Ventricular dysfunction in_critically_ill

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Ventricular dysfunction in_critically_ill

  1. 1. Ventricular dysfunction in Critically Ill 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW &ULWLFDO &DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  2. 2. How much have we deciphered Mother Nature? “And the LV volume is a surrogate for LV wall tension And the LV wall tension a surrogate for LV stroke volume And the LV stroke volume determines CO And the LV CO is a surrogate for tissue blood flow And tissue blood flowis a surrogate for tissue oxygenation And the tissue oxygenation is a surrogate for ATP generation And ATP generation powers cellular function” critical care clinic 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  3. 3. Ventricular function DIASTOLIC COMPLIANCE PRELOAD HEART RATE CONTRACTILITY AFTERLOAD VALVE FUNCTION 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  4. 4. VENTRICULAR PRESSURE- VOLUME RELATIONSHIP 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  5. 5. LV PRESSURE VOLUME CURVE LVESPVR - index of contractility 150 LV Pressure 100 50 LVESDVR - index of compliance LV volume 50 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  6. 6. ESPVR index of contractility All ESPV points lie along a line All ejection from different diastolic volumes end on ESPVR ESPVR shifts to left when contractility increases decreased ejection at any given preload and afterload ESPVR shifts to right when contractility decreases increased ejection at any given preload and afterload 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  7. 7. EDPVR index of compliance All EDPV points lie along a line EDPVR shifts to left and up when ventricular compliance decreases diastolic dysfunction EDPVR shifts to right and down when ventricular compliance increases dilated cardiomyopathy 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  8. 8. LV PRESSURE VOLUME CURVE a-MV opens b-MV closes c-AV opens d-AV closes LVESPVR 150 100 d Isovolemic contraction 50 isovolemic relaxation LV Pressure c a a-b = preload b-c = afterload c-d = stroke volume LVESDVR b LV volume 50 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  9. 9. CARDIAC MUSLCE LENGTH TENSION CURVE Isometric contraction Isometric relaxation Muscle tension End systolic length End diastolic length Muscle length 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  10. 10. Decreased ventricular contractility systolic dysfunction 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  11. 11. Decreased Contractility = ventricular systolic dysfunction Considering normal preload, afterload and ventricular compliance LVESPVR 150 c-d= stroke volume 130-50= 80 d d’ 50 Isovolemic contraction c isovolemic relaxation LV Pressure 100 a a’ c-d’= stroke volume 130-80= 50 LVESDVR b LV volume 50 80 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  12. 12. Decreased Contractility = ventricular systolic dysfunction Increased LVESV: decreased SV and EF EF or FS dependent on Preload Contractility afterload Increased LV end systolic volume with Normal or decreased afterload 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  13. 13. Decreased Contractility = ventricular systolic dysfunction Compensatoryresponse of Nature c-d’= stroke volume 130-80= 50 LVESPVR 150 d’ 100 LV Pressure Increased SVR Increased MSFP Increased VR Increased LVEDV Increased HR c c’ c’-d’= stroke volume 150-80= 70 50 a’ b b’ LVESDVR Increased O2 cost Pulmonary oedema LV volume 50 80 130 150 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  14. 14. Decreased Contractility = ventricular systolic dysfunction Causes: Acute Myocardial ischemia Myocardial Intracelluar Acidosis Decreased affinity of Calcium to contractile proteins 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  15. 15. Decreased Contractility = ventricular systolic dysfunction Causes: Acute Respiratory acidosis causes intracelluar acidosis Significantly decreases contractility at PaCO2 level of 60 Chronic respiratoryacidosis leads to metabolic compensation leading to nearly normal intracellular pH Metabolic acidosis Less effect as minimal change in intracellular pH Only metabolic anions permeate cell membrane Organic anions like lactate, ketoacides do not easliy cross cell membrane Lactic acidosis begins to depress contractility at pH 7.1 to 7.2 but even at pH 7.0 this depression is quiet small 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  16. 16. Decreased Contractility = ventricular systolic dysfunction Causes: Acute Ionized hypocalcemia Massive PRBC transfusion: citrate bind to Ca Lactic acid also binds to Ca Bicarbonate infusion also decreased Ca Hypokalemia or hyperkalemia Hypomagnesimia hypophosphatemia Bicarbonate infusion Increases PaCO2: decreases intracellular pH Increased lactic acid production: by increasing rate limiting step of glycolysis Decreases ionized Calcium 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  17. 17. Decreased Contractility = ventricular systolic dysfunction Causes: Acute Proinflammatory cytokines TNF ᾳ, IL 1, 2, 6 Increased NO production Reactive oxygen intermediates Released by leucocytes 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  18. 18. Decreased Contractility = ventricular systolic dysfunction Causes: Chronic Idiopathic Coronary arterydisease Inflammatory: viral, toxoplasmosis, chagas disease Alcoholic Infective: HIV Postpartum Uremic Diabetic Nutritional deficiency: selenium deficiency Metabolic disorders: fabry disease, Gaucher disease Toxic: Adriamycin, cobalt 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  19. 19. Decreased Contractility = ventricular systolic dysfunction Management Correcting acute reversible causes Ishemia Acidosis Dyselectrolytemia hypothermia 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  20. 20. Decreased Contractility = ventricular systolic dysfunction Management Increasing PRELOAD Increasing CONTRACTILITY Decreasing AFTERLOAD 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  21. 21. Increasing preload increasing MSFP: increasing Stress volume Increased venous tone by sympathetic nervous system Fluid retention by kidneys Volume optimization 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  22. 22. Increasing preload increasing MSFP 12 Guytonian Cardiac function Curve 10 Cardiac output 8 6 4 2 -5 0 5 10 15 20 25 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD Pra
  23. 23. Increasing preload increasing MSFP LVESPVR 150 c-d= stroke volume 130-80= 50 d’ LV Pressure 100 c c’ c-d’= stroke volume 160-80= 80 50 b’ LVESDVR a’ b LV volume 50 80 130 160 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  24. 24. Increasing preload increasing MSFP Can be increased by Fluid crystalloid vs colloid Safety margin: interstitial oedema vasopressures 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  25. 25. Increasing preload increasing ventricular compliance Increasing EDV without further increase in EDP Stress relaxation of pericardium and myocardium Usual response in dilated cardiomyopathies In septic shock patients, response of surviving patients is increasing ventricular diastolic compliance 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  26. 26. Heart in sepsis, Textbook of Critical Care Medicine, Shoemaker 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  27. 27. Increasing preload increasing ventricular compliance LVESPVR 150 c-d= stroke volume 130-80= 50 d’ LV Pressure 100 c c’ c-d’= stroke volume 160-80= 80 50 LVESDVR a’ b LVESDVR’ b’ LV volume 50 80 130 160 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  28. 28. Increasing preload increasing ventricular compliance: double edged sword parietal pericardium has high extensibility at lowlevel of stretch with an abrupt transition to relative inextensibility at higher stretch. Pericardium acts as limiting membrane, restricting cardiac filling at high intracardiac volume Therfore decreasing ventricular compliance: diastolic dysfunction 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  29. 29. Pericardial P- V curve of dead canine heart Ppc vs intracardiac volume Intracardiac Pericardial disease, P.S. Reddy Donald F.Leon, James A.Shaver, Raven Press , 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  30. 30. Pericardial P- V curve of isolated dog heart Role of pericardium Intact pericardium ----Intrapericardial volume …Intracardiac volume Pericardium removed ( intracardiac volume) Pericardial disease, P.S. Reddy Donald F.Leon, James A.Shaver, Raven Press , 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  31. 31. Increasing preload increase Pra = increase Ppc = Pulmonary odema Ponc = 21 21 21 21 21 Ppc = 15 13 11 9 7 Ppc-Ponc = -6 -8 -10 -12 -14 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  32. 32. Increasing preload at normal s.albumin and normal pulmonary capillary permeability pulmonary starts to develop at Ppaw value of 20-25 mmHg In critically ill patients s. albumin is decreased and pulmonary capillary permeability Is increased Pulmonary oedema will develop at lower Ppaw Ppaw has many reasons to increase in critically ill patients Optimal Ppaw has to be identifies which leads to increased stroke volume With minimal or no pulmonary oedema formation 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  33. 33. Increasing preload In critically ill patients without previous cardiac dysfunction major factor limiting cardiac output is limited venous return Limited venous return Increased venous capacitance: increase unstressed volume Positive pressure ventilation Ventricular diastolic dysfunction Venous return can be increased with Ionotropes and vasopressors: increase MSFP and decreased resistance to VR Volume expansion: increasing stressed volume Benefit and safety margin of vasopressor vs volume expansion has to be evaluated To avoid ineffective flogging of empty heart To avoid flooding of lungs and interstitial tissues 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  34. 34. Decreased Contractility = ventricular systolic dysfunction Increasing contractility LVESPVR 150 c-d’= stroke volume 130-80= 50 LV Pressure 100 d’’ d’ c-d= stroke volume 130-50= 80 c 50 LVESDVR b a’’ a’ LV volume 50 80 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  35. 35. Decreased Contractility = ventricular systolic dysfunction Decreasing afterload LVESPVR 150 c-d’= stroke volume 130-80= 50 LV Pressure 100 d’’ d’ c c’ c-d’’= stroke volume 130-55= 75 50 LVESDVR a’ a’’ b LV volume 55 50 80 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  36. 36. Decreased ventricular compliance diastolic dysfunction 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  37. 37. Decreased ventricular compliance: diastolic dysfunction LVESPVR 150 c-d= stroke volume 130-50= 80 LV Pressure 100 d c’ c’-d= stroke volume 100-50= 50 c LVESDVR’ 50 b’ a LVESDVR b LV volume 50 100 130 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  38. 38. Decreased ventricular compliance: diastolic dysfunction End diastolic volume decreased: decreased SV and EF EF or FS dependent on Preload Contractility afterload decreased LV end diastolic volume with Normal or increased Pra/ LVEDP 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  39. 39. Decreased ventricular compliance: diastolic dysfunction In the absence of Echocardiography Should be suspected when decreased LV pump function is not responding to fluid expansion/ vasopressors, ionotropic agents and reduction of afterload Cardiac output is unusually sensitive to changes in heart rate Late diastolic filling of LV is small in stiff LV little contribution in EDV by this phase Increase in HR has less impact on reduction in EDV and therefore SV Increase in HR, increases C.O. ( CO= SV *HR) 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  40. 40. Decreased ventricular compliance: diastolic dysfunction Causes: Acute Myocardial ischemia delayed systolic relaxation leading to stiffness Diastolic stiffness precedes depressed contractility Increased intrathoracic pressure Increased intrapericardial pressure positive pressure ventilation, pneumothorax, massive pleural effusion Increased intraperitoneal pressure Catecholemines and calcium infusion hypothermia 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  41. 41. Decreased ventricular compliance: diastolic dysfunction Causes: Chronic Concentric ventricular hypertrophy HOCM Restrictive CMP Constrictive pericarditis 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  42. 42. Decreased ventricular compliance: diastolic dysfunction Management: Treatment of causes Ischemia, pneumothorax Increased pleural, pericardial, abdominal pressures Optimized intrathoracic pressure in PPV patients: lowtidal ventilation strategy Identify Optimal filling pressures that maximizes LVEDV without causing substantial pulmonary odema Optimizes volume status correct hypovolemia aggressively and promptly not overlooking safety margin Optimize Ionotropes and vasopressor doses smallest dose that achieves desired systolic and vascular effect Tachycardia, arrhythmias should be treated early Hypothermia should be avoided 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  43. 43. The Right Ventricle 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  44. 44. Some facts right ventricle is thin walled pump, with large radius of curvature Built for lowpressure system: afterload Right venricle contraction moves sequentially from apex to pulmonary outflowtract like peristaltic pump During diastole RV at normal diastolic pressure lies belowits stressed volume allowing it to increase preload 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  45. 45. RV incrased afterload acute • Pulmonaryembolism • Hypoxic pulmonary vasoconstriction • Acidemic pulmonary vasoconstriction • ARDS • Sepsis • Positive pressure ventilation Chronic • Chronic hypoventilation • Recurrent pulmonary embolism • PPH • Chronically elevated LA pressure: MS, LVF 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  46. 46. RV incrased afterload Management • Management of acute cause • Management of ventricular interdependence Decrease parallel coupling of LV and RV 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  47. 47. Some facts to remember In heart failure, evidence of dependent pulmonary crackles on physical examination, suggest that LV filling pressure is elevated, usually to more than 20-25mmHg. However in Chronic heart failure crackles may not be heard even at Pla more than 30 mmHg as pulmonary lymphatic drainage is increased. Interstitial odema clearance lags decrease in Pla by hours, so rapid decrease in Pla is not accuratelyreflected by pulmonary auscultation. Even before diuresis is established, frusemide reduces Pla by a venodilatory effect and also reduced intrapulmonary shunt 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  48. 48. “The success of intensive care is not, therefore, to be measured only by the statistics of survival, as though each death were a medical failure. It is to be measured by the quality of lives preserved or restored; and by the quality of the dying of those in whose interest it is to die; and by the quality of human relationships involved in each death.” Gordon Dunstan 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD
  49. 49. THANK YOU 8EDLGXU 5DKDPDQ 6HQLRU 5HVLGHQW ULWLFDO DUH 0HGLFLQH 6*3*,06 /XFNQRZ ,QGLD

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