MODULE FOUR

BLOOD PRESSURE
SUGAR and SAFE Care

T EMPERATURE
A I R WAY
BLOOD PRESSURE

LAB WORK

E MOTIONAL SUPPORT

129
 BLOOD PRESSURE – Module Objectives
Upon completion of this module, participants will gain
increased understanding of:
1. The causes, presentation, and initial treatment of the
three major types of shock seen in infants: hypovolemic,
cardiogenic, and septic shock.
2. The physical examination to evaluate for shock.
3. The principles of cardiac output and heart rate as they
relate to shock.
4. Indications for, mixing, and safe administration of dopamine.

What Is Shock?
Shock is defined as "inadequate vital organ perfusion and
oxygen delivery" (Corneli, 1993, p.303) or, "a complex state
of circulatory dysfunction resulting in insufficient oxygen and
nutrient delivery to satisfy tissue requirements"
(Kourembanas, 2004, p.181). Failure to promptly recognize
and treat shock may lead to multiple organ failure and
even death in newborns, thus treatment must be prompt
and aggressive.

The Three Types of Shock:

Hypovolemic, Cardiogenic, Septic
Hypovolemic Shock
Hypovolemic shock results from a low circulating blood
volume. Causes of hypovolemic shock include:
• Acute blood loss during the intrapartum period
ª Fetal-maternal hemorrhage
ª Placental abruption or previa
ª Umbilical cord injury
ª Twin-to-twin transfusion
ª Organ laceration (liver or spleen)

130
 • Postnatal hemorrhage
ª Brain
ª Lung
ª Adrenal glands
ª Scalp (subgaleal hemorrhage)
• Non-hemorrhagic causes
ª Severe capillary leak secondary to infection
p.147
ª Dehydration
• Functional hypotension
ª Tension pneumothorax (impairs cardiac output)
ª Pneumopericardium (impairs cardiac output)
Some etiologies of postnatal hemorrhages may also occur prenatally or during the intrapartum
period. Infants in hypovolemic shock present with signs of poor cardiac output: tachycardia, weak

BLOOD PRESSURE
pulses, prolonged capillary refill time, mottling, and cyanosis. If there is severe blood loss they will
appear pale or white, and have acidosis and hypotension (a late sign of poor cardiac output).
Table 4.1 describes physical exam components when assessing for presence of shock.

Cardiogenic Shock
Cardiogenic (heart failure) shock results when the heart
muscle functions poorly and may occur in infants with:
• Intrapartum or postpartum asphyxia
• Hypoxia and/or metabolic acidosis
• Bacterial or viral infection
• Severe respiratory distress (requiring assisted ventilation)
• Severe hypoglycemia
• Severe metabolic and / or electrolyte disturbances
• Arrhythmias
• Congenital heart defects, especially those with severe hypoxemia or obstruction of blood flow
into the systemic circulation

131
 Septic (distributive) Shock
Severe infection may lead to a third type of shock known as
septic or distributive shock. Infants who are in septic shock
become rapidly and critically ill. In the presence of bacterial
infection, a host of complicated systemic reactions occur that
result in circulatory insufficiency. A hallmark of this type of
shock is hypotension that responds poorly to fluid
resuscitation. Loss of vascular integrity allows fluid to leak out
of the blood vessels and into the tissue spaces (also a cause
of hypovolemic shock). Poor myocardial contractility leads to
poor tissue perfusion and oxygenation. These infants often
need blood pressure medication to treat the severe hypotension. The risk for organ injury and death
is very high.
Not infrequently, infants may have a combination of the three types of shock.

Table 4.1. Physical examination for shock.

An infant in shock may exhibit the following signs:

Respiratory effort
ª Increased work of breathing (retractions, grunting,

nasal flaring)
ª Tachypnea
ª Apnea
ª Gasping (an ominous sign of impending
cardiorespiratory arrest)

Pulses
ª Weak peripheral pulses (the pulses feel decreased or the

pulses are not palpable)

ª Brachial pulses stronger than femoral pulses (consider
coarctation of the aorta or interrupted aortic arch)

(continued on page 133)

132
Table 4.1. Physical examination for shock. (continued)

Peripheral perfusion
ª Poor perfusion (results from vasoconstriction and poor

cardiac output)
ª Prolonged capillary refill time (greater than 3 seconds in a
sick infant is generally considered abnormal)
ª Mottled skin
ª Cool skin
Color
ª Cyanosis
ª Pale, white skin color (may indicate very low hemoglobin
secondary to hemorrhage)
ª Evaluate oxygenation and saturation
ª Evaluate the blood gas for the presence of respiratory,
metabolic, or mixed acidosis
Heart rate
ª Bradycardia (< 100 beats per minute) with evidence of

BLOOD PRESSURE
poor perfusion
▫ Hypoxemia, hypotension, and acidosis all depress
the conduction system
▫ Bradycardia combined with severe shock is an ominous
sign of impending cardiorespiratory arrest
▫ Rule out complete heart block
ª Tachycardia (sustained heart rate > 180 beats per minute
at rest)
▫ Tachycardia may indicate poor cardiac output and / or
congestive heart failure
▫ A normal heart rate is between 120 and 160 beats per
minute, but may range between 80 and 200 depending
upon the infant’s activity level
▫ If the heart rate is above 220 beats per minute, consider
supraventricular tachycardia (SVT)
Heart
ª Enlarged heart size on chest x-ray (correlates with myocardial dysfunction and development of
congestive heart failure)
ª Smaller than normal, or compressed heart on chest x-ray (may reflect poor filling or pre-load)
ª Evaluate for the presence or absence of a heart murmur
Note: structural congenital heart disease may be present even if there is no heart murmur

(continued on page 134)

133
 Table 4.1. Physical examination for shock. (continued)

Blood pressure
ª May be normal or low: hypotension is a late sign of

cardiac decompensation
Note: the blood pressure reading may be within normal
range because of vasoconstriction and centralization of
blood pressure. In other words, blood is “shunted away”
from non-vital organs to allow for perfusion of vital
organs. By the time the blood pressure drops and
hypotension becomes apparent, the patient is usually in
an advanced state of shock.
ª Evaluate the pulse pressure by subtracting the diastolic
from the systolic measurement. A normal pulse pressure in a term infant is between 25 and
30 mmHg and in a preterm infant between 15 and 25 mmHg. A narrow pulse pressure may
indicate peripheral vasoconstriction, heart failure, or low cardiac output. A wide pulse pressure
may indicate a large aortic runoff, as seen with a significant patent ductus arteriosus or large
arteriovenous malformation. A narrow or wide pulse pressure should be reported to the infant’s
healthcare practitioner.

Figure 4.1. Average systolic, diastolic, and mean blood pressures during the first 12 hours of life in normal
newborn infants according to birth weight. Evaluation of blood pressure is an important component of patient
evaluation, however, the decision to treat shock should be based on history, physical and laboratory exam, and patient
condition, not just blood pressure.

The shaded yellow area is considered normal.

Graphs adapted with permission from Versmold, HT, et al. (1981). Aortic blood pressure during the first 12 hours of life in infants
with birth weight 610 to 4,220 grams. Pediatrics, 67(5), 607-613.

134
Figure 4.2. Evaluation of capillary filling time. To check capillary filling time, press firmly for five
seconds and release. Count how many seconds the skin takes to re-fill. Compare the upper to lower
body. If greater than 3 seconds on the upper or lower body, or if the lower body is greater than the
upper body, report these findings to the infant’s healthcare practitioner.

Table 4.2. Laboratory evaluation for shock.

The following lab tests are useful to evaluate shock and, if abnormal, they
help determine appropriate corrective therapy:
Blood gas
Metabolic acidosis is present if the pH and bicarbonate are low. If the infant is
experiencing respiratory insufficiency, then the PCO2 will also be elevated and the infant will
have a mixed respiratory and metabolic acidosis.
ª pH < 7.30 is abnormal.

BLOOD PRESSURE
ª pH < 7.25 is concerning especially if in combination with poor perfusion, tachycardia,

and/or low blood pressure.

ª pH < 7.20 is significantly abnormal.

ª pH < 7.10 indicates the infant is in severe crisis.

Other labs that are useful in the evaluation of shock

ª Glucose

▫ In response to stress, the infant may initially be hyperglycemic. Evaluate the blood

sugar frequently until a pattern of stability is demonstrated.

ª Electrolytes (hypo or hypernatremia, hypo or hyperkalemia)
▫ If metabolic acidosis present, calculate the anion gap as follows:
[(Na + K)] – [Cl + HCO3)]. (Use the serum CO2 on the electrolyte panel for the HCO3).
The normal value in a neonate is 5 to 15 mEq/L.
ª Ionized calcium
ª Liver function tests
ª Renal function tests
ª Coagulation studies (prothrombin time, partial thromboplastin time, fibrinogen, D-dimer)
ª Blood lactate to confirm lactic acidosis
Other tests and observations
ª Echocardiogram to evaluate cardiac function and to rule out structural congenital
heart disease
ª Evaluate urine output for oliguria or anuria

ª Evaluate for sepsis (CBC with differential and blood culture)

ª If concerned about an inborn error of metabolism, obtain an ammonia level and other
metabolic screens (urine and serum amino acids and organic acids)
135
 The Principles of Cardiac Output
Cardiac output (CO) is influenced by heart rate (HR) and
stroke volume (SV) such that:
Heart rate multiplied by stroke volume equals cardiac output or
HR X SV = CO
The neonatal myocardium is poorly compliant and has
limited capacity to increase stroke volume on its own,
therefore, in response to shock the infant will attempt to
increase cardiac output by increasing heart rate. This results
in tachycardia.

Factors that Negatively Affect Heart Function

In addition to electrolyte, mineral, or energy imbalances, factors that can reduce cardiac output
include the following:
• Decreased volume of venous return to the heart (preload) – the heart has less to “pump”
with each contraction.
• Increased systemic vascular resistance (afterload) – requires extra work to pump blood to
the body.
• Decreased myocardial contractility – heart squeeze or contraction is poor so less blood is
ejected with every beat.

Treatment of Shock
The first step in the treatment of shock is to identify its source or sources. The second step is to
identify and correct any related or underlying problems that may impair heart function, such as
poor cardiac filling because of hypovolemia, tamponade, excessive airway pressure, electrolyte
disturbances, hypoglycemia, hypoxemia, arrhythmias, etc. Figure 4.3 illustrates the principles
underlying an improvement in blood pH.

136
 pH

Lactic
Acid Buildup

Anaerobic
Metabolism

Tissue Oxygenation

Tissue Perfusion

BLOOD PRESSURE
Cardiac Output
Volume Support, Inotropes

Increase cardiac output (by administering volume infusions and, if necessary, inotropic
medications), which will…
Improve tissue perfusion, which will…
Improve tissue oxygenation, which will…
Decrease anaerobic metabolism in the tissues, which will…
Decrease lactic acid buildup in the tissues, which will…
Improve pH of the blood (acidosis will improve or resolve)

Figure 4.3. Treatment goals. Supporting oxygenation and ventilation is critically important when infants are in
shock. Oxygen supply to the tissues must improve in order to reverse the effects of shock.

137
 Treatment of Hypovolemic (low blood volume) Shock
The goal of treatment is to improve the circulating blood volume. This can be accomplished by
administering the following crystalloids or blood products.

IF THERE IS NO ACUTE BLOOD LOSS

Normal Saline (NS) (0.9% saline)
Ringer's Lactate
Dose: 10 ml per kilogram per dose (10 ml/kg/dose)*
Route: IV, UVC, intraosseous
Time interval: Administer over 15 to 30 minutes
Note: The administration time is dependent
upon the severity of the situation and may
need to be more rapid.
*For treatment of severe shock, it may be necessary to provide two, three or more volume boluses. Evaluate
the infant’s response to treatment (changes in heart rate, perfusion, and blood pressure) following each
bolus and decide if more volume is necessary.

If there is a history of chronic blood loss, some infants in severe shock may not
tolerate volume boluses. Consultation with the tertiary center neonatologist is
advised if in doubt about whether to administer volume.

IF THERE IS ACUTE BLOOD LOSS

Normal saline to begin volume resuscitation while awaiting Packed Red Blood Cells (PRBCs), or
Whole Blood (usually reconstituted with PRBCs and Fresh Frozen Plasma)
Dose: 10 ml per kilogram per dose (10 ml/kg/dose)
Route: IV, UVC, intraosseous
Time interval: Administer over 30 minutes to 2 hours
Note: The administration time is dependent upon the severity of the situation,
and may need to be more rapid than 30 minutes.

138

What blood type can be administered
during an emergency when there
is not enough time to perform a type
and cross-match?
Type O-negative packed red blood cells may be
provided during an emergency when time does not
allow for cross matching of blood. Whenever possible,
transfuse neonates with PRBCs that are less than one
week old, CMV negative, and leuko-reduced.
Assignment:
Goal: To know how to rapidly access emergency
blood supplies.

Call the blood bank and inquire about the procedure to obtain 0-negative packed red blood cells for
emergencies in the delivery room or nursery (when cross-matching is not possible). This includes any
paperwork that is necessary, whether a written order is required, and who may place the order for the
blood (nurses, unit secretary, or physician). Ask whether this emergency supply of blood is available
24-hours per day and how long it will take to receive emergency blood once it is requested.

Clinical Tip

BLOOD PRESSURE
Practice Session: How to calculate the volume bolus
Desired Dose: 10 ml per kilogram per dose (10 ml/kg/dose)
Weight: 1800 grams or 1.8 kg
Final Dose: 10 (ml) X 1.8 (kg) = 18 ml
Give 18 ml of volume over 15 to 30 minutes IV, UVC, or intraosseous (IO) route

Crystalloid solutions, such as normal saline and Ringer’s

lactate, are isotonic and contain water and electrolytes.
They pass easily through semi-permeable membranes
and therefore stay in the intravascular (circulating)
compartment for shorter periods of time than colloids.
Advantages of crystalloid solutions are that they are
What is the difference between
readily available for the immediate treatment of shock,
crystalloids and colloids?
they require no special compatibility testing, they do
not produce sensitivity reactions, they are inexpensive, and there are no religious objections to their use.

Colloid solutions have a large molecular weight and do not pass easily through semi-permeable
membranes. Colloid solutions include the plasma protein, albumin, and synthetic colloid solutions such as
Plasmanate®. Colloid solutions stay in the intravascular (circulating) compartment longer than crystalloids.
The disadvantages of colloids include sensitivity reactions, their increased expense, and the need for
compatibility testing (in some cases), before they can be administered.

Clinical Tip
139
 Treatment of Cardiogenic (heart failure) Shock
Evaluate the infant for tachycardia, bradycardia, hypotension,
oliguria, hypoxemia, acidosis, and hypoglycemia, because
these signs may be present when an infant is in cardiogenic
shock. Treatment is aimed at correcting the underlying
problems that may negatively affect heart function. These
include (but are not limited to), hypoxia, hypoglycemia,
hypothermia, hypotension, acidosis, arrhythmias, infection,
and electrolyte or mineral imbalances.

Treatment of Septic (distributive) Shock

Treatment involves a combination of hypovolemic and cardiogenic shock therapies. The septic
infant may require more fluid boluses than in other types of shock given the movement of fluid
from the intravascular compartment into the interstitial space, or extravascular compartment. This is
due to capillary injury as well as pooling of blood in the capillary bed. A continuous drip infusion of
dopamine will be necessary to treat severe hypotension. It is critically important to optimize
oxygenation and ventilation when treating septic shock.

Medications Used to Treat Cardiogenic

and Septic Shock
Volume Infusions (0.9% normal saline or Ringer’s lactate)
Indications: To improve the circulating blood volume
Dose: The dose recommendations are the same as for
hypovolemic shock: 10 ml/kg per dose
Route: IV, UVC, Intraosseous

Sodium Bicarbonate 4.2% solution (0.5 mEq/mL)

Indications: To treat severe metabolic acidosis (consider using if arterial pH is less than 7.15 and
the infant is adequately ventilated)
Note: The use of this medication is controversial, so consult your transport control
physician if unsure whether sodium bicarbonate is indicated. Most important is to
identify the potential causes of metabolic acidosis and institute appropriate
corrective therapies.
Dose: 1 to 2 milliequivalent per kilogram per dose (1 to 2 mEq/kg/dose)
When the 4.2% solution is used, this equals 2 to 4 ml/kg/dose
Route: Give over 30 to 60 minutes IV
Sodium bicarbonate is a very hypertonic solution and if given too rapidly may lead to
intraventricular hemorrhage in preterm infants

140
Dopamine Hydrochloride
Indications: Poor cardiac contractility
Dose: 5 to 20 micrograms per kg per minute
(mcg/kg/minute)
Route: IV continuous infusion (IV pump)

Do not give via any arterial route or through

an endotracheal tube

Table 4.3. Dopamine dose and effect.

Dosage Receptors Effect

0.5 to 2 mcg/kg/min Dopaminergic (stimulation of Renal and mesenteric
dopaminergic receptors) vasodilatation; little effect on
blood pressure

BLOOD PRESSURE
2-10 mcg/kg/min Beta-adrenergic (beta1 Beta-adrenergic (beta1
receptors activated) receptors activated)

Greater than 10 mcg/kg/min Alpha-adrenergic (alpha Vasoconstriction; increased

receptors activated) systolic and diastolic
blood pressure
From Osborn et al. (2004). NeoReviews, Vol. 5, No. 3, p. e114.

141
 Dopamine Dosing for Newborns
How to Calculate a Final Standardized Concentration of
800 Micrograms per ml IV Fluid
As many nurses and physicians will have limited experience using dopamine, the recommended
dopamine infusion described below is a relatively dilute one. More concentrated solutions are usually
provided in the neonatal intensive care unit.
Step 1: Select the pre-mixed dopamine solution as
described in option one, or mix the solution as
described in option two.
Option One
A commercially prepared pre-mixed dopamine drip
solution with a concentration of 800 micrograms
(mcg) per milliliter (ml) in D5W IS available.
To determine the appropriate rate, go to Step 2
on the next page. Infuse dopamine on an
infusion pump.

Option Two
A commercially prepared pre-mixed dopamine
solution IS NOT available.
Mix the dopamine drip as follows:
1. Select a dopamine vial containing dopamine
40 milligrams (mg) per ml.
2. From this vial draw up 5 ml (or 200 mg)
of dopamine.
3. Add this amount (5 ml or 200 mg of dopamine) to a 250 ml bag of D10W.
4. This will provide a dopamine concentration of 800 mcg per ml of IV fluid (or 200 mg per
250 ml IV fluid).
5. Label the IV bag with the following: This 250 ml bag of D10W contains 800 mcg dopamine per
ml IV fluid.
6. Infuse dopamine on an infusion pump.

142
Dopamine Dosing for Newborns (continued)
Step 2: Using the graph, select the infusion rate.
1. Find the patient’s weight in the first column marked Weight in kg. Round up
or down as needed if the weight is in between the 0.5 kilogram increments.
2. Read across the row to the ordered infusion dose in mcg/kg/min.
3. Result = infusion pump setting in ml/hr.

Double check all calculations and reconstitution with another nurse or physician
before administering dopamine to the infant.

Ordered Dose (mcg/kg/min)

using a dopamine solution containing 800 mcg per ml of IV fluid

Weight 5 7.5 10 12.5 15 17.5 20 25

in kg mcg/kg/min mcg/kg/min mcg/kg/min mcg/kg/min mcg/kg/min mcg/kg/min mcg/kg/min mcg/kg/min

0.5 kg 0.2 ml/hr 0.3 ml/hr 0.4 ml/hr 0.5 ml/hr 0.6 ml/hr 0.7 ml/hr 0.8 ml/hr 0.9 ml/hr

BLOOD PRESSURE
1 kg 0.4 ml/hr 0.6 ml/hr 0.8 ml/hr 0.95 ml/hr 1.1 ml/hr 1.3 ml/hr 1.5 ml/hr 1.9 ml/hr

1.5 kg 0.6 ml/hr 0.8 ml/hr 1.1 ml/hr 1.4 ml/hr 1.7 ml/hr 2 ml/hr 2.3 ml/hr 2.8 ml/hr

2 kg 0.8 ml/hr 1.1 ml/hr 1.5 ml/hr 1.9 ml/hr 2.3 ml/h 2.6 ml/hr 3 ml/hr 3.8 ml/hr

2.5 kg 0.95 ml/hr 1.4 ml/hr 1.9 ml/hr 2.3 ml/hr 2.8 ml/hr 3.3 ml/hr 3.8 ml/hr 4.7 ml/hr

3 kg 1.1 ml/hr 1.7 ml/hr 2.3 ml/hr 2.8 ml/hr 3.4 ml/hr 3.9 ml/hr 4.5 ml/hr 5.6 ml/hr

3.5 kg 1.3 ml/hr 2 ml/hr 2.6 ml/hr 3.3 ml/hr 3.9 ml/hr 4.6 ml/h 5.3 ml/hr 6.6 ml/hr

4 kg 1.5 ml/hr 2.3 ml/h 3 ml/hr 3.8 ml/hr 4.5 ml/h 5.3 ml/hr 6 ml/hr 7.5 ml/hr

4.5 kg 1.7 ml/hr 2.5 ml/hr 3.4 ml/hr 4.2 ml/h 5.1 ml/hr 5.9 ml/hr 6.8 ml/hr 8.4 ml/hr

5 kg 1.9 ml/hr 2.8 ml/hr 3.8 ml/hr 4.7 ml/hr 5.6 ml/hr 6.6 ml/hr 7.5 ml/hr 9.4 ml/hr

Note: some rounding has occurred to simplify infusion rate.

If a pre-mixed dopamine solution is not available, place the following items in a plastic bag or
container and keep with emergency medications:
250 ml bag of D10W
Dopamine hydrochloride 40 mg/ml solution (5 ml vial = 200 mg)
This instructional information
Expert consultation regarding dopamine mixing and instructions provided by: Vinay Vaidya, MD; Director, Pediatric Critical Care Fellowship
Program; Assistant Professor Pediatrics; University of Maryland School of Medicine; 22 S. Greene Street, Room N5E13B; Baltimore, MD 21201;
Research website: www.icudrips.org 143
 Rules for Dopamine Infusion
1. In most cases, volume boluses are administered before it
is determined that dopamine is necessary.
2. The starting dose for dopamine should be selected based
on the infant’s clinical status and reason for hypotension.
Dopamine is usually started at 5 mcg/kg/minute and
can be increased (or decreased) by 2.5 mcg/kg/minute
as shown in the graph in Table 4.1.
Note: In many neonatal intensive care units, dopamine is
mixed to yield a more concentrated solution than
presented in this module, and the rate of increase (or decrease) is usually limited to
1 mcg/kg/minute, each time the rate is changed.
3. Monitor the blood pressure and heart rate every 1 to 2 minutes for 15 minutes then every 2 to 5
minutes depending upon response to the medication. If an infant is failing to respond to a dose
of 20 mcg/kg/minute, then increasing the dose further is not recommended.
4. Infuse dopamine on an infusion pump and to increase safety, use “smart pump” technology
whenever possible.
5. Administer through an umbilical venous site if the catheter’s position has been confirmed by chest
x-ray and the tip is appropriately located above the liver at the inferior vena cava/right atrial
junction. If no central venous access is available, infuse dopamine through a peripheral IV. Carefully
monitor the infusion site for extravasation (infiltration) and change infusion sites if the IV should
infiltrate. If unsure how to treat a dopamine infiltration, consult your tertiary center for guidance.
6. Never infuse dopamine through any arterial site including the Umbilical Artery Catheter.
7. Do not flush dopamine or lines containing dopamine, as this will cause the blood pressure to
surge up and the heart rate to abruptly slow down.

In most cases, the amount of dopamine in ml per hour can be

safely added to the infant’s maintenance infusion rate, especially
if the dopamine is mixed in a D5W solution. If however, the
infant must receive a restricted amount of IV fluid, then:
Do I need to adjust the IV rate
1. Dopamine should be mixed in D10W (so that the glucose
when administering dopamine?
infusion rate is not affected), and

2. Dopamine infusion amount can be subtracted from the maintenance IV infusion amount.
Example:
3 kg infant on D10W at 80 ml/kg/day = 10 ml per hour infusion rate
Dopamine ordered at 10 mcg/kg/minute = 2.3 ml per hour
10 (ml per hour) minus 2.3 (ml per hour) = 7.7 ml per hour
Run the dopamine at 2.3 ml per hour and the regular D10W at 7.7 ml per hour for a combined hourly
infusion rate of 10 ml per hour.

144 Clinical Tip

Practice Session: Dopamine rate
A dopamine standardized concentration of 800 mcg per ml
IV fluid has been prepared.
Using the infusion graph on page 143 answer the follow
questions:
1. A dose of 10 mcg/kg/minute of dopamine is ordered for
a 3.8 kg infant. What infusion rate will this infant require? p.149

2. A dose of 5 mcg/kg/minute of dopamine is ordered for a

1.4 kg infant. What infusion rate will this infant require?

BLOOD PRESSURE

145
146
Appendix 4.1 HYPERLINK: Evaluation of Scalp Swelling

Slide 1 Slide 2

APPENDICES
Slide 3 Slide 4

Slide 5 Slide 6

147
 APPENDIX 4.1 (continued)

Slide 7 Slide 8

Slide 9 Slide 10

Slide 11

148
Appendix 4.2 HYPERLINK: Case Study: Baby Doe
The full case study may be found on page 151.

Slide 1 Slide 2

APPENDICES
Slide 3 Slide 4

Slide 5 Slide 6

149
 Appendix 4.2 (continued)

Slide 7 Slide 8

Slide 9

150
Appendix 4.2 (continued)
It Isn’t Just the Lungs:
A Case Presentation
Lynn E. Lynam, RNC, MS, NNP
When I began this column last year, I
promised to try to use it as a forum to
get back to the basics and present
interesting case studies. This article
represents my first attempt to combine
those goals. The following true case
occurred during the transport of a
critically ill neonate to a Level III East
Coast facility. The patient’s name has
been changed for legal protection of
that facility.
M s Long, a 15-year-old, gravida 1,
para 0, black teen, delivered a
29-week 1,200-gm male fetus precipi-
tously from a double-footling breech
presentation shortly after her arrival at a
Level I obstetrical facility. Just prior to
delivery, the fetal heart rate had been
assessed at 140 beats per minute with
excellent variability. Amniotic mem-
branes ruptured at delivery, and the fluid
was noted to be normal in volume, color,
and odor.
On initial physical assessment, the
neonate’s heart rate was auscultated at
60 beats per minute despite vigorous
tactile stimulation and oropharyngeal
suctioning. Hence, bag-mask ventilation
with 100 percent oxygen and chest com-
pressions were initiated, followed by
successful endotracheal intubation with
NEONATAL NETWORK / APRIL 1992
Reproduced with permission from Lynam, L.E. (1992). It isn’t just the lungs: A case presentation.
Neonatal Network 11(3): 65-68.
CONTRIBUTING EDITOR
a 2.0 endotracheal tube by three minutes
of life. The infant’s heart rate increased
to 120 almost immediately, and no fur-
ther resuscitative efforts were necessary.
Apgars were 1 and 7 at one and five
minutes, respectively. A 10 percent dex-
trose infusion was started via an umbili-
cal venous catheter at 80 cc/kg/day.
After obtaining blood specimens for
culture and hematologic analysis, ampi-
cillin and gentamicin were administered
intravenously.
By 25 minutes of life, the infant’s
oxygen saturation by pulse oximetry
was consistently in the 90-100 percent
range as long as a respiratory therapist
delivered positive pressure ventilation to
the endotracheal tube with an anesthesia
bag. The initial chest x-ray film showed
that the endotracheal tube was
positioned at the carina and that the
infant had severe respiratory distress
syndrome. No other cardiorespiratory
abnormalities were appreciated. After
the endotracheal tube was repositioned
at 35 minutes of life, a referral call was
placed to the tertiary care facility
requesting transport services.
When the transport team (neonatal
nurse practitioner and nurse) arrived, the
two and a half hour old premature infant
was found lying in an open radiant
warming bed located in the same room
APPENDICES
where he had been born, loosely covered
by a sterile drape. The circulating nurse
and respiratory therapist were present,
but the referring pediatrician had been
called away to another emergency.
They reported that no significant
problems had occurred since the initial
telephone call except for the attending
physician being unsuccessful in
obtaining an arterial blood gas before
being called away. Hence, the infant’s
acid base status was undocumented. The
transport nurse found that the
circulating nurse had removed the bed’s
temperature sensor from skin contact
because of “frequent alarms” and placed
the bed on manual control mode.
Because almost an hour had elapsed
since the last vital signs assessment, the
transport nurse promptly obtained them.
The infant’s axillary temperature
measured 88.7°F, and his blood pressure
would not register on a noninvasive
monitor. The Dextrostix measurement
was 40-80. His other vital signs were
within the expected normal range for his
weight and gestational age.
After reviewing the chest x-ray
examination, the transport team elect-
Vol. 11 No. 3 65
151
 ed to replace the 2.0 endotracheal tube
with a 3.0 and to administer exoge-
nous surfactant. Baby Long was then
placed on a transport ventilator set at the
following parameters: PIP 22, PEEP 5,
IMV 60, I-time 0.4 seconds, FiO 2 100
percent.
The following blood gas values were
obtained from a right radial artery
specimen ten minutes later: pH 7.38,
PCO 2 19.7, PO 2 151, bicarbonate 11.4,
oxygen saturation 100 percent. Based on
these values, the PIP was decreased to
20, the IMV was decreased to 40
breaths and the FiO 2 was decreased to
95 percent.
After visiting briefly with Ms. Long
and discussing the infant’s condition
with her, the transport team left the
referring hospital. Arrival time to
departure time was 40 minutes. Vital
signs and physical examination on
departure from the referring hospital
were recorded as follows:
Vital signs: Temperature 89°F, pulse rate
136, respiratory rate 40. Dextrostix
had increased to 180; blood pressure
continued to be nonrecordable.
Maternal medical history: No recollec-
tion of serious childhood illness.
Denied personal drug or alcohol use,
although the baby’s father had been
recently jailed for selling and dis-
tributing cocaine. Ms. Long had had
no contact with him for the last four
months. There was no familial histo-ry
of congenital anomalies, and the
mother could not recall any expo-
sure to communicable diseases dur-
ing her pregnancy.
General: Length 39 cm, head circumfer-
ence 27 cm, weight 1,200 gm. No
obvious anomalies. Abundant lanugo.
Skin turgor fair. Color pallid.
Head, eyes, ears, nose, throat: Normo-
cephalic. Anterior fontanel open,
flat, soft. Posterior fontanel not
appreciated. Sutures overlapping.
Pupils sluggishly reactive. Red reflex
elicited. Pinna aligned above eye-
occiput line with slow recoil. Nares
patent without drainage. Palate
intact. Mucous membranes pink. Neck
supple without masses.
66 Vol. 11 No. 3
152
Chest: Clear to auscultation. Point of
maximal impulse nondisplaced.
Nipples visualized. No palpable areo-
lar tissue.
Cardiovascular: Regular rate and
rhythm without murmur. Femoral
pulses +1/4. Brachial and radial puls-
es not appreciated. Capillary refill 6
seconds.
Gastrointestinal: Soft, nontender,
nondistended abdomen. No organ-
omegaly. Absent bowel sounds. Anus
grossly patent.
Extremities: All digits present. No sacral
dimples or hair tufts. Hip check
deferred. Full range of motion.
Extensive bruising of lower extremi-
ties.
Neurological: Lethargic. Absent Moro
reflex. Weak gag and palmar reflexes
Intact plantar and Babinski reflexes.
Laboratory data: CBC: hemoglobin
14.1; hematocrit 39.6; WBC 8,200;
platelets 218,000; neutrophils 22
percent; lymphocytes 64 percent;
monocytes 12 percent; eosinophils 1
percent; basophils 1 percent.
Glucose: 67 mg/dL.
Approximately 16 minutes after
departing from the referring hospital,
the infant’s heart rate dropped precipi-
tously to 60. The FiO2 was immediately
increased to 100 percent, and the
infant’s chest was auscultated.
Decreased breath sounds were heard on
the left side. Slight tension was placed
on the endotracheal tube, and resusci-
tation was initiated. The ambulance
driver was instructed to return immed-
iately to the referring hospital.
After 30 seconds, no improvement
was observed, so 0.3 cc epinephrine
1:10,000 was given via the umbilical
venous line. Because decreased breath
sounds continued to be heard over the
left chest, a 25-gauge butterfly needle
was placed in the left, anterior second
intercostal space at the midclavicular
line. No air was obtained. Resuscitation
continued, and two subsequent doses of
epinephrine were given per AHA-AAP
guidelines for neonatal resuscitation.
Chest compressions were halted 13
minutes into the code when the infant’s
heart rate reached 100. A chest x-ray
film in the referring hospital emergency
room showed no evidence of pneu-
mothorax and was essentially unchanged
from the previous film—severe respira-
tory distress syndrome persisted. A right
radial arterial blood gas specimen was
profoundly acidotic: pH 7.06, PCO2
41.8, PO2 98.9, bicarbonate 11.8, oxy-
gen saturation 97 percent.
A peripheral catheter was placed in the
left antecubital vein, and 2.4 mEq
sodium bicarbonate was infused while an
umbilical artery catheter was insert-ed.
The repeat arterial blood gas 20 minutes
after the infusion demonstrated a
worsening situation: pH 7.00, PCO2
80.5, PO2 11.5, bicarbonate 19.9, oxy-
gen saturation 12 percent. Despite
aggressive ventilatory and pharmacolog-
ic maneuvers, the neonate expired soon
thereafter.
What Is Your Assessment?
In a premature neonate with the his-
tory just presented, consideration must
be given to the following possible clini-
cal problems: (1) severe respiratory dis-
tress syndrome, (2) sepsis, (3) perinatal
asphyxia, and (4) other.
Many clues were offered that lead to
the conclusion that Baby Long had
severe respiratory distress syndrome.
Not only were several perinatal risk fac-
tors for the disease present, including
prematurity and male gender, but fac-tors
likely to acutely impair surfactant
production, release, or function (possi-
ble perinatal asphyxia and precipitous
delivery) could also be identified.1,2
Furthermore, in the postnatal period, the
chest x-ray examination demonstrat-ed
the classic radiographic appearance of
low-volume lungs with a reticulogranu-
lar pattern and air bronchograms.3
The keys to successful management of
neonates with respiratory distress syn-
drome are (1) to prevent hypoxemia
and acidemia in order to optimize
endogenous surfactant production, (2)
to reduce metabolic demands so as to
minimize oxygen requirements and car-
bon dioxide production, (3) to improve
lung function, and (4) to minimize
APRIL 1992 / NEONATAL NETWORK
barotrauma.2,3 In this case, it seemed history suggested no clues, and the That leaves the dreaded “other” cat-
that early implementation of mechanical leukocyte or differential counts revealed egory to be considered. According to
ventilation and appropriate use of an no abnormalities. Blood cultures subse- AHA-AAP guidelines, one of the cardi-
exogenous surfactant preparation were quently proved negative by 72 hours nal initial steps after delivery involves
initially effective in accomplishing these postmortem and discounted septic preventing heat loss by placing the infant
goals, as evidenced by the first arterial shock as the etiology of the metabolic under a radiant heat source and drying
blood gas results. However, the acute acidosis. off the amniotic fluid.6 These steps
clinical deterioration that occurred dur- Perinatal asphyxia should also be become even more crucial for the
ing transport after surfactant administra- considered as a possible etiology of the premature neonate who is compro-
tion, made it necessary for the team to metabolic acidosis and central nervous mised by decreased amounts of subcu-
look for other, concomitant taneous fat to act as insula- tion
FIGURE 1 • The effects of cooling
problems. against the cold, reduced
Because decreased breath Cooling amounts of mitochodria-
sounds were heard over the left enriched brown fat to serve
chest and because some as a heat source, increased
Norepinephrine
infants respond rapidly to sur- Release
surface area/body weight
factant replacement therapy Brown Fat Increased ratio from which to lose heat,
with improved lung compli- Utilization Metabolic Rate and compromised oxygen
ance and subsequent pneu- Pulmonary Peripheral resources due to immature
Vasoconstriction Vasoconstriction
mothorax, the initial thera- lungs.7
peutic goal was to rule out The recommended inter-
this possibility. As noted, nei- Increased Right- Decreased Oxygen ventions eliminate potential
ther direct needle aspiration to-Left Shunting Delivery to Tissues radiant and conductive losses of
nor radiograph supported this body heat and minimize
hypothesis. Closer inspection evaporative losses.8 Undoubt-

APPENDICES
Free Fatty Increased Oxygen
of both the initial arterial Acid Release Consumption
edly, the initial stabilization
blood gas results obtained Hypoxemia Hypoxia measures at the referring hos-
before surfactant administra- pital included these cardinal
tion and transport and subse- steps. Retrospectively though,
quent blood gas results ob- Dependence on it became obvious that further
Anerobic Metabolism
tained after deterioration of heat losses were not or could
the infant made it obvious not be prevented, as evi-
that a profound primary Lactic Acidosis
denced by the axillary temper-
metabolic acidosis was pre- ature of 88.7°F at two and a half
sent. Respiratory compensa- hours of life. As Figure 1
tion with mechanical ventila- ? Death suggests, this cold stress had
tion had all but obscured it on the potential to significantly
the first blood gas results. complicate the infant’s respira-
What was the source? Why was tory status by the time of the
the infant hypotensive and lethargic? system depression, especially in the face final blood gas results and probably was
The possibility of fulminant septic of prematurity and a breech presenta- an important contributing factor leading
shock should always be considered in tion.5 However, because the fetal heart to his demise.
the preterm infant who deteriorates rate and beat-to-beat variability did not
suddenly with severe metabolic acidosis, seem to be compromised prior to the Conclusion
signs of systemic hypoperfusion, unex- birth and appropriate resuscitative mea- It is a sad fact that in 1992, infants
plained lethargy, and intractable sures, including prompt assisted ventila- continue to die of hypothermia more
hypotension.4 Because initial clinical tion, were initiated at delivery, it was than 30 years after Dr. W.A. Silverman
signs of septic shock are commonly sub- unlikely that perinatal asphyxia was the and his colleagues described its effects on
tle and nonspecific, a high index of sus- overriding problem for Baby Long. morbidity and mortality.9 This case study
picion, a thorough investigation, and Additionally, although the infant did represents one of two cases of document-
prompt initiation of appropriate treat- present in a breech manner, delivery ed intractable hypothermia encountered
ment are essential to improve the out- occurred in an uncomplicated fashion, by the aforementioned transport team
come. Although not discounted at the and the Apgar scores did not reflect during the last year. Because it is not an
time of clinical deterioration, maternal ongoing perinatal depression. uncommon problem, nurses must recog-

NEONATAL NETWORK / APRIL 1992 Vol. 11 No. 3 67

153
 nize the danger signs and symptoms of
hypothermia, including pallid skin, cyan-
otic extremities, poor tissue perfusion,
central nervous system depression,
metabolic acidosis, alterations in glucose
homeostasis, and compromised respir-
atory function.7,8
More important is preventing this
complication by using common sense.
Because heat loss cannot occur in the
absence of a thermal gradient, it is
essential to avoid exposing the baby to a
cold environment by warming the envi-
ronment (delivery room or nursery) to
avoid radiant and conductive losses, by
covering the baby with a clear plastic
sheet or acrylic heat shield to mini-
mize evaporative losses in a radiant bed,
and by using equipment properly. A
radiant warmer provides free access to
infants who require frequent unimpeded
procedures. It allows these procedures
to be performed with minimal changes
in an infant’s skin temperature—as long
as the temperature probe is firmly
attached to the infant’s skin and the
heat source is not blocked by drapes or
68 Vol. 11 No. 3
154
other unnecessary paraphernalia. Finally
the value of frequent vital signs assess-
ments in the first hours of life cannot be
overemphasized.
REFERENCES
1. Farrel PM, and ME Avery. 1975. Hyaline
membrane disease. American Review of
Respiratory Diseases 111: 657-688.
2. Liley HG, and AR Stark. 1991.
Respiratory distress syndrome/hyaline
membrane disease. In Manual of
Neonatal Care, ed. JP Cloherty and AR
Stark, 189-195. Boston: Little, Brown.
3. Martin RJ, MH Klaus, and AA Fanaroff.
1986. Respiratory problems. In Care of
the High Risk Neonate, ed. MH Klaus and
AA Fanaroff, 171-201. Philadelphia:
WB Saunders.
4. Laurenti F. 1990. Granulocyte transfu-
sion. In Current Therapy in Neonatal-
Perinatal Medicine, ed. NM Nelson,
427-430. Philadelphia: BC Decker.
5. Phibbs R. 1990. Delivery room manage-
ment of the newborn. In Neonatology:
Pathophysiology and Management of the
Newborn, ed. GB Avery, 212-231.
Philadelphia: JB Lippincott.
6. Bloom RS, and C Cropley 1987.
Textbook of Neonatal Resuscitation.
Elk Grove: American Heart Association/
American Academy of Pediatrics.
7. Washington S. 1978. Temperature con-
trol of the neonate. Nursing Clinics of
North America 13: 23-28.
8. Perlstein P. 1987. The thermal environ-
ment: Temperature and survival. In
Neonatal-Perinatal Medicine: Diseases of
the Fetus and Infant, ed. AA Fanaroff and
RH Martin, 398-416. St. Louis: CV
Mosby.
9. Silverman WA, JW Fertig, and AP Berger.
1958. The influence of thermal environ-
ment upon the survival of newly born
premature infants. Pediatrics 22: 876.
About the Author
Lynn E. Lyman is currently employed as a
neonatal nurse practitioner at the Medical
Center of Delaware in Newark. She received
her masters degree in maternal-child nursing
from the University of Delaware and her
neonatal nurse practitioner certificate from
Georgetown University Hospital. She is a
member of NAACOG and is president of
NANN’s Special Interest Group for Advanced
Practice in Neonatal Nursing.
APRIL 1992 / NEONATAL NETWORK