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Cardiovascular Physiology Concepts, 2nd Edition by Richard E Klabunde PhD

By Richard E Klabunde PhD

Now in its moment version, this hugely available monograph lays a starting place for figuring out of the underlying strategies of ordinary cardiovascular functionality. scholars of medication and comparable disciplines welcome the book’s concise insurance as a pragmatic companion or replacement to a extra mechanistically orientated process or an encyclopedic body structure textual content. a spotlight on well-established cardiovascular ideas displays fresh, largely approved examine from the sphere.

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A. Ventricles prior to depolarization; isoelectric (zero) voltage recorded by electrodes aVL and II. B. Septal depolarization; voltage aVL < II. C. Apical depolarization; voltage aVL < II. D. Left ventricular depolarization (primarily); voltage aVL > II. E. Left ventricular depolarization; voltage in aVL > II. F. Ventricles depolarized; isoelectric voltage in aVL and II; red arrow represents mean electrical axis. In contrast, the mean vector is heading almost directly towards the lead II positive electrode, which results in a very tall, positive deflection (R wave of the QRS).

At low resting heart rates, vagal influences are dominant over sympathetic influences. This is termed vagal tone. Autonomic nerves increase SA nodal firing rate by both decreasing vagal tone and increasing sympathetic activity on the SA node in a reciprocal manner. An increase in heart rate is a positive chronotropic response (or positive chronotropy), whereas a reduction in heart rate is a negative chronotropic response (or negative chronotropy). Autonomic influences alter the rate of pacemaker firing through the following mechanisms: (1) changing the slope of phase 4; (2) altering the threshold voltage for triggering phase 0; and (3) altering the degree of hyperpolarization at the end of phase 3.

When these ionic currents are sufficient to rapidly depolarize the adjoining cell to its threshold potential, an action potential is elicited in the second cell. This is repeated in every cell, thereby causing action potentials to be propagated throughout the atria. 5 m/s (Fig. 10). , Bachmann bundle). As action potentials originating from the SA node spread across and depolarize the atrial muscle, excitation–contraction coupling is initiated (see Chapter 3). Nonconducting connective tissue separates the atria from the ventricles.

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