Bài giảng dành cho sinh viên y khoa, bác sĩ đa khoa, sau đại học. ĐH Y Dược TP Hồ Chí Minh. Introduction Definition Incidence Pathophysiology Causes and Risks factors Diagnosis Treatment
POSTOPERATIVE LOW CARDIAC OUTPUT SYNDROME Vu Minh Phuc MD CONTENTS Introduction Definition Incidence Pathophysiology Causes and Risks factors Diagnosis Treatment 1- INTRODUCTION Postoperative complications of cardiac surgery Cardiovascular subsystem Low cardiac output syndrome (LCOS) Cardiac arrest Arrhythmias Myocardial ischemia and infarction 1- INTRODUCTION Postoperative complications of cardiac surgery Pulmonary subsystem Atelectasis Bronchospasm Phrenic nerve injury Prolonged respiratory Insufficiency Acute respiratory distress syndrome Pneumothorax Pleural effusions 1- INTRODUCTION Postoperative complications of cardiac surgery Renal acute dysfunction Neuropsychological acute dysfunction Gastrointestinal subsystem Gastrointestinal bleeding Acute cholecystitis Acute pancreatitis Hepatic necrosis Intestinal necrosis Esophagitis Watery diarrhea Abdominal distention 1- INTRODUCTION Postoperative complications of cardiac surgery Endocrine subsystem Hematologic subsystem Immune subsystem 2- DEFINITION Significant LCOS following heart surgery is the following: the requirement for intra-aortic balloon counterpulsation or significant doses of inotropic drug support for longer than 30 minutes to maintain the systolic BP > 90 mmHg (70+2n) and the CI > 2.2 L/min/m2 3- INCIDENCE 10-20% of cardiac surgery patients Up to 25% in postoperation of dTGA Depends on cardiac lesion undergoing repair preoperative ventricular function adequacy of myocardial preservation during procedure adequacy of the surgical repair the 4- PATHOPHYSIOLOGY Cardiac output (CO) is the quantity of blood delivered to the systemic circulation per unit time CO (liters) = stroke volume (SV) × heart rate (HR) Cardiac index (CI) (L/min/m2) CI = CO/BSA normal CI in children at rest = 4-5 L/min/m2 normal CI in adults at rest = 2,5 L/min/m2 4- PATHOPHYSIOLOGY Determinants of cardiac output preload afterload myocardial contractility heart rate 4- PATHOPHYSIOLOGY Ventricular afterload is defined as systolic wall stress, the load that resists shortenning in the isolated papillary muscle Increased In afterload # decreased stroke volume the intact ventricle, afterload relate is related to Ventricular transmural pressure during systole Ventricular curvature, as determined by ventricular volume Ventricular wall thickness Shape of the ventricle 4- PATHOPHYSIOLOGY Ventricular afterload after cardiac surgery Changes in intraventricular pressure during systole # proximal aortic and pulmonary aterial systolic pressure Arterial hypertension: early postop Pulmonary hypertension Follow up ventricular afterload through Mean arterial blood pressure (intraarterial BP) Pulmonary aretrial pressure (echocardiogram) 4- PATHOPHYSIOLOGY Myocardial contractility after cardiac surgery The most important factor determining the incidence of postoperative LOCS Depends on Ventricular function prior to CPB Myocardial preservation during operation CPB time Follow up by echovardiogram 4- PATHOPHYSIOLOGY Heart rate: LCOS occurs in arrhythmias Sinus tachycadia Tachycardia arrhythmias Bradycardia arrhythmias 5- CAUSES – RISK FACTORS LCOS “Pre-factors” Surgical anatomy for correction Size of lesion Long standing pulmonary hypertension Congestive heart failure before surgery Ventricular function prior to CPB Others (probably have some effect) Nutritional status Previous infection 5- CAUSES – RISK FACTORS LCOS intra-operative factors CBP time (less is obviously better) also degree of hypothermia Aortic cross clamp time (less is obviously better) Residual Any lesions (size) ventricular dysfunction Arrhythmias 5- CAUSES – RISK FACTORS LCOS post operative factors Arrhythmias (heart rate) Inadequate filling pressure (preload) Inadequate inotropic support (myocardial contractility) Sepsis Significant Change lesions residual lesions NOT appreciated in OR in hemodynamics due to opening of new 6- DIAGNOSIS Clinical information about LCOS Mental status (limited by sedation, anesthesia, neuromuscular blockade and mechanical ventilation) Lethargy or Decreased responsiveness or Irritability Vital signs Core hyperthermia Tachycardia or bradycardia Tachypnea Hypotension Narrow pulse pressure 6- DIAGNOSIS Clinical information about LCOS Peripheral perfusion Cool temperature or pale color of skin in extremities Prolonged distal extremity capillary refill (>3 seconds) Poorly palpable pulses Cardiac impulse Abnormally increased Outflow tract obstruction Shunt lesion Decreased poor systolic dysfunction Liver size: enlarge, normal or small 6- DIAGNOSIS Bedside monitoring and laboratory data ECG : rhythm other than normal sinus? Arterial wave form : blunted upstroke, narrow pulse pressure RAP or CVP, LAP Low in hypovolemia High with Ventricular dysfuction Decreased ventricular compliance Cardiac tamponade Urine output < mL/kg/h 6- DIAGNOSIS Bedside monitoring and laboratory data Mixed venous O2 saturation < 65-70% because of Acid-base balance Increased arterial lactate concentration, > 2.2 mmol Metabolic acidosis on ABG Electrolyes Renal : hyperkalemia function : BUN, creatinine increase 6- DIAGNOSIS Bedside monitoring and laboratory data Chest X ray Cardiac enlargement Dilatation from decreased systolic function Large volume load Pericardial effusion Abnormal pulmonary blood flow Increased in large left-to-right shunt Decreased with severe pulmonary stenosis Pulmonary edema : elevated pulmonary venous pressure 6- DIAGNOSIS Bedside monitoring and laboratory data Transthoracic echocardiography or TEE with the following goals Throughly image all areas of haert manipulated during the operation Confirm the anatomic details of the operation Scan for any possible residual defects Shunts Valve stenosis or regurgitation Obstructed anastomosis Rate ventricular function Image for potential complications of the operation 7- TREATMENT Management of causes Mild to moderate hypotension Evaluate for significant residuel anatomic lesions Assess need for cardiac catheterization or reoperation Management the complication of LCOS Acidosis Electrolyte disturbances Renal dysfunction Coagulation dysfunction Hepatic dysfunction: D.I.C Gastrointestinal hemorrhage ↓ BP, ↓ CVP/RAP, ↓ PCWP, ↓ CI Fluid bolus, raise PCWP to 18 mmHG RESOLVED ↓ CI, ↑ PCWP, ↑ SVR CONTINUED LOW CI Neosynephrine Rhythm -Rate ↓ CI, ↑ PCWP ↑ CVP/RAP CVP/RAP normal = LV failure SBP > 90+2n or > 110 BP LOW, CI HIGH Rule ou and treat temponade SBP < 90+2n or < 110 RESOLVED Milrinone +/- NTG Epinephrine Dopamine Continued low CI BP low BP normal or high - Norepinephrine and NTG - Milrinone if BP allows Continued low CI ↓ CI, PCWP normal ↑ CVP/RAP = RV failure Volume loading - Dobutamine - Isoproterenol if rate allows - Adenosine - PGE1 - Nitric oxide - Consider IABP Milrinone +/- NTG IABP Continued low CI Consider LVAD +/- RAVD ... factors Diagnosis Treatment 1- INTRODUCTION Postoperative complications of cardiac surgery Cardiovascular subsystem Low cardiac output syndrome (LCOS) Cardiac arrest Arrhythmias Myocardial... INTRODUCTION Postoperative complications of cardiac surgery Endocrine subsystem Hematologic subsystem Immune subsystem 2- DEFINITION Significant LCOS following heart surgery is the following:... Milrinone +/- NTG Epinephrine Dopamine Continued low CI BP low BP normal or high - Norepinephrine and NTG - Milrinone if BP allows Continued low CI ↓ CI, PCWP normal ↑ CVP/RAP = RV failure Volume