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Myocardial contraction reffers to the contraction of the heart muscle. The contraction is propagated through a system of intricate fibers and nodules each with their specific function and characteristics. Impulses generated by the SA node (sinoatrial node) - located medial to the opening of the vena cava - are passed to the AV node (atrioventricular node) - located medial to the right AV valve. The AV node further branches into two nerve bundles (left and right) that terminate at the apex of the heart into highly conductive Purkinje fibers that innervate the tip of the ventricles. Signal transduction from SA to AV node takes about 0.04s, because the two nodes are located on the same atrial wall. At the AV node, a critical delay of 0.11s is experienced before the signal reaches the left and right bundles, accumulating a total delay of 0.15s before the ventricles contract. The delay is critical, as it allows full contraction of the atria before the ventricles begin contracting. The highly conducting Purkinje fibers innervating the heart from the apex upwards cause contraction of the myocardium from the bottom up, allowing for complete or near complete evacuation of blood from the heart. The strength of the cardiac contraction is regulated by Ca++ ions, while the unusually long depolarization period of the muscle is regulated by increased permeability to both Ca++ and Na+ ions. Typical signal transduction carries an action potential along the membrane of myocardial muscle, by opening voltage gated Na+ channels and facilitating exchange of ions with K+. This activation of channels creates a temporary refractory period in which Na+/K+ exchange continues to occur along with Ca++ release inside the sarcoplasm. The ions further stimulate the thick muscle fillaments to contract by sliding of the thin and thick fibers past one another. Relaxation of the muscle occurs by a reverse process in which Na+ influx replaces K+ and Ca++; when Ca++ concentration decreases, the muscle relaxes.
1. Due to physical damage, the myocardium was deprived of Ca++ ions. What would the effect be on a) contractibility of the myocardium, b) heart rate, c) cardiac output.
2. A "defective" heart lacks the necessary 0.11s delay in signal transduction from AV node to the nerve bundles, the signal being "short circuited" to the Purkinje fibers. What is the immediate and most devastating effect?
1. a) contractibility not significantly affected b) heart rate increased due reduced depolarization time c) CO increased, as HR increases
2. Since the signal is shorted to the ventricles directly from the atria, they both contract simultaneously, causing reduced output due to partial evacuation of blood from the chambers. Insufficient circulation results.
For more information on this topic, please refer to Berne & Levy , pg. 63
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This page was written by Emil Istoc, a student in this course.
BME 403 Pages maintained by the T.A., Douglas Miles.