individually stimulated

    • Abundance of T tubules

    • Elaborate SR with terminal cisterns

    • Ca for contraction comes from SR

    • CA binds to troponin

    • No pacemaker cells

    • Tetanus possible

    • Gets ATP from aerobic and anaerobic respiration

  • Cardiac

    • Striated, short, branchedd, 1-2 nuclei per cell

    • Has gap junctions

    • Gap junctions create functional syncytium (contracts as unit)

    • T tubules are less numerous, wider

    • SR less elaborate, no terminal cisterns

    • Ca for contraction from SR and ECF

    • Ca binds to troponin

    • Tetanus not possible

    • ATP from aerobic respiration (more mitochondria)

<ul><li><p><span>Skeletal</span></p><ul><li><p><span>Striated, long, cylindrical, multinucleate</span></p></li><li><p><span>No gap junctions</span></p></li><li><p><span>No motor units, must be individually stimulated</span></p></li><li><p><span>Abundance of T tubules</span></p></li><li><p><span>Elaborate SR with terminal cisterns</span></p></li><li><p><span>Ca for contraction comes from SR</span></p></li><li><p><span>CA binds to troponin</span></p></li><li><p><span>No pacemaker cells</span></p></li><li><p><span>Tetanus possible</span></p></li><li><p><span>Gets ATP from aerobic and anaerobic respiration</span></p></li></ul></li><li><p><span>Cardiac</span></p><ul><li><p><span>Striated, short, branchedd, 1-2 nuclei per cell</span></p></li><li><p><span>Has gap junctions</span></p></li><li><p><span>Gap junctions create functional syncytium (contracts as unit)</span></p></li><li><p><span>T tubules are less numerous, wider</span></p></li><li><p><span>SR less elaborate, no terminal cisterns</span></p></li><li><p><span>Ca for contraction from SR and ECF</span></p></li><li><p><span>Ca binds to troponin</span></p></li><li><p><span>Tetanus not possible</span></p></li><li><p><span>ATP from aerobic respiration (more mitochondria)</span></p></li></ul></li></ul><p></p>
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Sequence of Excitation ***

  1. The sinoatrial (SA) node generates impulses (pacemaker)

  2. The impulses pause (0.1 s) at the atrioventricular (AV) node

  3. The atrioventricular bundle connects the atria to the ventricles

  4. The bundle branches conduct the impulses through interventricular septum

  5. The subendocardial conducting network depolarizes the contractile cells of both ventricles

<ol><li><p>The<strong> sinoatrial (SA) node </strong>generates impulses (pacemaker)</p></li><li><p>The impulses pause (0.1 s) at the<strong> atrioventricular (AV) node</strong></p></li><li><p>The <strong>atrioventricular bundle</strong> connects the atria to the ventricles</p></li><li><p>The <strong>bundle branches</strong> conduct the impulses through interventricular septum</p></li><li><p>The <strong>subendocardial conducting network </strong>depolarizes the contractile cells of both ventricles</p></li></ol><p></p>
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Autonomic Nervous System

  • Fibers of ANS modify the beat of the heart

  • Sympathetic NS increases heart rate

  • Parasympathetic NS decreases heart rate

  • Cardiac centers are located in medulla oblongata. The cardioacceleratory center projects to sympathetic neurons in the spinal cord. The postganglionic fibers run thru cardiac plexus to heart where they innervate the SA + AV nodes, heart muscle + coronary arteries

  • The cardioinhibitory center sends impulses to sympathetic dorsal vagus nucleus in the medulla which sends inhibitory impulses to heart via branches of vagus nerves

    • Most parasympathetic postganglionic motor neurons are in ganglia in heart wall

      • Fibers project to SA and AV nodes

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ECG/EKG


  • Electrocardiogram: graphic record of heart activity

  • The electrical currents generated in and transmitted through the heart spread throughout the body and can be detected with an electrocardiograph

  • And ECG is a composite of all the APs generated by nodal and contractile cells at a given time

  • To record an ECG, electrodes are placed at various sites on body surfaces → typical 12 lead ECG:

    • 3 electrodes form bipolar leads that measure voltage between arms or between an arm and leg

    • 9 electrodes form unipolar leads

    • Together, 12 provide a comprehensive picture of heart electrical activity

  • Typical ECG has 3 waves/deflections:

    • P wave: 1st wave, small, lasts 0.09 seconds. Results from movement of the depolarization wave from SA node through atria; approximately 0.1 seconds after P wave begins the atria contracts

    • QRS complex: large, results from ventricular depolarization and precedes ventricular contraction, complicated shape be the paths of depolarization waves through ventricular walls change contraction and produces corresponding changes in current direction

    • T wave: caused by ventricular repolarization, lasts 0.16s, more spread out and has a lower amplitude than QRS complex because repolarization is slower.

  • P-R interval: time from beginning of atrial excitation to beginning of ventricular excitation

  • S-T segment: APs of ventricular myocytes are in plateau phases

<ul><li><p>Electrocardiogram: graphic record of heart activity</p></li><li><p>The electrical currents generated in and transmitted through the heart spread throughout the body and can be detected with an electrocardiograph</p></li><li><p>And ECG is a composite of all the APs generated by nodal and contractile cells at a given time</p></li><li><p>To record an ECG, electrodes are placed at various sites on body surfaces → typical 12 lead ECG:</p><ul><li><p>3 electrodes form bipolar leads that measure voltage between arms or between an arm and leg</p></li><li><p>9 electrodes form unipolar leads</p></li><li><p>Together, 12 provide a comprehensive picture of heart electrical activity</p></li></ul></li><li><p><strong><u>Typical ECG has 3 waves/deflections:</u></strong></p><ul><li><p><strong>P wave: </strong>1st wave, small, lasts 0.09 seconds. Results from movement of the depolarization wave from SA node through atria; approximately 0.1 seconds after P wave begins the atria contracts</p></li><li><p><strong>QRS complex</strong>: large, results from ventricular depolarization and precedes ventricular contraction, complicated shape be the paths of depolarization waves through ventricular walls change contraction and produces corresponding changes in current direction</p></li><li><p><strong>T wave:</strong> caused by ventricular repolarization, lasts 0.16s, more spread out and has a lower amplitude than QRS complex because repolarization is slower.</p></li></ul></li><li><p><strong>P-R interval:</strong> time from beginning of atrial excitation to beginning of ventricular excitation</p></li><li><p><strong>S-T segment:</strong> APs of ventricular myocytes are in plateau phases</p></li></ul><p></p>
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Phases of cardiac cycle

  1. Ventricular filling: mid to late diastole

    1. Ventricles fill with blood and the aortic + pulmonary valves are closed

    2. Atria contract and propels residual blood into ventricles

  2. Isovolumetric contraction

    1. Ventricles contract and pressure increases

    2. Phase is when ventricles are completely closed chambers

    3. SL valves are forced open

  3. Ventricular ejection

    1. Blood rushes from ventricles into aorta + pulmonary trunk

  4. Isovolumetric relaxations: early diastole

    1. Ventricles relax and the SL valves close

    2. End is the beginning of isovolumetric relaxation phase

<ol><li><p><strong>Ventricular filling: mid to late diastole</strong></p><ol><li><p>Ventricles fill with blood and the aortic + pulmonary valves are closed</p></li><li><p>Atria contract and propels residual blood into ventricles</p></li></ol></li><li><p><strong>Isovolumetric contraction</strong></p><ol><li><p>Ventricles contract and pressure increases</p></li><li><p><strong>Phase </strong>is when ventricles are completely closed chambers</p></li><li><p>SL valves are forced open</p></li></ol></li><li><p><strong>Ventricular ejection</strong></p><ol><li><p>Blood rushes from ventricles into aorta + pulmonary trunk</p></li></ol></li><li><p><strong>Isovolumetric relaxations: early diastole</strong></p><ol><li><p>Ventricles relax and the SL valves close</p></li><li><p>End is the beginning of isovolumetric relaxation phase</p></li></ol></li></ol><p></p>
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Heart Sounds

  • 2 sounds

  • First: closing of AV valves at beginning of ventricular systolic

  • Second: closing of SL valves at beginning of ventricular diastole

  • Pause between (lub-dub) indicates heart relaxation

  • Mitral valve closes slightly before tricuspid, and aortic closes slightly before pulmonary valve

  • Differences allow auscultation of each valve when the stethoscope is placed in 4 diff regions.

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Cardiac Output


  • Amount of blood pumped out by each ventricle in 1 minute

  • CO = HR (heart rate) x SV (stroke volume)

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Stroke volume 


  • Volume of blood pumped out by 1 ventricle with each beat 

    • Correlated with force of ventricular contraction

  • Measured in LPM

  • Increases with increase in SV or HR

  • Cardiac reserve: difference between resting and maximal cardiac output

    • Higher in trained athletes

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Regulation of Stroke Volume


  • Difference between end diastolic volume (EDV) and end systolic volume (ESV)

    • end diastolic volume (EDV): amount of blood that collects in ventricle during diastole

    • end systolic volume (ESV): volume blood in ventricle after it contracted

  1. Preload

    1. Degree to which cardiac muscle cells are stretched just before they contract. Increase preload and increase SV

    2. Venous system: amt of blood returning to heart and distending its vesicles, most important factor stretching cardiac muscle. higher venous return is higher cardiac output.

    3. Frank-starling is relation between SV and preload

  2. Contractility

    1. Contractile strength achieved at given muscle length

    2. Rises when increased Ca enters cytoplasm from SR and EC fluid

  3. Afterload

    1. Pressure that the ventricles must overcome to eject blood

    2. Not a major determinant in SV
      In people with hypertension = important, afterload reduces ability of ventricles to eject blood

<ul><li><p>Difference between end diastolic volume (EDV) and end systolic volume (ESV)</p><ul><li><p>end diastolic volume (EDV): amount of blood that collects in ventricle during diastole</p></li><li><p>end systolic volume (ESV): volume blood in ventricle after it contracted</p></li></ul></li></ul><ol><li><p><strong>Preload</strong></p><ol><li><p>Degree to which cardiac muscle cells are stretched just before they contract. Increase preload and increase SV</p></li><li><p><u>Venous system:</u> amt of blood returning to heart and distending its vesicles, most important factor stretching cardiac muscle. higher <strong>venous return</strong> is higher cardiac output.</p></li><li><p>Frank-starling is relation between SV and preload</p></li></ol></li><li><p><strong>Contractility</strong></p><ol><li><p>Contractile strength achieved at given muscle length</p></li><li><p>Rises when increased Ca enters cytoplasm from SR and EC fluid</p></li></ol></li><li><p><strong>Afterload</strong></p><ol><li><p>Pressure that the ventricles must overcome to eject blood</p></li><li><p>Not a major determinant in SV<br>In people with hypertension = important, afterload reduces ability of ventricles to eject blood</p></li></ol></li></ol><p></p>
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Regulation of Heart Rate


  • Positive chronotropic factors increase heart rate, negative chronotropic decreases

  • HR is regulated by ANS, chemicals, other factors

    Increases

  • ANS: sympathetic NS activated by emotional/physical stressors

  • Norepinephrine release: pacemaker fires more rapidly, increased contractility

  • Atrial (bainbridge) reflex: sympathetic reflex initiated by increased venous return, hence increased atrial filling

  • Hormone release (epinephrine/thyroxine) influences HR

    Decreases

  • PNS has opposite effects

    • Acetylcholine release: opens K channels

  • Heart at rest exhibits vagal tone

    • Parasympathetic = dominant influence

      • Decreases rate about 25 bpm

      • Cutting vagal nerve leads to HR of 100

  • Intra/extracellular ion concentration need to be maintained

  • Age, gender, exercise, body temp also influences 

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Homeostatic imbalance of cardiac output

  • Hearts pumping action maintains balance between Cardiac output and venous return

  • In congestive heart failure, heart is an inefficient pumped blood circulation does not meet tissue needs

    • Reflects weakening of myocardium

  • Most common causes:

    • Coronary atherosclerosis: fatty build up that clogs arteries and impairs blood and oxygen delivery. Cells and heart becomes hypoxic

    • Increased Blood pressure: myocardium must exert more force to open aortic valve

      • Stress causes weaker myocardium

    • Multiple myocardial infarction: heart attack depresses pumping because noncontractile fibrous tissue replaces dead heart cells

    • Dilated cardiomyopathy: ventricles stretch and myocardium deteriorates

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intrinsic cardiac conduction system

  • noncontractile cardiac cells specialized to initiate and distribute impulses throughout the heart, so that it depolarizes and contracts in an orderly, sequential manner

  • Cardiac pacemaker cells: having the special ability to depolarize spontaneously and so pace the heart

  • Pacemaker potentials: initiate action potentials that spread throughout the heart to trigger contractions

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cardiac reserve

different between resting and maximal cardiac output

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Angina pectoris

  • thoracic pain caused by a fleeting deficiency in blood to myocardium

  • blockage of coronary arterial circulation

  • may result from spasms of coronary arteries or increased physical demands of heart

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Myocardial infarction

  • Heart attack

  • prolonged coronary blockage in which cells do die

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Cardiac Muscle differences

  • Some cardiac muscle cells are self-excitable

  • Heart contracts as a unit

  • Influx of Ca from extracellular fluid triggers Ca release from SR

  • Tetanic contractions cannot occur (multiple contractions)

  • Relies on aerobic respiration

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3 Parts of action potential in pacemaker cells

  1. Pacemaker potential: Slow Na channels open and Na influx occurs. (depolarization in action potential tracing)

  2. Depolarization: Ca channels open and influx of Ca occurs. (plateau in action potential tracing)

  3. Repolarization: Ca channels inactivate and K efflux from the cell