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A positive chronotropic agentis a drug that increases heart rate. Stimulation of the sympathetic nervous system increases the chronotropic, dromotropic,and inotropic state of the heart, whereas the parasympatheticnervous system mainly reduces the chronotropic and dromotropic state.102Cardiovascular Physiologycurrents created during action potentials, and unidirectionaldepolarization is maintained due to the refractory periods ofcells once they have depolarized.three augmented limb leads (AVL, AVR, and AVF). A normalECG consists of a:■■■THE ELECTROCARDIOGRAMAn electrocardiogram (ECG or EKG) is a recording of changesin surface potential on the body, produced by the depolarization and repolarization of the heart.
Electrocardiography mayreveal the following:■■■■Abnormal cardiac rhythms and conduction.Presence, location, and extent of ischemia or infarction.Orientation of the heart in the thoracic cavity and sizeof chambers.Effects of abnormal electrolyte levels and some drugs.These observations are facilitated by recording of the ECGwith multiple lead configurations. A 12-lead ECG includesstandard leads I, II, and III; six unipolar leads (V1–V6); andIn the normal ECG, each P wave leads to a QRS complexand T wave. The heart is considered to be in “sinus rhythm,”because the rhythm is being regulated by the SA node.
Bradycardia refers to a resting heart rate below 60 beats perminute; tachycardia is a resting heart rate above 100 beatsper minute. Some causes of bradyarrhythmias in the presenceof normal sinus rhythm include high vagal (parasympathetic)tone; drugs; and various metabolic, endocrine, and neurological disorders.
Some causes of tachyarrhythmias with sinusrhythm include high sympathetic tone; drugs; low bloodvolume (dehydration); and metabolic, endocrine, and neurological disorders. The specific electrical events leadingto the components of the ECG are detailed in Figures 9.2to 9.4.CLINICAL CORRELATEAtrioventricular BlockThe normal conducting pathway in the heart is:SA → AV → Bundle of His → Bundle branches → Purkinjefibers → Ventricular muscleWhen conduction is disrupted in this pathway, arrhythmias result.Atrioventricular block (heart block) is a group of cardiac arrhythmias associated with altered conduction through the AV node:■■First-degree AV block is abnormally delayed conductionthrough the AV node (PR interval on the ECG exceeding200 msec). Each P wave results in a QRS complex and thusventricular contraction, as in normal sinus rhythm, but AVconduction is delayed.
By itself, first-degree block does notproduce bradycardia and is usually benign if not caused byunderlying heart disease.Second-degree AV block is characterized by intermittent conduction through the AV node. As a result, some P waves on theECG are followed by a QRS complex, whereas others are not.P wave, caused by atrial depolarization.QRS complex, representing ventricular depolarization.T wave, representing ventricular repolarization.■Thus, the ventricles contract less frequently than the atria.Myocardial ischemia or infarction may produce second-degreeblock.Third-degree AV block (complete block) occurs when the waveof depolarization is not conducted through the AV node (fromatria to ventricles). On the ECG, both P-P intervals and R-Rintervals are regular, but P waves are dissociated from the QRScomplexes. When atrial pacemaker activity fails to be conducted to the ventricle, an escape pacemaker may arise in theAV node below the site of block or in the bundle of His, producing a ventricular rate of 40 to 55 beats per minute (as determined by the R-R interval) that is only partially responsive tosympathetic stimulation.
When the conduction block occurs inthe bundle of His, the ventricular escape rhythm will producean inadequate heart rate of 20 to 40 beats per minute; cardiacoutput (flow rate from one ventricle) may be insufficient evenat rest, and activity will be greatly restricted due to inability toadequately adjust output. The usual therapy is implantation ofa cardiac pacemaker.Impulses originate at SA node (P waves) and below siteof block in AV node (junctional rhythm), conducting toventricles.PRRRTPP TPRPAtria and ventricles depolarize independently.
QRS complexes lessfrequent; regular at 40 to 55 beats/min but normal in shape.BlockThird-Degree Heart BlockPCardiac ElectrophysiologyAction potentialsSA nodeAtrial muscleAV nodeCommon bundleBundle branchesPurkinje fibersVentricular muscleTPUQR SA0.2Action potential of SA node cells0.4SecondsAction potential of ventricular myocytes10200Potential(mV)Potential(mV)⫺80⫺65OutwardiK⫹IoniccurrentsifInwardiCa2⫹B0.643ERPRRP4iK⫹OutwardIoniccurrentsiCa2⫹InwardiNa⫹Figure 9.1 Electrical Activity of the Heart Action potentials vary as the wave of depolarizationproceeds through the conducting pathway of the heart, beginning at the SA node and ending in the ventricular muscle. The ECG records changes in surface potential on the body associated with depolarizationand repolarization of the heart.
P waves, QRS complexes, and T waves constitute the normal ECG. In 50%to 70% of individuals, a U wave will also be recorded. Its origin is not well defined (A). Differences in morphology of the action potentials are based on differences in specific ion currents (B). In AV nodal cells, notethe spontaneous depolarization from the resting membrane potential that results in the action potential. Inventricular myocytes (and also the His-Purkinje system), note the sharp phase 0 upstroke that producesrapid conduction of the wave of depolarization.
The phase 2 plateau is important in preventing prematuredepolarization. The effective refractory period (ERP) is the period during which another action potentialcannot be elicited; during the relative refractory period (RRP), it is more difficult to elicit an action potentialthan during phase 4.103104Cardiovascular PhysiologyNormal Sequence of Cardiac Depolarization and Repolarizationand Derivation of ECGPLead IA. Impulse origin and atrial depolarizationImpulse originates at SA node, and wave ofdepolarization spreads over atria, resultingin electrical vector directed downward andto left.
This causes upward (positive) deflectionin ECG tracing in leads I and aVF (P wave).SA nodeRecording axis oflead I (horizontal,right to left)Resultant vectorof electricalactivityRecording axis oflead aVF (vertical,downward)Lead aVFPLead IPB. Septal depolarizationAfter brief delay at AV node, impulse traverses commonbundle of His and right and left bundle branches and thenenters interventricular septum, causing myocardialdepolarization with electrical vector directed to right anddownward. This results in small negative (downward)deflection in lead I (Q wave) and positive (upward)deflection in lead aVF (R wave).QRecording axis oflead I (horizontal,right to left)Resultant vectorof electricalactivityRecording axis oflead aVF (vertical,downward)Lead aVFAV nodePCommon bundleof HisRRight and leftbundle branchesFigure 9.2 Cardiac Depolarization and Repolarization Part I This series of figures (Figs.
9.2 to 9.4) depicts the sequence of cardiacelectrical events during the cardiac cycle and the surface recordings that result from these events and constitute the ECG. The initial events aredepicted above, in which the firing of the SA node results in depolarization of the atria, recorded on the ECG as the P wave.
This depolarizationspreads to the AV node, the bundle of His, and bundle branches, with the resultant electrical activity vectors and surface ECG recordings. Note thatthe morphology of the ECG recording varies with lead placement.Cardiac ElectrophysiologyNormal Sequence of Cardiac Depolarization and Repolarizationand Derivation of ECG (continued)PRC. Apical and early ventricular depolarizationImpulse continues along conduction system, causingdepolarization of apical ventricular myocardium withelectrical vector directed downward and to left. Thisresults in large positive (upward) deflection (R wave) inlead I and extends R wave in lead aVF.105Lead IQRecording axis oflead I (horizontal,right to left)Resultant vectorof electricalactivityRecording axis oflead aVF (vertical,downward)Lead aVFRPRPD.
Late ventricular depolarizationAs depolarization progresses over ventricles, vector shiftsto become directed superiorly as well as to left, thusextending upward R wave in lead I and causing negative(downward) deflection (S wave) in lead aVF.QPurkinje fibersResultant vectorof electricalactivityRecording axis oflead I (horizontal,right to left)Recording axis oflead aVF (vertical,downward)Lead aVFRPSFigure 9.3 Cardiac Depolarization and Repolarization Part II Septal depolarization (see Fig. 9.2) is followed by apical and ventricularwall depolarization; resultant vectors of electrical activity produce the QRS complex of the ECG.106Cardiovascular PhysiologyNormal Sequence of Cardiac Depolarization and Repolarizationand Derivation of ECG (continued)RE.
RepolarizationWhen heart is fully depolarized, there is no electrical activityfor brief period (ST segment). Then repolarization begins fromepicardium to endocardium, producing electrical vectordirected downward and to left, causing upward (positive)deflection in both leads I and aVF (T waves). A period of noelectrical activity follows, with tracing at baseline until nextimpulse originates at SA node.Lead ITPQRecording axis oflead I (horizontal,right to left)Resultant vectorof electricalactivityRecording axis oflead aVF (vertical,downward)Lead aVFRTPSF.
Summary of cardiac electrical activitySA nodeAtrialdepolarizationvector1Late ventriculardepolarization vector4AV node (pausein conduction)5Common bundleof HisRepolarizationvector2Apical andearly leftventriculardepolarizationvectorLeft and rightbundle branches3Septal depolarizationvectorFigure 9.4 Cardiac Depolarization and Repolarization Part III Ventricular depolarization (see Fig. 9.3) is followed by ventricular repolarization; the resultant vector of electrical activity produces the T wave of the ECG. The cardiac electrical activity and resultant vectors (1-5) throughthe cycle are summarized in F.107CHAPTER10Flow, Pressure, and ResistanceHemodynamics is the study of the forces involved in circulation of blood.
Although arterial blood pressure is a convenientand readily measured parameter, understanding the broaderhemodynamic state of an individual is essential when assessing cardiovascular disease.BASIC HEMODYNAMICSThe rate of flow through the circulation (Q) is determined bythe pressure gradient across the circulation (ΔP) and the resistance of the circulation (R):Q = ΔP/RPressure is defined as force per unit area. For example, in anauto tire, pressure is measured as pounds per square inch(PSI).
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