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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
    Noninvasive:
    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)
    Invasive:
    Inserting a catheter into the thoracic great veins
    Direct pressure reading
  • 4. Microcirculation
    Capillaries
    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
    Causes:
    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
    Local:
    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:
    SNS
    Histamine, bradykinin, & prostaglandins
  • 12. Acute Mechanisms
    Autoregulation
    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
    Example:
    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
    Example:
    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
    VEGF
    Fibroblast growth factor
    Angiogenin
    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
  • 19. ARTERIAL BLOOD PRESSURE CONTROL
  • 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
    Timeline:
    Acute
    Intermediate
    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.
    Normally,
    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
    Renin-Angiotensin-Aldosterone
  • 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
    Cardiac
    Heart rate
    Contractibility
    Coupling factors*
    Preload
    Afterload
    Ancillary factors
    All factors affecting venous return
  • 43. CO Regulation: DetailedCO = SV x HR
    Stroke Volume
    SV = EDV – ESV
    = 120 – 50 = 70 ml
    EDV
    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
    ESV
    Afterload (Aortic pressure – arterial BP)
    Affects myocardial fiber shortening ability
    Contractility
    SNS (NE via β1)
    Heart Rate
    HR and SV are inversely proportional
    ANS
  • 44. CO Regulation: Another angle
  • 45. Conditions affecting CO
    No change
    Sleep
    Moderate changes in temperature
    Increased
    Anxiety/Excitement
    Exercise
    Increased temperature
    Pregnancy
    Epinephrine/histamine
    Anemia & hyperthyroidism
    Decreased
    Sitting/standing
    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
    However!
    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:
    C1V1=C2V2
    A=CxV
    C=A/V
  • 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:
    Rises
    Peaks
    Declines
    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