Cardiovascular System5


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Cardiovascular System5

  1. 1. <ul><li>Lecture 5 </li></ul><ul><li>Cardiac Output </li></ul>
  2. 2. Cardiac Output <ul><li>Volume of blood ejected by each ventricle in 1 minute </li></ul><ul><li>Cardiac Output = Heart Rate (beats/minute) x Stroke Volume (mL/beat) </li></ul><ul><li>Cardiac output varies with the body’s state of activity. </li></ul><ul><li>Cardiac reserve is the difference between resting and maximal CO </li></ul>
  3. 3. Cardiac output <ul><li>Cardiac Index: the cardiac output per square meter of body surface area. </li></ul><ul><ul><li>the normalized data for different size individuals </li></ul></ul><ul><ul><li>the normal range is about 3.0 – 3.5 L/min/m2 </li></ul></ul>
  4. 4. MEASUREMENT OF CARDIAC OUTPUT 1. THE FICK METHOD: VO 2 = ([O 2 ] a - [O 2 ] v ) x Flow Flow = VO 2 [O 2 ] a - [O 2 ] v Spirometry (250 ml/min) Arterial Blood (20 ml%) Pulmonary Artery Blood (15 ml%) CARDIAC OUTPUT PERIPHERAL BLOOD FLOW VENOUS RETURN PULMONARY BLOOD FLOW
  5. 5. CARDIAC OUTPUT (Q) = VO 2 [O 2 ] a - [O 2 ] v 250 ml/min 20 ml% - 15 ml% = = 5 L/min . Q = HR x SV . SV = Q HR . = 5 L/min 70 beats/min = 0.0714 L or 71.4 ml CARDIAC INDEX = Q m 2 body surface area . 5 L/min 1.6 m 2 = = 3.1 L/min/m 2
  6. 6. Measurement of cardiac output 2. Indicator dilution method 3. Doppler Echocardiography
  7. 7. Factors Affecting Cardiac Output
  8. 8. Heart Rate <ul><li>Pulse = surge of pressure in artery </li></ul><ul><ul><li>Infants have HR of 120 bpm or more </li></ul></ul><ul><ul><li>Normal range of the heart rate 60 – 100 beats/min </li></ul></ul><ul><li>Tachycardia: resting adult HR above 100 </li></ul><ul><ul><li>stress, anxiety, drugs, heart disease or  body temp. </li></ul></ul><ul><li>Bradycardia: resting adult HR < 60 </li></ul><ul><ul><li>in sleep and endurance trained athletes </li></ul></ul>
  9. 9. Regulation of Heart Rate <ul><li>Positive chronotropic factors increase heart rate </li></ul><ul><li>Negative chronotropic factors decrease heart rate </li></ul>
  10. 10. Regulation of Heart Rate <ul><li>1. Vital centers of medulla </li></ul><ul><li>Cardiac Center </li></ul><ul><ul><li>Cardioaccelerator center </li></ul></ul><ul><ul><ul><li>Activates sympathetic neurons that increase HR </li></ul></ul></ul><ul><ul><li>Cardioinhibitory center </li></ul></ul><ul><ul><ul><li>Activates parasympathetic neurons that decrease HR </li></ul></ul></ul><ul><li>Cardiac center receives input from higher centers (hypotha-lamus), monitoring blood pressure and dissolved gas concentrations </li></ul>
  11. 11. Regulation of the Heart rate <ul><li>2. Neural regulation </li></ul><ul><ul><li>Parasympathetic stimulation - a negative chronotropic factor </li></ul></ul><ul><ul><ul><li>Supplied by vagus nerve, decreases heart rate, acetylcholine is secreted and hyperpolarizes the heart </li></ul></ul></ul><ul><ul><li>Sympathetic stimulation - a positive chronotropic factor </li></ul></ul><ul><ul><ul><li>Supplied by cardiac nerves. </li></ul></ul></ul><ul><ul><ul><li>Innervate the SA and AV nodes, and the atrial and ventricular myocardium. </li></ul></ul></ul><ul><ul><ul><li>Increases heart rate and force of contraction . </li></ul></ul></ul><ul><ul><ul><li>Epinephrine and norepinephrine released. </li></ul></ul></ul><ul><li>3.Hormonal regulation </li></ul><ul><ul><li>Epinephrine and norepinephrine from the adrenal medulla. </li></ul></ul><ul><ul><ul><li>Occurs in response to increased physical activity, emotional excitement, stress </li></ul></ul></ul>
  12. 12. <ul><li>SA node establishes baseline (sinus rhythm) </li></ul><ul><li>Modified by ANS </li></ul><ul><li>If all ANS nerves to heart are cut, heart rate jumps to about 100 b/min </li></ul>Basic heart rate established by pacemaker cells
  13. 13. Regulation of Stroke Volume <ul><li>SV: volume of blood pumped by a ventricle per beat </li></ul><ul><ul><li>SV= end diastolic volume (EDV) minus end systolic volume (ESV); SV = EDV - ESV </li></ul></ul><ul><li>EDV = end diastolic volume </li></ul><ul><ul><li>amount of blood in a ventricle at end of diastole </li></ul></ul><ul><li>ESV = end systolic volume </li></ul><ul><ul><li>amount of blood remaining in a ventricle after contraction </li></ul></ul><ul><li>Ejection Fraction - % of EDV that is pumped by the ventricle; important clinical parameter = stroke volume / end diastole volume X 100%,it s hould be about 55-60% or higher </li></ul>
  14. 14. Factors Affecting Stroke Volume <ul><li>EDV - affected by </li></ul><ul><ul><li>Venous return - vol. of blood returning to heart </li></ul></ul><ul><ul><li>Preload – amount of stretch on the ventricular myocardium prior to contraction (=EDV ) </li></ul></ul><ul><li>ESV - affected by </li></ul><ul><ul><li>Contractility – myocardial contractile force due to factors other than EDV. </li></ul></ul><ul><ul><li>After load – back pressure exerted by blood in the large arteries leaving the heart. </li></ul></ul>
  15. 15. Frank-Starling Law of the Heart <ul><li>Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume;  EDV leads to  stretch of myocardium. </li></ul><ul><ul><li> preload   stretch of muscle   force of contraction   SV </li></ul></ul><ul><ul><li>If SV is increased, then ESV is decreased!! </li></ul></ul><ul><li>Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV </li></ul><ul><ul><li>VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output </li></ul></ul><ul><ul><li> VR   EDV and  in VR   in EDV </li></ul></ul><ul><li>Blood loss and extremely rapid heartbeat decrease SV </li></ul>
  16. 16. Frank –starling curve <ul><li>Left ventricle (LV) function curve, or Frank - Starling curve (1914): </li></ul><ul><ul><li>Normal range of the LVEDP, 5-6 mmHg </li></ul></ul><ul><ul><li>Optimal initial preload, 15-20 mmHg (Sarcomere, 2.0 – 2.2 µm ) </li></ul></ul>
  17. 17. Factors influencing Venous return
  18. 18. Total Peripheral Resistance ( TPR) <ul><li>Total Peripheral Resistance: </li></ul><ul><ul><li>Impedance to the ejection of blood from ventricle. </li></ul></ul><ul><ul><li>Afterload. </li></ul></ul><ul><ul><ul><li>In order to eject blood, pressure generated in the ventricle must be greater than pressure in the arteries. </li></ul></ul></ul><ul><ul><li>Pressure in arteries before ventricle contracts is a function of TPR. </li></ul></ul><ul><li>SV inversely proportional to TPR. </li></ul><ul><ul><li>Greater the TPR, the lower the SV. </li></ul></ul>
  19. 19. Contractility- Extrinsic factors influencing SV <ul><li>Contractility is the increase in contractile strength, independent of stretch and EDV </li></ul><ul><li>Referred to as extrinsic since the influencing factor is from some external source </li></ul><ul><li>Increase in contractility comes from: </li></ul><ul><ul><li>Increased sympathetic stimuli </li></ul></ul><ul><ul><li>Certain hormones </li></ul></ul><ul><ul><li>Ca 2+ and some drugs </li></ul></ul><ul><li>Agents/factors that decrease contractility include: </li></ul><ul><ul><li>Acidosis </li></ul></ul><ul><ul><li>Increased extracellular K + </li></ul></ul><ul><ul><li>Calcium channel blockers </li></ul></ul>
  20. 20. Effects of Hormones on Contractility <ul><li>Epi, NE, and Thyroxine all have positive ionotropic effects and thus  contractility </li></ul><ul><li>Digitalis elevates intracellular Ca ++ concentrations by interfering with its removal from sarcoplasm of cardiac cells </li></ul><ul><li>Beta-blockers ( propanolol, timolol ) block beta-receptors and prevent sympathetic stimulation of heart (neg. chronotropic effect) </li></ul>
  21. 21. Unbalanced Ventricular Output
  22. 22. Unbalanced Ventricular Output
  23. 23. Factors Involved in Regulation of Cardiac Output
  24. 24. RIGHT ATRIAL PRESSURE AND VENOUS RETURN Venous return RA pressure Venous return from the periphery depends on the pressure difference between the peripheral pressure and right atrial pressure. Thus as right atrial pressure (central venous pressure) rises venous return will fall Venules Right atrium 25 mm Hg ∆P = 25 mm Hg 0 mm Hg 25 mm Hg ∆P = 20 mm Hg 5 mm Hg
  25. 25. GUYTON’S ANALYSIS OF THE INTACT CIRCULATION Two relationships have been established: A rise of right atrial pressure will more effectively fill the heart in diastole, increase stroke work and thus increase flow in the circulation (assume afterload and heart rate are constant) A rise of right atrial pressure will hinder venous return and thus decrease flow in the circulation. But in the intact circulation venous return must equal cardiac output Venous return RA pressure Cardiac output RA pressure
  26. 26. GUYTON’S ANALYSIS OF THE INTACT CIRCULATION Thus right atrial pressure exerts conflicting effects on flow in the intact circulation. But: cardiac out put = venous return. Thus: the two curves can be superimposed to yield an equilibrium point for the circulation. Cardiac output = venous return RA pressure cardiac function curve equilibrium point vascular function curve