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Cardiac Physiology

BYU PdBio 305 Rhees Cardiac Physiology

QuestionAnswer
How much blood does the heart pump? L/min 5
How long does it take for all the blood to be pumped through? one minute
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 the moment when all 4 valves are closed and no blood can enter or leave the ventricles.
Minimum diastolic pressure on both sides 10mm Hg and 80 mm Hg
Normal resting condition pressure 24 mm Hg and 120 mm Hg
Stroke volume volume of blood ejected from either ventricle; 70 to 80 ml
End-systolic volume Amount of blood remaining in either ventricle at the end of systole; 50 ml
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
Sphygmomanometer the mercury manometer to take blood pressure
Auscultatory method method to take blood pressure using atrial sounds
Sounds of Korotkoff the turbulent flow of the blood with each beat creates vibrations that are heard in the stethoscope when taking blood pressure using the auscultatory method
Pulse pressure the difference between the systolic and diastolic pressures; this pressure difference is what drives blood along the arteries to the capillaries.
SA node rate 72-75 beats/min
AV node rate 50-60 beats/min
ventricles rate 30-40 beats/min
factors that increase heart rate excitement, anger, pain, hypoxia, exercise, epinephrine, norepinephrine, thyroid hormones, fever, inspiration
bradycardia less than 60 beats/min
tachycardia more than 100 beats/min
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 contractin during systole
catecholamines epinephrine and norepinephrin
xanthines caffeine, theophylline
digitalis drug used for cardiac failure
factors that have a positive inotropic effect frank starling, catecholamines, xanthines, digitalis
chronotropic rate of contraction
dromotropic rate of conduction of impulse
two ways nerves contrals the heart chronotropic and inotropic
sympathetic control of heart increase rate and force of contraction, uses norepinephrine to increase permeability to Na and Ca
max sympathetic stimulation 250 beats/min
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+
max parasympathetic stimulation 20-30 beats/min
stroke volume 60-80 ml; amount of blood pumped out of each ventricle per beat
cardiac output CO= stroke volume X heart rate
caradiac output of average person 5.76 Liters/minute
factors causing an increase in cardiac output axiety, eating, exercies, increased body temperture, pregnancy
fick method blood flow=cardiac output; the amount of oxygen consumed by the body in a perdod of time is divided by the AV difference
fick equation for cardiad output CO=(oxygen consumed in ml/min)/(arterial O2-venous O2)
factors that may alter the heartbeat rate sympathetic/parasympathetic impulses, hormones, body temperature, exercise, drugs, emotions, stimulation from exteroceptors
ectopic pacemakers out of place pacemakers
einthoven's triangle electrodes attached to the left shoulder, right shoulder, and left leg, forming a triangle to take ECGs
cardiac arrhythmia deviations from nromal heart rate or from normal electrical activity of the conduction system
causes of ectopic pacemakers ischemia, heart damage, dilation of heart, toxic irritants (nicotine, caffeine, alcohol), lack of sleep, anxiety, extremes in body temp, change in body pH
atrial premature beat premature depolarization of SA node or ectopic pacemaker; some P waves are weird; little clinical significance
AV nodal premature beat ectopic discharge of the AV node; normal QRS but no P wave before
Premature Ventricular Depolarization PVD or PVC; ectopic pacemaker in ventricles; no P wave, wide QRS, high voltage, inverted T wave, pause afterwords like a skipped beat
bigeminy one normal and one PVD
trigeminy two normal and one PVD
SA block pacemaker stops for at least one cycle and then resumes; all is identical before and after
first degree AV block (incomplete) prolonged PR interval; caused by digitalis or vagal stimulation
second degree AV block type I (Wenckeback or Mobitz's type 1) PR intervals lengthen progressively until a ventricle beat is dropped; can be caused by digitalis
second degree AV block type 2 (Mobitz's type 2) takes 2 or more atrial impulses to stimulate the ventricles; usually 2:1, 3:1, or 4:1; caused by myocardial infarction or myocarditis; may lead to 3rd degree block
third degree AV block (complete) none of the atrial impulses stimulate the AV node; ventricles are paced independently from the atria; ventricular rate is slower than the atrial rate of contraction; totally random ECG
atrial flutter ectopic atrial pacemaker; p waves are very rapid and coordinated; 2:1, 3:1, 4:1; treatment-digitalis
Atrial fibrillation many ectopic pacemakers in atria; irregular p waves; decrease in cardiac output; QRST look normal
Ventricular flutter single ectopic pacemaker in ventricles; smooth sine wave; extremely dangerous; heart does not fill properly, decreased cardiac output, leads to fibrillation; decreased coronary flow
ventricular fibrillation caused by many ventricular ectopic pacemakers, uncoordinated, chaotic twitching, bag of worms, 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
classical triad 3 phases of myocardial infarction 1)ischemia 2)injury 3)infarction
ischemia as a ecg symmetrical inversion of the T wave; most obvious in chest leads; caused by delay in the recovery at the epicardial regions; altered repolarization; take nitroglycerin to correct
injury as a ecg ST elevation means infarction is fresh (acute)
infarction as a ecg significant Q wave-much wider than normal; Q may be 1/3 height of QRS; may last for years; some drugs can cause similar effects
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
treatment of myocardial infarction aspirin, heparin, sublingual nitroglycerine, morphine, sulfate, oxygen administration
blood flow equation pressure/resistance
resistance equation (length)(viscosity)/((radius)^4)
how does radius of arterioles change? vasoconstriction and vasodilation
laminar flow flow is greater at the center of the vessel than along the outer edges
blood vessel diameter is mainly regulated by autonomic nervous system
angiotensin II causes vasoconstriction; produced as a result of secretion of renin from the kidneys, it may functiont o help maintain adequate filtration pressure in kidneys when systemic blood flow and pressure are reduced
ADH (vasopressin) causes vasoconstriction
Histamine causes vasodilation; promotes localized vasodilation during inflammation and allergic reactions
% circulation in systemic, pulmonary, and heart systems 79% systemic, 12% pulmonary, 9% max heart
percent breakdown of 79% of blood in systemic circulation 15% in arteries, 5% in capillaries, 59% in veins
blood pressure in different vessels large arteries 100-95; small arteries 95-85; arterioles 85-30; capillaries 30-10; veins 10-0
where does most regulation of blood pressure occur arterioles
precapillary sphincters regulate blood flow to capillary. Use myogenic and metabolic mechanisms to regulate blood flow in relation to the local tissues need for oxygen called autoregulation
autoregulation myogenic and metabolic mechanisms to regulate blood flow in relation to the local tissues need for oxygen
capillary hydrostatic pressure CP; blood pressure in the capillary
osmotic force usually stays the same in capillaries due to albumin
edema excess interstitial fluid in the tissues
three main cuases of edema 1)increased capillary hydrostatic pressure 2)decreased plasma proteins (albumin) 3)increased interstitial fluid protein
causes of increased capillary hydrostatic pressure edema venous obstruction, cardiac failure (congestive heart failure), retention of body salt and fluid
causes of decreased plasma protein edema kidney damage resulting in loss of plasma proteins, liver damage-decreased plasma protein production, malnutrition-not enough protein in diet
causes of increased interstitial fluid protein edema increased capillary permeability-inflammation, decreased lymphatic flow
blood pressure can be changed by changing cardiac output, peripheral resistance, or total blood volume
long term regulation of blood pressure is regulated by hormones
ADH (vasopressin) effects decreases urine formation in kidneys which increases blood pressure
diuretic agent effecs inhibit release of ADH, increase urine, decrease blood pressure
alcohol effect on ADH inhibits ADH increasing urine to dump the alcohol
renin angiotensin system releases aldosterone which raises blood pressure
aldosterone hormone which raises blood pressure
steps of renin-angiotensin system up to angiotensin II formation decrease in blood pressure->decrease in blood flow to kidney->juxtaglomerular apparatus in the kidney secretes renin->renin converts angiotensinogen to angiotensin I which is converted to angiotensin II
steps of renin-angiotensin system from angiotensin II to increased blood pressure 3 mxnsms;1)angiotensin II->increased ADH->water retention->higher bp 2)angiotensin II->adrenal cortex secretes aldosterone->salt and water retention->yep 3)angiotensin II->vasoconstriction of arterioles->increased resistance->higher bp
primary aldosteronism (Conn's syndrome) results from hypersecretion of aldosterone from the adrenals->hypertension, increased exracellular fluid volume, hypernatremia and potassium depletion; mostly occurs because of an adrenal adenoma (tumor in adrenal cortex)
short term regulation of bp nervous system controls to mechanism 1)baroreceptors 2)chemoreceptors; both are in medulla
baroreceptors cardioinhibitory center->parasympathetic->HR down+CO down+vasodilation up->BP down
chemoreceptors vasomoter center->sympathetic->HR up+CO up+vasocontriction=BP up
where are baroreceptors located aortic arch, pulmonary veins, right and left atria, superior and inferior vena cava and in the carotid sinuses
how are baroreceptors stimulated a change in pressure causes the walls of these arterial regions to stretch or relax and stimulate sensory receptors which stimulate or inhibit the cardioinhibitory center and the opposite to the vasomoter center
where are chemoreceptors located aortic bodies and in the carotid bodies
how are chemoreceptors stimulated decreased levels of oxygen and increased levels of CO2 and H+ in the blood; impulses sent through the same nerves as the baroreceptors where they stimulat the vasomoter center
what is circulatory shock inadequate blood flow and/or oxygen delivered to the tissues
4 types of circulatory shock hypovolemic, anaphylactic, neurogenic, cardiogenic
hypovolemic shock reduced blood volume as a result of hemorrhage, dehydration, or burns; symptoms: low blood pressure, rapid pulse, cold, clammy skin, little urine formation, increased respiration rate, and intense thirst
anaphylactic shock rapid drop in bp from a severe allergic reaction causing an extreme release of histamine which causes vasodilation and a drop in bp
neurogenic shock spinal cord damage causes decreased sympathetic activity
cardiogenic shock inadequate circulation of blood in body tissues due to cardiac failure
body's compensation for circulatory shock vasoconstriction (except for heart and brain), venoconstriction, increased heart rate and respiration and thirst and hematopoiesis, secretion of epinephrine and norep and adh, spleen contracts, renin-angiotensin system activated
time frame the body restores homeostasis plasma volume restored in hours, plasma proteins restored in days, blood cells restored in 3-4 weeks
hypertension high bp; 1/5 people; 12% of all deaths by rupturing a vessel in a vital organ or by causing the heart or kidneys to fail; two types: primary (essential) and secondary
essential or primary hypertension facts no cause;90% of all hypertensive patients; 25-50 years old; females more often; hereditory; blacks more often; from high salt intake; psycho emotional stress contributes
essentail or primary hypertenstion characteristics asymptomatic (people don't know they have it); CO and extracellular fluid volumes are normal but total peripheral resistance is high; increased sensitivity to epi and norepi; many have left ventricular hypertrophy
secondary hypertension definable causes; 10% of cases; renal artery disease, excess catecholamines (tumor of adrenal medulla), or excess aldosterone (Conn's syndrome)
symptoms of essential hypertension headaches, dizziness, fatigue, blurring of vision, polyuria, polydipsia, muscle weakness, hypokalemia
dangers of hypertension may lead to congestive heart failure, cerebral blood vessel damage and stroke; atherosclerosis
general treatment of hypertension exercise, weight loss, low refined carb diet, not-smoking, restrict salt intake, reduce psycho-emotional stress
Created by: droid on 2008-02-26



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