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How do we measure heart performance? Cardiac Output = Blood Volume per Minute!

How do we measure heart performance? Cardiac Output = Blood Volume per Minute!. Cardiac Output = heart rate x stroke volume. Heart rate = # of beats per minute; can measure by taking pulse; normally ~ 75 b/min Stroke Volume = volume of blood ejected by L. Ventricle in one cardiac cycle.

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How do we measure heart performance? Cardiac Output = Blood Volume per Minute!

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  1. How do we measure heart performance?Cardiac Output = Blood Volume per Minute! Cardiac Output = heart rate x stroke volume Heart rate = # of beats per minute; can measure by taking pulse; normally ~ 75 b/min Stroke Volume = volume of blood ejected by L. Ventricle in one cardiac cycle Stroke volume = end DIASTOLIC volume – end SYSTOLIC volume Stroke Volume = 135 mL – 65 mL = 70 mL per beat Cardiac Output = 75 beat/min x 70 mL/beat = 5250 mL/min = 5.2 L/min

  2. Normal Cardiac Output Total Blood Volume = ~ 5 liters CO @ Rest: 5 L/min All blood in body is completely circulated every minute at rest! CO @ Exercise: 30-35 L/Min How does your body alter Cardiac Output to meet metabolic demands?

  3. How does your body Alter Cardiac Output? Cardiac Output = heart rate x stroke volume • Autonomic Nervous System • Endocrine (Hormonal) Control • Mechanically (Stroke Volume only)

  4. Somatic vs. Autonomic Somatic motor output is consciously controlled Autonomic motor output is NOT consciously controlled

  5. Functional subdivisions of ANS:Parasympathetic vs. Sympathetic Parasympathetic = Cranio-Sacral Division SLOWING, RELAXING effect Sympathetic = Thoraco-Lumbar Division SPEED-UP, EXCITE, FIGHT

  6. Autonomics are everywhere Autonomics are Reflex Arcs

  7. Autonomic Nervous System: General Anatomy • 5 Parts: • Origin of neural signal • Preganglionic neuron • Autonomic ganglion • Postganglionic neuron • Target organ

  8. Main Differences: Postganglionic neuron Cholinergic vs Adrenergic Target tissue receptor Muscarinic vs α-adrenergic β-adrenergic

  9. Adrenal Medulla releases Epinephrine Epi = Adrenaline Epi Produces a Sympathetic-like Effect

  10. How does your body Alter Cardiac Output? Cardiac Output = heart rate x stroke volume

  11. Heart rate is controlled by AUTONOMIC NERVOUS SYSTEM & Hormones! Altering Cardiac Output: Heart Rate 2) Parasympathetic ANS decreases HR 3) Symapthetic ANS increases HR 4) Sympathetic stimulates Adrenal Gland Epinephrine (hormone) released to blood increases HR Remember: Heart electrical signals are initiated by Pacemaker cells (Autorhymicity) Their rate of depolarization is altered by ANS & Hormones

  12. Cardiac Output = heart rate x stroke volume

  13. Mechanisms of Altered Stroke Volume Stroke Volume is directly related to contraction force Stroke Volume (EDV – ESV) What effects the FORCE of Myocardial Contraction? Force of Ventricular Contraction

  14. Mechanisms of Altered Stroke Volume Stroke Volume is directly related to contraction force • Myocardium Muscle Fiber Length More STRETCH = longer fibers = greater contraction force = more blood expelled Frank-Starling Law of the Heart EDV determines STRETCH

  15. What determines EDV? Venous Return: amount of blood entering R. Atrium • Increase Venous Return by: • Skeletal Muscle Pump • Return MORE Blood from Muscle Veins • 2) Constriction of Veins via Sympathetic ANS • Forces Blood in Veins Back to RA

  16. Compression Tights

  17. What determines EDV? Venous Return: amount of blood entering R. Atrium • Increase Venous Return by: • 3) Respiratory Pump • Lower Pressure is created in Inf. Vena Cava & Right Atrium during inspiration • Bulk Flow pushes more blood towards RA

  18. Cardiac Output = heart rate x stroke volume 1) Venous Return > EDV > Fiber Length > Contractile Force

  19. Mechanisms of Altered Stroke Volume Stroke Volume is directly related to contraction force 1) Myocardium Muscle Fiber Length 2) Contractility Controlled by Autonomics (Neurotransmitters) & Endocrine (Hormones) Norepinephrine (Neuro) Epinephrine (Hormone) Acetylcholine (Neuro) Acetylcholine Mechanism: Altered Calcium Concentrations in Myocardium

  20. Summary: Altering Heart Performance

  21. Homeostasis and Heart Function Cardiac Output is altered in response to: Blood Pressure, pH, and/or CO2 1) O2, CO2 and pressure receptors carry sensory info to Brain Stem 2) Parasympathetic ANS decreases HR venous return contractility 3) Symapthetic ANS increases HR venous return contractility 4) Sympathetic stimulates Adrenal Gland Epinephrine (hormone) released to blood increases HR contractility

  22. Cardiovascular Physiology • Blood • Heart • Peripheral Circulation - tubes The primary function of the Cardiovascular system is to 1) deliver nutrients/oxygen and 2)remove wastes/CO2 from the cells in your body

  23. Basic Anatomy of Circulation Systemic Circuit Pulmonary Circuit

  24. Heart Artery SYSTOLE Heart Artery DIASTOLE

  25. MEAN ARTERIAL PRESSURE (MAP) :is responsible for bulk flow of blood :is measured on ARTERIES Cardiac Output = generates MAP Arteriole Resistance Controls Flow & Impacts MAP HIGH R = narrow arteriole = low flow LOW R = wide arteriole = high flow

  26. MAP = CO x R R = Arteriole Resistance to Flow More Cardiac Output = larger MAP Less Cardiac Output = smaller MAP More Resistance = smaller arteriole = greater MAP but slower flow Less Resistance = larger arteriole = lower MAP but greater flow

  27. Vascular Anatomy effects Resistance Arteries have more smooth muscle & elastic material than veins!

  28. Smooth Muscle Contraction varies with chemical input and varies widely! Neurotransmitters from ANS Hormones from Endocrine Glands Vasoactive Chemicals from Blood Vessels & Tissues

  29. Control of Vascular Resistance & Flowvia smooth muscle • Chemical Control • Neural Control • Endocrine Control

  30. Local Control SHUNTS blood to different parts of body Note: Cardiac output = the total flow to all organs Shunting just redistributes the flow!

  31. Local Control of Blood Flow: Meta-Arterioles feeding into capillaries Metabolically ACTIVE tissue Results in: Low levels in O2, Glucose High Levels in CO2, Lactic Acid, ADP Resting tissue Results in: INCREASE in O2, Glucose DECREASE in CO2, Lactic Acid, ADP Leading to VASODILATION Leads to VASOCONSTRICTION

  32. 2) Neural control of Blood Flow: Widespread Blood Vessels ONLY have SYMPATHETIC INNERVATION! MAP = CO x R Alpha receptors are located on most of the vasculature

  33. Endocrine Control of Blood Flow:Epinephrine, Widespread Epinephrine enters circulation and binds β2-receptors β2-receptors are ONLY located Heart, Liver, Skeletal Muscles Epi on β2-receptors lead to VASODILATION β2-receptors are not innervated by ANS!!!!! Not located elsewhere! Epi MAP = CO x R

  34. Local Control = Precapillary sphincters- local, chemical controlWidespread = vascular Smooth Muscle – sympathetic, adrenal

  35. MAP drives blood flow…..So the body carefully monitors and maintains MAP • Short Term maintenance of MAP – Cardiovascular Regulation • Long Term maintenance of MAP – Kidney & Hormonal Regulation MAP = CO x R Short & long term mechanisms will alter cardiac output & vascular resistance

  36. Short-Term Mechanisms for MAP homeostasis:ANS/ADRENAL via BARORECEPTOR REFLEX • Baroreceptors in Carotid Body & Aorta • Signal processed in Brainstem • IF High MAP • Stimulates Parasym. • Decrease in HR, Stroke Vol. • MAP = CO x R • 4&5) IF Low MAP • Stimulates Sympathetics & Adrenal Gland • Increase in HR, Stroke Volume • Peripheral Vasoconstriction • Vasodilatation at Heart, Skel. Musc. Liver • MAP = CO x R

  37. Long-Term Mechanisms for MAP homeostasis • Renin-Angiotensin-Aldosterone • Vasopressin (Anti-diuretic Hormone) • Atrial-Natriuretic Hormone We will discuss these AFTER kidney physiology……because they all involve the kidney!

  38. Pathological MAP: Hypertension Systolic > 130 Diastolic > 100 Hypertensive, MAP > 130 mm Hg Normal, MAP = 100 mm Hg Normal = 120/80

  39. Increase Length Main Consequences: Heart Failure/Attack, Emboli (broken off blood clots) Poor Vision, Cerebral Hemorrhage Main Causes Hardening Increase in R Decrease Diameter (clogging, thrombi, Atheroscelrosis) LOSS of Elasticity

  40. Fluid Volume

  41. Blood: Functions • Transport of nutrients, gases, wastes • Transport of processed molecules (Vitamin precursors, recycled products) • Transport of hormones & enzymes • Buffer for pH and Fluid/Ion Balance • Body Temperature Homeostatis • Immune Response

  42. Blood: Composition We will talk RBC, Gases, Globulins with Respiratory physiology!

  43. Clotting: dealing with extensive damage Injury: Cut, Wound, etc. Activation of Clotting Cascade, Tissue Factors, Platelets + feedback loop Blood Clot Dissolves

  44. Atherosclerosis Damage to Endothelium = initiation of disease process Chemically: LDL, toxins Mechanically: Hypertension

  45. Normal Moderate Atherosclerosis Severe Atherosclerosis

  46. Inflammatory-Immune-Clotting Ruptured Atheroscelortic Plaque Initiates Clot (Thrombus) Formation

  47. Too much clotting results in Thrombus and/or Embolus! Thrombus breaks free = Embolus Emboli are a major cause of heart attack & stroke! Can originate from anywhere….e.g. varicose veins!

  48. Emboli can get lodged in any small artery Results in ISCHEMIA >>> Infarct >>>> Cell Necrosis

  49. Anti-Coagulants: Clot Inhibitors Aspirin: blocks thromboxane synthesis Platelet Factors = ADP & Thromboxane W/out Thromboxane fewer platelets are attracted to injury Fewer clots form; existing clots shrink Clot Intiation

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