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
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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
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Knowledge of the pre-op condition allows you to anticipate postop problems
Pre-op anatomy
Pre-op physiology
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Non cardiac problems
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Ex: L R shunt, PHTN, RVOT obstruction
Ex: FTT, airway/vocal cord issues, genetic (ex: DiGeorge), feeding
intolerance/dysfunction
PMH, medications, recent illness
Past surgeries and any complications
Pre-op studies
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Cath data
EKG
CXR – most recent
In the OR…Cardiopulmonary
Bypass
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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
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Mandatory for brain and organ protection during
circulatory arrest (maintains cellular ATP stores with low
oxygen delivery)
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Keeps the heart cold in-between cardioplegia doses
Surgical exposure:
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decreased flow=decreased collateral blood flow back to
the heart
Cardiopulmonary Bypass
Effects of CPB
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Abnormal Circulatory Environment
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Non-pulsatile arterial flow
Blood trauma - hemolysis
Hemodilution
Foreign surface exposure
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Activates inflammatory mediators and coagulation pathways
General stress response
Systemic Inflammatory Response (SIRS)
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Activation and interaction of many systems and cellular
elements in the body
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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
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Very critical period involving both the transfer
of the patient AND pertinent information
What do I need to know?
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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
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Extremely important to know where you are starting from
Vital signs:
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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:
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ABG, Lactate, CBC, BMP, Mag, Phos, iCa,
coags, LFT, ?SvO2
Before we go further…Let’s Review
Cardiac Physiology
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What is the overall purpose of the heart?
O2 !
Oxygen Delivery
Oxygen Delivery
DO2= CO x CaO2
Cardiac Output =
Arterial Oxygen Content (CaO2)
Heart Rate x Stroke Volume
(Hgb x 1.34 x SaO2) + (0.003 x PaO2)
Delivery of oxygen (DO2) is a direct function of
cardiac output (CO) and arterial oxygen content
(CaO2)
Cardiac Physiology
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Cardiac output is the quantity of blood
delivered to the systemic circulation per
unit of time
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Cardiac Output = Heart Rate x Stroke
Volume
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Stroke volume = Preload + afterload +
contractility
Stroke Volume
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Preload:
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Afterload:
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atrial filing pressure or volume of blood in ventricle
during diastole, reflects circulating intravascular
blood volume
impedance to ventricular emptying or resistance to
ventricular ejection
Contractility:
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intrinsic ability of the heart to contract
independent of preload and afterload
The first 24 hours
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What are we trying to achieve?
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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
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Clinical condition caused by transient
decrease in systemic perfusion secondary to
myocardial dysfunction
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Outcome  imbalance between oxygen delivery
and oxygen consumption at the cellular level
which leads to metabolic acidosis
Occurs 9-16 hours post op
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Predictable fall in CO and pulmonary function
during the first 24 hours after neonatal and infant
surgery
Low Cardiac Output Syndrome
(LCOS)
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Causes:
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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
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Systemic vasoconstriction
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Resting tachycardia
Oliguria
Pulmonary venous congestion
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Poor perfusion, cold extremities, weak pulses
Rales/rhonci
Systemic venous congestion
 Hepataomegaly, anasarca, ascites
Hypotension
Signs of LCOS
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Lab/monitoring findings:
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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
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Low preload:
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Causes:
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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
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Treatment: volume (albumin 5%, NS or blood product)
Cardiac
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High Afterload:
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With increasing afterload, shortening is
decreased and slowed
Causes:
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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
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Tx: Avoidance of known etiologies, ventilation
manipulation for PVR, vasodilating agents to decrease
SVR
Cardiac
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Depressed Contractility
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Secondary to myocardial injury during CPB
and aortic cross clamp
Myocardial edema
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Optimize arterial oxygen saturation
Treat anemia and acidemia
Inotropes
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Milrinone, epinephrine, dopamine
Reduce myocardial O2 consumption
Hemostasis
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Platelet dysfunction and coagulation abnormalities occur post CPB
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All patients are coagulopathic
Correction with appropriate blood product
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Hemoglobin/Hematocrit
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Platelets, FFP, cryoprecipitate, factor VII
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
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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
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Pericardial Effusion
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Accumulation of fluid in pericardial sac
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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
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Tachycardia, hypotension, increased CVP, narrowed pulse
pressure
Treated with urgent decompression of the cardiac space
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Response to volume and inotropes is minimal
Arrhythmias
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Post op cardiac patients always at risk
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Increased with certain surgeries
Sinus bradycardia or tachycardia may be detrimental in post op
patients with little reserve
Look at HR and rhythm
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Bradycardia
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Tachycardia
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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
Will increase myocardial consumption
Etiology: pain, fever, agitation, CHF, hypovolemia, conduction disturbance
Junctional ectopic tachycardia (JET)
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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
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Gas exchanged compromised due to:
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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
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Ventilation management will vary based on
type of lesion and surgical repair
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Who should be kept intubated?
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Who should be extubated quickly?
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Long pump runs
Poor function
Hemodynamically unstable
Pulmonary hypertension
Passive pulmonary blood flow (Glenn, Fontan)
Know what sats are supposed to be!!!
Pulmonary Hypertension
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Acute rise in pulmonary artery pressure followed by a
decrease in CO and O2 saturations
Exacerbated by
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Alveolar hypoxia, hypothermia, hypercarbia, acidosis, alpha
adrenergic agents
Best treatment prevention!!
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Adequate analgesia and sedation/paralysis?
Hyperoxia
Low PEEP
Alkalosis
Avoidance of measures which exacerbate PVR
Inhaled NO
IV vasodilators
Renal
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Acute Tubular Necrosis (ATN) due to hypothermia, low flow or
circulatory arrest, hypotension, decreased CO
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Decrease in urine output due to decrease GFR and SIADH
As ADH surge resolves  improved response to diuretics
Monitor:
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Adequate urine output
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Evidence of adequate solute excretions
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Goal >1ml/kg/hr
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
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Bolus vs. continuous
If inadequate--> think 2nd agent
Metabolic System
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Fluids restricted to 2/3 maintenance
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Unless shunt or non CPB cases
Accurate I/O’s
Monitor electrolytes and acid-base status closely
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Treat metabolic acidosis if base deficit >5
Lactic acedemia in LCOS may ensue poor cerebral and
intestinal perfusion
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Avoid post op hypothermia
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Treatment aimed at improving CO
Avoid hypo/hyperglycemia
Interference with hemostasis and coagulopathy
Follow CT output closely
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?albumin/total protien
GI
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Adequate caloric intake is essential
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120-150 kcal/kg/day
Parenteral nutrition when enteral may be delayed
Gastric/ulcer prophylaxis
Enteral feeding individualized
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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
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Monitor for NEC when feeding:
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S/S: abdominal distention/discoloration, guiac + stools, metabolic
acidosis, thrombocytopenia, pneumotosis intestinalas
 Tx: NPO, serial KUB and blood cx, wide spectrum abx
Neuro
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Should respond appropriately for the level of sedation
without evidence of neurologic defects
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Monitor NIRS: Cerebral O2 sats (combined cerebral arterial and
venous vascular beds)
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Incidence of central nervous system anomalies increased
in patients with congenital heart defects
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CPB risk for cerebral dysfunction due to:
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VERY HELPFUL TO DETECT CEREBRAL HYPOXIA DURING LCOS
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
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May require EEG and video monitoring
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Treat with anticonvulsant therapy
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Lorazepam, Fosphenytoin, Phenobarbital (follow levels)
Infection
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All patients who have been on CPB are functionally
immune suppressed
Consider sepsis in pts with hemodynamic instability
refractory to usual measures
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Consider adrenal stimulation testing
Anti-staphylococcal therapy for all patients
Preventive strategies
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Sterile technique
Deintensify ASAP
Handwashing
Cohorting colonized/infected patients
In Summary…
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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:
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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?