Overview
Definition:
Low cardiac output syndrome (LCOS) in the pediatric postoperative period refers to a state where the heart is unable to generate sufficient cardiac output to meet the body's metabolic demands, leading to inadequate tissue perfusion
It is a common and serious complication following congenital or acquired cardiac surgery in children.
Epidemiology:
LCOS complicates approximately 10-30% of pediatric cardiac surgical procedures, with incidence varying based on the complexity of the surgery, patient's preoperative condition, and specific surgical techniques
Mortality rates can range from 5-20% depending on the severity and management.
Clinical Significance:
LCOS significantly increases morbidity and mortality in pediatric cardiac surgery patients
Early recognition and aggressive management are crucial to prevent irreversible organ damage, prolonged mechanical ventilation, and increased length of hospital stay, directly impacting patient outcomes and healthcare resource utilization.
Clinical Presentation
Symptoms:
Tachypnea
Increased work of breathing
Cool extremities
Mottled skin
Delayed capillary refill time (>3 seconds)
Decreased urine output (<1 ml/kg/hr)
Lethargy or irritability
Hypotension (may be a late sign).
Signs:
Worsening respiratory distress
Gallop rhythm (S3, S4)
Murmurs of new or worsening mitral/tricuspid regurgitation
Peripheral edema
Pulses: weak, thready, or absent peripheral pulses
Hepatojugular reflux
Ascites
Altered mental status
Persistent oliguria or anuria.
Diagnostic Criteria:
No single universally accepted criteria exist
Diagnosis is typically made based on a combination of clinical signs of inadequate tissue perfusion, abnormal hemodynamic parameters, and exclusion of other causes
Often defined by impaired cardiac index (<2.5 L/min/m²) with evidence of end-organ dysfunction.
Diagnostic Approach
History Taking:
Detailed surgical history: type of cardiac defect, duration of cardiopulmonary bypass, cross-clamp time, intraoperative complications
Preoperative cardiac function
Fluid balance
Urine output trends
Medications administered (vasopressors, inotropes).
Physical Examination:
Thorough cardiovascular exam focusing on heart sounds, peripheral pulses, capillary refill, and presence of edema
Respiratory assessment for work of breathing and air entry
Neurological assessment for mentation
Abdominal examination for hepatomegaly and ascites.
Investigations:
Arterial blood gas (ABG) with lactate: to assess tissue perfusion and metabolic acidosis
Complete blood count (CBC): to assess for anemia or infection
Serum electrolytes, BUN, creatinine: for renal function
Liver function tests (LFTs): for hepatic congestion
Echocardiography: essential for assessing ventricular function, valvular function, and intracardiac shunts
Central venous pressure (CVP) monitoring: to assess preload
Pulmonary artery catheterization (if available): for advanced hemodynamic monitoring (cardiac output, PVR, SVR)
Chest X-ray: to assess for cardiomegaly and pulmonary edema.
Differential Diagnosis:
Hypovolemia
Sepsis
Anemia
Tamponade
Residual shunts
Pulmonary hypertension
Arrhythmias
Myocardial stunning
Air embolism
Sepsis leading to myocardial depression.
Management
Initial Management:
Optimize preload: fluid boluses if hypovolemic, judicious fluid restriction if fluid overloaded
Optimize afterload: titrate vasoactive agents to maintain adequate mean arterial pressure (MAP) to perfuse vital organs
Optimize contractility: administer inotropic support
Ensure adequate oxygenation and ventilation
Correct electrolyte abnormalities and acid-base disturbances.
Medical Management:
Inotropes: Dopamine (2-10 mcg/kg/min), Dobutamine (2-10 mcg/kg/min), Milrinone (0.25-0.75 mcg/kg/min infusion)
Vasopressors: Epinephrine (0.01-0.1 mcg/kg/min), Norepinephrine (0.01-0.1 mcg/kg/min) if hypotension persists despite inotropes
Vasodilators: Sodium nitroprusside (0.5-10 mcg/kg/min) or Nitroglycerin (0.5-10 mcg/kg/min) for afterload reduction if afterload is elevated
Pulmonary vasodilators: Inhaled nitric oxide (iNO) or sildenafil for pulmonary hypertension
Sedation and analgesia to reduce metabolic demand.
Surgical Management:
Rarely indicated acutely for LCOS unless there is a correctable surgical lesion such as residual shunt, valvular dysfunction, or mechanical obstruction
Re-exploration for tamponade may be necessary.
Supportive Care:
Continuous hemodynamic monitoring (ECG, arterial line, central venous line)
Close monitoring of urine output
Mechanical ventilation as needed
Nutritional support (enteral or parenteral)
Pain and anxiety management
Strict fluid balance
Temperature control.
Complications
Early Complications:
Multi-organ dysfunction (renal failure, hepatic dysfunction, neurological deficits)
Arrhythmias
Myocardial ischemia
Pulmonary edema
Pleural effusions
Ascites
Sepsis.
Late Complications:
Chronic renal insufficiency
Growth and developmental delay
Neurodevelopmental deficits
Recurrent heart failure
Need for re-intervention.
Prevention Strategies:
Meticulous surgical technique
Minimizing cardiopulmonary bypass time
Careful fluid management
Early recognition and aggressive treatment of hemodynamic derangements
Optimal anesthetic management
Prompt treatment of hypothermia and acidosis.
Prognosis
Factors Affecting Prognosis:
Severity and duration of LCOS
Underlying cardiac defect complexity
Patient's preoperative physiological state
Presence of comorbidities
Promptness and appropriateness of management
Development of multi-organ dysfunction.
Outcomes:
With prompt and effective management, many children recover from LCOS and achieve good outcomes
However, severe or prolonged LCOS is associated with significant morbidity and mortality, leading to prolonged PICU stay and potential long-term sequelae.
Follow Up:
Regular cardiology follow-up is essential to monitor cardiac function, assess for complications, and manage any long-term sequelae
Developmental assessment and neurodevelopmental follow-up may be required for children with significant LCOS episodes.
Key Points
Exam Focus:
LCOS is a diagnosis of inadequate perfusion
Management is hemodynamic optimization: preload, afterload, contractility
Recognize LCOS early by signs of poor perfusion, not just hypotension
Milrinone and epinephrine are cornerstones of medical therapy
Echocardiography is vital for diagnosis and monitoring.
Clinical Pearls:
Always consider hypovolemia as a reversible cause of low cardiac output
Differentiate LCOS from pure vasodilation
Aggressive afterload reduction may worsen hypotension if contractility is severely impaired
Monitor trends in lactate, urine output, and mental status closely
Consider mechanical circulatory support (ECMO) for refractory LCOS.
Common Mistakes:
Attributing hypotension solely to vasodilation without assessing preload and contractility
Delaying initiation of inotropic support
Inadequate fluid resuscitation in the face of suspected hypovolemia
Over-reliance on single hemodynamic parameters
Failure to consider other causes of low cardiac output.