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Control of Cardiac Output

Reading. Klabunde, Cardiovascular Physiology ConceptsChapter 4 (Cardiac Function). Basic Theory of Circulatory Function. The blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue needsThe cardiac output is controlled mainly by the sum of all the local tissue flowsFrank-Starling Relationship is the predominant factor in matching venous return and cardiac outputIn general, the arterial pressure is controlled independently of either local blood flow or cardiac output control.

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Control of Cardiac Output

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    1. Control of Cardiac Output

    2. Reading Klabunde, Cardiovascular Physiology Concepts Chapter 4 (Cardiac Function)

    3. Basic Theory of Circulatory Function The blood flow to each tissue of the body is almost always precisely controlled in relation to the tissue needs The cardiac output is controlled mainly by the sum of all the local tissue flows Frank-Starling Relationship is the predominant factor in matching venous return and cardiac output In general, the arterial pressure is controlled independently of either local blood flow or cardiac output control

    4. Definitions Cardiac Output The quantity of blood pumped into the aorta each minute Venous Return The quantity of blood flowing from the veins into the right atrium each minute

    5. Cardiac Output CO = HR x SV SV = EDV – ESV

    7. Determinants of Cardiac Output

    9. Heart Rate

    10. Heart Rate Changes in heart rate are generally more important quantitatively in producing changes in cardiac output than are changes in stroke volume Changes in heart rate alone inversely affect stroke volume

    11. Heart Rate At low HR Increase in HR is greater than decrement in SV At high HR The decrease in SV is greater than the increase in HR (decreased filling time)

    12. Effects of Heart Rate on Cardiac Output

    13. Bowditch (Treppe) Effect An increase in heart rate will also cause positive inotropy (Bowditch effect, Treppe or “staircase” phenomenon). This is due to an increase in intracellular Ca++ with a higher heart rate: More depolarizations per minute Inability of Na+/K+-ATPase to keep up with influx of Na+, thus, the Na+-Ca++ exchange pump doesn’t function as well

    14. Factors Affecting Stroke Volume

    16. Preload

    17. Preload Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. It is related to the sarcomere length at the end of diastole. Because we cannot measure sarcomere length directly, we must use indirect indices of preload. LVEDV (left ventricular end-diastolic volume) LVEDP (left ventricular end-diastolic pressure) PCWP (pulmonary capillary wedge pressure) CVP (central venous pressure)

    18. Determinants of Preload Venous Blood Pressure Venomotor tone (Venous compliance) Venous volume Venous Return Total Blood Volume Respiration Exercise/Muscle contraction Gravity Filling time (Heart rate) Ventricular compliance Atrial contraction Inflow or outflow resistance Ventricular systolic failure

    19. Frank-Starling Mechanism

    20. Frank-Starling Mechanism When venous return to the heart is increased, ventricular filling increases, as does preload. This stretching of the myocytes causes an increase in force generation, which enables the heart to eject the additional venous return and thereby increase stroke volume. Simply stated: The heart pumps the blood that is returned to it

    21. Frank-Starling Mechanism Allows the heart to readily adapt to changes in venous return. The Frank-Starling Mechanism plays an important role in balancing the output of the 2 ventricles. In summary: Increasing venous return and ventricular preload leads to an increase in stroke volume.

    22. Frank-Starling Mechanism

    23. Frank-Starling Relationship

    24. Frank-Starling Mechanism There is no single Frank-Starling Curve for the ventricle. Instead, there is a family of curves with each curve defined by the existing conditions of afterload and inotropy.

    25. Frank-Starling Curves

    26. Afterload

    27. Afterload Afterload can be viewed as the "load" that the heart must eject blood against. In simple terms, the afterload is closely related to the aortic pressure.

    28. Afterload More precisely defined in terms of ventricular wall stress: LaPlace’s Law: Wall stress = Pr/h P = ventricular pressure R = ventricular radius h = wall thickness

    29. Afterload is better defined in relation to ventricular wall stress LaPlace’s Law

    30. Afterload Afterload is increased by: Increased aortic pressure Increased systemic vascular resistance Aortic valve stenosis Ventricular dilation

    31. Effects of Afterload

    32. Anrep Effect An abrupt increase in afterload can cause a modest increase in inotropy. The mechanism of the Anrep Effect is not fully understood.

    33. Contractility

    34. Contractility The inherent capacity of the myocardium to contract independently of changes in afterload or preload. Changes in contractility are caused by intrinsic cellular mechanisms that regulate the interaction between actin and myosin independent of sarcomere length. Alternate name is inotropy.

    35. Contractility Force of contraction Increased rate and/or quantity of Calcium delivered to myofilaments during contraction Heart functions at lower end-systolic volume and lower end-diastolic volume

    37. Factors Regulating Inotropy

    38. Ancillary Factors

    39. Ancillary Factors Affect the Venous System and Cardiac Output Gravity Venous pooling may significantly reduce CO Muscular Activity and Venous Valves Respiratory Activity

    40. Effects of Gravity on the Venous System and Cardiac Output Gravity Venous pooling may significantly reduce CO

    41. Muscular Activity and Venous Valves

    42. Effects of Respiration Spontaneous respiration Decreased intra-thoracic pressure results in a decreased right atrial pressure which enhances venous return Mechanical ventilation Increased intra-thoracic pressure during positive-pressure lung inflation causes increased right atrial pressure which decreases venous return Valsalva Maneuver Causes a large increase in intra-thoracic pressure which impedes venous return to the right atrium

    43. Summary of Factors That Influence Cardiac Output and Mean Arterial Pressure

    45. Myocardial Oxygen Consumption

    46. Myocardial Oxygen Consumption Oxygen consumption is defined as the volume of oxygen consumed per minute (usually expressed per 100 grams of tissue weight)

    47. Myocardial Oxygen Demand is Related to Wall Stress LaPlace’s Law

    48. Factors Increasing Myocardial Oxygen Consumption Increased Heart Rate Increased Inotropy (Contractility) Increased Afterload Increased Preload Changes in preload affect myocardial oxygen consumption less than do changes in the other factors

    49. The End

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