Hemodynamics advanced orientation, july 2008 - copy


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Hemodynamics advanced orientation, july 2008 - copy

  1. 1. Advanced Hemodynamics Kathleen Brownrigg, RN, MN Pediatric Critical Care Unit
  2. 2. Objectives Discuss invasive monitoring lines Review Indications Understand normal hemodynamics Gain competency in monitoring Interpret hemodynamic data
  3. 3. Objectives Understand hemodynamic variations of congenital cardiac disease Review hemodynamic waveforms and intracardiac pressures Describe complications of invasive lines Correlate hemodynamic data with clinical assessment Discuss the impact of preload, afterload, contractility and ventricular compliance
  4. 4. History1st measurements in 1773by Stephen Hale, an Englishtheologian/scientist andassistantMeasuring directly 1stmean BP on anunanesthetized horseMeasurement of BPevolved slowly
  5. 5. Cardiac Output Measure of performance Volume of blood ejected in 1 min C.O. = HR X SV Varies with size CI = CO BSA
  6. 6. Heart Rate Vital for good cardiac performance Children are less able to vary stroke volume as their myocardial performance is working near max under basal conditions SV is less dynamic – HR influences CO to a greater extent that in adults Tachycardia – shortening of diastolic component of cardiac cycle = 30% of total cycle time
  7. 7. Indications For Hemodynamic Monitoring Shock states: Cardiogenic, hypovolemic, distributive Surgical patients Respiratory patients Multiple trauma
  8. 8. Invasive MonitoringProvides objective quantitative data:  Cardiac output  Preload  Afterload  Rt & Lt heart function  Assessment of intracardiac shunting  Assessment of pharmacologic response
  9. 9. Risk vs Benefit Necessity vs risk assessment Embolism Vessel thrombosis Vessel patency - palliative cavopulmonary connection, cardiac transplantation and repeated biopsy
  10. 10. Goal Increase stroke volume Increase cardiac output Maximize filling pressures Decrease pulmonary congestion
  11. 11. Monitoring Tailored to the individual infant, defect & reparative surgical intervention - Line placement – ie left radial art line and repair of coarctation with subclavian flap is inappropriate Information outweighs risks/complications – remove lines ASAP Line should be transduced for a waveform prior to potent or corrosive drugs. i.e. cyanosed & hypotensive patient, …..color or force of ejection may not be helpful in determining ART vs venous line
  12. 12. Invasive Monitoring Oxygenated blood (ABP, UAC, Pulmonary veins - LAP) Deoxygenated blood (CVL, PA Lines, UVC) Requires a fluid filled system (catheter & tubing) Requires a pressure transducer to transmit one energyform to another – ie physical energy to an electrical signalthat is amplified
  13. 13. Transducing Solutions ART Lines: 0.9 NaCl with 100 units of Heparin/50 ml Run at 1.5 to 2ml/hr. Cardiac neonate rate 1.0 ml/hr All other: D5W & 0.2 NaCl with 100 units of Heparin/ 50 ml Run at 2ml/hr (minimum rate 1.5 ml/hr). May decrease to 0.5ml/hr if sufficient fluid infusing through line to keep vein open. DO NOT TURN TRANSDUCING FLUID OFF completely -stagnation of fluid in transducer
  14. 14. Proper Leveling/Rezeroing Point? Must be leveled to an anatomically consistent point Phlebostatic axis provides an external reference point Reference point that approximates the anatomic level ofthe atria and PA Ensures accuracy of readings Must be zeroed to eliminate effects of hydrostatic &atmospheric pressures Zeroing stopcock should be used
  15. 15. Phlebostatic AxisMidpoint between the anterior and posterior surfaces of thechest at the 4th intercostal space midaxillary line
  16. 16. Zeroing/CalibratingInaccurate transducer position can result in large errors inreading!!!!!
  17. 17. Zeroing
  18. 18. Zeroing
  19. 19. Causes of Error? Air bubbles in the system = underestimation of systolicpressure and overestimation of diastolic pressure Blood clots Use of non-compliant tubing Tighten loose fitting connections Catheter lodged again vessel wall Improper zero Interpretive
  20. 20. Arterial Pressures? Moment by moment pressure Visual display of systolic, diastolic and MAP MAP = 2X(DAP) + SAP 3
  21. 21. Dicrotic Notch
  22. 22. Intrathoracic Lines Directly positioned at time of surgery RA, LA PA, RV Fixed to the thorax by a suture Maintained with 1.5-2.0 ml/hr
  23. 23. RA Lines Information about: systemic venous return vascular volume right heart events Reported as a mean pressure Ideal location is within the body of RA where venous blood return is mixed RA line is a low pressure line
  24. 24. RA Lines Reflects preload or right ventricular end diastolic pressure (RVEDP) Placed through RA appendage during surgery or Threaded into the RA by venous cannulation or umbilical venous line
  25. 25. RA Line Low RAP: hypovolemia waveform dampening faulty positioning of transducer line placement in the coronary sinus or low in IVC
  26. 26. RA Line High RAP: RV dysfunction Tricuspid stenosis or insufficiency Hypervolemia Tamponade Constrictive pericarditis Pericardial effusion LV to RA shunt Pulmonary hypertension
  27. 27. LA Catheters Provides a measurement of pulmonary venous pressure Indicates systemic volume, LV preload, LV function Placement: Posteriorly through the wall of LA at the junction of superior pulmonary vein and advanced across the LA Xray display a straight line across the chamber
  28. 28. LA Catheters Low pressure: hypovolemia Increased LAP: Deep inspiration PEEP Hypervolemia Mitral valve insufficiency Loss of AV conduction Ventricular dysfunction Coronary artery occlusion Pericardial effusion/tamponade
  29. 29. Cardiac Output Cardiac Output is a product of stroke volume X HR SV 60-130 ml Adult Factors affecting SV: preload, afterload contractility Cardiac Index: adjusts CO to individual persons body size = blood flow relative to a square meter of body surface area. 1/3 cardiac cycle – consuming O2 2/3 diastolic & perfusing coronary arteries Cardiac index is highest in childhood and diminishes with age
  30. 30. Principles of Hemodynamics Blood Pressure = C.O. X SVR C.O. & SVR have an inverse relationship: If bloodpressure drops, SVR increases to compensate = equilibrium SVR is the strongest component regulating BP A vasoconstrictor has a greater effect than an inotrope Cardiac medications manipulate the: Contractility (improve/depress) Preload (increase/decrease) Afterload (increase/decrease)
  31. 31. Alpha Adrenergic Receptors Receptors in the peripheral and coronary arteries. Peripheral vasoconstriction - skin, lungs, GI tract, and kidneys Increases sweating Dilates pupils Norepinephrine, Epinephrine, Dopamine
  32. 32. Beta 1 AdrenergicReceptorsB1: Receptors in the heart, lungs and coronary arteries.(lesser in vessels)Found largely in the heartIncreases: HR, contractility, conductivityNorepinephrine, Epinephrine, Dopamine, Dobutamine, Isuprel
  33. 33. Beta 2 Adrenergic ReceptorsFound largely in the lungsBronchodilationPeripheral vasodilation: skeletal muscles, heart andlungsArteriolar dilation = O2 delivery to the cellsAdrenalin, Isuprel, VentolinCaution: B-Blockers:Propanolol, Esmolol, Labetolol, Atenolol
  34. 34. Preload Preload: End diastolic stretch of the muscle fibres. Voland pressures in ventricle just prior to systole Frank Starling principle: The greater the muscle fibresare stretched in diastole, the more they will shorten andwith > force in systole If preload increases so does C.O. to an optimum level
  35. 35. Preload The ideal preload is associated with optimal cardiac output What is that norm for your patient?????? Influencing factors: circulating blood volume, distribution of blood volume, atrial contraction Estimating preload: PAD LAP RAP
  36. 36. Afterload Resistance to blood flow as it leaves the ventricles Major influences – vascular compliance & outflowobstruction A function of: Arterial pressure Ventricular size An increase in vascular resistance (PVR or SVR) resultsin an increased contractility in order to maintain: strokevolume and C.O Increase in SVR or PVR - more energy required forejection - myocardial O2 demand increases
  37. 37. Afterload Systemic hypertension (functional) Pulmonary hypertension (functional) Aortic stenosis/Coarctation (structural) Pulmonary stenosis (structural)
  38. 38. SVRSVR (Woods units) = MAP – Mean RAP(CVP) Cardiac output = 10 – 15 Woods unitsSVRI (dynes-sec-cm -5) = MAP – Mean RAP(CVP) X 80 Cardiac index = 800-1600 dynes/sec/cm-5
  39. 39. PVRPVR (Woods units) = MAP – Mean RAP Cardiac output = 1-3 Woods units over 8 wks of age 8-10 Woods units < 8 weeks of agePVRI (dynes-sec-cm -5) = MAP – Mean PCWP (or LA ) X 80 Cardiac index = 80-240 dynes/sec/cm-5
  40. 40. Factors Causing Increased PVR Alveolar hypoxia and PA vasoconstriction: hypoventilation ETT obstruction pneumothorax Obstruction to flow: pulmonary venous obstruction mitral valve stenosis, severe left ventricular failure
  41. 41. Potential Vasoconstrictors for PVR Potential Vasoconstrictors Acidosis Body temperature – hypothermia Stimulation – Pain Potential Vasodilators: Good oxygenation Alkalosis Mild hyperventilation Sedation Inhaled nitric oxide
  42. 42. Contractility Inotropic state of the muscle. The ability of the myofibrilsto shorten in length and produce a contraction for any givenpreload and afterload. Preload & afterload Drugs – concentrations of circulating catecholamines, inotropic agents, pharmacologic depressants Cardiac oxygenation Physiological depressants: hypoxia, hypercapnia, acidosis Functional myocardium Ionized Ca++
  43. 43. ContractilityNot measured directlyUse SWI (stroke work index) to assess ventricular contractilitySVI 33-47 cm/m2/beatRVSWI 7-12 gm/m2/beat (6 - 7 Curley)LVSWI 35-85 gm/m2/beat (50 - 62 Curley)If high: B-blockers: PropanololIf low: +ve inotropes: Dopamine, Milrinone, Epinephrine
  44. 44. Normal SaturationsMay be falsely high or lowdepending on catheterplacement or residual lesions 70% 75% 95% 35% 95% Coronary 75% sinus 75% 75%
  45. 45. Step UpCorrelation of RA to PA sat with residual lesions
  46. 46. LA Saturations Can not really beDecreased LA O2 SAT: assumed - intrapulmonary shunting as a result of atelactasis, lung collapse, consolidation - R to L cardiac shunt
  47. 47. Cardiac Function Adequate C.O. and balance between: O2 DELIVERY & O2 Consumption or DEMAND If balance is altered then anaerobic glycolysis (lacticacidosis) Blood leaves heart 100% O2 saturated Tissue extraction is 25% SvO2 (mixed venous oxygen saturation) is 75% (60-80%)….blood returning to right side of heart
  48. 48. Tissue Metabolism Systemic O2 balance is critical! O2 Delivery O2 Consumption (DO2) (VO2) Is it an O2 delivery or tissue extraction problem?An increase in O2 consumption(VO2) is usually seen 4 hrspost op due to a rise in central body temperature
  49. 49. SvO2 Monitoring: Too High SvO2 > 80%High O2 supply: FiO2 too highLow O2 demand: Anesthesia/sedation - little muscle activity Hypothermia lowers metabolic demands Sepsis impairs utilization of O2 – early high output state L to R shunt PAPVD or TAPVD LV-RA shunt Aorto pulmonary collaterals
  50. 50. SvO2 Monitoring: Too Low SvO2 < 60%Low O2 supply: Hypoxemia (lung disease or poor supply) Low cardiac output Catheter position in the coronary sinus or low in IVCHigh O2 demand: Consumption high (demand > supply) Shivering, Seizures Hyperthermia Nursing activities Pain, anxiety
  51. 51. Conditions That Increase VO2Minor Surgery 7%Fever – for each degree rise 10%Agitation 16%Increased WOB 40%Severe infection 60%Multiple organ failure 20-80%Shivering 50-100%Burns 100%Sepsis 50-100% Darovic
  52. 52. Medications That Increase VO2Norepinephrine (0.1-0.3 10-21%mcg/kg/min)Dopamine 5 mcg/kg/min 6%Dopamine 10 mcg/kg/min 15%Epinephrine 0.1 mcg/kg/min 23-29%Ace inhibitors for systolic Used when pump not strongfailure enough or SVR too highB blocker –slow hr anddecrease O2 requirements. Darovic
  53. 53. Procedures/Activities Increase VO2Dressing change 10%Nursing assessment 12%ECG 16%Physical exam 20%Bath 23%Chest Xray 25%ET suctioning 27%Turn 31%Nasal intubation 25-40% Darovic
  54. 54. Factors that Decrease VO2Hypothermia (for each 10%degree C)Morphine Sulphate 9-21%Anesthesia 50%Assist control ventilation 30%Neuromuscular blockade Abolishes the increase in VO2 incurred by shivering Darovic
  55. 55. Cardiac Function If you have decreased C.O tissues, will extract moreO2 so the MvO2 will drop If there is a patch leak (ASD, VSD, AVSD) thenMvO2 will increase
  56. 56. PA CathetersProvides information about:Mixed venous oxygen saturationsRV functionRVOT patencyPulmonary vascular reactivityVenous pressure in the lungsPlacement: via RVOT into main PA
  57. 57. Elevated PAPHypervolemiaIncreased pulmonary blood flow with L to R shuntLung diseaseMitral stenosisObstructed TAPVDPulmonary embolus
  58. 58. Understanding Waveforms
  59. 59. Waveform analysisScale?
  60. 60. Modified StarlingCurve Relationship between ventricularfilling pressure and stroke volumeCurve BNormal FunctionAs PCWP increases – SV increasesCurve A –Enhanced Sympathetic stimulationCurve C & D – Depressed contractility – curve shifts to right. In response to an increased filling pressure only minimal augmentation of stroke volume and addition of appropriate pharmacology is required.
  61. 61. Volume administration andaugmentation of preloadimproves stroke volumeVentricular compliancerefers to the distensibility ofthe ventricle and is related tothe changes in volumeIf the ventricle is compliantie distensible then a largeincrease in LVEDV can beaccommodated with minchange in VEDP Modified Starling Curve
  62. 62. LVEDP The relationship between of ventricular filling volume and ventricular filling pressure to changes in stroke volume are not consistent between patients and are not the same over time in the same patient. These relationships are prone to changes
  63. 63. Non-Compliant Stiff Ventricles A noncompliant stiff ventricle such as a hypertrophic ventricle - even a small increase in ventricular end diastolic volume may produce significant increase in LVEDP High filling pressures lead to pulmonary edema, increased systemic venous pressure on RV.
  64. 64. Intravascular Lines & Swan Ganz Catheters
  65. 65. EKG and Atrial Waveform Record atrial pressure waveform & EKG simultaneously a wave occurs at approx the same time as the QRS v wave occurs near the T wave
  66. 66. A, C & V waves The atria do not have systolic & diastolic pressures Mean atrial pressure is the average pressure in the atrium during the cardiac cycle 3 positive deflections during each cardiac cycle – a, c & v
  67. 67. A, C & V Waves a – wave produced by atrial contractions during atrialsystole c – wave produced due to the rapid rise in ventricularpressure in early systole, causing the AV valve leaflets tobulge back into the atria so that the atrial pressureincreases briefly v – wave produced by blood entering the atriumduring late systole.
  68. 68. CVP & LAPA waveC waveV wave C wave is a notch on the a wave or may be absent
  69. 69. A & C & V wavesAtrial Contraction Bulging of valve Atrial filling into atria Ventricular contraction * A wave * C wave * V wave
  70. 70. A & C & V WavesAtrialfibrillation =no A -wave
  71. 71. A & C & V Waves Usually atrial contraction (a-wave) produces a taller wavethan ventricular filling (v-wave) in the RA and reverse in the LA
  72. 72. LAP A and V waves are a little away or delayed incomparison to RAP pressure waveforms.
  73. 73. Cannon A WavesRight SideTricuspid AtresiaEbstein’sPulmonary StenosisPulmonary venous occlusivediseasePulmonary hypertensionVentricular hypertrophyVentricular dysfunction Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm
  74. 74. Cannon A WavesLeft SideMitral stenosisVSDPDAAortic stenosis Cannon waves occur when the atria contracts against a closed valve, loss of normal sinus rhythm
  75. 75. Cannon V WavesRight sideTricuspid regurgitationASDCongestive heart failure
  76. 76. Cannon V WavesLeft sideMitral regurgitationCHF
  77. 77. Mitral Valve Regurgitation LAPLAP5 ½ yr old Ross ProcedureMitral, trivial tricuspid and aortic regurgitationLAP V V V V V
  78. 78. Mitral Regurgitation LAPMitral Regurgitation & Cannon v- wavesLAP
  79. 79. 3 ½ yr Old CardiomyopathyRAP3 ½ yr old cardiomyopathyARTRAP Cannon A – poor ventricular function Cannon V – tricuspid valve regurgitation
  80. 80. LA Waves3 ½ cardiomyopathy awaiting a hearttransplantCannon v due to mitral regurgitationCannon a waves due to ventricular failure 1 2 3
  81. 81. RV Line 1 RV 2 3RVP 58/3 (Note subsytemic RV systolic pressures)RV
  82. 82. RV Line ART RVInfantART 1 2 3 1RV No dicrotic knotch 3
  83. 83. PAP Waveform PA waveform in the pulmonary artery – differs fromthe RV PA diastolic pressure higher than RV – pulmonaryvalve closes preventing PA diastolic from becominglower
  84. 84. Swan Ganz Catheter4-5 lumens1) RAP (right atrial pressure)2) PAP (pulmonary artery pressure)3) PCWP (pulmonary capillary wedge pressure)4) Cardiac output measurement via thermodilution5) Lumen for drug/fluid administration
  85. 85. Swan Ganz Catheters:AdvantagesAllows for real time determination of systemic oxygendelivery and consumptionInvasive (right heart)Measures pressures in the heart and in the lungsDifferentiates pulmonary disease vs left ventricularfailureGuides treatment: drugs/fluidsMultilumen balloon tipped catheter
  86. 86. PA Lines
  87. 87. PAP
  88. 88. X-ray of PA LineCommonly in the rightmain PAThe tip of the cathetershould not be visiblebeyond the silhouette ofmediastinal structures
  89. 89. Swan Ganz: Complications Pulmonary embolism Thrombus formation Infection PA perforation Dysrhythmias Dislodged & wedged Balloon bursts Catheter kinked
  90. 90. Waveform Changes5-10 mmHg 20-30 mmHg 20-30 mmHg 6-12 mmHg 5-10 6-12 Mean PAP (10-20) mmHg
  91. 91. PA Waveform 1 2 3
  92. 92. Swan Ganz
  93. 93. RAPLAP slightly higher thanRAP.RAP can be used to assessvolume and function in thehealthy person as theycorrelate well….. but notone with cardiopulmonarydysfunctionAcidosis, hypoxemia,positive pressure ventilationat high pressures and CHDalter the relationship
  94. 94. RVPElevated inPulmonary hypertensionPulmonic stenosisVSDRV diastolic pressureelevated due to RVdysfunction
  95. 95. RV CathetersRV linePA catheter that slips back? Vs purposeful placementDocumentation of pressures and waveformsWatch for ventricular arrhythmias
  96. 96. PAPElevated in pulmonaryemboliCOPDVSDIncreased PBF – L to RshuntPA hypertensionSevere heart failure
  97. 97. PCWP
  98. 98. What Are Your Pressures?
  99. 99. PA Wedge (PWCP) Left heart pressure Measured by the SWAN Measures LVEDP Read when inflated balloon lodges in a smallerbranch of the PA – occlusion of the branch Pressure of the distal catheter will be the same as theLA In the absence of lung disease Wedge should be 1- 5mmHg < than PAD
  100. 100. PAP to Wedge 1 2 Dicrotic notch 3 End diastoleIntentional or Not? Spontaneous wedging in the PA = pulmonaryinfarction!
  101. 101. PAD not equal PCWP Pulmonary diastolic pressure do not equal LVEDP PCWP is a static reading during diastole and systole When wedge higher consider ARDS in the face of high ventilator settings > 4mm difference between PAD and wedge then likely not accurately measuring LVED but more likely the lung disease Measure over again and compare to BP, and U/O Identify which wedge get the best C.O/pt
  102. 102. Anatomy
  103. 103. PAD & PCWP AnalysisWhen PCWP is > true LVEDPMitral stenosisMyxomaMitral valve regurgitationPulmonary embolism0
  104. 104. Computation Constant
  105. 105. Thermodilution
  106. 106. Thermodilution
  107. 107. Errors Quantity of injectate Injection time Rewarming of injectate
  108. 108. Calculating EquationsC.O. = HR X SV = 4-6 L/minC.I. = C.O. = 3-5 L/min/m2 BSASVR = MAP - RAP X 80 dynes/sec/cm -5 C.O.PVR = mPAP - PCWP X 80 dynes/sec/cm -5 C.O.
  109. 109. Cardiac VolumesC.O. = 4-8 L/minC.I. = 3-5 L/min Adult – 2.5-4 L/minStroke volume = 60 - 100 ml/beatStroke volume in children 1.5 ml/kg/beatEjection fraction = > 60 %
  110. 110. PressuresCVP 5-10 mmHg LAP 6-12 mmHgRAP 5-10 mmHg PCWP 6-12 mmHgRVP 15 - 25 mmHg MAP (age related) 5-10PAP 15 - 30 mmHg 8-12mPAP (10-20) mmHg or < 1/2 to 1/3 systemic
  111. 111. Making Sense of PressuresIncreased RAP: Right ventricular failure(>10 mm Hg) Hypervolemia Tricupid stenosis/regurgitation Pulmonary stenosis/regurgitation Cardiac tamponadeDecreased RAP Hypovolemia(< 5 mm Hg) Vasodilation
  112. 112. Making Sense of PressuresPCWP reflects LVEDP only when there is no obstruction(pulmonary disease or mitral valve disease)Increased PCWP: Left ventricular failure(>12 mm Hg) Hypervolemia Mitral stenosis/regurgitation Aortic stenosis/regurgitation Cardiac tampondeDecreased PCWP Hypovolemia(< 6mmHg) Vasodilation
  113. 113. Making Sense of PressuresElevation & Equalization of pressures: RAP = PCWPFilling problems - tamponade/constriction - restrictive cardiomyopathy BEWARE!!
  114. 114. Assessment of TamponadeIncreasing tachycardiaAgitationHypotensionElevated intracardiac pressuresAbrupt cessation of chest tube drainageCardiac arrest
  115. 115. Systolic/Diastolic PAP PA systolic pressure equals RV systolic pressure unless RVOT obstruction is present PA diastolic pressure corresponds to LA pressure if no gradient exists across the mitral valve Oxygen Saturation: Reflects total mixed venous sample
  116. 116. ShuntingDetermination of L to R shunt by calculating Qp:Qs (pulmonary to systemic blood flow ratio)Uses saturation data from the intracardiac linesQp:Qs = Art Sat – RA Sat Pulm ven sat – PA satQp:Qs = 100 – 75 = 25 Normal = 1:1 100 – 75 25
  117. 117. Complications of ThoracicLinesInfectionHemorrhageMalpositionEntrapmentFragmentationEmbolusDeath
  118. 118. Guidelines for Intrathoracic LineRemoval Volume available Determine clotting factors Stop Heparin infusion in preparation for removal Assess patency of chest tubes CVS removes OBSERVE FOR CARDIAC TAMPONADE
  119. 119. PAPPVR drops by 80 % after birthPVR progressively falls & reaches adult levels within a few weeksPulmonary arteries are very reactive in neonatal periodVasoconstriction due to alveolar hypoxia, acidosis, over-distension of the alveoli, or hypothermiaVasodilation is promoted by alveolar oxygenation, an alkalotic pH
  120. 120. Wedged PA catheter• Occluded segment – looks through the non-active segment
  121. 121. PA Wedge
  122. 122. PA WedgeIf wedge waveform were to be on an incline = over wedgingBalloon will be overdilated – build up of pressure within the flushsystem.
  123. 123. PA Line Wedged PAPPAP 12Wedged 3PAP
  124. 124. PCWPPCWP is used to assess: Intravascular volume (preload) Function of the left ventricleIs a measurement of the pressure in the left atriumIs NOT a measurement of left ventricular preload but isa reflection of LVEDPCan reflect the pressure in the surrounding alveoliIs NOT a measure of capillary hydrostatic pressureIs NOT a transmural pressure
  125. 125. PAD & PCWP AnalysisWhen PAD is < LVEDPLeft ventricular failureAortic valve regurgitation
  126. 126. PAD & PCWP analysisWhen PAD = PCWPIncreased PVRMitral valve diseasePulmonary hypertensionPulmonary venous diseaseHigh Peep >10mmHgCor pulmonalePulmonary embolism
  127. 127. Cardiac Output
  128. 128. Case 12 yr old post op cardiac surgical repair of VSDHR 166/minC.O 3.0 SVR 1712CI 1.8 PVR 350BP 60/35 PAP 46/22CVP 16 RVSWI 4PCWP 22 LVSWI 21
  129. 129. Case 212 yr old patient who underwent a Ross Konnoprocedure for LVOT and aortic valve reconstructionHR 136C.O 3.4 SVR 1905CI 2.2 PVR 150BP 65/38 PAP 13/5CVP 1 RVSWI 5PCWP 4 LVSWI 29
  130. 130. Case 316 yr old post op cardiac surgical repair of mitral valveHR 166/minC.O 3.3 SVR 1689CI 2.1 PVR 175BP 70/48CVP 19 RVSWI 5PCWP 19 LVSWI 18
  131. 131. Case 42 yr old previous AVSD repair at 4 weeks of ageadmitted with SOB post RSV.HR 168C.O 5.0 SVR 1200CI 3.0 PVR 385BP 98/67 PAP 46/22CVP 14 RVSWI 5PCWP 6 LVSWI 42
  132. 132. Case 5A 10 yr old cardiomyopathic patient in critical careawaiting heart transplant. This is her hemodynamic data.She has a CVL, PA line, LA line. You have justreturned from the cardiac catheterization lab and thefollowing data is available for you to interpret.HR 126C.O 10 SVR 356CI 5.7 PVR 302BP 91/39 PAP 46/22CVP 13 RVSWI 8PCWP 15 LVSWI 24
  133. 133. Sepsis Patient7 yr old sepsis patientGram negative septic shockMulti-organ failure: respiratory, renal, liverSvO2 = 75%Lactate of 2.2Vasopressin 0.0002 units/kg/hrEpinephrine .03 mcg/kg/minDopamine 7.5 mcg/kg/minStarted on Milrinone .66 mcg/kg/min Nipride of 1.0 mcg/kg/min
  134. 134. Sepsis PatientPAP = 37.8 deg. TempEsophageal = 37.2 deg. TempWt 25 kgHt 126 cm
  135. 135. Sepsis 21:00 01:03 04.22 11:00CO 3.87 6.29 6.27 2.07CI 4.07 6.62 6.60 2.18SI 30.97 48.3 47 15.7SVRI 1060 918 787 2385PVRI 314 85 194 550HR 132 137 140 139BP 110/59 148/76 123/63 116/74PAP 43/34 (37) 44/36 (31) 46/37 (32) 46/36 (31)(mean)PCWP 21 29 21 21RAP 19 17 16 21SvO2 72 69 70 50SVR 2511PVR 579SV 14.9
  136. 136. Intramural MI 14 yr old sudden loss of consciousness while playing sports SOB + O2. On oxygen. O2 sat 99% Marked ST segment depression on EKG 59.0 kg Ht 177 cm Computation constant - .547 Swan Ganz inserted. Nitroglycerine infusion started wwwemedicine.com/med/topic2956.c?htm
  137. 137. coronary 1320 Insert 1325 13:29 13:38 1435CO ST depressed 4.84 HOB 45CI 2.86SISVRIPVRI 279HR 90 92 92BP 92/69 (78) 94/70 94/57PAP 38/10 RV 39/18 PAP 37/21 42/28 30/20(mean) (21) (27) (27) (33) (24)PCWP 20 17 22 18RAP 9 4 6SvO2SVR 1041PVR 165LVSWI 35.8 21.2RVSWI 16.46 9.74
  138. 138. Intramural MI ST segment depression in the night BP okay Wedge increased from 14 mm Hg -19 mm Hg Awoke – suddenly SOB – sat bolt upright O2 sats in the 80’s on 100% O2 Nitroglycerine increased to 3 mcg/kg/min Morphine 12 lead done 5:20 am Esmolol 400 mcg/kg/min Tachycardia PAP 55/22 reflecting Marked LV failure
  139. 139. Intramural MI LOC decreased Emergent intubation Systole of 40 mm Hg Epi - .02 mcg/kg/min Vasopressin .0004 units/kg/hr Nitroglycerine 6 mcg/kg/min Bicarb Ca++ Volume 2 units PRBC Troponin and CPK increased Esmolol off V tachycardia
  140. 140. Intramural MI Reimplantation of intramural LCA Good function LCA origin in middle of L coronary sinus Abherrent LMCA from tight sinus of aorta Unroof the LMCA off the ostium Bipass 91 min XClamp 41 min Nitroglygerine 0.5 mcg/kg/min Milrinone Tylenol and Ketorolac Esmolol Day 2 – Post op ST depression and diastolic dysfunction