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As the pacing frequency increases, the decrease in stroke volume must be approximately equal to the increase in heart rate. Generalized vascular autoregulation helps maintain constant tissue blood flow. This adaptation leads to changes in preload and afterload, which also keep cardiac output nearly constant.

At excessively high pacing frequencies (above 200 beats/minute), further increases in heart rate actually decrease cardiac output. This occurs because the decrease in stroke volume exceeds the increase in heart rate at these high frequencies. The limited ventricular filling time fails to adequately compensate, resulting in a sharp decrease in cardiac output. While the relationship between cardiac output and heart rate is typically an inverted U shape in the general population, it varies quantitatively among individuals and physiological states.

Strong correlations between heart rate and cardiac output must be interpreted with caution. During exercise, for instance, cardiac output and heart rate usually increase proportionately, and stroke volume may remain constant or only slightly increase. It may be tempting to attribute the increase in cardiac output solely to the observed increase in heart rate. However, a wide range of heart rates shown in Figure 19.14 demonstrates that a change in heart rate may have little influence on cardiac output. The primary increase in cardiac output during exercise is attributed to other factors, such as reduced peripheral vascular resistance due to vasodilation in active skeletal muscles and increased contractility of cardiac muscle associated with sympathetic neural activity. Nonetheless, the increase in heart rate still plays an important role. Abundant data show that if the heart rate cannot increase normally during exercise, the capacity for exercise and augmentation of cardiac output are severely limited. Since stroke volume changes only slightly during exercise, the increase in heart rate may have a crucial permissive role in enhancing cardiac output during physical activity.

The distinct relationship between cardiac output and heart rate explains the urgent need for treatment in patients with excessively slow or excessively fast heart rates. Profound bradycardia (slow rate) may occur as a result of very slow sinus rhythm in patients with sick sinus syndrome or as a consequence of a slow idioventricular rhythm in patients with complete atrioventricular block. In either rhythm disturbance, the limited capacity of the ventricles to fill during prolonged diastole (often due to the noncompliant pericardium) substantially reduces cardiac output since the very slow heart rate cannot be counterbalanced by a sufficiently large stroke volume. Consequently, such bradycardia often requires the implantation of an artificial pacemaker. In patients with supraventricular or ventricular tachycardia, excessively high heart rates frequently necessitate emergency treatment because cardiac output may be critically low and the filling time is severely restricted at these very high heart rates, causing disproportionate reductions in filling volume. Slowing the heart rate to a more normal rhythm can generally be achieved pharmacologically, but electrical cardioversion may be required in emergencies. (see Ancillary Factors That Affect the Venous System﻿ and Cardiac Output)

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19.14B ). Hence, as pacing frequency is increased, the decrease in stroke volume must be approximately equal to the increase in heart rate. In addition, generalized vascular autoregulation tends to keep tissue blood flow constant (see also ). This adaptation leads to changes in preload and afterload that also keep cardiac output nearly constant.
Moreover, at excessively high pacing frequencies (above 200 beats/minute; see
Fig. 19.14 ), further increases in heart rate decrease cardiac output. Therefore, the induced decrease in stroke volume must have exceeded the increase in heart rate at this high range of pacing frequencies. At such high pacing frequencies, the ventricular filling time is so severely restricted that compensation is inadequate, and cardiac output decreases sharply. Although the relationship of cardiac output to heart rate is characteristically that of an inverted U in the general population, the relationship varies quantitatively among subjects and among physiological states.
Strong correlations between heart rate and cardiac output must be interpreted cautiously. In people who are exercising, for example, cardiac output and heart rate usually increase proportionately, and stroke volume may remain constant or increase only slightly (see the later section ”). It is tempting to conclude that the increase in cardiac output during exercise must be caused solely by the observed increase in heart rate. However,
Fig. 19.14 shows that over a wide range of heart rates, a change in heart rate may have little influence on cardiac output. The principal increase in cardiac output during exercise must therefore be attributed to other factors. Such ancillary factors include the pronounced reduction in peripheral vascular resistance because of the vasodilation in the active skeletal muscles and the increased contractility of cardiac muscle associated with the generalized increase in sympathetic neural activity. Nevertheless, the increase in heart rate is still an important factor. Abundant data show that if the heart rate cannot increase normally during exercise, the augmentation in cardiac output and the capacity for exercise are severely limited. Because stroke volume changes only slightly during exercise, the increase in heart rate may play an important permissive role in augmenting cardiac output during physical exercise.
Thecharacteristicrelationshipbetweencardiacoutputandheartrateexplainstheurgentneedoftreatmentbypatientswhohaveexcessivelysloworexcessivelyfastheartrates.Profoundbradycardia (slowrate)mayoccurasaresultofaveryslowsinusrhythminpatientswithsick sinus syndrome orasaresultofaslowidioventricularrhythminpatientswithcomplete atrioventricular block. Ineitherrhythmdisturbance,thecapacityoftheventriclestofillduringprolongeddiastoleislimited(oftenbythenoncompliantpericardium).Hence,cardiacoutputusuallydecreasessubstantiallybecausetheveryslowheartratecannotbecounterbalancedbyasufficientlylargestrokevolume.Asaconsequence,suchbradycardiaoftennecessitatestheimplantationofanartificialpacemaker.Inpatientswithsupraventricular orventricular tachycardia, excessivelyhighheartratesfrequentlynecessitateemergencytreatmentbecauseinsuchpatients,cardiacoutputmaybecriticallylow,andthefillingtimeissorestrictedatveryhighheartratesthatevensmalladditionalreductionsinfillingtimecausedisproportionatelyseverereductionsinfillingvolume.Slowingtheheartratetoamorenormalrhythmcangenerallybeaccomplishedpharmacologically,butelectricalcardioversionmayberequiredinemergencies(see
Ancillary Factors That Affect the Venous System﻿ and Cardiac Output