CHAPTER

10
Cardiovascular Disorders: Heart
Disease
Fred M. Kusumoto, MD, FACC

Diseases of the cardiovascular system frequently confront the physician involved

in the day-to-day care of patients. Knowledge of the underlying
pathophysiologic processes associated with diseases of the heart and blood
vessels provides a critical framework for patient management. This chapter deals
with diseases of the heart, with the following chapter focusing on diseases of the
blood vessels. Normal cardiac structure and function are summarized here, and
pathophysiologic mechanisms for commonly encountered cardiac problems are
then discussed, with emphasis on arrhythmias, heart failure, valvular heart
disease, coronary artery disease, and pericardial disease.

NORMAL STRUCTURE & FUNCTION OF THE

HEART

ANATOMY
The heart is a complex organ whose primary function is to pump blood through
the pulmonary and systemic circulations. It is composed of four muscular
chambers: the main pumping chambers, the left and right ventricles, and the left
and right atria, which act like “priming pumps” responsible for the final 20–30%
of ventricular filling (Figure 10–1A). Peripheral venous return from the inferior
and superior venae cavae fills the right atrium and ventricle (through the open
tricuspid valve) (Figure 10–1B). With atrial contraction, additional blood flows
through the tricuspid valve and completes the filling of the right ventricle.
Unoxygenated blood is then pumped to the pulmonary artery and lung by the
right ventricle through the pulmonary valve (Figure 10–1C). Oxygenated blood
returns from the lung to the left atrium via four pulmonary veins (Figure 10–1D).
Sequential left atrial and ventricular contraction pumps blood back to the
peripheral tissues. The mitral valve separates the left atrium and ventricle, and
the aortic valve separates the left ventricle from the aorta (Figures 10–1D and
10–1E).
FIGURE 10–1 Anatomy of the heart. A: Anterior view of the heart. B: View of the right heart with
the right atrial wall reflected to show the right atrium. C: Anterior view of the heart with the anterior wall
removed to show the right ventricular cavity. D: View of the left heart with the left ventricular wall turned
back to show the mitral valve. E: View of the left heart from the left side with the left ventricular free wall
and mitral valve cut away to reveal the aortic valve. (Redrawn, with permission, from Cheitlin MD et al, eds. Clinical
Cardiology, 6th ed. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.)

The heart lies free in the pericardial sac, attached to mediastinal structures
only at the great vessels. During embryologic development, the heart invaginates
into the pericardial sac like a fist pushing into a partially inflated balloon. The
pericardial sac is composed of a serous inner layer (visceral pericardium)
directly apposed to the myocardium and a fibrous outer layer called the parietal
pericardium. Under normal conditions, approximately 40–50 mL of clear fluid,
which probably is an ultrafiltrate of plasma, fills the space between the layers of
the pericardial sac.
The left main and right coronary arteries arise from the root of the aorta and
provide the principal blood supply to the heart (Figure 10–2). The large left main
coronary artery usually branches into the left anterior descending artery and the
circumflex coronary artery. The left anterior descending coronary artery gives
off diagonal and septal branches that supply blood to the anterior wall and
septum of the heart, respectively. The circumflex coronary artery continues
around the heart in the left atrioventricular groove and gives off large obtuse
marginal arteries that supply blood to the left ventricular free wall. The right
coronary artery travels in the right atrioventricular groove and supplies blood to
the right ventricle via acute marginal branches. The posterior descending artery,
which supplies blood to the posterior and inferior walls of the left ventricle,
arises from the right coronary artery in 80% of people (right-dominant
circulation) and from the circumflex artery in the remainder (left-dominant
circulation).

FIGURE 10–2 Coronary arteries and their principal branches in humans. (Redrawn, with permission, from
Ross G. The cardiovascular system. In: Ross G, ed. Essentials of Human Physiology. Copyright © 1978 by Year Book Medical
Publishers, Inc., Chicago. Copyright © Elsevier.)

Contraction of the heart chambers is coordinated by several regions in the

heart composed of myocytes with specialized automaticity (pacemaker) and
conduction properties (Figure 10–3). Cells in the sinoatrial (SA) node and the
atrioventricular (AV) node have fast pacemaker rates (SA node: 60–100 bpm;
AV node: 40–70 bpm), and the His bundle and Purkinje fibers are characterized
by rapid rates of conduction. Because it has the fastest intrinsic pacemaker
rhythm, the SA node is usually the site of initiation of the cardiac electrical
impulse during a normal heartbeat. The impulse then rapidly depolarizes both
the left and right atria as it travels to the AV node. Conduction velocity slows
from 1 m/s in atrial tissue to 0.05 m/s in nodal tissue. After the delay in the AV
node, the impulse moves rapidly down the His bundle (1 m/s) and Purkinje
fibers (4 m/s) to simultaneously depolarize the right and left ventricles. The atria
and ventricles are separated by a fibrous framework that is electrically inert, so
under normal conditions the AV node and the contiguous His bundle form the
only electrical connection between the atria and ventricles. This arrangement
allows the atria and ventricles to beat in a synchronized fashion and minimizes
the chance of electrical feedback between the chambers.

FIGURE 10–3 Conducting system of the heart. Typical transmembrane action potentials for the SA
and AV nodes, other parts of the conduction system, and the atrial and ventricular muscles are shown along
with the correlation to the extracellularly recorded electrical activity (ie, the electrocardiogram [ECG]). The
action potentials and ECG are plotted on the same time axis but with different zero points on the vertical
scale. The PR interval is measured from the beginning of the P wave to the beginning of the QRS. (LAF,
left anterior fascicle.) (Redrawn, with permission, from Barrett KE et al, eds. Ganong’s Review of Medical Physiology, 25th ed.
McGraw-Hill, 2016.)
 The electrical activity of the heart can be measured from the body surface at
standardized positions by electrocardiography. On the electrocardiogram (ECG),
the P wave represents depolarization of atrial tissue; the electrocardiographic
wave (QRS) interval, ventricular depolarization; and the T wave, ventricular
repolarization (see Figure 10–3). Because normal ventricular depolarization
occurs almost simultaneously in the right and left ventricles—usually within 60–
100 ms—the QRS complex is narrow. Although the electrical activity of the
small specialized conduction tissues cannot be measured directly from the
surface, the interval between the P wave and the start of the QRS complex (PR
interval) primarily represents the conduction time of the AV node and His
bundle.

HISTOLOGY
Ventricular myocytes are normally 50–100 mm long and 10–25 mm wide. Atrial
and nodal myocytes are smaller, whereas myocytes of the Purkinje system are
larger in both dimensions. Myocytes are filled with hundreds of parallel striated
bundles termed myofibrils. Myofibrils are composed of repeating units, termed
sarcomeres, that form the major contractile unit of the myocyte (Figure 10–4).
Sarcomeres are complex structures composed of contractile proteins, myosin and
actin, which are connected by cross-bridges, and a regulatory protein complex,
tropomyosin. (See Cellular Physiology section later.)
FIGURE 10–4 A: Electron photomicrograph of cardiac muscle. The fuzzy thick lines are
intercalated disks (×12,000). (Reproduced, with permission, from Bloom W et al. A Textbook of Histology, 10th ed. Saunders,
1975. Copyright © Elsevier.) B: Diagram of cardiac muscle as seen under the light microscope (top) and the
electron microscope (bottom). (N, nucleus.) (Redrawn, with permission, from Braunwald E et al. Mechanisms of
contraction of the normal and failing heart. N Engl J Med. 1967;277:794. Copyright © 1967 Massachusetts Medical Society. Reprinted
with permission from Massachusetts Medical Society.)