2Heart Anatomy Approximately the size of a fist Location In the mediastinum between second rib and fifth intercostal spaceOn the superior surface of diaphragmTwo-thirds to the left of the midsternal lineAnterior to the vertebral column, posterior to the sternumEnclosed in pericardium, a double-walled sac
3Midsternal line 2nd rib Sternum Diaphragm Point of maximal intensity (PMI)(a)Figure 18.1a
5Pericardium 3 layers Fibrous pericardium (superficial) Serous pericardium (2 layers)Parietal layerVisceral layerlines the internal surface of the fibrous pericardiumVisceral layer (epicardium) on external surface of the heart
6Pericardium: Layer Functions Fibrous layerProtects, anchors, and prevents overfillingSerous parietal layerlines the internal surface of the fibrous pericardiumParietal means relating to or forming the wall of a body part, organ, or cavitySerous visceral layeron external surface of the heart, known as the epicardiumVisceral means organs
7Percardium: Layer Functions The parietal and visceral serous pericardium form a sac or cushion of space around the heartThis sac is called the pericardial cavityFilled with fluidPurpose = decrease friction
9Layers of the Heart Wall Epicardium—visceral layer of the serous pericardium
10Layers of the Heart Wall MyocardiumMyo = muscleSpiral bundles of cardiac muscle cellsFibrous skeleton of the heart: crisscrossing, interlacing layer of connective tissueAnchors cardiac muscle fibersSupports great vessels and valvesLimits spread of action potentials to specific paths
11Layers of the Heart Wall Endocardium is continuous with endothelial lining of blood vessels
14Chambers Four chambers Two atria (receiving chambers) and two ventricles (discharging chambers)Left and right atrium, left and right ventricleCoronary sulcus (atrioventricular groove, AV groove) encircles the junction of the atria and ventriclesSulcus = deep, narrow grooveAuricles (ears) increase atrial volume
15Two ventricles (discharging chambers) Separated by the interventricular septumPumping chambersR ventricle pumps blood into the lungsL ventricle pumps blood into the bodyInter = betweenIntra = within
16Direction of blood flow A note on vesselsDirection of blood flowArtery = Away from the heartVein = to the heartThis is important to remember when looking at the heart; arteries do not always carry oxygenated blood and veins do not always carry deoxygenated bloodi.e., pulmonary artery carries deoxygenated bloodPulmonary veins carry oxygenated blood
19Atria: The Receiving Chambers Walls are ridged by pectinate musclesVessels entering right atriumSuperior vena cavaInferior vena cavaCoronary sinusVessels entering left atriumRight and left pulmonary veins
20Ventricles: The Discharging Chambers Walls are ridged by trabeculae carneaePapillary muscles project into the ventricular cavities (anchor valves)Vessel leaving the right ventriclePulmonary trunkVessel leaving the left ventricleAorta
22Pathway of Blood Through the Heart The heart is two side-by-side pumpsRight side is the pump for the pulmonary circuitVessels that carry blood to and from the lungsLeft side is the pump for the systemic circuitVessels that carry the blood to and from all body tissues
23Capillary beds of lungs where gas exchange occurs Pulmonary Circuit Pulmonary veinsPulmonary arteriesAorta and branchesVenae cavaeLeft atriumLeft ventricleRight atriumHeartRight ventricleSystemicCircuitOxygen-rich,CO2-poor bloodCapillary beds of allbody tissues wheregas exchange occursOxygen-poor,CO2-rich bloodFigure 18.5
24Pathway of Blood Through the Heart Right atriumRight ventriclePulmonary trunkPulmonary arteriesLungsPulmonary veinsLeft atriumLeft ventricleAortaSystemic circulation
25Pathway of Blood Through the Heart Pulmonary circuit is a short, low-pressure circulationSystemic circuit blood encounters much resistance in the long pathwaysAs a result, the left ventricle has a much thicker wall (stronger muscle)
28Heart Valves Ensure unidirectional blood flow through the heart Atrioventricular (AV) valves (balloons)Prevent backflow into the atria when ventricles contractTricuspid valve (right)Between R atrium and R ventricleMitral valve (left)Between L atrium and L ventricleChordae tendineae anchor AV valve cusps to papillary muscles
29Semilunar (SL) valves (cups) Heart ValvesSemilunar (SL) valves (cups)Prevent backflow into the ventricles when ventricles relaxPulmonary valvebetween R ventricle and pulmonary trunkAortic valveBetween L ventricle and aorta
30Aorta Left pulmonary artery Superior vena cava Right pulmonary artery Left atriumLeft pulmonaryveinsPulmonary trunkRight atriumMitral (bicuspid)valveRight pulmonaryveinsAortic valvePulmonary valveTricuspid valveLeft ventricleRight ventriclePapillary muscleChordae tendineaeInterventricularseptumTrabeculae carneaeEpicardiumInferior vena cavaMyocardiumEndocardium(e) Frontal sectionFigure 18.4e
41Coronary CirculationThe functional blood supply to the heart muscle itselfArterial supply varies considerably and contains many anastomoses (junctions) among branches
42Coronary Circulation Arteries Veins Right and left coronary (in atrioventricular groove)VeinsSmall cardiac, anterior cardiac, and great cardiac veins, coronary sinusCoronary sinus is where dexoygenated blood from coronary circulation pools and is returned to venous circulation via the inferior vena cava
43(a) The major coronary arteries Left atrium Pulmonary trunk Figure 18.7aRightventriclecoronaryarteryatriumPosteriorinterventricularAnteriorCircumflexLeftAortaAnastomosis(junction ofvessels)Superiorvena cava(a) The major coronary arteriesLeft atriumPulmonarytrunk
44(b) The major cardiac veins Figure 18.7bSuperiorvena cavaAnteriorcardiacveinsGreatveinCoronarysinus(b) The major cardiac veins
46Homeostatic Imbalances Angina pectorisThoracic pain caused by a fleeting deficiency in blood delivery to the myocardiumCells are weakenedMyocardial infarction (heart attack)Prolonged coronary blockageAreas of cell death are repaired with noncontractile scar tissue
48Microscopic Anatomy of Cardiac Muscle Cardiac muscle cells are striated, short, fat, branched, and interconnectedConnective tissue matrix (endomysium) connects to the fibrous skeletonT tubules are wide but less numerousSR (sarcoplasmic reticulum) is simpler than in skeletal muscleSR stores Ca++, which plays an important part in cardiac cell APs and contractionNumerous large mitochondriaMultiple nuclei per cell
49Microscopic Anatomy of Cardiac Muscle Intercalated discs: junctions between cells anchor cardiac cells, cause heart to beat as a functional syncytium (as a group)Desmosomes prevent cells from separating during contractionGap junctions allow ions to pass; electrically couple adjacent cells
50Nucleus Intercalated discs Cardiac muscle cell Gap junctions Desmosomes(a)Figure 18.11a
51Cardiac muscle cell Mitochondrion Intercalated disc Nucleus T tubule SarcoplasmicreticulumZ discNucleusSarcolemmaI bandI bandA band(b)Figure 18.11b
54Cardiac Muscle Contraction Depolarization opens voltage-gated fast Na+ channels in the sarcolemmaReversal of membrane potential from –90 mV to +30 mVSlow Ca2+ channels open (delayed), about 20% of Ca2+ enters cell this wayDepolarization wave in T tubules causes the SR to release Ca2+; 80% of Ca2+ released thru SRCa2+ surge prolongs the depolarization phase (plateau)K+ channels open and Ca2+ channels close, repolarizing the membraneCa2+ is pumped back into the SR and ECF
55Cardiac Muscle Contraction Because of influx of Ca2+ from slow Ca2+ channels and the SR, the duration of the AP and the contractile phase is much greater in cardiac muscle than in skeletal muscleSkeletal muscleAP is 1-2msContraction is msCardiac muscleAP is 200msContraction is 200ms
56Cardiac AP and Ca++ Channel Ca++ Channel OpenUsually 200 mv action potential....drug that blocks calcium cause to pump less……shorter action potential less potential for rhythm issues
571 2 3 Action Depolarization is potential due to Na+ influx through fast voltage-gated Na+channels. A positivefeedback cycle rapidlyopens many Na+channels, reversing themembrane potential.Channel inactivation endsthis phase.1Plateau2Tensiondevelopment(contraction)Membrane potential (mV)13Tension (g)Plateau phase isdue to Ca2+ influx throughslow Ca2+ channels. Thiskeeps the cell depolarizedbecause few K+ channelsare open.2AbsoluterefractoryperiodRepolarization isdue to Ca2+ channelsinactivating and K+channels opening. Thisallows K+ efflux, whichbrings the membranepotential back to itsresting voltage.3Time (ms)Figure 18.12
58Cardiac Muscle Physiology EPIBeta blockersB-1AdrenergicreceptorAdenylate cyclaseEPIcAMPCyclase-aATPProt. KinaseCA++ ChannelsCA++InfluxProt.Kinase-aCa++B1: make heart pump harder…..also open Ca2+ channels….potentiates NaHTN, chronic angina, most common arrhythmiasCross BridgeFormation“Phosphorylation”TensionGenerationCA++Channel Blockers
60Heart Physiology: Electrical Events Intrinsic cardiac conduction systemA network of noncontractile cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heartThe independent but coordinated activity of the heart is a function ofGap junctionsIntrinsic conducting system
62Cardiac Pacemaker Cells Found in SA node, AV node, AV bundle, R and L bundle branches, Purkinje fibers; part of conduction system of the heartAutorhythmic cells (1% of cardiac muscle cells)Have unstable RMP (resting membrane potential)Cells continously depolarize because they drift toward thresholdDepolarization of the heart is rhythmic and spontaneousGap junctions ensure the heart contracts as a unit
63Cardiac Pacemaker Cells Unstable resting potentials = pacemaker potentialPacemaker potential is due to slow Na+ channels and closing of K+ channelsSlow Na+ channels leak positive ions into the cell, causing the RMP to creep upAt threshold, Ca2+ channels openExplosive Ca2+ influx produces the rising phase of the action potential (not Na+)Repolarization results from inactivation of Ca2+ channels and opening of voltage-gated K+ channels
64Action potential Threshold Pacemaker potential 2 2 3 1 1 1 2 3 This slow depolarization isdue to both opening of Na+channels and closing of K+channels. Notice that themembrane potential isnever a flat line.1Depolarization Theaction potential begins whenthe pacemaker potentialreaches threshold.Depolarization is due to Ca2+influx through Ca2+ channels.2Repolarization is due toCa2+ channels inactivating andK+ channels opening. Thisallows K+ efflux, which bringsthe membrane potential backto its most negative voltage.3Figure 18.13
65Heart Physiology: Sequence of Excitation Sinoatrial (SA) node (pacemaker)Generates impulses about 75 times/minute (sinus rhythm)Depolarizes faster than any other part of the myocardiumAtrial contraction
66Heart Physiology: Sequence of Excitation Atrioventricular (AV) nodeSmaller diameter fibers; fewer gap junctionsDelays impulses approximately 0.1 secondWant a delay between contract of atria and ventriclesDepolarizes 50 times per minute in absence of SA node input
67Heart Physiology: Sequence of Excitation Atrioventricular (AV) bundle (bundle of His)Only electrical connection between the atria and ventricles
68Heart Physiology: Sequence of Excitation Right and left bundle branchesTwo pathways in the interventricular septum that carry the impulses toward the apex of the heart
69Heart Physiology: Sequence of Excitation Purkinje fibersComplete the pathway into the apex and ventricular wallsAV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input
70(a) Anatomy of the intrinsic conduction system showing the Figure 18.14a(a) Anatomy of the intrinsic conduction system showing thesequence of electrical excitationSuperior vena cavaRight atriumLeft atriumPurkinjefibersInter-ventricularseptum1The sinoatrial (SA)node (pacemaker)generates impulses.2The atrioventricular(AV) node.(AV) bundle4The bundle branches3The Purkinje fibers5
71Homeostatic Imbalances Defects in the intrinsic conduction system may result inArrhythmias: irregular heart rhythmsUncoordinated atrial and ventricular contractionsFibrillation: rapid, irregular contractions; useless for pumping blood because atria, and more importantly ventricles, are not getting filled with blood
72Homeostatic Imbalances Defective SA node may result inEctopic focus: abnormal pacemaker takes overIf AV node takes over, there will be a junctional rhythm (40–60 bpm)Defective AV node may result inPartial or total heart blockFew or no impulses from SA node reach the ventricles
74ElectrocardiographyElectrocardiogram (ECG or EKG): a composite of all the action potentials generated by nodal and contractile cells at a given timeThree wavesP wave: depolarization of SA nodeQRS complex: ventricular depolarizationT wave: ventricular repolarization
76Atrial depolarization, initiated by the SA node, causes the P wave. RepolarizationPTQSAtrial depolarization, initiated by the SA node, causes the P wave.1Figure 18.17, step 1
77Atrial depolarization, initiated by the SA node, causes the P wave. RepolarizationPTQSAtrial depolarization, initiated by the SA node, causes the P wave.1RAV nodePTQS2With atrial depolarization complete, the impulse is delayed at the AV node.Figure 18.17, step 2
78Atrial depolarization, initiated by the SA node, causes the P wave. RepolarizationPTQSAtrial depolarization, initiated by the SA node, causes the P wave.1RAV nodePTQS2With atrial depolarization complete, the impulse is delayed at the AV node.RPTQS3Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs.Figure 18.17, step 3
79Ventricular depolarization is complete. RepolarizationPTQSVentricular depolarization is complete.4Figure 18.17, step 4
80Ventricular depolarization is complete. RepolarizationPTQS4Ventricular depolarization is complete.RPTQSVentricular repolarization begins at apex, causing the T wave.5Figure 18.17, step 5
81Ventricular depolarization is complete. RepolarizationPTQSVentricular depolarization is complete.4RPTQSVentricular repolarization begins at apex, causing the T wave.5RPTQSVentricular repolarization is complete.6Figure 18.17, step 6
82Atrial depolarization, initiated by the SA node, causes the P wave. Q RepolarizationRRPTQPTS1Atrial depolarization, initiated by the SA node, causes the P wave.QSVentricular depolarization is complete.4AV nodeRRPTPTQSWith atrial depolarization complete, the impulse is delayed at the AV node.2QSVentricular repolarization begins at apex, causing the T wave.5RRPTPTQSQ3SVentricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs.6Ventricular repolarization is complete.Figure 18.17
83(a) Normal sinus rhythm. (b) Junctional rhythm. The SAnode is nonfunctional, P wavesare absent, and heart is paced bythe AV node at beats/min.(c) Second-degree heart block.Some P waves are not conductedthrough the AV node; hence moreP than QRS waves are seen. Inthis tracing, the ratio of P wavesto QRS waves is mostly 2:1.(d) Ventricular fibrillation. Thesechaotic, grossly irregular ECGdeflections are seen in acuteheart attack and electrical shock.
85Mechanical Events: The Cardiac Cycle Cardiac cycle: all events associated with blood flow through the heart during one complete heartbeatSystole—contractionDiastole—relaxationNormal heart rate (HR) = bpm
86Two sounds (lub-dub) associated with closing of heart valves Heart SoundsTwo sounds (lub-dub) associated with closing of heart valvesFirst sound occurs as AV valves close and signifies beginning of systoleSecond sound occurs when semilunar valves close at the beginning of ventricular diastoleHeart murmurs: abnormal heart sounds most often indicative of valve problems
87Tricuspid valve sounds typically heard in right sternal margin of Figure 18.19Tricuspid valve sounds typicallyheard in right sternal margin of5th intercostal spaceAortic valve sounds heardin 2nd intercostal space atright sternal marginPulmonary valvesounds heard in 2ndintercostal space at leftsternal marginMitral valve soundsheard over heart apex(in 5th intercostal space)in line with middle ofclavicle
88Cardiac Cycle: A Note on Pressure REMEMBER:Blood will always flow from high pressure to low pressure
89Phases of the Cardiac Cycle Ventricular filling—takes place in mid-to-late diastoleAV valves are open80% of blood passively flows into ventriclesAtrial systole occurs, delivering the remaining 20%End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole
90Phases of the Cardiac Cycle Ventricular systoleRising ventricular pressure results in closing of AV valvesIsovolumetric contraction phase (all valves are closed)In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves openEnd systolic volume (ESV): volume of blood remaining in each ventricle
91Phases of the Cardiac Cycle Isovolumetric relaxation occurs in early diastoleVentricles relaxBackflow of blood in aorta and pulmonary trunk closes semilunar valves and causes brief rise in aortic pressure
92(mid-to-late diastole) Left heartQRSPTPElectrocardiogramHeart sounds1st2ndDicrotic notchAortaPressure (mm Hg)Left ventricleAtrial systoleLeft atriumEDVVentricularvolume (ml)SVESVAtrioventricular valvesOpenClosedOpenAortic and pulmonary valvesClosedOpenClosedPhase12a2b31Left atriumRight atriumLeft ventricleRight ventricleVentricularfillingAtrialcontractionIsovolumetriccontraction phaseVentricularejection phaseIsovolumetricrelaxationVentricularfilling12a2b3Ventricular filling(mid-to-late diastole)Ventricular systole(atria in diastole)Early diastoleFigure 18.20
93Volume of blood pumped by each ventricle in one minute Cardiac Output (CO)Volume of blood pumped by each ventricle in one minuteCO = heart rate (HR) x stroke volume (SV)HR = number of beats per minuteSV = volume of blood pumped out by a ventricle with each beat
94Regulation of Stroke Volume SV = EDV – ESVThree main factors affect SVPreloadContractilityAfterload
95Regulation of Stroke Volume Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart)Cardiac muscle exhibits a length-tension relationshipAt rest, cardiac muscle cells are shorter than optimal length (as opposed to skeletal muscle fibers which are kept near optimal length)This degree of stretch produces more contractile forceIncreased venous return distends (stretches) the ventricles and increases contraction forceHigher preload = higher SV
96Regulation of Stroke Volume Contractility: contractile strength at a given muscle length, independent of muscle stretch and EDVContractility rises when more Ca2+ is released into the ICF via the SRPositive inotropic agents increase contractilityIno = muscle, fiberCa2+, hormones (thyroxine, glucagon, and epinephrine)Negative inotropic agents decrease contractilityAcidosis (increased H+)Increased extracellular K+Calcium channel blockers
97Regulation of Stroke Volume Afterload: pressure that must be overcome for ventricles to eject bloodThe back pressure that arterial blood exerts on the aortic (80mg) and pulmonary (10mg) valvesHypertension increases afterload, resulting in increased ESV and reduced SV
98Regulation of Heart Rate Positive chronotropic factors increase heart rateChrono = timeNegative chronotropic factors decrease heart rateCan be neural, chemical, or physical factors
100Autonomic Nervous System Regulation Exerts the most important extrinsic controls affecting HRSympathetic nervous system is activated by emotional or physical stressorsSympathetic nerves release norepinephrine which binds to β1 adrenergic receptors on the heart, causing the pacemaker to fire more rapidlyIt also increases contractility
101Autonomic Nervous System Regulation Parasympathetic nervous system opposes the sympathetic effects and reduces HR when a stressful situation has passeParasympathetic-initiated cardiac responses are mediated by Acetylcholine (ACh)ACh hyperpolarizes the membranes by opening K+ channels
102Autonomic Nervous System Regulation At rest, the heart exhibits vagal toneAt rest, both SNS and PNS send impulses to SA node, but the dominant influence is inhibitory (PNS)The heart rate is slower than if the vagus nerve was not innervating it
103Dorsal motor nucleus of vagus The vagus nerve (parasympathetic) decreases heart rate.Medulla oblongataCardio-acceleratorycenterSympathetic trunk ganglionThoracic spinal cordSympathetic trunkSympathetic cardiacnerves increase heart rateand force of contraction.AV nodeSA nodeParasympathetic fibersSympathetic fibersInterneuronsFigure 18.15
104Exercise (by skeletal muscle and respiratory pumps; see Chapter 19) Heart rate(allows moretime forventricularfilling)Bloodborneepinephrine,thyroxine,excess Ca2+Exercise,fright, anxietyVenousreturnSympatheticactivityParasympatheticactivityContractilityEDV(preload)ESVStrokevolumeHeartrateCardiacoutputInitial stimulusPhysiological responseResultFigure 18.22
105Chemical Regulation of Heart Rate HormonesEpinephrine from adrenal medulla increases HR and contractilityThyroxine increases HR and enhances the effects of norepinephrine and epinephrineIntra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart functionElectrolyte imbalances pose serious danger to the heart
106Other Factors that Influence Heart Rate AgeGenderExerciseBody temperature
107Homeostatic Imbalances Tachycardia: abnormally fast heart rate (>100 bpm)If persistent, may lead to fibrillationBradycardia: heart rate slower than 60 bpmMay result in grossly inadequate blood circulationMay be desirable result of endurance training
108Congestive Heart Failure (CHF) Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needsCaused byCoronary atherosclerosisPersistent high blood pressureMultiple myocardial infarctsDilated cardiomyopathy (DCM)
109Ventricular septal defect. The superior part of the inter- Occurs inabout 1 inevery500 birthsevery 1500birthsNarrowedaortaevery 2000Ventricular septal defect.The superior part of the inter-ventricular septum fails toform; thus, blood mixesbetween the two ventricles.More blood is shunted fromleft to right because the leftventricle is stronger.(a)Coarctation of theaorta. A part of theaorta is narrowed,increasing the workloadof the left ventricle.(b)Tetralogy of Fallot.Multiple defects (tetra =four): (1) Pulmonary trunktoo narrow and pulmonaryvalve stenosed, resultingin (2) hypertrophied rightventricle; (3) ventricularseptal defect; (4) aortaopens from both ventricles.(c)Figure 18.24
111The principle of complementary structure and function is evident when examining the coverings of the heart. In what way is this relationship evident?The pericardium surrounds the heart.The epicardium and visceral layer of the pericardium are synonymous.The pericardial cavity surrounds the heart.The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement.Answer: d. The visceral and parietal membranes of the pericardium are smooth and slide past each other, providing a low-friction environment for heart movement.
112Of the following layers of the heart wall, which consumes the most energy? EpicardiumMyocardiumEndocardiumVisceral pericardiumAnswer: b. Myocardium
113Which of the following structures is an exception to the general principle surrounding blood vessel oxygenation levels?Pulmonary arteryAortaPulmonary veinsBoth a and cAnswer: d. Both a and c
114What purpose does the coronary circuit serve? None; it is a vestigial set of vessels.It delivers 1/20 of the body’s blood supply to the heart muscle itself.It delivers blood to the anterior lung surface for gas exchange.It feeds the anterior thoracic wall.Answer: b. It delivers 1/20 of the body’s blood supply to the heart muscle itself.
115right atrium; right ventricle; tricuspid valve A heart murmur would be detected when blood is heard flowing from the ________ to the __________ through the ___________.right atrium; right ventricle; tricuspid valveright atrium; left atrium; tricuspid valveleft ventricle; left atrium; mitral valveleft atrium; left ventricle; mitral valveAnswer: d. left atrium; left ventricle; mitral valve
116contractile myofibril desmosome functional syncytium The presence of intercalated discs between adjacent cardiac muscle cells causes the heart to behave as a _____________.single chambercontractile myofibrildesmosomefunctional syncytiumAnswer: d. functional syncytium
117The cells are each innervated by a nerve ending. Cardiac muscle cells have several similarities with skeletal muscle cells. Which of the following is not a similarity?The cells are each innervated by a nerve ending.The cells store calcium ions in the sarcoplasmic reticulum.The cells contain sarcomeres.The cells become depolarized when sodium ions enter the cytoplasm.Answer: a. The cells are each innervated by a nerve ending.
118an increased potassium permeability. an influx of calcium ions. The plateau portion of the action potential in contractile cardiac muscle cells is due to:an increased potassium permeability.an influx of calcium ions.an influx of sodium ions.exit of calcium ions from the sarcoplasmic reticulum.Answer: b. an influx of calcium ions.
119a neuromuscular junction a pacemaker potential The stimulus for the heart’s rhythmic contractions comes from _________.intercalated discsacetylcholinea neuromuscular junctiona pacemaker potentialAnswer: d. a pacemaker potential
120The major ionic change that initiates the rising phase of the autorhythmic cell action potential is __________.potassium ion exitsodium ion entrycalcium ion entrycalcium ion exitAnswer: c. calcium ion entry
121For which type of heart condition might a doctor prescribe calcium channel blockers? Depressed heart rateHeart irritabilityHeart murmurWeak heart rateAnswer: b. Heart irritability
122Atrioventricular node Atrioventricular bundle Purkinje fibers In a normal heart, which of the following structures is responsible for setting the heart’s pace?Sinoatrial nodeAtrioventricular nodeAtrioventricular bundlePurkinje fibersAnswer: a. Sinoatrial node
123There would continue to be a normal sinus rhythm. Predict the nature of an ECG recording when the atrioventricular node becomes the pacemaker.There would continue to be a normal sinus rhythm.The P wave would be much larger than normal.The rhythm would be slower.The T wave would be much smaller than normal.Answer: c. The rhythm would be slower.
124sinoatrial node and atrioventricular node Purkinje fibers The primary input to the heart by the cardioinhibitory center is primarily found in the ___________.sinoatrial node and atrioventricular nodePurkinje fibersthe cardiac contractile fibersbundle of HisAnswer: a. sinoatrial node and atrioventricular node
125The “lub-dup” heart sounds are produced by: the walls of the atria and ventricles slapping together during a contraction.the blood hitting the walls of the ventricles and arteries, respectively.the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”).the closing of the semilunar valves (“lub”) and the closing of the atrioventricular valves (“dup”).Answer: c. the closing of the atrioventricular valves (“lub”) and the closing of the semilunar valves (“dup”).
126Atrial systole occurs _______ the firing of the sinoatrial node. beforeaftersimultaneously withalternately withAnswer: b. after
127The majority (80%) of ventricular filling occurs ___________. during late ventricular systolepassively through blood flow alonewith atrial systoleboth a and bAnswer: d. both a and b
128The atria need that time to prepare for the next contraction. In terms of blood flow, why is it important that atrial diastole occurs just as ventricular systole begins?Blood is continually propelled in a forward motion down its pressure gradient.The atria need that time to prepare for the next contraction.Ventricular systole pulls the remaining 20% of blood volume from the atria.Blood would flow too fast otherwise.Answer: a. Blood is continually propelled in a forward motion down its pressure gradient.
129Cardiac output is determined by________. heart ratestroke volumecardiac reserveboth a and bAnswer: d. both a and b
130It would remain constant. ESV is not affected by contraction force. Predict what would happen to the end systolic volume (ESV) if contraction force were to increase.It would decrease.It would increase.It would remain constant.ESV is not affected by contraction force.Answer: a. It would decrease.
131the heart expands during inhalation. The Frank-Starling law of the heart can be demonstrated when an individual takes a deep breath. This is because:the heart expands during inhalation.the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle.sympathetic impulses are sent to the heart during inspiration.both a and c occur.Answer: b. the negative intrathoracic pressure induces a larger than normal venous return to the right atrium, thereby stretching the wall of the right ventricle.
132because you were startled. Your heart seems to “pound” after you hear a sudden, loud noise. This increased contractility is:because you were startled.because when a gasp of surprise is emitted, the Frank-Starling law of the heart is evident.due to norepinephrine causing threshold to be reached more quickly.because acetylcholine release is inhibited.Answer: c. due to norepinephrine causing threshold to be reached more quickly.
133End diastolic volume is increased. End diastolic volume is decreased. Predict what happens to end diastolic volume when an increase in heart rate is not accompanied by an increase in contractility.End diastolic volume is increased.End diastolic volume is decreased.End diastolic volume is unchanged.End diastolic volume is not affected by heart rate.Answer: b. End diastolic volume is decreased.
134What is the nature of acetylcholine’s inhibitory effect on heart rate? Acetylcholine induces depolarization in the sinoatrial node.Acetylcholine causes closing of sodium channels in the sinoatrial node.Acetylcholine causes opening of fast calcium channels in contractile cells.Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it.Answer: d. Acetylcholine causes opening of potassium channels in the sinoatrial node, thereby hyperpolarizing it.
135Why is high blood pressure damaging to the heart? With high blood pressure, the blood is more viscous and harder to pump.The heart rate slows down to dangerously low levels if blood pressure is too high.Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood.Sodium concentration increases during high blood pressure and is toxic to the myocardium.Answer: c. Due to increased afterload, the left ventricle must contract more forcefully to expel the same amount of blood.