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Cardiac Arrhythmias(Part 2)

Hemodynamic Sequelae of Cardiac ArrhythmiasBy PHILIP SAMET, M.D.

SUMMARYThe hemodynamic consequences of cardiac arrhythmias depend on various factors, including

the ventricular rate and the duration of the abnormal rate, the temporal relationship betweenatrial and ventricular activity, the sequence of ventricular activation, the functional state of theheart, the irregularity of the cycle length, associated drug therapy, the peripheral vascular vaso-motor system, disease in organ systems other than the heart, and the degree of anxiety caused bythe disease processes. Sinus bradyeardia, even with rates as low as 40 beats/min, may not be asso-ciated with significant hemodynamic consequences unless the stroke volume is limited by myo-cardial or valvular disease, as in acute myocardial infarction. Cardiac output usually, but notinvariably, falls when atrial fibrillation replaces normal sinus rhythm, even at comparable ven-tricular rates, both at rest and during exercise. Similar observations have been made during thedevelopment of atrial flutter despite the persistence of effective mechanical atrial activity in atleast some cases. Marked hemodynamic changes are frequent in the course of ventricular tachy-cardia with systemic arterial hypotension, a decrease in cardiac output, and evidence of cerebral,coronary, and renal vascular insufficiency. Cyclic variations in systemic and pulmonary arterialpressures are common during atrioventricular dissociation. Cardiac output is generally depressedduring the severe bradyeardia of acquired complete heart block with evidence of atrioventric-ular valvular insufficiency. Increase of the heart rate by ventricular pacing reverses all or someof these abnormalities. The changes in congenital complete heart block are considerably less se-vere because myocardial insufficiency is less frequently seen in congenital complete heart block.

T HE PAST DECADE has witnessed a rebirthof interest in cardiac arrhythmias. This devel-

opment has extended beyond considerations of theclinical and electrocardiographic differential diag-nosis to evaluation of the hemodynamic and clinicalsequelae of the arrhythmias.A number of investigatorsl-5 have stressed the

concept that the physiologic consequences ofcardiac arrhythmias are caused by: (1) changes inventricular rate and the duration of these changes;(2) the effect of atrial function including thetemporal relationships between atrial and ventricu-lar activity, atrioventricular valvular function,strength and effectiveness of atrial mechanical

From the Division of Cardiology, Department ofMedicine, Mount Sinai Hospital of Greater Miami, MiamiBeach, Florida, and the University of Miami School ofMedicine, Miami, Florida.

Circulation, Volume XLVII, February 1973

activity, and storage function of the atria; (3) thesequence of ventricular activation; (4) functionalstate of the heart; (5) the irregularity of the cyclelength of the arrhythmia; (6) drug therapy;(7) preservation of vasomotor control mechanisms;(8) The superimposed presence or absence of an-xiety; and (9) disease in other organ systems.

Changes in Ventricular Rate

Modest increments in ventricular rate (185-230beats/min) produced by atrial pacing result in onlysmall and transient decreases in cardiac output inthe dog.6 7 The changes in systemic arterial bloodpressures and coronary blood flow are minimal.Further increments in ventricular rate followingatrial pacing caused clear-cut decrements in theseparameters.A substantial body of data has accumulated in

man as to the effect of variations in heart rate. Rosset al.8 reported "no striking alterations in the

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cardiac index occurred" during the use of rightatrial pacing alone to increase the ventricular rate:increases in heart rate from 80 to 121 beats/minaltered cardiac index from 3.67 to 3.72 liters/min/m2. Further increases in atrial pacingrate caused a small decrease in flow to 3.2liters/min/m2. Stein et al.9 reported similar results.On the other hand Samet et al.10 reported data onthe effect of right atrial pacing in 33 normalsubjects and 136 patients with cardiac or pulmonarydisease. These latter data demonstrated that cardiacoutput increases in a statistically (but not physio-logically) significant manner as the ventricular rateis increased modestly (to rates of 60-89 beats/min).Further rate increments produced no further outputchanges as the rate was increased to levels of 90-110and 110-140 beats/min. Yoshida et al.11 came tosimilar conclusions. The therapeutic value oftemporary right atrial pacing in management ofthe patient after open-heart surgery has beenstressed.12' 13 Augmentation of cardiac output isprobably the primary beneficial hemodynamiceffect of postoperative pacing. Increase in atrial andventricular rate to 180 beats/min in man followingright atrial pacing was followed by a fall in cardiacoutput in normal subjects; output fell at pacingrates above 140 in cardiac patients.'4 Inadequatediastolic ventricular filling periods are the probablecause of these results. Data as to the effect of long-tern increases in atrial and ventricular rate uponcardiovascular dynamics in man are not available.An experimental study on the effects of increasing

heart rate on the force-velocity relationships of theleft ventricle has provided a basis for understandingthe small increases in output observed by someinvestigators during atrial pacing. While meanaortic and left ventricular end-diastolic pressureswere maintained constant, the heart rate wasincreased by atrial pacing. This shifted theisovolumic force-velocity curve up to the right withincrease ii, maximum contractile element velocityand maximum isovolumic tension. These effectswere evident despite shortening of the phases ofsystole.'5 These changes probably provide thesubstrate for an increase in output.

Effect of Atrial FunctionThe basic function of the atrium is to aid in blood

transport into the ventricle by atrial systole and toaid in closure of the atrioventricular valves therebyfacilitating ventricular filling while left atrial meanpressure is maintained at a normal level.

Temporal Relationships between Atrial andVentricular Activity

It has long been appreciated that significantchanges in cardiac dynamics follow interruption ofnormal sequential atrioventricular electrical andmechanical activity both in the experimental animaland in man.'-3, 5 6. 16. 17 The so-called "boosterpump action of the atria" in increasing ventricularvolume at end-diastole is 15-20% larger during atrialthan during ventricular pacing.5 P-wave synchro-nous pacing (in complete heart block) elevatescardiac output by 10-15% more than does ventricularpacing at the same ventricular rates.18 Theseobservations apply to ventricular rates of 60-100beats/min as well as faster ventricular rates as highas 130-140 beats/min. The optimal P-R interval is0.10-0.20 sec.'9 As the heart rate increases, the P-Rinterval effect is increased.20 The atrial contributionmay also be more significant in the presence ofmyocardial dysfunction.

Atrioventricular Valvular FunctionA properly timed atrial systole results in essential-

ly a presystolic reversed atrioventricular gradient,21placing the atrioventricular valve leaflets in aposition to close early with the onset of ventricularsystole and thus prevent atrioventricular valvularregurgitation. Such regurgitation, in addition to theabsence of the booster pump action of the atrium(atrial kick) may be responsible for the lowercardiac output during ventricular as compared toatrial pacing.

Atrial Mechanical ActivityDissociation between the effects of the ventricu-

lar irregularity per se, the rapid ventricular rate,and the lack of effective atrial mechanical activityis not always achieved in studies of atrial fibrillationand flutter. Skinner et al.22 studied the effects ofatrial fibrillation at constant ventricular rates in thedog during ventricular pacing. Removal of theeffective atrial contribution resulted in a rise of leftatrial mean pressure despite a decrease in leftventricular and end-diastolic pressure, a fall inaortic pressure, and a decrease in output. Aventricular systolic rise in left atrial pressure wasseen only during atrial fibrillation. These effects canalso be observed in man.The effect of loss of atrial mechanical activity in

atrial fibrillation in man is somewhat difficult toanalyze because of the multiplicity of factorsinvolved in the studies in the literature. Theseinclude the effect of drugs and anesthesia plus the


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SEQUELAE OF ARRHYTHMIAS

problems mentioned above, i.e. the increase inventricular rate and ventricular irregularity changesper se in addition to the loss of atrial mechanicalactivity. Morris et al.23 studied 11 patients beforeand after cardioversion under light thiobarbiturateanesthesia (duration 12-30 min). The averageventricular rate and cardiac index before and 2hours after cardioversion were 78 beats/min and4.41 liters/min/m2 before and 86 and 5.31 after-ward, P <0.05 for the output increase. Oxygenconsumption was identical (316 ml/min/m2 control,318 after cardioversion) in the two studies. Outputrose more than 0.5 liters/min in seven of the 11patients after conversion. Five of the 11 patientswere also exercised before and after electricalshock. The control exercise data was oxygenconsumption 1002 ml/min/m2, heart rate 110beats/min, and output 8.36 liters/min; the postcon-version figures were 988, 118, and 9.80, respectively.The average output changes were significant,P < 0.01. All five patients exhibited a significantoutput rise during exercise. Rodman et al. studied19 patients (generally without anesthesia) before,immediately after, and 1, 2, and 3 hours aftercardioversion from atrial fibrillation to sinusrhythm.24 Despite considerable individual variation,cardiac index rose from a control level of 2.36 to2.40, 2.45, 2.56, and 2.65 liters/min/m2 at the fourstated times after cardioversion. The average heartrate was 73 control and 70-74 beats/min aftercardioversion. Full interpretation of the availabledata poses problems ranging from contradictorydata reporting no change in output at rest followingcardioversion without a fall in ventricular rate,25 toobservations at rest showing output increment notimmediately after conversion but only days later,26to observations reporting more significant effects oncardioversion during exercise than at rest.27 Carltonand co-workers have stressed that atrial systoleaugments cardiac output and left ventricular dp/dtin patients without valvular heart disease but doesnot do so in the presence of mitral stenosis; study of11 patients with mitral stenosis and atrial fibrillationduring right ventricular pacing to induce artificialtachycardia led to the conclusion that the functionaldeterioration often seen in patients with mitralstenosis with atrial fibrillation is due to ventricularrate increase rather than loss of atrial systole.28 Ithas been noted that following successful cardiover-sion right atrial a waves may occur in the absenceof left atrial a waves even in the presence of Pwaves on the electrocardiogram;29 i.e., right atrialCi(rculation, Volume XLVII, February 1973

function recovers more rapidly than left atrialfunction.

Storage Function of the AtriumThe atria also serve as conduit and storage areas

between the great veins and the ventricles.

Sequence of Ventricular Activation

It has been stated that the sequence of ventricu-lar activation and contraction has significant effectson cardiovascular dynamics. The fact that somecardiac pacing studies demonstrate differences instroke output of up to 100% secondary to changingthe site of ventricular stimulation has been inter-preted as demonstrating the importance of alteredventricular sequence of contraction. However,studies in man have suggested that an abnormalpathway of ventricular depolarization is of littlehemodynamic import.5 In analysis of the cause ofthe hemodynamic differences between atrial andventricular pacing, two possible explanations weresuggested-the absence of the atrial kick andabnormal depolarization during ventricular pacing.Observations were therefore made during atrial,ventricular, and sequential atrioventricular pacingto separate these two factors. The latter was doneby applying paired pacing stimuli to the rightatrium and right ventricle, at an interval less thanthe control P-R interval for a given subject. Duringsequential atrioventricular pacing the effect of theatrial kick is preserved in the face of abnormalventricular depolarization. The results of studies inpatients with normal hearts and with heart diseasedemonstrated that the cardiac outputs duringsequential atrioventricular pacing were only slightlyless than those during atrial pacing and that bothwere significantly greater than the outputs duringventricular pacing. Abnormal ventricular depolar-ization per se produced little effect on cardiacoutput.The data suggest that asynchronous ventricular

activation has relatively little hemodynamic effect,and are consistent with older observations thatsignificant mechanical ventricular asynchronism isnot a necessary consequence of the electricalventricular asynchronism of bundle-branch block orventricular premature beats.30 Braunwald andMorrow31 studied five patients with complete leftbundle-branch block and 10 with complete rightbundle-branch block. None of the former exhibiteddelay in onset of left ventricular contraction, andonly four of the latter patients had as much as a

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0.04-sec delay in onset of right ventricular contrac-tion. Bourassa et al. have, however, presented datato the contrary in a patient with intermittent leftbundle-branch block.32

Functional State of the Heart

It can readily be appreciated that any givencardiac arrhythmia may be better tolerated whenthe underlying myocardium is normal. Patients withcongenital complete heart block are better able totolerate severe bradyeardia than patients withacquired complete heart block. In the former groupthe ability to compensate for bradyeardia byincreasing the stroke volume is greater than inpatients with acquired block. Even minor arrhyth-mias may be hemodynamically significant in theface of severe myocardial disease.

Irregularity of Cycle Length of the Arrhythmia

The irregular pulse rate observed in manyarrhythmias, especially atrial fibrillation, may per sehave definite hemodynamic effects. Potentiation is akey mechanism for some of these effects. Potentia-tion is a mechanism in which an early ventriculardepolarization augments the force of contraction ofthe succeeding contraction.33 4 Greenfield et al.35noted that peak flow, peak power, and stroke workcorrelated best with the two previous R-R intervals,not simply the preceding cycle length. A secondmechanism whereby cardiac irregularities producehemodynamic effects is via Starling's law of theheart. Braunwald et al.36 performed studies in 26adult patients with atrial fibrillation at operation.Measurements of the length of a segment of the leftventricle by means of a mercury-filled resistancegauge were made together with arterial pressureand left ventricular end-diastolic pressure. Varia-tions of end-diastolic segment length and pressuredue to changing duration of diastole were mea-sured. Changes in end-diastolic segment lengthcorrelated with peak systolic ventricular pressures.The longer the preceding cycle length in the atrialfibrillation, the greater is the length of the leftventricular segment.A third mechanism is change in the refractory

period of various cardiac tissues associated withsudden rate changes. As many as the 12 precedingcycles may affect the refractory period. An abruptchange from slow to rapid ventricular rates shortensthe refractory period maximally in the first beat andprogressively less in subsequent beats.37 Suchchanges in refractory period may be responsible forrate changes in arrhythmias.

Drug Therapy

Just as the state of the myocardium may influencethe hemodynamic effects of cardiac arrhythmias, somay drugs alter the consequence of arrhythmias.These effects may result from direct drug effect onthe myocardium or from effects on the peripheralvascular system. In addition, the drug involved mayitself cause an arrhythmia.

Preservation of Vasomotor Control Mechanisms

The response to similar cardiac arrhythmias maybe quite varied in different patients. At least part ofthese differences may be due to the status of theperipheral vascular system and its control mecha-nism. For example, Skinner et al.22 noted thatbilateral vagotomy, with control of carotid sinuspressure, blunted the compensatory mechanismswhich modified the hemodynamic consequences ofacute induced atrial fibrillation in the dog. Drugs,circulating catecholamines, altered blood volume,redistribution of blood volume, venous tone,neurogenic reflexes, or intrinsic disease may thusalter the effects of cardiac arrhythmias.

Superimposed Mental Status of the Patient,i.e. Level of Anxiety

Cardiac arrhythmias may result in anxietyresponses on the part of the patient. Outpouring ofcatecholamines may result38 with secondary effectson the cardiac rhythm as well as the peripheralvascular system.

Disease in Other Organ Systems

The hemodynamic effect of arrhythmias may alsobe conditioned by disease processes in other organs.Atherosclerosis of the bowel vessels may result insymptoms secondary to the arrhythmia which mightbe absent in patients without such vascularinvolvement. Mild pulmonary congestion in apatient with obstructive pulmonary emphysemamay result in more profound symptomatology thanin the presence of otherwise normal lungs. Anemiamay also modify the hemodynamic result of cardiacarrhythmias.

Effect of Arrhythmias onRegional Blood Flow

Several lines of evidence indicate that thecerebral circulation may be compromised bycardiac arrhythmias. The electromagnetic flowmeterwas employed to measure cerebral blood flow(carotid artery flow) during the control sinusrhythm, and various arrhythmias in the dog.39 Theflow decrement averaged 7-12% during premature


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beats, 14% during supraventricular tachycardia, 23%during atrial fibrillation, and 40-75% during ventric-ular tachycardia. The clinical counterpart of theseexperimental observations is well established.40 A10-hour taped electrocardiogram was recorded in 39adult patients with symptoms of cerebral ischemia.Ten of the 39 patients exhibited arrhythmias withbradyeardia below 40 beats/min or heart ratesabove 150 beats/min. Morgagni-Stokes-Adams epi-sodes in complete heart block have, of course, beenwell known for many years. Electrical pacing withcorrection of the bradyeardia was associated with a

significant increase in cerebral blood flow.41 Coro-nary artery flow may be reduced by atrial or

ventricular premature systoles, atrial and ventricu-lar tachycardia, and atrial fibrillation.42 The clinicalcounterparts of these experimental data are wellknown.43 Posttachyeardia T-wave inversion is fre-quently seen even in young individuals with normalcoronary circulations. Cardiac arrhythmias may alsobe associated with reduction in renal and mesenter-ic blood flow in the dog. Marked polyuria44 is oftenseen in patients during supraventricular tachycar-dia. Lower rhythm nephrosis may complicatearrhythmias.45

Specific Arrhythmias

Sinus BradycardiaEven ventricular rates below 40-45 beats/min are

often not associated with severe hemodynamicconsequences if the stroke volume is not limited bymyocardial or valvular disease. In one group of 17patients with only sinus bradyeardia (Hildner FJ,Narula OS, Samet P: Unpublished data), theventricular rate ranged from 37 to 59 beats/min(average 49). The average cardiac index was

1.93.Patients with acute myocardial infarction and

sinus bradyeardia are often prone to increasedvagal and vasovagal reactions with hypotensiveepisodes. Bradycardia, inability to increase strokevolume due to decreased myocardial reserve, andinadequate peripheral vasomotor controls all con-

tribute to the problem.46 The bradyeardia andhypotension may, in turn, predispose to seriousventricular arrhythmias and ventricular standstillespecially in the presence of an acute myocardialinfarction.

Supraventricular TachycardiaThe hemodynamic differences between nodal-and

atrial tachycardia relate primarily to the incidenceof atrioventricular dissociation in the former but not

Cifculation, Volume XLVII, February 1973

the latter and to ventricular rate differences. Theeffects of atrial tachycardia depend on the myocar-dial state, duration of the rhythm, and heart rate.As the heart rate increases in atrial tachycardia,there is, at most, only a small change in cardiacoutput in the experimental laboratory, until rates of160-230 beats/min are recorded, at least in normalhearts; at faster rates the output may then fall. Thefall in output may occur at slower rates in thediseased heart. Several studies in man2' 47 haverevealed little change in cardiac output at the onsetof atrial tachycardia. A fall in systemic arterialpressure may occur especially when in the uprightposition. Right atrial and pulmonary artery wedgepressures rose especially at the onset of tachycardiaprobably secondary to inadequate diastolic ventric-ular filling. Systemic pulsus alternans has beenreported.47 The occasional development of heartfailure or angina pectoris during supraventriculartachycardia is the clinical counterpart of thephysiologic hemodynamic changes. Study of twopatients with nodal tachycardia and the Wolff-Parkinson-White syndrome3 revealed evidence oftricuspid regurgitation with right atrial hyperten-sion.

Atrial FlutterMechanical atrial activity may persist in atrial

flutter unlike atrial fibrillation. Atrial contractions atrates of 300/min may be present. Cardiac outputwas decreased in nine patients with atrial flutter,five with heart failure (index 1.48-2.48), three withheart disease not in failure (index 1.67-2.10), andone without heart disease, cardiac index 2.57.48 Infive patients studied in flutter and sinus rhythm, theindex rose 40% on conversion to sinus rhythm as theventricular rate also fell.48 Digitalization in fourpatients resulted in a significant rise in output witha significant decrease in heart rate and persistenceof atrial flutter. A single patient was studied in sinusrhythm, atrial fibrillation, and atrial flutter duringboth rest and exercise,49 with comparable oxygenconsumptions during the three rest and threeexercise periods. The three resting ventricular rateswere virtually identical. The cardiac indices wereidentical during sinus rhythm and atrial fibrillationbut fell slightly in atrial flutter. During exercise, thecardiac index was greater during sinus rhythm thanduring the atrial arrhythmias.

Atrial FibrillationThe development of the right atrial electrogram

has demonstrated that differentiation between atrial

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fibrillation and supraventricular tachycardia is notalways possible on the basis of the surfaceelectrocardiogram. Intracardiac recordings may berequired for this purpose. Comments on thehemodynamic changes during atrial fibrillationwere made above.The hemodynamic data observed in patients with

atrial fibrillation during exercise deserve comment.Most studies have revealed significant hemodynam-ic improvement after conversion to sinus rhythm.Graettinger et al.25 studied 17 patients duringexercise in both atrial fibrillation and normal sinusrhythm. Oxygen consumption was very similarduring both rhythms, but the average cardiac indexrose from 2.98 to 3.20 while the respective heartrates fell from 127 to 98 on conversion. Benchimolet al.50 studied eight patients during exercise inboth rhythms and observed an 8% rise in cardiacoutput after conversion with a 30% rise in strokevolume since the heart rate fell 24%. Separation ofthe effects of rhythm change from heart rate changeis difficult. Another observer reported that, inselected patients, exercise tolerance may not beaffected by atrial fibrillation.5'

Ventricular TachycardiaThe hemodynamic effects of spontaneous rapid

ventricular tachycardia in the experimental animalinclude hypotension, a fall in cardiac output, andevidence of cerebral, coronary, and renal vascularinsufficiency.6 38 Pulmonary arterial and left andright atrial pressures may increase.38 The effect ofventricular tachycardia may also be observed inman by simulated ventricular tachycardia, i.e.ventricular pacing.' 2 5. 6 13 16 These studies clearlyreveal that systemic hypotension, cyclic variationsin systemic and right heart pressures, and decreasesin cardiac output regularly occur even when theeffect of rate, per se, is eliminated by comparingatrial and ventricular pacing at similar ventricularrates. The abnormal dynamics during ventricularpacing or ventricular tachycardia are probably dueto both the rapid rates and the absence ofsequential atrial-ventricular activity. Thus, thehemodynamic abnormalities seen in ventriculartachycardia are often more severe than those insupraventricular tachycardia even at the sameoverall ventricular rate. The importance of theventricular rate per se in the hemodynamics ofventricular rhythms has been stressed by recogni-tion of the relatively benign course of someventricular rhythms (rates 60-90) in the course ofacute myocardial infarction. The abnormal dynam-

ics of ventricular tachycardia are accentuatedduring ventricular fibrillation when effective circu-lation ceases.

Brady-Tachyarrhythmia Syndrome (Sick Sinus Syndrome)The frequency of this syndrome in which slow

and rapid ventricular rates alternate has recentlybeen recognized.5` The hemodynamic effects varywith the different arrhythmias present in a givencase.

Complete Heart BlockLevinson et al.53 studied five patients in acquired

heart block not in failure. Right heart pressureswere elevated. Systemic and right heart pulsepressures are widened. The heart rates are 45-55when the QRS complex is narrow, i.e. originatesabove the bifurcation of the His bundle. The rate is30-45 when the ventricular focus is idioventricularin origin. The cardiac output was decreased but thestroke volume was elevated. Stark et al.54 madecomparable observations in eight patients. Rightventricular end-diastolic pressure was generallynormal. In the presence of heart failure, markedfurther decrease in cardiac output was observed.Samet'5 reported low cardiac indices in 24 subjectsnot in failure. The abnormalities observed in thesepatients probably result from a slow rate, myocardi-al disease, plus abnormal P-QRS temporal relation-ships. The hemodynamic data in congenital heartblock are somewhat different from those inacquired complete heart block. The effects ofassociated myocardial disease are probably absentin these patients. The heart rates are somewhatfaster (40-80/min). The cardiac output is usuallynormal. Right heart pressures are generally close tonormal. Right ventricular end-diastolic pressure isnormal or minimally elevated.56

Exercise studies in acquired complete heart blockhave revealed a further increase in the already largestroke volume and a rise in cardiac output if leftventricular function is relatively normal. If myocar-dial function is depressed, the stroke volume maybe fixed during exercise.57 The heart rate isgenerally constant during exercise in acquiredcomplete heart block. In congenital complete heartblock, the ventricular rate and cardiac outputusually rise during exercise, as myocardial functionis commonly normal.58When the heart rate is increased by ventricular

pacing in patients in complete heart block, thecardiac output generally rises.4 ' 59 A bell-shaped curve is often noted and the output may fall


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as the rate rises above 100 beats/min. P-wavesynchronous pacing results in larger cardiac outputsthan obtained during ventricular pacing at similarventricular rates.18

Atrial, Nodal, and Ventricular Premature BeatsThe effect of premature beats depends on several

factors including the underlying heart disease, thedegree of prematurity of the beat, the frequencyand the site, i.e. atrial or ventricular, and the P-QRStemporal relationship.1 A very early premature beatmay have little or no mechanical effect, with evenlittle effect on the ventricular pressure curve. Theelectrical heart rate is then greater than theeffective mechanical heart rate, as in the postextra-systolic potentiation phenomena.33 34 If the prema-ture beat is somewhat later in the cardiac cycle, amechanical ventricular pressure curve may begenerated, but the level of pressure achieved maynot be sufficient to open the correspondingsemilunar valve. Premature beats in mid-to-latediastole will usually have less abnormal hemody-namic effects than earlier beats. The left ventricularpulse pressure and systolic pressure peak and thesystemic arterial pulse pressure increase after thecompensatory pause of a ventricular prematurebeat except for patients with idiopathic hyper-trophic subaortic stenosis. In these individuals thesystemic arterial pulse pressure falls after aventricular premature beat due to the increasedcontractility observed after the premature beat.60The hemodynamic sequelae of premature beats

also depend on the site of origin, i.e. whether or notnormal atrioventricular sequential activity is main-tained. The site of origin of ventricular prematurebeats is believed by some investigators to influencethe hemodynamic effect of such beats.6' Otherstudies have, however, cast doubt on the importanceof the sites of ventricular stimulation.62

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PHILIP SAMETHemodynamic Sequelae of Cardiac Arrhythmias

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cardiac arrhythmias (part 2) -...

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