9. HEMODYNAMIC DISORDERS IN ARRHYTHMIAS Flashcards
Cause of hemodynamic changes?
The causes of hemodynamic changes during arrhythmias include the effects of alterations in
ventricular rate, loss of synchronized atrial systole, changes in the sequence of ventricular activation,
and depend somewhat on the underlying functional condition of the heart and the background
vasomotor tone. In addition, the hemodynamic effects of anxiety and the drugs used in treating the
arrhythmia must be considered. From this it can be seen that an arrhythmia with no adverse effect in
one patient could be quite harmful to another.
Heart Rate?
Stroke volume increases progressively with slowing of the heart rate so that cardiac output can be
maintained. Ventricular dilatation in such bradyarrhythmias results in increased fiber length at enddiastole, and the increased force of contraction due to the Frank-Starling mechanism compensates
for the need for increased wall tension to maintain pressure.
Decreases in the heart rate beyond the ability of the stroke volume to increase will reduce
cardiac output despite increases in filling pressure of both ventricles. With acceleration of the heart
rate, stroke volume is, at first, decreased proportionately less, and this results in an early increase in
cardiac output before compensatory mechanisms return cardiac output to baseline. With faster
heart rates and marked shortening in the filling period of the ventricles, cardiac output starts to
decline. In normal hearts this usually does not occur until rates of 180 to 190 beats per min are
reached, but in abnormal hearts this decline in cardiac output may occur at much lower rates.
Heart rate ( regional blood flow)?
Regional blood flow may be altered during arrhythmias, and organs having less capacity to adjust
their flow with alterations in pressure may develop symptoms and signs of ischemia. An occasional
premature beat has little effect on the cerebral circulation, while frequent premature beats may
reduce cerebral blood flow as much as 7 to 12 per cent. In supraventricular tachycardias with
moderately fast ventricular response, the average reduction in cerebral blood flow is 23 per cent,
while with extremely fast ventricular responses the reduction may reach 40 per cent. Under such
circumstances, if there is accompanying vascular disease, symptoms of cerebral insufficiency will
appear
Heart rate ( regional blood flow) Stokes-Adams attacks?
Stokes-Adams attacks in complete heart block are due to complete cessation of
cerebral blood flow and should not be confused with cerebral ischemia, which occurs during slow
ventricular rates and produces varying levels of obtundation. Symptoms of cerebral ischemia are of
dizziness, syncope, weakness, convulsions, blurring of vision, paresis or paralysis. Psychotic episodes
should be added to this list.
Heart rate (coronary blood flow)?
Coronary blood flow has a cyclic pattern different from that in the rest of the circulation. This flow
pattern is determined by aortic pressure, the impedance to coronary perfusion secondary to
coronary vascular resistance, and the obliteration of the intramyocardial arteries during myocardial
contraction. Thus, 80 to 90 per cent of the coronary arterial blood flow occurs during diastole.
Arrhythmias may jeopardize coronary blood flow, lowering mean or diastolic arterial pressure,
vasodilating areas of non-ischemic myocardium or shortening diastole.
Supraventricular tachycardias with fast ventricular response shorten diastole, lower aortic pressure, and thus decrease total
coronary blood flow by as much as 35 per cent. Varying ventricular rates in the presence of atrial
flutter or atrial fibrillation can alter coronary blood flow. The elevated mean left ventricular diastolic
pressure needed to compensate for the loss of atrial booster function may significantly decrease the
transmyocardial pressure gradient (aortic diastolic pressure-left ventricular diastolic pressure) which
determines flow through these vessels. An occasional atrial premature beat may reduce the coronary
blood flow by 5 percent.
An occasional premature ventricular beat,
on the other hand, may reduce coronary blood flow by 12 per cent, a prominent effect which is
related in part to the drop in aortic perfusion pressures. During ventricular tachycardia, reductions of
coronary flow as high as 60 per cent have been documented. In ventricular fibrillation, the
myocardial fibers will be contracting and not compressing the coronary vessels, but may cause a
redistribution of flow throughout the myocardium. With the absence of aortic perfusion pressure this
is of little consequence, but during aortocoronary bypass this maybe an important determinant of
preservation of myocardium.
Heart rate ( renal circulation)?
Renal circulation may be altered by arrhythmias either as a change in total flow or a redistribution of
flow within the kidneys. Frequent premature atrial or ventricular systoles cause an average drop in
renal blood flow of 8 to 10 per cent, while paroxysmal atrial tachycardia and atrial fibrillation may
reduce renal blood flow by as much as 20 per cent. Renal blood flow may decrease 60 per cent
during ventricular tachycardia.
Little change in the mesenteric circulation results from a premature beat, but paroxysmal atrial
tachycardia and atrial fibrillation have been shown to reduce mesenteric blood flow 28 and 34
percent respectively. Rapid restoration of normal mesenteric perfusion follows the correction of
dysrhythmias, in contrast to the cerebral and renal circulations, in which vasoconstriction continues
after the arrhythmias are abolished.
Heart rate (Musculocutaneous circulation)?
The cold, clammy skin seen in patients in shock is a manifestation of
decreased flow and increased peripheral vascular resistance. A similar clinical picture is not
infrequently encountered in patients with ventricular tachycardia, and is a protective mechanism to
maintain perfusion pressures of the vital organ. Following circulatory arrest, however, the sudden
build-up of arterial lactate and carbon dioxide may cause momentary vasodilatation and be
responsible for the flush occasionally seen in patients recovering from a Stokes-Adams episode.
Hemodynamics in specific arrhythmias
(Sinus Bradycardia)?
Sinus bradycardia is usually not harmful in young persons with a normal heart because stroke volume
increases and cardiac output and blood pressure are maintained. In addition, the response of heart
rate to stress is maintained. In older individuals with sinus bradycardia caused by malfunction of the
sinus node, cerebrovascular symptoms may appear because stroke volume cannot compensate for
the decreased rate, and rate cannot increase during periods of stress. Young patients with vasovagal
syncope are symptomatic because of the accompanying decrease in vascular resistance and venous
pooling.
Hemodynamics in specific arrhythmias
(Paroxysmal Atrial Tachycardia)?
Stroke volume decreases with paroxysmal atrial tachycardia, unlike the sustained or increased stroke
volume seen in exercise-induced tachycardia of the same rate. With paroxysmal tachycardia, cardiac
output does not need to increase, and arterial pressure may decline in the standing position because
of reflex inhibition of normal vasoconstriction.
Congestive heart failure, angina, or ischemia of vital organs, may appear or worsen after
the onset of such dysrhythmias. Polyuria has been reported to develop after the onset of paroxysmal
atrial tachycardia, atrial flutter and atrial fibrillation and to last about an hour. Left atrial receptors
have been implicated in causing changes in renal blood flow and diuresis.
Hemodynamics in specific arrhythmias
(Atrial Flutter)?
The presence of coordinated atrial contraction in atrial flutter makes its hemodynamic effects
different from those of atrial fibrillation.
At rates lower than 100 per minute, little change in cardiac
output will develop. Cardiac output was assessed in 3 patients with atrial flutter and an average
ventricular response of 155 beats per minute.
Ventricular, arterial and pulmonary artery
pressures were not significantly different from those determined at the same rate and sinus rhythm.
If ventricular rates are rapid, cardiac output is decreased, arterial pressure drops, and atrial pressure
rises.
Hemodynamics in specific arrhythmias
(Atrial Fibrillation)?
The loss of atrial contraction in atrial fibrillation, added to the variation in cycle length with frequent
short cycles, especially at exercise, significantly alters ventricular filling and may result in marked
hemodynamic deterioration, is particularly evident in the presence of underlying myocardial or
valvular disease. The difficulty in separating the effect of the arrhythmia from that of the underlying
disease makes assessment of the hemodynamic effects of the arrhythmia itself difficult.
Hemodynamics in specific arrhythmias
(Ventricular Tachycardia)?
Rapid ventricular tachycardia results in hypotension, low cardiac output, and ischemia to the vital
organs. The pulmonaryartery pressure and atrial pressures increase.
Mild to moderate mitral regurgitation developed in only one third of the patients during ventricular
tachycardia.
The duration of ventricular fibrillation, the overall status of the heart, and the factor that precipitated
this arrhythmia are all determinants of the hemodynamic status after return to sinus rhythm.
Hemodynamic derangements in premature ventricular beats are transient and depend upon the
degree of prematurity, frequency, and the site of origin of the beat. Very early premature
contractions are unable to open the aortic valve and generate a stroke output. Premature beats may produce a normal or only slightly decreased pressure and stroke output if they occur after the rapid
ventricular filling phase. The first beat that follows the premature beat has an elevated stroke
volume and a shorter period of isometric contraction, reflecting increased contractility. The
potentiation is related to the degree of prematurity. The prolonged filling during the compensatory
pause is not the only mechanism by which potentiation develops, since the phenomenon also occurs
after interpolated beats.
Complete Heart Block definition?
Circulatory effects of complete heart block depend upon several factors including: ventricular rate,
duration of the slow rate, status of the heart, age of the patient, rest, and exercise.
Complete heart block symptomes?
Experimentally
induced heart block in the dog has been demonstrated to cause slight diastolic mitral and tricuspid
regurgitation immediately after the rate slows. Pulse pressures increase markedly as stroke volume
increases. Cardiac output is proportional to ventricular rate after maximum stroke volume is reached.
Right atrial, right ventricular, and pulmonary wedge pressures are all elevated. Arterial systolic and
left ventricular end-diastolic pressures are all increased. The cardiac output and cardiac indeks fall
despite the elevated stroke volume.The ever-changing atrial and ventricular contraction relationship
explains the beat-to-beat variation of pulse amplitudes in complete heart block. Oxygen consumption
remains the same with higher oxygen extraction at tissue level during accelerated demands, an effect
that leads to a widened arterial-venous oxygen difference
In complete atrioventricular block?
In complete
atrioventricular block, especially the acquired type, any increase in cardiac outputis dependent upon
increased stroke volume, and much ofthe increased oxygen deliveryis accomplished by increasing the
percent age of oxygen extracted in the periphery.
