BYU PdBio 305 Rhees Cardiac Physiology
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| Endocardium | a thin layer of endothelium in the heart
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| Myocardium | muscle layer (cardiac muscle)
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| Epicardium | thin external layer covering the heart
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| Sinoatrial node | SA node or pacemaker;located within the posterior wall of the right atrium; rhythmic impulses originate in the SA node and spread through the atria
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| Atrioventricular node | AV node; located within the lower right interatrial septum; an impulse is delayed there for about 1/10 of a second to allow the atria to contract before ventricular contraction
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| Atrioventricular bundle | AV bundle or bundle of HIS; originiates in the AV node, dividing into two bundle branches which extend down the two sides of the interventricualr septum
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| Purkinje fibers | originate from the right and left branches, extending to the papillary muscles and lateral walls of the ventricles
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| Factors that may alter the heartbeat rate | sympathetic and parasympathetic impulses, hormones, body temp., exercise, and emotions
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| Systole | the phase of contraction
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| Diastole | the phase of relaxation
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| 4 steps of cardiac cycle | 1)mid-diastole 2)Atrial systole 3)Ventricular systole 4)Early diastole
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| mid-diastole | the atria and ventricles are relaxed, the tricuspid and mitral valves are open, and the aortic and pulmonary valves are closed. Blood flows passively from the atria into the ventricles, with 65% to 85% of ventricular filling occurring before the end of t
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| atrial systole | atria contract ad pump the additional 20-30% of the blood into the ventricles. As the atria contract, the vena cava and pulmonary veins narrow; there is some regurgitation. There is about 135 ml of blood in each ventricle.
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| ventricular systole | pressure changes and the AV valves close “lub”. All 4 valves are closed (isovolumetric ventricular contraction phase). When the pressure on the right exceeds 10 mm Hg and the left exceeds 80 mm Hg the pulmonary and aortic valves open.
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| Isovolumetric ventricular contraction phase | Atria repolarize/relax, ventricles depolarize, QRS complex in ECG, ventricles contract, rising pressure closes AV valves, first heart sound (lupp) all 4 valves closed, no blood can leave/enter the ventricles.
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| Stroke volume | volume of blood ejected from either ventricle, around 70ml (EDV-ESV=stroke volume)
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| End-systolic volume | Amount of blood remaining in either ventricle at the end of systole, about 60ml
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| Early diastole | as the ventricles relax, pressure drops; the pulmonary and aortic valves close, preventing backflow “dub”. The tricuspid and mutral valves open, and blod flows from the atria into the ventricles
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| Pulse pressure | the difference between the systolic and diastolic pressures; this pressure difference is what drives blood along the arteries to the capillaries.
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| factors that increase heart rate | excitement, anger, pain, hypoxia, exercise, epinephrine, norepinephrine, thyroid hormones, fever, inspiration
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| bradycardia | less than 60 beats/min-sleep, endurance athletes.
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| tachycardia | more than 100 beats/min-stress, anxiety, drugs, heart disease or ↑ body temp.
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| factors that decrease heart rate | expiration, fear, grief
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| inotropic | strength of contraction
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| franks starling's law of the heart | the greater the filling during diastole, the greater the force of contraction during systole
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| catecholamines | epinephrine and norepinephrin
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| digitalis | drug used for cardiac failure
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| factors that have a positive inotropic effect | frank starling, catecholamines, xanthines, digitalis
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| chronotropic | rate of contraction- Positive is anything speeding heart rate and Negative is anything slowing heart rate down
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| two ways nerves contracts the heart | chronotropic and inotropic
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| sympathetic control of heart | increase rate and force of contraction, uses norepinephrine to increase permeability to Na and Ca
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| parasympathetic control of heart | decrease rate and force of contraction, S.A node-right vagus, A.V. node- left vagus, uses acetylcholine to increase permeability to K+
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| stroke volume factors | Preload, contractility, and afterload. Increase preload or contractility = increase SV. Increased afterload = decreased SV
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| cardiac output | CO= stroke volume X heart rate
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| factors causing an increase in cardiac output | axiety, eating, exercies, increased body temperture, pregnancy
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| factors that may alter the heartbeat rate | sympathetic/parasympathetic impulses, hormones, body temperature, exercise, drugs, emotions, stimulation from exteroceptors
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| cardiac arrhythmia | deviations from normal heart rate or from normal electrical activity of the conduction system
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| Atrial fibrillation | many ectopic pacemakers in atria; irregular p waves; decrease in cardiac output; QRST look normal
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| ventricular fibrillation | caused by many ventricular ectopic pacemakers, uncoordinated, chaotic twitching, blood pressure drops, unless stopped, death will occur in short time
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| myocardial infarction | lack of blood flow to an area of the heart, may be caused by thrombus formation with blockage of vessels, spasms in the coronary arteries without total occlusion, narrowing caused by atherosclerosis; area is electrically dead
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| symptoms of myocardial infarction | pain in neck, jaw, back, shoulder, and left arm; vomiting; catecholamines released, increased blood sugar; cardiac troponins in blood; released enzymes; amount of troponin and creatine kinase correlate with severity of infarction
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| What vessel sends oxygenated blood to left atrium from lungs | Right/left pulmonary veins
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| What vessel sends deoxygenated blood to lungs from the heart | Pulmonary trunk/right & left pulmonary arteries
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| What vessels sends deoxygenated blood to right atrium from the body | Superior/inferior vena cava and coronary sinus
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| Left ventricle | Apex of heart/most of mass on posterior side. Pumps oxy blood through aortic semilunar valve to the body.
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| What vessels send oxygenated blood to the rest of the body from the heart | Aorta (subclavian, carotids, etc.)
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| Left atrium | Revieves oxygenated blood from lungs. 4 pulmonary veins, Pumps blood to left ventricle from mitral/bicuspid valve (left AV)
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| Right atrium | Receives deoxygented blood from superior/inferior vena cava and coronary sinus. Pumps blood to right ventricle through the tricuspid valve (right AV)
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| Right ventricle | Pumps deoxy blood through pulmonary semilunar valve to the lungs to become oxygenated (via pulmonary trunk)
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| What does the Q-T interval represent | Electrical depolarization and repolarization of the ventricles (very fast heart rates shorten Q-T length)
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| What does the QRS complex represent | AV node fires, ventricular depolarization, ventricular systole (atrial repolarization and diastole - signal obscured by strong QRS complex)
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| P wave | SA node fires, atrial depolarization, atrial systole
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| T wave | Ventricular repolarization
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| What does the P-Q interval represent | Electrical depolarization and repolarization of the atrium
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| Cardiac cycle | A full contraction/relaxation of all four heart chambers
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| What happens when you have Congestive Heart Failure on the right side of the heart | Left side (systemic circuit) is pumping more blood to the body causing pitting edema
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| What happens when you have Congestive Heart Failure on the left side of the heart | Right side (pulmonary circuit) is pumping more blood to lungs causing fluid to fill the lungs
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| Isovolumetric ventricular relaxation phase | Ventricles repolarize/relax, semi-lunar valves close, AV valves remain closed, 2nd heart sound occurs (dupp), T wave in ECG, no change in volume
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| Coronary circulation | blood supply to the heart
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| Anastomoses in coronary circulation | Many connections between arteries supplying blood to the heart, provide alternate routes if one artery
becomes occluded
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| What causes constant and rapid action potentials/brief depolarization in cardiac muscle vs AP in neurons | Rapid Na2+ voltage-gated channels opening and leaking Na2+ into the cells(peaks at 30mv), Na+2 channels close quikly/neurons need a strong stimulus to activate opening of Na2+ channels
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| What is cardiac muscle's resting membrane potential vs. neuron's | -90 mv/-70 mv
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| What happens during the plateau phase of cardiac muscles AP | Slow Ca2+ channels open and let Ca2+ into cell while K+ channels close. Also called "absolute refractory period." 250msec long (only 1msec in neurons.)
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| What happens to the heart during the plateau phase | The plateau phase is quite long, allowing the heart to fill, contract, and relax before starting another AP starts
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| What happens during the repolarization of the AP in cardiac muscle | Ca2+ channels close, K+ channels open causing rapid K+ outflow and AP returning to the RMP
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| End-diastolic volume | Volume in ventricle at the end of the diastole, about 130ml
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| The steps of the cardiac cycle in sequence are... | Ventricle filling (atrial systole), isovolumetric contraction, ventricular ejection, isovolumetric relaxation
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| When the pressure in the ventricles becomes lower than the pressure in the atria... | The AV valves open
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| Ach with the parasympathetic NS and heart rate | Ach releases from Vagus nerve onto SA node causing K+ channels to open. So you have K+ and Na2+ leaking in at the same time causing it to take longer to get to threshold =slower heart rate
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| Norepinephrine with the sympathetic NS and heart rate | Norepine. opens up Ca2+ channels, so you have Ca2+ and Na2+ leaking in at the same time, causing faster depolar. = increases heart rate AND force of contraction
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| What is the pathway of the conduction system | 1. SA node sets rate of depolar. & generates impulses for contraction, 2. Impulse pauses at AV node to let atria finish contracting, 3. Impulse passes through bundle of his, R/L bundle branches, and perkinje fibers, 4. Ventricular depolar. complete
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| Autorhythmicity of cardiac muscle | Regular, spontaneous depolarization from SA node
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| Automaticity of cardiac muscle | Heart beat originates within the heart
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