How to maintain optimal perfusion during Cardiopulmonary By-pass Herdono Poernomo, MD
Cardiopulmonary By-pass Target Physiologic condition as a healthy person Everything is in Normal Limit How to maintain normal limit during abnormal conditions? Compensate the non physiologic conditions Realized there is an abnormal conditions Need sensor and monitoring devices
Cardiopulmonary By-pass Maintain whole body perfusion CPB Monitoring Machine Human Effects and results Human physiology monitoring General monitoring Not specific? Organ selective Other organs?
Monitoring devices DO2 VO2 Flow MAP SvO2 NIRS EEG etc UOP Lactate Hct Hb ph CO2 O2
Critical organs Brain Heart Renal Splanic Optimal perfusion
Tissue perfusion monitoring End result Oxygenation metabolic marker tissue blood flow Global oxygenation Blood analisis ScvO2, delivery and uptake balance Lactate, inadequate oxygenation CO2, product of cellular respiration NADH fluorescence, oxidorecudtive status of mitochondria Laser Doppler, local tissue blood flow
Contact free tissue monitoring Hyperspectral imaging Near Infrared Spectroscopy
hyperspectral imaging technology in the Visible (VIS) Near infrared (NIR) high spectral and spatial resolution hemoglobin oxygenation (SpO 2 ) relative concentration of hemoglobin tissue hemoglobin index (THI) NIR-perfusion index
Maintain adequate perfusion Cannula placement and size 75 to 100 cc/kilo/min perfusion rate mean arterial pressures (60-70 mmhg) foreign blood along with hypotensive situations as with poor perfusions DIC and organ failure Hypokalemia (plasma and intracellular) Excessively high po2 (over 150) and/or excessively low pco2 (under 35) CNS aberrations
HUMAN BODY Maintain adequate perfusion
Factors of adequate perfusion Cardiac Vascular Microcirculatory Humoral
Cardiac Stroke volume: pre-load Afterload Contractility CPB machine Heart rate: sympathetic para-sympathetic Anesthetist
Factors of adequate perfusion Cardiac Vascular Microcirculatory Humoral
Vascular Resistence vessel length, blood viscosity and vessel radius Tone epinephrine and nor-epinephrine Local metabolic factors adenosine and prostaglandins low PO 2 (causing prostaglandin release) endothelial relaxing factor (nitric oxide, NO)
Microcirculatory leukocyte/platelet adhesion and coagulation can result in microvessel occlusion Flow colloid forces (tending to retain intravascular fluid volume) capillary hydrostatic pressure (tending to force fluid into extravacular space) Vasoconstriction of precapillary resistance vessels reduce capillary hydrostatic pressure vasoconstiction of postcapillary venules tend to increase hydrostatic pressure gradients hypoxic states, arteriolar metabolic effects may dominate causing precapillary vasodilation and with vasoconstriction of postcapillary venules, movement of fluid into extravascular spaces is favored. Tissue edema may be further worsened by circulating toxins which enhances capillary permeability. Intravascular plasma protein loss decreases oncotic (colloid) forces which causes additional intravascular fluid loss
Humoral CNS, cellular and immunological responses to shock cause an increase in levels of epinephrine and other catecholamines, renin, vasopressin, prostaglandins
Optimal setup Flow vs. Pressure optimal blood flow requirements optimal blood pressure needs venous saturation Haemoglobin lactate can be used as the markers of optimal perfusion
Optimal setup Flow Normothermic 2.2 2.5 L/min/m2 Hypothtermic 1.0 2.4 L/min/m2 MAP 65 100 mmhg SvO2, continuously monitored 75 percent Arterial blood gases, base deficit and lactate levels Every 30 mnts Arterial po2: 150 to 250 mmhg Alpha-stat management of arterial blood gases PaCO 35-45 mmhg and ph 7.35 7.45 Cerebral blood flow
Optimal setup Severe systemic vasodilation (vasoplegia) ACE inhibitors, heparin, calcium channel blockers, prebypass hemodynamic instability heparin anticoagulation ACT > 480 seconds Awareness during rewarming Benzodiazepine neuromuscular blocking agent 10% / *C Rewarming >30 C is limited to 0.5 C/minute
Urine output > 0.5 ml/kg per hour Hb > 7.5 g/dl (Hct > 22 %) Special Populations AR Anti-inflammatory steroids, statins Deep hypothermic circulatory arrest 16 to 18 C ph stat Cerebral embolization & edema
Inflammatory response Contact of blood with nonendothelial surfaces Platelet activation Decrease circulating coagulation factors Endothelial cells and leukocytes are activated capillary leakage and tissue edema myocardial dysfunction, Vasodilation, bleeding Hemodilution temporary or persistent anemia and coagulopathy
Conclusion CPB need several good monitoring devices Keep in physiologic conditions, or compensate it Ideal monitoring devices Localized Every organ Real time User friendly
Thank you