The conduction of the cardiac impulse throughout the heart is traced by the ECG, which is recorded from the surface of the body. The ECG is useful in detecting and analyzing various cardiac arrhythmias, including altered SA rhythms, AV conduction blocks, premature depolarizations, ectopic tachycardias, and atrial and ventricular fibrillation.

On excitation, voltage-gated calcium channels open, allowing extracellular Ca++ to enter the cardiac myocytes. This influx of Ca++ triggers the release of Ca++ from the sarcoplasmic reticulum, resulting in elevated intracellular [Ca++]. The increased intracellular [Ca++] leads to the contraction of the myofilaments. Relaxation is achieved by pumping Ca++ back into the sarcoplasmic reticulum and exchanging it with extracellular Na+ across the sarcolemma, which restores the resting cytosolic [Ca++]. The velocity and force of contraction depend on intracellular [Ca++]. Force and velocity have an inverse relationship, with maximal velocity occurring in the absence of any load during contraction.

During ventricular contraction, preload refers to the stretch of the fibers caused by blood during ventricular filling, while afterload refers to the arterial pressure against which the ventricle ejects the blood. Increased myocardial fiber length, which occurs during augmented ventricular filling (preload) in diastole, results in a more forceful ventricular contraction. This relationship between fiber length and the strength of contraction is known as the Frank-Starling law of the heart.

Contractility is an expression of cardiac performance at a given preload and afterload, and it can be influenced by the autonomic nervous system.

According to the Fick principle, cardiac output can be determined by measuring the O2 consumption of the body (q2) and the oxygen content of arterial blood ([O2]a) and mixed venous blood ([O2]v). Cardiac output is calculated as q2/([O2]a - [O2]v). It can also be measured noninvasively using Doppler echocardiography.

In the normal heart, the rate of ATP hydrolysis is balanced by the rate of ATP synthesis. ATP is generated through oxidative phosphorylation of fatty acids and glucose, which requires O2. During exercise, when the rate of ATP hydrolysis increases, the O2 consumption for oxidative phosphorylation also increases. The rate of O2 utilization is thus linked to the rate of cardiac work. The myocardium primarily functions aerobically and utilizes substrates in proportion to their arterial concentration.

After studying this chapter, the student should be able to answer the following questions:

1. What physical properties of blood vessels and blood determine hemodynamics, and how are they defined by Poiseuille's law?
2. How does arterial compliance relate to stroke volume and pulse pressure? How does arterial compliance impact the arterial pulse wave and cardiac work?
3. What are mean, systolic, diastolic, and pulse pressures, and how are they measured?
4.
The ECG, which is recorded from the surface of the body, traces the conduction of the cardiac impulse throughout the heart. The ECG may be used to detect and analyze certain cardiac arrhythmias, such as altered SA rhythms, AV conduction blocks, premature depolarizations, ectopic tachycardias, and atrial and ventricular fibrillation.
8.
On excitation, voltage-gated calcium channels open to admit extracellular Ca++ into the cardiac myocytes. The influx of Ca++ triggers the release of Ca++ from the sarcoplasmic reticulum. The elevated intracellular [Ca++] elicits contraction of the myofilaments. Relaxation is accomplished through the restoration of resting cytosolic [Ca++] by the pumping of Ca++ back into the sarcoplasmic reticulum and the exchange of Ca++ for extracellular Na+ across the sarcolemma. Velocity and force of contraction are functions of intracellular [Ca++]. Force and velocity are inversely related, and so with no load, velocity is maximal. In
Abriel H, Rougier J-S, Jalife J. Ion channel macromolecular complexes in cardiomyocites: Roles in sudden cardiac death. Circ Res. 2015;116:1971.
Bers DM, Guo T. Calcium signaling in cardiac ventricular myocytes. Ann N Y Acad Sci. 2005;1047:86. Cannell MB, Kong CH. Local control in cardiac E-C coupling. J Mol Cell Cardiol. 2012;52:298.
an isovolumic contraction, no external shortening occurs.
9.
In ventricular contraction, preload is stretch of the fibers by blood during ventricular filling. Afterload is the arterial pressure against which the ventricle ejects the blood. An increase in myocardial fiber length, as occurs with augmented ventricular filling (preload) during diastole, produces a more forceful ventricular contraction. This relationship between fiber length and strength of contraction is known as the Frank-Starling law of the heart.
10.
Contractility is an expression of cardiac performance at a given preload and afterload. Contractility can be modulated by the autonomic nervous system.
11.
To determine cardiac output, according to the Fick principle, the O2 consumption of the body (q2) and the oxygen content of arterial blood ([O2]a) and mixed venous blood ([O2]v) are measured. Cardiac output = q2/([O2]a − [O2]v). It can also be measured noninvasively by Doppler echocardiography.
12.
In the normal heart, the rate of ATP hydrolysis is matched by the rate of ATP synthesis. ATP is generated by oxidative phosphorylation of fatty acids and glucose, a process that requires O2. When the rate of ATP hydrolysis increases, as during exercise, the consumption of O2 for oxidative phosphorylation also increases. The rate of O2 utilization is thereby coupled to the rate of cardiac work. The myocardium functions only aerobically, and in general it uses substrates in proportion to their arterial concentration.
Gima K, Rudy Y. Ionic current basis of electrocardiographic waveforms. Circ Res. 2003;90:889.
Priori SG. The fifteen years of discoveries that shaped molecular electrophysiology: time for appraisal. Circ Res. 2010;107: 451.
Upon completion of this chapter, the student should be able to answer the following questions: 1.
What physical properties of blood vessels and blood determine hemodynamics, and how are they defined by Poiseuille’s law?
2.
How is arterial compliance related to stroke volume and pulse pressure? How does arterial compliance affect the arterial pulse wave and cardiac work?
3.
What are mean, systolic, diastolic, and pulse pressures, and how are they measured?
4.