 | Term | Definition |
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cardiac cycle |
on complete contraction and relaxation of all four chambers of the heart |
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sphygmomanometer |
tool to measure blood pressure. Consists of a calibrated tube filled with mercury and attached to an inflatable pressure cuff wapped around the arm |
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pressure gradient |
a pressure difference between two points which makes the fluid flow |
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auscultation |
listening to the sounds made by the body |
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first heart sound |
"S1" aka "Lubb," is louder and a little longer, produced mainly by the left ventricle |
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second heart sound |
S2 aka Dubb, a little softer and sharper |
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third heart sound |
often times only audible in childern and adolescents |
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ventricular filling |
ventricles expand and their pressure drops below the artia's. The AV valve therefore opens and blood flows into the ventricles, causing ventricular pressure to rise and the atrial pressure to fall. There are three phases to this process of the heart: 1) rapid ventricular filling, 2) diastasis, and c) atrial systole. As the ventricles fill, the AV valves float to a closed postition. |
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rapid ventricular filling |
blood enters the ventricles especialy quickly. This is one of the phases of ventricular filling. |
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diastasis |
a slower filling of the ventricles. The second phase of ventricular filling, the completion of this phase is marked by the p wave. |
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atrial systole |
the last 1/3 of ventricular filling. only provides about 31% of blood contributions. |
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end-diastolic volume |
the amount of blood at the end of ventricular filling. each ventricle contains about 130mL. |
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Isovolumetric contraction |
the atria repolarize, relax, and remain in diastole for the remainder of the cardiac cycle, but the ventricles depolarize, generate the QRS complex, and begin to contract. Pressure in the ventricles rises sharply and reverses the pressure gradient between the atria and the ventricles. The AV valves close and the blood surges back against the cusps and produces the S1. Even though the ventricles are contracted, they do not eject the blood because the pressure in the aorta and the pulmonary trunk are still greater and oppose the opening of the semiulnar valves. |
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ventricular contraction |
ventricular pressure exceeds arterial pressure and forces the semiulnar valves open. Blood spurts out rapidly at first, and then flows out more slowly under pressure. This phase corresponds to the plateau of the myocardial action potential but lags somewhat behind it. The T wave also occurs late in this phase, beginning at the moment of peak ventricular pressure. The ventricles do not expell all of their blood |
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stroke volume |
the amount of blood ejected, about 70 mL |
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ejection fraction |
the percentage of the end-diastolic volume ejected, about 54%. This value is an important measur of cardiac health |
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end-systolic volume |
the blood remaining behind, about 60 mL |
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isovolumetric relaxation |
this phase is early ventricular diastole. when the T wave ends and the ventricles begin to expand. There are two hypotheses as to why the ventricles expand: 1) blood flow into the ventricles inflates them, and 2) the fibrous skeleton which was deformed from compression, springs back to its shape because of elsastic recoil. At the beginning blood from the aorta and pulmonary trunk breifly flow backward through the semiulnar valves, which quickly fills the cusps and closes them, this slight pressure rebound is called the dicrotic notch of the aortic pressure curve. S2 occurs as a result of blood rebounding from the closed semiulnar valves and the ventricles expand. This phases got its name from the fact that the semiulnar valves are closed, and the AV valves have not yet opened. |
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quiescent period |
all four chambers of the heart are in diastole |
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cardiac output |
the amount of blood ejected by each ventricle in one minute. Is equivalent to heart rate times stroke volume. THis amount varies with the body's state of activity |
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cardiac reserve |
the difference between the maximum and resting cardiac output. Peoplewith severe heart disease may have little or none of this... and little tolerace of physical exertion |
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pulse |
easiest measurement of someone's heart rate. Commonly taken at the radial artery in the wrist, or common carotid artery in the neck |
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tachycardia |
a persisent, resting adult heart rate above 100 bpm. can be caused by stress, anxiety, drugs, heart disease, and fever. The heart rate may also increase in order to compensate for a drop in stroke volume, for example, when a body has lost a significant amount of blood. |
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congestive heart failure |
the failure of either ventricle to eject blood effectively. Typically caused by a heart that is weakened because of myocardial infarction, chronic hyoertension, valvular insufficiency, or defects in the cardiac structure. If either of the ventricles blood can back up in the pulmonary or systemic circuit. Failure of one ventricle increases the workload of the other ventricle. |
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bradycardia |
a persistent, resting adult heart rate below 60 bpm endurance training enlarges the heart and increases its stroke volume...it can maintain the same cardiac output with fewer beats. Hypothermia also slows the heart and may be induced in preparation for cardiac surgery. |
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positive chronotropic agents |
factors that raise the heart rate |
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negative chronotropic agents |
factors that lower the heart rate |
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cardiac center |
portion of the medulla oblongata that modulates the heart rhythm and force. it is composed of two pools: a cardioacceleratory center and cardioinhibitory center. |
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cardioacceleratory center |
sends signals to the SA node, AV node, and myocardium through cardiac nerves. Secretes norepinnephrin, which increases the heart rate. Cardiac output peaks when the heart rate is 160-180 bpm, this limit is set because of the refractory period of the SA node. At such a high rate the ventricles have little time to fill between beats. |
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cardioinhibitory center |
sends signals to the heart by way of parasympathetic fibers in the vagus nerves to the SA and AV nodes, it secretes ACh which opens the K+ channels in the nodal cell. As the cell becomes hyperpolarized it fires less, so the heart slows down. |
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vagal tone |
a background firing rate which inhibits the nodes maintained by the vagus nerves. If the vagus nerve is severed, the SA node fires at its own intrinsic frequency, but with the vagus nerve intact, vagal tone holds the heart rate down to about 70-80 bpm |
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proprioceptors |
receptors found int he muscles and joints which can inform the cardiac center of changes in physical activity and the heart rate will increase the output before the metabolic demands of the muscles rise. |
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baroreceptors |
pressure sensors in the aorta and internal carotid arteries that send a continual stream of signals to the cardiac center. A negative feedback loop incorporating cardioacceleratory and cardioinhibitory factors prevents the blood pressure from deviating too far from the normal. |
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chemoreceptors |
sensors that are sensative to blood pH, CO2, and oxygen that are found in the aortic arch. Too much CO2 accumulated in the blood increases acidity and can be dangerous, the cardiac center is therefore signaled and cardioacceleratory factors increase the heart rate. Oxygen deficiency, like suffocation, tends to slow down the heart. |
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hyperkalemia |
a potassium excess, where K+ diffuses quickly into the myocytes, making the membrane potential less negative and interfereing with monocyte repolorization. The myocardium becomesless excitable and the heart rate becomes slow and irregular, and the heart rate may arrest in diastole |
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hypokalemia |
deficiency of K+. The K+ diffuses out of the myocytes, their membrane potential is more negative than normal, and they are harder to stimulate |
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hypercalcemia |
state of Ca++ excess which the heart beats abnormally slow |
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hypocalcemia |
state of Ca++ deficiency which the heart beats rapidly |
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preload |
the amount of tension in the ventricular myocardium immediately before it begins to cantract. The more blood that enters the heart, the greater the stretch of the myocardium, the more forceful the eventual contraction when the blood is expelled. |
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Frank-Starling law of the heart |
the principle that states the stroke volume is proportional to the end-diastolic volume. The ventricles tend to eject as much blood as they receive. The more they receive, the harder they contract when they are stimulated. |
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contractility |
refers to how hard the myocarium contracts for a given preload. Describes the increase caused by factors that make the myocytes more responsive to stimulation. |
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positive inotropic agents |
factors that increase contractility. Ca++ |
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negative inotropic agents |
factors that reduce the contractility. excess K++ because it reduces the strength of myocardial action potentials and thus reduces the release of Ca++ into the sarcoplasm; the vagus nerves have a negative inotropic affect on the atria |
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afterload |
the blood pressure in the arteries just outside the semilunar valves and opposes the opening of the valves. if this factor is increased, stroke volume will decrease |
