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Lab #10: Cardiovascular Physiology p.1Lab #10: Cardiovascular Physiology Background The heart serves as a pump to drive the flow of blood through the body. It does so by undergoing a cycle of contraction and relaxation called the cardiac cycle. During the initial portion of the cardiac cycle, an electrical signal is generated in so-called “pacemaker cells” that is distributed through the heart through an electrical conduction system. In response to electrical stimulation, the myocardium of first the atria and then the ventricles undergoes contraction (systole), followed by sequential relaxation (diastole) of the two sets of chambers a fraction of a second later. This cycle of compressing on the blood in the ventricles during systole followed by the filling of the ventricles during diastole induces pressure changes in the ventricles that cause one-way valves in the heart to close audibly at different intervals of the cardiac cycle. The result of the injection of blood into the arteries by the ventricles undergoing systole is the generation of blood pressure, the primary driving force for the flow of blood through the body. In this exercise we will examine both electrical and mechanical events that take place during the cardiac cycle as well as measure the resultant blood pressure generated through this contractile activity. Electrical stimulation of the heart and electrocardiograms. The heart is auto-excitatory. Action potentials are formed spontaneously at regular intervals in specialized cells called pacemaker cells. These cells are arranged in a network that enables signals to be conducted throughout the myocardium from the point of origin. Four major structures are found within the conduction network (Fig 10.1). The sinoatrial node (SA node), which is located in the right atrial wall near the junction for the superior vena cava, contains pacemaker cells that undergo spontaneous depolarizations at a higher rate than any of the other pacemaker cells in the heart. As a result, the SA node sets the basic tempo for heart contraction (the sinus rhythm), and thus is often referred to as the pacemaker of the heart. Action potentials originating in the SA node are conducted rapidly through both atria through tracts of pacemaker cells. Located in the medial wall of the right atrium, near its junction with the right ventricle, is the atrioventricular node (AV node). The AV node contains the only pacemaker cells that lead out of the ventricles, thus normally electrical signals originating in the SA node and passing through the atria can only be conducted to the ventricles through this structure. The pacemaker cells in the AV node have very low conduction velocities, thus electrical signals pass through this region very slowly. Once the signal passes through the AV node, it is transferred to a structure called the Fig 10.1. The conduction system of the heart and the path of cardiac excitation. Typically, action potentials originate in the sinoatrial node (1) and are conducted rapidly through the atria (2) to the atrioventricular node (3). Once having passed through the AV node, the action potential propagates through the Bundle of His (4) and the lateral branches that arise from it (5). Once the signal has reached the apex of the heart, Purkinje fibers distribute the depolarization to the ventricular myocardium. Image from http://www.merck.com /mmhe/Lab #10: Cardiovascular Physiology p.2atrioventricular bundle (AV bundle) or Bundle of His, which conducts the signal through the interventricular septum towards the apex of the heart. Soon after entering the interventricular septum the AV bundle bifurcates into two separate branches. The conduction of the electrical signal through the interventricular septum, coupled with the slow conduction velocity of the AV node, causes a delay from when action potentials form in atrial myocardium and when they form in the ventricular myocardium (and subsequently in when the two sets of chambers contract) called the atrioventricular delay. This delay ensures that atrial systole is complete at the onset of ventricular systole. Once the signal reaches the apex of the heart it is conducted up the lateral walls of the ventricle through branched tracts of pacemaker cells called Purkinje fibers, which distribute the electrical signal to the ventricular myocardium. Electrical changes occurring during the cardiac cycle can be monitored from the surface of the body in a recording called an electrocardiogram (ECG, or EKG). A normal ECG recording associated with a single cardiac cycle contains three distinctive waveforms (Fig 10.2). The P wave is generated when the atria depolarize as the action potential wave spreads out from the sinoatrial node. The QRS complex (which consists of the Q, R, and S waves) is triggered by the depolarization of the ventricles just before ventricular systole. During the QRS wave the atria are repolarizing, but the small electrical disturbance caused by this is masked by the massive change in extracellular charge caused by the ventricles depolarizing. The last waveform, the T wave, is triggered by the repolarization of the ventricles at the end of ventricular systole. A number of important intervals can be measured from an ECG recording. A simple measure of the duration of the cardiac cycle can be measured simply as the time that elapses between a particular point in one cardiac to that same point in the next cardiac cycle (e.g., from R wave to R wave). The P-R interval, (which here we will measure as from the start of the P wave to the peak of the R wave), indicates the duration of time that the atria are depolarized, which is roughly equal to the duration of atrial systole. In addition, the P-R interval indicates how long it takes electrical signals to travel from the atria to the ventricles (i.e., the AV delay). During the R-T interval (here measured as the duration from the peak of the R wave to the start of the T wave), the ventricles remain in a depolarized state. The duration of this interval is roughly the duration of ventricular systole, thus the amount of time that blood is being forced out of the heart and into the arteries. Conversely, the T-R interval (here measured as the duration between the start of the T wave of one cardiac cycle to the peak of the R wave of the next cycle) indicates how long the ventricles remain in a polarized state between depolarizations, corresponding


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IUB PHSL-P 215 - Cardiovascular Physiology

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