The peak of the R wave on an ECG, the initiation of the first heart sound, and the earliest rise in ventricular pressure on the ventricular pressure curve after atrial contraction all coincide with the onset of isovolumic contraction (Fig. 16.39). The onset of the ventricular ejection phase is marked by the opening of the semilunar valves. This phase can be divided into an earlier, shorter phase known as rapid ejection, and a later, longer phase called reduced ejection. The rapid ejection phase is characterized by a sharp rise in ventricular and aortic pressure, which ends at peak ventricular and aortic pressure. Additionally, there is an abrupt decrease in ventricular volume and a pronounced increase in aortic blood flow (see Fig. 16.39).

In cases of congestive heart failure, when the ventricular volume is very large and the ventricular walls are maximally stretched, a third heart sound is often heard. It is important to note that a third heart sound in patients with heart disease is typically a grave sign. Abnormal conditions can lead to the accentuation of both the third and fourth (atrial) sounds, resulting in triplet sounds resembling the sound of a galloping horse (referred to as gallop rhythms). Mitral insufficiency and mitral stenosis produce systolic and diastolic murmurs, respectively, which are best heard at the cardiac apex. On the other hand, aortic insufficiency and aortic stenosis produce diastolic and systolic murmurs, respectively, which are best heard in the second intercostal space just to the right of the sternum. The characteristics of these murmurs are valuable in diagnosing valvular disease.

During the rapid ejection period, left ventricular pressure slightly exceeds aortic pressure, resulting in the acceleration of aortic blood flow. However, during the reduced ventricular ejection phase, aortic pressure is higher and aortic blood flow decelerates. This reversal of the ventricular-aortic pressure gradient while blood continues to flow from the left ventricle to the aorta is due to the storage of potential energy in the stretched arterial walls. The stored potential energy causes the blood flow from the left ventricle into the aorta to decelerate. The peak of the flow curve aligns with the point at which the left ventricular pressure curve intersects the aortic pressure curve during ejection. Subsequently, the flow decelerates because the pressure gradient has been reversed.

Fig. 16.39 displays a tracing of a venous pulse curve recorded from a jugular vein. It shows three apparent waves. The a wave occurs during the rise in pressure caused by atrial contraction. The c wave is a result of the impact of the common carotid artery with the adjacent jugular vein, and to some extent, the abrupt closure of the tricuspid valve in early ventricular systole. The v wave reflects the rise in pressure associated with atrial filling. Apart from the c wave, the venous pulse curve closely resembles the left atrial pressure curve.

At the end of ventricular ejection, a volume of blood approximately equal to that ejected during systole remains in the ventricular cavities. This residual volume remains relatively constant in normal hearts, although it may decrease slightly with an increase in heart rate or a decrease in peripheral vascular resistance.
Fig. 16.39 ). The onset of isovolumic contraction also coincides with the peak of the R wave on an ECG, initiation of the first heart sound, and the earliest rise in ventricular pressure on the ventricular pressure curve after atrial contraction.
Opening of the semilunar valves marks the onset of the ventricular ejection phase, which may be subdivided dWith inspiration, intrathoracic pressure is reduced (see
Chapter 21), which then increases venous blood flow to the right atrium.
Inoverloadedhearts,asincongestiveheartfailure,whenventricularvolumeisverylargeandtheventricularwallsarestretchedmaximally,athirdheartsoundisoftenheard.Athirdheartsoundinpatientswithheartdiseaseisusuallyagravesign.Whenthethirdandfourth(atrial)soundsareaccentuated,asoccursincertainabnormalconditions,tripletsofsoundsresemblingthesoundofagallopinghorse(calledgallop rhythms)mayoccur.Mitralinsufficiencyandmitralstenosisproduce,respectively,systolicanddiastolicmurmursthatareheardbestatthecardiacapex.Aorticinsufficiencyandaorticstenosis,incontrast,produce,respectively,diastolicandsystolicmurmursthatareheardbestinthesecondintercostalspacejusttotherightofthesternum.Thecharacteristicsofthemurmursserveasanimportantguideinthediagnosisofvalvulardisease.
into an earlier, shorter phase (rapid ejection) and a later, longer phase (reduced ejection). The rapid ejection phase is distinguished from the reduced ejection phase by three characteristics: (1) a sharp rise in ventricular and aortic pressure that terminates at peak ventricular and aortic pressure, (2) an abrupt decrease in ventricular volume, and (3) a pronounced increase in aortic blood flow (see
Fig. 16.39 ). The sharp decrease in left atrial pressure at the onset of ventricular ejection results from descent of the base of the heart and consequent stretching of the atria. During the reduced ejection period, runoff of blood from the aorta to the peripheral blood vessels exceeds the rate of ventricular output, and aortic pressure therefore declines. Throughout ventricular systole, the blood returning from the peripheral veins to the atria produces a progressive increase in atrial pressure.
During the rapid ejection period, left ventricular pressure slightly exceeds aortic pressure and aortic blood flow accelerates (continues to increase), whereas during the reduced ventricular ejection phase, aortic pressure is higher and aortic blood flow decelerates. This reversal of the ventricular-aortic pressure gradient in the presence of continuous flow of blood from the left ventricle to the aorta is the result of storage of potential energy in the stretched arterial walls. This stored potential energy causes blood flow from the left ventricle into the aorta to decelerate. The peak of the flow curve coincides with the point at which the left ventricular pressure curve intersects the aortic pressure curve during ejection. Thereafter, flow decelerates (continues to decrease) because the pressure gradient has been reversed.
Fig. 16.39 shows a tracing of a venous pulse curve recorded from a jugular vein. Three waves are apparent. The a wave occurs with the rise in pressure caused by atrial contraction. The c wave is caused by impact of the common carotid artery with the adjacent jugular vein and, to some extent, by the abrupt closure of the tricuspid valve in early ventricular systole. The v wave reflects the rise in pressure associated with atrial filling. Except for the c wave, the
CHAPTER 16 Elements of Cardiac Function venous pulse curve closely resembles the left atrial pressure curve.
At the end of ventricular ejection, a volume of blood approximately equal to that ejected during systole remains in the ventricular cavities. This residual volume is fairly constant in normal hearts. However, residual volume decreases somewhat when the heart rate increases or when peripheral vascular resistance has diminished.