The heart lies in the center of the thoracic cavity and is suspended by its attachments to the great vessels within a thin fibrous sac called the pericardium. A small amount of fluid in the sac lubricates the surface of the heart and allows it to move freely during contraction and relaxation. Blood flow through all organs is passive and occurs only because arterial pressure is kept higher than venous pressure by the pumping action of the heart. The right heart pump provides the energy necessary to move blood through the pulmonary vessels, and the left heart pump provides the energy to move blood through the systemic organs.
The pathway of blood flow through the chambers of the heart is indicated in Figure 1–4. Venous blood returns from the systemic organs to the right atrium via the superior and inferior venae cavae. This “venous” blood is deficient in oxygen because it has just passed through systemic organs that all extract oxygen from blood for their metabolism. It then passes through the tricuspid valve into the right ventricle and from there it is pumped through the pulmonic valve into the pulmonary circulation via the pulmonary arteries. Within the capillaries of the lung, blood is “reoxygenated” by exposure to oxygen-rich inspired air. Oxygenated pulmonary venous blood flows in pulmonary veins to the left atrium and passes through the mitral valve into the left ventricle. From there it is pumped through the aortic valve into the aorta to be distributed to the systemic organs.
Pathway of blood flow through the heart.
Although the gross anatomy of the right heart pump is somewhat different from that of the left heart pump, the pumping principles are identical. Each pump consists of a ventricle, which is a closed chamber surrounded by a muscular wall, as illustrated in Figure 1–5
. The valves are structurally designed to allow flow in only one direction and passively
open and close in response to the direction of the pressure differences across them. Ventricular pumping action occurs because the volume of the intraventricular chamber is cyclically changed by rhythmic and synchronized contraction and relaxation of the individual cardiac muscle cells that lie in a circumferential orientation within the ventricular wall.
Ventricular pumping action.
When the ventricular muscle cells are contracting, they generate a circumferential tension in the ventricular walls that causes the pressure within the chamber to increase. As soon as the ventricular pressure exceeds the pressure in the pulmonary artery (right pump) or aorta (left pump), blood is forced out of the chamber through the outlet valve, as shown in Figure 1–5. This phase of the cardiac cycle during which the ventricular muscle cells are contracting is called systole. Because the pressure is higher in the ventricle than in the atrium during systole, the inlet or atrioventricular (AV) valve is closed. When the ventricular muscle cells relax, the pressure in the ventricle falls below that in the atrium, the AV valve opens, and the ventricle refills with blood, as shown on the right side in Figure 1–5. This portion of the cardiac cycle is called diastole. The outlet valve is closed during diastole because arterial pressure is greater than intraventricular pressure. After the period of diastolic filling, the systolic phase of a new cardiac cycle is initiated.
The amount of blood pumped per minute from each ventricle (the cardiac output
, CO) is determined by the volume of blood ejected per beat (the stroke volume
, SV) and the number of heartbeats per minute (the heart rate
, HR) as follows:
It should be evident from this relationship that all influences on cardiac output must act through changes in either the heart rate or the stroke volume.
An important implication of the above is that the volume of blood that the ventricle pumps with each heartbeat (ie, the stroke volume, SV) must equal the blood volume inside the ventricle at the end of diastole (end-diastolic volume, EDV) minus ventricular volume at the end of systole (end-systolic volume, ESV). That is:
Thus, stroke volume can only be changed by changes in EDV and/or ESV. The implication for the bigger picture is that cardiac output can only be changed by changes in HR, EDV, and/or ESV.
Efficient pumping action of the heart requires a precise coordination of the contraction of millions of individual cardiac muscle cells. Contraction of each cell is triggered when an electrical excitatory impulse (action potential) sweeps over its membrane. Proper coordination of the contractile activity of the individual cardiac muscle cells is achieved primarily by the conduction of action potentials from one cell to the next via gap junctions that connect all cells of the heart into a functional syncytium (ie, acting as one synchronous unit). In addition, muscle cells in certain areas of the heart are specifically adapted to control the frequency of cardiac excitation, the pathway of conduction, and the rate of the impulse propagation through various regions of the heart. The major components of this specialized excitation and conduction system are shown in Figure 1–6. These include the sinoatrial node (SA node), the atrioventricular node (AV node), the bundle of His, and the right and left bundle branches made up of specialized cells called Purkinje fibers.
Electrical conduction system of the heart.
The SA node contains specialized cells that normally function as the heart’s pacemaker and initiate the action potential that is conducted through the heart. The AV node contains slowly conducting cells that normally function to create a slight delay between atrial contraction and ventricular contraction. The Purkinje fibers are specialized for rapid conduction and ensure that all ventricular cells contract at nearly the same instant. The overall message is that HR is normally controlled by the electrical activity of the SA nodal cells. The rest of the conduction system ensures that all the rest of the cells in the heart follow along in proper lockstep for efficient pumping action.
Control of Cardiac Output
Autonomic Neural Influences
Although the heart can inherently beat on its own, cardiac function can be influenced profoundly by neural inputs from both the sympathetic and parasympathetic divisions of the autonomic nervous system. These inputs allow us to modify cardiac pumping as is appropriate to meet changing homeostatic needs of the body. All portions of the heart are richly innervated by adrenergic sympathetic fibers.
When active, these sympathetic nerves release norepinephrine
(noradrenaline) on cardiac cells. Norepinephrine
interacts with β1
-adrenergic receptors on cardiac muscle cells to increase the heart rate, increase the action potential conduction velocity, and increase the force of contraction and rates of contraction and relaxation. Overall, sympathetic activation acts to increase cardiac pumping.
Cholinergic parasympathetic nerve fibers travel to the heart via the vagus nerve and innervate the SA node, the AV node, and the atrial muscle. When active, these parasympathetic nerves release acetylcholine on cardiac muscle cells. Acetylcholine interacts with muscarinic receptors on cardiac muscle cells to decrease the heart rate (SA node) and decrease the action potential conduction velocity (AV node). Parasympathetic nerves may also act to decrease the force of contraction of atrial (not ventricular) muscle cells. Overall, parasympathetic activation acts to decrease cardiac pumping. Usually, an increase in parasympathetic nerve activity is accompanied by a decrease in sympathetic nerve activity, and vice versa.
Diastolic Filling: Starling’s Law of the Heart
One of the most fundamental causes of variations in stroke volume was described by William Howell in 1884 and by Otto Frank in 1894 and formally stated by E. H. Starling in 1918. These investigators demonstrated that, with other factors being equal, if cardiac filling increases during diastole, the volume ejected during systole also increases. As a consequence, and as illustrated in Figure 1–7
, stroke volume increases nearly in proportion to increases in end-diastolic volume. This phenomenon is commonly referred to as Starling’s law of the heart
. In a subsequent chapter, we will describe how Starling’s law is a direct consequence of the intrinsic mechanical properties of cardiac muscle cells. However, knowing the mechanisms behind Starling’s law is not ultimately as important as appreciating its consequences. The primary consequence is that stroke volume (and therefore cardiac output) is strongly influenced by cardiac filling during diastole. Therefore, we shall later pay particular attention to the factors that affect cardiac filling and how they participate in the normal regulation of cardiac output.
Starling’s law of the heart.
Requirements for Effective Operation
For effective efficient ventricular pumping action, the heart must be functioning properly in five basic respects:
The contractions of individual cardiac muscle cells must occur at regular intervals and be synchronized (not arrhythmic).
The valves must open fully (not stenotic).
The valves must not leak (not insufficient or regurgitant).
The muscle contractions must be forceful (not failing).
The ventricles must fill adequately during diastole.
In the subsequent chapters, we will study in detail how these requirements are met in the normal heart.