Chapter 14 Cardiac Output, Blood Flow, and Blood Pressure

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Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.Chapter 14 Cardiac Output, Blood Flow, and Blood Pressure

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I. Cardiac Output

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IntroductionCardiac output – the volume of blood pumped from each ventricle per minute: CO = SV x HR cardiac output = stroke volume X heart rate (ml/minute) (ml/beat) (beats/min) Average heart rate = 70 bpm Average stroke volume = 70−80 ml/beat Average cardiac output = 5,500 ml/minute

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Regulation of Heart RateSpontaneous depolarization occurs at SA node when HCN channels open, allowing Na+ in. Open due to hyperpolarization at the end of the preceding action potential Sympathetic norepinephrine and adrenal epinephrine keep HCN channels open, increasing heart rate. Parasympathetic acetylcholine opens K+ channels, slowing heart rate. Controlled by cardiac center of medulla oblongata that is affected by higher brain centers

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Regulation of Cardiac RateActual pace comes from the net affect of these antagonistic influences Positive chronotropic effect – increases rate Negative chronotropic effect – decreases rate

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Effects of ANS on the SA NodeCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.= Pacemaker potentialControlThresholdSympathetic nerve effectParasympathetic nerve effect1000Time (msec)750500250–50mV–50mV–50mV

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Effects of ANS Activity on the Heart

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Regulation of Stroke VolumeRegulated by three variables: End diastolic volume (EDV): volume of blood in the ventricles at the end of diastole Sometimes called preload Stroke volume increases with increased EDV. Total peripheral resistance: Frictional resistance in the arteries Inversely related to stroke volume Called afterload

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Regulation of Stroke VolumeContractility: strength of ventricular contraction Stroke volume increases with contractility. Ejection fraction (EF) – percentage of the EDV that is ejected per cardiac cycle Stroke volume = EDV – ESV EF% = (SV / EDV) x 100 Normal ejection fraction is about 50-65%

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Frank-Starling Law of the Heart

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Intrinsic Control of Contraction StrengthDue to myocardial stretch Increased EDV stretches the myocardium, which increases contraction strength. Due to increased myosin and actin overlap and increased sensitivity to Ca2+ in cardiac muscle cells

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Intrinsic Control of Contraction StrengthAdjustment for rise in peripheral resistance Increased peripheral resistance will decrease stroke volume More blood remains in the ventricles, so EDV increases Ventricles are stretched more, so they contract more strongly

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Frank-Starling Law of the HeartCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.AHII0Tension (g)StretchZZTimemsec(a)1.5 μm2.0 μm2.2 μm(c)(b)Resting sarcomere lengths(d)2.4 μmActinMyosin(d)(c)(b)(a)1000500

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Extrinsic Control of ContractilityContractility – strength of contraction at any given fiber length Sympathetic norepinephrine and adrenal epinephrine (positive inotropic effect) can increase contractility by making more Ca2+ available to sarcomeres. Also increases heart rate. Parasympathetic acetylcholine (negative chronotropic effect) will decrease heart rate which will increase EDV  increases contraction strength  increases stroke volume, but not enough to compensate for slower rate, so cardiac output decreases

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Effect of muscle length & epinephrine on contractilityCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.0Relative tension (%)Skeletal muscle10080Cardiac muscle with epinephrine (inotropic effect)60Cardiac muscle without epinephrine4020100Length of muscle (as percent of optimum at 100%)5060708090

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*Regulation of Cardiac OutputCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.=XCardiac outputHeart rateStroke volumeTotal peripheral resistance and mean arterial pressureContraction strengthEnd- diastolic volume (EDV)Frank- StarlingParasympathetic nervesSympathetic nervesStretch

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Venous ReturnEnd diastolic volume is controlled by factors that affect venous return: Total blood volume Venous pressure (driving force for blood return) Veins have high compliance – stretch more at a given pressure than arteries (veins have thinner walls). Veins are capacitance vessels – 2/3 of the total blood volume is in veins They hold more blood than arteries but maintain lower pressure.

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Distribution of blood at restCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.Lungs (10%–12%)Heart (8%–11%)Systemic arteries (10%–12%)Capillaries (4%–5%)Large veinsSystemic veins (60%–70%)Small veins and venules

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Factors in Venous ReturnPressure difference between arteries and veins (about 10mm Hg) Pressure difference in venous system - highest pressure in venules vs. lowest pressure in venae cavae into the right atrium (0mm Hg) Sympathetic nerve activity to stimulate smooth muscle contraction and lower compliance Skeletal muscle pumps Pressure difference between abdominal and thoracic cavities (respiration) Blood volume

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Factors in Venous ReturnCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.End-diastolic volumeVenous returnVenous pressureSkeletal muscle pumpSympathetic nerve stimulationTissue-fluid volumeUrine volumeVenoconstrictionBreathingNegative intrathoracic pressureBlood volume

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II. Blood Volume

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Body Water Distribution2/3 of our body water is found in the cells (intracellular). Of the remaining, 80% exists in interstitial spaces and 20% is in the blood plasma (extracellular). Osmotic forces control the movement of water between the interstitial spaces and the capillaries, affecting blood volume. Urine formation and water intake (drinking) also play a role in blood volume. Fluid is always circulating in a state of dynamic equilibrium

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Body Water DistributionCopyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display.Cell membraneIntracellular 27–30 LExtracellular 14–16.5 LCapillary wallWater excretion per 24 hrsKidneys 0.6–1.5 LLungs 0.3–0.4 LSkin (sweat glands) 0.2–1.0 LFeces 0.1–0.2 L H2OGI tractBlood plasma volume 3.0–3.5 LInterstitial fluid volume 11–13 LCytoplasmWater intake per 24 hrs (drink + food) 1.5–2.5 L H2O

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Tissue/Capillary Fluid ExchangeNet filtration pressure is the hydrostatic pressure of the blood in the capillaries minus the hydrostatic pressure of the fluid outside the capillaries Hydrostatic pressure at arteriole end is 37 mmHg and at the venule end is 17 mmHg Hydrostatic pressure of interstitial fluid is 1 mmHg Net filtration pressure is 36 mmHg at arteriole end and 16 mmHg at venule end

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Colloid osmotic pressureDue to proteins dissolved in fluid Blood plasma has higher colloid osmotic pressure than interstitial fluid. This difference is called oncotic pressure. Oncotic pressure = 25 mmHg This favors the movement of fluid into the capillaries.

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Starling ForcesCombination of hydrostatic pressure and oncotic pressure that predicts movement of fluid across capillary membranes Fluid movement is proportional to: (pc + πi) - (pi + πp) or (BHP + IFOP) – (IFHP + BCOP) fluid out fluid in fluid out fluid in pc = Hydrostatic pressure in capillary (BHP) πi = Colloid osmotic pressure of interstitial fluid (IFOP) pi = Hydrostatic pressure of interstitial fluid (IFHP) πp = Colloid osmotic pressure of blood plasma (BCOP)

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Last Updated: 8th March 2018

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