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Hematocrit, plasma & serum

Hematocrit, plasma & serum

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Hematocrit, plasma & serum

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  1. Hematocrit, plasma & serum Hematocrit = volume of red cells (~45%) Plasma = fluid in fresh blood Serum = fluid after blood has clotted Plasma = serum + fibrinogen (& other clotting factors) Normal volumes: blood ~5.5L, plasma ~3L, rbc’s ~2.5L fig 12-1

  2. Systemic, pulmonary circulations 2 hearts, each with 2 chambers Left heart to all body except lungs (systemic) Right heart to lungs (pulmonary) Systemic arteries: oxygenated blood Pulmonary arteries: deoxygenated blood Systemic veins: deoxygenated blood Pulmonary veins: oxygenated blood Atria: receive blood from veins Ventricles: pump blood to arteries fig 12-2

  3. Pressure, flow & resistance flow = Δ pressure / resistance It is Δ pressure that drives flow Later you will see that: blood pressure = cardiac output (flow) x peripheral resistance

  4. Resistance resistance = 8 x  x L  x r4 where:  = viscosity (“eta” mostly depends on hematocrit) L = length of vessel r = radius of vessel conclusion: the body regulates blood flow by altering vessel radius halving the radius  16x resistance

  5. Heart structure fig 12-6

  6. Heart valve structure fig 12-7 atrioventricular valves: like parachutes aortic & pulmonary valves: like pockets

  7. Heart muscle structure fig 12-9 striated, branched cells, 1 nucleus/cell, connected by intercalated discs spontaneous contraction, regulated by autonomic NS, hormones coronary blood flow regulated by active hyperemia (see later)

  8. Conducting system consists of modified cardiac muscle cells Sequence: sinoatrial node atrial pathways atrioventricular node Bundle of His only path to ventricles R & L bundle branches Purkinje fibers fig 12-10

  9. Conducting system properties Spontaneous depolarization all conducting system shows spontaneous depolarization intrinsic rates: SA node (70/min), AV node (40/min), Purkinje fibers (20/min) therefore SA node sets heart rate Conduction rates slowest: AV node, ~ 100 msec delay between atrial & ventricular contraction fastest: Purkinje fibers all ventricular muscle contracts together (apex slightly ahead)

  10. Cardiac action potential (ventricular muscle) RMP close to K+ equilibrium potential depolarization: Na+ channels open/inactivate plateau phase: Ca++ channels open, K+ channels close repolarization: Ca++ channels close, K+ channels open refractory period ~250 milliseconds value of plateau & refractory period: heart must relax before contracting again fig 12-12

  11. Cardiac action potential (conducting tissue) RMP drifts to threshold (pacemaker potential) K+ channels closing funny Na+ channels open/close T-type Ca++ channels open depolarization: L-type Ca++ channels open repolarization: Ca++ channels close, K+ channels open plateau phase: Ca++ channels open, K+ channels close repolarization: Ca++ channels close, K+ channels open refractory period ~250 milliseconds fig 12-13

  12. Excitation contraction coupling fig 12-18

  13. Excitation contraction coupling L-type channel Ca++ channel acts as voltage gated channel Ca++ enters cytosol from T tubules Ca++ from T tubules stimulates opening of ryanodine receptor Ca++ channel Ca++ enters cytosol from sarcoplasmic reticulum  contraction fig 12-17

  14. Excitation contraction: cardiac vs. skeletal muscle Ca++ channels 1. L-type Ca++ channels (DHP receptor) in T tubule membrane 2. Ryanodine receptor Ca++ channels in wall of sarcoplasmic reticulum Skeletal muscle: L-type (DHP) Ca++ channel acts as voltage sensor (not as channel) L-type (DHP) mechanically opens ryanodine receptor channel Ca++ enters cytosol from sarcoplasmic reticulum  contraction Cardiac muscle L-type channel Ca++ channel acts as voltage gated channel Ca++ enters cytosol from T tubules Ca++ from T tubules stimulates opening of ryanodine receptor Ca++ channel Ca++ enters cytosol from sarcoplasmic reticulum  contraction Why is this important? Skeletal muscle will contract even if there is no extracellular Ca++ Ca++ channel blocking drugs (DHP derivatives): cardiac contractility, but do not  skeletal muscle strength

  15. Electrocardiogram P wave: atrial depolarization QRS complex: ventricular depolarization T wave: ventricular repolarization Atrial repolarization wave obscured by QRS complex note voltage (compare with ic electrode) fig 12-14

  16. Cardiac cycle Systole = contraction (~ *0.3 sec) Diastole = relaxation (~ *0.5 sec) *resting rate 4 phases: 1. ventricular filling (diastole) 2. isovolumetric ventricular contraction (systole) 3. ventricular ejection (systole) 4. isovolumetric ventricular relaxation (diastole)

  17. 1. Ventricular filling AV valves A&P valves atrial P > ventricular P AV valves open aortic P > ventricular P A&P valves closed atrial contraction adds ~15% more blood

  18. 2. Isovolumetric ventricular contraction ventricular P > atrial P  AV valves closed aortic P > ventricular P  A&P valves closed 1st heart sound: closing of AV valves

  19. 3. Ventricular ejection AV valves A&P valves ventricular P > atrial P  AV valves closed ventricular P > aortic P  A&P valves open

  20. 3. Isovolumetric ventricular relaxation ventricular P > atrial P  AV valves closed aortic P > ventricular P  A&P valves close 2nd heart sound: closing of A&P valves

  21. Right heart mechanics fig 12-21 Notes: Volumes, valves, sounds, & times are the same as left heart Pressures are lower because peripheral resistance of lung is lower

  22. Cardiac output & ejection fraction Cardiac output = stroke volume x heart rate Stroke volume = end diastolic volume (EDV) – end systolic volume (ESV) Hence: cardiac output = (EDV – ESV) x heart rate at rest: EDV = ~130 ml, ESV = 60 ml, heart rate = 70/min so: resting cardiac output = (130 – 60) x 70 = 4900 ml/min = ~5L/min Ejection fraction = percentage of blood ejected with each beat = stroke volume/EDV = 70/130 = 54%

  23. Regulation of cardiac output Heart rate: sympathetic nervous activity epinephrine parasympathetic nervous activity Stroke volume: end diastolic volume (Frank-Starling effect) sympathetic nervous activity (contractility epinephrine (contractility)

  24. Regulation of heart rate: autonomics & epinephrine fig 12-24

  25. Regulation of heart rate: autonomics & epinephrine fig 12-23 Curve b: sympathetic nerves end on sinoatrial node  funny Na+ channels  rate of depolarization (cAMP 2nd messenger) Curve c: parasympathetic nerves end on sinoatrial node AcCh open K+ channels (hyperpolarization),  funny Na+ channels  rate of depolarization

  26. Regulation of cardiac output Heart rate: sympathetic nervous activity epinephrine parasympathetic nervous activity Stroke volume: end diastolic volume (Frank-Starling effect) sympathetic nervous activity (contractility epinephrine (contractility)

  27. Regulation of stroke volume: Frank-Starling effect Mechanism:  end diastolic volume  stretch of ventricle  better alignment of X-bridges and binding sites on actin Important for balancing output of left & right heart

  28. Regulation of stroke volume: sympathetic NS & epinephrine Contractility  contraction at a given end diastolic volume i.e. same EDV,  ESV,  stroke volume

  29. Frank Starling vs. sympathetic/epinephrine These numbers are just examples Frank Starling:  end diastolic volume   stroke volume Sympathetic NS-epinephrine:  stroke volume at given end diastolic volume

  30. Sympathetic effects on contraction  rate & force of contraction  rate of relaxation

  31. Autonomic nerves on heart Sympathetic nervous system & epinephrine (all via 1 receptors, cAMP, protein kinase A, phosphorylation)  heart rate ( funny Na+ channels,  Ca++ channels)  contractility ( Ca++ channels)  relaxation rate ( Ca++ ATPase activity, faster Ca++ release from troponin) Parasympathetic nervous system  heart rate minimal effects on contractility

  32. Regulation of cardiac output

  33. Arteries Functions: Structure: low resistance conduit large diameter  resistance pressure reservoir  elastic tissue in walls fig 12-29

  34. Arteries as pressure reservoirs fig 12-30

  35. Mean arterial pressure Mean arterial pressure = diastolic pressure + 1/3 pulse pressure fig 12-31a

  36. Arterial compliance Compliance = ease of distension, i.e. larger volume change for given pressure change Mathematically: compliance = Δvolume / Δpressure fig 12-31b Aging & hypertension  arterial compliance (arteriosclerosis)

  37. Arterioles Functions: regulate blood flow to organs main component of peripheral resistance Structure:  smooth muscle in walls rich autonomic supply, especially sympathetic NS fig 12-33a

  38. Regulation of arteriolar tone 1. active & reactive hyperemia 2. flow autoregulation 3. sympathetic, parasympathetic nerves 4. hormones (epinephrine, angiotensin II, ADH/vasopressin, NO) Note: “injury” is in the objectives, but will not be on the test

  39. Regulation of arteriolar tone: active hyperemia fig 12-34a Metabolites ( relaxation of smooth muscle  blood flow to organ) decreased: O2 increased: CO2, adenosine, K+, H+ (from CO2 & lactate), osmolality Important in regulating blood flow to heart (coronaries) & skeletal muscle Reactive hyperemia block blood flow, metabolites accumulate, arterioles dilate release block, high blood flow until metabolites washed out

  40. Regulation of arteriolar tone: flow autoregulation Mechanism 1: metabolite accumulation fig 12-34b Mechanism 2: myogenic response Especially important in brain & kidney

  41. Regulation of arteriolar tone: autonomics Sympathetics: Generally vasoconstrictor ( receptors) Intrinsic tone (basal discharge)  constriction or relaxation possible Important in constricting GI, kidney, skin arterioles Parasympathetics: Not important Nonadrenergic, noncholinergic (NANC) neurons: NO is neurotransmitter; important in genitals, GI tract

  42. Regulation of arteriolar tone: hormones Epinephrine: Generally vasoconstrictor ( receptors) Vasodilator in skeletal muscle ( receptors) Angiotensin II Powerful vasoconstrictor Additional action to  aldosterone release ADH (aka vasopressin) Powerful vasoconstrictor Additional role to cause water retention by kidneys (antidiuresis) Nitric oxide NO Acts as neurotransmitter & paracrine: vasodilator

  43. Capillaries: anatomy fig 12-37 permeability: permeable to all molecules except proteins, transport by diffusion via intercellular clefts & transcellular vesicles & fused vesicle channels: uncertain function

  44. Microcirculation structure fig 12-38 precapillary sphincters: regulated by metabolite levels metarterioles: potential short circuits between arterioles & venules

  45. Capillary flow velocity fig 12-39 Distinguish between: flow volume of blood (ml/min) & flow velocity of single red cell (cm/min) flow velocity in capillaries is slowest because total XS area is greatest Consequence: blood lingers in capillaries for nutrient & waste exchange

  46. Fluid exchange across capillary wall Permeability of capillary endothelium: freely permeable to molecules < ~ 5000 MWt (gases, ions, glucose, amino acids, hormones) relatively impermeable to protein Therefore, interstitial fluid = plasma without the protein & red cells Transport of solutes: mostly by simple diffusion via intercellular clefts & some transcellular some “bulk flow” ( fluid flow carries solutes across endothelium) Edema: excessive accumulation of fluid in interstitial fluid space

  47. Fluid exchange across capillary wall (Starling forces) fig 12-42a Balance of fluid between plasma & interstitium controlled by 4 forces Outward forces: plasma  interstitial fluid (“filtration”), given +ve sign capillary hydrostatic pressure (PC) interstitial fluid protein osmotic pressure (IF) Inward forces: interstitial fluid  plasma (“reabsorption”), given –ve sign plasma protein protein osmotic pressure (P) interstitial fluid hydrostatic pressure (PIF)

  48. Starling forces: the numbers fig 12-42b The most important forces are capillary hydrostatic pressure (PC) & plasma protein protein osmotic pressure (P) 3-4 L/day more fluid is filtered than is absorbed That 3-4 L re-enters blood via the lymph (lymph composition = interstitial fluid composition) Edema develops if net filtration > lymph flow

  49. Veins Function: capacitance vessels contain ~60% of blood regulate venous flow to heart Structure: thin walls, smooth muscle valves large diameter, low resistance fig 12-44

  50. Regulation of venous return (VR) to heart 1. sympathetic activity  SNS  vein compression VR 2. muscle pump  muscle activity  vein compression  VR 3. ventilation  inspiration  atrial pressure  VR 4. blood volume  blood volume (kidney)  VR fig 12-45