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The Heart -more info

The Heart: Study Stack for Test (more info)

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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