9. Summarize the events of the cardiac cycle including, diastole, Systole, valve
ID: 3519103 • Letter: 9
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9. Summarize the events of the cardiac cycle including, diastole, Systole, valve opening in closings, chamber volumes and pressures, and heart sounds 11. Define automaticity, describe the structure and function of the conduction system and relate it to the components of the ECG (p waves QRS complex t wave pr interval, and QT interval) 12. relate ECG to cardiac cycle 13. Explain how following influence cardiac output and the concept of cardiac reverse: Stroke volume, heart rate, venous return, end systolic volume, end diastolic volume, fill time, preload, after load, contractility 15. Predict how these chemicals influence cardiac output: Natriuretic peptides, epinephrine norepinephrine and acetylcholine. Anatomy & Physiology II Comprehensive Final Exam Study Guide Cardiovascular Systenm Blood (Martini Chapter 19) 1. CV2. Explain the roles of formed elements, plasma, and plasma proteins in the funet ion of blood. 2. CV4- Descri be hemopoiesis including the location, myleoid and lymphoid tissues, significant cells (hemocytoblasts, reticulocytes, megakaryocytes) and regulatory hormones (erythropoietin, colony stimulating factors). 3. CV7- Describe the structure and function of hemoglobin and define these related terms: oxyhemoglobin, deoxyhemoglobin, carboaminohemoglobin. 4. CV8-Trace the process of RBC breakdown and component recycling including locations and products created 5. cv9- Perform and explain ABO and Rh blood typing, the role of surface antigens, and antibodies 6. CV10- Predict which blood types are compatible and what happens when the incorrect ABO or Rh blood type is transfused 7. CV11-Outline the three phases of hemostasis and describe the steps in coagulation including the three pathways, hormones, major enzymes from initial damage to fibrinolysis using this vocabulary: Intrinsic, Extrinsic, Common pathway, Factor X, Thrombin, Fibrin, Plasmin The Heart (Martini Chapter 20) 8. CV 12- Describe the position and anatomy of the heart including the following: Pericardium (Parietal, Visceral), Chambers (Atria, Ventricles), Chordac Tendineae, Papillary Muscles, interventricular septum, Valves (Tricuspid, Bicuspid/Mitral, Pulmonary, Aortic), Epicardium, Myocardium, Endocardium, and arteries the supply (Right Coronary, Marginal, Posterior Interventricular, Left Coronary, Anterior Interventricular, Circumflex) and veins that drain (Great Cardiac, Middle Cardiac, Coronary Sinus) 9. CV13-Summarize the events of a cardiac cycle including, Diastole, Systole, Valve opening and closings, chamber Volumes & Pressures, and heart sounds 10. CV14- Trace the flow of blood through the heart chambers and great vessels 11. CV15-Define automaticity, describe the structure and function of the conduction system and relate it to the components of the ECG (P wave QRS complex T wave PR interval, and QT interval). 12. CV16- Relate the ECG to the cardiac cycle. 13. CV17-Explain how following influence Cardiac output and the concept ofcardiac reserve: Stroke Volume, Heart Rate, Venous Return, End Systolic Volume, End Diastolic Volume, Fill Time, Preload, Afterload, Contractility 14. SECOND QUESTION OVER ABOVE 15. CV18- Predict how these chemicals influence Cardiac output: Natriuretic Peptides, Epinephrine/ Norepinephrine, Acetylcholine Blood Vessels and Circulation (Martini Chapter 21) 16. CV20- Identify vessel structures and pressures (osmotic, hydrostatic, net) that determine capillary exchange of fluid, cells and solutes.Explanation / Answer
9) The cardiac events that occur from the beginning of one heartbeat to the beginning of the next are called the cardiac cycle. Each cycle is initiated by spontaneous generation of an action potential in the sinus node. This node is located in the superior lateral wall of the right atrium near the opening of the superior vena cava, and the action potential travels from here rapidly through both atria and then through the A-V bundle into the ventricles. Because of this special arrangement of the conducting system from the atria into the ventricles, there is a delay of more than 0.1 second during passage of the cardiac impulse from the atria into the ventricles. This allows the atria to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins. Thus, the atria act as primer pumps for the ventricles, and the ventricles in turn provide the major source of power for moving blood through the body’s vascular system.
Diastole and Systole The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills with blood, followed by a period of contraction called systole. The total duration of the cardiac cycle, including systole and diastole, is the reciprocal of the heart rate. For example, if heart rate is 72 beats/min, the duration of the cardiac cycle is 1/72 beats/min—about 0.0139 minutes per beat, or 0.833 second per beat.
When the ventricles contract, one first hears a sound caused by closure of the A-V valves. The vibration is low in pitch and relatively long-lasting and is known as the first heart sound. When the aortic and pulmonary valves close at the end of systole, one hears a rapid snap because these valves close rapidly, and the surroundings vibrate for a short period. This sound is called the second heart sound.
11)Some cardiac fibers have the capability of self-excitation, a process that can cause automatic rhythmical discharge and contraction. This is especially true of the fibers of the heart’s specialized conducting system, including the fibers of the sinus node. For this reason, the sinus node ordinarily controls the rate of beat of the entire heart,
Internodal Pathways and Transmission of the Cardiac Impulse Through the Atria.
The ends of the sinus nodal fibers connect directly with surrounding atrial muscle fibers. Therefore, action potentials originating in the sinus node travel outward into these atrial muscle fibers. In this way, the action potential spreads through the entire atrial muscle mass and, eventually, to the A-V node. The velocity of conduction in most atrial muscle is about 0.3m/sec, but conduction is more rapid, about 1m/sec, in several small bands of atrial fibers. One of these, called the anterior interatrial band, passes through the anterior walls of the atria to the left atrium. In addition, three other small bands curve through the anterior, lateral, and posterior atrial walls and terminate in the A-V node, these are called, respectively, the anterior, middle, and posterior internodal pathways. The cause of more rapid velocity of conduction in these bands is the presence of specialized conduction fibers. These fibers are similar to even more rapidly conducting “Purkinje fibers” of the ventricles. Atrioventricular Node and Delay of Impulse Conduction from the Atria to the Ventricles The atrial conductive system is organized so that the cardiac impulse does not travel from the atria into the ventricles too rapidly; this delay allows time for the atria to empty their blood into the ventricles before ventricular contraction begins. It is primarily the A-V node and its adjacent conductive fibers that delay this transmission into the ventricles. The A-V node is located in the posterior wall of the right atrium immediately behind the tricuspid valve,the impulse, after traveling through the internodal pathways, reaches the A-V node about 0.03 second after its origin in the sinus node. Then there is a delay of another 0.09 second in the A-V node itself before the impulse enters the penetrating portion of the A-V bundle, where it passes into the ventricles. A final delay of another 0.04 second occurs mainly in this penetrating A-V bundle, which is composed of multiple small fascicles passing through the fibrous tissue separating the atria from the ventricles. Thus, the total delay in the A-V nodal and A-V bundle system is about 0.13 second. This, in addition to the initial conduction delay of 0.03 second from the sinus node to the A-V node, makes a total delay of 0.16 second before the excitatory signal finally reaches the contracting muscle of the ventricles. Cause of the Slow Conduction. The slow conduction in the transitional, nodal, and penetrating A-V bundle fibers is caused mainly by diminished numbers of gap junctions between successive cells in the conducting pathways, so there is great resistance to conduction of excitatory ions from one conducting fiber to the next. Therefore, it is easy to see why each succeeding cell is slow to be excited. Rapid Transmission in the Ventricular Purkinje System Special Purkinje fibers lead from the A-V node through the A-V bundle into the ventricles. Except for the initial portion of these fibers where they penetrate the A-V fibrous barrier, they have functional characteristics that are quite the opposite of those of the A-V nodal fibers. They are very large fibers, even larger than the normal ventricular muscle fibers, and they transmit action potentials at a velocity of 1.5 to 4.0m/sec, a velocity about 6 times that in the usual ventricular muscle and 150 times that in some of the A-V nodal fibers. This allows almost instantaneous transmission of the cardiac impulse throughout the entire remainder of the ventricular muscle. The rapid transmission of action potentials by Purkinje fibers is believed to be caused by a very high level of permeability of the gap junctions at the intercalated discs between the successive cells that make up the Purkinje fibers. Therefore, ions are transmitted easily from one cell to the next, thus enhancing the velocity of transmission. The Purkinje fibers also have very few myofibrils, which means that they contract little or not at all during the course of impulse transmission. One-Way Conduction Through the A-V Bundle. A special characteristic of the A-V bundle is the inability, except in abnormal states, of action potentials to travel backward from the ventricles to the atria. This prevents re-entry of cardiac impulses by this route from the ventricles to the atria, allowing only forward conduction from the atria to the ventricles. Furthermore, it should be recalled that everywhere, except at the A-V bundle, the atrial muscle is separated from the ventricular muscle by a continuous fibrous barrier This barrier normally acts as an insulator to prevent passage of the cardiac impulse between atrial and ventricular muscle through any other route besides forward conduction through the A-V bundle itself. (In rare instances, an abnormal muscle bridge does penetrate the fibrous barrier elsewhere besides at the A-V bundle. Under such conditions, the cardiac impulse can re-enter the atria from the ventricles and cause a serious cardiac arrhythmia.) Distribution of the Purkinje Fibers in the Ventricles— The Left and Right Bundle Branches. After penetrating the fibrous tissue between the atrial and ventricular muscle, the distal portion of the A-V bundle passes downward in the ventricular septum for 5 to 15 millimeters toward the apex of the heart. Then the bundle divides into left and right bundle branches that lie beneath the endocardium on the two respective sides of the ventricular septum. Each branch spreads downward toward the apex of the ventricle, progressively dividing into smaller branches. These branches in turn course sidewise around each ventricular chamber and back toward the base of the heart. The ends of the Purkinje fibers penetrate about one third of the way into the muscle mass and finally become continuous with the cardiac muscle fibers. From the time the cardiac impulse enters the bundle branches in the ventricular septum until it reaches the terminations of the Purkinje fibers, the total elapsed time averages only 0.03 second. Therefore, once the cardiac impulse enters the ventricular Purkinje conductive system, it spreads almost immediately to the entire ventricular muscle mass. Transmission of the Cardiac Impulse in the Ventricular Muscle Once the impulse reaches the ends of the Purkinje fibers, it is transmitted through the ventricular muscle mass by the ventricular muscle fibers themselves. The velocity of transmission is now only 0.3 to 0.5m/sec, one sixth that in the Purkinje fibers. The cardiac muscle wraps around the heart in a double spiral, with fibrous septa between the spiraling layers; therefore, the cardiac impulse does not necessarily travel directly outward toward the surface of the heart but instead angulates toward the surface along the directions of the spirals. Because of this, transmission from the endocardial surface to the epicardial surface of the ventricle requires as much as another 0.03 second, approximately equal to the time required for transmission through the entire ventricular portion of the Purkinje system. Thus, the total time for transmission of the cardiac impulse from the initial bundle branches to the last of the ventricular muscle fibers in the normal heart is about 0.06 second.
The normal electrocardiogram is composed of a P wave, a QRS complex, and a T wave. The QRS complex is often, but not always, three separate waves: the Q wave, the R wave, and the S wave. The P wave is caused by electrical potentials generated when the atria depolarize before atrial contraction begins. The QRS complex is caused by potentials generated when the ventricles depolarize before contraction, that is, as the depolarization wave spreads through the ventricles. Therefore, both the P wave and the components of the QRS complex are depolarization waves.The T wave is caused by potentials generated as the ventricles recover from the state of depolarization. This process normally occurs in ventricular muscle 0.25 to 0.35 second after depolarization, and the T wave is known as a repolarization wave.
12) The electrocardiogram shows the P, Q, R, S, and T waves. They are electrical voltages generated by the heart and recorded by the electrocardiograph from the surface of the body. The P wave is caused by spread of depolarization through the atria, and this is followed by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after the electrocardiographic P wave. About 0.16 second after the onset of the P wave, the QRS waves appear as a result of electrical depolarization of the ventricles, which initiates contraction of the ventricles and causes the ventricular pressure to begin rising, as also shown in the figure. Therefore, the QRS complex begins slightly before the onset of ventricular systole. Finally, one observes the ventricular T wave in the electrocardiogram. This represents the stage of repolarization of the ventricles when the ventricular muscle fibers begin to relax. Therefore, the T wave occurs slightly before the end of ventricular contraction.
15) natriuretic pepetides reduces cardiac output by decreasing ventricular preload.
Norepinephrine, produced by the adrenal medulla, is a stress hormone that increases cardiac output.
ACH decreases cardiac output by decreasing both stroke volume and heart rate.
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