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Arsalan Khan
Other Co-operations:
Guahar Rahman and Rahat Ullah
BS Anesthesia
3rd batch, 6th semester, IPMS, KMU.
 Technique that takeovers the cardiac and pulmonary
function during open heart surgeries.
 Maintains circulation and oxygenation.
 Certain patho-physiologies are involved in CPB during
pregnancy.
 Hypothermia
 Hemodilution
 Inhibition of coagulation
 Complement activation
 Non- pulsatile flow
 Acid base changes
 Much more chances of poor neonatal outcomes.
 Maternal out comes are similar to those in non-pregnant
women’s cardiac surgeries.
 10-15% of maternal mortality, if cardiac disease during
pregnancy is untreated.
 With maternal CPB, 16-33% of fetal mortality.
 60-80% pregnant women with rheumatic heart disease, in
low income countries.
 Optimization of maternal cardiovascular status.
 Preop. Fetal monitoring.
 Optimization of CPB machine.
 Delivery of viable fetus before operation.
 During second trimester, elective cardiac surgery.
 Cardiac valve disease
 Prosthetic valve malfunction
 Cardiac myxoma
 Congenital heart disease
 Pulmonary embolism
 Aneurism
 Coronary artery disease
 Fetal arterial blood is not fully saturated.
 Hb in fetal blood is 65 % saturated b/c of arteriovenous mixture.
 Oxy-fetal Hb dissociation curve shifts to left.
 Improves placental uptake.
 But still dissociation is somehow restricted.
 Develops early fetal distress.
 fetal cardiac output, pH and maternal hematocrit are to be maintained.
 Fetal cardiac output is rate dependent i.e. fetal bradycardia leads to fetal distress
immediately.
 placental function is dependent on maternal and fetal circulation both.
 sustained uterine contraction, decreased uterine blood flow and intervillous
perfusion results feto-placental insufficiency, leading to fetal hypoxia.
 After 30-60 min. of removal of CPB progressive acidosis due to increase in placental
vascular resistance by activation of eicosoid products.
 Low CO, secondary to fetal SVR due to increased catecholamine due to fetal
manipulation during surgery, anesthesia and fetal hypo perfusion.
 Hemodilution due to;
 Decreased O2 content
 Physiological anemia during pregnancy
 Also depends on maternal hematocrit
 CPB results in low placental flow and pressure
 Worsened by hypothermia
 Results in impaired placental perfusion and respirator gas exchange
 Hence, increase CPB flow rates
 Administer sympathomimetics i.e. ephedrine and phynlephrine
(safe in pregnancy)
 This will maintain perfusion pressure and improve placental
perfusion
 Avoid vasoconstrictors.
 Pump flow rate, type of flow and MAP during CPB mostly
influences fetal oxygenation.
 Vasodilators are used to overcome placental vascular
resistance.
 Non-pulsatile flow increases SVR in fetus.
 Lactate level are stable in pulsatile flow, while increases
continuously in non-pulsatile flow.
 Intra-aortic balloon pump electively used with CPB to
change non-pulsatile into pulsatile flow.
 Mild hypothermia can be tolerated by fetus.
 Severe hypothermia leads to arrhythmias and cardiac arrest
with 24% fetal mortality.
 0% fetal mortality with normothermic flow.
 Warm cardioplegic flow is preferred.
 Cardioplegic solution increases potassium level, which
diffuses into fetal circulation.
 High level of potassium will cause cardiac arrest.
 It is maintained by keeping the level <5mmol/L.
 High flow, high pressure, normothermic and a short CPB to
maintain placental homeostasis. ( best choices )
 Hemodilution disturbs drug pharmacology.
 Increased variability of unbound drug.
 Transfer to fetus across placenta occurs as per drug conc.
gradient from maternal to fetal circulation.
 And transfer also depends on placental membrane
characteristics.
 All inhalational/some IV agents are lipid soluble, so easily cross
placental barrier, showing effects on fetus as well.
 Volatiles are potent uterine relaxants so decreases uterine blood
flow.
 Studies have shown that most adverse maternal and fetal
outcomes are not due to anesthetics but due to CPB and
underlying cardiac status of mother.
 Cardiopulmonary bypass in pregnancy
 Annals of Cardiac Anesthesia. Vol. 17:1 Jan-Mar/2014
CPB during pregnancy and Anesthesia considration by Arsalan

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CPB during pregnancy and Anesthesia considration by Arsalan

  • 1. Arsalan Khan Other Co-operations: Guahar Rahman and Rahat Ullah BS Anesthesia 3rd batch, 6th semester, IPMS, KMU.
  • 2.  Technique that takeovers the cardiac and pulmonary function during open heart surgeries.  Maintains circulation and oxygenation.  Certain patho-physiologies are involved in CPB during pregnancy.  Hypothermia  Hemodilution  Inhibition of coagulation  Complement activation  Non- pulsatile flow  Acid base changes
  • 3.  Much more chances of poor neonatal outcomes.  Maternal out comes are similar to those in non-pregnant women’s cardiac surgeries.  10-15% of maternal mortality, if cardiac disease during pregnancy is untreated.  With maternal CPB, 16-33% of fetal mortality.  60-80% pregnant women with rheumatic heart disease, in low income countries.
  • 4.  Optimization of maternal cardiovascular status.  Preop. Fetal monitoring.  Optimization of CPB machine.  Delivery of viable fetus before operation.  During second trimester, elective cardiac surgery.
  • 5.  Cardiac valve disease  Prosthetic valve malfunction  Cardiac myxoma  Congenital heart disease  Pulmonary embolism  Aneurism  Coronary artery disease
  • 6.  Fetal arterial blood is not fully saturated.  Hb in fetal blood is 65 % saturated b/c of arteriovenous mixture.  Oxy-fetal Hb dissociation curve shifts to left.  Improves placental uptake.  But still dissociation is somehow restricted.  Develops early fetal distress.  fetal cardiac output, pH and maternal hematocrit are to be maintained.  Fetal cardiac output is rate dependent i.e. fetal bradycardia leads to fetal distress immediately.  placental function is dependent on maternal and fetal circulation both.  sustained uterine contraction, decreased uterine blood flow and intervillous perfusion results feto-placental insufficiency, leading to fetal hypoxia.  After 30-60 min. of removal of CPB progressive acidosis due to increase in placental vascular resistance by activation of eicosoid products.  Low CO, secondary to fetal SVR due to increased catecholamine due to fetal manipulation during surgery, anesthesia and fetal hypo perfusion.
  • 7.  Hemodilution due to;  Decreased O2 content  Physiological anemia during pregnancy  Also depends on maternal hematocrit  CPB results in low placental flow and pressure  Worsened by hypothermia  Results in impaired placental perfusion and respirator gas exchange  Hence, increase CPB flow rates  Administer sympathomimetics i.e. ephedrine and phynlephrine (safe in pregnancy)  This will maintain perfusion pressure and improve placental perfusion
  • 8.  Avoid vasoconstrictors.  Pump flow rate, type of flow and MAP during CPB mostly influences fetal oxygenation.  Vasodilators are used to overcome placental vascular resistance.  Non-pulsatile flow increases SVR in fetus.  Lactate level are stable in pulsatile flow, while increases continuously in non-pulsatile flow.  Intra-aortic balloon pump electively used with CPB to change non-pulsatile into pulsatile flow.
  • 9.  Mild hypothermia can be tolerated by fetus.  Severe hypothermia leads to arrhythmias and cardiac arrest with 24% fetal mortality.  0% fetal mortality with normothermic flow.  Warm cardioplegic flow is preferred.  Cardioplegic solution increases potassium level, which diffuses into fetal circulation.  High level of potassium will cause cardiac arrest.  It is maintained by keeping the level <5mmol/L.  High flow, high pressure, normothermic and a short CPB to maintain placental homeostasis. ( best choices )
  • 10.  Hemodilution disturbs drug pharmacology.  Increased variability of unbound drug.  Transfer to fetus across placenta occurs as per drug conc. gradient from maternal to fetal circulation.  And transfer also depends on placental membrane characteristics.  All inhalational/some IV agents are lipid soluble, so easily cross placental barrier, showing effects on fetus as well.  Volatiles are potent uterine relaxants so decreases uterine blood flow.  Studies have shown that most adverse maternal and fetal outcomes are not due to anesthetics but due to CPB and underlying cardiac status of mother.
  • 11.  Cardiopulmonary bypass in pregnancy  Annals of Cardiac Anesthesia. Vol. 17:1 Jan-Mar/2014