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27 Cards in this Set
- Front
- Back
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PV loop (Point A) |
-Mitral valve opens |
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PV Loop |
-Rapid ventricular filling -Diastasis -Atrial contraction |
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PV loop (Point B) |
-Mitral valve closes (S1) -Beginning of systole -EDV (preload)
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PV loop (Segment B-C) |
Isovolumetric contraction |
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PV loop (point C) |
-Aortic valve opens -Pressure corresponds to diastolic pressure |
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PV loop (segment C-D) |
-Rapid ventricular ejection -reduce ventricular ejection
Highest point - Max afterword and systolic pressure |
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PV loop (point D) |
-Aortic valve closes (S2) -Begins diastole -end systolic volume |
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PV loop (segment D-A) |
Isovolumetric relaxation |
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Increase Preload |
-Increase stroke volume -Segment B-C shifts to right
Increase venous return---> Increase left atrial filling---> Increase EDV---> Increase sarcomere length ----> increase force of contraction----> increase Left ventricle stroke volume ---> Increase cardiac output |
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End systolic pressure volume relationship (ESPVR) |
-Increase inotropy (contractility) = Steeper and shift to left -Decrease inotropy = flatter and shifts to the right |
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Increase afterload |
-Stroke volume reduced -Segment A-D is shifted to right ; C-D elevated
-aortic valve stenosis -Increase aortic diastolic pressure |
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Increase contractility |
-Increase ability of cardiac muscles to shorten -A-D shifted to left
-increase sympathetic activity of heart |
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Positive intropic agents |
-Increase contractility -Increase sarcoplasmic Calcium concentrations |
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PIA - Adrenergic agonists |
-norepinephrine and epinephrine -Stimulate beta 1 adrenergic receptors |
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PIA-Cardiac glycosides |
-digitalis -Inhibit sodium potassium pump which leads to increase in intracellular calcium -Heart failure -Arrhythmias |
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Sympathetic stimulation |
-Increase force of contraction 1.L type calcium channel flux increased 2.RYR enhanced calcium released 3.Phospholamban - faster Ca2+ uptake and levels 4. Troponin I released quicker |
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Negative Intropic agents |
-decrease contractility -Decrease sarcoplasmic calcium concentrations
-Calcium channel blockers or beta blockers -treat hypertension |
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Increase activity in SNS |
-Increase cAMP--->Increase I(f) ---> pacemaker accelerated ---> decreased K+ permeability --->Increase L type Calcium ---> Tachycardia ---->increase conduction through AV node
-Systolic duration reduced -Each contraction is reduced in time but reduced in force |
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Increase activity in PNS |
-Release of ACh ----> Decreased I(f) ---> pacemaker slowed ---> Increase K+ permeability of SA node
-SA node produces fewer action potentials per unit time -Bradycardia |
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Cardiac output |
CO=SV x HR
-Stroke volume affected by preload, afterload, contractility
Heart rate affected by SNS (+), PNS (-) |
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Stroke volume |
SV=EDV-ESV |
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Ejection fraction |
EJ=SV/EDV
-Measures heart efficiency - normal is 55-65% |
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ESV |
-Volume at D or A on pressure loop
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EDV |
-Volume at B on PV loop |
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Max afterload |
Peak of phase III
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Blood pressure |
-sys - peak of phase III
-Dias- Point C |
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Stroke work |
-energy required to eject blood -Area in PV loop -Greater area = greater stroke work |
