Introduction to Cardiovascular Physiology (eBook)

J R Levick (Autor)

eBook Download: PDF | EPUB

2013 | 1. Auflage
288 Seiten
Elsevier Science (Verlag)
978-1-4831-8384-8 (ISBN)

Infos

An Introduction to Cardiovascular Physiology is designed primarily for students of medicine and physiology. This introductory text is mostly didactic in teaching style and it attempts to show that knowledge of the circulatory system is derived from experimental observations. This book is organized into 15 chapters. The chapters provide a fuller account of microvascular physiology to reflect the explosion of microvascular research and include a discussion of the fundamental function of the cardiovascular system involving the transfer of nutrients from plasma to the tissue. They also cover major advances in cardiovascular physiology including biochemical events underlying Starling's law of the heart, nonadrenergic, non-cholinergic neurotransmission, the discovery of new vasoactive substances produced by endothelium and the novel concepts on the organization of the central nervous control of the circulation. This book is intended to medicine and physiology students.

Textauszug

Chapter 2

Cardiac cycle

Publisher Summary

This chapter discusses mechanical events underlying cardiac cycle. The mature heart is built upon a collagenous skeleton in the shape of a fibrotendinous ring (the annulus fibrosus), which is located at the atrioventricular junction. The atria and ventricles contract in sequence, resulting in a cycle of pressure and volume changes, and a thorough knowledge of the cycle is needed for the diagnosis of valvular defects. The volume of blood in a ventricle at the end of the filling phase is called the end-diastolic volume and is typically around 120 ml in an adult human. With the closure of the aortic and pulmonary valves, each ventricle once again becomes a closed chamber. Intracardiac pacing is a therapeutic application of the cardiac catheter in which a wire catheter is wedged in the ventricle and used to stimulate each heart beat from an external electrical device, thereby replacing the heart’s own pacemaker.

2.1 Gross structure of the heart

2.2 Mechanical events of the cardiac cycle

2.3 Atrial cycle and central venous pressure cycle

2.4 Effect of heart rate on phase duration

2.5 Clinical aspects of the human cardiac cycle

The adult human heart weighs only 300—350 g, yet most of us can reasonably expect it to pump out around 200 million litres of blood over our allotted ‘three score years and ten’. In this chapter the mechanical events underlying this remarkable performance are described.

2.1 Gross structure of the heart

The mature heart is built upon a collagenous ’skeleton’ in the shape of a fibrotendinous ring (the annulus fibrosus) which is located at the atrioventricular junction (Figure 2.1). The muscular atria and ventricles are attached to either side of this ring, and the ring is perforated by four apertures, each containing a valve. As well as functioning as the mechanical base of the heart, the fibrotendinous ring insulates the ventricles electrically from the atria.

Figure 2.1 The heart lies obliquely across the chest. The fibrotendinous ring (black) forms the base of the heart. It contains the tricuspid (t), mitral (m), aortic and pulmonary valves grouped in an oblique plane beneath the sternum. The apex of the heart is formed by the left ventricle (LV), and the anterior surface is formed by the right ventricle (RV) and right atrium (RA). The inferior surface of the heart and the pericardium (not shown) rest on the central tendon of the diaphragm

Right atrium and tricuspid valve

The right atrium is a thin-walled muscular chamber which receives the venous return from the venae cavae and the coronary sinus (the main vein draining heart muscle; see Figure 2.2a). The wall near the entrance of the superior vena cava also contains the cardiac pacemaker, the ’sparking plug’ that initiates each heart beat (see Chapter 3). The right atrium communicates with the right ventricle through the tricuspid valve which, as its name implies has three cusps, although it is sometimes difficult to distinguish all three. It is the large anterior cusp which is mainly responsible for valve closure. Each cusp is a flexible flap of connective tissue, roughly 0.1mm thick, covered by endothelium. The free margin of the cusp is tethered by tendinous strings, called chordae tendineae, to an inward projection of the ventricle wall, the papillary muscle. The papillary muscle contracts and tenses the chordae tendineae during systole and this helps to prevent the valve from inverting into the atrium during systole.

Figure 2.2 Sections through the heart, (a) Schematic diagram of an oblique section, (b) Section across the ventricles to illustrate mode of emptying, (c) Arrangement of muscle fibres in the ventricle wall. RA, LA, right and left atrium. The opening just below the label RA is the coronary sinus. RV, LV, right and left ventricle; T, M, tricuspid and mitral valves; P, papillary muscle with chordae tendineae; A, aorta; PA, PV, pulmonary artery and veins; SVC, IVC, superior and inferior venae cavae

Right ventricle and pulmonary valve

The anterior wall of the right ventricle is about 0.5 cm thick in man, and resembles a pocket tacked around the septum (Figure 2.2b). Expulsion of blood is produced chiefly by the free anterior wall approaching the septum, rather like an old-fashioned bellows. The outlet from the ventricle into the pulmonary artery is guarded by the pulmonary valve which, like the aortic valve, consists of three equal sized, baggy cusps.

Left atrium and mitral valve

The left atrium receives blood from the pulmonary veins and transmits it into the left ventricle through a bicuspid valve. The large anterior and small posterior cusps are thought to look like a bishop’s mitre, hence the name ‘mitral valve’. The cusp margins are attached by chordae tendineae to two papillary muscles in the left ventricle.

Left ventricle and aortic valve

The chamber of the left ventricle is conical and ejection of blood is produced by a reduction in both diameter and length. The wall is around three times thicker than that of the right ventricle because it has to generate higher pressures. The innermost (endocarp-dial) muscle fibres are orientated longitudinally, running from the base of the heart (the fibrotendinous ring) to the apex (tip of left ventricle); the central fibres run circumferentially; the outermost or epicardial fibres again run longitudinally; and intermediate fibres run obliquely (Figure 2.2c). In other words, the muscle orientation changes progressively across the wall. When the chamber contracts, it twists forwards and the apex taps against the chest wall, producing the apex beat. This can be felt in the fifth, left intercostal space, about 10 cm from the midline. The root of the aorta contains a three-cusp valve similar to the pulmonary valve.

The heart is enclosed in a fibrous sac or pericardium, which is lined by a layer of mesothelium and is lubricated by pericardial fluid. The lower surface of the pericardium is fused to the diaphragm, and as the diaphragm descends during inspiration it pulls the heart into a more vertical orientation.

2.2 Mechanical events of the cardiac cycle

The atria and ventricles contract in sequence, resulting in a cycle of pressure and volume changes, and a thorough knowledge of the cycle is needed for the diagnosis of valvular defects. The cardiac cycle has four phases and we will begin, arbitrarily, at a moment when both the atria and ventricles are in diastole (relaxed). The timings below refer to a human cycle of 0.9 s duration (67 beats/min) and the data have been acquired by a combination of echocardiography (Section 2.5), cardiac catheterization (Section 2.5), electrocardiography (see Chapter 4) and cardiometry (Section 6.3).

Ventricular filling

Duration: 0.5 s

Inlet valves (tricuspid and mitral): open

Outlet valves (pulmonary and aortic): closed

Ventricular diastole lasts for nearly two-thirds of the cycle at rest, providing ample time for refilling the chamber. Initially the atria too are in diastole and blood flows passively from the great veins through the open atrioventricular valves into the ventricles. There is an initial phase of rapid filling, lasting about 0.15 s (Figure 2.3), which has a curious feature; even though ventricular volume is increasing, ventricular pressure is falling (see Figure 2.4; also Figure 6.10). The reason is that the ventricle wall is recoiling elastically from the deformation of systole, and is in effect sucking blood into the chamber. As the ventricle reaches its natural volume, filling slows down and further filling requires distension of the ventricle by the pressure of the venous blood; ventricular pressure now begins to rise. In the final third of the filling phase, the atria contract and force some additional blood into the ventricle. In resting subjects, this atrial boost is quite small and enhances ventricular filling by only 15—20%: indeed, the absence of an atrial boost in patients suffering from atrial fibrillation (ineffective atrial contractions; Section 4.8) makes little difference to resting cardiac output. During exercise, however, when heart rate is high the time available for passive ventricular filling is curtailed (see later), and the atrial boost becomes important.

Figure 2.3 The changes in valve setting and ventricular volume during one cardiac cycle lasting 0.9 s. EDV, end-diastolic volume; ESV, end-systolic volume; SV, stroke volume. The ejection fraction is SV/EDV. The heart sounds on the phonocardiogram are numbered 1 to 4 and the second sound is split here into an aortic component (A) and pulmonary component (P). The electrocardiogram waves are described in the text

Figure 2.4 Diagram of pressure and outflow on the left side of the human heart, based on data from intracardiac catheters and velocity measurements at...

Produkt-Details

• Erscheint lt. Verlag: 22.10.2013
• Sprache: englisch
• Themenwelt: Studium ► 1. Studienabschnitt (Vorklinik) ► Physiologie
• Themenwelt: Naturwissenschaften ► Biologie ► Humanbiologie
• ISBN-10: 1-4831-8384-X / 148318384X
• ISBN-13: 978-1-4831-8384-8 / 9781483183848