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Cardiac Physiology I, V. Systole=.25-.3 s Isovol contraction-develop P all valves closed at EDV -120-130 mL vol reached Ejection-between open/close SL valve 1. Rapid ejection-1/3 ejection, 70%vol PᢈmmHg, aortic v. opens -P⇑ to 120, then aorticP=ventP 2. Reduced ejection-2/3 ejec. 30%vol Vpressure falls, aortaP>ventP -brief reversal of flow, valves close 2ND HEART SOUND-heard at base S2-aortic valve before pulm. -splits during insp.S1-A2-P2 V. diastole=.5-.55s Isovol relaxation- all valves closed at ESV aorta backflow closes valve ->incisura, then aorta P⇓ with recoil V. Filling 1. Rapid Filling-1/4 interval, most vol Vs still relaxing, so ventP still falls 2. Reduced Filling-'diastasis'-1/2 int. 3. Atrial Systole-1/4 int.-atria contract -'a' wave in atrial/vent pressure not nec. in normal heart-enough filling helps w/ exercise or debilitated hearts Isovol contraction closes AV valves FIRST HEART SOUND-heard at apex, Change contractility -increase Vpressure at given EDV -F-S curved moved up and left -↑peak tension, tension rate, relax rate -reduction by ischemia negative inotropic ⇑ with NE, epi, force-freq digitalis, other drugs ⇓ -anoxia, hypercapnia,acidosis ischemia, depressants, Murmurs-white noise -due to turbulence -prolonged duration -non-musical Descriptors -timing-pan-systolic, etc. -location-rt. base, mitral=apex -radiation-neck, back, axilla -quality-harsh, blowing, pitch -loudness-grade I to IV or VI ???? AV valve stenosis -diastolic-during rapid filling -after S2, isovol relax -start with AV valve opening, Frank-Starling Mech -↑m. length,↑active tension -so ⇑EDV, ⇑systole vent pressure -max filling pressure=12mmHg -max active tension -til ~2.2um sarcomeres -maximize x-bridge linking -resting tension ⇑⇑ at Lmax -stronger Titin than sk. m -same time from stim to max tension -contractility not increased Stretch Myocardium ↑total blood vol ↑atrial filling, 1. sympa stim-NE or catachols from adrenal phos'ate Ca channel pros -↑ Ca into cytosol 2. Force-freq relationship -Treppe Phenomenon -⇑HR, ⇑contractility -more Ca in cytosol/min 3. Digitalis (cardiac glycosides) -inhibit Na/K pump, Na grad. -Na/Ca exchange can't work -⇓Na in->⇓Ca out Intrinsic regulation -increased contractility Postextrasystolic Potentiation -premature beat weaker than normal -insuff Ca released from SR b/c Ca can't go from uptake to release sites fast enough NOT BECAUSE OF REDUCED FILLING -PES beat has enough time to get enough Ca so a stronger beat NOT BECAUSE ACCUM. OF Ca (Treppe), ECG APs P wave-atrial depol (AP) causes atrial systole QRS complex-AP of vents endo->epicardium causes isovol contraction repol of atrium not seen T wave-vent repol- during 'reduced ejection' from epi->endocard Heart Blocks 1st degree incomplete P-R interval>.2s (normal=.16s) 2nd degree incomplete-drop beats atria beat faster than Vs. 3rd deg complete- P waves sep from QRS-T As, Vs contract at own rate, Cardiac Physiology I Cycle V. Systole=.25-.3 s Isovol contraction-develop P all valves closed at EDV -120-130 mL vol reached Ejection-between open/close SL valve 1. Rapid ejection-1/3 ejection, 70%vol PᢈmmHg, aortic v. opens -P⇑ to 120, then aorticP=ventP 2. Reduced ejection-2/3 ejec. 30%vol Vpressure falls, aortaP>ventP -brief reversal of flow, valves close 2ND HEART SOUND-heard at base, AV valve stenosis -diastolic-during rapid filling -after S2, isovol relax -start with AV valve opening ???? Regurgitation -systolic-WITH S1 -persist throughout, Use bell for low freq -S3, S4, low murmur ???? Diaphragm for high freq -S1, S2, high murmurs -high freq heard more easily, Cardiac Physiology I Flow Elastic aa to musc. aa. -sharp ⇑R, ⇓P in arterioles -HENCE, CAUSE STEADY FLOW -to caps- higher x-area->lower V -nutrient exchange A1V1=A2V2 75%pressure on artery side large venous capacity, 67% of blood