Term
| what is the fick method for CO measurement? |
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Definition
| cardiac output (L/min) = VO2/([O2]pv - [O2]pa) |
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Term
| how are the three necessary measurements for the fick CO measurement method gathered? |
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Definition
| [O2]pa is mixed venous blood taken through a catheter through the brachial vein->subclavian vein->R atrium->R ventricle/pulmonary artery. [O2]pv is obtained from any systemic artery, and the rate of O2 absorption by the lungs, VO2, is measured by the rate of O2 disappearance from respired air |
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Term
| what is the indicator dilution technique? |
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Definition
| a more current technique of monitoring cardiac output, where a dye of known conc. is injected into a systemic vein or RA |
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Term
| how is cardiac output calculated with the indicator dilution method? |
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Definition
| cardiac output = (mg of dye injected)/((avg dye conc./dL blood for duration of curve)(duration of curve in sec)). you may have to x60 to convert L/sec to L/min. T1 is when dye appears, T2 is when the dye decreases; T2-T1 = duration of the curve |
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Term
| what determines the cardiac output? |
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Definition
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Term
| what are the intrinsic determinants of stroke volume? |
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Definition
| 1) preload: end-diastolic fiber length, ventricular filling, end-diastolic pressure -> all basically how much blood is in the ventricle before it starts contracting. 2) afterload: contractile force, the force against which the heart must pump (aortic pressure) |
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Term
| what are the extrinsic determinants of stroke volume? |
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Definition
| 1) contractility; can be affected by various hormone stimulation, *sympathetic and parasympathetic stimulation, drugs, and disease states 2) hypertrophy |
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Term
| where does cardiac muscle operate on the length tension curve? |
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Definition
| on the ascending limb, b/c cardiac muscle's contractility needs to increase with the level of blood it needs to pump (skeletal works on the plateau) |
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Term
| how does sarcomere length affect Ca++ sensitivity in cardiac tissue? |
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Definition
| at increased length, contractile proteins become more sensitive to Ca++ and there is a slight increase in Ca++ released from the SR |
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Term
| what is titin? what 2 functions does it play in cardiac muscle? |
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Definition
| titin is a large protein in the I-band that connects the A-band and Z-line in all striated muscle. when stretched, it induces passive motion (its resting length is on the short side of the conventional length-tension relation), and it also prevents myocytes from going beyond the plateau portion of the length-tension curve (prevents cell from being ripped apart/blown out/tetanus - it *cannot go down the descending limb) |
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Term
| what are the normal pressure/volume relationships for the LV? |
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Definition
| phase 1) start in diastole, mitral valve opens LV fills to 65 to 140 mL (total SV) and the QRS complex occurs -> pressure increase. phase 2) isometric contractile phase, pressure is rising, volume stays the same, then aortic valve opens when LV pressure > aortic. phase 3) LV volume decreases, as does pressure, *T wave occurs, and the aortic valve closes when LV pressure < aortic pressure, (volume doesnt change when valves are closed). phase 4) isovolumetric relaxation. |
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Term
| how does an increase in pre-load affect the pressure/volume relationships for the LV? |
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Definition
| more filling occurs in phase 1 (160 as opposed to 140 mL - main difference), more pressure is created in phase 2 (isometric contraction), more volume is ejected in phase 3 = overall, larger systolic pressure, but diastolic unchanged. the aortic valve closes at about the same point |
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Term
| can the heart modify its preload levels to match performance demands? |
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Definition
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Term
| anything that increases preload increases ______? |
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Definition
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Term
| what is the major determinant of ventricular preload/cardiac output? |
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Definition
| ***central venous pressure/tone |
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Term
| how does total blood volume affect preload/cardiac output? |
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Definition
| increased total blood volume (increased venous tone usually due to sympathetics) should increase cardiac output |
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Term
| can peripheral skeletal muscle pumping affect preload/cardiac output? |
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Definition
| yes by increasing venous return |
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Term
| how does intrathoracic pressure affect preload/cardiac output? |
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Definition
| this will generate more negative pressure, which increases preload |
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Term
| how does standing up affect preload/cardiac output? |
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Definition
| standing up quickly causes pooling in legs, which decreases venous return and therefore preload/cardiac output/SV |
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Term
| how does ventricular pericardial pressure affect preload/cardiac output? how might this happen? |
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Definition
| if the pericardial sac becomes fibrotic, or infections/fluid gets between sac and heart -> the heart cannot fill as much and decreased preload/cardiac output/SV results |
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Term
| how do decreases in ventricular compliance affect preload/cardiac output? |
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Definition
| if ventricular wall compliance decreases, the heart will not be able to fill as much and preload/cardiac output will decrease |
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Term
| how does increasing afterload (aortic pressure) decrease SV? |
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Definition
| increased afterload increases load on muscle (as seen on the force-velocity curve), which causes shortening/contracture to occur slower and SV is thus decreased b/c it has to happen within a certain amount of time |
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Term
| what are the 3 determinants of cardiac afterload? what is the end result of this? |
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Definition
| aortic diastolic pressure, aortic compliance, and aortic valve resistance. increased afterload will decrease SV and increase LV work, increasing its O2 demand |
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Term
| does aortic diastolic pressure determine afterload? |
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Definition
| yes aortic diastolic pressure is the major determinant of afterload. MAP is a more general index of afterload and HTN (increase in diastolic or systolic pressure) may be involved |
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Term
| how does decreased aortic compliance increase afterload? |
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Definition
| if the aorta is more rigid, it cannot distend during ejection - increasing afterload and systolic pressure. this is seen with atherosclerosis. |
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Term
| how does aortic valve resistance increase afterload? |
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Definition
| if the aortic valve is stenosed, this places more pressure on the heart to eject blood |
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Term
| in situations where afterload is increased, how much pressure is generated before the aortic valve opens? |
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Definition
| more than if afterload was not increased |
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Term
| in situations where afterload is increased, how does end systolic volume compare to when afterload is not increased? |
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Definition
| end systolic volume is higher than normal, and this is why SV is lower |
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Term
| if afterload is decreased, what happens to SV (assuming the same preload for each)? |
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Definition
| SV will increase, and isovolumetric contraction pressure will be less |
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Term
| how does increased afterload affect subsequent beats? |
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Definition
| at same ventricular EDV (LVEDV), if you increase afterload, SV goes down for 1st beat but in subsequent beats, it starts to go up a little b/c filling volume has gone up and you don’t eject it all in initial beat (opposite occurs if you decrease afterload) |
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Term
| what are characteristics of a hypodynamic heart? hyperdynamic? |
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Definition
| hypodynamic: elevated EDP and a slowly rising ventricular pressure. hyperdynamic: reduced EDP and a fast-rising ventricular pressure (can be measured on dP/dt curve) |
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Term
| how does a increase in contractility affect SV? |
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Definition
| since aortic pressure is no different, the aortic valve opens at the same time, but the ejection fraction is increased, which leads to an increased SV. the aortic valve then closes on a much lower ventricular ESV |
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Term
| what is the cellular basis for an increase in contractility? |
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Definition
the predominant underlying mechanism is a transient increase in amount of Ca2+ -> this increases the
rate of contraction, peak force
developed, and rate of relaxation |
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Term
| how is venous pressure affected by a drop in cardiac output? |
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Definition
| it will increase, because the pump is down. (however, this should increase preload, which should then increase cardiac output) |
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Term
| how is arterieal pressure affected by a drop in cardiac output? |
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Definition
| it will increase, b/c the pump action of the heart is down |
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Term
| how are cardiac output and venous pressure intertwined? |
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Definition
| as cardiac output increases, venous pressure decreases (can happen to where veins collapse) and the equilibrium point is where CO is about 5 L/min which sustains venous pressure at about 2 mm Hg |
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Term
| what happens in the body if there is an acute increase in venous pressure? |
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Definition
| initially; venous pressure increases, preload increases, CO increases - but then with each beat, the system will equilibriate back to where it was |
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Term
| what happens in the body if there is an acute increase in blood volume? |
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Definition
| venous pressure and cardiac output will both increase to a point slightly higher on the curve (everything shifts up) |
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Term
| how does increased sympathetic stimulation affect cardiac function and venous pressure? |
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Definition
| CO increases, increasing venous pressure, which then drops a little b/c of the shift from venous to arterial w/the CO uptick, but eventually a new venous pressure/CO equilibrium is reached at a higher state than previous to sympathetic stimulation |
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Term
| when CO goes up, what happens to pressure in the RA? |
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Definition
| it will decrease b/c blood is moving from the venous to arterial side |
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Term
| what vessels contain the highest % if blood in the body? |
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Definition
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Term
| how does the CV respond to increased arterial resistance due to only sympathetic stimulation of the arterioles? |
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Definition
| the venous pressure and CO will drop due to increased retention of blood in the arteries and increased afterload respectively |
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Term
| how does the CV respond to increased arterial resistance due to only sympathetic stimulation of the arterioles, followed by increased contractility by sympathetic stimulation on the heart? |
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Definition
| venous pressure and CO will increase slightly |
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Term
| how does the CV respond to increased arterial resistance due to only sympathetic stimulation of the arterioles, followed by increased contractility by sympathetic stimulation on the heart, and finally followed by increased venous tone via sympathetic stimulation? |
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Definition
| the venous pressure and CO will increase greatly |
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Term
| how do you "jump" to different curves? move up and down curves? |
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Definition
| "jump" to different curves: change contractility. move up and down curves: change EDV via preload, afterload |
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