regulation of cardiac out put

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  • 09/30/11
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  • Humoral regulation refers to the effect of hormones in the heart and how hormones that are released into the bloodstream under certain physiological states may regulate cardiac function. Catecholamines released from the adrenal medulla increase the dP/dt of the heart. This effect is potentiated by steroid hormones. Calorigenic hormones like insulin, glucagon and thyroxine also increase cardiac contractility. Thyroxine produces a permissive effect on the action of catecholamines. In hypothyroidism the effect of catecholamines in the heart is depressed by the absence of thyroxine.
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Transcript

  • 1. Addis Ababa University Collage of Health Science Department of Physiology By : Robel Abay September 19 09/30/11 Regulation of cardiac out put
  • 2. Objectives
    • Define cardiac output
    • Out line normal values of CO in different conditions
    • Describe intrinsic and extrinsic regulation of cardiac output
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  • 3. Cardiac output
    • Cardiac output is the quantity of blood pumped into the aorta each minute by the heart.
    • This is also the quantity of blood that flows through the circulation.
    • CO = SV x HR
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  • 4.
    • Normal values for cardiac output at rest and during activity
    • Cardiac output varies widely with the level of activity of the body.
    • The following factors, among others, directly affect cardiac output:
    • (1) The basic level of body metabolism,
    • (2) Whether the person is exercising,
    • (3) The person’s age, and
    • (4) Size of the body
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  • 5. Normal values cont…
    • For young, healthy men, resting cardiac output averages about 5.6 L/min.
    • For women, this value is about 4.9 L/min.
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  • 6. Regulation of cardiac out put
    • Under most normal unstressful conditions , the cardiac output is controlled almost entirely by peripheral factors that determine venous return.
    • If the returning blood does become more than the heart can pump, then the heart becomes the limiting factor that determines cardiac output
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  • 7. Regulation cont….
    • Heart is not the primary controller of cardiac output.
    • Instead, factors of the peripheral circulation affecting venous return, are the primary controllers.
    • The main reason peripheral factors are usually more important than the heart itself in controlling cardiac output is that the heart has a built-in mechanism that normally allows it to pump automatically whatever amount of blood that flows into the right atrium from the veins.
    09/30/11
  • 8. Venous Return
    • The greater the difference between the mean systemic filling pressure and the right atrial pressure, the greater becomes the venous return.
    • Therefore, the difference between these two pressures is called the pressure gradient for venous return .
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  • 9. Factors aiding venous return
    • Venous return is aided by the:
      • Respiratory “ pump ” – pressure changes created during breathing suck blood toward the heart by squeezing local veins
      • Muscular “ pump ” – contraction of skeletal muscles “milk” blood toward the heart
    • Valves prevent backflow during venous return
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  • 10. Body position 09/30/11
  • 11. Factors resisting venous return
    • Right atrial pressure
    • Resistance to blood flow
  • 12.
    • Venous return can be calculated by the following formula: VR= Psf –PRA/ RVR
    • in which VR is venous return, Psf is mean systemic filling pressure, PRA is right atrial pressure, and RVR is resistance to venous return
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  • 13. 09/30/11
  • 14. 09/30/11
  • 15. Regulation cont….
    • A combination of factors together determine cardiac output.
    • These include preload, afterload, contractility and heart rate
    • Intrinsic:
    • filling pressure(preload)
    • Arterial pressure (afterload)
    • Extrinsic :
    • Parasympathetic, sympathetic effects and hormonal
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  • 16. Determinants of cardiac output
    • Preload = initial stretching of the cardiac myocytes prior to contraction (related to sarcomere length)
    • Afterload = “load ” that the heart must eject blood against (related to aortic pressure)
    • Contractility (inotropy) = inherent ability of myocardial cells to develop force at given muscle lengths (related to calcium)
    • Heart rate autonomic nervous system
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  • 17. 09/30/11
  • 18. Cardiac output is controlled by venous return
    • Increased venous return causes increased stretch of cardiac muscle fibers. (Intrinsic effects)
      • increased cross-bridge formation
      • increased calcium influx
        • both increases force of contraction
      • increased stretch on SA node
        • increases heart rate
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  • 19. Increase in preload 09/30/11
  • 20. Increased after load 09/30/11
  • 21. Factors effecting cardiac performance 09/30/11
    • Preload
    • ( LV diastolic volume)
    • Total blood volume
    • Venous tone (sympathetic tone)
    • Body position
    • Intra thoracic / intra pericardial Press.
    • Atrial contraction
    • Pumping action of skeletal muscle
    • After load
    • (Impedance)
    • Peripheral vascular resistance
    • Physical characteristics of arteries
    • (e.g., elasticity of vessels or pressure
    • of outflow obstruction)
  • 22. Factors affecting preload
    • Posture
    • Blood volume
    • Intrinsic Venous Tone
    • Sympathetic neural tone to veins and vaso active drugs
    • Atrial Contraction
    • Muscular Activity
    • Intrapleural Pressure
    • Intrapericardial Pressure
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  • 23. Factors Affecting End-diastolic Volume Ventricular EVD Ventricular performance Total blood volume Body position Intrathoracic pressure Atrial contrib. to vent. filling Pumping action to skeletal muscle Venous tone Intrapericardial pressure ventricular compliance STRETCHING OF MYOCARDIUM 09/30/11
  • 24. Preload vs Afterload Venules / veins Arterioles Capacitance vessels Resistance vessels Affect preload Affect afterload 09/30/11
  • 25. 09/30/11
  • 26. 09/30/11
  • 27. Regulation of heart rate
    • Sympathetic nervous system
      • sympathetic nerves release norepinephrine
      • plus circulating epinephrine from adrenal medulla
      • both act on ß-receptors on sinoatrial node
      • increases slope of the pacemaker potential
      • increases heart rate = tachycardia
    09/30/11 +25 0 -25 -50 -75 mV
  • 28. Regulation of heart rate
    • Parasympathetic nervous system
      • vagus releases ACh
      • acts on muscarinic receptors on sinoatrial node
      • hyperpolarizes cells and decreases slope of pacemaker potential
      • decreases heart rate = bradycardia
    09/30/11 +25 0 -25 -50 -75 mV
  • 29. 09/30/11
  • 30. 09/30/11
  • 31. Effect of Bainbridge and Baroreceptor Reflex on HR Intravenous infusion Increased right atrial pressure Stimulate atrial receptors Bainbridge reflex Increased cardiac output Increased arterial pressure Baroreceptor reflex Heart rate 09/30/11
  • 32. C. Humoral regulation HR/CO INSULIN THYROID GLUCAGON CATECHOLAMINES STEROIDS POTENTIATION
  • 33. CARDIAC OUTPUT HEART RATE MYOCARDIAL CONTRACTILITY PRELOAD AFTERLOAD CARDIAC FACTORS COUPLING FACTORS 09/30/11
  • 34. 09/30/11
  • 35. Reference
    • 1. David E. Mohrman . Lois Jane Heller .(2006). Cardiovascular Physiology, Sixth Edition. New York: McGraw-Hill Companies, Inc.
    • Vander et al. (2007).Human Physiology: The Mechanism of Body Function,(8 th edition). New York: McGraw-Hill Companies, Inc
    • Internet sources
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  • 36. Thank you