In previous sections of this chapter, we simplified the descriptions of the interrelationships between Pv and cardiac output by focusing on the effects caused by individual variables. However, due to the complex nature of the cardiovascular system, its responses are often not straightforward. For example, a change in blood volume not only directly affects cardiac output through the Frank-Starling mechanism, but it also triggers reflexes that impact other aspects of cardiac function, such as heart rate, atrioventricular conduction, and myocardial contractility, as well as characteristics of the vascular system, including peripheral resistance and venomotor tone. Additionally, other factors like gravity and respiration also play a role in regulating cardiac output.

Respiratory activity has circulatory effects on the body. The rhythmic variations in vena caval flow are caused by the periodic activity of the respiratory muscles. During respiration, the reduction in intrathoracic pressure is transmitted to the thoracic blood vessels, leading to a decrease in Pv during inspiration. This decrease in pressure creates a higher pressure gradient between extrathoracic and intrathoracic veins, resulting in an increase in venous return to the right atrium. This increase in superior vena caval blood flow is evident during inspiration compared to expiration.

During a strong inspiratory effort against a closed glottis, known as Müller's maneuver, the reduction in intrathoracic pressure does not proportionately increase venous return. The extrathoracic veins collapse near their entry into the chest when their internal pressures fall below the ambient level. This collapse momentarily stops the flow, causing upstream pressure to rise and reopen the collapsed segment.

Normal expiration decelerates flow into the central veins, but the mean rate of venous return during normal respiration still exceeds the flow during a brief period of apnea. Therefore, normal inspiration seems to facilitate venous return more than normal expiration impedes it. Valves in the veins of the extremities also contribute to facilitating venous return by preventing any reversal of flow during expiration. Thus, the respiratory muscles and venous valves serve as an auxiliary pump for venous return.

Coughing, which induces a dramatic increase in intrathoracic pressure, acts as an auxiliary pumping mechanism for blood despite its potential to impede venous return. Certain diagnostic procedures, such as coronary angiography or electrophysiological testing of cardiac function, carry a risk of ventricular fibrillation. To mitigate this risk, patients undergoing such procedures are trained to cough rhythmically on command. In the event of ventricular fibrillation, each cough can generate substantial increases in arterial blood pressure, promoting enough cerebral blood flow to sustain consciousness. The cough raises intravascular pressure equally in the intrathoracic arteries and veins. Blood is propelled through the extrathoracic tissues because the increased pressure is transmitted to the extrathoracic arteries but not to the extrathoracic veins, thanks to the venous valves that prevent backward flow from the intrathoracic to the extrathoracic veins.
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.