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The sequence of valve openingand closure during the cardiac cycle is as follows:■■■Left heart: Mitral closure, aortic opening, aortic closing,mitral opening.Right heart: Tricuspid closure, pulmonic opening, pulmonic closure, tricuspid opening.Aggregate sequence: Mitral closure, tricuspid closure,pulmonic opening, aortic opening, aortic closure, pulmonic closure, tricuspid opening, mitral opening.Isovolumetric periods in the cardiac cycle refer to shortintervals when all of the valves are closed.
On the leftside of the heart during isovolumetric contraction, ventricularpressure exceeds atrial pressure, and thus the mitral valve hasclosed. Ventricular pressure rises as the heart contracts, but ithas not yet exceeded aortic pressure, and thus the aortic valveis still closed. During isovolumetric relaxation, ventricular pressure is less than aortic pressure, and thus the aortic valve isclosed. However, ventricular pressure has not yet fallen belowatrial pressure, and therefore the mitral valve is still closed. Theoverall sequence in the cardiac cycle in the ventricles consists ofisovolumetric contraction, followed by ejection, isovolumetricrelaxation, ventricular filling, isovolumetric contraction, and soforth.The asynchrony between the left- and right-side valves iscaused by differences in the pressure gradients between thesides of the circulation, and the degree of asynchrony variesduring the respiratory cycle, because of the effects of thoracicpressure on filling and pressures within the heart and centralcirculation.Ventricular PressureThe cardiac cycle is initiated by the P wave of the electrocardiogram (ECG).
Depolarization of the atria results in atrialcontraction and final filling of the ventricles; this accounts forthe slight increase in left ventricular pressure (LVP). Whenthe wave of depolarization reaches the ventricle (QRS complexof the ECG) and ventricular contraction is initiated, LVP risesabove left atrial pressure (LAP), producing mitral valveclosure and marking the beginning of isovolumetric contraction. Left ventricular end-diastolic pressure (LVEDP) is normally about 5 mm Hg (RVEDP is normally about 2 mm Hg).From this point, LVP rises rapidly, as the ventricle attemptsto contract against a fixed volume.
When LVP rises aboveaortic pressure, the aortic valve opens, marking the end ofisovolumetric contraction and the beginning of ventricularejection. If aortic pressure is 120/80 mm Hg, this occurs at80 mm Hg. LVP continues to rise for a period, but as thestroke volume is ejected, LVP reaches a peak (at approximately 120 mm Hg when aortic pressure is 120/80 mm Hg)and begins to fall. The T wave of the ECG occurs at this time,120Reducedventricular filling(diastasis)RapidventricularfillingIsovolumetricrelaxationReduced ejectionRapid ejectionIsovolumetriccontractionCardiovascular PhysiologyAtrial systole114Aortic valve closesAorticvalveopens100Aorticpressure80Pressure (mm Hg)Left ventricularpressure60Mitralvalveclosesa4020Mitral valve opensLeft atrialpressurecv0Aortic blood flow (L/min)543210130Ventricular volume (mL)110907050S1S2S4Heart soundsaVenous pulsecS3vRElectrocardiogramTPQ00.1SPVentricularsystole0.20.30.40.5Time (seconds)0.60.70.8Figure 11.1 The Cardiac Cycle The cardiac cycle (or Wiggers diagram) is a simultaneous depictionof several parameters related to blood flow and volume, the electrocardiogram, and the echocardiogramthrough a cycle of cardiac systole and diastole.
Ventricular systole begins with a short period of isovolumetriccontraction, during which all of the heart valves are closed. This is followed by the ejection phase of systole,and then isovolumetric relaxation when the heart valves are again all closed. Cardiac filling occurs afterisovolumetric relaxation. The temporal relationships between features of these various curves or tracingsare predictable, based on functional relationships within the cycle. The a, c, and v waves are identified onboth the venous pulse and atrial pressure curves.as ventricular repolarization takes place.
LVP falls below aorticpressure, but aortic valve closure is not immediate, due to themomentum associated with ventricular ejection. Closure ofthe aortic valve marks the end of ejection and the beginningof isovolumetric relaxation. During this period, the ventricleis beginning to relax, but the valves are closed, resulting inrapid fall of LVP. When LVP falls below LAP, the mitral valveopens, and ventricular filling begins. During the remainder ofdiastole, LVP remains slightly below LAP, consistent with thedirection of blood flow during ventricular filling.The Cardiac PumpAortic PressureThe aortic pressure curve falls during diastole as blood flowsto the peripheral circulation (see Fig.
11.1). The upstroke inthis curve begins (at 80 mm Hg if aortic pressure is120/80 mm Hg) with the opening of the aortic valve. As ejection proceeds, pressure rises to the systolic aortic pressure(120 mm Hg in this example), and then begins to fall. Thedicrotic notch, a high frequency deflection in the aortic pressure curve, occurs when the aortic valve closes. Aortic flowreaches a peak during rapid ejection and is lowest duringdiastole when no ejection is occurring.Ventricular VolumeThe left ventricular volume curve illustrates the filling andemptying of the ventricle (see Fig.
11.1). At the time of the Pwave, ventricular filling is nearly complete, but the final filling(approximately 15%) is produced by atrial contraction. Thisphase of ventricular filling is known as active ventricularfilling. Ventricular filling ends when the mitral valve closes, atthe left ventricular end-diastolic volume (EDV). Of course,ventricular volume remains constant during isovolumetriccontraction. With opening of the aortic valve, rapid ejection ofblood begins, and ventricular volume falls quickly. This is followed by a period of reduced ejection, which ends with aorticvalve closure.
At this point, left ventricular end-systolic volume(ESV) has been reached, and this volume remains constantduring isovolumetric relaxation. The stroke volume is the difference between EDV and ESV. Normal EDV is approximately140 mL and normal stroke volume is approximately 70 mL,although these values vary considerably. Opening of the mitralvalve initiates a period of rapid passive filling. This is followedby a period of slow passive filling (also known as diastasis), asthe ventricle fills more slowly with the diminished pressuregradient between the atrium and ventricle.115the ECG, atrial contraction produces the first rise in atrialpressure, the a wave (see Fig. 11.1).
During isovolumetriccontraction, there is another upward wave in the LAP curve,the c wave, caused by bulging of the mitral valve back into theleft atrium, as the ventricle attempts to contract against a fixedvolume. During the ejection phase of the left ventricle, LAPrises slowly while venous return from the pulmonary circulation fills the atrium (the mitral valve is closed during thisperiod), producing the v wave. When LVP falls below LAP,the mitral valve opens and LAP falls as blood flows into theleft atrium. For the remainder of diastole, LAP remains aboveLVP as the heart fills. Because there are no valves between thevena cavae and right atrium (or the pulmonary vein and leftatrium), the venous pulse and the atrial pressure curve aresimilar in shape.PhonocardiogramThe phonocardiogram is an acoustical recording reflectingthe heart sounds generated during the cardiac cycle (seeFig.
11.1). S1, the first heart sound, is generated by closure ofthe mitral and tricuspid valves (the mitral valve closes slightlybefore the tricuspid valve). S2 is associated with closure of theaortic and pulmonic valves; again, the valve on the left sidecloses just before the right-side valve. During inspiration,closure of the pulmonic valve is delayed more distinctly, normally resulting in audible physiological splitting of S2. Thisdelay is caused by increased filling of the right ventricle, dueto reduced intrathoracic pressure during inspiration. S3, thethird heart sound, is normal in children, and is associated withrapid ventricular filling. It is not heard in normal adults, andmay be a sign of volume overload, as in congestive heartfailure.
S4, caused by active ventricular filling, also is notaudible in normal adults, but may be present in a variety ofdisease states.Atrial PressureREGULATION OF CARDIAC OUTPUTThe shape of the left atrial pressure curve reflects both cardiacevents and venous return (flow of blood back to the atrium);it consists of the a, c, and v waves. Following the P wave onCardiac output is 5 liters (L) per minute (min) in the average,resting adult. The cardiac output formula is a key physiological concept, relating cardiac output (CO) to heart rate (HR)and stroke volume (SV):The events of the cardiac cycle are initiated when anaction potential is generated in the sinoatrial (SA) node,producing depolarization and contraction of the atria, followedby contraction of the ventricles.
When heart rate is increased,diastole is shortened, because the P wave (and thus, atrial andventricular contraction) occurs earlier. As a result, the time forventricular filling is diminished. However, at a resting heart rateof 70 beats per minute, there is a significant period of diastasis(slow ventricular filling), and, up to a point, increasing heartrate will not limit the time for rapid passive filling, the periodduring which most ventricular filling occurs. Very rapid heartrates allow insufficient time for ventricular filling and can evencompromise cardiac output.CO = HR × SVAt rest, HR is approximately 70 beats per minute and SV isapproximately 70 mL, yielding CO of approximately 5000 mL/min (5 L/min). In order to maintain adequate arterial bloodpressure and blood flow at rest, during increased activity, orduring challenges to homeostasis such as exercise, CO mustbe adjusted through regulation of HR and SV.
Many of themechanisms that regulate HR or SV affect both parameters,and furthermore, are closely linked to mechanisms involvedin blood pressure regulation.The autonomic nervous system (ANS) plays an importantrole in regulation of cardiac output, through modulation ofCardiovascular PhysiologyCervical BrainstemPARASYMPATHETICSYMPATHETICCervical Brainstem116GanglionVagusnervesAChACh SA NEGanglionACh AV NEACh2/3 E1/3 NEAdrenal medullaThoracicThoracicNEAChAChAChSacralAChSomevascular bedsSpinalcordLumbarNEChange in posture(standing to lying)Venous returnSympathetic efferent nerveactivity (% baseline)LumbarSmall arteriesand arterioles200100Stroke volumeParasympatheticefferent output0MAPSA nodeFiring rate ofbaroreceptorafferent fibersHeart rateCNS (medulla)0100MAP (mm Hg)200Sympatheticefferent outputArteriolesVeinsVentricleVenous toneContractilityPeripheralresistanceCardiac outputMAPCardiac outputStroke volumeFigure 11.2 Autonomic Nervous System and Arterial Baroreceptor Reflexes Both sympathetic and parasympathetic nerves innervate the SA and AV nodes.
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