650 likes | 1.58k Views
General Post Operative Management of the Child with Congenital Heart Disease The first 24 hours. Pediatric Cardiac Intensive Care Unit Levine Children’s Hospital. Objectives. Understand importance of pre-op data for post-op management
E N D
General Post Operative Management of the Child with Congenital Heart DiseaseThe first 24 hours Pediatric Cardiac Intensive Care Unit Levine Children’s Hospital
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
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
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
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
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
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
Before we go further…Let’s Review Cardiac Physiology • What is the overall purpose of the heart? O2!
Oxygen Delivery Delivery of oxygen (DO2) is a direct function of cardiac output (CO) and arterial oxygen content (CaO2)
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
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
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!!!!
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
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)
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
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!
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)
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
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
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!!
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
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
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
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!!!
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
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
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
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
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)
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
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
Thank You for your Attention! Questions?