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Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
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Chapter 5
Clinical Assessment of
Cardiovascular Structure,
Function, and Dysfunction
Patricia Bastero, MD, and Ronald Bronicki, MD
Key words: physical examination, radiography,
electrophysiology, echocardiography,
hemodynamics, biomarkers
Disclosures: The authors have not disclosed any potential
conflicts of interest.
Physical Examination
Although the physical examination is fundamental
in the diagnosis and management of cardiovascular
disease, studies in children and adults have demonstrated
significant discordance between estimations of cardiac
function and cardiac output based on the physical
examination and objective measurements. Additional
information can be obtained by the methods described
in this chapter and used in conjunction with the physical
examination in assessing cardiovascular function.
Table 1 on page 64 shows signs and symptoms of congenital
heart diseases by anatomical classification, and Table 2
on page 66 lists common clinical findings in acquired heart
diseases.
Radiographic Evaluation
Chest Radiograph
The chest radiograph is part of our routine assessment
of cardiopulmonary function in the ICU. A systematic
approach is important to retrieve the relevant diagnostic
information and focuses on heart size, heart shape, and
pulmonary vascular markings, contributing to the diagnosis
and the hemodynamic status.
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Chapter 5 | Comprehensive Critical Care: Pediatric
Table 1.
Signs and Symptoms of Congenital Heart Diseases by Anatomical Classification
Signs and Symptoms
Lesions
Left-Sided Obstructive Lesions and HLHS
CHF, circulatory collapse: pallor, mottling,
cool extremities, weak pulses, prolonged
capillary refill time, dyspnea, tachypnea,
poor feeding
Critical aortic stenosis, coarctation of the aorta, interrupted aortic arch,
HLHS
•Prostaglandin E–dependent lesion with symptoms becoming more
obvious when the ductus arteriosus closes
•Pulse difference between upper and lower limbs
•Possible differential cyanosis (ductus arteriosus supplying
deoxygenated blood to lower extremities)
Right-Sided Obstructive Lesions
Cyanosis with oligemia on chest
radiograph
Critical PS, hypoplastic right heart syndrome (eg, tricuspid atresia)
•PS: systolic murmur, second left intercostal space, radiates to neck
or back
Shunt Lesions
Left-to-right shunting: CHF, cardiomegaly,
hepatomegaly, pulmonary edema
(interstitial), lower airway obstruction,
flattened diaphragms, dyspnea, poor
feeding.
Right-to-left shunting: cyanosis
ASD, VSD, AVSD
ASD: shunt in diastole
•Wide split of S2 without respiratory variation, absent or minimal
murmur (systolic)
•RA dilation, RV overload, and pulmonary edema
VSD: shunt in systole
•Systolic murmur, LLSB
•LA enlargement, LV overload, pulmonary edema
•Pulmonary hypertension
Partial and total anomalous pulmonary venous drainage
•Obstructed: clinical emergency (severe early cyanosis)
•Unobstructed: right-to-left shunt, RA and RV dilation
•Partial: similar to ASD
Truncus arteriosus
•Biventricular pressure and volume overload
•Pulmonary overcirculation
•Mild cyanosis
•Risk for coronary ischemia
•More severe if truncal valve regurgitation or stenosis
Table 3 on page 66 lists cardiovascular silhouettes and their
related diagnoses, and Table 4 on page 67 relates lung fields
to diagnoses. Figure 1 on page 67 provides some examples of
characteristic chest radiographs.
Electrocardiography
The initial approach to a rhythm change or anomaly in
pediatric intensive care is not to discern the mechanism of
the cardiac arrhythmia but rather to determine whether it
has hemodynamic consequences.
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Table 1. Continued
Signs and Symptoms of Congenital Heart Diseases by Anatomical Classification
Signs and Symptoms
Lesions
Miscellaneous
Mitral valve lesions: Failure to thrive, recurrent pneumonias, tachypnea, chronic cough, wheeze
•Stenosis: LA enlargement, pulmonary venous hypertension, LCOS. Diastolic murmur at the apex.
•Regurgitation: CHF, LCOS with LA enlargement, LV overload, pulmonary venous hypertension. Systolic murmur,
apex with axillary irradiation.
ALCAPA
•Progressive ischemia and ventricular dilation with or without mitral regurgitation
•CHF, angina, sudden death
Ebstein anomaly
•Neonatal presentation: severe tricuspid regurgitation, compromised LV filling
•Cyanosis, with or without CHF, circulatory collapse, arrhythmias
Vascular rings and slings
•Tracheal compression
•Esophageal compression
•Stridor, wheeze, respiratory distress
•Feeding problems
Other Conotruncal Lesions
Dextro-transposition of the great arteries
Cyanosis (reverse differential cyanosis)
Abbreviations: ALCAPA, anomalous left coronary artery from the pulmonary artery; ASD, atrial septal defect;
AVSD, atrioventricular septal defect; CHF, congestive heart failure; HLHS, hypoplastic left heart syndrome; LA,
left atrium; LCOS, low cardiac output syndrome; LLSB, left lower sternal border; LV, left ventricle; MR, mitral
regurgitation; MS, mitral stenosis; PS, pulmonary stenosis; RA, right atrium; RV, right ventricle; VSD, ventricular
septal defect.
It is also important to differentiate true dysrhythmia
from artifact. In the ICU, pulse oximetry, central venous
pressure, and atrial and/or arterial pressure waveforms can
help in the diagnosis of dysrhythmias.
Table 5 on page 68 lists ECG characteristics of newborns.
Tables 6 through 12 on page 68 through page 71 summarize
some of the most common electrocardiographic (ECG)
alterations in cardiac disease.
Echocardiography
Echocardiography is a powerful tool used to diagnose
and monitor cardiac performance, cardiac disease, and
intrathoracic and extrathoracic abnormalities. Therefore,
focused, goal-directed echocardiography helps provide
high-quality care in the ICU.1
Hemodynamic assessment is a constant process in
critically ill patients. Echocardiography is a reliable tool
to interrogate pressures, ventricular systolic and diastolic
function, ventricular interaction, fluid status, and effusions.2
However, its use in the assessment of a dynamic process
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Table 2.
Common Clinical Findings in Acquired Heart Diseases
Diseases of the Myocardium
Myocarditis, dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy. Difficult to
differentiate based only on clinical findings most times. Common findings:
•Congestive heart failure: tachycardia, tachypnea, difficulty feeding, failure to thrive, cough, wheeze (left-sided,
cardiac asthma), palpitations (arrhythmia), edema, hepatomegaly, ascites and pleural effusions, dizziness
•Shock
•Sudden death
Diseases of the Pericardium
Pericarditis: chest pain (worsens with inspiration and cough, worse lying down), fever, discomfort, septic (bacterial
pericarditis), rub on auscultation
Pericardial effusion: tachycardia, tachypnea, poor perfusion, hepatomegaly, decreased cardiac sounds
Tamponade: pulsus paradoxus, tachycardia, tachypnea, hypotension, altered level of consciousness
Table 3.
Function
Specific Cardiovascular Silhouettes
Systolic
Silhouette
Diagnosis
Snowman sign
Total anomalous pulmonary
venous drainage
Narrow mediastinum
with “egg-shaped”
heart
Dextro-transposition of the
great arteries
“Boot-shaped” heart
Tetralogy of Fallot
Severe cardiomegaly
Anomalous left coronary
artery from pulmonary artery
is limited by the fact that echocardiographic studies are
intermittent.
Volume Status
Left ventricle end-diastolic volume and inferior vena cava
size, among others, can be used for preload assessment.
End-systolic cavity obliteration, or the “kissing papillary
muscle sign,” is a useful sign of hypovolemia. This is a
very sensitive predictor of decreases in the end-systolic
area (100%), but the specificity for predicting decrease in
preload is low (30%).3
There is no perfect measure for left ventricular (LV)
function due to its complex volumetric and geometric
functions. In addition, an assessment of ventricular ejection
is sensitive to changes in ventricular loading conditions.
The routinely used parameters to assess systolic function
are the ejection phase indices, ejection fraction (EF)
and fractional shortening (FS),4 derived from M-mode
calculations and analyzed in the parasternal long and/or
short axis. Normal average FS is about 28%.
The American Society of Echocardiography recommends
the modified Simpson method, which calculates EF in
2 planes and averages them. However, EF estimated
by experienced echocardiographers, without formal
measurement, has been shown to have excellent
correlation with formal measurement.3
The information provided by standard echocardiography is
mostly qualitative. Studies such as tissue Doppler imaging
allow for quantitative assessment of regional and global
myocardial function by detecting changes in myocardial
deformation based on tissue velocities. Myocardial
function is represented by strain (percentage change in
length of a segment of myocardium) and strain rate (speed
at which such changes occur).4
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Table 4.
Lung Fields
Lung Field
Diagnosis
Oligemia: decreased vascular shadows
Critical pulmonary stenosis, tetralogy of
Fallot, severe pulmonary hypertension
Plethora: numerous vascular shadows
Left-to-right shunts, dextro-transposition
of the great arteries
Pulmonary venous hypertension:
Left ventricular failure, mitral stenosis,
congestive heart failure
•PVP >12-15 mm Hg equalization of upper and lower lobe vascularity
•PVP >15-20 mm Hg Kerley B lines (lateral septal lines), Kerley A lines
(longer linear lines reaching hilum)
•PVP >20-25 mm Hg pulmonary interstitial edema
Pulmonary edema:
•PVP >25-28 mm Hg pulmonary alveolar edema reaching hilum
(“bat wing” or “butterfly” appearance)
Pleural effusions: bilateral and transudative
Obstructed total anomalous pulmonary
venous drainage, cardiogenic shock,
severe mitral stenosis
Elevated left atrial pressure or elevated
pulmonary wedge pressure: congestive
heart failure
Abbreviation: PVP, pulmonary venous pressure.
Wall and septal motion abnormalities are useful in
the assessment of right ventricular (RV) performance.
Examination of ventricular septal motion is useful in
differentiating volume overload (maximal septal distortion
occurs at end-diastole) from pressure overload (septal
distortion in end-systole and early diastole) of the RV.
by Doppler, calculation of the peak A and peak E ratio,
pulmonary vein Doppler, and A-wave reversal. All the
studied methods have their strengths and weaknesses,
so it is better to use all modalities to gather an overall
impression. Right ventricular diastolic function is more
problematic to assess. Myocardial tissue Doppler has had
some success.4
Diastolic
Several methods for the measurement of LV diastolic
performance have been assessed, such as transmitral flow
Figure 1.
Examples of Characteristic Chest Radiographs.
(a) Anomalous left coronary artery from the pulmonary artery. (b) Tetralogy of Fallot. (c) Dextro-transposition of
the great arteries. (d) Total anomalous pulmonary venous drainage.
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Table 5.
Pressures
Electrocardiographic Characteristics of the Newborn
Echocardiography does not measure intracardiac pressures
directly but instead uses a simplified form of the Bernoulli
equation to calculate pressure differences, or gradient,
between cardiac chambers.
Measurement
Normal
Abnormal
PR interval
<110 ms
>110 ms
QRS axis
+45 to +180
0 to –90
V3R and V1
Rs, R wave <15 mm
qR, rS
Negative T wave
>7 days (V1)
Positive T
waves in infants
(V1-V2)
qrS
Rs
V6 and V7
Positive T wave
>7 days (V5-V6)
Right ventricular pressures can be estimated in the
presence of a tricuspid regurgitation jet. The peak
velocity is measured and then a gradient between the
right ventricular and right atrium is derived using the
Bernoulli equation. The right atrial pressure and central
venous pressure (CVP) are added to the estimated
gradient to determine RV systolic pressure. In the
absence of an obstruction to RV outflow, the RV systolic
pressure correlates well with measured pulmonary artery
(PA) systolic pressures. In the absence of a tricuspid
Table 6.
Chamber Enlargements
Right atrial enlargement
Tall (>2.5) peak P wave, best in II and V2
Left atrial enlargement
Flat, notched P waves, in I, aVF, and V6
Right ventricular enlargement
Volume overload rsR' in V3R and V1
Pressure overload tall R or R' in V3R and V1
Left ventricular enlargement
Volume overload deep Q, tall R in V6 and V7
Pressure overload small q, tall R in V6 and V7
Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
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Table 7.
ST-Segment Abnormalities
Elevation
Acute ischemia
Depression
Subendocardial ischemia
Osborne wave
Hypothermia, hypercalcemia, VF, brain injury
Table 8.
T-Wave Abnormalities
Peak
Hyperkalemia (diffuse) (infarction if localized)
Flat with U-wave
Hypokalemia
Inversion
Ischemia
Table 9.
QT-Segment Abnormalitiesa
Long QT
Hypocalcemia, hypothyroidism, myocarditis, hypokalemia, central
nervous system events (tumor, trauma) prolonged QT syndrome (familial),
quinidine
Short QT
Hypercalcemia, digoxin, hyperkalemia
QT segment duration depends on heart rate. Estimated for heart rate 60-100/min: 0.4 seconds. For calculation
based on heart rate, refer to Lepeschkin’s diagram.26
a
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Chapter 5 | Comprehensive Critical Care: Pediatric
Table 10.
Ischemia and Pericarditis
Ischemia
Inverse T wave, elevated ST segment, Q waves
Pericarditis
Flat P wave, concave ST-segment elevation
(depression in aVR), elevated T wave, low-voltage
QRS (pericardial effusions)
Table 11.
Bradyarrhythmias
Second-degree AV block Mobitz I
(Wenckebach)
Progressive increase in PR interval, until
nonconducted p wave
Second-degree AV block Mobitz II
Constant PR interval and sudden nonconducted
p wave
Second-degree AV block 2:1; 3:1
Two p waves for every QRS
Complete (third-degree) AV block
AV dissociation, atrial rate faster than ventricular
Abbreviation: AV, atrioventricular
regurgitation jet, RV systolic pressure is estimated by
observing the behavior of the septum during systole. A
midline septum has been shown by catheterization to
correlate with an RV systolic pressure that is at least halfsystemic.
Intracardiac pressures can be assessed both qualitatively
and quantitatively using a combination of 2-dimensional,
M-mode, and Doppler parameters. This should take into
account the clinical context, as these parameters are very
sensitive to external factors such as image quality, position
of the probe, Doppler angle, and position of the heart in
the body. Therefore, no measurement should stand alone
as proof of the filling pressures; instead, an integrated
approach should be used to arrive at the most likely
conclusion.2
Effusions
Echocardiography is the primary tool for diagnosing
and quantifying pericardial effusions. Two-dimensional
echocardiography allows delineation of the size and
distribution of pericardial effusion and the detection of
loculated fluid. Small effusions have an echo-free space of
less than 5 mm, moderate-sized effusions range between
5 and 10 mm and are circumferential, and a large effusion
is greater than 10 mm. The diagnostic feature on M-mode
echocardiography is the persistence of an echo-free space
Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
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Table 12.
Tachyarrhythmiasa
Narrow QRS
Atrial ectopic tachycardia
HR 120-300/min (usually >200/min),
rapid p waves
Reentry
Atrial flutter
AR 300 > VR 75-100, negative
sawtooth
Reentry
Atrial fibrillation
Chaotic, irregular rhythm, no
p waves, ectopic atrial peaks,
AR 300‑600 > VR 150-200
Chaotic atrial depolarization
Supraventricular tachycardia
(paroxysmal)
Fixed rate, no p waves,
HR >180‑200/min
Reentry (most common)
Junctional ectopic tachycardia
AV dissociation with more p waves
than QRS or nonvisible p waves,
HR ≥180/min
Increased automaticity
Wolff-Parkinson-White
Short PR (<120 ms), delta waves
Extraconduction pathway
Ventricular tachycardia
HR >120/min, AV dissociation
Ischemia, electrolyte abnormalities, toxics
structural damage, systemic diseases
Ventricular fibrillation
Rapid disorganized polymorphic
rhythm
Same as ventricular tachycardia, hypoxia
Torsade de pointes
Polymorphic with gradual amplitude Drugs, prolonged QT
change
Wide QRS
Abbreviations: AR, atrial rate; AV, atrioventricular; HR, heart rate; VR, ventricular rate.
a
Normal QRS: 100 ms
between parietal and visceral pericardium throughout the
cardiac cycle. Separations that are observed only in systole
represent clinically insignificant accumulations.5
Tamponade
Diastolic collapse of the compliant RV signifies that
pericardial pressure exceeds early diastolic RV pressure.
Although this sign is a relatively sensitive and specific
marker for tamponade, it may not be seen in the presence
of RV hypertrophy. In addition, collapse of the right
heart chamber occurs with smaller collections of fluid
and higher pericardial pressures when there is coexisting
LV dysfunction. Right atrial collapse is virtually 100%
sensitive for tamponade but is less specific. Duration of
right atrial collapse exceeding one-third of the cardiac
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Chapter 5 | Comprehensive Critical Care: Pediatric
cycle increases specificity without sacrificing sensitivity.
Left atrial collapse is seen in about 25% of patients and is
very specific for tamponade. Left ventricular collapse is less
common because the wall of the LV is more muscular.5
Doppler Flowmetry
Doppler echocardiography can accurately and
quantitatively assess regional and global cardiac function.
It is routinely used to measure velocity and direction
of flow (color Doppler). Calculations derived from
Doppler measurements provide quantitative estimations
of stroke volume and cardiac output, pressure gradients,
cross-sectional flow area, and prediction of intracardiac
pressures.
The principle of Doppler ultrasound flowmetry states
that the change in frequency of the reflected ultrasound
will be proportional to the velocity of the reflecting blood
cells. Doppler flow can be applied to any blood vessel,
but for measurement of cardiac output (CO), it is usually
performed in the aorta (transthoracic or transesophageal
approach).
Doppler flow to measure CO correlates best with other
methods of measuring CO (thermodilution, Fick principle,
dye dilution) when used as a trend monitor more than
an absolute measure and when it is performed as an
esophageal rather than suprasternal Doppler.6
Measurement of Vascular
Pressures and Resistances
Pressures
Invasive pressure measurement is common in the
management of cardiac surgical patients. Pressure and
waveform monitoring guides the titration of vasoactive
drugs, helps direct inspired oxygen and volume or diuretic
therapy, and serves as a surrogate of cardiac performance,
volume status, and possible residual defect assessment.
However, invasive pressure measurement carries potential
risks, such as bleeding, pain (arterial insertion), infection,
arrhythmias (right atrial lines), air emboli, thrombus
formation, and ischemia (arterial lines).
Central Venous Pressure and Right Atrial
Pressure
Although widely used, the values obtained from CVP
monitoring can be misinterpreted to suggest actual
intravascular volume status. The indicator of ventricular
filling is the ventricular end-diastolic volume.7 The CVP
approximates ventricular filling pressures; however, the
relationship between volume and pressure is compliance,
which is altered by changes in intrathoracic pressure as
well as myocardial and pericardial disease. An estimation
of ventricular compliance and the optimal filling pressure
can be made based on the response to administered
fluid volume. Additionally, CVP waveform analysis can
be used to monitor for dysrhythmias (cannon A waves
in atrioventricular dissociation, absent A wave and
prominent C wave in atrial fibrillation); atrioventricular
valve regurgitation (CVP resembles RV pressure wave, tall
systolic C-V wave); and tamponade (all pressures elevated
with absent descent y wave).7,8
Central venous pressure monitoring may also be
accomplished with femoral cannulas, as studies have
demonstrated a strong correlation between pressures read
in the inferior vena cava (below the renal veins) and those
obtained from the right atrium.9
Table 13 on page 73 shows the changes in right atrial
pressure (RAP) that occur with specific lesions. Normal
values for RAP are 1 to 8 mm Hg.
Figure 2 on page 73 shows an atrial pressure waveform. The
a wave represents the atrial contraction (coincides with p
wave in ECG). The c wave represents the atrioventricular
valve protrusion toward the atria with ventricular
contraction (coincides with QRS in ECG). The x' descent
shows the atrioventricular valve pulled downward at
end-ventricular contraction. The v wave represents atrial
filling (end of T wave on ECG). The y descent shows the
atrioventricular valve opening and ventricular diastole.
Left Atrial Pressure
Studies have demonstrated that in the presence of cardiac
or pulmonary disease, RAP does not correlate well
with left atrial pressure (LAP). As is the case with RAP
monitoring, LAPs do not correlate well with LV enddiastolic volume in the presence of cardiac and pulmonary
disease.
Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
Table 13.
Table 14.
Changes in Right Atrial Pressure
Changes in Left Atrial Pressure
Lesion
RA Pressure
Lesion
LA Pressure
RV dysfunction
­↑
Mitral valve stenosis or regurgitation
­↑
RV hypertrophy
­↑
LV dysfunction
­↑
Tricuspid valve stenosis or regurgitation
↑­
LV hypertrophy
↑­
Volume overload
­↑
Left-to-right shunt
­↑
LV-to-RA shunt
↑­
Tachyarrhythmias
­↑
AV dissociation
↑­
Volume overload
­↑
Tachyarrhythmias
­↑
Tamponade
­↑
Tamponade
­↑
Hypovolemia
↓
Artifact
↓ or ↑ ­
Artifact
↓ or ↑
Hypovolemia
↓
73
Abbreviations: LA, left atrium; LV, left ventricle.
Abbreviations: AV, atrioventricular; LV, left ventricle;
RA, right atrium; RV, right ventricle.
Normal values for LAP range from to 4 to 10 mm Hg and
LAP is usually 1 to 2 mm Hg higher than RAP. Values for
LAP are usually slightly elevated in postoperative patients
(8‑10 mm Hg).
In cardiogenic pulmonary edema, LAP is elevated
(>20 mm Hg in adults), whereas in permeability
pulmonary edema the LAP should be normal. Table 14 on
page 73 shows changes in LAP related to specific lesions.
Figure 2.
Right Atrial Pressure Waveform.
Invasive Arterial Blood Pressure
Invasive arterial blood pressure monitoring is the gold
standard blood pressure measurement in critically ill
patients.8 The arterial pressure waveform is a combination
of factors such as stroke volume, vascular resistance,
arterial compliance and impedance, inertia, and wave
reflection. All these factors vary along the arterial tree,
and the changes are more pronounced in children than
in adults. Centrally measured arterial pressures will have
lower systolic values and higher diastolic values than
peripheral measurements but will have the same mean
values overall. Common sites of cannulation for invasive
arterial blood pressure measurement are radial, femoral,
umbilical, and posterior tibial arteries. Less commonly
used cannulation sites include brachial and axillary arteries,
because of their higher rate of complications.7
When the systemic vascular resistance is high, more flow
and pressure are transmitted to the aorta in systole and
diastole, creating a narrower pulse pressure in the arterial
blood pressure wave. In tamponade, pulsus paradoxus will
be represented as variation of 10 mm Hg or greater in the
systolic blood pressure with inspiration.
Pulmonary Artery Pressure
Pulmonary artery catheters are helpful to evaluate not
only PA pressure but also mixed venous oxygen saturation
and pulmonary vascular resistance.
Similar waveforms are represented in the left atrium.
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Chapter 5 | Comprehensive Critical Care: Pediatric
Normal PA pressure values are less than 25 mm Hg
(except in the first weeks of life). Despite the lack of
evidence suggesting that the use of PA catheters increases
mortality in pediatric patients, use of these catheters
is limited.10 However, PA catheters may be useful in
the management of patients with known pulmonary
hypertension, or in whom pulmonary hypertension may
be anticipated, and for the diagnosis and management of
significant residual left-to-right shunting.
If there is an inflated balloon close to the end of the
PA catheter, occluding the upstream flow, the clinician
can measure pulmonary wedge pressure (or occlusion
pressure), which is a reflection of LV filling pressures.
There has been significant improvement in noninvasive
diagnostic cardiac imaging in recent years, with new
echocardiographic, computed tomography, and magnetic
resonance techniques. Nonetheless, cardiac catheterization
is still the gold standard for making certain hemodynamic
and anatomical diagnoses.
The following data can be collected by cardiac
catheterization:
• Cardiac index
• Shunts (intracardiac and extracardiac)
• Oxygen content and saturation
• Pressures: right atrium, left atrium, PA, RV, LV,
pulmonary venous pressure, PA wedge pressure,
pulmonary venous wedge pressure, aortic pressure
• Vascular resistances (systemic vascular resistance,
pulmonary vascular resistance)
• Pulmonary and systemic flows, ratio of pulmonary (Qp)
to systemic flow (Qs)
Resistances
Cardiac catheterization is the gold standard for
resistance.11 It provides information on vascular resistance
calculation based on Ohm’s law: Voltage = Current ×
Resistance; therefore, Resistance = Voltage/Current. In the
hemodynamic setting, the potential difference is replaced
with transpulmonary or transsystemic gradient, and current
is replaced with blood flow through the pulmonary or
systemic circuits. Therefore, Resistance = Gradient/Flow.
Then the calculation is indexed to body surface area:
Systemic Vascular Resistance =
(Mean Aortic Pressure – Mean Right Atrial Pressure)/
Systemic Flow (or Cardiac Index),
where normal values approximate 15 to 25 Wood
units × m2. Also,
Pulmonary Vascular Resistance =
(Mean Pulmonary Artery Pressure – Mean Left Atrial
Pressure or Pulmonary Wedge Pressure)/Pulmonary Flow,
where normal values are less than 4 Wood units × m2.
Quantification of Cardiac
Output and Blood Flow
Invasive Techniques
Measurement of cardiac output is uncommon in pediatric
intensive care because of technical difficulties and
controversy regarding the risk–benefit ratio.
Thermodilution
Blood flow and cardiac output can be calculated with
central venous (right atrium) injection of an indicator,
most commonly a cold solution of normal saline 0.9% or
dextrose 5%, followed by measurement of the temperature
change over time, sensed by thermostats (thermistor ports)
present at both the injection site and a point downstream.
The distal measurement can be the PA (using a SwanGanz catheter or PA thermodilution) or the femoral artery
(transpulmonary thermodilution). Several readings are
taken for a more accurate determination.
The transpulmonary technique does not require a catheter
in the PA (central venous and arterial line required),
and commercial devices are available that combine
transpulmonary thermodilution with pulse contour
analysis for the assessment of continuous cardiac output.
The result is reflected in a composite curve, where the y
axis is the decrease in temperature and the x axis is time, as
shown in Figure 3 on page 75.
Low CO states yield a larger area under the curve because
it takes longer for the temperature to return to baseline,
whereas normal CO states give a smaller area under the
curve.
Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
Figure 3.
Thermodilution Composite Curve.
75
Studies in critically ill pediatric patients show good
correlation in the measurement of CO by transesophageal
Doppler echocardiography12 and good correlation with
CO estimated by thermodilution, indirect calorimetry
(Fick principle), and suprasternal echocardiography.13
Newer techniques such as 3-dimensional echocardiography
and 2-dimensional strain echocardiography require further
study before their use in hemodynamic assessment can be
recommended.
Doppler Flowmetry
∆T (°C): Increase in temperature (Celsius degrees); t(s):
time (seconds)
Fick Technique
The Fick principle calculates blood flow and cardiac output
by measuring the amount of oxygen consumed divided by
the change in oxygen between the aorta and mixed venous
saturation.
Metabolic monitors are accurate in measuring oxygen
consumption in the pediatric patient but are limited by
gas loss, the need for cuffed intratracheal tubes, and the
potential for lung injury (an alveolar–arterial oxygen
gradient needs to be present).
Noninvasive Techniques
Echocardiography
Echocardiography is paramount in the diagnosis and
management of cardiac diseases. It is a very attractive tool
because it is widely and easily used, can be performed
at the bedside, and is noninvasive. The disadvantage in
the intensive care setting is that multiple factors affect
cardiac performance (eg, inotropic infusions, mechanical
ventilation), limiting the utility of intermittent assessment.
Echocardiography provides only a single measure in time.
Echocardiography as a hemodynamic monitor has a class
II recommendation by the American Heart Association
and the American College of Cardiology Task Force on
Practice Guidelines, with limited evidence to support its
utility for pediatric hemodynamic monitoring.4
Color-coded and spectral Doppler flow mapping is used
to measure direction and velocity of blood flow. Doppler
calculations provide quantitative estimation of flow and
therefore of stroke volume and cardiac output. Tissue
Doppler imaging is a very reliable tool to assess myocardial
performance and can be used to trend alterations in
cardiac function.4
Quantification and
Detection Of Shunts
Thermodilution
The presence of intracardiac shunts presents challenges in
the measurement of CO by thermodilution. The presence
of a left-to-right shunt creates an early recirculation of
the indicator (cooled saline), affecting the composite
curve. Left-to-right shunting influences the validity of
thermodilution measurements for the calculation of
flow.14 Recent studies have raised the possibility of using
transpulmonary thermodilution to diagnose left-toright shunts in the pediatric patient. Transpulmonary
thermodilution allows for CO, extravascular lung
water, and volumetric variable measurements. These
studies propose that changes in the transpulmonary
thermodilution curve and overestimation in the
extravascular lung water, in the absence of gas exchange
abnormalities, suggest the presence of a left-to-right
shunt.14,15
Fick Equation
The Fick equation can measure CO when there is an
anatomical shunt, via the following formulas:
Systemic Flow (Qs) = VO2/(Caorta – Cmixed venous)
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Chapter 5 | Comprehensive Critical Care: Pediatric
Pulmonary flow (Qp) = VO2/(Cpulmonary vein – Cpulmonary artery),
where VO2 is oxygen consumption and C refers to oxygen
content.
In the absence of shunts, Qp should be equal to Qs, and
so the formulas can be interchanged. We measure mixed
venous oxygen saturation from the PA, and the oxygen
content in the pulmonary veins is similar to that in the
systemic arteries. When there is a left-to-right shunt, the
blood in the PA will be highly saturated, hence the need to
measure Cmixed venous proximally to the shunt (right atrium,
or weighted average between superior and inferior vena
cava). When there is a right-to-left shunt, oxygen content in
the systemic arteries will be lower than in the pulmonary
veins; therefore, to measure Qp, we need to sample blood
from the pulmonary veins.
The combination of both formulas gives us a Qp to Qs
ratio:
Qp:Qs = (Caorta – Cmixed venous)/(Cpulmonary vein – Cpulmonary artery).
Following is an example of Qp:Qs calculation at the
bedside: You have a single-ventricle patient with arterial
oxygen of 85% in room air and mixed venous saturation of
55%. Assuming a PV saturation of 100%,
Qp:Qs = (Aortic Saturation – Mixed Venous Saturation)/
(Pulmonary Venous Saturation – PA Saturation)
Qp:Qs = (85 – 55)/(100 – 85) = 2:1.
Contrast Echocardiography
Contrast echocardiography has been used widely to detect
intracardiac shunts. The IV injection of a solution results
in a contrast effect that is detectable with ultrasound. If
an agitated bolus of saline is injected into a peripheral
vein, it creates contrast in the right atrium but disappears
completely after running through the pulmonary capillary
bed. Therefore, the presence of contrast in the left atrium
indicates right-to-left shunting, at either the atrial or
intrapulmonary level.
Biomarkers
B-Type Natriuretic Peptide
B-type natriuretic peptide (BNP) is a neurohormone
excreted mainly by ventricular myocytes in response to
volume and/or pressure loads and has diuretic, natriuretic,
and vasodilatory effects; in addition, BNP inhibits the
renin–angiotensin–aldosterone axis.16-19 Levels of BNP
are elevated in adults with congestive heart failure and
correlate with the severity of congestive heart failure
and the risk for hospitalization and death. Studies have
demonstrated that serial BNP plasma levels are useful
for diagnosing and stratifying adults with heart failure.19
Measurement of BNP is also a good adjuvant tool in the
management of pediatric patients with cardiac disease,
as there is strong evidence correlating BNP levels to
heart failure in pediatric patients with either acquired
or congenital heart disease.17,20 Evidence demonstrates
a positive correlation between BNP levels and Qp:Qs
measurements and an inverse relation with ventricular IF.
Troponin
Cardiac troponin subunits are released after myocardial
cell injury, the levels being highly sensitive and specific
of myocardial damage. Troponin level in the pediatric
population has some limitations, especially in the neonatal
period, due to the uncertainty of normal range values21
and differences in normal values among different assays.16
Troponin levels are elevated after almost every cardiac
surgery (surgical trauma, defibrillation, reperfusion
injury). The association with postoperative outcomes is
uncertain.16 Cardiac troponin levels are also elevated in
systemic disease, where there may also be direct or indirect
myocardial injury (sepsis, trauma, hypoxic respiratory
distress).22-24 Elevated cardiac troponin levels in systemic
illness may indicate poor prognosis, regardless of the
underlying cause.14 The recommendation in all situations is
to follow the trend with serial measurements.
Creatine Kinase and Free Myoglobin
Along with cardiac troponin, creatine kinase, especially
CK-MB (myocardium-specific) isoenzyme, and myoglobin
are well-known markers of myocardial injury. Both CKMB and myoglobin have lower sensitivity and specificity
for myocardial infarction than troponin.25 However,
increasing levels of both biomarkers warrant special
attention.
Clinical Assessment of Cardiovascular Structure, Function, and Dysfunction | Chapter 5
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