hemodynamics.kiran rai

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basis of hemodynamics

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Page 1: Hemodynamics.kiran rai
Page 2: Hemodynamics.kiran rai

HemodynamicsHemodynamics

Physics of Blood flow in the Physics of Blood flow in the circulationcirculation

Page 3: Hemodynamics.kiran rai

Circulatory SystemCirculatory SystemHeart:Heart:

Has 2 collecting chambers - (Left, Right Has 2 collecting chambers - (Left, Right Atria) Atria)

Has 2 Pumping chambers - (Left, Right Has 2 Pumping chambers - (Left, Right Ventricles) Ventricles)

Page 4: Hemodynamics.kiran rai
Page 5: Hemodynamics.kiran rai

Left Side of Heart Left Side of Heart

LungsLungs TissuesTissues

Circulation SchematicCirculation Schematic

Right Side of HeartRight Side of Heart

AA VV

VV AA

Pulmonary VeinPulmonary Vein

Pulmonary ArteryPulmonary Artery

AortaAorta

Sup. & Inf. Vena CavaSup. & Inf. Vena Cava

Pulmonary ValvePulmonary Valve

Aortic ValveAortic Valve

Tricuspid ValveTricuspid Valve

Mitral Mitral ValveValve

Page 6: Hemodynamics.kiran rai

Blood VesselsBlood VesselsArteriesArteriesCapillariesCapillariesVeinsVeins

Systemic Pathway:Systemic Pathway:Left Ventricle of Heart Aorta Arteries ArteriolesLeft Ventricle of Heart Aorta Arteries Arterioles

CapillariesCapillariesVenulesVenules VeinsVeins Right Atrium of the heart Right Atrium of the heart

Page 7: Hemodynamics.kiran rai

BloodBloodComposition:Composition:

Approx 45% by Vol. Solid ComponentsApprox 45% by Vol. Solid ComponentsRed Blood Cells (12Red Blood Cells (12m x 2 m x 2 m)m)

White CellsWhite Cells

PlateletsPlatelets

Approx 55% Liquid (plasma)Approx 55% Liquid (plasma)91.5% of which is water91.5% of which is water

7% plasma proteins7% plasma proteins

1.5% other solutes1.5% other solutes

\\

Page 8: Hemodynamics.kiran rai

Viscosity of Blood = 3 3.5 times of Viscosity of Blood = 3 3.5 times of waterwater

Page 9: Hemodynamics.kiran rai

Hemodynamic Hemodynamic PrinciplesPrinciplesCO = SV X HRCO = SV X HR

Stroke VolumeStroke Volume: : Amount of blood ejected by the Amount of blood ejected by the left ventricle with each Cardiac Contraction.left ventricle with each Cardiac Contraction.

PreloadPreload - Ventricular filling pressure at end - Ventricular filling pressure at end diastole.diastole.

AfterloadAfterload - Resistance the ventricle has to - Resistance the ventricle has to overcome to eject it’s content.overcome to eject it’s content.

ContractilityContractility - Heart muscles pumping ability. - Heart muscles pumping ability.

Page 10: Hemodynamics.kiran rai

Cardiac OutputCardiac OutputStroke volume X Heart rate. Stroke volume X Heart rate.

Normal CO = 4-8 liters/minNormal CO = 4-8 liters/min

CI=CO/BSACI=CO/BSA

Body surface area = Weight in Kg. x Height in Body surface area = Weight in Kg. x Height in cm.cm.

Normal CI=2.8-4.2 L/min/m2Normal CI=2.8-4.2 L/min/m2

A CI of 2.0 or less should be immediately A CI of 2.0 or less should be immediately reported to the physician!!reported to the physician!!

Page 11: Hemodynamics.kiran rai

Four determinants of Four determinants of cardiac outputcardiac output

Heart Rate x Stroke VolumeHeart Rate x Stroke Volume

ContractilityContractility

AfterloadAfterloadPreloadPreload

Page 12: Hemodynamics.kiran rai
Page 13: Hemodynamics.kiran rai

Starling’s LawStarling’s Law

The strength of The strength of the contraction is the contraction is proportionate to proportionate to the stretch the stretch applied---applied---

Up to a point!Up to a point!

An overstretched An overstretched heart cannot heart cannot contract back well contract back well at all.at all.

Page 14: Hemodynamics.kiran rai

Preload is the stretch of the balloon as air is blown into it. The more air, the greater the stretch.

The stretching The stretching of muscle fibers of muscle fibers in the in the ventriclesventricles

Results from Results from blood volume in blood volume in the ventricles the ventricles at end-diastoleat end-diastole

The greater the The greater the stretch during stretch during diastole, the diastole, the more forcefully more forcefully they contract they contract during systoleduring systole

PreloadPreload

Page 15: Hemodynamics.kiran rai

Preload and Cardiac Preload and Cardiac OutputOutput

Preload will generally Preload will generally INCREASEINCREASE CO CO

Myocardial fibers stretch and increase the Myocardial fibers stretch and increase the force of contractionforce of contraction

Too much preload: heart becomes Too much preload: heart becomes overstretched; results in diminished overstretched; results in diminished contraction and contraction and DECREASEDECREASE CO CO

Decrease in preload, heart and vessels are Decrease in preload, heart and vessels are underfilled, results in underfilled, results in DECREASEDDECREASED CO CO

Page 16: Hemodynamics.kiran rai

PreloadPreload

Central Venous Pressure ( CVP) Measures the Central Venous Pressure ( CVP) Measures the filling pressure of the Right Atrium at end diastole. filling pressure of the Right Atrium at end diastole.

Normal CVP is 0-8 mmHg.Normal CVP is 0-8 mmHg.

Pulmonary Artery (PCWP) reflects the filling Pulmonary Artery (PCWP) reflects the filling pressure of the Left Ventricle at end diastole.pressure of the Left Ventricle at end diastole.

Normal PCWP is 6-12 mmHg. Normal PCWP is 6-12 mmHg.

The amount of blood in a ventricle before it The amount of blood in a ventricle before it contracts.contracts.

Page 17: Hemodynamics.kiran rai

Increasing Preload:Increasing Preload:

Crystalloids & colloidsCrystalloids & colloids

Crystalloids: NS or LRCrystalloids: NS or LR

Takes 1000 ml to increase blood volume by Takes 1000 ml to increase blood volume by 200 ml200 ml

Colloids used when acute vascular loss exists Colloids used when acute vascular loss exists

Page 18: Hemodynamics.kiran rai

Low CVPLow CVP

Decreased Venous return to the heart.Decreased Venous return to the heart.

Hypovolemia.Hypovolemia.

Volume LossVolume Loss

Page 19: Hemodynamics.kiran rai

Elevated CVPElevated CVP

Fluid Overload.Fluid Overload.

Heart Failure.Heart Failure.

Cardiac Tamponade.Cardiac Tamponade.

Tricuspid valve Regurgitation.Tricuspid valve Regurgitation.

Increased Intrathoracic/Pulmonic pressures.Increased Intrathoracic/Pulmonic pressures.

Page 20: Hemodynamics.kiran rai

Left Heart Left Heart PreloadPreload

The amount of blood in the LV at the end of The amount of blood in the LV at the end of diastolediastole

Measured by the pulmonary capillary wedge Measured by the pulmonary capillary wedge pressure (PCWP)pressure (PCWP)

Normal PCWP 6-12mmHgNormal PCWP 6-12mmHg

Obtained when PA balloon is inflated.Obtained when PA balloon is inflated.

This blocks off all pressures from right side and This blocks off all pressures from right side and all the PA catheter “see” is the filling pressure all the PA catheter “see” is the filling pressure of Left side of heart.of Left side of heart.

Page 21: Hemodynamics.kiran rai

The pressure that the The pressure that the ventricles must ventricles must generate to overcome generate to overcome the higher pressure in the higher pressure in the aorta to get the the aorta to get the blood out of the heartblood out of the heart

AfterloadAfterload

Resistance is the knot on the Resistance is the knot on the end of the balloon, which the end of the balloon, which the balloon has to work against to balloon has to work against to

get the air out.get the air out.

Page 22: Hemodynamics.kiran rai

Factors Affecting Factors Affecting AfterloadAfterload

Compliance of the aortaCompliance of the aorta

Mass/viscosity of the blood: how thick or thin is it?Mass/viscosity of the blood: how thick or thin is it?

Vascular resistance: Are the blood vessels constricted Vascular resistance: Are the blood vessels constricted or dilated?or dilated?

Oxygen level: Hypoxemia will cause vasoconstriction.Oxygen level: Hypoxemia will cause vasoconstriction.

The afterload force opposes muscle The afterload force opposes muscle contraction”contraction”

Afterload is inversely proportional to stroke Afterload is inversely proportional to stroke volume.volume.

Page 23: Hemodynamics.kiran rai

Afterload Reduction:Afterload Reduction:Improves cardiac performance by reducing Improves cardiac performance by reducing the resistance facing the ventricle during the resistance facing the ventricle during contraction.contraction.

Other factors, such as blood viscosity and valvular Other factors, such as blood viscosity and valvular resistance, can influence afterloadresistance, can influence afterload

Agents that reduce arterial resistance:Agents that reduce arterial resistance:

Calcium channel blockersCalcium channel blockers

ACE inhibitorsACE inhibitors

Arteriolar dilatorsArteriolar dilators

Beta blockersBeta blockers

Page 24: Hemodynamics.kiran rai

Afterload Increase and Afterload Increase and Increasing the BP:Increasing the BP:

Increasing afterload with vasopressors is the most Increasing afterload with vasopressors is the most potent method.potent method.

Hypovolemia must be corrected before using Hypovolemia must be corrected before using vasopressorsvasopressors

Vasopressors increase myocardial oxygen Vasopressors increase myocardial oxygen consumptionconsumption

May increase the BP but not the blood flowMay increase the BP but not the blood flow

Common agents: norepinephrine, dopamine, Common agents: norepinephrine, dopamine, phenylephrinephenylephrine

Page 25: Hemodynamics.kiran rai

IABPIABP

Decreases afterloadDecreases afterload

Improves coronary perfusionImproves coronary perfusion

Page 26: Hemodynamics.kiran rai
Page 27: Hemodynamics.kiran rai

The ability of the The ability of the myocardium to myocardium to contract normallycontract normally

Influenced by Influenced by preloadpreload

The greater the The greater the stretch, the more stretch, the more forceful the forceful the contractioncontraction

ContractilityContractility

The more air in the balloon, the The more air in the balloon, the greater the stretch, the farther the greater the stretch, the farther the

balloon will fly when air is balloon will fly when air is released.released.

Page 28: Hemodynamics.kiran rai

Determined by force and velocity of muscle Determined by force and velocity of muscle contraction when loading conditions (preload and contraction when loading conditions (preload and afterload) are held constant.afterload) are held constant.

Can be influenced by neural, humoral or Can be influenced by neural, humoral or pharmacological factors.pharmacological factors.

ContractilityContractility

Page 29: Hemodynamics.kiran rai

Increased ContractilityIncreased Contractility

““Fight or Flight”Fight or Flight”

Sympathetic responseSympathetic response

Catecholamine releaseCatecholamine release

Increased contractility also increased myocardial Increased contractility also increased myocardial oxygen demandoxygen demand

Page 30: Hemodynamics.kiran rai

Decreased contractilityDecreased contractilityDecreased contractility Decreased contractility

Decreased stroke volumeDecreased stroke volume

Decreased myocardial oxygen demandDecreased myocardial oxygen demand

Contractility decreases with:Contractility decreases with:

HypoxiaHypoxia

Metabolic acidosisMetabolic acidosis

Myocardial infarctionMyocardial infarction

HyperkalemiaHyperkalemia

HypercapniaHypercapnia

HypocalcemiaHypocalcemia

Page 31: Hemodynamics.kiran rai

Improving Contractility:Improving Contractility:

Can occur through:Can occur through:

Preload reductionPreload reduction

Afterload reductionAfterload reduction

Direct contractile stimulationDirect contractile stimulation

Contractile stimulating drugs in the ICU setting:Contractile stimulating drugs in the ICU setting:

DobutamineDobutamine

DopamineDopamine

AmrinoneAmrinone

Page 32: Hemodynamics.kiran rai

Hemodynamic Hemodynamic MonitoringMonitoring

•Practical ApplicationsPractical Applications

Page 33: Hemodynamics.kiran rai

Examples of Examples of hemodynamic hemodynamic monitoring devices:monitoring devices:

Arterial LinesArterial Lines

RA/CVPRA/CVP

Pulmonary Artery CatheterPulmonary Artery Catheter

SvO2/CCO CatheterSvO2/CCO Catheter

Bedside BP cuffBedside BP cuff

Page 34: Hemodynamics.kiran rai

Arterial Line MonitoringArterial Line Monitoring

Arterial lines provide direct and continuous Arterial lines provide direct and continuous measurement of the patients systolic and diastolic measurement of the patients systolic and diastolic BP via an electrical waveform and digital readout BP via an electrical waveform and digital readout displayed on a monitor.displayed on a monitor.

Page 35: Hemodynamics.kiran rai

Anacrotic rise: Initial steep Anacrotic rise: Initial steep upward slope, Ventricular upward slope, Ventricular contraction, opening of contraction, opening of aortic valveaortic valve

Peak slope: continued Peak slope: continued stroke volume ejection stroke volume ejection from left ventriclefrom left ventricle

Down slope: peripheral Down slope: peripheral runoffrunoff

Dicrotic notch: Aortic Dicrotic notch: Aortic valve closes, diastole valve closes, diastole beginsbegins

Arterial Line waveformArterial Line waveform

Page 36: Hemodynamics.kiran rai

Leveling and Zeroing Leveling and Zeroing SystemSystem

Page 37: Hemodynamics.kiran rai

Central Venous Pressure/Central Venous Pressure/RA Pressure MonitoringRA Pressure Monitoring

Tip of the catheter located in right atrium or Tip of the catheter located in right atrium or superior vena cavasuperior vena cava

RA pressure (AKA CVP) measures venous return to RA pressure (AKA CVP) measures venous return to the right heartthe right heart

RA/CVP pressure is used to determine the RA/CVP pressure is used to determine the “preload” or volume status of the right heart“preload” or volume status of the right heart

Page 38: Hemodynamics.kiran rai

RA/CVP Catheter RA/CVP Catheter PlacementPlacement

Page 39: Hemodynamics.kiran rai

RA/CVP MonitoringRA/CVP MonitoringNormal RA/CVP is between 2-6 mm hg (read as a Normal RA/CVP is between 2-6 mm hg (read as a “mean” value)“mean” value)

Most critically ill patients require a RA pressure of Most critically ill patients require a RA pressure of 6-12 mm hg 6-12 mm hg

RA pressures elevated > 15 - 20 mm hg caused byRA pressures elevated > 15 - 20 mm hg caused by

Fluid OverloadFluid Overload

Pulmonary Problems Pulmonary Problems

Right Heart failureRight Heart failure

Elevated RA pressures indicates hypervolemia; Elevated RA pressures indicates hypervolemia; “Preload” in the right heart is too high “Preload” in the right heart is too high

Page 40: Hemodynamics.kiran rai

Use brown port for CVP monitoring.Use brown port for CVP monitoring.

Arrow triple lumen CVCArrow triple lumen CVC

Page 41: Hemodynamics.kiran rai

PA Pressure & Waveform PA Pressure & Waveform AnalysisAnalysis

PA Pressure (PAP) – tip of the catheter is at the PA Pressure (PAP) – tip of the catheter is at the distal tip of the pulmonary artery (yellow port) distal tip of the pulmonary artery (yellow port) with the balloon downwith the balloon down

Normal PA Pressure isNormal PA Pressure is

20 - 30 mm hg (Systolic) 20 - 30 mm hg (Systolic)

6 – 12 mm hg (Diastolic)6 – 12 mm hg (Diastolic)

PA pressures:PA pressures:

Document Q4 hours: wedge, CO, CI, SVR, PVRDocument Q4 hours: wedge, CO, CI, SVR, PVR

PA waveform needs to be monitored for PA waveform needs to be monitored for spontaneous wedging.spontaneous wedging.

Page 42: Hemodynamics.kiran rai

Pulmonary Artery CatheterA 110 cm flow-directed, balloon tipped, multi-lumen catheter positioned in the distal branch of the pulmonary artery

Yellow Port – PA distal lumen

Blue Port – Proximal (RA/CVP) lumen

White Port = Venous infusion lumen

Balloon Port – Inflate with NO more than 1.5 cc air to obtain INTERMITTENT PA wedge pressures

Thermistor Port – Core blood temperature

Thermal coil port - provides Continuos Cardia Output

Used to obtain derived parameters of CI, Systemic (SVR) & Pulmonary Vascular Resistance (PVR); Sv02/CCO monitoring

Page 43: Hemodynamics.kiran rai

PA Catheter Inflated for Wedge PA Catheter Inflated for Wedge PressurePressure

Page 44: Hemodynamics.kiran rai

PA Waveform ProgressionPA Waveform Progression

Page 45: Hemodynamics.kiran rai

PA Wedge Pressure PA Wedge Pressure PA wedge pressure – obtained by inflating distal PA wedge pressure – obtained by inflating distal balloon port w/ no more than 1.5 ccballoon port w/ no more than 1.5 cc

Inflate the balloon slowly observe for a change in Inflate the balloon slowly observe for a change in waveform from PA to “Wedge”.waveform from PA to “Wedge”.

Only use as much air as needed to obtain Only use as much air as needed to obtain wedge.wedge.

Make a mental note of how much air is needed to Make a mental note of how much air is needed to wedgewedge

Inflation will block off all pressures from Inflation will block off all pressures from right side of heart – it “sees” ahead to the right side of heart – it “sees” ahead to the left side of the heartleft side of the heart

Do NOT inflate for longer than 15 seconds Do NOT inflate for longer than 15 seconds (prolonged inflation will result in pulmonary (prolonged inflation will result in pulmonary infarction, PA rupture & hemorrhage) infarction, PA rupture & hemorrhage)

Page 46: Hemodynamics.kiran rai

• Hemodynamic data obtained by 2-D Doppler echo

• Volumetric measurements

• SV and CO

• Regurgitant volume and fraction

• Qp/Qs

• Pressure gradients

• Maximal instantaneous gradient

• Mean gradient

Page 47: Hemodynamics.kiran rai

• Valve area

• Stenotic valve area

• Regurgitant orifice area

• Intracardiac pressures

• PA pressures, LAP, LVEDP

Page 48: Hemodynamics.kiran rai

• Volumetric Measurments• Stroke Volume and Cardiac Output

• Flow velocity varies during ejection in a pulsatile system so flow velocity is summed as VTI or velocity-time integral

• VTI = area enclosed by baseline and doppler spectrum

• Flow = area x velocity

• SV = CSA x VTI

• CSA = π r2

• CSA = D2 x 0.785

• CO = SV x HR

Page 49: Hemodynamics.kiran rai

What the hell are you talking about ?What the hell are you talking about ?

Page 50: Hemodynamics.kiran rai
Page 51: Hemodynamics.kiran rai

1.PRELOAD-venous blood return to the heart Controlled by; Diuretics-

lasix,bumex Thiazides

Ace inhibitors ♥. Venous Dilation Nitroglycerine Ca+ channel blockers clonidine (Catapress) methyldopa trimethaphan (arfonad) ↓ Dobutamine Morphine

2. CONTRACTILITY-forcefulness of contractilityCa+ channel blockersDigoxinDopamine/DobutamineMilrinone/amrinone

3.AFTERLOAD – work required to open aortic valve and eject blood – resistance to flow in arteries

° Dopamine (at higher doses)

Ace inhibitors Nipride/lesser extent

Nitro Calcium channel

blockers

Labetalol

Drugs of Hemodynamics

4. HEART RATE – 11 Beta blockers11 Calcium

channel blockers

11 Atropine11 Dopamine11 Dobutamine

Page 52: Hemodynamics.kiran rai

Q & A......Q & A......

Whew....Glad thats over !!!!Whew....Glad thats over !!!!

Page 53: Hemodynamics.kiran rai