General Post Operative Management of the Child with Congenital Heart Disease The first 24 hours

1. General Post Operative Management of the Child with Congenital Heart DiseaseThe first 24 hours Pediatric Cardiac Intensive Care Unit Levine Children’s Hospital

2. Objectives • Understand importance of pre-op data for post-op management • Discuss the basic principles of cardiopulmonary bypass and its effects on post-op patients • Review essential information needed in handoff communication • Briefly review cardiac physiology • Review low cardiac output syndrome and treatment in the immediate post op period through a systems based approach

3. Before the patient arrives • Knowledge of the pre-op condition allows you to anticipate post-op problems • Pre-op anatomy • Pre-op physiology • Ex: L R shunt, PHTN, RVOT obstruction • Non cardiac problems • Ex: FTT, airway/vocal cord issues, genetic (ex: DiGeorge), feeding intolerance/dysfunction • PMH, medications, recent illness • Past surgeries and any complications • Pre-op studies • Cath data • EKG • CXR – most recent

4. In the OR…Cardiopulmonary Bypass • A mechanical means of circulating and oxygenating blood volume while diverting most of the circulation away from the cardiopulmonary system • Why do we use it? • Reduces metabolic rate and O2 consumption • Mandatory for brain and organ protection during circulatory arrest (maintains cellular ATP stores with low oxygen delivery) • Keeps the heart cold in-between cardioplegia doses • Surgical exposure: • decreased flow=decreased collateral blood flow back to the heart

5. Cardiopulmonary Bypass

6. Effects of CPB • Abnormal Circulatory Environment • Non-pulsatile arterial flow • Blood trauma - hemolysis • Hemodilution • Foreign surface exposure • Activates inflammatory mediators and coagulation pathways • General stress response • Systemic Inflammatory Response (SIRS) • Activation and interaction of many systems and cellular elements in the body • The complement system, neutrophils, cytokines, the arachidonic acid pathway, and the coagulation cascade • This response promotes increased capillary permeability and interstitial edema

7. OR to ICU Handoff • Very critical period involving both the transfer of the patient AND pertinent information • What do I need to know? • Surgical repair and times • Separation from CPB • Intubation/ventilation/oxygenation • Arrhythmias • Lines and tubes • Drugs: meds, product and ? reversal • Bleeding • Lab values and vitals during intraop period • Intraoperative ECHO (TEE) findings

8. Initial Assessment • Extremely important to know where you are starting from • Vital signs: • Temperature, Heart Rate, Blood Pressure, Saturation, NIRS • CVP, RA/LA/PA pressures • EKG Rhythm - ? pacing • Ventilator Settings and compliance • Cardiac and Respiratory Exam • ? Open sternum • Degree of cardiac support - inotropes? • Sedation and analgesia, muscle relaxation - pupil size/neuro exam • Bleeding: Chest tube losses and incision • CXR – eval lung fields, ett position, wires and tubes • Labs: • ABG, Lactate, CBC, BMP, Mag, Phos, iCa, coags, LFT, ?SvO2

9. Before we go further…Let’s Review Cardiac Physiology • What is the overall purpose of the heart? O2!

10. Oxygen Delivery Delivery of oxygen (DO2) is a direct function of cardiac output (CO) and arterial oxygen content (CaO2)

11. Cardiac Physiology • Cardiac output is the quantity of blood delivered to the systemic circulation per unit of time • Cardiac Output = Heart Rate x Stroke Volume • Stroke volume = Preload + afterload + contractility

12. Stroke Volume • Preload: • atrial filing pressure or volume of blood in ventricle during diastole, reflects circulating intravascular blood volume • Afterload: • impedance to ventricular emptying or resistance to ventricular ejection • Contractility: • intrinsic ability of the heart to contract independent of preload and afterload

13. The first 24 hours • What are we trying to achieve? • Maximize O2 delivery • Provide adequate end organ perfusion • Maintain BP The goal in all cases is to maximize oxygen delivery and perfusion at an acceptable blood pressure!!!!

14. Low Cardiac Output Syndrome • Clinical condition caused by transient decrease in systemic perfusion secondary to myocardial dysfunction • Outcome  imbalance between oxygen delivery and oxygen consumption at the cellular level which leads to metabolic acidosis • Occurs 9-16 hours post op • Predictable fall in CO and pulmonary function during the first 24 hours after neonatal and infant surgery

15. Low Cardiac Output Syndrome (LCOS) • Causes: • Residual/unrecognized defects • Continuation of pre-op ventricular dysfunction • Myocardial dysfunction related to circulatory arrest, hypothermia, aortic cross-clamp time, reperfusion injury • Inflammatory response triggered by CPB • Changes in SVR/PVR • Type of surgical repair - ventriculotomy • Complication of surgery (compromised coronary artery perfusion) • Dysrhythmia • Cardiac tamponade • Pulmonary hypertension (especially without intra atrial or ventricular communization)

16. Signs of LCOS • Systemic vasoconstriction • Poor perfusion, cold extremities, weak pulses • Resting tachycardia • Oliguria • Pulmonary venous congestion • Rales/rhonci • Systemic venous congestion • Hepataomegaly, anasarca, ascites • Hypotension

17. Signs of LCOS • Lab/monitoring findings: • Lactic acidemia • Metabolic acidosis • Azotemia • Decreased creatinine clearance • Rising serum K+ • Arterial waveform: blunted upstroke • RAP/CVP: decreased with hypovolemia, increased with ventricular dysfunction and cardiac tamponade • Mixed venous sats: decreased with increased O2 extraction • Decrease in NIRS TREATMENT IS DIRECTED AT THE CAUSE!

18. Cardiac • Low preload: • Causes: • Decreased venous return due to fluid loss or insufficient volume replacement with postoperative bleeding • Vasodilation with re-warming • Third spacing of fluids related to a systemic vascular response after CPB or diuresis • Treatment: volume (albumin 5%, NS or blood product)

19. Cardiac • High Afterload: • With increasing afterload, shortening is decreased and slowed • Causes: • Increase in PVR or SVR may be triggered by acidosis, hypoxemia, pain, hypothermia • SVR increase as compensatory mechanism of low cardiac output state • Residual RV or LV outflow tract obstruction • Reactive pulmonary bed in neonates • Afterload reduction increases fiber shortening • Decreasing afterload helps the heart contract • Tx: Avoidance of known etiologies, ventilation manipulation for PVR, vasodilating agents to decrease SVR

20. Cardiac • Depressed Contractility • Secondary to myocardial injury during CPB and aortic cross clamp • Myocardial edema • Optimize arterial oxygen saturation • Treat anemia and acidemia • Inotropes • Milrinone, epinephrine, dopamine • Reduce myocardial O2 consumption

21. Hemostasis • Platelet dysfunction and coagulation abnormalities occur post CPB • All patients are coagulopathic • Correction with appropriate blood product • Platelets, FFP, cryoprecipitate, factor VII • Hemoglobin/Hematocrit • Identify source of low Hgb/Hct • Monitor incision line and CT sites • Adequate hematocrit important for CaO2 • Use cell saver for volume expansion if available • Maintain HCT 40mg/dl for cyanotic lesions • Bleeding • Expect CT output to be sanguinous then serous • Chest tube losses should not be >3 cc/kg/hr for 3 hours OR > 5cc/kg/hr total • Notify CT surgery for pulsatile bright red blood or > 10cc/kg/hr for several hours • Be wary of abrupt stop to CT output!!

22. Effusion and Tamponade • Pericardial Effusion • Accumulation of fluid in pericardial sac • S/S: Muffled heart sounds, rub, low voltage on EKG • May see increased heart size on CXR • ECHO indicated to make diagnosis • Puts patient at risk for cardiac tamponade • Cardiac Tamponade: results from persistent surgical bleeding not properly drained by chest tubes • Tachycardia, hypotension, increased CVP, narrowed pulse pressure • Treated with urgent decompression of the cardiac space • Response to volume and inotropes is minimal

23. Arrhythmias • Post op cardiac patients always at risk • Increased with certain surgeries • Sinus bradycardia or tachycardia may be detrimental in post op patients with little reserve • Look at HR and rhythm • Bradycardia • Thorough investigation to unmask secondary causes of bradycardia (meds, hypoxia, hypoglycemia, electrolytes, increased ICP, hypothyroidism) • Injury to sinus node (fontan or atrial switch) • May need pacing or chronotropic agents • Tachycardia • Will increase myocardial consumption • Etiology: pain, fever, agitation, CHF, hypovolemia, conduction disturbance • Junctional ectopic tachycardia (JET) • Occurs early in post-op period • Treatment with cooling, sedation, paralysis • Avoid inotropes, correct electrolyte abnormalities and acidosis • Pacing to restore AV synchrony if possible • Amiodarone/Procainamide

24. Respiratory • Gas exchanged compromised due to: • Endothelial dysfunction • Left ventricular failure • Pulmonary edema related to fluid overload • Residual intracardiac shunt • Inadequate L heart decompression • Microatelectasis due to CPB lung collapse • Muscle weakness due to prolonged intubation/sedatives • Secretions • Phrenic nerve injury • Pre-op lung status

25. Respiratory • Ventilation management will vary based on type of lesion and surgical repair • Who should be kept intubated? • Long pump runs • Poor function • Hemodynamically unstable • Pulmonary hypertension • Who should be extubated quickly? • Passive pulmonary blood flow (Glenn, Fontan) • Know what sats are supposed to be!!!

26. Pulmonary Hypertension • Acute rise in pulmonary artery pressure followed by a decrease in CO and O2 saturations • Exacerbated by • Alveolar hypoxia, hypothermia, hypercarbia, acidosis, alpha adrenergic agents • Best treatment prevention!! • Adequate analgesia and sedation/paralysis? • Hyperoxia • Low PEEP • Alkalosis • Avoidance of measures which exacerbate PVR • Inhaled NO • IV vasodilators

27. Renal • Acute Tubular Necrosis (ATN) due to hypothermia, low flow or circulatory arrest, hypotension, decreased CO • Decrease in urine output due to decrease GFR and SIADH • As ADH surge resolves  improved response to diuretics • Monitor: • Adequate urine output • Goal >1ml/kg/hr • Evidence of adequate solute excretions • K<5 mEq/L • BUN <40 mg/dL • Creatinine < 1 mg/dL • Optimize preload • Adjust renal meds and protein in HAL accordingly • Response to lasix after 1st 12 hours • Bolus vs. continuous • If inadequate--> think 2nd agent

28. Metabolic System • Fluids restricted to 2/3 maintenance • Unless shunt or non CPB cases • Accurate I/O’s • Monitor electrolytes and acid-base status closely • Treat metabolic acidosis if base deficit >5 • Lactic acedemia in LCOS may ensue poor cerebral and intestinal perfusion • Treatment aimed at improving CO • Avoid hypo/hyperglycemia • Avoid post op hypothermia • Interference with hemostasis and coagulopathy • Follow CT output closely • ?albumin/total protien

29. GI • Adequate caloric intake is essential • 120-150 kcal/kg/day • Parenteral nutrition when enteral may be delayed • Gastric/ulcer prophylaxis • Enteral feeding individualized • Follow wt. gain (at least 20 g/day) • Monitor for s/s GER, delayed swallowing • May need supplemental tube feedings • Single ventricle defects, coarctation of aorta, arch abnormalities typically fed VERY SLOW for increased risk of NEC • Monitor for NEC when feeding: • S/S: abdominal distention/discoloration, guiac + stools, metabolic acidosis, thrombocytopenia, pneumotosis intestinalas • Tx: NPO, serial KUB and blood cx, wide spectrum abx

30. Neuro • Should respond appropriately for the level of sedation without evidence of neurologic defects • Monitor NIRS: Cerebral O2 sats (combined cerebral arterial and venous vascular beds) • VERY HELPFUL TO DETECT CEREBRAL HYPOXIA DURING LCOS • Incidence of central nervous system anomalies increased in patients with congenital heart defects • CPB risk for cerebral dysfunction due to: • Inadequate perfusion • Hypotension or low flow state • Embolization of air or other matter • Exposure to heparinization • Monitor for seizure activity in immediate post op period • May require EEG and video monitoring • Treat with anticonvulsant therapy • Lorazepam, Fosphenytoin, Phenobarbital (follow levels)

31. Infection • All patients who have been on CPB are functionally immune suppressed • Consider sepsis in pts with hemodynamic instability refractory to usual measures • Consider adrenal stimulation testing • Anti-staphylococcal therapy for all patients • Preventive strategies • Sterile technique • Deintensify ASAP • Handwashing • Cohorting colonized/infected patients

32. In Summary… • Post op complications are direct result of severity of CHD, age at time of presentation, duration of CPB and type of surgical intervention • Successful post op management is team approach and depends upon a thorough knowledge of: • Anatomic diagnosis of the cardiac defect and preoperative findings • Pathophysiologic effects of the defect on the cardiopulmonary system and other organs • Details of the surgery, CPB and anesthesia • Understating LCOS and how it affects patient care • Data obtained from the physical exam, invasive/noninvasive monitoring and imaging

33. Thank You for your Attention! Questions?