Transcript APLS Cardiovascular 1

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.
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
• 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”
• 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)
• 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)
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
Initial Assessment (2 of 2)
A:
B:
C:
D:
E:
No evidence of obstruction
Elevated RR and labored
Pale, diaphoretic, tachycardia, weak
pulse, cyanosis
GCS grossly normal but in distress and
inconsolable
No signs of head injury, fractures, or
bruising
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
Question
What is your general impression of this
patient?
General Impression
• Impending cardiopulmonary failure
(compensated shock)
– Cyanosis, diaphoresis
– Pale, tachycardia
What are your initial management
priorities?
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)
• 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)
• 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)
• 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)
• 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
• 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
• 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
• 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
• Age
• Progressive deterioration (mild)
followed by suddenly progressing to
critical condition
• Cyanosis
• Congestive Heart Failure (CHF)
• Consider concurrent sepsis
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)
• 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)
• 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)
• 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)
• 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.
Coarctation of the Aorta (1 of 2)
Coarctation
of the Aorta
(2 of 2)
Transposition
of the Great
Arteries
Differential Diagnosis: What
Else? (1 of 2)
• Other cyanotic and acyanotic
congenital structural heart disease
• Ductal dependent coarctation
• Hypothermia
• Sepsis
• TORCH
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
• 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
Newborn
1 month
3 months
6 months
1 year
2 years
4 years
6 years
8 years
10 years
12 years
14 years
HR
90-180
110-180
110-180
110-180
80-160
80-140
80-120
75-115
70-110
70-110
60-110
60-110
RR
40-60
30-50
30-45
25-35
20-30
20-28
20-26
18-24
18-22
16-20
16-20
16-20
BP (systolic)
60-90
70-104
70-104
72-110
72-110
74-110
78-112
82-115
86-118
90-121
90-126
92-130
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: 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
• 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)
•
•
•
•
•
Pulmonic stenosis
Aortic override
VSD
RVH
Right-to-left
shunting through
VSD dependent
on severity of
pulmonic stenosis
Tricuspid
Atresia
• RV is
hypoplastic.
• Right-to-left
shunt
through
VSD
Total
Anomalous
Pulmonary
Venous
Return
(TAPVR)
Cyanosis
• 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.
Central Cyanosis vs.
Acrocyanosis
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.
CHD
• 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 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
• 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
• CHF: Tachypnea, tachycardia,
diaphoresis, decreased feeding,
hepatomegaly, murmurs, gallop
rhythms, pulmonary edema
• Decreased activity or poor sleeping
with respiratory distress
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
•
•
•
•
•
•
•
•
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”
• 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
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
Initial Assessment
A:
B:
C:
D:
E:
Patent
Intermittently shallow and deep;
rapid respiratory rate
Pale; pulse rapid, thready, and
weak
No focal deficits, GCS 15
No signs of injury
Focused History
O:
P:
Q:
R:
S:
T:
Chest hurts for several days.
Provoked by cough and exertion; short of
breath whenever he gets up and walks
Burning, pressure
Substernal, some radiation to shoulders
3 to 8 out of 10
Pressure and SOB last almost all day,
exacerbations with exertion last 15 to 30
min.
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
Question
What is your general impression of this
patient?
What are your initial management
priorities?
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
•
•
•
•
•
•
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
• 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 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
• Radiology:
– CXR will reveal
cardiomegaly
and prominent
vasculature,
perhaps even
pulmonary
edema
– Laboratory:
• May not add
much
• Not specific
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
•
•
•
•
Gentle diuretic therapy
Afterload reduction
Possibly inotropic support
Echocardiogram
–
–
–
–
Intrinsic cardiac lesion?
Muscle hypertrophy?
Pericardial effusion?
Decreased contractility?
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 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)
Myocarditis
• 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
• Major criteria:
– Carditis: Most commonly valvulitis
– Migratory polyarthritis
– Chorea, erythema marginatum,
subcutaneous nodules
• Minor criteria:
– Fever, elevated CRP or ESR, prolonged
PR interval, arthralgia
Pericarditis
• Pericardial inflammation
• Viral versus bacterial
• Bacterial causes include
pneumococcus, S. aureus, H.
influenzae type B
• Cardiac tamponade possibly requiring
pericardiocentesis
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.
Endocarditis
• 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
• Fever
• Tachycardia, CHF, dysrhythmia, cardiogenic
shock
• History of recent cardiac surgery or
indwelling vascular catheter
• Heart murmur
• Petechiae, septic emboli, or splenomegaly
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
•
•
•
•
•
•
High fever
Conjunctivitis
Cervical lymphadenopathy
Gingivostomatitis
Polymorphous rash
Swelling of the hands with erythema of
the palms
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.