Ch. 20 cont'd & Ch 21
Ch. 20 cont'd & Ch 21 BIOL 224
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This 8 page Class Notes was uploaded by Gail Chernomorets on Friday September 30, 2016. The Class Notes belongs to BIOL 224 at University of Nevada - Las Vegas taught by Sean Neiswenter in Fall 2016. Since its upload, it has received 22 views. For similar materials see Human Anatomy and Physiology II in Biology at University of Nevada - Las Vegas.
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Date Created: 09/30/16
09/29 Chapter 20 cont’d * 2-3 questions on exam 2 The Energy for Cardiac Contractions Aerobic metabolism - Fatty acids - Glucose - Oxygen from circulating hemoglobin stored in myoglobin The Cardiac Cycle One heartbeat - Contraction and relaxation of each chamber Each chamber has two phases - Systole (contraction) - Diastole (relaxation) * Fluids move from higher to lower pressure - When pressure gradient present Blood pressure in any chamber - Rises (move blood) - Falls (blood flow in) - Alternate movement in and out Blood flows from high to low pressure (repeated) - Timing of contractions and one-way valves Phases of the Cardiac Cycle - Atrial systole - Atrial diastole - Ventricular systole - Ventricular diastole Cardiac Cycle begins with Atrial Systole Atrial Systole Pressure increases AP starts at AV node and atrium responds AV valves are open Small proportion of blood ejected 30% Short lived; top off ventricles End-diastolic volume (EDV) - Volume at the end of ventricular diastole Largest amount of blood in ventricles in the cycle Take blood coming back to it Pressure drops as atrial systole ends Atrial Diastole AV valves close * Atrial diastole and ventricular systole begin at the same time Atria fill during atrial diastole - Low pressure Ventricular Systole 2 phases Isovolumetric ventricular contraction - Ventricles contract - Valves closed - Volume of blood does not change Same volume during ventricle contraction - Pressure increases But does not exceed pressure of artery Ventricular ejection - Isotonic contraction - Exceeds pressure of artery - Ventricular pressure - Vessel pressure - Semilunar valves - Stroke volume (SV) Amount ejected per ventricular contraction Difference between end diastolic and end systolic - End-systolic volume (ESV) About 40% of end-diastolic volume What’s left after ejection (60% ejected) Ventricular Diastole 2 phases Isovolumetric ventricular relaxation - Valves closed - Vessels expand - Ventricles contracting Leads to relaxation - Pressure dropping Passive ventricular filling - Pressure in ventricles drops below atrium and allows them to open Ex. turkey pastor Squeezing it – active Suction that occurs – passive *Figure 20-17 Important * Recommend printing out from slides Different sounds of the heart Can be heard depending where you place your stethoscope Heart Sounds * Know names and what causes them S1 - Loud sound produced by AV valves closing - “lub” S2 - Loud sound produced by semilunar valves closing - “dub” S3 & S4 - Soft sounds as blood flows into ventricles and atrial contraction Heart murmur - Sounds produced by regurgitation through valves - Insufficient backflow - In between sounds Cardiodynamics End-diastolic volume (EDV) - Volume of blood in ventricle before it contracts - As much blood as you can pack before End-systolic volume (ESV) - Volume of blood remaining in ventricle after contraction - What’s left after Stroke volume (SV) - EDV – ESV - Amount of blood ejected from ventricle during one contraction Ejection fraction - % of EDV represented by SV, typically 60% at rest Model of Stroke Volume Example: hand pump ESV - allows creation of suction to allow passive filling Can eject a little more or less depending on what is needed Cardiac Output (CO) The volume pumped by left ventricle in 1 minute - pumps to systemic circuit CO = HR SV Anything that affects components affects CO CO = cardiac output (mL/min) HR = heart rate (beats/min) SV = stroke volume (mL/beat) Factors Affecting Cardiac Output - heart rate – ANS and/or hormones - stroke volume – adjust EDV or ESV - change BV – before and after it contracts Affecting HR - autonomic innervation - hormones Affecting SV - end-diastolic volume - end-systolic volume Autonomic Innervation adjusts Heart Rate Cardiac centers of medulla oblongata Cardioacceleratory center - norepinephrine - sympathetic neurons – stimulation - cervical and upper thoracic – more AP per minute - increase HR Cardioinhibitory center - Acetylcholine - Parasympathetic neurons – inhibiting HR - Vagus nerves – few AP per minute Cardiac reflexes Cardiac centers respond to: - Blood pressure (baroreceptors) - Arterial oxygen and carbon dioxide levels (chemoreceptors) Located in aorta and carotid artery - directly to brain - systemic side of heart * Aid in speeding or slowing of HR Autonomic tone Dual innervation maintains resting tone - Ach and NE - Gas and break adjusting at the same time - Adjustments on demand ANS effects on the SA Node Alter membrane permeability Ach (parasympathetic stimulation) - binds to ligand gated K+ channels - opens the channels - (+) ions move out & (-) ions inside - slow heart down by hyperpolarizing action potential NE (sympathetic stimulation) - by opening Na+/Ca 2+ - push membrane up closer to AP so occurs more often - increase HR Atrial Reflex Stretch receptors in right atrium sense venous return Increase HR – sympathetic stimulation of SA node Large return at once How much blood returning to RA Seen when relaxed and you jump up and run Hormonal effects on heart rate - increase HR E and NE Thyroid hormone Delivering blood to system Factors Affecting Stroke Volume Change EDV or ESV = change SV - EDV influenced by: Filling time – duration of ventricular diastole Venous return – rate during ventricular diastole; increase rate of blood flow return Preload – degree of ventricular stretching during diastole – directly proportional to EDV – right before it contracts – affects ability of muscle cells to produce tension – intrinsic property of cardiac muscle – don’t have to innervate; stretch a little more and contract harder and ejects more blood – fill longer or faster at end of diastole * Anything that affects the heart before and after contraction More on EDV and SV At rest EDV is low - myocardium is minimally stretched and stroke volume is low (won’t contract hard) Intrinsic factor of blood With exercise EDV increases - myocardium stretches more and stroke volume increases The Frank-Starling Principle As EDV increases, stroke volume increases - up to a point Ventricular expansion is limited by myocardial connective tissue, the cardiac (fibrous) skeleton, and the pericardial sac End-Systolic Volume (ESV) The amount of blood that remains in the ventricle at the end of ventricular systole Three Factors that Affect ESV - Preload Ventricular stretching during diastole Increase SV Affects what is left at the end Affected by venous return and filling time (longer or faster) - Contractility Force produced at a given preload Adjust through hormone and nervous stimulation, and preload Affected by autonomic activity and hormones or preload to contract harder - Afterload Tension required to open the semilunar valve Artery on other side of ventricle Decrease SV Inversely related to ESV and SV From the aorta Large pressure – more pressure/tension needed to overcome pressure – decrease amount of blood ejected Increased by restricting arterial blood flow Pressure that needs to be created to eject blood Makes it harder to push blood out Summary: The Control of Cardiac Output Heart rate control factors - ANS - Hormones - Atrial reflex Stroke volume control factors - EDV - ESV Chapter 21 Blood Vessels and Circulation Arteries Alter blood flow Elasticity - passive contraction - stretch and return - absorb the pressure waves from heart beating - return to original size/shape - will be lost or reduced when you get older - rebound and continue movement - vessels that carry blood away from heart Contractility - change diameter - sympathetic division of ANS - Vasoconstriction – smooth muscle contracts - Vasodilation – smooth muscle relaxes - Affects afterload, peripheral blood pressure, and perfusion - Change SV - Take blood from heart and pushed through with high pressure and returns pulse gets bounced - Smooth muscle = active control Capillaries * Are the only vessels that permit exchange between blood and interstitial fluid Small with thin walls and slow blood flow - layer of ET and apical & basal surface - profuse through tissue and allow exchange Networks permeate all active tissues of capillaries Consist of endothelium inside basement membrane No tunica media or tunica externa Diameter is similar to RBC or even smaller Continuous Capillaries Most common; found everywhere Basement membrane Complete endothelial lining All tissues except epithelia and cartilage; unless avascular tissue Diffusion of - small things & lipid soluble - water, small solutes, and lipid-soluble materials - not blood cells and plasma proteins Specialized in CNS and thymus - tight junctions - water tight barrier - selective membrane Diffusion around epithelial cells Fenestrated Capillaries Similar to continuous Specialized Biggest difference: pores in endothelial lining Rapid exchange of water and large solutes; no RBC - much faster - same size gets through it - larger things don’t get through Found in - specialized areas - choroid plexus, endocrine organs, kidneys, intestinal tract Sinusoids (Sinusoidal capillaries) Gaps between endothelial cells - large gaps - pores allow movement between and through the cells Free exchange of water, proteins, RBC - seen where need to move things in and out of blood (big things) - nothing prevents Found in liver, spleen, bone marrow - most extreme - don’t have basement membrane in many cases - make RBCs
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