Hemodynamics.kiran rai
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Hemodynamics.kiran rai



basis of hemodynamics

basis of hemodynamics



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  • Afterload is the pressure the ventricles must OVERCOME in order to pump the blood past the aorta.
  • Anacrotic rise is the initital upward slope of the waveform when the ventricle is contracting and forcing open the aortic valve.

Hemodynamics.kiran rai Hemodynamics.kiran rai Presentation Transcript

  • Hemodynamics Physics of Blood flow in the circulation
  • Circulatory System
    • Heart:
    • Has 2 collecting chambers - (Left, Right Atria)
    • Has 2 Pumping chambers - (Left, Right Ventricles)
  • Left Side of Heart Lungs Tissues Circulation Schematic Right Side of Heart A V V A Pulmonary Vein Pulmonary Artery Aorta Sup. & Inf. Vena Cava Pulmonary Valve Aortic Valve Tricuspid Valve Mitral Valve
  • Blood Vessels
    • Arteries
    • Capillaries
    • Veins
    • Systemic Pathway:
    • Left Ventricle of Heart Aorta Arteries Arterioles
    • Capillaries
    • Venules Veins Right Atrium of the heart
  • Blood
    • Composition:
      • Approx 45% by Vol. Solid Components
            • Red Blood Cells (12  m x 2  m)
            • White Cells
            • Platelets
      • Approx 55% Liquid (plasma)
            • 91.5% of which is water
            • 7% plasma proteins
            • 1.5% other solutes
    • Viscosity of Blood = 3 3.5 times of water
  • Hemodynamic Principles
    • CO = SV X HR
    • Stroke Volume : Amount of blood ejected by the left ventricle with each Cardiac Contraction.
    • Preload - Ventricular filling pressure at end diastole.
    • Afterload - Resistance the ventricle has to overcome to eject it’s content.
    • Contractility - Heart muscles pumping ability.
  • Cardiac Output
    • Stroke volume X Heart rate.
    • Normal CO = 4-8 liters/min
    • CI=CO/BSA
    • Body surface area = Weight in Kg. x Height in cm.
    • Normal CI=2.8-4.2 L/min/m2
    • A CI of 2.0 or less should be immediately reported to the physician!!
  • Four determinants of cardiac output Heart Rate x Stroke Volume Contractility Afterload Preload
  • Starling’s Law
    • The strength of the contraction is proportionate to the stretch applied---
    • Up to a point!
    • An overstretched heart cannot contract back well at all.
    • The stretching of muscle fibers in the ventricles
    • Results from blood volume in the ventricles at end-diastole
    • The greater the stretch during diastole, the more forcefully they contract during systole
    Preload Preload is the stretch of the balloon as air is blown into it. The more air, the greater the stretch.
  • Preload and Cardiac Output
    • Preload will generally INCREASE CO
    • Myocardial fibers stretch and increase the force of contraction
    • Too much preload: heart becomes overstretched; results in diminished contraction and DECREASE CO
    • Decrease in preload, heart and vessels are underfilled, results in DECREASED CO
  • Preload
    • Central Venous Pressure ( CVP) Measures the filling pressure of the Right Atrium at end diastole.
    • Normal CVP is 0-8 mmHg.
    • Pulmonary Artery (PCWP) reflects the filling pressure of the Left Ventricle at end diastole.
    • Normal PCWP is 6-12 mmHg.
    • The amount of blood in a ventricle before it contracts.
  • Increasing Preload:
    • Crystalloids & colloids
    • Crystalloids: NS or LR
      • Takes 1000 ml to increase blood volume by 200 ml
    • Colloids used when acute vascular loss exists
  • Low CVP
    • Decreased Venous return to the heart.
    • Hypovolemia.
    • Volume Loss
  • Elevated CVP
    • Fluid Overload.
    • Heart Failure.
    • Cardiac Tamponade.
    • Tricuspid valve Regurgitation.
    • Increased Intrathoracic/Pulmonic pressures.
  • Left Heart Preload
    • The amount of blood in the LV at the end of diastole
    • Measured by the pulmonary capillary wedge pressure (PCWP)
    • Normal PCWP 6-12mmHg
    • Obtained when PA balloon is inflated.
    • This blocks off all pressures from right side and all the PA catheter “see” is the filling pressure of Left side of heart.
    • The pressure that the ventricles must generate to overcome the higher pressure in the aorta to get the blood out of the heart
    Afterload Resistance is the knot on the end of the balloon, which the balloon has to work against to get the air out.
  • Factors Affecting Afterload
    • Compliance of the aorta
    • Mass/viscosity of the blood: how thick or thin is it?
    • Vascular resistance: Are the blood vessels constricted or dilated?
    • Oxygen level: Hypoxemia will cause vasoconstriction.
    • The afterload force opposes muscle contraction”
    • Afterload is inversely proportional to stroke volume.
  • Afterload Reduction:
    • Improves cardiac performance by reducing the resistance facing the ventricle during contraction.
    • Other factors, such as blood viscosity and valvular resistance, can influence afterload
    • Agents that reduce arterial resistance:
      • Calcium channel blockers
      • ACE inhibitors
      • Arteriolar dilators
      • Beta blockers
  • Afterload Increase and Increasing the BP:
    • Increasing afterload with vasopressors is the most potent method.
    • Hypovolemia must be corrected before using vasopressors
    • Vasopressors increase myocardial oxygen consumption
    • May increase the BP but not the blood flow
    • Common agents: norepinephrine, dopamine, phenylephrine
  • IABP
    • Decreases afterload
    • Improves coronary perfusion
    • The ability of the myocardium to contract normally
    • Influenced by preload
    • The greater the stretch, the more forceful the contraction
    Contractility The more air in the balloon, the greater the stretch, the farther the balloon will fly when air is released.
    • Determined by force and velocity of muscle contraction when loading conditions (preload and afterload) are held constant.
    • Can be influenced by neural, humoral or pharmacological factors.
  • Increased Contractility
    • “ Fight or Flight”
      • Sympathetic response
      • Catecholamine release
    • Increased contractility also increased myocardial oxygen demand
  • Decreased contractility
    • Decreased contractility
      • Decreased stroke volume
      • Decreased myocardial oxygen demand
    • Contractility decreases with:
      • Hypoxia
      • Metabolic acidosis
      • Myocardial infarction
      • Hyperkalemia
      • Hypercapnia
      • Hypocalcemia
  • Improving Contractility:
    • Can occur through:
      • Preload reduction
      • Afterload reduction
      • Direct contractile stimulation
    • Contractile stimulating drugs in the ICU setting:
      • Dobutamine
      • Dopamine
      • Amrinone
  • Hemodynamic Monitoring
    • Practical Applications
  • Examples of hemodynamic monitoring devices:
    • Arterial Lines
    • RA/CVP
    • Pulmonary Artery Catheter
    • SvO2/CCO Catheter
    • Bedside BP cuff
  • Arterial Line Monitoring
    • Arterial lines provide direct and continuous measurement of the patients systolic and diastolic BP via an electrical waveform and digital readout displayed on a monitor.
    • Anacrotic rise: Initial steep upward slope, Ventricular contraction, opening of aortic valve
    • Peak slope: continued stroke volume ejection from left ventricle
    • Down slope: peripheral runoff
    • Dicrotic notch: Aortic valve closes, diastole begins
    Arterial Line waveform
  • Leveling and Zeroing System
  • Central Venous Pressure/ RA Pressure Monitoring
    • Tip of the catheter located in right atrium or superior vena cava
    • RA pressure (AKA CVP) measures venous return to the right heart
    • RA/CVP pressure is used to determine the “preload” or volume status of the right heart
  • RA/CVP Catheter Placement
  • RA/CVP Monitoring
    • Normal RA/CVP is between 2-6 mm hg (read as a “mean” value)
    • Most critically ill patients require a RA pressure of 6-12 mm hg
    • RA pressures elevated > 15 - 20 mm hg caused by
      • Fluid Overload
      • Pulmonary Problems
      • Right Heart failure
    • Elevated RA pressures indicates hypervolemia; “Preload” in the right heart is too high
  • Use brown port for CVP monitoring. Arrow triple lumen CVC
  • PA Pressure & Waveform Analysis
    • PA Pressure (PAP) – tip of the catheter is at the distal tip of the pulmonary artery (yellow port) with the balloon down
    • Normal PA Pressure is
    • 20 - 30 mm hg (Systolic)
    • 6 – 12 mm hg (Diastolic)
    • PA pressures:
      • Document Q4 hours: wedge, CO, CI, SVR, PVR
      • PA waveform needs to be monitored for spontaneous wedging.
  • Pulmonary Artery Catheter
    • A 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
  • PA Catheter Inflated for Wedge Pressure
  • PA Waveform Progression
  • PA Wedge Pressure
    • PA wedge pressure – obtained by inflating distal balloon port w/ no more than 1.5 cc
    • Inflate the balloon slowly observe for a change in waveform from PA to “Wedge”.
    • Only use as much air as needed to obtain wedge.
    • Make a mental note of how much air is needed to wedge
    • Inflation will block off all pressures from right side of heart – it “sees” ahead to the left side of the heart
    • Do NOT inflate for longer than 15 seconds (prolonged inflation will result in pulmonary infarction, PA rupture & hemorrhage)
    • 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
    • Valve area
      • Stenotic valve area
      • Regurgitant orifice area
    • Intracardiac pressures
      • PA pressures, LAP, LVEDP
    • 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
  • What the hell are you talking about ?
    • 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 contractility  Ca+ channel blockers  Digoxin  Dopamine/Dobutamine  Milrinone/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 –
    •  Beta blockers
    •  Calcium channel blockers
    •  Atropine
    •  Dopamine
    •  Dobutamine
  • Q & A...... Whew....Glad thats over !!!!