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  • Capillary filtration coefficient: number & size of pores in each capillary + number of capillaries
  • *in response to the stretch, arteriolar vascular smooth muscle contracts, decreasing the arteriolar radius and returning wall tension back to normal. This relationship is explained by the law of Laplace, which states that T = P × r. If pressure (P) increases and radius (r) decreases, then wall tension (T) can remain constant. (Of course, the other consequence of the decreased radius, discussed previously, is increased arteriolar resistance; in the face of increased pressure, increased resistance allows blood flow to be maintained constant, i.e., autoregulation.)
  • Normally SNS is active…..baroR mechanism increases parasympathetic NS and ‘snubs’ SNS
  • Discharges (vertical lines) in a single afferent nerve fiber from the carotid sinus at various levels of mean arterial pressures, plotted against changes in aortic pressure with time.Baroreceptors are very sensitive to changes in pulse pressure as shown by the record of phasic aortic pressure.*esp at lower pressures….at higher pressures they seem to respond during both systolic and diastolic pressure phases
  • *The degree of sympathetic vasoconstriction caused by intense cerebral ischemia is often so greatthat some of the peripheral vessels become totally or almost totally occluded.
  • *discussed in detail later
  • * Nearly equal due to low compliance of pulmonary tree
  • Coupling of heart & circulation: corollary-1*Consider a situation in which the heart pumps blood at a constant flow of 100 mL/sec (6 L/min) into rigid arteries with a resistance of 16.6 peripheral resistance units (PRUs) for 4 seconds. This would then generate a constant pressure of 100 mm Hg, and cardiac work over the 4 seconds would be simply pressure (P) × volume (V) or 100 mm Hg × 400 mL = 40,000. If the heart pumped intermittently and ejected blood at 100 mL/sec into noncompliant arteries during the first half-second of the cycle only (i.e., 200 mL/sec for 0.5 seconds), pressure would rise to 200 mm Hg during each ejection and drop to 0 mm Hg during relaxation. Although no work would be done during relaxation, work done during the contraction would be 80,000. If this same intermittent flow was ejected into arteries with infinite compliance (flexibility), pressure would not rise during systole or fall during diastole and would remain at an average of 100 mm Hg. Work in this situation would then again equal 40,000. In reality, arteries are neither totally rigid nor infinitely compliant. **even if all other factors, such as arterial pressure, stroke volume, and heart rate, do not change. For this reason, the heart of an older person is confronted by increased oxygen demand from the simple fact that arterial compliance decreases with aging.
  • *CO Is Increased by an Increase in Venous Filling Pressure, but Venous Filling Pressure Is Decreased by an Increase in CO
  • Normal equilibrium point
  • *Changes in venous compliance produce effects similar to those produced by changes in blood volume. Decreases in venous compliance cause a shift of blood out of the unstressed volume and into the stressed volume and produce changes similar to those caused by increases in blood volume, a parallel shift to the right. Likewise, increases in venous compliance cause a shift of blood into the unstressed volume and out of the stressed volume and produce changes similar to those caused by decreased blood volume, a parallel shift to the left.
  • In applying this Fick procedure for measuring cardiac output in the human being, mixed venous blood is usually obtained through a catheter inserted up the brachial vein of the forearm, through the subclavian vein, down to the right atrium, and, finally, into the right ventricle or pulmonary artery. And systemic arterial blood can then be obtained from any systemic artery in the body. The rate of oxygen absorption by the lungs is measured by the rate of disappearance of oxygen from the respired air, using any type of oxygen meter.
  • This is why angina pectoris due to deficient delivery of O2 to the myocardium is more common in aortic stenosis than in aortic insufficiency
  • Difference between loading-induced enhanced contraction Vs contractibility (inotropism)!
  • Transcript

    • 1.
    • 2. Veins
      Reservoir function
      60% blood in veins
      Specific reservoirs in spleen, liver, skin, lungs and heart!
      Effect of gravity
      Venous pump
      Valves (varicose veins)
      Abdominal pump
      Thorax pump
      Central venous pressure (CVP) – Right Atrial Pressure
      Ability of the heart to pump
      Venous return
      Values: normal is 0 mmHg
      Increased (straining, heart failure, massive transfusion)
      Decreased (extraordinary heart contractions, haemorrhage)
    • 3. Veins
      Measuring CVP
      Height to which external jugular veins are distended when the subject lies in recumbent position
      Vertical distance b/w rt. atrium and the place the vein collapses (the place where the pressure =0) =venous pressure (in mm of Hg)
      Inserting a catheter into the thoracic great veins
      Direct pressure reading
    • 4. Microcirculation
      Arterial end
      Venous end
      Filtration across capillaries: Starling Forces
      Capillary pressure (Pc)
      Interstitial fluid pressure (Pif)
      Plasma colloid osmotic pressure (πp)
      Interstitial colloid osmotic pressure (πif)
      NFP = Pc – Pif – πp + πif
      Filtration = NFP x Kf
      Where, Kf is Capillary filtration coefficient
    • 5. Starling’s Forces
    • 6. Edema
      Accumulation of interstitial fluid in abnormally large amounts
      Increased filtration pressure    
      Arteriolar dilation
      Venular constriction  
      Increased venous pressure (heart failure, incompetent valves, venous obstruction, increased total ECF volume, effect of gravity, etc)
      Decreased osmotic pressure gradient across capillary    
      Decreased plasma protein level
      Severe liver failure, Protein malnutrition, Nephrotic syndrome  
       Accumulation of osmotically active substances in interstitial space
    • 7. Edema
      Increased capillary permeability    
      Substance P  
      Histamine and related substances   
      Kinins, etc
      Inadequate lymph flow (lymphedema)
      Elephantiasis (In filariasis, parasitic worms migrate into lymphatics & obstruct them)
    • 8. Lymphatics
      Normal 24-h lymph flow is 2 - 4 L
      Lymphatic vessels divided into 2 types:
      Initial lymphatics
      Lack valves
      Lack smooth muscle
      Found in regions such as intestine or skeletal muscle
      Fluid enters thru loose junctions
      Drain into collecting lymphatics
      Collecting lymphatics
    • 9. Lymphatics
      Return of filtered proteins
      Very important fn
      amount of protein returned in 1 day = 25–50% of the total circulating plasma protein
      Transport of absorbed long-chain fatty acids and cholesterol from the intestine
    • 10. Local Control of Blood Flow
      Why control blood flow?
      Blood flow is variable between one organ and another,
      Depends on overall demands of each organ system
      These inter-organ differences in blood flow are the result of differences in vascular resistance
    • 11. Local Control of Blood Flow:Mechanisms
      Matching blood flow to metabolic needs
      Exerted through direct action of local metabolites on arteriolar resistance
      Acute: rapid changes in local vasoconstriction/ dilation of arterioles, metarterioles, precap-sphincters
      Long-term: slow, controlled (days, weeks & months) – increase in physical size, number
      Nervous / Hormonal:
      Histamine, bradykinin, & prostaglandins
    • 12. Acute Mechanisms
      Reactive hyperemia
      Active hyperemia
    • 13. Acute Mechanisms:Autoregulation
      Maintenance of constant blood flow to an organ in the face of changing arterial pressure
      Kidneys, brain, heart, & skeletal muscle + others exhibit autoregulation
    • 14. Acute Mechanisms:Active hyperemia
      Blood flow to an organ is proportional to its metabolic activity
      Metabolic activity in skeletal muscle increases as a result of strenuous exercise
      Blood flow to muscle will increase proportionately to meet the increased metabolic demand
    • 15. Acute Mechanisms:Reactive hyperemia
      Increase in blood flow in response to or reacting to a prior period of decreased blood flow
      Arterial occlusion to an organ occurs
      During the occlusion, an O2 debt is accumulated
      Longer the period of occlusion, the greater the O2 debt
      Greater the subsequent increase in blood flow above the preocclusion levels.
      The increase in blood flow continues until the O2 debt is "repaid."
    • 16. Explanation
      Myogenic hypothesis
      Explains autoregulation
      Not active or reactive hyperemia
      If arterial pressure - suddenly increased - arterioles are stretched - vascular smooth muscle - contracts in response to this stretch*
      Metabolic hypothesis
      O2 demand theory
      Vasodilator theory
      CO2, H+, K+ lactate, and adenosine
    • 17. Long-term Mechanisms for Blood Flow Control
      Vascularity changed – acc. to metabolic profile
      Role of oxygen
      Role of vascular endothelial growth factors
      Fibroblast growth factor
      Vascularity is determined by max. tissue need (not average)
      Collateral circulation
    • 18. Humoral control of Blood Flow
      Vasocontrictor agents (NE, epinephrine, Angiotensin-II)
      Vasodilatory agents (bradykinin, histamine)
      Ions & other agents
      Increase in Ca++: vasoconstriction
      Increase in K+: vasodilation
      Increase in Mg++: powerful vasodialtion
      Increase in H+: vasodilation
      Acetate and citrate: vasodilation
      Increase in CO2: vasodilation
    • 20. General
      The ‘large water tower’ example
      MAP is maintained – hence tissues can ‘tap into’ the general blood flow
      CVS needs to maintain just MAP !
      Nervous and hormonal factors play major roles
      Long term
    • 21. CNS areas controlling BP
    • 22.
    • 23.
    • 24.
    • 25.
    • 26.
    • 27. Baroreceptor Reflex
    • 28. Baroreceptor Features: Sensitivity
      Carotid sinus baroR are not stimulated at all by pressures between 0 and 50 to 60 mm Hg
      Above these levels, they respond rapidly and reach a maximum at ~180 mm Hg
      Around 100 mmHg – very sensitive
      Responses of the aortic baroR – similar
      But they operate about 30 mm Hg higher
    • 29. Baroreceptor Features: Speed
      Respond extremely rapidly to BP changes
      Increases in the fraction of a second during each systole
      Decreases again during diastole
      BaroRs respond much more to rapidly changing pressure than to a stationary pressure
    • 30. Baroreceptor Features: Posture
      Standing – BP in head and upper body falls
      Marked reduction may cause cause loss of consciousness.
      Falling BP at the baroreceptors elicits – BaroR reflex
      Resulting in strong sympathetic discharge
      Maintenance of BP!
    • 31. Baroreceptor Features: Buffer Control
      BaroR reflex is a pressure buffer system
    • 32. Baroreceptor Features: Accomodation
      Role in long-term regulation of BP
      ‘Resets’ in 1-2 days to ‘new’ pressure
    • 33.
    • 34. Baroreceptors are more sensitive to pulsatile pressure than to constant pressure*
      Especially at lower pressures
    • 35. CNS Ischemic Response
      Cerebral ischemia
      Vasoconstrictor & cardioaccelerator neurons in the vasomotor center b/c strongly excited
      Accumulating local concentration of CO2
      Causes strong neuronal +++
      This BP elevation in response to cerebral ischemia is known as the CNS ischemic response*
      Emergency pressure control system only
      Kicks in only when BP falls 60 mm Hg and below
      Cushing’s reaction
    • 36. Intermediate Control Mechanisms
      Fluid shift
      Stress relaxation
      Renin-angiotensin vasoconstrictor mechanism
      Biogenic amines
      Vasoconstrictors (Epinephrine via α1, Serotonin etc)
      Vasodilators (Epinephrine via β2, Histamine, ANP etc)
    • 37. Long-term BP Control Mechanism
      Pressure natriuresis
      Pressure diuresis
    • 38. Long-term BP Control Mechanism
    • 39. Cardiac Output
      Quantity of blood pumped into the aorta each minute by the left ventricle
      Normal values: 5.6 L/min (males), 4.9 L/min (females)
      Cardiac index: C.O./min/m2
      Average: 3.2 L (@ rest)
      Maximum value @ age 10 – then decreases
    • 40. Cardiac Output
    • 41. Cardiac Output
      Mean circulatory filling pressure
    • 42. CO Regulation: Conceptual Overview
      Heart rate
      Coupling factors*
      Ancillary factors
      All factors affecting venous return
    • 43. CO Regulation: DetailedCO = SV x HR
      Stroke Volume
      SV = EDV – ESV
      = 120 – 50 = 70 ml
      Preload (Myocardial fiber length)
      Affected by VR
      Filling time of diastole
      Rapid HR – diastole time decreases – EDV decreases
      Atrial contraction
      Inadequate contraction affects EDV
      Ventricular distensibility
      if decreases – EDV decreases
      Afterload (Aortic pressure – arterial BP)
      Affects myocardial fiber shortening ability
      SNS (NE via β1)
      Heart Rate
      HR and SV are inversely proportional
    • 44. CO Regulation: Another angle
    • 45. Conditions affecting CO
      No change
      Moderate changes in temperature
      Increased temperature
      Anemia & hyperthyroidism
      Rapid arrhythmias
      Heart disease
    • 46. Mean Circulatory Filling Pressure
      With heart stopped – after pressure equilibrates – pressure throughout CVS – MCFP
      MSFP Vs MCFP*
      Factors affecting:
      BV (more raises MCFP)
      Sympathetic +++ (raises MCFP)
      Directly proportional to VR
    • 47. Venous Return
      VR = MSFP* – Rt. Atrial Pressure / Resistance in venous return
      VR = 7 – 0/1.4 = 5 litres
      VR is affected by:
      Blood volume
      Skeletal muscle contraction
      Venous valves
      Thoracoabdominal pump
      Myocardial contractibility
    • 48. Coupling of Cardiac & Vascular Function
      Characteristics of arteries and veins (vascular compliance, BV & vascular resistance)
      affect heart fn & its other variables
      However, it is also true that performance of the heart influences volumes and pressures within the vasculature
      So vasculature affects heart & vice versa
      Equilibrium must exist between cardiac and vascular function
    • 49. Changes in Arterial Compliance Change Cardiac Work
      One of the more important consequences of the elastic nature of large arteries is that it reduces cardiac work*
      Increased arterial compliance (increase in arterial elasticity / afterload reduction)
      Reduces cardiac work
      Decreased compliance
      Increases cardiac work
      Myocardial O2 demand will be increased by any factor that reduces arterial compliance**
    • 50. Relationship b/w Venous filling P. & CO : Tricky!*
      CVP - key determinant of filling of the right heart - key determinant of cardiac output
      Starling's Law
      Increased cardiac output into the arterial segment should result in ‘depletion’ in venous pressure & volume
      Q(1) How are values of cardiac output above or below the resting level ever achieved or maintained,
      Q(2) What determines the resting equilibrium between cardiac output and central venous pressure?
    • 51. Cardiac & Vascular fn Curves
      Cardiac fn Curve
      plots CO as a function of CVP
      An extension of Starling's law
      Position and slope depends on ‘cardiac’ factors
      Vascular fn Curve
      shows how CVP changes as a function of VR
      Position and slope depends on ‘vascular’ factors (BV,SVR,compliance)
    • 52. Cardiac & Vascular fn Curves
      Combining the curves provides a useful tool for predicting the changes in CO
      That will occur when various CVS parameters are altered
      CO can be altered by:
      Changes in the cardiac function curve
      By changes in the vascular function curve
      By simultaneous changes in both curves
    • 53. Inotropic agents alter cardiac fn curve
      Vice versa
      CO is increased and CVP is decreased
    • 54. Changes in BV* alter MSP : alter vascular fn curve
      CO is increased and CVP is increased
      Vice versa
    • 55. Changes in TPR alter both curves
      Cardiac fn curve shifts downward (increased afterload)
      Counterclockwise rotation of vascular fn curve
      Vice versa
    • 56. CO Measurement
      Principle of mass balance
      Introducing a known conc. of a dye (A) into an unknown volume of a fluid (V)
      By calculating conc. of dye in fluid (C) along with A – V can be calculated via:
    • 57. CO Measurement
      Indicator dilution method
      Known amount of indicator (Indocyanine green – Cardiogreen) injected into venous circulation (A)
      Blood sampled serially from distal artery
      Concentration of dye (C) in serial samples:
      C is then averaged between T1 (time of appearance of dye in blood) and T2 (time of appearance of dye in blood) - Cave
    • 58. CO Measurement
      Thermodilution method
      Variation of indicator dilution method
      More used in clinical practice
      Swan-Ganz catheter placed via vein – threaded to the pulmonary artery
      Catheter releases ice-cold saline into right heart via a side port
      Saline changes temperature of the blood coming in contact with it – reflected by CO – to be measured by thermistor on catheter tip (placed downstream into pulmonary artery)
      Equations similar to indicator dilution technique employed here
    • 59. CO Measurement
      Fick’s principle – principle of mass balance taking into account oxygen entry/exit
      1 liter blood can take 40 ml O2
      How many 1-liter ‘units’ will it take to carry 200 ml in a min? – 5 L
      This much needs to supplied by heart – CO!
    • 60. Energetics of Cardiac Function
      Oxidative phosphorylation of either carbohydrates or fatty acids
      Steady supply of O2 required (via coronary blood flow)
      Cardiac energy consumption = cardiac O2 consumption
      Work done by heart
      External: ejection of blood from the ventricles (Volume work)
      Internal: stretching elastic tissue, overcoming internal viscosity, rearranging muscular architecture of heart as it contracts (Pressure work)
    • 61. “Pressure Work” Vs “Volume Work”
      Ventricles have to do external & internal work:
      If the external work of the heart is raised by increasing SV, but not MAP, the O2 consumption of heart increases very little
      Alternatively, if MAP is increased, O2 consumption/beat goes up much more
      Pressure work by the heart is far more expensive in terms of O2 consumption than volume work
      In other words, an increase in afterload causes greater increase in cardiac O2 consumption than does an increase in preload
    • 62. “Pressure Work” Vs “Volume Work”
      Which one would produce angina due to less O2 delivery to myocardium?
      Aortic stenosis or Aortic regurgitation
    • 63. “Pressure Work” Vs “Volume Work”
      Increase in O2 consumption produced by increased SV (when myocardial fibers are stretched) – preload increase
      An example of operation of law of Laplace
      More the stretch – bigger the radium – more the tension developed – more the O2 consumption
      In comparison, SNS induced increase in cardiac performance
      Via intracellular Ca++ manipulation – not so much to do with radius – less O2 consumption