| Flap 1 |
Flap 2 |
| 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 |
