Blood Volume: Vascular and Systemic

Transcription

1 Various examples and supplementary slides that may be used in lecture. These are provided as a resource for M1 students by Dr. HN Mayrovitz Fall Note that all of the following slides may or may not actually be presented in lecture depending on time available and planned emphasis and overall objectives. Blood Volume: Vascular and Systemic PreCapillary PostCapillary 30% 70% 2/3 of systemic % =86% Left Heart Aorta Arteries Venules Arterioles & Capillaries Veins Vena Cava Right Heart Lungs 14% Senario #1: An angiogram performed on the thoracic aorta of a pateint reveals a longitudinal and crosssectional pattern as shown in the figure. Q In which segment would you expect the blood velocity to be greatest? Why? 2. In which segment would you expect the greatest loss of pressure? Why? 3. In which segment would you expect to measure the greatest blood flow? Why? 4. In which segment is the local Reynolds number the greatest? Why? Senario #2: A patient with a history of polycythemia presents with cyanosis of the fingers. This is most clearly seen in the capillary beds of the nail fold which cause a bluish tint. 1. Can the cyanosis be explained by the polycythemia? Mechanism? 2. If due to increased viscosity, what happens to Q & shear rate in the capillaries? Dr. HN Mayrovitz Supplementary slides and examples 3. What is the effect of decreased shear rate on blood viscosity in capillaries? 1

2 Scenario #3. The following data were measured in a patient. Heart Rate (HR) Stroke Volume (SV) Mean Aortic (MAP) Kidney Blood Flow Central Venous (CVP) 60 beats/min 100 ml 95 mmhg 1200 ml/min 5 mmhg 1. What is her cardiac output? 2. What is her total peripheral resistance (TPR)? 3. What is the resistance of the kidney vascular bed? Resistance Calculation 5 mmhg R. Heart Lungs Rkidney Rgi.. TPR = P/CO Rmuscle L. Heart 1200 ml/min CO = 6000 ml/min Peripheral Resistance Unit (pru) TPR=? R Kidney =? 95 mmhg TPR = 90/6000 = mmhg/ml/min = pru R kidney = 90/1200 = pru Distensibility vs. Compliance Aortic Segment C = 5 ml 5 mmhg 2.54 cm Volume Vo ~ 20 ml 4 cm Inject 5 ml and measure pressure change P = 5 mmhg This has half the C of the full segment & appears to be stiffer 2.54 Volume Vo ~ 10 ml C = 5 ml 10 mmhg 2 cm Inject 5 ml and measure pressure change P = 10 mmhg This is due to a smaller initial volume receiving the V The Distensibility ( V/Vo)/ P of both is the same! Distensibility = C/Vo Dr. HN Mayrovitz Supplementary slides and examples 2

3 CARDIO P Cardiac PUMP Pump Q V Example MAP = CO x TPR k (V/C) Measuring Aortic P true = E 1/2ρU 2 R What happens to P=MAP if: Cardiac Output Compliance (Arterial) TPR. U Aortic Arch P measured = E Measuring Catheter K i 120 mm Na 10 mm 4.5 mm K o V m =88mv 145 mm Nao V m =72mv E K Equilibrium Potential E k =(61.5) log [K ] i /[K ] o E Na =(61.5) log [Na ] i /[Na ] o K K Na 2. Resting Membrane Potential V m ~90mv Na V m = E k E na (g na /g k ) 1 (g na /g k ) K K Na V m ~90mv 4. Depolarization Na Resting V m = E k E na (g na /g k ) (1 g na /g k ) V 0 m Slight depolarization of V m opens voltagegated Na fast channels g na /g k that rapidly increase g na Depolarizes Phase 0 Fast Na Channels Open then Close: VoltageGated Na Example of Channel Model m I Na h Activation Open Closes Inactivation 1. Initial depolarization 2. mgates start to open 3. Further depolarization 4. mgates wide open 5. g na /g K high 1. hgates start to close 2. fully closed inactivated Dr. HN Mayrovitz Supplementary slides and examples 3

4 Rectification Concept Membrane/Channel passes current more readily in one direction than the other K 1 Membrane K Outwardly rectifying channel: Channel passes current most readily in outward direction if membrane is depolarizing Example: I K channel/current (outward) increases with increasing membrane depolarization (G K increases). Delayed: Develops maximum near end of plateau Delayed outward rectifier current... Repolarization 2 Plateau Repolarization Inwardly rectifying channel: Channel passes inward current more readily than outward current (but physiologically may only be outward) V m I K1 4 0 I K 3 Upstroke (Depolarization) Example: I K1 channel/current (outward) is inactivated (channels close) during depolarization (g K1 decreases) 2 Plateau Repolarization Outwardly Rectifying K Channel I K V m 0 3 Upstroke E I K = 94 K1 (Depolarization) 4 E m = 90 Ohmic (linear) outward voltage 60 inward E K = 94 Inwardly Rectifying K Channel Small outward K current E m = 90 I K1 Inwardly rectifying channel (IR) current outward inward Ohmic (linear) 60 SUMMARY of AV Block Slowed or Absent Conduction AN AV Node N NH Many Possible Causes Refractory Inhibition of Ca channel opening voltage Start Repolarization Total K current = I K I K1 E K = 94 I K1 Inwardly rectifying channel (IR) E m = 90 current Total K Current Depolarization I K current Outwardly rectifying channel outward inward Repolarization Ohmic (linear) K 1 60 Membrane voltage K Repolarized 1 o = Abnormal Delay 2 o = Some Impulses Conducted 3 o = No Impulses Conducted Complete Heart Block A B C D E Repolarization begins at site most recently depolarized Dr. HN Mayrovitz Supplementary slides and examples 4

5 Example Turned Around 1.2 mv in lead I Thus ~ mv II mv LL I III 0.1 Example of D ~ Perpendicular to av R If the frontal plane QRS Vector (MEA) is 90 o which limb lead records the largest Rwave? 150 avr avr MEA III 120 III 120 II avf To which lead is this MEA most parallel? avf Largest rojection! 30 avl I II avf o 30 avl I Is the EKG deflection or in Lead II? 0 o Positive! If normal axis why in I and II? All projections of the MEA are along the positive axis of each of the leads Normal MEA Therefore all Rwaves are positive Simple Method For Quick Assessment Axis Example Question What is approximate axis? AXIS Normal Lead I Lead II Left Axis Deviation 90 o to av L Right Axis Deviation ~ 60 o Dr. HN Mayrovitz Supplementary slides and examples 5

6 Cardiac Pump Function Afterload Higher Translation reload Effect to Heart Can eject against larger afterload Little effect on intrinsic muscle contraction properties Input Lower PUMP Filling Strength Speed Output Preload SV HR Contractility Vel Afterload PRELOAD: Big effect on Max Developed Force PRELOAD: Minor effect on V max The Calcium Pool and Contractility Size of Ca Pool at next Systole Determines Cardiac Contraction Vigor Pool depends on Ca influx during Phase 2 versus Ca expelled during previous diastole Vigor of contraction INCREASES if: Magnitude of I CA Relative duration of Ca influx vs. efflux Extracellular Ca concentration TensionTime Integral (TTI) Load on muscle P r / w ~ avg Tension Myocardial Energy (O 2 ) Need TTI Increased Energy Need if Increases in: Arterial Ventricular (aortic stenosis) Heart Rate Chamber Size (dilated ventricle) Muscle Mass (hypertrophy) Internal Energy Minimization Increasing Cardiac Efficiency work: more costly then flow work CO by TPR better than HR: more energetically costly than SV CO by SV better than HR Double Product: HR x P correlates with myocardial O 2 consumption Cardiac Contractility Intrinsic ability of myocardial cells to develop force at a given muscle cell length Amount of force Rate of force development LV A B LV A B LV (mmhg) 80 Your patient Jim has this PV loop LV Volume Patients A & B have PV loops as shown. Which best describes patient A vs. patient B? 1) B has a greater contractility than A 2) B has a greater EDV than A 3) B has a greater afterload than A 4) 1 & 2 5) 2 & 3 LV Volume Patients A & B have PV loops as shown. Which best describes patient A vs. patient B? 1) A has a greater SV than B 2) A has a greater EF than B 3) A has has a greater contractility than B 4) 1 & 2 5) 1, 2 & LV Volume (ml) Which best describes Jim s SV? 1. It is abnormally low 2. It is abnormally high 3. It is equal to 100 ml 4. It is equal to 150 ml 5. 2 & 4 Dr. HN Mayrovitz Supplementary slides and examples 6

7 Aortic Stenosis Systemic Mitral Stenosis Venous HTN Systemic Edema RV Pulmonary Ao Systolic Diastolic LV LVH (concentric) wall mass Outflow R compliance RVH/ Failure Further in RV TV Right Ventricle (RV) ulmonary resistance (medial hypertrophy) PV R Ao Left Ventricle (LV) M Pulmonary Edema/congestion Enlarged afib Thrombi Aortic Regurgitation RV Systemic Pulmonary Ao LV EDV EDP Mitral Diastole Diastole Large PP Acute P Pulmonary congestion Chronic LV enlarges Chamber dilatation LVH enlarges Mitral Regurgitation RV Systemic Reduced SV systole V Pulmonary M Ao EDV Acute Edema/congestion FS RV Output AS or HTN Normal MR or AR Normal LVH (AS) Dilated (AR) LVH is often associated with an LV pressure overload. Commonly due to aortic stenosis or HTN. RVH is often associated with an RV pressure overload commonly due to RV outflow obstruction or pulmonary HTN. Can be caused by leftside dysfunction such as with mitral stenosis Ventricular Dilatation often due to chronic volume overload as in Aortic or Mitral regurgitation. Ventricular Systolic Myocyte D No L change # of parallel myocytes Wall Mass Chamber Volume Concentric Hypertrophy Overload σ % pr/w Volume Overload Cardiac Output EDV and EDP Myocyte D and L # serial myocytes Wall Mass Chamber Volume = K Eccentric Hypertrophy Dr. HN Mayrovitz Supplementary slides and examples 7

8 Examples sec Examples 140 mmhg Arterial 110 A B C D 90 mmhg 90 What is systolic pressure? What is diastolic pressure? What is pulse pressure? What is MAP? What is HR? Which is (are) hypertensive? Which is (are) isolated systolic hypertension? If SV all same, which aorta is probably the stiffest? If CO all same, which has highest TPR? If TPR & SV same, which has highest HR? Pulse Wave Generation & Propagation F V 1 2 c 0 2 ~ Compliance C Inertia Resistance c0 1 ρc Vessel Wall Blood Filled Pulse wavespeed inverse to Compliance Stiffer arteries ~ higher speed Gradient Produces Flow Femoral Artery P u P d dx P u P d x gradient (space derivative) P u t 1 0 P d wave x Gradient Time Flow Remember: P u & P d are composite waves that include the effects of reflection P T =6, Π T =5 P C =26, Π C =20 Example Q f Interstitial Tissue Capillary Q f ~ [(P C P T ) (Π C Π T )] Q f ~ [(266) (20 5)] = 5 Dr. HN Mayrovitz Supplementary slides and examples 8

9 Scenario: A vascular bed with a perfusion pressure of 100 mmhg has a measured blood flow of 100 ml/min as shown below in A. The pre and post capillary resistances are 0.75 and 0.25 pru respectively. A vasoactive drug is then given to this person that results in figure B. A 100 mmhg 100 ml/min B What was the drug s effect on the precapillary vasculature? 2. What was the drug s effect on the postcapillary vasculature? 3. What is the new value of blood flow in this vascular bed? 4. What is the effect of the drug on the capillary pressure? Senario Summary of Directional Changes in Capillary P A PreCapillary PostCap P V R A P C R V P C ~ P V P A (R V /R A ) Ratio is important Capillary pressure increases if: Venous Increases Arteriole Resistance Decreases Venous Resistance Increases Arterial Increases Specific conditions in notes in section 29.0 On page 53 A D.O. student, lost in the wilderness, eats an herb that is known to slightly constrict all arterioles that supply the fingers. Soon after eating the herb she observes that her fingers are beginning to swell and become edematous as would occur if her capillary pressure was rising. She takes out her trusty blood pressure cuff, measures her arterial pressure and finds that it is unchanged and normal. 1. Could this effect be due to increased capillary pressure? If so explain how. Suppose it is indeed due to a vascularly related increase in capillary pressure. 2. What definite statements could you make about the blood flow to her fingers? Suppose you knew that the finger blood flow was in fact decreased. 3. What definite statement could be made about blood velocity in her capillaries? Negative Feedback Set Point T 0 Desired Thermostat Disturbance or Altered Function Air Conditioner Feedback Gainβ Form Stabilization δt T=(δT/β) Room Temp (T) T 0 δt T Change without Feedback Net T Change reduced by a factor of β β is called the feedback gain Dr. HN Mayrovitz Supplementary slides and examples 9