Download Cardiac Arrhythmias (Part 2)

SYMPOSIUM
Cardiac Arrhythmias
(Part 2)
Hemodynamic Sequelae of Cardiac Arrhythmias
By PHILIP SAMET, M.D.
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
SUMMARY
The hemodynamic consequences of cardiac arrhythmias depend on various factors, including
the ventricular rate and the duration of the abnormal rate, the temporal relationship between
atrial and ventricular activity, the sequence of ventricular activation, the functional state of the
heart, the irregularity of the cycle length, associated drug therapy, the peripheral vascular vasomotor system, disease in organ systems other than the heart, and the degree of anxiety caused by
the disease processes. Sinus bradyeardia, even with rates as low as 40 beats/min, may not be associated with significant hemodynamic consequences unless the stroke volume is limited by myocardial or valvular disease, as in acute myocardial infarction. Cardiac output usually, but not
invariably, falls when atrial fibrillation replaces normal sinus rhythm, even at comparable ventricular rates, both at rest and during exercise. Similar observations have been made during the
development of atrial flutter despite the persistence of effective mechanical atrial activity in at
least some cases. Marked hemodynamic changes are frequent in the course of ventricular tachycardia with systemic arterial hypotension, a decrease in cardiac output, and evidence of cerebral,
coronary, and renal vascular insufficiency. Cyclic variations in systemic and pulmonary arterial
pressures are common during atrioventricular dissociation. Cardiac output is generally depressed
during the severe bradyeardia of acquired complete heart block with evidence of atrioventricular valvular insufficiency. Increase of the heart rate by ventricular pacing reverses all or some
of these abnormalities. The changes in congenital complete heart block are considerably less severe because myocardial insufficiency is less frequently seen in congenital complete heart block.
T HE PAST DECADE has witnessed a rebirth
of interest in cardiac arrhythmias. This development has extended beyond considerations of the
clinical and electrocardiographic differential diagnosis to evaluation of the hemodynamic and clinical
sequelae of the arrhythmias.
A number of investigatorsl-5 have stressed the
concept that the physiologic consequences of
cardiac arrhythmias are caused by: (1) changes in
ventricular rate and the duration of these changes;
(2) the effect of atrial function including the
temporal relationships between atrial and ventricular activity, atrioventricular valvular function,
strength and effectiveness of atrial mechanical
From the Division of Cardiology,
activity, and storage function of the atria; (3) the
sequence of ventricular activation; (4) functional
state of the heart; (5) the irregularity of the cycle
length of the arrhythmia; (6) drug therapy;
(7) preservation of vasomotor control mechanisms;
(8) The superimposed presence or absence of anxiety; and (9) disease in other organ systems.
Changes in Ventricular Rate
Modest increments in ventricular rate (185-230
beats/min) produced by atrial pacing result in only
small and transient decreases in cardiac output in
the dog.6 7 The changes in systemic arterial blood
pressures and coronary blood flow are minimal.
Further increments in ventricular rate following
atrial pacing caused clear-cut decrements in these
parameters.
A substantial body of data has accumulated in
man as to the effect of variations in heart rate. Ross
et al.8 reported "no striking alterations in the
Department of
Medicine, Mount Sinai Hospital of Greater Miami, Miami
Beach, Florida, and the University of Miami School of
Medicine, Miami, Florida.
Circulation, Volume XLVII, February 1973
399
SAMET
400
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
cardiac index occurred" during the use of right
atrial pacing alone to increase the ventricular rate:
increases in heart rate from 80 to 121 beats/min
altered cardiac index from 3.67 to 3.72 liters/
min/m2. Further increases in atrial pacing
rate caused a small decrease in flow to 3.2
liters/min/m2. Stein et al.9 reported similar results.
On the other hand Samet et al.10 reported data on
the effect of right atrial pacing in 33 normal
subjects and 136 patients with cardiac or pulmonary
disease. These latter data demonstrated that cardiac
output increases in a statistically (but not physiologically) significant manner as the ventricular rate
is increased modestly (to rates of 60-89 beats/min).
Further rate increments produced no further output
changes as the rate was increased to levels of 90-110
and 110-140 beats/min. Yoshida et al.11 came to
similar conclusions. The therapeutic value of
temporary right atrial pacing in management of
the patient after open-heart surgery has been
stressed.12' 13 Augmentation of cardiac output is
probably the primary beneficial hemodynamic
effect of postoperative pacing. Increase in atrial and
ventricular rate to 180 beats/min in man following
right atrial pacing was followed by a fall in cardiac
output in normal subjects; output fell at pacing
rates above 140 in cardiac patients.'4 Inadequate
diastolic ventricular filling periods are the probable
cause of these results. Data as to the effect of longtern increases in atrial and ventricular rate upon
cardiovascular dynamics in man are not available.
An experimental study on the effects of increasing
heart rate on the force-velocity relationships of the
left ventricle has provided a basis for understanding
the small increases in output observed by some
investigators during atrial pacing. While mean
aortic and left ventricular end-diastolic pressures
were maintained constant, the heart rate was
increased by atrial pacing. This shifted the
isovolumic force-velocity curve up to the right with
increase ii, maximum contractile element velocity
and maximum isovolumic tension. These effects
were evident despite shortening of the phases of
systole.'5 These changes probably provide the
substrate for an increase in output.
Effect of Atrial Function
The basic function of the atrium is to aid in blood
transport into the ventricle by atrial systole and to
aid in closure of the atrioventricular valves thereby
facilitating ventricular filling while left atrial mean
pressure is maintained at a normal level.
Temporal Relationships between
Ventricular Activity
Atrial and
It has long been appreciated that significant
changes in cardiac dynamics follow interruption of
normal sequential atrioventricular electrical and
mechanical activity both in the experimental animal
and in man.'-3, 5 6. 16. 17 The so-called "booster
pump action of the atria" in increasing ventricular
volume at end-diastole is 15-20% larger during atrial
than during ventricular pacing.5 P-wave synchronous pacing (in complete heart block) elevates
cardiac output by 10-15% more than does ventricular
pacing at the same ventricular rates.18 These
observations apply to ventricular rates of 60-100
beats/min as well as faster ventricular rates as high
as 130-140 beats/min. The optimal P-R interval is
0.10-0.20 sec.'9 As the heart rate increases, the P-R
interval effect is increased.20 The atrial contribution
may also be more significant in the presence of
myocardial dysfunction.
Atrioventricular Valvular Function
A properly timed atrial systole results in essentially a presystolic reversed atrioventricular gradient,21
placing the atrioventricular valve leaflets in a
position to close early with the onset of ventricular
systole and thus prevent atrioventricular valvular
regurgitation. Such regurgitation, in addition to the
absence of the booster pump action of the atrium
(atrial kick) may be responsible for the lower
cardiac output during ventricular as compared to
atrial pacing.
Atrial Mechanical Activity
Dissociation between the effects of the ventricular irregularity per se, the rapid ventricular rate,
and the lack of effective atrial mechanical activity
is not always achieved in studies of atrial fibrillation
and flutter. Skinner et al.22 studied the effects of
atrial fibrillation at constant ventricular rates in the
dog during ventricular pacing. Removal of the
effective atrial contribution resulted in a rise of left
atrial mean pressure despite a decrease in left
ventricular and end-diastolic pressure, a fall in
aortic pressure, and a decrease in output. A
ventricular systolic rise in left atrial pressure was
seen only during atrial fibrillation. These effects can
also be observed in man.
The effect of loss of atrial mechanical activity in
atrial fibrillation in man is somewhat difficult to
analyze because of the multiplicity of factors
involved in the studies in the literature. These
include the effect of drugs and anesthesia plus the
Circulation, Volume XLVII, February 1973
401
SEQUELAE OF ARRHYTHMIAS
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
problems mentioned above, i.e. the increase in
ventricular rate and ventricular irregularity changes
per se in addition to the loss of atrial mechanical
activity. Morris et al.23 studied 11 patients before
and after cardioversion under light thiobarbiturate
anesthesia (duration 12-30 min). The average
ventricular rate and cardiac index before and 2
hours after cardioversion were 78 beats/min and
4.41 liters/min/m2 before and 86 and 5.31 afterward, P <0.05 for the output increase. Oxygen
consumption was identical (316 ml/min/m2 control,
318 after cardioversion) in the two studies. Output
rose more than 0.5 liters/min in seven of the 11
patients after conversion. Five of the 11 patients
were also exercised before and after electrical
shock. The control exercise data was oxygen
consumption 1002 ml/min/m2, heart rate 110
beats/min, and output 8.36 liters/min; the postconversion figures were 988, 118, and 9.80, respectively.
The average output changes were significant,
P < 0.01. All five patients exhibited a significant
output rise during exercise. Rodman et al. studied
19 patients (generally without anesthesia) before,
immediately after, and 1, 2, and 3 hours after
cardioversion from atrial fibrillation to sinus
rhythm.24 Despite considerable individual variation,
cardiac index rose from a control level of 2.36 to
2.40, 2.45, 2.56, and 2.65 liters/min/m2 at the four
stated times after cardioversion. The average heart
rate was 73 control and 70-74 beats/min after
cardioversion. Full interpretation of the available
data poses problems ranging from contradictory
data reporting no change in output at rest following
cardioversion without a fall in ventricular rate,25 to
observations at rest showing output increment not
immediately after conversion but only days later,26
to observations reporting more significant effects on
cardioversion during exercise than at rest.27 Carlton
and co-workers have stressed that atrial systole
augments cardiac output and left ventricular dp/dt
in patients without valvular heart disease but does
not do so in the presence of mitral stenosis; study of
11 patients with mitral stenosis and atrial fibrillation
during right ventricular pacing to induce artificial
tachycardia led to the conclusion that the functional
deterioration often seen in patients with mitral
stenosis with atrial fibrillation is due to ventricular
rate increase rather than loss of atrial systole.28 It
has been noted that following successful cardioversion right atrial a waves may occur in the absence
of left atrial a waves even in the presence of P
waves on the electrocardiogram;29 i.e., right atrial
Ci(rculation, Volume XLVII, February 1973
function recovers more rapidly than left atrial
function.
Storage Function of the Atrium
The 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 ventricular activation and contraction has significant effects
on cardiovascular dynamics. The fact that some
cardiac pacing studies demonstrate differences in
stroke output of up to 100% secondary to changing
the site of ventricular stimulation has been interpreted as demonstrating the importance of altered
ventricular sequence of contraction. However,
studies in man have suggested that an abnormal
pathway of ventricular depolarization is of little
hemodynamic import.5 In analysis of the cause of
the hemodynamic differences between atrial and
ventricular pacing, two possible explanations were
suggested-the absence of the atrial kick and
abnormal depolarization during ventricular pacing.
Observations were therefore made during atrial,
ventricular, and sequential atrioventricular pacing
to separate these two factors. The latter was done
by applying paired pacing stimuli to the right
atrium and right ventricle, at an interval less than
the control P-R interval for a given subject. During
sequential atrioventricular pacing the effect of the
atrial kick is preserved in the face of abnormal
ventricular depolarization. The results of studies in
patients with normal hearts and with heart disease
demonstrated that the cardiac outputs during
sequential atrioventricular pacing were only slightly
less than those during atrial pacing and that both
were significantly greater than the outputs during
ventricular pacing. Abnormal ventricular depolarization per se produced little effect on cardiac
output.
The data suggest that asynchronous ventricular
activation has relatively little hemodynamic effect,
and are consistent with older observations that
significant mechanical ventricular asynchronism is
not a necessary consequence of the electrical
ventricular asynchronism of bundle-branch block or
ventricular premature beats.30 Braunwald and
Morrow31 studied five patients with complete left
bundle-branch block and 10 with complete right
bundle-branch block. None of the former exhibited
delay in onset of left ventricular contraction, and
only four of the latter patients had as much as a
SAMET
402
0.04-sec delay in onset of right ventricular contraction. Bourassa et al. have, however, presented data
to the contrary in a patient with intermittent left
bundle-branch block.32
Functional State of the Heart
It can readily be appreciated that any given
cardiac arrhythmia may be better tolerated when
the underlying myocardium is normal. Patients with
congenital complete heart block are better able to
tolerate severe bradyeardia than patients with
acquired complete heart block. In the former group
the ability to compensate for bradyeardia by
increasing the stroke volume is greater than in
patients with acquired block. Even minor arrhythmias may be hemodynamically significant in the
face of severe myocardial disease.
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
Irregularity of Cycle Length of the Arrhythmia
The irregular pulse rate observed in many
arrhythmias, especially atrial fibrillation, may per se
have definite hemodynamic effects. Potentiation is a
key mechanism for some of these effects. Potentiation is a mechanism in which an early ventricular
depolarization augments the force of contraction of
the succeeding contraction.33 4 Greenfield et al.35
noted that peak flow, peak power, and stroke work
correlated best with the two previous R-R intervals,
not simply the preceding cycle length. A second
mechanism whereby cardiac irregularities produce
hemodynamic effects is via Starling's law of the
heart. Braunwald et al.36 performed studies in 26
adult patients with atrial fibrillation at operation.
Measurements of the length of a segment of the left
ventricle by means of a mercury-filled resistance
gauge were made together with arterial pressure
and left ventricular end-diastolic pressure. Variations of end-diastolic segment length and pressure
due to changing duration of diastole were measured. Changes in end-diastolic segment length
correlated with peak systolic ventricular pressures.
The longer the preceding cycle length in the atrial
fibrillation, the greater is the length of the left
ventricular segment.
A third mechanism is change in the refractory
period of various cardiac tissues associated with
sudden rate changes. As many as the 12 preceding
cycles may affect the refractory period. An abrupt
change from slow to rapid ventricular rates shortens
the refractory period maximally in the first beat and
progressively less in subsequent beats.37 Such
changes in refractory period may be responsible for
rate changes in arrhythmias.
Drug Therapy
Just as the state of the myocardium may influence
the hemodynamic effects of cardiac arrhythmias, so
may drugs alter the consequence of arrhythmias.
These effects may result from direct drug effect on
the myocardium or from effects on the peripheral
vascular system. In addition, the drug involved may
itself cause an arrhythmia.
Preservation of Vasomotor Control Mechanisms
The response to similar cardiac arrhythmias may
be quite varied in different patients. At least part of
these differences may be due to the status of the
peripheral vascular system and its control mechanism. For example, Skinner et al.22 noted that
bilateral vagotomy, with control of carotid sinus
pressure, blunted the compensatory mechanisms
which modified the hemodynamic consequences of
acute induced atrial fibrillation in the dog. Drugs,
circulating catecholamines, altered blood volume,
redistribution of blood volume, venous tone,
neurogenic reflexes, or intrinsic disease may thus
alter the effects of cardiac arrhythmias.
Superimposed Mental Status of the Patient,
i.e. Level of Anxiety
Cardiac arrhythmias may result in anxiety
responses on the part of the patient. Outpouring of
catecholamines may result38 with secondary effects
on the cardiac rhythm as well as the peripheral
vascular system.
Disease in Other Organ Systems
The hemodynamic effect of arrhythmias may also
be conditioned by disease processes in other organs.
Atherosclerosis of the bowel vessels may result in
symptoms secondary to the arrhythmia which might
be absent in patients without such vascular
involvement. Mild pulmonary congestion in a
patient with obstructive pulmonary emphysema
may result in more profound symptomatology than
in the presence of otherwise normal lungs. Anemia
may also modify the hemodynamic result of cardiac
arrhythmias.
Effect
of Arrhythmias on
Regional Blood Flow
Several lines of evidence indicate that the
cerebral circulation may be compromised by
cardiac arrhythmias. The electromagnetic flowmeter
was employed to measure cerebral blood flow
(carotid artery flow) during the control sinus
rhythm, and various arrhythmias in the dog.39 The
flow decrement averaged 7-12% during premature
Circulation, Volume XLVII, February 1973
403
SEQUELAE OF ARRHYTHMIAS
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
beats, 14% during supraventricular tachycardia, 23%
during atrial fibrillation, and 40-75% during ventricular tachycardia. The clinical counterpart of these
experimental observations is well established.40 A
10-hour taped electrocardiogram was recorded in 39
adult patients with symptoms of cerebral ischemia.
Ten of the 39 patients exhibited arrhythmias with
bradyeardia below 40 beats/min or heart rates
above 150 beats/min. Morgagni-Stokes-Adams episodes in complete heart block have, of course, been
well known for many years. Electrical pacing with
correction of the bradyeardia was associated with a
significant increase in cerebral blood flow.41 Coronary artery flow may be reduced by atrial or
ventricular premature systoles, atrial and ventricular tachycardia, and atrial fibrillation.42 The clinical
counterparts of these experimental data are well
known.43 Posttachyeardia T-wave inversion is frequently seen even in young individuals with normal
coronary circulations. Cardiac arrhythmias may also
be associated with reduction in renal and mesenteric blood flow in the dog. Marked polyuria44 is often
seen in patients during supraventricular tachycar-
dia. Lower rhythm nephrosis
arrhythmias.45
may
complicate
Specific Arrhythmias
Sinus Bradycardia
Even ventricular rates below 40-45 beats/min are
often not associated with severe hemodynamic
consequences if the stroke volume is not limited by
myocardial or valvular disease. In one group of 17
patients with only sinus bradyeardia (Hildner FJ,
Narula OS, Samet P: Unpublished data), the
ventricular 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 increased
vagal and vasovagal reactions with hypotensive
episodes. Bradycardia, inability to increase stroke
volume due to decreased myocardial reserve, and
inadequate peripheral vasomotor controls all contribute to the problem.46 The bradyeardia and
hypotension may, in turn, predispose to serious
ventricular arrhythmias and ventricular standstill
especially in the presence of an acute myocardial
infarction.
Supraventricular Tachycardia
The hemodynamic differences between nodal-and
atrial tachycardia relate primarily to the incidence
of atrioventricular dissociation in the former but not
Cifculation, Volume XLVII, February 1973
the latter and to ventricular rate differences. The
effects of atrial tachycardia depend on the myocardial 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 cardiac
output in the experimental laboratory, until rates of
160-230 beats/min are recorded, at least in normal
hearts; at faster rates the output may then fall. The
fall in output may occur at slower rates in the
diseased heart. Several studies in man2' 47 have
revealed little change in cardiac output at the onset
of atrial tachycardia. A fall in systemic arterial
pressure may occur especially when in the upright
position. Right atrial and pulmonary artery wedge
pressures rose especially at the onset of tachycardia
probably secondary to inadequate diastolic ventricular filling. Systemic pulsus alternans has been
reported.47 The occasional development of heart
failure or angina pectoris during supraventricular
tachycardia is the clinical counterpart of the
physiologic hemodynamic changes. Study of two
patients with nodal tachycardia and the WolffParkinson-White syndrome3 revealed evidence of
tricuspid regurgitation with right atrial hypertension.
Atrial Flutter
Mechanical atrial activity may persist in atrial
flutter unlike atrial fibrillation. Atrial contractions at
rates of 300/min may be present. Cardiac output
was decreased in nine patients with atrial flutter,
five with heart failure (index 1.48-2.48), three with
heart disease not in failure (index 1.67-2.10), and
one without heart disease, cardiac index 2.57.48 In
five patients studied in flutter and sinus rhythm, the
index rose 40% on conversion to sinus rhythm as the
ventricular rate also fell.48 Digitalization in four
patients resulted in a significant rise in output with
a significant decrease in heart rate and persistence
of atrial flutter. A single patient was studied in sinus
rhythm, atrial fibrillation, and atrial flutter during
both rest and exercise,49 with comparable oxygen
consumptions during the three rest and three
exercise periods. The three resting ventricular rates
were virtually identical. The cardiac indices were
identical during sinus rhythm and atrial fibrillation
but fell slightly in atrial flutter. During exercise, the
cardiac index was greater during sinus rhythm than
during the atrial arrhythmias.
Atrial Fibrillation
The development of the right atrial electrogram
has demonstrated that differentiation between atrial
SAMET
404
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
fibrillation and supraventricular tachycardia is not
always possible on the basis of the surface
electrocardiogram. Intracardiac recordings may be
required for this purpose. Comments on the
hemodynamic changes during atrial fibrillation
were made above.
The hemodynamic data observed in patients with
atrial fibrillation during exercise deserve comment.
Most studies have revealed significant hemodynamic improvement after conversion to sinus rhythm.
Graettinger et al.25 studied 17 patients during
exercise in both atrial fibrillation and normal sinus
rhythm. Oxygen consumption was very similar
during both rhythms, but the average cardiac index
rose from 2.98 to 3.20 while the respective heart
rates fell from 127 to 98 on conversion. Benchimol
et al.50 studied eight patients during exercise in
both rhythms and observed an 8% rise in cardiac
output after conversion with a 30% rise in stroke
volume since the heart rate fell 24%. Separation of
the effects of rhythm change from heart rate change
is difficult. Another observer reported that, in
selected patients, exercise tolerance may not be
affected by atrial fibrillation.5'
Ventricular Tachycardia
The hemodynamic effects of spontaneous rapid
ventricular tachycardia in the experimental animal
include hypotension, a fall in cardiac output, and
evidence of cerebral, coronary, and renal vascular
insufficiency.6 38 Pulmonary arterial and left and
right atrial pressures may increase.38 The effect of
ventricular tachycardia may also be observed in
man by simulated ventricular tachycardia, i.e.
ventricular pacing.' 2 5. 6 13 16 These studies clearly
reveal that systemic hypotension, cyclic variations
in systemic and right heart pressures, and decreases
in cardiac output regularly occur even when the
effect of rate, per se, is eliminated by comparing
atrial and ventricular pacing at similar ventricular
rates. The abnormal dynamics during ventricular
pacing or ventricular tachycardia are probably due
to both the rapid rates and the absence of
sequential atrial-ventricular activity. Thus, the
hemodynamic abnormalities seen in ventricular
tachycardia are often more severe than those in
supraventricular tachycardia even at the same
overall ventricular rate. The importance of the
ventricular rate per se in the hemodynamics of
ventricular rhythms has been stressed by recognition of the relatively benign course of some
ventricular rhythms (rates 60-90) in the course of
acute myocardial infarction. The abnormal dynam-
ics of ventricular tachycardia are accentuated
during ventricular fibrillation when effective circulation ceases.
Brady-Tachyarrhythmia Syndrome (Sick Sinus Syndrome)
The frequency of this syndrome in which slow
and rapid ventricular rates alternate has recently
been recognized.5` The hemodynamic effects vary
with the different arrhythmias present in a given
case.
Complete Heart Block
Levinson et al.53 studied five patients in acquired
heart block not in failure. Right heart pressures
were elevated. Systemic and right heart pulse
pressures are widened. The heart rates are 45-55
when the QRS complex is narrow, i.e. originates
above the bifurcation of the His bundle. The rate is
30-45 when the ventricular focus is idioventricular
in origin. The cardiac output was decreased but the
stroke volume was elevated. Stark et al.54 made
comparable observations in eight patients. Right
ventricular end-diastolic pressure was generally
normal. In the presence of heart failure, marked
further decrease in cardiac output was observed.
Samet'5 reported low cardiac indices in 24 subjects
not in failure. The abnormalities observed in these
patients probably result from a slow rate, myocardial disease, plus abnormal P-QRS temporal relationships. The hemodynamic data in congenital heart
block are somewhat different from those in
acquired complete heart block. The effects of
associated myocardial disease are probably absent
in these patients. The heart rates are somewhat
faster (40-80/min). The cardiac output is usually
normal. Right heart pressures are generally close to
normal. Right ventricular end-diastolic pressure is
normal or minimally elevated.56
Exercise studies in acquired complete heart block
have revealed a further increase in the already large
stroke volume and a rise in cardiac output if left
ventricular function is relatively normal. If myocardial function is depressed, the stroke volume may
be fixed during exercise.57 The heart rate is
generally constant during exercise in acquired
complete heart block. In congenital complete heart
block, the ventricular rate and cardiac output
usually rise during exercise, as myocardial function
is commonly normal.58
When the heart rate is increased by ventricular
pacing in patients in complete heart block, the
cardiac output generally rises.4 ' 59 A bellshaped curve is often noted and the output may fall
Circulation, Volume XLVII, February 1973
405
SEQUELAE OF ARRHYTHMIAS
as the rate rises above 100 beats/min. P-wave
synchronous pacing results in larger cardiac outputs
than obtained during ventricular pacing at similar
ventricular rates.18
Atrial, Nodal, and Ventricular Premature Beats
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
The effect of premature beats depends on several
factors including the underlying heart disease, the
degree of prematurity of the beat, the frequency
and the site, i.e. atrial or ventricular, and the P-QRS
temporal relationship.1 A very early premature beat
may have little or no mechanical effect, with even
little effect on the ventricular pressure curve. The
electrical heart rate is then greater than the
effective mechanical heart rate, as in the postextrasystolic potentiation phenomena.33 34 If the premature beat is somewhat later in the cardiac cycle, a
mechanical ventricular pressure curve may be
generated, but the level of pressure achieved may
not be sufficient to open the corresponding
semilunar valve. Premature beats in mid-to-late
diastole will usually have less abnormal hemodynamic effects than earlier beats. The left ventricular
pulse pressure and systolic pressure peak and the
systemic arterial pulse pressure increase after the
compensatory pause of a ventricular premature
beat except for patients with idiopathic hypertrophic subaortic stenosis. In these individuals the
systemic arterial pulse pressure falls after a
ventricular premature beat due to the increased
contractility observed after the premature beat.60
The hemodynamic sequelae of premature beats
also depend on the site of origin, i.e. whether or not
normal atrioventricular sequential activity is maintained. The site of origin of ventricular premature
beats is believed by some investigators to influence
the hemodynamic effect of such beats.6' Other
studies have, however, cast doubt on the importance
of the sites of ventricular stimulation.62
References
1. BELLET S: Clinical Disorders of the Heart Beat, ed 3.
Philadelphia, Lea & Febiger, 1971, p 105
2. MCINTOSH HD, MORRIS JJ JR: The hemodynamic
consequences of arrhythmias. Progr Cardiovasc Dis
8: 330, 1966
3. FERRER MI, HARVEY RM: Some hemodynamic aspects
of cardiac arrhythmias in man: A clinico-physiologic
correlation. Amer Heart J 68: 153, 1964
4. SAMET P, BERNSTEIN WH, MEDOW A, NATHAN DA:
Effects of alterations in ventricular rate on cardiac
output in complete heart block. Amer J Cardiol 14:
477, 1964
Circulation, Volume XLVII; February 1973
5. SAMET P, CASTILLO C, BERNSTEIN WH: Hemodynamic
sequelae of atrial, ventricular and sequential atrioventricular pacing in cardiac patients. Amer Heart J 72:
725, 1966
6. WEGRIA R, FRANK CW, WANG H, LAMMERANT J: The
effect of atrial and ventricular tachycardia on cardiac
output, coronary blood flow and mean arterial blood
pressure. Circ Res 6: 624, 1958
7. SUGEMOTO T, SAGAWA K, GUYTON AC: Effect of
tachycardia on cardiac output during normal and
increased venous return. Amer J Physiol 211: 288,
1966
8. Ross J JR, LINHART JW, BRAUNWALD E: Effect of
changing heart rate in man by electrical stimulation
of the right atrium. Circulation 32: 549, 1965
9. STEIN E, DAMATO AN, KosowsKY BD, LAU SH,
LISTER JW: The relation of heart rate to cardiovascular dynamics: Pacing by atrial electrodes. Circulation 33: 925, 1966
10. SAMET P, CASTILLO C, BERNSTEIN WH, FERNANDEZ P:
Hemodynamic results of right atrial pacing in cardiac
subjects. Dis Chest 53: 133, 1968
11. YOSHIDA S, GANZ W, DONOso R, MARCUS HS, SWAN
HJC: Coronary hemodynamics during successive
elevation of heart rate by pacing in subjects with
angina pectoris. Circulation 44: 1062, 1971
12. HODAM RP, STARR A: Temporary postoperative
epicardial pacing electrodes: Their value and
management after open heart surgery. Ann Thorac
Surg 8: 506, 1969
13. DESANCTIS RW: Diagnostic and therapeutic uses of
atrial pacing. Circulation 43: 748, 1971
14. BENCHIMOL A, LIGGETT MS: Cardiac hemodynamics
during stimulation of the right atrium, right ventricle
and left ventricle in normal and abnormal hearts.
Circulation 33: 933, 1966
15. COVELL JW, Ross J JR, TAYLOR R, SONNENBLICK EH,
BRAUNWALD E: Effects of increasing frequency of
contraction on the force velocity relation of the left
ventricle. Cardiovasc Res 1: 2, 1967
16. GESELL RA: Auricular systole and its relation to
ventricular output. Amer J Physiol 29: 32, 1911
17. SKINNER NS JR, MITCHELL JH, WALLACE AG, SARNOFF
SJ: Hemodynamic effects of altering the timing of
atrial systole. Amer J Physiol 205: 499, 1963
18. SAMET P, BERNSTEIN WH, NATHAN DA, LOPEZ A:
Atrial contribution to cardiac output in complete
heart block. Amer J Cardiol 16: 1, 1965
19. BROCKMIAN SK: Cardiodynamics of complete heart
block. Amer J Cardiol 16: 72, 1965
20. RESNEKOV L: Circulatory effects of cardiac arrhythmias.
In Cardiovascular Clinics, edited by Dreifus LS.
Philadelphia, F. A. Davis Co., 1970, p 23
21. MITCHELL JH, GUPTA DN, PAYNE RG: Influence of
atrial systole on effective ventricular stroke volume.
Circ Res 17: 11, 1965
22. SKINNER NS, MITCHELL JH, WALLACE AG, SARNOFF
SJ: Hemodynamic consequences of atrial fibrillation
at constant ventricular rates. Amer J Med 36: 342,
1964
406
SAMET
23. MORRIS JJ JR, ENTIMANT G, NORTH WC, KONG Y,
24.
25.
26.
27.
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
MCINTOSH H: The changes in cardiac output with
reversion of atrial fibrillation to sinus rhythm.
Circulation 31: 670, 1965
RODMAN T, PASTOR BH, FIGUF;ROA W: Effect on
cardiac output of cardioversion from atrial fibrillation
to normal sinus mechanism. Amer J Med 41: 249,
1966
GRAETTINCER JS, CARLETON RA, MUENSTER JJ:
Circulatory consequences of changes in cardiac
rhythm produced in patients by transthoracic direct
current shock. J Clin Invest 43: 2290, 1964
ScoT-r ME, PATTERSON GC: Cardiac output after direct
current cardioversion of atrial fibrillation. Brit Heart J
31: 87, 1969
SHAPIRO W, KLEIN G: Alterations in cardiac function
immediately following electrical conversion of atrial
fibrillation to normal sinus rhythm. Circulation 38:
1074, 1968
ARANI DT, CARLTON RA: The deleterious role of
tachycardia in mitral stenosis. Circulation 36: 511,
1967
LOGAN WF, ROWLANDS DJ, HOwITT G, HOLMES AM:
Left atrial activity following cardioversion. Lancet
2: 471, 1965
SAMET P, BERNSTEIN WH, LITWAK RS: Electrical
activation and mechanical asynchronism in the
cardiac cycle of the dog. Cire Res 7: 228, 1959
BRAUNWALD E, MORROW AG: Sequence of ventricular
contraction in human bundle branch block: A study
based on simultaneous catheterization of both
ventricles. Amer J Med 23: 205, 1957
BOURASSA G, BOITEAU GM, ALLENSTEIN BJ: Hemodynamic studies during intermittent left bundle branch
block. Amer J Cardiol 10: 792, 1962
KOCH-WESER J, BLINKS JR: The influence of the
interval between beats on myocardial contractility.
Pharmacol Rev 15: 601, 1963
BRAUNWALD E, Ross J JR, FROMMER PL, WILLIAMS
JF, SONNENBLICK EH, GAULT JH: Clinical observations on paired electrical stimulation of the heart:
Effect on ventricular performance and heart rate.
Amer J Med 37: 700, 1964
GREENFIELD JC JR, HARLEY A, THOMPSON HK,
WALLACE AG: Pressure flow studies in man during
atrial fibrillation. J Clin Invest 47: 2411, 1968
BRAUNWALD E, FRYE RL, AYGEN MM, GILBERT JW JR:
Studies on Starling's law of the heart: III.
Observations in patients with mitral stenosis and
atrial fibrillation on the relationship between left
ventricular end-diastolic segment length, filling
pressure and the characteristics of ventricular
contraction. J Clin Invest 39: 1874, 1960
JANSE MJ, VAN DER STEEN ABM, VAN DAM RT,
DURRER D: Refractory period of the dog's ventricular
myocardium following sudden changes in frequency.
Circ Res 24: 251, 1969
NAKANO J: Effects of atrial and ventricular tachyeardias
on cardiovascular dynamics. Amer J Physiol 206:
547, 1964
39. CORDAY E, IRVING DW: Effect of cardiac arrhythmias
on the cerebral circulation. Amer J Cardiol 6: 803,
1960
40. WALTER PF, REED SD, WENGER NK: Transient cerebral
ischemia due to arrhythmias. Ann Intern Med 72:
471, 1970
41. SHAPIRO W, CHARLES NPS: Observations on the
regulation of cerebral blood flow in complete heart
block. Circulation 40: 863, 1969
42. CORDAY E, GOLD H, DEVERA LB, WILLIAMS JH,
FIELDS J: Effect of the cardiac arrhythmias on the
coronary circulation. Ann Intern Med 50: 535,
1959
43. ELIAKIM M, BRAUN K: Observations on the relation of
electrical and mechanical events in cardiac arrhythmias. Amer Heart J 51: 61, 1956
44. WOOD P: Polyuria in paroxysmal tachycardia and
paroxysmal atrial flutter and fibrillation. Brit Heart J
25: 273, 1963
45. CALBRAITH BT: Lower nephron nephrosis associated
with prolonged shock from ventricular tachycardia.
Amer Heart J 42: 766, 1951
46. ZIPES DP: The clinical significance of bradyeardic
rhythms in acute myocardial infarction. Amer J
Cardiol 24: 814, 1969
47. SAUNDERS DE, Oiw JW: The hemodynamic effects of
supraventricular tachycardia in patients with the
Wolff-Parkinson-White syndrome. Amer J Cardiol 9:
223, 1962
48. HARVEY RM, FERRER MI, RICHARDS DW, COURNAND
A: Cardio-circulatory performance in atrial flutter.
Circulation 12: 507, 1955
49. MCINTOSH HD, KONG Y, MORLS JJ JR: Hemodynamic
effects of supraventricular arrhythmias. Amer J Med
37: 712, 1964
50. BENCHIMOL A, LOWE HM, AKRE PR: Cardiovascular
response to exercise during atrial fibrillation and after
conversion to sinus rhythm. Amer J Cardiol 16: 31,
1965
51. HORNSTEIN TR, BRUCE RA: Effects of atrial fibrillation
on exercise performance in patients with cardiac
disease. Circulation 37: 543, 1968
52. SCHULMAN CL, RUBENSTEIN JJ, YURCHAK PM,
DESANCTIS RW: The "sick" sinus syndrome: Clinical
spectrum. Circulation 42 (suppl III): III-42, 1970
53. LEVINSON DC, GUNTHER L, MECHAN JP, GRIFFITH
CC, SPRITZLER RJ: Hemodynamic studies in five
patients with heart block and slow ventricular rates.
Circulation 12: 739, 1955
54. STARK MF, RADER B, SOBOL BJ, FARBER SJ, EICHNA
LW: Cardiovascular hemodynamic function in complete heart block and the effect of isopropylnorepinephrine. Circulation 17: 526, 1958
55. SAMET P, BERNSTEIN WH: Hemodynamic alterations
due to A-V block. In Mechanisms and Therapy of
Cardiac Arrhythmias, edited by Dreifus LS, Likoff
W. New York, Grune and Stratton, 1966, p 498
56. SCARPELLI FM, RUDOLPH AM: The hemodynamics of
congenital complete heart block. Progr Cardiovasc
Dis 6: 327, 1964
Circulation, Volume XLVII, February 1973
SEQUELAE OF ARRHYTHMIAS
57. MCGREGOR M, KLASSEN GA: Observations on the effect
of heart rate on cardiac output in patients with
complete heart block at rest and during exercise. Circ
Res 14 (suppl II): 11-215, 1964
58. IKKos D, HANSON JS: Response to exercise in congenital
complete atrioventricular block. Circulatioii 22: 583,
1960
59. SEGEL N, HUDSON WA, HARRIS P, BIsHoP JM: The
circulatory effect of electrically induced changes in
ventricular rate at rest and during exercise in
complete heart block. J Clin Invest 43: 1541, 1964
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
Circulation, Volume XLVII, February 1973
407
60. BROCKENBROUGH EC, BRAUNWALD E, MORROW AG: A
hemodynamic technique for the detection of hypertropic subaortic stenosis. Circulation 23: 189, 1961
61. MILLER K, EICH RH, ABILDSKOV JA: Relation of
variations in activation order to intraventricular
pressures during premature beats. Circ Res 19: 481,
1966
62. BAROLD SS, LINHART JW, HILDNER FJ, SAMET P:
Hemodynamic comparison of endocardial pacing of
outflow and inflow tracts of the right ventricle. Amer
J Cardiol 23: 697, 1969
Hemodynamic Sequelae of Cardiac Arrhythmias
PHILIP SAMET
Circulation. 1973;47:399-407
doi: 10.1161/01.CIR.47.2.399
Downloaded from http://circ.ahajournals.org/ by guest on June 18, 2017
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1973 American Heart Association, Inc. All rights reserved.
Print ISSN: 0009-7322. Online ISSN: 1524-4539
The online version of this article, along with updated information and services, is located on the World
Wide Web at:
http://circ.ahajournals.org/content/47/2/399
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in
Circulation can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office.
Once the online version of the published article for which permission is being requested is located, click Request
Permissions in the middle column of the Web page under Services. Further information about this process is available
in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Circulation is online at:
http://circ.ahajournals.org//subscriptions/