Haemodynamics. Milan Chovanec Department of Physiology 2.LF UK

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Haemodynamics Milan Chovanec Department of Physiology 2.LF UK

Major types of blood vessels Blood flow: 50cm/s 0.05cm/s

Flow, pressure, resistance

Flow, pressure, resistance ΔU = I x R Blood and vessels are not rigidig tubes and ideal liquid! Q = (Pa Pv)/R

F Low vessel resistance (vasodilation) High vessel resistance (vasoconstriction) Vasodilation = increased blood flow, more blood in organ Vasoconstriction = decreased blood flow, less blood in organ ( P)

Flow, pressure, resistance Hagen - Poiseuille law ƞ viskosity L vessel lenght r radius

Flow, pressure, resistance F r 4

Critical closing flow pressure Extramural pressure Rigid tubes Blood vessls Intramural pressure flow flow Critical closing pressure Flow in the vessels starts when intramural pressure exceed extramural pressure pressure pressure

Flow measurement Electromagnetic method Ultrasound (doppler effect) The dye dilution methods Fick priciple

Electromagnetic flowmeter

Ultrasound dopple effect (echo)

The dilution methods Dye dilution: methylene green, Evans blue AUC represents the value of CO Thermodilution: cold salt solution MacIntyre et al, Circulation 1958

Fick principle

The types of blood flow: laminar vs. turbulent a normal blood flow in majority of vessels Energically the most effective The smallest loose of energy inaudible Energetically less effective Present in high flow velocity above critical point Audible - murmur Able to injure the vessel wall Stenosis, aterosclerosis.

Changing from laminar to turbulent flow murmur Reynolds number ρ - density η - viskosity D diameter V velocity

Relationship between vessel kinetic and potential energy Bernouli law Flow in all segments is constant Energy of the blood is constant Sum of the flow velocity and pressure is constant Increasing flow velocity leads to decreasing of the flow pressure and vice versa P + v = const. Stenosis, suction, spray, airplane wings,.

Serial and Parallel arragement of the vasculature Serial Parallel R T = R 1 + R 2 + R 3 + R 4 + R 5 e.g. Systemic and pulmonary circulation The total resistace equals the sum of the individual segmental resistances R T = R A + R a + R c + R v + R V 1% + 70% + 20% + 8% + 1% = 100% depends on which vessel region is affected Parallel vessels decrease total vascular resistance The total resistance of a network of parallel resistances is less than the resistance of the single lowest resistance An example: R 1 = 5, R 2 = 10, R 3 = 20 R T = 1/0.2+0.1+0.05 = 1/0.35 = 2.86

Arterial blood pressure Arterial pressures: o Systolic: end of the systole, approx. 120mmHg o Diastolic: end of the diastole, approx. 80mmHg o Pulse pressure aplitude: difference between systolic and diastolic pr., approx. 40-45mmHg o Mean geometric mean: is less than arithmetric mean (systole is shorter than diastole) - influences of the organ blood flow MAP = P diast + 1/3 (P syst - P diast )

Mean arterial pressure Measurement of the MAP by integration of AUC

Mean arterial pressure Transmission of the pressure pulse along the aorta reduction of the blood pressure and flow fluctuation Pathology: atherosclerosis

Blood pressure measurement Non-invasive: ausculatory method Invasive:

Systemic vascular resistance (SVR) Resistance to blood flow offered by all of the systemic vasculature SVR is determined by changes in: vascular diameters, viscosity, m (Hagen - Poiseuille law) SVR represents resistance for left ventricle (AFTERLOAD) Vasoconstriction = increase SVR Vasodilation = decrease SVR Small arteries + arterioles = resistent vessels MAP mean arterial pressure CVP central venous pressure CO cardiac output

SVR: systemic vascular resistance CVP: central venous pressure (pressure in IVC)

Vascular tone Resistance vessels (small arteries and arterioles) are normaly in a partially constricted state vascular tone. A partially constricted state of resistace vessels could: Increase vasoconstriction increase SVR, increase BP decrease vasoconstriction (vasodilation) decrease SVR, decrease BP A regulation of vascular tone: Inner: products of the endothelial cells, autocrinne substances, local metabolites (O 2, CO 2, lactate, teplota, ph ) Outer: hormones (ATII, ET), sympathetic nerves Mechanisms of vasoconstriction: maintain of MAP Mechanisms of vasodilation: regulation of blood flow in particular organs

Arthur Guyton s experiments on vascular tone

Venous blood pressure central venous pressure (CVP) Blood pressure within venous compartment CVP determines the filling pressure of the right ventricle (PRELOAD) and affects cardiac output (Frank-Starling mechanism) Factors affecting CVP: Cardiac output* Sympathetic activation* Respiratory activity Skeletal muscle pump gravity

Cetral venous pressure Changes of CVP are determined by changes of venous volume nad tone/compliance: Increase of venous volume leads to increase of venous pressure Increase of venous pressure is determined by venous tone/compliance

Respiratory activity and CVP

Valsalvův manévr (externí komprese DDŽ) = zvýšení CVP Gravity and CVP

Skeletal muscle pump and CVP

Cardiac output vs. Venous return Cardiovascular system closed system. Amount of blood from the left heart have to return back to the right heart. Cardiac output = venous return Transitional imbalance (beginning of run, stand up...) is very fast repaired by regulation mechanisms Vascular system significantly affects cardiac output and venous return (relationship among CO, MAP and CVP)

Relationship among CO, MAP and RAP Decrease of CO = decrease MAP and increase of RAP = less amount of blood is moved from veins to the aorta If CO = 0, then RAP=MAP = Pmc RAP = CVP Cardiac Output (L/min) Pmc mean filling pressure - BP in venous system when flow is zero - depends on blood volume nad venous compiance

Relathioship between CO and RAP (CVP) Vascular functional curves Increase blood volume/decrease venous compliance leads to increase Pmc and increase of RAP (changes in the whole system) Changes of SVR (arterioles) does not change of Pmc (changes in the part of the system) Increasing of SVR leads to increase of RAP but not Pmc CVP CVP P RA right atrium pressure P mc mean filling pressure, depends on volume and compliance of the veins Vol blood volume Cv venous compliance SVR systemic vascular compliance

...disequilibrium... Arteriolar dilation decreasing of SVR (constant CO) moving blood from arteries to capilaries and veins more blood leave arteries than will flow into them (constant CO).increased pressure in veins + decreased pressure in arteries. Increased venous volume and pressure (PRELOAD) increased heart filling increased CO (Frank-Starling mechanism changes CO) = equilibrium

Increased sympathetic activity (increased heart stimulation + veanous splanchnic vasoconstriction + arteriolar vasodilation) Combination of the heart and the vascular curves The heart functions curve A equilibrium between CO and venous return

Heart failure

Increased sympathetic activity (increased heart stimulation + veanous splanchnic vasoconstriction + arteriolar vasodilation) Combination of the heart and the vascular curves The heart functions curve A equilibrium between CO and venous return

15:1mmHg = 1 + 70 + 20 + 8 + 1 = 100