Chap 1 Circulatory Blood Flow Preload stretch of relaxed muscle based on the end-diastolic volume, which is measured by end

ed by end diastolic pressure EDP easily. diastolic vol governs strength of contraction ventricular hypertrophy & ischemic heart disease can decrease compliance and increase EDP, EDV remains constant EDP accurate only when ventricular compliance normal and constant decreasing myocardial contractility = increases end diastolic pressure diastolic heart failure diuretic worsens decreases preload which decreases EDP (EDV constant) which decreases cardiac output preload component of afterload b/c volume load must be moved by ventricles during systole

Afterload force that opposes muscle contraction pulmonary & systemic vascular resistance, chamber radius, vascular compliance, pleural pressure Law of Leplace T= Pr. Transmural tension, pressure and radius at end diastole Neg pleural pressure will increase transmural pressure and increase ventricular afterload Neg pressures surrounding heart can impeded ventricular emptying via inward displacement of ventricular wall during systole pulsus paradoxus transient drop systolic pressure of >15mmHg during inspiration decrease cardiac output Pos pleural pressure can help ventricular emptying inward movement of ventricular wall during systole pos pressure mech vent to increase systolic BP unloading the ventricle o Minor effect only, possible tx for cardiogenic shock

Impedance Aorta impedance is the major afterload force for LV, pulm artery for RV Dependent on compliance and resistance Compliance plays effect in large arteries pulsatile Resistance plays effect in peripheral arteries flow steady/non pulsatile (plays less effect to ventricular emptying downstream) Resistance = pressure gradient across surface/rate of flow Systemic vasc resistance SVR = mean systemic arterial pressure SAP mean R atrial pressure RAP/CO pulm vasc resistance PVR = mean pulm artery pressure PAP mean L atrial pressure LAP/CO SAP measured with arterial catheter, PAP measure with pulm art cath SVR and PVR are clinical measures of afterload but are unreliable abandoned o SVR and PVR measures of total vascular resistance (arterial and venous) less likely to contribute to vent afterload than arterial resistance

Contractility Dependent on preload and afterload No reliable measures clinically. In theory acceleration rate of ven pressure during isovolumic contraction (onset systole Ao open and preload and afterload constant card cath can measure)

All above theory based on laminar flow in a system of non-rigid compressible vessels Flow in rigid tubes Flow dependent on pressure gradient x r4/ (viscosity of fluid x length of tube) Resistance dependent on viscosity x length/ r4 Law of continuity flow must be the same at all points in circulatory sys preservation of flow across varying diameters of vessel by changing velocities

Flow in rigid tubes When tube compressed by ext pressure, driving force for flow independent of pressure gradient along tube Driving force = pressure gradient b/w inlet pressure and external pressure (if ext pressure > outlet pressure)

Pulmonary circulation Pos pressure mech vent alveolar pressure > hydrostatic pressure in pulm cap so driving force for flow through lungs is no longer pressure gradient from pulm arteries to L atrium PAP-LAP, but PAP-Palv. o Decreases pulm flow o Affects pulm vasc resistance PVR= PAP-LAP/CO becomes PAP-Palv/CO

Blood Viscosity Rarely measure with viscometer clinically b/c in vitro measurement unreliable. No circulatory system effects (shear thinning) accounted for. o Serial measurements may be helpful Increase viscosity = increase force to initiate flow Blood viscosity dependent on concentration of circulating erythrocytes (hematocrit) Viscosity of some fluids change with change in velocity o Blood decreases in viscosity with increase flow in small vessels o Caused by shear thinning velocity plasma increase more than velocity of erythrocytes o Evident in vessels w/ diameter <0.3mm Dec viscosity causes far greater inc in cardiac output o Blood viscosity varies inversely with flow rate dec viscosity = increase flow further dec viscosity = further increase flow etc amplification

Chap 2 Oxygen and Carbon Dioxide Transport Page 31