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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.
Instructor Information
Begin discussion of assessment and management of a patient with compensated shock
and cardiopulmonary failure.
The child was slow to breastfeed since birth. He would gasp and cry after sucking for a
short time. Difficulty feeding. He had 3 to 4 wet diapers per day. There was no
congestion or fever. He had no vomiting with feedings. He had two yellow seedy stools
since passing meconium after birth.
The child is ill-appearing, in respiratory distress, fussy, and has a weak cry. Additionally,
there is nasal flaring and occasional grunting. The child is pale, cyanotic centrally and in
all extremities, and sweaty to touch.
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Cardiovascular System I
• Weight: 3.4 kg
• Oxygen saturation: 90% on room air
Initial assessment:
• A: No evidence of obstruction.
• B: Elevated respiratory rate and labored.
• C: Pale, diaphoretic, tachycardia, weak pulse, cyanosis.
• D: Glasgow Coma Scale (GCS) grossly normal but in distress and inconsolable.
• E: No signs of head injury, fractures, or bruising.
Key Questions
What is your general impression of this patient?
Key Questions
What are your initial management priorities?
Critical Actions
ABCs.
Give 15L oxygen by nonrebreather mask or 100% oxygen by bag-mask ventilation
(BMV), or perform endotracheal intubation.
Start an IV and obtain blood glucose.
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Cardiovascular System I
If blood pressure and perfusion do not improve, add an inotropic agent, such as:
• Dobutamine: 2 to 20 mcg/kg/min
• Epinephrine: 0.1 to 1.5 mcg/kg/min
Case Development
This infant is in congestive heart failure (CHF):
• Poor feeding and easy fatigability
• Gallop rhythm and enlarged liver
• Diminished pulses
The infant is in shock, showing altered mental status and compensated shock
(tachycardia, diaphoresis, respiratory distress, and normal blood pressure in upper
extremities).
Version 1:
A blood pressure differential is noted in the lower extremities.
Oxygenation improves to 99% with supplemental oxygen.
A chest radiograph shows cardiomegaly and pulmonary edema.
An echocardiogram demonstrates coarctation of the aorta.
The infant improves with PGE1 infusion, diuretics, and inotropes.
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Cardiovascular System I
Version 2:
Oxygenation fails to improve with supplemental oxygen (remains 90%).
Oxygenation declines further to <80%.
The chest radiograph is nonspecific.
An echocardiogram demonstrates transposition of the great vessels.
The infant improves with PGE1 infusion.
Surgical intervention is scheduled.
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Cardiovascular System I
• Left axis: Hypoplastic right heart, tricuspid atresia, endocardial cushion defect
(AV canal)
• ST-T changes, strain, ischemia
• Dysrhythmia
• Prolonged QT
• Low voltage
Oxygenated blood preferentially shunts across the foramen ovale (FO) to the left atrium
(LA).
The left ventricle ejects the most oxygenated blood to the 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.
The right ventricle (RV) pumps less oxygenated blood into the pulmonary artery (PA).
The pulmonary vascular bed is vasoconstricted, so most of the blood is shunted through
the ductus arterious to mix with the systemic arterial circulation in the descending aorta
(distal to the coronary and carotid arteries), thus delivering less oxygenated blood to the
rest of the systemic arterial circulation.
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Cardiovascular System I
A shunt between the left and right circulations is required to maintain sufficient
oxygenation. In the diagram, a ventricular septal defect (VSD) permits mixing between
the left and right ventricles to permit some oxygenated blood from the lungs to reach the
systemic circulation.
Without a VSD, the ductus arteriosus must remain patent to maintain sufficient
oxygenation. Once the ductus closes, oxygenation will markedly decline. Ductus patency
can be maintained with a prostaglandin E1 infusion.
Many physiological parameters such as the heart rate, stroke volume, mean arterial blood
pressure, and vascular resistance affect the cardiac output. Stroke volume is the quantity
of blood ejected from the heart with each contraction and is a function of the pumping
action of the ventricle, which is dependent on preload, afterload, and contractility of the
ventricle.
Infants and young children rely mainly on the heart rate to increase cardiac output, as
they have limited capacity to change stroke volume. Children older than 8 to 10 years of
age develop the capacity of adults to change the stroke volume and heart rate to improve
cardiac output. Oxygen delivery is the amount of oxygen delivered to the entire body per
minute and is an essential component for adequate cardiac function. If the oxygen
delivery falls for any reason, supplemental oxygen is required and/or the cardiac output
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Cardiovascular System I
must increase to maintain adequate oxygen delivery to the tissues. Oxygen delivery to the
tissues is determined by the amount of blood flow through the lungs, the arterial oxygen
content (dependent on oxygenation and hemoglobin concentration), and the cardiac
output. Without adequate delivery, the metabolic demand of tissues is not met and shock
(inadequate substrate delivery to meet metabolic demands) begins.
The newborn becomes hypoxic with the discontinuation of the placental flow that they
relied on in utero. This causes an increase in blood pressure, heart rate, and the start of
spontaneous respirations. The respirations help decrease pulmonary vascular resistance
and increase the pulmonary blood flow.
The pulmonary artery pressure decreases and there is an increase in pulmonary venous
return and left atrial pressure, which closes the foramen ovale.
Finally, the increase in systemic arterial pressure and decrease in pulmonary artery
pressure cause flow through the ductus arteriosus to reverse.
This initial rapid change slows down over the first 24 hours of life and pulmonary artery
pressures continue to decrease toward adult levels over the next 6 weeks of life. Some of
this change in pressure is aided by the anatomic structure of pulmonary vessels in the
fetus and newborn, which have a thicker medial smooth muscle layer with increased
vasoreactivity.
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Cardiovascular System I
In children with structural congenital heart disease, the changes that occur at birth and the
interruption of intrauterine flow place great stress on the infant's cardiovascular system.
Oxygenation is not possible for the infant who relied on the extraneous shunting (in
utero) that they received from the ductus arteriosus.
The normal oxygen saturation on the right side is from 70% to 75% and on the left side
from 95% to 98%.
The infant shunts deoxygenated blood into the systemic circulation; this is called "right-
to-left shunting." Some cyanotic heart disease conditions are highly dependent on
shunting through the ductus arteriosus (e.g., transposition of great arteries [TGA]), in
which case complete closure of the ductus is a terminal event.
Cyanosis may present shortly after birth, when the ductus arteriosus begins to close.
The lesions most commonly seen that are cyanotic in presentation include the five Ts
(truncus arteriosus, tetralogy of Fallot, transposition of the great vessels, tricuspid atresia,
and total anomalous pulmonary venous return), severe aortic stenosis, hypoplastic left
heart, and severe coarctation of the aorta.
The degree of cyanosis and the severity of the TOF is largely dependent on the degree of
pulmonary blood flow achieved (and hence the severity of the pulmonic stenosis).
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Cardiovascular System I
Both right and left ventricles pump blood into a common outflow vessel (common trunk).
Right-to-left shunting occurs through an atrial septal defect (ASD), VSD, or patent ductus
arteriosis (PDA).
Normal newborns will have cyanosis of the hands and feet. This is called acrocyanosis
and is caused by cold stress and peripheral vasoconstriction.
In infants with respiratory and hemoglobin disorders, the PaO2 will increase significantly.
The child with a cyanotic heart disease from a significant right to left shunt will have a
low PaO2 to start, which will only increase slightly with 100% oxygen because
deoxygenated blood bypasses the lungs and goes directly to the left side of the heart. This
dilutes the fully oxygenated blood coming from the lungs with deoxygenated blood. The
oxygen saturation of the resultant mixture will never reach 100% (hence, PaO2 will never
rise significantly above 100 mm Hg despite 100% inspired oxygen).
This is called the hyperoxia test and may help to distinguish cyanotic heart disease from
respiratory causes, although severe respiratory illness may also result in low oxygen
saturation despite the application of oxygen.
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Cardiovascular System I
It is infused at 0.05 to 0.1 mcg/kg/min with an increase to 0.2 mcg/kg/min over several
minutes.
Side effects of the infusion include apnea, pulmonary congestion, fever, hypotension,
seizures, and diarrhea.
They may be divided into left-to-right shunts and obstructive lesions. The left-to-right
shunt lesions, which can show an increase in pulmonary circulation, include atrial septal
defects, ventricular septal defects, and patent ductus arteriosus.
Obstructive lesions include aortic stenosis, coarctation of the aorta, pulmonary stenosis,
and mitral stenosis.
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Cardiovascular System I
Most of these patients present during the first 6 months of life when the shunt or
obstruction overwhelms the cardiac compensation and function.
Clinical features include signs of congestive heart failure, such as tachypnea, tachycardia,
diaphoresis, decreased feeding, hepatomegaly, various systolic flow murmurs, and gallop
rhythms, depending on the specific lesion.
The child may present with decreased activity or poor sleeping with respiratory distress.
The chest radiograph will show an abnormal cardiac shadow or increased pulmonary
vascular flow.
The ECG may show an abnormal axis, QRS changes, ST segment changes, and chamber
enlargement.
The definitive testing is the two-dimensional echocardiogram that will define the
abnormality and the degree of congestive heart failure.
Critical Actions
Provide supplemental oxygen and assist ventilation as needed.
Elevate the head and shoulders about 45 degrees.
Place cardiorespiratory and pulse oximetry monitoring
Obtain IV access.
Send laboratories (electrolytes, blood urea nitrogen [BUN], creatinine, complete blood
count).
Obtain chest radiograph and ECG.
Administer furosemide, nitroglycerin, and digoxin.
Administer inotropic agent for signs of shock.
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Cardiovascular System I
Instructor Information
Begin discussion of a patient with respiratory distress and cardiogenic shock.
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
Key Questions
What is your general impression of this patient?
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Cardiovascular System I
Overall he demonstrates normal appearance, but increased work of breathing and signs of
shock.
Critical Actions
Check ABCs.
Give oxygen 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.
He may need inotropic support.
Case Development
He may have an acquired cardiac problem due to a respiratory illness during winter
months causing secondary myocarditis.
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Cardiovascular System I
A second possibility is a congenital heart lesion that had been asymptomatic until this
illness, such as an anomalous coronary artery or valvular disease.
Critical Actions
Management should include:
• Gentle diuretic therapy
• Afterload reduction
• Possibly inotropic support
• Echocardiogram
– Intrinsic cardiac lesion?
– Muscle hypertrophy?
– Pericardial effusion?
– Decreased contractility?
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Cardiovascular System I
Case Development
Myocarditis is a global infection/inflammation of the myocardium – the degree to which
each child is affected is variable. Two potential courses of the disease are described.
Version 1:
A chest radiograph reveals cardiomegaly.
The echocardiogram reveals poor cardiac contractility.
The diagnosis for this patient is myocarditis.
He is maintained on inotropes and pressor agents.
He recovered to a point that he could be discharged 2 weeks later.
Will be followed closely for years to assess the degree to which he regains cardiac
function
Version 2:
A chest radiograph reveals cardiomegaly.
The echocardiogram reveals poor cardiac contractility.
He is diagnosed with myocarditis.
His condition deteriorated in the ED, and he suffered progressive shock.
He required inotropic support but developed ventricular tachycardia and ventricular
fibrillation.
Talk students through the ventricular fibrillation algorithm. Discuss the AHA Guidelines
2000.
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Cardiovascular System I
Minor criteria include fever, elevated CRP or ESR, prolonged PR interval, and arthralgia.
Between visceral and parietal pericardium is a fluid layer to help protect the heart and its
contractility. The usual fluid volume in the pericardial sac is 10 to 30 mL. When there is
a sudden increase in fluid, or constriction of the pericardial sac, chamber-filling volume
is restricted, which results in stroke volume reduction and hypotension (a process known
as tamponade). This increases the end-diastolic pressure in the ventricle, which impairs
ventricular filling and the ejection volume. Cardiac tamponade may require
pericardiocentesis.
The most common etiology is infectious, with approximately 30% resulting from a
bacterial cause. The most common viral etiology is Coxsackie virus. Other causes include
autoimmune disease, trauma, and neoplasms. The most common cause of constrictive
pericarditis is tuberculosis. Other bacterial causes of pericarditis include pneumococci,
staphylococci, and Haemophilus influenzae pericarditis.
Clinical features:
Clinically, the child may present with chest pain and respiratory distress.
If they have altered cardiac function from either an increase in pericardial fluid or
constriction of the pericardial sac, they will present with signs of congestive heart failure
as well as a 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.
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Cardiovascular System I
Endocarditis is an infection of the endothelial surface of the heart, with a propensity for
the valves.
Clinical features:
Patients typically present with fever, tachycardia, and signs of cardiac failure or
dysrhythmia with a history of recent cardiac surgery or indwelling vascular catheter.
Other signs include myalgias, heart murmur or petechiae, septic emboli, or splenomegaly.
They may present with signs indistinguishable from myocarditis with poor cardiac
contractility and inadequate perfusion with cool extremities, or symptoms similar to
pericarditis, with pain in addition to congestive heart failure.
The etiology is unknown, but it is seen most often in children less than 5 years of age,
during the winter and spring months, and with boys more susceptible than girls. There is
also a predilection for Asian and African children.
These patients may present with cardiac abnormalities that present in similar manner to
children with decreased myocardial contractility, myocarditis, or coronary insufficiency.
The child may present or go on to develop congestive heart failure and shock with chest
pain. Without treatment, 15% to 20% of children with Kawasaki disease will develop
coronary artery aneurysms within 1 to 3 weeks from the onset of illness, which can
eventually lead to a myocardial infarction or ischemia-induced dysrhythmias.
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Cardiovascular System I
A child that presents with a myocardial infarction may have more nonspecific findings
than an adult. They can present with nausea, vomiting, and abdominal pain. They may be
diaphoretic and crying, or asymptomatic.
Clinical features:
Clinically, the child presents with a history of fever for 5 days or more. The diagnostic
criteria are the presence of conjunctivitis, cervical lymphadenopathy, gingivostomatitis,
maculopapular exanthem (called polymorphous, which means that it can have many
different patterns), and swelling of the hands with erythema of the palms.
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