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Cardiac Physiology

BYU PdBio 305 Rhees Cardiac Physiology

Endocardium a thin layer of endothelium in the heart
Myocardium muscle layer (cardiac muscle)
Epicardium thin external layer covering the heart
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
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
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
Purkinje fibers originate from the right and left branches, extending to the papillary muscles and lateral walls of the ventricles
Factors that may alter the heartbeat rate sympathetic and parasympathetic impulses, hormones, body temp., exercise, and emotions
Systole the phase of contraction
Diastole the phase of relaxation
4 steps of cardiac cycle 1)mid-diastole 2)Atrial systole 3)Ventricular systole 4)Early diastole
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
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.
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.
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.
Stroke volume volume of blood ejected from either ventricle, around 70ml (EDV-ESV=stroke volume)
End-systolic volume Amount of blood remaining in either ventricle at the end of systole, about 60ml
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
Pulse pressure the difference between the systolic and diastolic pressures; this pressure difference is what drives blood along the arteries to the capillaries.
factors that increase heart rate excitement, anger, pain, hypoxia, exercise, epinephrine, norepinephrine, thyroid hormones, fever, inspiration
bradycardia less than 60 beats/min-sleep, endurance athletes.
tachycardia more than 100 beats/min-stress, anxiety, drugs, heart disease or ↑ body temp.
factors that decrease heart rate expiration, fear, grief
inotropic strength of contraction
franks starling's law of the heart the greater the filling during diastole, the greater the force of contraction during systole
catecholamines epinephrine and norepinephrin
digitalis drug used for cardiac failure
factors that have a positive inotropic effect frank starling, catecholamines, xanthines, digitalis
chronotropic rate of contraction- Positive is anything speeding heart rate and Negative is anything slowing heart rate down
two ways nerves contracts the heart chronotropic and inotropic
sympathetic control of heart increase rate and force of contraction, uses norepinephrine to increase permeability to Na and Ca
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+
stroke volume factors Preload, contractility, and afterload. Increase preload or contractility = increase SV. Increased afterload = decreased SV
cardiac output CO= stroke volume X heart rate
factors causing an increase in cardiac output axiety, eating, exercies, increased body temperture, pregnancy
factors that may alter the heartbeat rate sympathetic/parasympathetic impulses, hormones, body temperature, exercise, drugs, emotions, stimulation from exteroceptors
cardiac arrhythmia deviations from normal heart rate or from normal electrical activity of the conduction system
Atrial fibrillation many ectopic pacemakers in atria; irregular p waves; decrease in cardiac output; QRST look normal
ventricular fibrillation caused by many ventricular ectopic pacemakers, uncoordinated, chaotic twitching, blood pressure drops, unless stopped, death will occur in short time
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
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
What vessel sends oxygenated blood to left atrium from lungs Right/left pulmonary veins
What vessel sends deoxygenated blood to lungs from the heart Pulmonary trunk/right & left pulmonary arteries
What vessels sends deoxygenated blood to right atrium from the body Superior/inferior vena cava and coronary sinus
Left ventricle Apex of heart/most of mass on posterior side. Pumps oxy blood through aortic semilunar valve to the body.
What vessels send oxygenated blood to the rest of the body from the heart Aorta (subclavian, carotids, etc.)
Left atrium Revieves oxygenated blood from lungs. 4 pulmonary veins, Pumps blood to left ventricle from mitral/bicuspid valve (left AV)
Right atrium Receives deoxygented blood from superior/inferior vena cava and coronary sinus. Pumps blood to right ventricle through the tricuspid valve (right AV)
Right ventricle Pumps deoxy blood through pulmonary semilunar valve to the lungs to become oxygenated (via pulmonary trunk)
What does the Q-T interval represent Electrical depolarization and repolarization of the ventricles (very fast heart rates shorten Q-T length)
What does the QRS complex represent AV node fires, ventricular depolarization, ventricular systole (atrial repolarization and diastole - signal obscured by strong QRS complex)
P wave SA node fires, atrial depolarization, atrial systole
T wave Ventricular repolarization
What does the P-Q interval represent Electrical depolarization and repolarization of the atrium
Cardiac cycle A full contraction/relaxation of all four heart chambers
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
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
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
Coronary circulation blood supply to the heart
Anastomoses in coronary circulation Many connections between arteries supplying blood to the heart, provide alternate routes if one artery becomes occluded
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
What is cardiac muscle's resting membrane potential vs. neuron's -90 mv/-70 mv
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.)
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
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
End-diastolic volume Volume in ventricle at the end of the diastole, about 130ml
The steps of the cardiac cycle in sequence are... Ventricle filling (atrial systole), isovolumetric contraction, ventricular ejection, isovolumetric relaxation
When the pressure in the ventricles becomes lower than the pressure in the atria... The AV valves open
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
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
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
Autorhythmicity of cardiac muscle Regular, spontaneous depolarization from SA node
Automaticity of cardiac muscle Heart beat originates within the heart
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