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Review PSIO 420 CARDIO.docx

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University of Arizona
PSIO 420
Douglas Keen

Review PSIO 420 CARDIO Lecture 28: Heart anatomy Facts: • Beats 100,00 times a day • 60,000 miles of blood vessels • Heart develops autorhythmicity after gestation. Cardiac cells: Cardiac muscle • 25% mitochondrial density - Therefore the heart is continually generating ATP so that it does not have to use anaerobic respiration. This would be bad. Cardiac muscle is a aerobic muscle. Compare to skeleton muscle which only has 2% Mitochondria. • Intercalated disks allow for the heart as a whole to function as one big pump per contraction. • Gap junctions - allow for a rapid dispersal of action potentials that generate a contraction. • Desmosomes - Physical connection between fibers. Conduction system of HEART: SA node (Cardiac myocytes) • Sets autorythmicity of heart • Important in generating HR • Affected by autonomic nervous system  Sympathetic nervous system increases HR, Contractility with an increase in Norepinephrine and epinephrine.  Parasympathetic nervous system affects depolarization, by releasing Acetylcholine which reduces Camp and ultimately reduces HR - example of rest AV node (atrioventricular) • Slows conduction of electrical signals before the spreading the signals to the ventricles. Allows for maximal filling of the ventricles. Bundle of His • Electrical conduit between atria and ventricles Right and left bundle branches • Signal spreads rapidly through to the perkinjie fibers (end) Draw pacemaker potentials and action potentials in autorhythmic fibers of SA node. (funny current, resting membrane potential =intracellular voltage) Influence of Total cross sectional area of the vascular system:  Aorta - velocity fast, 2.5 diameter (not largest diameter)  Arteries - bulk flow (responsible vessels), Fairly elastic (expansion), Expand during systole, and recoil during diastole - aids in blood flow  Arterioles - These are the resistance vessels, responsible for redistribution of blood, hence they contain smooth muscle which can be vasodialated ( very important for exercise) or vasoconstricted (NE/E, increase in resistance to flow) depending on what the situation is.  Capillaries - Diffusion cite, small, thin, slowest velocity of blood flow, and largest cross sectional area.  Veins - Very low pressure, at rest they are the blood reservoir (about 60% of blood). They also contain some one way valves which stop the blood from moving down with the pull of gravity. Makes blood move to the heart. Without one way valves we have varicose veins. Flow = Change in pressure/ resistance or Cardiac output (L/min) = mean arterial pressure (mmHg)/ Systemic vascular resistance (mmHg/L/min) * This is the sum of all the blood flow resistance in the network Parallel arrangement of organ blood flow:  Tissue is connected in parallel, except the hepatic portal vein.  Arterioles all contain stopcock which allows for the redistribution of blood during exercise and rest. These stop cocks represent different arterial resistance to blood flow which is regulated by the sympathetic and parasympathetic nervous system. Lecture 29: Cardiac performance (stroke volume) Stroke volume: changes with exercise, Maximal HR does not change with - stays around age (220-age)  The about of blood ejected from the heart per heart beat (L/beat)  Resting CO = 5L/min  Resting HR - 60-80 Beats/min  Resting SV untrained - 60-80 ml/beat  Maximal exercise for UT - 100-120 ml/beat  Maximal exercise for T - up to 180 ml/beat SV= End diastolic volume - Ends systolic volume = Amount of blood left in ventricle after diastole - the amount of blood left in ventricle after systole 1. Systolic (systole) - time when heart is contracting (generating pressure, emptying) 1/3 time 2. Diastolic (diastole) - time when heart is relaxing ( filling with blood) 2/3 time of Cardiac cycle Factors affecting SV:  Preload - venous return - how much blood is returned to the heart after diastole  Afterload - affects ESV - Mean arterial pressure affects this, The higher the blood pressure the harder the heart has to work to push the blood out of the ventricle. This can also be the resistance from the arterioles/arteries. Therefore the afterload is the pressure needed to push the blood out of the left ventricle.  contractility - degree of forcefulness which doesn't affect EDV or preload, however it affects the End systolic volume. More force more blood leaves the left ventricle, the smaller the End systolic volume the greater the SV. Mechanism - Sympathetic nervous system release of NE. NE binds to B-adrenergic receptors, which increases Calcium release which increases the crossbridge formation increasing contractility - only affects ESV Factors affecting EDV: Stretching of myocardium Pe rf -Stretch of myocardium is associated with Sv an increase in the filling which is an increasem in EDV. L Factors:  increase in blood volume - increase EDV and Preload  Body position - Prolonged standing decreases EDV - blood pools in legs (vein reservoir). Ventricular EDV (ml) Laying down prone position causes the EDV to increase. When we go from prone to standing our EDV decreases and we get a fainting response.  Respiratory pump - increased ventilation will cause blood to be sucked back to the heart which increases the venous return.  Venous tone - Venoconstriction (mediated by SNS)- contraction of the veins so that there is a push of blood back to the heart. Increases with trained individuals more venous tone.  Muscle pump - pumping action of skeletal muscles causes blood to be pumped back to the heart. Happens when we contract our muscles - exercise.  Time of filling - (HR) decrease in HR increase in EDV, increase in HR decrease in EDV. The relationship between CO and HR and how it relates to SV: Graph RELATIONSHIP: With Increases in HR, there is less filling time therefore the stroke volume decreases. This is with exercise and a "denervated" heart -No PNS or SNS Relationship between SV (ml/beat), EDV (ml) and Aortic Pressure( mmHg):Graph Lecture: 30 FACTS: HR (beats/min)  resting HR: 60 - 80 beats/min - below 60 bradycardia, above 100 tachycardia.  Maximal HR 220-age  Maximal HR for trained is lower than heart rate of untrained an maximal VO2  Increase metabolic work, increase HR relationship Stroke volume  Rest SV: 60-80 ml/beats  Maximal untrained 100-120 ml/beat  Maximal trained up to 180 ml/beat  Maximal SV reached at 50% of VO2 max. VO2  Resting: 0.3 L/min, 300ml/min, 5ml/kg*min  Maximal trained athlete, heavy person - 6-7 L/min absolute  Maximal trained althetes only - 60-85ml/kg*min relative  Maximal untrained maybe - 45ml/kg*min, 4-5 L/min Power watts  rest 0 W  Maximal trained 800Watts  Maximal untrained 300-500 Watts % VO2  Rest 5-10%  Maximal 100% for both trained and untrained. Fick equation Q(L/min) = VO2L/min/(CaO2 - CvO2)/100 Q = SV(mL/min) x HR (beats/min) RELATIONSHIP: between VO2 and extr
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