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Ehab Khairy

A 72-year-old female with diabetes underwent coronary angiography revealing multi-vessel disease. She underwent CABG with complications during protamine administration including pulmonary hypertension, RV failure, and cardiac arrest. Maximum inotropes and vasopressors were used to support blood pressure until protamine was finished, after which the patient developed ventricular arrhythmias and acidosis but ultimately survived after intensive care. The case highlights the complex hemodynamic effects of protamine and importance of strict protocols to manage complications.

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Name: Al SUFIANY RUZAIGAH Date of birth: 25/7/1941 Gender: Female Word: FS 434B
A 72-year-old female, with a history of diabetes mellitus, with no allergy. Coronary angiography revealed: LAD: tight lesion at the bifurcation with D1& D2 has tight ostial lesion. LCX: Diffusely disease. OM: Diffusely disease.
LV: Normal size and wall thickness Moderately impaired LV systolic function. Moderate global hypokinesia. EF= 40%. Other chambers and valves were normal.
Premedication: Pt was pre medicatated by P.O. valium 5 mg at midnight and 6 Am, plus 10 mg morphine on calling to OR. Arterial cannulation was done before induction of GA, while venous CVP and large bore cannula were inserted after smooth un eventual induction of
Maintenance of anesthesia was carried by Propofol, nimbex infusion, and supplemental titrated doses of midazolam, Fentanyl, and Morphine guided by BSI, and the operative steps. Heparin achieved satisfactory ACT result.
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Ventilator was kept on with - A low tidal volume 150 ML - FI02 50% - Frequency 12/min. Maintenance of Anesthesia by Propofol, Nimbex infusion, and supplemental of midazolam, Fentanyl,
Preparing adequate equivalent Protamine dose ready for infusion Preparing blood and its product. Adrenaline 50 n g started during the second proximal anastomosis. Reassume normal mechanical ventilation. Achieving HR. 108 and BP 130/ 80 CVP reading had a mean of 10. It was temporally elevated with the filling
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Insulin infusion together with K correction was the second natural inotropic to be administrated. Drop by drop Protamine started very slowly while Bp was 156/90. According to protocol; Platelets infusion started, and were to be followed by blood and FFP according to CVP reading guide and surgeon advice.
Blood pressure was gradually dropping and accordingly inotropic adrenaline does was increased to maximum 200 ng , Noradrenalin was administrated and also reached maximum 200 ng in order to keep the systolic Bp in the range of
When 遜 Protamine had been given, Anesthetist requested to discontinue protamine infusion, Surgeon insisted to finish Protamine before removing the aortic cannula. Maximum doses of nor and adrenaline infusion were able to maintain a
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Increasing insulin infusion to 6U/H Running maximum K infusion 40 MEq/hr Protamine was finished Considering NaHC03 for correction of acidosis. Discussing nitroglycerin infusion with the surgeon to lower the CVP reading,
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Despite Maximum inotrope and vasopressors Systolic BP started rapid dropping 120- 100- 80- till 67 mmHg RV Distension 40 mmHg reading of CVP Sluggish myocardial contractility Ventricular arrhythmia Bradycardia
Hyperventilation Inotropic and vasopressors kept maximum Bolus Adrenaline 1 mg Surgeon regretted, & incriminated nitroglycerine to be the cause of the catastrophe, and requested to administrate bolus 1 g Calcium chloride. Internal cardiac massage for less than 遜 min was effective to over come
Bp restored to 240/130 Development of ventricular arrhythmia necessitate bolus lidocaine followed by 2 mg /kg / hr infusion Marked acidosis necessitated administration of a total dose of 200
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Pt was weaned form IABP and Pacemaker and extubated successfully within 24 hr. Elevated Renal function tests were returned to normal with in 5 days.
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Protamine remains the mainstay drug for heparin neutralization during cardiac surgery. Frequently, protamine causes transient hypotension from histamine release, which is more apparent if rapidly injected
The systemic hypotension typically occurs secondary to poor LV filling associated with the severe RV dysfunction. In our case maximum inotropes and vasopressors were able to maintain BP and coronary perfusion till the
Protamine systemic hypotension mediated by: 1- Histamine release 2- Endothelium derived relaxing factor, i.e., NO This vasodilating effect is not observed in the presence of a heparin- protamine complex. Protamine-induced severe pulmonary
During CPB, complement activation takes place. The production of prostacyclin, a potent vasodilating prostaglandin, increases during the early stages of CPB, but decreases progressively during re warming and reperfusion of the lungs. The production vasoconstricting thromboxane A2 and B2 follows an opposite pattern, reaching the
Thromboxane are at their highest levels at the time of Protamine administration Acid-base interaction between protamine and heparin polyanionic polycationic interaction further more activate complement and potentiate the pulmonary vasoconstricting effect of thromboxane possibly aggravated by concomitant platelets administration.
Inotropic support of the failing myocardium may combine calcium with adrenaline in an attempt to augment the haemodynamic actions of each drug. Calcium blunts adrenaline induced increases in blood pressure and cardiac output in animals and human. Ca blunts epinephrine's beta- adrenergic actions in postoperative cardiac surgery patients.
During myocardial ischemia there is a Membrane depolarization Fall in ATP and loss of Rise in lactate excitability Decrease in intracellular pH Increase in the intracellular Ca which further consumes ATP. Membrane ionic pumps and Ventricular channels are disrupted fibrillation
The main causes of reperfusion injury following prolonged ischemia Cytosolic Ca2+ loading Exacerbate Generation of mitochondrial reactive oxygen species dysfunction
Ventricular fibrillation Myocardial stunning Loss of intracellular proteins Further Promoting an compromise inflammatory response the cardiac function Cytokine release Complement activation
1- Stop Protamine administration if it was not finished. 2- Re heparinization to decrease heparin-protamine complexes and stopping thromboxane release from macrophages 3- Hyper ventilation with 100% FI02 4- Maximum inotropic and vasopressors given through a left atrial catheter Why?
1- Inhaled: prostacyclin, nitric oxide. 2- Nitroglycerin, but it increases pulmonary shunt 3- Cyclic AMP-specific phosphodiesterase inhibitors e.g. milrinone amrinone, enoximone, but they result in systemic hypotension 4- Ketanserin
Nitroglycerine exerts a direct effect on the pulmonary circulation in doses that do not affect systemic resistance vessels or the myocardium and do not activate neurohumoral reflexes Uniquely it reduces pulmonary artery pressures in addition to pulmonary vascular resistance due to its ability to dilate venous capacitance vessels.
Ketanserin is a quinazoline derivative that selectively blocks S2-serotonergic receptors. it has 留1 receptor blocking and H1 histaminergic antagonistic properties. Unlike Nitroglycerine the use of I.V ketanserin 1.0 to 2.0 mg, over a period of 10 minutes, does not change, shunt fraction, does not block hypoxic
The fear of postoperative bleeding, the urge to transfuse blood products for haemostatic purposes, the over looking of the developing clinical status; were the reasons beyond all of these catastrophes happened in this case. Settled appropriate protocols for management of possible complications and sticking to it is much more prudent
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  • 3. Name: Al SUFIANY RUZAIGAH Date of birth: 25/7/1941 Gender: Female Word: FS 434B
  • 4. A 72-year-old female, with a history of diabetes mellitus, with no allergy. Coronary angiography revealed: LAD: tight lesion at the bifurcation with D1& D2 has tight ostial lesion. LCX: Diffusely disease. OM: Diffusely disease.
  • 5. LV: Normal size and wall thickness Moderately impaired LV systolic function. Moderate global hypokinesia. EF= 40%. Other chambers and valves were normal.
  • 6. Premedication: Pt was pre medicatated by P.O. valium 5 mg at midnight and 6 Am, plus 10 mg morphine on calling to OR. Arterial cannulation was done before induction of GA, while venous CVP and large bore cannula were inserted after smooth un eventual induction of
  • 7. Maintenance of anesthesia was carried by Propofol, nimbex infusion, and supplemental titrated doses of midazolam, Fentanyl, and Morphine guided by BSI, and the operative steps. Heparin achieved satisfactory ACT result.
  • 9. Ventilator was kept on with - A low tidal volume 150 ML - FI02 50% - Frequency 12/min. Maintenance of Anesthesia by Propofol, Nimbex infusion, and supplemental of midazolam, Fentanyl,
  • 10. Preparing adequate equivalent Protamine dose ready for infusion Preparing blood and its product. Adrenaline 50 n g started during the second proximal anastomosis. Reassume normal mechanical ventilation. Achieving HR. 108 and BP 130/ 80 CVP reading had a mean of 10. It was temporally elevated with the filling
  • 12. Insulin infusion together with K correction was the second natural inotropic to be administrated. Drop by drop Protamine started very slowly while Bp was 156/90. According to protocol; Platelets infusion started, and were to be followed by blood and FFP according to CVP reading guide and surgeon advice.
  • 13. Blood pressure was gradually dropping and accordingly inotropic adrenaline does was increased to maximum 200 ng , Noradrenalin was administrated and also reached maximum 200 ng in order to keep the systolic Bp in the range of
  • 14. When 遜 Protamine had been given, Anesthetist requested to discontinue protamine infusion, Surgeon insisted to finish Protamine before removing the aortic cannula. Maximum doses of nor and adrenaline infusion were able to maintain a
  • 16. Increasing insulin infusion to 6U/H Running maximum K infusion 40 MEq/hr Protamine was finished Considering NaHC03 for correction of acidosis. Discussing nitroglycerin infusion with the surgeon to lower the CVP reading,
  • 18. Despite Maximum inotrope and vasopressors Systolic BP started rapid dropping 120- 100- 80- till 67 mmHg RV Distension 40 mmHg reading of CVP Sluggish myocardial contractility Ventricular arrhythmia Bradycardia
  • 19. Hyperventilation Inotropic and vasopressors kept maximum Bolus Adrenaline 1 mg Surgeon regretted, & incriminated nitroglycerine to be the cause of the catastrophe, and requested to administrate bolus 1 g Calcium chloride. Internal cardiac massage for less than 遜 min was effective to over come
  • 20. Bp restored to 240/130 Development of ventricular arrhythmia necessitate bolus lidocaine followed by 2 mg /kg / hr infusion Marked acidosis necessitated administration of a total dose of 200
  • 22. Pt was weaned form IABP and Pacemaker and extubated successfully within 24 hr. Elevated Renal function tests were returned to normal with in 5 days.
  • 24. Protamine remains the mainstay drug for heparin neutralization during cardiac surgery. Frequently, protamine causes transient hypotension from histamine release, which is more apparent if rapidly injected
  • 25. The systemic hypotension typically occurs secondary to poor LV filling associated with the severe RV dysfunction. In our case maximum inotropes and vasopressors were able to maintain BP and coronary perfusion till the
  • 26. Protamine systemic hypotension mediated by: 1- Histamine release 2- Endothelium derived relaxing factor, i.e., NO This vasodilating effect is not observed in the presence of a heparin- protamine complex. Protamine-induced severe pulmonary
  • 27. During CPB, complement activation takes place. The production of prostacyclin, a potent vasodilating prostaglandin, increases during the early stages of CPB, but decreases progressively during re warming and reperfusion of the lungs. The production vasoconstricting thromboxane A2 and B2 follows an opposite pattern, reaching the
  • 28. Thromboxane are at their highest levels at the time of Protamine administration Acid-base interaction between protamine and heparin polyanionic polycationic interaction further more activate complement and potentiate the pulmonary vasoconstricting effect of thromboxane possibly aggravated by concomitant platelets administration.
  • 29. Inotropic support of the failing myocardium may combine calcium with adrenaline in an attempt to augment the haemodynamic actions of each drug. Calcium blunts adrenaline induced increases in blood pressure and cardiac output in animals and human. Ca blunts epinephrine's beta- adrenergic actions in postoperative cardiac surgery patients.
  • 30. During myocardial ischemia there is a Membrane depolarization Fall in ATP and loss of Rise in lactate excitability Decrease in intracellular pH Increase in the intracellular Ca which further consumes ATP. Membrane ionic pumps and Ventricular channels are disrupted fibrillation
  • 31. The main causes of reperfusion injury following prolonged ischemia Cytosolic Ca2+ loading Exacerbate Generation of mitochondrial reactive oxygen species dysfunction
  • 32. Ventricular fibrillation Myocardial stunning Loss of intracellular proteins Further Promoting an compromise inflammatory response the cardiac function Cytokine release Complement activation
  • 33. 1- Stop Protamine administration if it was not finished. 2- Re heparinization to decrease heparin-protamine complexes and stopping thromboxane release from macrophages 3- Hyper ventilation with 100% FI02 4- Maximum inotropic and vasopressors given through a left atrial catheter Why?
  • 34. 1- Inhaled: prostacyclin, nitric oxide. 2- Nitroglycerin, but it increases pulmonary shunt 3- Cyclic AMP-specific phosphodiesterase inhibitors e.g. milrinone amrinone, enoximone, but they result in systemic hypotension 4- Ketanserin
  • 35. Nitroglycerine exerts a direct effect on the pulmonary circulation in doses that do not affect systemic resistance vessels or the myocardium and do not activate neurohumoral reflexes Uniquely it reduces pulmonary artery pressures in addition to pulmonary vascular resistance due to its ability to dilate venous capacitance vessels.
  • 36. Ketanserin is a quinazoline derivative that selectively blocks S2-serotonergic receptors. it has 留1 receptor blocking and H1 histaminergic antagonistic properties. Unlike Nitroglycerine the use of I.V ketanserin 1.0 to 2.0 mg, over a period of 10 minutes, does not change, shunt fraction, does not block hypoxic
  • 37. The fear of postoperative bleeding, the urge to transfuse blood products for haemostatic purposes, the over looking of the developing clinical status; were the reasons beyond all of these catastrophes happened in this case. Settled appropriate protocols for management of possible complications and sticking to it is much more prudent