The electrocardiogram shown in Figure 18.11 was taken from a quadriplegic patient who was unable to breathe on their own and required tracheal intubation and artificial respiration. When the tracheal catheter was briefly disconnected to allow for nursing care, the patient experienced a significant decrease in heart rate after 9 heartbeats. Prior to the disconnection, the patient's heart rate was 65 beats per minute. Within 10 seconds of artificial respiration cessation, the heart rate dropped to approximately 20 beats per minute. This bradycardia could be prevented by blocking the effects of efferent vagal activity with atropine, and its onset could be delayed by hyperventilating the patient before disconnecting the tracheal catheter.

The heart rate and peripheral resistance can be diminished by the excitation of endocardial receptors, such as arterial baroreceptors. Additional sensory receptors have been found in the epicardial regions of the ventricles. Although these ventricular receptors are stimulated by various mechanical and chemical stimuli, their specific physiological functions are still not fully understood.

The heart can generate its own beat even without nervous or hormonal control, and it can also adapt to changes in hemodynamic conditions through intrinsic mechanisms within the cardiac muscle itself. For instance, denervated hearts in racing greyhounds perform nearly as well as those with intact innervation. The maximal running speed of denervated greyhounds only decreases by 5% after complete cardiac denervation. During exercise, the increase in cardiac output is typically accompanied by a proportional increase in heart rate, with stroke volume remaining relatively stable. In denervated hearts, the increase in cardiac output is primarily achieved by an increase in stroke volume. However, intrinsic mechanisms alone are not solely responsible for this adaptation in denervated hearts; circulating catecholamines also contribute. When β-adrenergic receptor antagonists are administered to greyhounds with denervated hearts, their racing performance is significantly impaired.

Ventricular receptors have been implicated in the initiation of vasovagal syncope, which is characterized by lightheadedness or brief loss of consciousness that may be triggered by psychological or orthostatic stress. It is believed that these receptors are stimulated by reduced ventricular filling volume in combination with vigorous ventricular contraction. When a person is standing quietly, ventricular filling is diminished due to blood pooling in the veins of the abdomen and legs. This leads to a decrease in cardiac output and arterial blood pressure, resulting in an overall increase in sympathetic neural activity through the baroreceptor reflex. The heightened sympathetic activity to the heart triggers a forceful ventricular contraction, which then stimulates the ventricular receptors. Excitation of these receptors initiates autonomic neural changes that induce vasovagal syncope, including a profound, vagally-mediated bradycardia and generalized arteriolar vasodilation mediated by a reduction in sympathetic neural activity.
Fig.18.11 wasrecordedfromaquadriplegicpatientwhocouldnotbreathespontaneouslyandrequiredtrachealintubationandartificialrespiration.Whenthetrachealcatheterwasbrieflydisconnected(nearthebeginningofthetopstripinthefigure,indicatedbythearrow)toallownursingcare,profoundbradycardiadevelopedafter9heartbeats.Thepatient’sheartratewas65beatsperminutejustbeforethetrachealcatheterwasdisconnected.Inlessthan10secondsaftercessationofartificialrespiration,hisheartratedroppedtoapproximately20beatsperminute.Thisbradycardiacouldbepreventedbyblockingtheeffectsofefferentvagalactivitywithatropine,anditsonsetcouldbedelayedconsiderablybyhyperventilationofthepatientbeforethetrachealcatheterisdisconnected.
by the arterial baroreceptors. Excitation of these endocardial receptors causes the heart rate and peripheral resistance to diminish. Other sensory receptors have been identified in the epicardial regions of the ventricles. Although all these ventricular receptors are excited by various mechanical and chemical stimuli, their exact physiological functions remain unclear.
Regulation of Myocardial Performance
Intrinsic Regulation of Myocardial Performance
As noted previously, the heart can initiate its own beat in the absence of any nervous or hormonal control. The myocardium can also adapt to changing hemodynamic conditions by means of mechanisms that are intrinsic to cardiac muscle itself. For example, racing greyhounds with •Fig. 18.11 Electrocardiogram of a 30-Year-Old Quadriplegic Man Who Could Not Breathe Spontaneously and Required Tracheal Intubation and Artificial Respiration. Thetwostripsarecontinuous.(ModifiedfromBerkJL,LevyMN.Eur Surg Res. 1977;9:75.) denervated hearts perform almost as well as those with intact innervation. Their maximal running speed decreases by only 5% after complete cardiac denervation. In these dogs, the threefold to fourfold increase in cardiac output during a race is achieved principally by an increase in stroke volume. Normally, the increase in cardiac output with exercise is accompanied by a proportionate increase in heart rate; stroke volume does not change much (see ). This adaptation in the denervated heart is not achieved entirely by intrinsic mechanisms; circulating catecholamines undoubtedly contribute. For example, if β-adrenergic receptor antagonists are given to greyhounds with denervated hearts, their racing performance is severely impaired.
Ventricularreceptorshavebeenimplicatedintheinitiationofvasovagal syncope, afeelingoflightheadednessorbrieflossofconsciousnessthatmaybetriggeredbypsychologicalororthostaticstress.Theventricularreceptorsarebelievedtobestimulatedbyreducedventricularfillingvolumeincombinationwithvigorousventricularcontraction.Inapersonstandingquietly,ventricularfillingisdiminishedbecausebloodtendstopoolintheveinsintheabdomenandlegs,asexplainedin
Chapter17.
Consequently,thereductionincardiacoutputandarterialbloodpressureleadstoageneralizedincreaseinsympatheticneuralactivitythroughthebaroreceptorreflex(see
Fig.18.5 ).Theenhancedsympatheticactivitytotheheartevokesavigorousventricularcontractionthatstimulatestheventricularreceptors.Excitationoftheventricularreceptorsinitiatestheautonomicneuralchangesthatevokevasovagalsyncope:namely,acombinationofprofound,vagallymediatedbradycardiaandgeneralizedarteriolarvasodilationmediatedbyareductioninsympatheticneuralactivity.