Cardiovascular System I - PowerPoint PPT Presentation

• 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.

• Rapid cardiopulmonary assessment to recognize and manage life-threatening illness caused by heart disease
• Understand the physiology of different conditions to optimize treatment plans.

• 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.

• 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

• 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

PAT:

• 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

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

• 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?

• Impending cardiopulmonary failure (compensated shock)
• Cyanosis, diaphoresis
• Pale, tachycardia

What are your initial management priorities?

• 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

• 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.

• 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

• 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)

• 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

• 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.

• 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.

• 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.

• Age
• Progressive deterioration (mild) followed by suddenly progressing to critical condition
• Cyanosis
• Congestive Heart Failure (CHF)
• Consider concurrent sepsis

• 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

• 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

• 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

• 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.

• 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.

• Other cyanotic and acyanotic congenital structural heart disease
• Ductal dependent coarctation
• Hypothermia
• Sepsis
• TORCH

• Congenital adrenal hyperplasia (CAH)
• Hypoglycemia
• Shaken baby syndrome/intracranial lesion
• Catastrophic gastrointestinal process, e.g., volvulus

• 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).

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

• 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: 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.

• 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

• Pulmonic stenosis
• Aortic override
• VSD
• RVH
• Right-to-left shunting through VSD dependent on severity of pulmonic stenosis

• 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.

• 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

• 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.

• 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

• CHF: Tachypnea, tachycardia, diaphoresis, decreased feeding, hepatomegaly, murmurs, gallop rhythms, pulmonary edema
• Decreased activity or poor sleeping with respiratory distress

• CXR: Cardiomegaly, pulmonary vascular congestion
• ECG: Abnormal axis, ST segment changes
• Echocardiogram: Definitive anatomic diagnosis, degree of congestive heart failure (chamber sizes, contractility)

• 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

• 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

PAT:

• 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

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

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.

• 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?

• Child is in respiratory distress and in cardiogenic shock.
• Demonstrates abnormal appearance with increased work of breathing and signs of shock.

• 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.

• 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

• 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

• Radiology:
• CXR will reveal cardiomegaly and prominent vasculature, perhaps even pulmonary edema
• Laboratory:
• May not add much
• Not specific

• 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

• Gentle diuretic therapy
• Afterload reduction
• Possibly inotropic support
• Echocardiogram
• Intrinsic cardiac lesion?
• Muscle hypertrophy?
• Pericardial effusion?
• Decreased contractility?

• 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

• 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).

• 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

• 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

• Fever
• Tachycardia, CHF, dysrhythmia, cardiogenic shock
• History of recent cardiac surgery or indwelling vascular catheter
• Heart murmur
• Petechiae, septic emboli, or splenomegaly

• 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

• High fever
• Conjunctivitis
• Cervical lymphadenopathy
• Gingivostomatitis
• Polymorphous rash
• Swelling of the hands with erythema of the palms

• 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.