4_stable blood pressure

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MODULE FOUR BLOOD PRESSURE S UGAR and SAFE Care T EMPERATURE A IRWAY B LOOD PRESSURE L AB WORK E MOTIONAL SUPPORT 129

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S U G A R a n d S A F E C a r e

T E M P E R A T U R E

A I R W A Y

B L O O D P R E S S U R E

L A B W O R K

E M O T I O N A L S U P P O R T

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Upon completion of this module, participants will gainincreased understanding of:

1. The causes, presentation, and initial treatment of thethree 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 theyrelate to shock.

4. Indications for, mixing, and safe administration of dopamine.

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

The Three Types of Shock:Hypovolemic, Cardiogenic, Septic

Hypovolemic ShockHypovolemic shock results from a low circulating bloodvolume. 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)

BLOOD PRESSURE – Module Objectives

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• Postnatal hemorrhage

ª Brain

ª Lung

ª Adrenal glands

ª Scalp (subgaleal hemorrhage)

• Non-hemorrhagic causes

ª Severe capillary leak secondary to infection

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 intrapartumperiod. Infants in hypovolemic shock present with signs of poor cardiac output: tachycardia, weakpulses, prolonged capillary refill time, mottling, and cyanosis. If there is severe blood loss they willappear 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 ShockCardiogenic (heart failure) shock results when the heartmuscle 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 flowinto the systemic circulation

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An infant in shock may exhibit the following signs:

Respiratory effortª Increased work of breathing (retractions, grunting,

nasal flaring)

ª Tachypnea

ª Apnea

ª Gasping (an ominous sign of impending cardiorespiratory arrest)

Pulsesª Weak peripheral pulses (the pulses feel decreased or the

pulses are not palpable)

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

(continued on page 133)

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Septic (distributive) ShockSevere infection may lead to a third type of shock known asseptic or distributive shock. Infants who are in septic shockbecome rapidly and critically ill. In the presence of bacterialinfection, a host of complicated systemic reactions occur thatresult in circulatory insufficiency. A hallmark of this type ofshock is hypotension that responds poorly to fluidresuscitation. Loss of vascular integrity allows fluid to leak outof the blood vessels and into the tissue spaces (also a causeof hypovolemic shock). Poor myocardial contractility leads topoor tissue perfusion and oxygenation. These infants oftenneed blood pressure medication to treat the severe hypotension. The risk for organ injury and deathis very high.

Not infrequently, infants may have a combination of the three types of shock.

Table 4.1. Physical examination for shock.

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Peripheral perfusion ª Poor perfusion (results from vasoconstriction and poor

cardiac output)

ª Prolonged capillary refill time (greater than 3 seconds in asick infant is generally considered abnormal)

ª Mottled skin

ª Cool skin

Color

ª Cyanosis

ª Pale, white skin color (may indicate very low hemoglobinsecondary 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 ofpoor 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 minuteat rest)

▫ Tachycardia may indicate poor cardiac output and / orcongestive heart failure

▫ A normal heart rate is between 120 and 160 beats perminute, but may range between 80 and 200 dependingupon 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 ofcongestive 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)

Table 4.1. Physical examination for shock. (continued)

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

The shaded yellow area is considered normal.

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

cardiac decompensation

Note: the blood pressure reading may be within normalrange because of vasoconstriction and centralization ofblood pressure. In other words, blood is “shunted away”from non-vital organs to allow for perfusion of vitalorgans. By the time the blood pressure drops andhypotension becomes apparent, the patient is usually inan advanced state of shock.

ª Evaluate the pulse pressure by subtracting the diastolicfrom 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 mayindicate peripheral vasoconstriction, heart failure, or low cardiac output. A wide pulse pressuremay indicate a large aortic runoff, as seen with a significant patent ductus arteriosus or largearteriovenous malformation. A narrow or wide pulse pressure should be reported to the infant’shealthcare practitioner.

Table 4.1. Physical examination for shock. (continued)

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

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Figure 4.2. Evaluation of capillary filling time. To check capillary filling time, press firmly for fiveseconds and release. Count how many seconds the skin takes to re-fill. Compare the upper to lowerbody. If greater than 3 seconds on the upper or lower body, or if the lower body is greater than theupper 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 gasMetabolic acidosis is present if the pH and bicarbonate are low. If the infant isexperiencing respiratory insufficiency, then the PCO2 will also be elevated and the infant willhave a mixed respiratory and metabolic acidosis.

ª pH < 7.30 is abnormal.

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 shockª Glucose

▫ In response to stress, the infant may initially be hyperglycemic. Evaluate the bloodsugar 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 calciumª Liver function testsª Renal function testsª Coagulation studies (prothrombin time, partial thromboplastin time, fibrinogen, D-dimer)ª Blood lactate to confirm lactic acidosis

Other tests and observationsª 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 othermetabolic screens (urine and serum amino acids and organic acids)

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The Principles of Cardiac OutputCardiac output (CO) is influenced by heart rate (HR) andstroke 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 haslimited capacity to increase stroke volume on its own,therefore, in response to shock the infant will attempt toincrease cardiac output by increasing heart rate. This resultsin tachycardia.

Factors that Negatively Affect Heart FunctionIn addition to electrolyte, mineral, or energy imbalances, factors that can reduce cardiac outputinclude 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 isejected with every beat.

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

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LacticAcid Buildup

Cardiac OutputVolume Support, Inotropes

pH

Tissue Oxygenation

Tissue Perfusion

AnaerobicMetabolism

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 inshock. Oxygen supply to the tissues must improve in order to reverse the effects of shock.

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Treatment of Hypovolemic (low blood volume) Shock

The goal of treatment is to improve the circulating blood volume. This can be accomplished byadministering 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 dependentupon the severity of the situation and mayneed to be more rapid.

*For treatment of severe shock, it may be necessary to provide two, three or more volume boluses. Evaluatethe infant’s response to treatment (changes in heart rate, perfusion, and blood pressure) following eachbolus and decide if more volume is necessary.

If there is a history of chronic blood loss, some infants in severe shock may nottolerate volume boluses. Consultation with the tertiary center neonatologist isadvised 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.

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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

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

What blood type can be administeredduring an emergency when there

is not enough time to perform a type and cross-match?

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

readily available for the immediate treatment of shock,

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

What is the difference between crystalloids and colloids?

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Treatment of Cardiogenic (heart failure) ShockEvaluate the infant for tachycardia, bradycardia, hypotension,oliguria, hypoxemia, acidosis, and hypoglycemia, becausethese signs may be present when an infant is in cardiogenicshock. Treatment is aimed at correcting the underlyingproblems that may negatively affect heart function. Theseinclude (but are not limited to), hypoxia, hypoglycemia,hypothermia, hypotension, acidosis, arrhythmias, infection,and electrolyte or mineral imbalances.

Treatment of Septic (distributive) ShockTreatment involves a combination of hypovolemic and cardiogenic shock therapies. The septicinfant may require more fluid boluses than in other types of shock given the movement of fluidfrom the intravascular compartment into the interstitial space, or extravascular compartment. This isdue to capillary injury as well as pooling of blood in the capillary bed. A continuous drip infusion ofdopamine will be necessary to treat severe hypotension. It is critically important to optimizeoxygenation and ventilation when treating septic shock.

Medications Used to Treat Cardiogenicand 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 forhypovolemic 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 controlphysician if unsure whether sodium bicarbonate is indicated. Most important is toidentify 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 tointraventricular hemorrhage in preterm infants

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Dopamine HydrochlorideIndications: Poor cardiac contractility

Dose: 5 to 20 micrograms per kg per minute(mcg/kg/minute)

Route: IV continuous infusion (IV pump)

Table 4.3. Dopamine dose and effect.

Do not give via any arterial route or throughan endotracheal tube

Dosage Receptors Effect

0.5 to 2 mcg/kg/min Dopaminergic (stimulation ofdopaminergic receptors)

Renal and mesentericvasodilatation; little effect onblood pressure

2-10 mcg/kg/min Beta-adrenergic (beta1

receptors activated)Beta-adrenergic (beta1

receptors activated)

Greater than 10 mcg/kg/min Alpha-adrenergic (alphareceptors activated)

Vasoconstriction; increasedsystolic and diastolic blood pressure

From Osborn et al. (2004). NeoReviews, Vol. 5, No. 3, p. e114.

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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 recommendeddopamine infusion described below is a relatively dilute one. More concentrated solutions are usuallyprovided in the neonatal intensive care unit.

Step 1: Select the pre-mixed dopamine solution asdescribed in option one, or mix the solution asdescribed in option two.

Option OneA commercially prepared pre-mixed dopamine dripsolution 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 TwoA commercially prepared pre-mixed dopaminesolution 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 per250 ml IV fluid).

5. Label the IV bag with the following: This 250 ml bag of D10W contains 800 mcg dopamine perml IV fluid.

6. Infuse dopamine on an infusion pump.

Dopamine Dosing for Newborns

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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.

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Ordered Dose (mcg/kg/min) using a dopamine solution containing 800 mcg per ml of IV fluid

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

Weightin kg

5mcg/kg/min

7.5mcg/kg/min

10mcg/kg/min

12.5mcg/kg/min

15mcg/kg/min

17.5mcg/kg/min

20mcg/kg/min

25mcg/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

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

If a pre-mixed dopamine solution is not available, place the following items in a plastic bag orcontainer and keep with emergency medications:

250 ml bag of D10WDopamine 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 FellowshipProgram; Assistant Professor Pediatrics; University of Maryland School of Medicine; 22 S. Greene Street, Room N5E13B; Baltimore, MD 21201;Research website: www.icudrips.org

Note: some rounding has occurred to simplify infusion rate.

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Rules for Dopamine Infusion

1. In most cases, volume boluses are administered before itis determined that dopamine is necessary.

2. The starting dose for dopamine should be selected basedon 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 ismixed to yield a more concentrated solution thanpresented 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 5minutes depending upon response to the medication. If an infant is failing to respond to a doseof 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” technologywhenever possible.

5. Administer through an umbilical venous site if the catheter’s position has been confirmed by chestx-ray and the tip is appropriately located above the liver at the inferior vena cava/right atrialjunction. If no central venous access is available, infuse dopamine through a peripheral IV. Carefullymonitor the infusion site for extravasation (infiltration) and change infusion sites if the IV shouldinfiltrate. 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 tosurge 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:

1. Dopamine should be mixed in D10W (so that the glucose

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 hourlyinfusion rate of 10 ml per hour.

Clinical Tip

Do I need to adjust the IV ratewhen administering dopamine?

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Practice Session: Dopamine rate

A dopamine standardized concentration of 800 mcg per mlIV fluid has been prepared.

Using the infusion graph on page 143 answer the followquestions:

1. A dose of 10 mcg/kg/minute of dopamine is ordered fora 3.8 kg infant. What infusion rate will this infant require?

2. A dose of 5 mcg/kg/minute of dopamine is ordered for a1.4 kg infant. What infusion rate will this infant require?

p.149

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Appendix 4.1 HYPERLINK: Evaluation of Scalp Swelling

APPEN

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Slide 1

Slide 3

Slide 5

Slide 2

Slide 4

Slide 6

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APPENDIX 4.1 (continued)

Slide 7

Slide 9

Slide 11

Slide 8

Slide 10

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

APPEN

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Slide 1

Slide 3

Slide 5

Slide 2

Slide 4

Slide 6

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Appendix 4.2 (continued)

Slide 7

Slide 9

Slide 8

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APPEN

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When I began this column last year, Ipromised to try to use it as a forum toget back to the basics and presentinteresting case studies. This articlerepresents my first attempt to combinethose goals. The following true caseoccurred during the transport of acritically ill neonate to a Level III EastCoast facility. The patient’s name hasbeen changed for legal protection ofthat facility.

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 breechpresentation shortly after her arrival at aLevel I obstetrical facility. Just prior todelivery, the fetal heart rate had beenassessed at 140 beats per minute withexcellent variability. Amniotic mem-branes ruptured at delivery, and the fluidwas noted to be normal in volume, color,and odor.

On initial physical assessment, theneonate’s heart rate was auscultated at60 beats per minute despite vigoroustactile stimulation and oropharyngealsuctioning. Hence, bag-mask ventilationwith 100 percent oxygen and chest com-pressions were initiated, followed bysuccessful endotracheal intubation with

a 2.0 endotracheal tube by three minutesof life. The infant’s heart rate increasedto 120 almost immediately, and no fur-ther resuscitative efforts were necessary.Apgars were 1 and 7 at one and fiveminutes, respectively. A 10 percent dex-trose infusion was started via an umbili-cal venous catheter at 80 cc/kg/day.After obtaining blood specimens forculture and hematologic analysis, ampi-cillin and gentamicin were administeredintravenously.

By 25 minutes of life, the infant’soxygen saturation by pulse oximetrywas consistently in the 90-100 percentrange as long as a respiratory therapistdelivered positive pressure ventilation tothe endotracheal tube with an anesthesiabag. The initial chest x-ray film showedthat the endotracheal tube waspositioned at the carina and that theinfant had severe respiratory distresssyndrome. No other cardiorespiratoryabnormalities were appreciated. Afterthe endotracheal tube was repositionedat 35 minutes of life, a referral call wasplaced to the tertiary care facilityrequesting transport services.

When the transport team (neonatalnurse practitioner and nurse) arrived, thetwo and a half hour old premature infant

was found lying in an open radiantwarming bed located in the same roomwhere he had been born, loosely coveredby a sterile drape. The circulating nurseand respiratory therapist were present,but the referring pediatrician had beencalled away to another emergency.

They reported that no significantproblems had occurred since the initialtelephone call except for the attendingphysician being unsuccessful inobtaining an arterial blood gas beforebeing called away. Hence, the infant’sacid base status was undocumented. Thetransport nurse found that thecirculating nurse had removed the bed’stemperature sensor from skin contactbecause of “frequent alarms” and placedthe bed on manual control mode.

Because almost an hour had elapsedsince the last vital signs assessment, thetransport nurse promptly obtained them.The infant’s axillary temperaturemeasured 88.7°F, and his blood pressurewould not register on a noninvasivemonitor. The Dextrostix measurementwas 40-80. His other vital signs werewithin the expected normal range for hisweight and gestational age.

After reviewing the chest x-rayexamination, the transport team elect-

It Isn’t Just the Lungs:A Case Presentation

Lynn E. Lynam, RNC, MS, NNP

CONTRIBUTING EDITOR

M

NEONATAL NETWORK / APRIL 1992 Vol. 11 No. 3 65Reproduced with permission from Lynam, L.E. (1992). It isn’t just the lungs: A case presentation. Neonatal Network 11(3): 65-68.

Appendix 4.2 (continued)

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ed to replace the 2.0 endotracheal tubewith a 3.0 and to administer exoge-nous surfactant. Baby Long was thenplaced on a transport ventilator set at thefollowing parameters: PIP 22, PEEP 5,IMV 60, I-time 0.4 seconds, FiO2 100percent.

The following blood gas values wereobtained from a right radial arteryspecimen ten minutes later: pH 7.38,PCO2 19.7, PO2 151, bicarbonate 11.4,oxygen saturation 100 percent. Based onthese values, the PIP was decreased to20, the IMV was decreased to 40breaths and the FiO2 was decreased to95 percent.

After visiting briefly with Ms. Longand discussing the infant’s conditionwith her, the transport team left thereferring hospital. Arrival time todeparture time was 40 minutes. Vitalsigns and physical examination ondeparture from the referring hospitalwere recorded as follows:Vital signs: Temperature 89°F, pulse rate

136, respiratory rate 40. Dextrostixhad increased to 180; blood pressurecontinued 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 beenrecently jailed for selling and dis-tributing cocaine. Ms. Long had hadno contact with him for the last fourmonths. There was no familial histo-ryof congenital anomalies, and themother 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. Noobvious anomalies. Abundant lanugo.Skin turgor fair. Color pallid.

Head, eyes, ears, nose, throat: Normo-cephalic. Anterior fontanel open,flat, soft. Posterior fontanel notappreciated. Sutures overlapping.Pupils sluggishly reactive. Red reflexelicited. Pinna aligned above eye-occiput line with slow recoil. Narespatent without drainage. Palateintact. Mucous membranes pink. Necksupple without masses.

Chest: Clear to auscultation. Point ofmaximal impulse nondisplaced.Nipples visualized. No palpable areo-lar tissue.

Cardiovascular: Regular rate andrhythm without murmur. Femoralpulses +1/4. Brachial and radial puls-es not appreciated. Capillary refill 6seconds.

Gastrointestinal: Soft, nontender,nondistended abdomen. No organ-omegaly. Absent bowel sounds. Anusgrossly patent.

Extremities: All digits present. No sacraldimples or hair tufts. Hip checkdeferred. Full range of motion.Extensive bruising of lower extremi-ties.

Neurological: Lethargic. Absent Mororeflex. Weak gag and palmar reflexesIntact plantar and Babinski reflexes.

Laboratory data: CBC: hemoglobin14.1; hematocrit 39.6; WBC 8,200;platelets 218,000; neutrophils 22percent; lymphocytes 64 percent;monocytes 12 percent; eosinophils 1percent; 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 immediatelyincreased to 100 percent, and theinfant’s chest was auscul ta ted.Decreased breath sounds were heard onthe left side. Slight tension was placedon the endotracheal tube, and resusci-tation was initiated. The ambulancedriver was instructed to return immed-iately to the referring hospital.

After 30 seconds, no improvementwas observed, so 0.3 cc epinephrine1:10,000 was given via the umbilicalvenous line. Because decreased breathsounds continued to be heard over theleft chest, a 25-gauge butterfly needlewas placed in the left, anterior secondintercostal space at the midclavicularline. No air was obtained. Resuscitationcontinued, and two subsequent doses ofepinephrine were given per AHA-AAPguidelines for neonatal resuscitation.

Chest compressions were halted 13minutes into the code when the infant’s

heart rate reached 100. A chest x-rayfilm in the referring hospital emergencyroom showed no evidence of pneu-mothorax and was essentially unchangedfrom the previous film—severe respira-tory distress syndrome persisted. A rightradial arterial blood gas specimen wasprofoundly acidotic: pH 7.06, PCO241.8, PO2 98.9, bicarbonate 11.8, oxy-gen saturation 97 percent.

A peripheral catheter was placed in theleft antecubital vein, and 2.4 mEqsodium bicarbonate was infused while anumbilical artery catheter was insert-ed.The repeat arterial blood gas 20 minutesafter the infusion demonstrated aworsening situation: pH 7.00, PCO280.5, PO2 11.5, bicarbonate 19.9, oxy-gen saturation 12 percent. Despiteaggressive ventilatory and pharmacolog-ic maneuvers, the neonate expired soonthereafter.

What Is Your Assessment?In a premature neonate with the his-

tory just presented, consideration mustbe given to the following possible clini-cal problems: (1) severe respiratory dis-tress syndrome, (2) sepsis, (3) perinatalasphyxia, and (4) other.

Many clues were offered that lead tothe conclusion that Baby Long hadsevere respiratory distress syndrome.Not only were several perinatal risk fac-tors for the disease present, includingprematurity and male gender, but fac-torslikely to acutely impair surfactantproduction, release, or function (possi-ble perinatal asphyxia and precipitousdelivery) could also be identified.1,2

Furthermore, in the postnatal period, thechest x-ray examination demonstrat-edthe classic radiographic appearance oflow-volume lungs with a reticulogranu-lar pattern and air bronchograms.3

The keys to successful management ofneonates with respiratory distress syn-drome are (1) to prevent hypoxemiaand acidemia in order to optimizeendogenous surfactant production, (2)to reduce metabolic demands so as tominimize oxygen requirements and car-bon dioxide production, (3) to improvelung function, and (4) to minimize

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barotrauma.2,3 In this case, it seemedthat early implementation of mechanicalventilation and appropriate use of anexogenous surfactant preparation wereinitially effective in accomplishing thesegoals, as evidenced by the first arterialblood gas results. However, the acuteclinical deterioration that occurred dur-ing transport after surfactant administra-tion, made it necessary for the team tolook for other, concomitantproblems.

Because decreased breathsounds were heard over the leftchest and because some infants respond rapidly to sur-factant replacement therapywith improved lung compli-ance and subsequent pneu-mothorax, the initial thera-peutic goal was to rule out this possibility. As noted, nei-ther direct needle aspiration nor radiograph supported thishypothesis. Closer inspection of both the initial arterial blood gas results obtainedbefore surfactant administra-tion and transport and subse-quent blood gas results ob-tained after deterioration of the infant made it obvious that a profound primarymetabolic acidosis was pre-sent. Respiratory compensa-tion with mechanical ventila-tion had all but obscured it onthe first blood gas results. What was the source? Why wasthe infant hypotensive and lethargic?

The possibility of fulminant septicshock should always be considered in the preterm infant who deterioratessuddenly with severe metabolic acidosis,signs of systemic hypoperfusion, unex-plained lethargy, and intractablehypotension.4 Because initial clinicalsigns of septic shock are commonly sub-tle and nonspecific, a high index of sus-picion, a thorough investigation, andprompt initiation of appropriate treat-ment are essential to improve the out-come. Although not discounted at thetime of clinical deterioration, maternal

history suggested no clues, and theleukocyte or differential counts revealedno abnormalities. Blood cultures subse-quently proved negative by 72 hourspostmortem and discounted septic shock as the etiology of the metabolicacidosis.

Perinatal asphyxia should also beconsidered as a possible etiology of themetabolic acidosis and central nervous

system depression, especially in the faceof prematurity and a breech presenta-tion.5 However, because the fetal heartrate and beat-to-beat variability did notseem to be compromised prior to thebirth and appropriate resuscitative mea-sures, including prompt assisted ventila-tion, were initiated at delivery, it wasunlikely that perinatal asphyxia was theoverriding problem for Baby Long.Additionally, although the infant didpresent in a breech manner, deliveryoccurred in an uncomplicated fashion,and the Apgar scores did not reflectongoing perinatal depression.

That leaves the dreaded “other” cat-egory to be considered. According toAHA-AAP guidelines, one of the cardi-nal initial steps after delivery involvespreventing heat loss by placing the infantunder a radiant heat source and drying off the amniotic fluid.6 These stepsbecome even more crucial for thepremature neonate who is compro- mised by decreased amounts of subcu-

taneous fat to act as insula- tionagainst the cold, reducedamounts of mitochodria-enriched brown fat to serve as a heat source, increasedsurface area/body weightratio from which to lose heat,and compromised oxygenresources due to immaturelungs.7

The recommended inter-ventions eliminate potentialradiant and conductive losses ofbody heat and minimizeevaporative losses.8 Undoubt-edly, the initial stabilizationmeasures at the referring hos-pital included these cardinalsteps. Retrospectively though,it became obvious that furtherheat losses were not or couldnot be prevented, as evi-denced by the axillary temper-ature of 88.7°F at two and a halfhours of life. As Figure 1suggests, this cold stress hadthe potential to significantlycomplicate the infant’s respira-tory status by the time of the

final blood gas results and probably wasan important contributing factor leadingto his demise.

ConclusionIt is a sad fact that in 1992, infants

continue to die of hypothermia morethan 30 years after Dr. W.A. Silvermanand his colleagues described its effects onmorbidity and mortality.9 This case studyrepresents one of two cases of document-ed intractable hypothermia encounteredby the aforementioned transport teamduring the last year. Because it is not anuncommon problem, nurses must recog-

FIGURE 1 • The effects of cooling

Cooling

NorepinephrineRelease

Brown Fat IncreasedUtilization Metabolic Rate

Pulmonary PeripheralVasoconstriction Vasoconstriction

Increased Right- Decreased Oxygento-Left Shunting Delivery to Tissues

Free Fatty Increased OxygenAcid Release Consumption

Hypoxemia Hypoxia

Dependence onAnerobic Metabolism

Lactic Acidosis

? Death

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nize the danger signs and symptoms ofhypothermia, including pallid skin, cyan-otic extremities, poor tissue perfusion,central nervous system depression,metabolic acidosis, alterations in glucosehomeostasis, and compromised respir-atory function.7,8

More important is preventing thiscomplication by using common sense.Because heat loss cannot occur in theabsence of a thermal gradient, it isessential to avoid exposing the baby to acold environment by warming the envi-ronment (delivery room or nursery) toavoid radiant and conductive losses, bycovering the baby with a clear plasticsheet or acrylic heat shield to mini-mize evaporative losses in a radiant bed,and by using equipment properly. Aradiant warmer provides free access toinfants who require frequent unimpededprocedures. It allows these proceduresto be performed with minimal changesin an infant’s skin temperature—as longas the temperature probe is firmlyattached to the infant’s skin and theheat source is not blocked by drapes or

other unnecessary paraphernalia. Finallythe value of frequent vital signs assess-ments in the first hours of life cannot beoveremphasized.

REFERENCES1. Farrel PM, and MEAvery. 1975. Hyaline

membrane disease. American Review ofRespiratory Diseases 111: 657-688.

2. Liley HG, and AR Stark. 1991.Respiratory distress syndrome/hyalinemembrane disease. In Manual ofNeonatal Care, ed. JP Cloherty and ARStark, 189-195. Boston: Little, Brown.

3. Martin RJ, MH Klaus, and AA Fanaroff.1986. Respiratory problems. In Care oftheHighRiskNeonate, ed.MHKlausandAA 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 theNewborn, 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 ofNorth America 13: 23-28.

8. Perlstein P. 1987. The thermal environ-ment: Temperature and survival. InNeonatal-Perinatal Medicine: Diseases ofthe Fetus and Infant, ed. AA Fanaroff andRH Martin, 398-416. St. Louis: CVMosby.

9. Silverman WA, JW Fertig, and AP Berger.1958. The influence of thermal environ-ment upon the survival of newly bornpremature infants. Pediatrics 22: 876.

About the AuthorLynn E. Lyman is currently employed as aneonatal nurse practitioner at the MedicalCenter of Delaware in Newark. She receivedher masters degree in maternal-child nursingfrom the University of Delaware and herneonatal nurse practitioner certificate fromGeorgetown University Hospital. She is amember of NAACOG and is president ofNANN’s Special Interest Group for AdvancedPractice in Neonatal Nursing.