In earlier sections of this chapter, the descriptions of the interrelationships between Pv and cardiac output were simplified by restricting the discussion to the effects evoked by individual variables. However, because the cardiovascular system is regulated by so many feedback control loops, its responses are rarely simple. A change in blood volume, for example, not only affects cardiac output directly through the Frank-Starling mechanism but also triggers reflexes that alter other aspects of cardiac function (such as the heart rate, atrioventricular conduction, and myocardial contractility) and other characteristics of the vascular system (such as peripheral resistance and venomotor tone). Several other factors, especially gravity (see ) and respiration, also regulate cardiac output.
Circulatory Effects of Respiratory Activity
The normal, periodic activity of the respiratory muscles causes rhythmic variations in vena caval flow (Fig. 19.15 ). During respiration, the reduction in intrathoracic pressure is transmitted to the lumens of the thoracic blood vessels. The reduction in Pv during inspiration increases the pressure gradient between extrathoracic and intrathoracic veins. The consequent acceleration in venous return to the right atrium is shown in
Fig. 19.15 as an increase in superior vena caval blood flow from 5.2 mL/sec during expiration to 11 mL/ sec during inspiration.
The exaggerated reduction in intrathoracic pressure achieved by a strong inspiratory effort against a closed glottis (called Müller’s maneuver) does not increase venous return proportionately. The extrathoracic veins collapse near their entry into the chest when their internal pressures fall below the ambient level. As the veins collapse, flow into the chest momentarily stops. The cessation of flow causes pressure upstream to rise, which forces the collapsed segment to reopen.
During normal expiration, flow into the central veins decelerates. However, the mean rate of venous return during normal respiration exceeds the flow during a brief period of apnea (cessation of respiration). Hence, normal inspiration apparently facilitates venous return more than normal expiration impedes it. In part, venous return is facilitated by the valves in the veins of the extremities. These valves prevent any reversal of flow during expiration. Thus the respiratory muscles and venous valves constitute an auxiliary pump for venous return.
•Fig. 19.15 Duringanormalinspiration,intrathoracicpressure,rightatrialpressure(RAP),andjugularvenous(JVP)pressuredecrease,andflowinthesuperiorvenacava(SVCF)increases(from5.2to11mL/sec).AllpressuresaregiveninmmH2O.Femoralarterialpressure(notshown)didnotchangesubstantiallyduringthenormalinspiration.Jugular vein 50 5.2 mL/sec 11 mL/sec SVCF JVP RAP 0 Atrial 0 –100
Thedramaticincreaseinintrathoracicpressureinducedbycoughingconstitutesanauxiliarypumpingmechanismfortheblooddespiteitsconcurrenttendencytoimpedevenousreturn.Certaindiagnosticprocedures,suchascoronaryangiographyorelectrophysiologicaltestingofcardiacfunction,increasetheriskforventricularfibrillation;therefore,patientsundergoingsuchproceduresaretrainedtocoughrhythmicallyoncommandduringthestudy.Ifventricularfibrillationdoesoccur,eachcoughcangeneratesubstantialincreasesinarterialbloodpressure,andenoughcerebralbloodflowmaybepromotedtosustainconsciousness.Thecoughraisesintravascularpressureequallyintheintrathoracicarteriesandveins.Bloodispropelledthroughtheextrathoracictissuesbecausetheincreasedpressureistransmittedtotheextrathoracicarteriesbutnottotheextrathoracicveinsbecausethevenousvalvespreventbackwardflowfromtheintrathoracictotheextrathoracicveins.