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Cardiovascular System I. Objectives. Present the clinical features and emergency management of cardiovascular disorders, including: Recognize congenital and acquired heart disease. Outline management of ductal dependent lesions. Identify patients with myocarditis.

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  • Present the clinical features and emergency management of cardiovascular disorders, including:
    • Recognize congenital and acquired heart disease.
    • Outline management of ductal dependent lesions.
    • Identify patients with myocarditis.
congenital heart disease recognition and stabilization
Congenital Heart Disease: Recognition and Stabilization
  • Rapid cardiopulmonary assessment to recognize and manage life-threatening illness caused by heart disease
  • Understand the physiology of different conditions to optimize treatment plans.
critical concepts
Critical Concepts
  • Dysrhythmias can cause serious cardiovascular compromise.
  • Structural congenital heart disease can present in many different ways at many different ages.
  • Acquired heart disease can be subtle yet life-threatening.
case study 1 rapid breathing
Case Study 1:“Rapid Breathing”
  • 10-day-old infant is brought to ED by mother for rapid breathing and not eating well.
  • Product of normal spontaneous vaginal delivery
    • Spent 2 days with mother in hospital
    • Uneventful course, including circumcision
    • Birth weight 3.2 kg
case study 1 continued
Case Study 1 (continued)
  • Slow to breastfeed since birth
  • Would gasp and cry after sucking for a short time. Difficulty feeding.
  • 3 to 4 wet diapers per day
  • No congestion, no fever
  • No vomiting with feedings
  • 2 yellow seedy stools since passing meconium after birth
initial assessment 1 of 2
Initial Assessment (1 of 2)


  • Abnormal appearance, abnormal breathing, abnormal circulation

Vital signs:

  • HR 170, RR 70, BP 82/40, T 37°C (rectal), Wt 3.4 kg, O2 sat 90% on room air
initial assessment 2 of 2
Initial Assessment (2 of 2)

A: No evidence of obstruction

B: Elevated RR and labored

C: Pale, diaphoretic, tachycardia, weak pulse, cyanosis

D: GCS grossly normal but in distress and inconsolable

E: No signs of head injury, fractures, or bruising

detailed physical exam
Detailed Physical Exam
  • Lung sounds equal bilaterally with rales in both bases
  • Hyperactive precordium with a gallop rhythm
  • Pulses weak in distal and lower extremities
  • Distended abdomen with liver palpable 4 cm below right costal margin

What is your general impression of this patient?

general impression
General Impression
  • Impending cardiopulmonary failure (compensated shock)
    • Cyanosis, diaphoresis
    • Pale, tachycardia

What are your initial management priorities?

management priorities 1 of 3
Management Priorities (1 of 3)
  • ABCs
  • Give 15L O2 by nonrebreather mask or 100% O2 by BMV, or perform endotracheal intubation.
  • Start IV, obtain blood glucose.
  • ECG and monitor rhythm on cardiac monitor
  • CXR
  • Administer fluid challenge: 10 cc/kg NS
management priorities 2 of 3
Management Priorities (2 of 3)
  • Administer prostaglandin E1 (PGE1):
    • 0.05 to 0.1 mcg/kg/min
    • Intubate to protect against apnea and relieve stress from work of breathing.
  • Consider furosemide (0.5 to 1 mg/kg).
  • Sepsis work-up and then antibiotics
    • Defer lumbar puncture.
management priorities 3 of 3
Management Priorities (3 of 3)
  • Cardiology consultation or transfer to pediatric cardiology center emergently:
    • Echocardiogram
  • If blood pressure and perfusion do not improve, add inotropic agent:
    • Dobutamine: 2 to 20 mcg/kg/min
    • Epinephrine: 0.1 to 1.5 mcg/kg/min
case discussion 1 of 2
Case Discussion (1 of 2)
  • This infant is in CHF.
    • Poor feeding and easy fatigability
    • Gallop rhythm and enlarged liver
    • Diminished pulses
  • Shock:
    • Altered mental status, compensated shock (tachycardia, diaphoresis, respiratory distress, normal BP in upper extremities)
case discussion 2 of 2
Case Discussion (2 of 2)
  • Possible ductal dependent lesion:
    • Right age for presentation of shock triggered by closure of the ductus arteriosus
    • Measure blood pressure in four extremities
    • Assess oxygenation response to supplemental oxygen
case progression version 1
Case Progression: Version 1
  • BP differential noted in lower extremities.
  • Oxygenation improves to 99% with supplemental oxygen.
  • CXR shows cardiomegaly and pulmonary edema.
  • Echocardiogram demonstrates coarctation of the aorta.
  • Infant improves with PGE1 infusion, diuretics, and inotropes.
case progression version 2
Case Progression: Version 2
  • Oxygenation fails to improve with supplemental oxygen (remains 90%).
  • Oxygenation declines further to <80%.
  • CXR is nonspecific.
  • Echocardiogram demonstrates transposition of the great vessels.
  • Infant improves with PGE1 infusion.
  • Surgical intervention is scheduled.
background structural congenital heart disease
Background: Structural Congenital Heart Disease
  • Congenital heart disease: 5 to 8 cases per 1,000 live births
  • Child with congenital anomaly usually does not show cardiovascular problems in utero.
  • Changes at birth place great stress on infant’s cardiovascular system.
  • Some cyanotic heart conditions are highly dependent on shunting through ductus arteriosus. Closure can be terminal event.
clinical features your first clue
Clinical Features: Your First Clue
  • Age
  • Progressive deterioration (mild) followed by suddenly progressing to critical condition
  • Cyanosis
  • Congestive Heart Failure (CHF)
  • Consider concurrent sepsis
diagnostic studies 1 of 3
Diagnostic Studies (1 of 3)
  • Radiology:
    • Pulmonary hypoperfusion: pulmonic stenosis, TOF, TA
    • CHF (if large VSD present to allow high-output failure, e.g., increased right-sided flow)
    • Some classic CXR appearances (more classic if condition is permitted to worsen):
      • TGA: Egg on side
      • TAPVR: Snowman
      • TOF: Boot shaped
diagnostic studies 2 of 3
Diagnostic Studies (2 of 3)
  • ECG:
    • Right axis (RVH): Normal for newborns
    • Left axis: Hypoplastic right heart, tricuspid atresia, endocardial cushion defect (AV canal)
    • ST-T changes, strain, ischemia
    • Dysrhythmia
    • Prolonged QT
    • Low voltage
diagnostic studies 3 of 3
Diagnostic Studies (3 of 3)
  • Laboratory:
    • Glucose: Any child in distress needs to have hypoglycemia excluded.
    • CBC: Look for anemia, signs of sepsis.
    • Electrolytes: Congenital adrenal hyperplasia, salt-wasting form
    • Arterial blood gas: Hyperoxia text
fetal circulation 1 of 2
Fetal Circulation (1 of 2)
  • Placenta oxygenates blood and returns to right atrium (RA) via IVC.
  • Preferentially shunts across FO to LA.
  • LV ejects most oxygenated blood to carotids and coronaries.
fetal circulation 2 of 2
Fetal Circulation (2 of 2)
  • Superior vena cava (SVC) returns deoxygenated blood to RA where it mixes with oxygenated blood from the placenta.
  • Preferentially enters RV.
  • RV ejects into PA.
  • No pulmonary capillary flow, so PA is shunted into the descending aorta via the ductus arteriosus.
differential diagnosis what else 1 of 2
Differential Diagnosis: What Else? (1 of 2)
  • Other cyanotic and acyanotic congenital structural heart disease
  • Ductal dependent coarctation
  • Hypothermia
  • Sepsis
differential diagnosis what else 2 of 2
Differential Diagnosis: What Else? (2 of 2)
  • Congenital adrenal hyperplasia (CAH)
  • Hypoglycemia
  • Shaken baby syndrome/intracranial lesion
  • Catastrophic gastrointestinal process, e.g., volvulus
normal cv system function
Normal CV System Function
  • Represented by vital signs (O2 sat included)
  • Factors affecting cardiac output (perfusion):
    • Heart rate
    • Stroke volume
    • Contractility
    • Vascular resistance
  • Children <8 years predominantly increase their HR to increase cardiac output (unable to increase stroke volume until >10 years).
normal vital signs for age
Normal Vital Signs For Age

HR RR BP (systolic)

Newborn 90-180 40-60 60-90

1 month 110-180 30-50 70-104

3 months 110-180 30-45 70-104

6 months 110-180 25-35 72-110

1 year 80-160 20-30 72-110

2 years 80-140 20-28 74-110

4 years 80-120 20-26 78-112

6 years 75-115 18-24 82-115

8 years 70-110 18-22 86-118

10 years 70-110 16-20 90-121

12 years 60-110 16-20 90-126

14 years 60-110 16-20 92-130

transition from fetal circulation
Transition from Fetal Circulation
  • Placental circulation is interrupted at birth:
    • Increase in systemic arterial blood pressure
    • Spontaneous respirations
  • Decreased pulmonary vascular resistance, increasing pulmonary blood flow
  • Foramen ovale closes.
  • Ductus arteriosus closes.
  • This initial rapid change slows down over first 24 hours of life.
cyanotic heart disease chd
Cyanotic Heart Disease (CHD)
  • Cyanotic: Refractory to oxygen
  • Right to left shunting
  • Some lesions (e.g., TGA) are highly dependent on a shunt (VSD, PDA)
  • Cyanosis usually presents shortly after birth.
cyanotic chd
Cyanotic CHD
  • 5 Ts:
    • Truncus arteriosus
    • Tetralogy of Fallot (TOF)
    • Transposition of the great arteries (TGA)
    • Tricuspid atresia
    • Total anomalous pulmonary venous return (TAPVR)
  • Severe aortic stenosis
  • Hypoplastic left heart
  • Severe coarctation of the aorta
tetralogy of fallot tof
Tetralogy of Fallot (TOF)
  • Pulmonic stenosis
  • Aortic override
  • VSD
  • RVH
  • Right-to-left shunting through VSD dependent on severity of pulmonic stenosis
tricuspid atresia
Tricuspid Atresia
  • RV is hypoplastic.
  • Right-to-left shunt through VSD
  • Respiratory disorder
  • Hemoglobin disorder
  • Acrocyanosis (normal newborns): Cold stress and peripheral vasoconstriction
  • Generalized or central cyanosis often due to cyanotic congenital heart disease. Often worsened by crying.
hyperoxia test
Hyperoxia Test
  • Administer 100% oxygen.
  • Significant increase in PaO2 seen with pulmonary and hemoglobin disorders.
  • In CHD, PaO2 will not increase or it will increase slightly.
    • Deoxygenated blood bypasses lungs and goes directly to left side of heart, diluting the fully oxygenated blood coming from lungs with deoxygenated blood.
  • Increased pulmonary vascularity:
    • Total anomalous pulmonary venous return
    • Truncus arteriosus
    • Transposition of the great arteries
    • Other complex lesions without pulmonic stenosis
  • Decreased pulmonary vascularity:
    • Tetralogy of Fallot
    • Ebstein’s anomaly
    • Hypoplastic right heart, tricuspid atresia
    • Complex lesions with pulmonic stenosis
prostaglandin e 1
Prostaglandin E1
  • Keeps the ductus open
  • 0.05 to 0.1 mcg/kg/min with an increase to 0.2 mcg/kg/min over several minutes
  • Side effects: Apnea, pulmonary congestion, fever, hypotension, seizures, and diarrhea
  • Consider elective intubation.
noncyanotic chd
Noncyanotic CHD
  • May present with CHF or heart murmurs heard during physical exam
  • Left-to-right shunts
    • Excess pulmonary vascularity
    • ASD, VSD, PDA
  • Obstructive lesions
    • Aortic stenosis, coarctation of the aorta, mitral stenosis, pulmonic stenosis
clinical features
Clinical Features
  • CHF: Tachypnea, tachycardia, diaphoresis, decreased feeding, hepatomegaly, murmurs, gallop rhythms, pulmonary edema
  • Decreased activity or poor sleeping with respiratory distress
diagnostic studies
Diagnostic Studies
  • CXR: Cardiomegaly, pulmonary vascular congestion
  • ECG: Abnormal axis, ST segment changes
  • Echocardiogram: Definitive anatomic diagnosis, degree of congestive heart failure (chamber sizes, contractility)
management of chf
Management of CHF
  • Give oxygen, assisted ventilation if needed.
  • Elevate head and shoulders 45 degrees.
  • Monitors, pulse oximetry
  • Obtain IV access.
  • Send laboratories.
  • CXR and ECG
  • Furosemide, nitroglycerin, digoxin
  • Inotropes (dobutamine) for signs of shock
case study 2 chest pain sob
Case Study 2:“Chest Pain, SOB”
  • 10-year-old boy presents with chief complaint of chest pain and shortness of breath.
  • 5 days of cold and cough symptoms
  • He has been lying around a lot and has missed 1 week of school.
    • Usually a very active child but complains that he is “just too tired” to play
initial assessment
Initial Assessment


  • Abnormal appearance, abnormal breathing, abnormal circulation

Vital signs:

  • HR 130, RR 44, BP 90/65, T 37.8°C, O2 sat 90% on room air, increases to 100% on O2
initial assessment50
Initial Assessment

A: Patent

B: Intermittently shallow and deep; rapid respiratory rate

C: Pale; pulse rapid, thready, and weak

D: No focal deficits, GCS 15

E: No signs of injury

focused history
Focused History

O: Chest hurts for several days.

P: Provoked by cough and exertion; short of breath whenever he gets up and walks

Q: Burning, pressure

R: Substernal, some radiation to shoulders

S: 3 to 8 out of 10

T: Pressure and SOB last almost all day, exacerbations with exertion last 15 to 30 min.

detailed physical exam52
Detailed Physical Exam
  • Neck: Jugular venous distention supine
  • Lungs: Diminished breath sounds with occasional end expiratory wheeze with deep breaths
  • Cardiac: Distant heart sounds, no murmurs, S3 gallop rhythm
  • Abdomen: Distended with palpable spleen and liver
  • Neuro: No focal deficits

What is your general impression of this patient?

What are your initial management priorities?

general impression54
General Impression
  • Child is in respiratory distress and in cardiogenic shock.
    • Demonstrates abnormal appearance with increased work of breathing and signs of shock.
management priorities
Management Priorities
  • ABCs
  • Give O2 by nonrebreather mask.
  • Obtain IV access.
  • Check rhythm on cardiac monitor.
  • Obtain blood glucose, lab studies.
  • Consider reducing preload and afterload with nitrates.
  • Consider diuretic therapy.
  • May need inotropic support.
case discussion differential diagnosis
Case Discussion:Differential Diagnosis
  • Acquired cardiac problem:
    • Respiratory illness during winter months causing secondary myocarditis
  • Congenital heart lesion that had been asymptomatic until this illness:
    • Anomalous coronary artery or valvular disease
  • Pericarditis
clinical features your first clue57
Clinical Features: Your First Clue
  • Consider myocarditis in any child with:
    • Weakness
    • SOB
    • Chest pain
    • Especially if associated with preceding prodromal viral illness
    • Distant heart sounds: “Silent Chest”
    • Enlarged heart on CXR
diagnostic studies myocarditis
Diagnostic Studies: Myocarditis
  • Radiology:
    • CXR will reveal cardiomegaly and prominent vasculature, perhaps even pulmonary edema
    • Laboratory:
      • May not add much
      • Not specific
differential diagnosis what else
Differential Diagnosis: What Else?
  • Pericarditis
  • Hypertensive crisis
  • Anomalous coronary artery and myocardial ischemia/infarction
  • Valvular disease
  • Structural cardiac disease (e.g., VSD, ASD)
  • Renal failure (e.g., glomerulonephritis)
  • Rheumatic fever
management myocarditis
Management: Myocarditis
  • Gentle diuretic therapy
  • Afterload reduction
  • Possibly inotropic support
  • Echocardiogram
    • Intrinsic cardiac lesion?
    • Muscle hypertrophy?
    • Pericardial effusion?
    • Decreased contractility?
case progression version 161
Case Progression: Version 1
  • CXR: Cardiomegaly
  • Echocardiogram: Poor cardiac contractility
  • Diagnosis: Myocarditis
  • Maintained on inotropes and pressor agents
  • Recovered to a point that he could be discharged 2 weeks later
  • Will be followed closely to assess the degree to which he regains cardiac function
case progression version 262
Case Progression: Version 2
  • CXR: Cardiomegaly
  • Echocardiogram: Poor cardiac contractility
  • Diagnosis: Myocarditis
  • Deteriorates in ED:
    • Progressive shock
    • Requires inotropic support
    • Develops V-tach and V-fib
    • Extracorporeal membrane oxygenation (ECMO)
  • Inflammatory disease of the myocardium:
    • Direct infection of the myocardium (e.g., viral myocarditis)
    • Toxin production (e.g., diphtheria)
    • Immune response as a delayed sequela of an infection (postviral or postinfectious myocarditis)
    • A common type of myocarditis is acute rheumatic fever (ARF).
acute rheumatic fever jones criteria
Acute Rheumatic Fever:Jones Criteria
  • Major criteria:
    • Carditis: Most commonly valvulitis
    • Migratory polyarthritis
    • Chorea, erythema marginatum, subcutaneous nodules
  • Minor criteria:
    • Fever, elevated CRP or ESR, prolonged PR interval, arthralgia
  • Pericardial inflammation
  • Viral versus bacterial
  • Bacterial causes include pneumococcus, S. aureus, H. influenzae type B
  • Cardiac tamponade possibly requiring pericardiocentesis
pericarditis clinical features
Pericarditis: Clinical Features
  • Chest pain
  • Respiratory distress, CHF, or tamponade
  • Precordial "knock" or rub (like the sound of shoes walking on snow)
  • The classic signs include exercise intolerance, fatigue, jugular distension, lower extremity edema, hepatomegaly, poor distal pulses, diminished heart tones, and pulsus paradoxus.
  • An infection of the endothelial surface of the heart, with a propensity for the valves
  • Increased risk in children with artificial valves and patches, and patients with central lines
  • 90% of cases are caused by gram-positive cocci.
    • Alpha strep, Staph aureus, pneumococcus, group A ß hemolytic streptococci
endocarditis clinical features
Endocarditis Clinical Features
  • Fever
  • Tachycardia, CHF, dysrhythmia, cardiogenic shock
  • History of recent cardiac surgery or indwelling vascular catheter
  • Heart murmur
  • Petechiae, septic emboli, or splenomegaly
kawasaki disease
Kawasaki Disease
  • Vasculitis: Propensity for coronary aneurysms
  • Aneurysms may subsequently scar, resulting in coronary stenosis (early onset coronary artery disease).
  • Coronary artery thrombosis and myocardial infarction
  • Myocarditis, dysrhythmia
kawasaki disease clinical features
Kawasaki Disease: Clinical Features
  • High fever
  • Conjunctivitis
  • Cervical lymphadenopathy
  • Gingivostomatitis
  • Polymorphous rash
  • Swelling of the hands with erythema of the palms
the bottom line
The Bottom Line
  • Assessment of congenital heart disease can be challenging; however, applying assessment skills with an understanding of normal physiology as well as pathophysiology of cardiovascular disorders in children will assist the clinician in management.