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Blood Pressure

Blood Pressure. Blood Pressure. Fig 15-4. Hydrostatic Pressure created by ventricular contractility becomes the driving force for blood flow Pulsatile blood flow in arteries  Elastic arteries expand and recoil for continuous blood flow. This is the “pulse” that we can feel.

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Blood Pressure

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  1. Blood Pressure

  2. Blood Pressure Fig 15-4 Hydrostatic Pressure created by ventricular contractility becomes the driving force for blood flow Pulsatile blood flow in arteries  Elastic arteries expand and recoil for continuous blood flow. This is the “pulse” that we can feel. Pulse wave disappears past arterioles and the precapillary sphincters

  3. Arteries vs. Veins • Endothelial lining throughout the cardiovascular system and heart • Less sticky than teflon • Arteries have more smooth muscle than veins • Arteries can vasoconstrict • Veins are “stretchy” or compliant • Veins have valves to prevent backflow of blood • Arteries don’t have backflow due to pressure gradient

  4. Cardiovascular System • Blood Flow • Aorta to major arteries to minor arteries entering organs to arterioles to capillaries to venules to veins leaving organs to vena cava • Cardiovascular system transports materials throughout the body • Nutrients, water, gases • Materials that move from cell to cell • Wastes that the cells eliminate

  5. Why Does Blood Flow? • Liquids and gases flow down pressure gradients (ΔP) • A region of higher pressure to a region of lower pressure • Blood can flow in the cardiovascular system only if one region develops higher pressure than other regions

  6. Pressure Gradients • Pressure is created in the chambers of the heart when they contract • Blood flows out of the heart • The higher region of pressure • As blood moves through the system pressure is lost due to friction between the fluid and the vessel walls • Pressure falls the farther the blood moves from the heart • Higher pressure in the aorta • Lowest pressure in the venae cavae just before they empty into the right atrium

  7. Blood Pressure (BP) Measurements • Ventricular pressure difficult to measure  measure arterial BP • BP highest in the arteries – falls continuously throughout systemic circulation (Why?) • Read as “Systolic over diastolic”– normal value  120 / 80 mm Hg • 2003: New range for blood pressure readings between 120/80 and 139/89 “Prehypertension” • Diastolic pressure in ventricle: ? mm Hg Blood Flow Rate P/ R

  8. Pressure of Fluid in Motion Decreases over Distance • Pressure in a fluid is the force exerted by the fluid on its container • The container is the wall of the artery for blood pressure • Hydrostatic Pressure • The pressure exerted if the fluid is not moving • Force is exerted equally in all directions on the container

  9. Capillaries • Capillaries contain sphincters • Sphincters are typically closed to 90% of the body • During exercise sphincters all open • Better perfusion

  10. Veins are Capacitance Vessels • Veins have little smooth muscle • Veins are “stretchy” • The stretch is called capacitance • The more the stretch the less pressure is exerted against the walls • Veins are located between muscle • Skeletal, smooth, cardiac • Veins contain valves • Varicose Veins • Venous Return • Blood flowing back to the heart through veins

  11. Cardiovascular Physiology • Blood Pressure is controlled by: • Heart Rate • Peripheral Resistance • Blood Viscosity • Blood Volume • Stroke Volume

  12. Heart Rate • Tachycardia • Faster than 60-100 bpm • Bradycardia • Slower than 60 bpm

  13. Cardiovascular Physiology • CO = HR X SV Cardiac Output = Heart Rate X Stroke Vol • SV = EDV – ESV • Stroke Vol = End Diastolic Vol – End Systolic Vol • BP = CO x PR • Blood Pressure = Cardiac Output X Peripheral Resistance • FRANK-STARLING’S LAW

  14. Hypovolemia Stimulates Compensatory Mechanisms • Baroreceptors • Aoritc arch, carotid arteries, kidneys • Detect blood pressure changes • Stimulates the medulla oblongata • MO stimulates the SNS to release Epi/Norepi • Myogenic Control • Arterial Spams

  15. Stroke Volume • The amount of blood pumped by one ventricle during a contraction (ml/beat) • SV=EDV-ESV • End Diastolic Volume • Volume of blood in ventricle before contraction • End Systolic Volume • Volume of blood in ventricle after contraction

  16. CO= HR xSV Force of contraction Length of muscle fibers (Starling curve/law) due to venous return, influenced by skeletal muscle pump and respiratory pump Sympathetic activity (and adrenaline) venous constriction by sympathetic NS and Increased Ca2+ availability

  17. Stroke Volume • Increase EDV • Increase Venous Return • Increase Contraction of Muscles • Skeletal muscle twitching • Increase Respiration Rate and Depth • Negative Intrathoracic Pressure • Afterload • The combined load of EDV and arterial resistance during ventricular contraction • The force necessary to push the blood out of the heart into the arteries

  18. Stroke Volume • Decrease ESV • Increase Force of Contraction in Cardiac Muscle • Sympathetic Nervous System Input • Epi/Norepi bind to receptors to open Calcium gates on the sarcolemma and sarcoplasmic reticulum

  19. Preload • The degree of myocardial stretch before contraction begins • This stretch represents the load placed on cardiac muscles before they contract • There is a relationship between stretch and force according to Drs. Frank and Starling

  20. Frank/Starling Law • Stretching muscle aligns actin and myosin better to achieve a greater force of contraction • Increasing EDV will stretch ventricle • Ventricle have greater force of contraction • Decreases ESV and thereby increases SV • Increases CO and BP

  21. Frank-Starling Law • SV α EDV • i.e., the heart pumps all the blood sent to it via venous return • Therefore, Venous Return = SV • Preload = the amount of load, or stretch of the myocardium before diastole • Afterload = Arterial resistance and EDV combined • Ejection Fraction = % of EDV that is actually ejected; e.g., 70 ml/135ml x 100 = 52% at rest

  22. Peripheral Resistance • Friction to flow against the walls of the arteries • Vasoconstrict the arteries by ½ the diameter and increase PR 4X • Laminar Flow

  23. BP Estimated by Sphygmomanometry Auscultation of brachial artery with stethoscope in cubital fossa Based on effects oflaminar flow vs. turbulent flow

  24. Blood Volume • Baroreceptors in the Kidney are stimulated due to low blood pressure • Renin and Angiotensinogen release • Angiotensin I • Angiotensin I is converted in the lungs to Angiotensin II by the enzyme Angiotensin Converting Enzyme (ACE) • ACE Inhibitors to reduce blood pressure

  25. Blood Volume • Angiotensin II stimulates the Adrenal Cortex to release Aldosterone • Aldosterone is a Mineralcorticoid • Controls Na + /K + concentrations in the blood • Aldosterone stimulates the kidneys to retain Na + in the blood and excrete K+

  26. Blood Volume • Increased concentration of Na + in the blood causes osmosis • Water moves from the intracellular and extracellular fluid into the blood stream • Increased concentration of Na in the blood stimulates Osmoreceptors in the Hypothalamus • Increased osmolarity or osmotic pressure in the blood • Anti-Diuretic Hormone Release • Decreased urine output • Unquenchable Thirst

  27. Blood Viscosity • Typically takes 2 weeks to change viscosity • Kidney release Erythropoietin • Erythropoietin stimulates erythropoiesis in the red bone marrow • Increases RBC formation and thickness in the blood • Increases PR and BP

  28. Mean Arterial Pressure Sometimes useful to have single value for driving pressure: Mean Arterial Pressure MAP  CO x Rarterioles A Calculation: MAP = PD+ 1/3 (PS – PD ) MAP is influenced by CO Peripheral resistance (mostly at arterioles) ANS and endocrine Metabolic Needs Total blood volume Blood distribution

  29. BP too low: Driving force for blood flow unable to overcome gravity O2 supply to brain  Symptoms?

  30. Shock Hypovolemic shock  volume loss (dehydration, blood loss, burns) Distributive shock  loss of vascular tone (anaphylactic, septic, toxic) Cardiogenic shock  pump failure Dissociative shock (not in book)  inability of RBC to deliver O2 (CO poisoning) Cell damage due to hypoxia Signs and symptoms? Management ? = generalized circulatory failure, may have a + feedback cycle

  31. BP too high: Weakening of arterial walls lead to Aneurysms Risk of rupture & hemorrhage Cerebral hemorrhage Rupture of major artery

  32. Pressures at which the Korotkoff . . . . . sound (= blood flow) first heard: . . . sound disappeared: CDAnimation Cardiovascular System: Measuring Blood Pressure

  33. Principles ofSphygmomanometry

  34. Slowly release pressure in cuff: turbulent flow

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