CVP physiology - exam I
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111 terms
Terms | Definitions |
|---|---|
 the major underlying cause of cardiovascular disease is due to | ischemia |
| a vasocontrictor and major secretory product of platelets, which potentiates release of granule contents | thromboxane A2 |
| contents of platelets | - actin & myosin - enzymes & calcium - ADP & ATP - thromboxane A2 - serotonin - growth factor |
| initiates clotting | thromboplastin |
| prevents platelet aggregation and produces prostacyclin | endothelium |
| aspirin and ibuprofen block what | fatty acid cyclooxygenase |
| cyclooxygenase is an enzyme needed for what conversions | - ARA to thromboxane A2 in platelets - ARA to prostacyclin in endothelium |
| - vasodilator - inhibits platelet degranulation | prostacyclin |
| - vasoconstrictor - potentiates platelet degranulation | thromboxane A2 |
| acts as an anticoagulant by enhancing the action of antithrombin III | heparin |
| important for lysis of clots | plasmin |
| endogenous activators of plasminogen are found in | - tissue - plasma - urine |
| exogenous activators of plasminogen are found in | - streptokinase - tPA (tissue plasminogen activator) |
| the ability to open up alternate routes of blood flow to compensate for a blocked vessel | collateralization |
| role of sympathetic nervous system in collateralization | - impede via vasoconstriction - augment via release of NPY |
| blood coagulation initiated by chemical factors released by damaged tissues | extrinsic mechanism |
| blood coagulation requiring only components in blood and trauma to blood or exposure to collagen | intrinsic mechanism |
| depresses liver formation by blocking action of vitamin K | coumarin |
| a key step in clotting that requires thrombin | fibrinogen to fibrin |
| risk factors in heart disease | - increasing age - male - heredity - tobacco smoke - high blood cholesterol, pressure, and homocysteine - physical inactivity - obesity - diabetes mellitus |
| high levels of this in the blood can be reduced by increasing intake of folic acid, B6, and B12 | homocysteine |
| amino acid in the blood that may irritate blood vessels promoting atherosclerosis and can make blood more likely to clot | homocysteine |
| allows the heart to behave as a syncytium | intercalated discs |
| sharp increase at onset of depolarization | Na+ |
| increased during the plateau | Ca++ |
| increased during the resting polarized state | K+ |
| increases at onset of depolarization and decreases during repolarization | Na+ and Ca++ |
| decreases at onset of depolarization and increases during repolarization | K+ |
| tetradotoxins block fast Na+ channels selectively changing what | a fast response into a slow response creating an increased time of depolarization |
| closed during resting membrane potential | - fast Na+ channels - slow Ca++/Na+ channels |
| open during resting membrane potential | K+ channels |
| the inhibiting effects of digitalis on the Na+/K+ pump does what to the Na+/Ca++ pump? what happens to Ca++ inside the cell? what happens to contractile strength | - digitalis reduces Na+/K+ pump. - Ca++ is built up inside of the cell - contractile strength is increased because of all of the built up Ca++ inside the cell |
| refractory period where the cell is unable to re-stimulate and occurs during the plateau | absolute refractory period |
| refractory period that requires a supra-normal stimulus and occurs during repolarization | relative refractory period |
| delays the wave of depolarization from entering the ventricle | AV node |
| TRUE or FALSE at resting heartrate diastole is greater than systole | TRUE |
| TRUE or FALSE both the duration of systole and diastole shorten when cycle length shortens, but systole shortens to a greater extent | FALSE; diastole shortens at a greater extent |
| what is the position of the mitral and aortic valves during isovolumic contraction | MV - closed AV - closed |
| what is the position of the mitral and aortic valves during ejection | MV - closed AV - open |
| isovolumic contraction and ejection are part of systole or diastole | systole |
| what is the position of the mitral and aortic valves during isovolumic relaxation | MV - closed AV - closed |
| what is the position of the mitral and aortic valves during rapid inflow to the LV (filling) | MV - open AV- closed |
| what is the position of the mitral and aortic valves during diastasis | MV - open AV - closed |
| what is the position of the mitral and aortic valves during atrial systole | MV- open AV - closed |
| the volume in the ventricles at the end of filling is called | end diastolic volume (EDV) |
| the volume in the ventricles at the end of ejection | end systolic volume (ESV) |
| volume ejected by ventricles (EDV-ESV) | stroke volume (SV) |
| percentage of EDV ejected | ejection fraction |
| stretch on the wall prior to contraction | preload |
| the changing resistance that the heart has to pump against as blood is ejected | afterload |
| wave associated with atrial contraction | A wave |
| wave associated with ventricular contraction | C wave |
| wave associated with atrial filling | V wave |
| what happens when the LV pressure is greater than the aortic pressure | the aortic valve opens |
| what happens when the aortic pressure is greater than the LV pressure | the aortic valve closes |
| valves that are - thin and filmy - contain chorda tendineae and papillary muscles | AV valves (bicuspid, tricuspid) |
| valves that are - strong in construction - lack chorda tendineae and papillary muscles | semilunar valves (aortic & pulmonary) |
| acts as check lines to prevent prolapse of a valve | chorda tendineae |
| increases tension on chorda tendineae | papillary muscle |
| valve that does not open fully is referred to as | stenotic |
| valve that does not close fully is referred to as | insufficient/leaky |
| when a valve creates a vibrational noise | murmur |
| heart murmurs in systole are caused by | - aortic & pulmonary stenosis - mitral & tricuspid insufficiency |
| heart murmurs in diastole are caused by | - aortic & pulmonary insufficiency - mitral & tricuspid stenosis |
| heart murmurs in both diastole and systole are caused by | - patent ductus arteriosis - combined valvular defect |
| a valve that is both insufficient and stenotic is said to have | combined valvular defect |
| (P)(r)/2 = | wall tension (law of laplace) |
| law of laplace states | wall tension = Pr/2 - In two chambers operating at the same pressure but with different chamber radii, the larger the chamber will have to generate more tension; consuming more energy & oxygen |
| anything that affects heart rate | chronotropic |
| anything that affects conduction velocity | dromotropic |
| anything that affects strength of contraction | inotropic |
| ability to increase strength of contractino independent of a length change | homeometric autoregulation |
| increased stroke volume maintained as EDV decreases | flow induced homeometric autoregulation |
| increase in aortic BP will increase force of contraction | pressure induced homeometric autoregulation |
| increased heart rate will increase force | rate induced homeometric autoregulation |
| direct stretch on the SA node will affect that heart rate in what way | increase heart rate; increases Ca and Na permeability |
| sympathetics control the heart in what ways | increase: - heart rate - strength of contraction - conduction velocity |
| parasympathetics control the heart in what ways | decrease: - heart rate - strength of contraction - conduction velocity |
| what happens when ANS effects on the heart are blocked | - heart rate increases - strength of contraction decreases |
| ACh from the parasympathetics inhibits what | Norepinephrine |
| NPY and norepinephrine from sympathetics inhibit what | ACh |
| TRUE or FALSE thyroid hormones are both positive inotropics and chronotropics | TRUE |
| effects of elevated K+ lead to | - dilation and flaccidity or cardiac muscle - decreasing resting membrane potential |
| effects of elevated Ca++ lead to | spastic contraction |
| effect of body temperature on heart | - for every degree F the temp. increases, the heartrate increases by 10 BPM - contractile strength increases temporarily - decrease in body temp. decreases heartrate and contractile strength |
| energy substrates for cardiac cells | - fatty acids (70%) - glucose - glycerol - lactate - pyruvate - amino acids |
| the energy produced by the heart is split up between heat production and work, what are the aspects of work | - pressurization of blood (99%) - acceleration of blood (1%) |
| greater than 100 BPM | tachycardia |
| less than 50 BPM | bradycardia |
| p wave | atrial depolarization |
| QRS complex | ventricular depolarization |
| T wave | ventricular repolarization |
| atrial repolarization is buried in the | QRS complex |
| when the wave of depolarization is moving toward the + electrode | positive deflection |
| when the wave of of depolarization is moving toward the - electrode | negative deflection |
| when the wave of of repolarization is moving toward the + electrode | negative deflection |
| when the wave of repolarization is moving toward the - electrode | positive deflection |
| lead I is perpendicular to | AvF |
| lead II is perpendicular to | AvL |
| lead III is perpendicular to | AvR |
| prolonged QT interval has what implications | increased incidence of sudden cardiac death |
| what the longest and shortest cycle length (RR) vary by more than .16 seconds | sinus arrhythmia |
| depolarization wave from atria to ventricle is delayed excessively | 1st degree AV block |
| the wave of depolarization is occasionally blocked form entering the ventricle | 2nd degree AV block |
| the atria and ventricles are beating independently, all depolarization waves from the atria to ventricles are blocked | 3rd degree AV block |
| no relationship between P waves and QRS complexes | 3rd degree AV block |
| PR interval is greater than .2 seconds | 1st degree AV block |
| dropped beat p wave with no associated QRS complex | 2nd degree AV block |
| when the QRS and T waves point in opposite directions | inverted T wave, implies ischemia |
| released only when myocardial necrosis occurs | cardiac troponins T and I |
| what do the SA node, AV node, and purkinje cells have in common | the all contract weakly and have few fibrils |
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