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The Heart -more info
The Heart: Study Stack for Test (more info)
| Term | Definition |
|---|---|
| Timing of Cardiac Cycle - in resting person: | atrial systole, ventricular systole, quiescent (when all four chambers are in diastole) |
| Cardiac Output (CO): | the amount ejected by ventricle in 1 minute (rate) |
| Cardiac Output: | heart rate x stroke volume |
| Cardiac Reserve: | the difference between a person's maximum and resting CO (increases with fitness, decreases with disease) CO can increase in an athlete |
| As you get older: | stroke volume will decrease, you still want to maintain a constant CO |
| Heart Rate: | is measured by taking a pulse. |
| Pulse: | surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips. |
| Tachycardia: | resting adult heart rate above 100 bpm (stress, anxiety, drugs, heart disease, fever, blood loss, damage to myocardium) |
| Bradycardia: | resting adult heart rate of less than 60 bpm (sleeping/rest, low blood temp, endurance trained athletes) |
| Positive Chronotropic Agents: | factors/agents that raise heart rate. |
| Negative Chronotropic Agents: | factors/agents that lower heart rate. |
| Common Carotid Artery: | neck |
| Radial Artery: | wrist |
| Cardiac Centers: | in the medulla oblongata initiate autonomic output to the heart. |
| Cardiostimulatory Effect: | some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways (increases heart rate) |
| Cardioinhibitory Effect: | others transmit parasympathetic signals by way of the vagus nerve. |
| Infant Heart Rate: | 120 bpm or more |
| Young adult female Heart Rate: | 72-80 bpm |
| Young adult male Heart Rate: | 64-72 bpm |
| Chronotropic Effects of the Autonomic Nervous System: | MEMORIZE |
| Chronotropic Effects of the Autonomic Nervous System: | MEMORIZE |
| Parasympathetic Vagus Nerves: | have cholinergic, inhibitory effects on the SA node and AV nods. [acetylcholine (ACh) binds to muscarinic receptors, opens K+ gates in the nodal cells, as K+ leaves the cells, they become hyperpolarized and fire less frequently, heart slows down] |
| What happens without influence from the cardiac centers? | The heart will still beat. The heart has an intrinsic heart rate of 100 bpm. |
| Cardiac Centers in the Medulla: | receive input input from many sources and integrate it into the decision to speed or slow the heart rate. |
| Higher Brain Centers: | affect heart rate & will respond to sensory/emotional stimuli [cerebral cortex, hypothalamus, limbic system] |
| Medulla: | also receives input from muscles, joints, arteries, and brain stem. |
| Proprioceptors in the muscles and joints: | informs the cardiac center about changes in activity. |
| Baroreceptors: | signal cardiac center when there is a pressure change. |
| Barorecptors: | pressure sensors in aorta & internal carotid arteries. |
| baro = | pressure |
| Chemoreceptors: | in aortic arch, carotid arteries and medulla oblongata |
| Chemoreceptors: | sensitive to blood pH, CO2, and O2 levels. |
| If blood pressure drops: | signal rate drops, and heart rate increases |
| If blood pressure rises: | signal rates increase, and heart rate decreases |
| Chemicals: | affect heart rate as well as neurotransmitters from cardiac nerves. |
| Drugs that stimulate heart: | Nicotine, thyroid hormone, caffeine |
| Nicotine: | stimulates catecholamine secretion (NE,EPI) |
| Thyroid hormone: | increases number of adrenergic receptors on heart so more responsive to sympatheitc stimulation. |
| Caffeine: | inhibits cAMP breakdown prolonging adrenergic effect. |
| All positive = | increases prolonged effect. |
| Three variables govern stroke volume: | Preload, contractility, afterload |
| Preload & Contractility: | etiher or can cause increase in stroke volume. |
| Afterload: | increase afterload which causes a decrease in stroke volume. |
| Preload: | the amount of tension in ventricular myocardium immediately before it begins to contract. |
| Increased preload: | causes increased force of contraction |
| Exercise: | increases venous return and stretches myocardium |
| Cardiocytes: | generate more tension during contraction |
| Increased cardiac output: | matches increased venous return |
| Frank-Starling Law of Heart: | Stroke volume is propportional to the end diastolic volume, ventricles eject as much blood as they recieve, the more they are stretched the harder they contract. |
| Contractility: | refers to how hard the myocardium contracts for a given preload. |
| Positive Inotropic Agents: | increase contractility. |
| Hypercalcemia: | can cause strong, prolonged contractions and even cardiac arrest in systole. |
| Catecholamines: | Increases calcium levels (examples of catecholamines are: dopamine EPI, NE) |
| Glucagon: | stimulates cAMP production |
| Digitalis: | raises intracellular calcium levels and contraction strength |
| Negative Inotropic Agents: | reduce contractility |
| Hypocalcemia: | can cause weak, irregular heartbeat and cardiac arrest in diastole |
| Hyperkalemia: | reduces strength of myocardial action potentials and the realease of Ca2+ into the sarcoplasm. |
| Vagus Nerves: | have effect on atria but too few nerves to ventricles for a significant effect |
| Afterload: | the blood pressure in the aorta and pulmonary trunk immediately diastal to the semilunar valves [opposes the opening of theses valves, limits stroke volume] |
| Hypertension: | increases afterload and opposes ventricular ejection. |
| Anything that impedes aterial circulation: | can also increase afterload. |
| Increase afterload: | will reduce stroke volume. |
| Exercise: | makes heart work harder and increases cardiac output. |
| Proprioceptors: signal cardiac center - | at beginning of exercise, signals from joints and muscles reach the cardiac center of the brain, & sympathetic output from cardiac center increases cardiac output |
| Increased muscular activity: | increases venous return [increase preload and ultimately cardiac output]. |
| Increase in heart rate and stroke volume: | cause an increase in cardiac output. |
| Exercise: | can produce ventricular hypertrophy. |
| The resting heart rates in athletes: | are lower |
| Increased stroke volume: | allows the heart to beat more slowly at rest (training athletes) |
Created by:
mr209368
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