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Field Treatment
1. Pediatric primary field survey.[1][2]
2. Pediatric airway management.
Normal Perfusion
3. Place on cardiac monitor.[3]
Diminished perfusion or respiratory distress
2. If signs of diminished perfusion and heart rate < 60 despite adequate oxygenation & ventilation:
a. begin chest compressions.[4]
b. obtain vascular access (IV or IO).
c. administer 20 ml/kg fluid bolus per Pediatric Resuscitation Chart and Fluid Resuscitation protocol.[5]
3. Place on cardiac monitor (and pulse oximeter, if available).
4. Drug therapy:
a. Epinephrine
IV/IO: 0.01 mg/kg (1:10,000, 0.1 ml/kg).
ETT: 0.1 mg/kg (1:1,000, 0.1 ml/kg).
Repeat every 3-5 minutes at same dose if no response.
b. Atropine
IV/IO: 0.02 mg/kg.
Minimum single dose:0.1 mg.
Maximum single dose: 0.5 mg (child), 1 mg (adolescent).
May repeat once.
Special Considerations:
[1] Hypoxia is the most common cause of bradycardia in children. Non-rebreather mask preferred.
[2] The decision to treat bradycardia depends on whether signs of shock are present:
poor capillary refill.
decreased peripheral pulses.
cool, mottled extremities.
altered level of consciousness: lethargy, hallucinations, agitation, coma.
[3] ECG shows slow rate. P waves may or may not be visible. QRS duration may be normal or prolonged.
[4] Special considerations may apply in the setting of severe hypothermia. Call for additional orders.
[5] Appendix: Pediatric Resuscitation
Chart
Appendix: Fluid Resuscitation.
Emergency Medical Services for Children
Pediatric Advanced Life Support Course Student Manual
Developed in Conjunction with the American Heart Association
Cardiovascular Emergencies
Objectives
Upon completion of this session, the participant will be able to:
Describe a systematic assessment of the cardiovascular system.
Recognize clinical signs of poor systemic perfusion in a child.
Identify causes, presentation, and management of the most common arrhythmias in the pediatric patient.
Demonstrate the correct procedure for cardioversion and defibrillation in the pediatric patient, including choice of paddles, energy dose, electrode placement, safety considerations and post-defibrillation care.
Differentiate between hypovolemic, cardiogenic, and septic shock using physical and laboratory findings and state the appropriate treatment for each type of shock.
Describe the management of a child in shock.
I. Assessment
Assessment of tissue perfusion requires an understanding of cardiovascular physiology as well as familiarity with several common parameters used to measure cardiovascular function. Cardiac output (CO) is the total amount of blood pumped by the ventricles each minute; it is the product of the heart rate (HR) and the stroke volume (SV). Stroke volume is the volume of blood ejected by the heart with each beat. In infants and children SV is approximately 1.5 ml/kg. Three components, preload, afterload and contractility, determine stroke volume.
Preload is the degree of heart muscle stretch at end-diastole (i.e. ventricular end-diastolic volume.) It is determined by intravascular volume, relative to intravascular space, and by ventricular compliance. Venous return to the heart is the principal determinant of preload and changes in circulatory blood volume and venous compliance most directly influence venous return. Preload is one determinant of stroke volume. Preload can be manipulated with volume, diuretics and vasodilators such as nitroglycerin.
Afterload is the resistance against which the ventricle must pump when ejecting blood. An increase in afterload (e.g. aortic obstruction or arterial hypertension) will increase ventricular workload and oxygen consumption. Therefore, resulting in decreased myocardial performance. With increased resistance, the ventricle cannot empty efficiently and fluid backs up into the ventricles and pulmonary syste 727e43h m; resulting in congestive heart failure and pulmonary edema. Afterload can be manipulated by vasodilators and vasopressor therapy.
Contractility is the inherent ability of the myocardium to develop force and/or shorten. Factors that decrease contractility include acidosis, hypoxia, hypoglycemia, hypocalcemia, hypokalemia, hyperkalemia, toxins, sepsis and primary myocardial disease. Increases in contractility may be due to endogenous catecholamines, or exogenous inotropic agents.
The assessment of adequate cardiovascular function includes the following objective measurements and clinical parameters.
Heart Rate - Normal heart rates in children vary by age and have a wide variation within each age group.
Age Group/ Normal Value (beats/minute)
Infant 120 - 160
Toddler 90 - 140
Preschooler 80 - 110
School age 75 - 100
Adolescent 60 - 90
* Children are extremely dependent on adequate heart rate. Extremely rapid or slow rates can be the cause of cardiovascular compromise.
Bradycardia in an ill child is usually a very ominous finding. Inadequate oxygenation is usually the primary cause of bradycardia in infants and children.
Tachycardia is a nonspecific abnormality. It may be seen with fever, pain, anxiety or shock. Tachycardia is often the first sign of shock in children; it also represents a compensatory mechanism to maintain CO when SV is low, since SV x HR = CO. Monitoring HR is helpful as a sign of effective resuscitation of shock.
B. Assessment of Systemic Perfusion
Pulses - The intensity and rhythm of peripheral and central pulses should be recorded. Absent peripheral pulses are an important finding that usually corresponds to decompensated shock.
Capillary Refill - This is normally 2-3 seconds. The site of assessment should be a distal extremity that is elevated above the level of the child's heart.
Technique - Pressure on the nailbed or skin will cause it to turn white or blanch. When the pressure is released, the color should return within 2-3 seconds. If the color does not return within that time, the capillary refill is said to be delayed. Capillary refill cannot be reliably assessed if the child is cold.
Skin color - Decreased perfusion of the skin is an early sign of shock. Mottled skin color in an ill child indicates high systemic vascular resistance. The skin is typically cool as well. Cyanosis may not be present, especially if hemoglobin is £ 10 gm%.
Level of Consciousness - Cardiovascular performance directly affects mental status, since brain tissue requires adequate perfusion to function properly. The child should respond to parents and interventions. He/she may be restless, agitated or lethargic when perfusion is inadequate. Recognition of and visual following of the parents is a good sign; with inadequate brain blood flow, failure to recognize parents or respond to noxious stimuli (needle sticks, etc) may be an early, ominous sign of cardiac hypoperfusion.
As cerebral blood flow diminishes, the child's level of consciousness progresses through the following stages:
alert
sleepy/combative
unable to recognize parents
unresponsive to painful stimuli
exhibition of fluctuating levels of consciousness from stupor to deep coma
5. Temperature -Cool extremities do not necessarily indicate that the child is hypothermic but that the child may be in shock. In shock, a decrease in systemic perfusion leads to cool extremities because of the shunting of blood from the periphery to vital organs. The line of demarcation between regions where the skin is warm versus cool should always be noted.
*Mottling and delayed capillary refill are often present when systemic perfusion is compromised (possibly due to peripheral vasoconstriction caused by a cold ambient temperature).
6. Blood Pressure (BP) - BP is determined by cardiac output and peripheral vascular resistance. Since the child's normal blood pressure is lower than an adult's, smaller quantitative changes in a child's blood pressure may represent significant qualitative changes in his/her clinical condition. Normal blood pressure has a wide range.
The lowest acceptable systolic BP by age:
Age Group Minimum Systolic Values (mmHg)
0 - 1 month
60
1 month - 1 year 70
> 1 year 0 + (2 x age in years)*
*This formula may be used in children over one year of age and up to ten years of age. After 10, the lowest acceptable systolic blood pressure is 90 mm/Hg.
a) The cuff size is the most critical variable in obtaining an accurate blood pressure reading. If the cuff is too large, the BP will be falsely low; if the BP cuff is too small, the reading will be falsely high. The cuff width should not exceed 2/3 of the length of the upper arm. In addition, the bladder should at least encircle the arm.
Usual sizes
Age Group Cuff Width (in.)
Cuff Length (in.)
Newborn 1 - 1.5
Infant 2 - 3 3 - 5
Child 3 - 4 6 - 8
b) Blood pressure may be normal despite the presence of shock. Hypotension is a very late sign of cardiovascular decompensation in children. As seen in Figure 2, vascular resistance increases as blood volume is lost so that blood pressure is maintained until at least 25% of the circulatory blood volume is lost. Hypotension is a sign of decompensated shock.
c) Pulse pressure is the difference between systolic and diastolic blood pressure. Normal pulse pressure is related to the constant relationship of diastolic to systolic blood pressure; diastolic blood pressure should be 2/3 of systolic blood pressure. (Remember 120/80 is normal adult BP; 80 is 2/3 of 120).
Narrow pulse pressure represents increased systemic vascular resistance, as seen in hypovolemic or cardiogenic shock.
Wide pulse pressure represents a low systemic vascular resistance as seen in septic shock.
7) Heart sounds
S1 occurs as the ventricles contract and AV (mitral and tricuspid) valves close.
S2 occurs early during ventricular filling as aortic and pulmonic valves close.
S3 occurs early in diastole and sounds like the "Y" in Kentucky or a galloping horse. This usually indicates failure of the left ventricle.
S4 occurs late in diastole and sounds like "Tenn" in Tennessee.
More than .5 of all children develop murmurs secondary to differing growth rates of the structures in the heart and to rapid blood flow.
8) Respiratory status - With increased left ventricular end-diastolic pressure and increased left atrial pressure, pulmonary capillary pressures rise; this results in pulmonary edema. Signs of respiratory distress secondary to pulmonary congestion include:
Difficulty with feedings
Tachypnea
Retractions
Nasal flaring
Rales
Quiet tachypnea (e.g. rapid breathing without an increase in the work of breathing) suggests respiratory compensation and metabolic acidosis.
9) Urine output should average 1 cc/kg/hr if the child is well hydrated. In the absence of renal pathology, urine output is a good indicator of tissue perfusion and cardiac output.
III. ARRHYTHMIAS
Life-threatening or unstable arrhythmias in children are those which compromise systemic perfusion, or have the potential to deteriorate into rhythms which compromise systemic perfusion. Incidence of these rhythms are rare. Always evaluate the heart rate in light of age and clinical condition.
Normal ECG - An ECG is a recording of the electrical forces produced by the heart. Electrical depolarization begins in the sinoatrial (SA) node (primary pacemaker), located at the junction of the superior vena cava and the right atrium, and advances to the atrioventricular (AV) node via atrial tissue and internodal pathways; here it is temporarily slowed. It then progresses along the Bundle of His, through the left and right bundle branches to the Purkinje fibers and, finally, to the surrounding cardiac muscle cells (Figure 3).
Figure 3: Electrical Pathways of the Heart
Figure 4: The electrocardiogram
P-wave = depolarization of both atria. Disruption in the configuration or timing of the P wave may indicate either an atrial dysrhythmia or atrial enlargement.
PR interval = conduction of the impulse through the A-V node, the Bundle of His, the bundle branches and the Purkinje fibers.
QRS wave = depolarization of the ventricles.
T wave = ventricular repolarization.
B. Arrhythmias - Dysrhythmias in children are generally a complication of a non-cardiac problem, and treatment is appropriately directed to the underlying cause. Arrhythmias are caused by acid-base problems (hypoxia, acidosis); drugs (digoxin, aminophylline, or tricyclic antidepressants); metabolic abnormalities; hypothermia; diseases of the CNS (e.g. those abnormalities that cause increased intracranial pressure); electrolyte abnormalities (derangements of calcium, potassium and magnesium); structural congenital heart defects; congenital abnormalities of automaticity or conduction (SA node dysfunction or ectopic foci); or myocarditis. There are 3 basic types of arrhythmias; these can be classified by heart rate.
Fast - The tachyarrhythmias include both ventricular and supraventricular arrhythmias. When the heart rate is markedly elevated, the heart cannot fill between beats and coronary perfusion is inadequate. Therefore, stroke volume and cardiac output are reduced (CO = HR x SV). The most common mechanisms that produce tachydysrhythmias are reentry and ectopic pacemakers. Reentry accounts for the majority of tachydysrhythmias. The reentrant pathways may be present in the atria, ventricles or anywhere along the conduction system. Therapy for the reentrant tachyarrhythmias is based on interruption of the reentry circuit or prevention of premature beats that trigger the cycle. Ectopic pacemaker tachycardias are treated by suppressing the focus.
Slow - This category includes sinus bradycardia and heart block with a slow ventricular rate. The product of a relatively normal stroke volume and an abnormally slow heart rate usually is an inadequate cardiac output (CO = HR x SV). Slow rates may be secondary to slowing of the intrinsic pacemaker (sinus bradycardia) or to a block in impulse conduction from the SA node to the ventricles. The block may be complete, in which case the lower pacemaker (AV node) takes over (usually at a slow rate), or it may be incomplete and allow only a few impulses to pass (resulting in a reduced number of ventricular contractions). Most slow rates in children are due to hypoxia or to an increase in vagal tone. Correction of these 2 factors is the basis for treatment.
Absent/Collapse - No cardiac output is produced. Examples include asystole, ventricular fibrillation, and pulseless electrical activity.
All unstable rhythms (fast, slow or absent) result in depressed cardiac output and inadequate perfusion:
Type of rhythm CO = HR X SV
slow low = low x normal
fast low = high x low
absent 0 = 0 x 0
C. Principles of Therapy - In children, rhythm disturbances are treated as an emergency only if:
1) They compromise cardiac output. Clinical criteria include the following signs and symptoms:
Signs: mottling; pallor; cyanosis; cool, moist skin; delayed capillary refill; increased respiratory rate; signs of congestive heart failure (rales, enlarged liver and edema)
Symptoms: irritability, sweating, poor feeding, vomiting, altered mental status, chest pain
2) They have the potential for deteriorating into a lethal rhythm.
D. Tachyarrhythmias
Sinus tachycardia is a heart rate greater than normal for age, secondary to an increased sinus node discharge rate. Tachycardia results from a variety of causes, some of which are unrelated to cardiovascular pathology. Causes of sinus tachycardia include anxiety, exercise, fever, infection, pain, certain drugs (theophylline), and blood loss. Therapy is directed at treating the underlying cause (e.g. antipyretics, analgesics).
Supraventricular tachycardia (SVT) (Paroxysmal atrial tachycardia - PAT) (Figure 5) - SVT is a narrow QRS complex tachycardia (HR > 220 beats/minute in infants and >180 beats/minute in children) usually caused by a reentry mechanism which originates above the bifurcation of the Bundle of His. Etiology includes congenital heart defects (AV canal defect or mitral valve prolapse), fever, sepsis, myocarditis and cardiomyopathy. P waves are often not identifiable. If the child has normal cardiovascular function, this heart rate may be tolerated for several hours before signs of congestive heart failure or shock will develop. SVT typically produces a fixed heart rate which may begin or end abruptly, but does not vary with activity.
Figure 5: Supraventricular tachycardia
Therapy for SVT depends on the presence or absence of hemodynamic compromise. All children should be given supplemental oxygen. If the child is stable, adenosine and consultation with a pediatric cardiologist is appropriate. The following vagal maneuvers may be attempted:
ice pack or ice cold water applied to the face with a washcloth
diving reflex; this is effective 90% of the time without any adverse effects.
pharyngeal suctioning or rectal stimulation
gag with a nasogastric tube
valsalva, which may be elicited by coaching the child to bear down, if the child is old enough to cooperate
unilateral carotid massage for 5 seconds if > 1 year of age (this procedure is less effective in children compared with adults).
eyeball pressure should not be performed because of the risk of retinal detachment.
Refer to the American Heart Association's Pediatric Advanced Life Support (PALS) manual for treatment of SVT.
SVT may be difficult to distinguish from sinus tachycardia. The following table may help to distinguish between these rhythms.
Table III: Sinus Tachycardia vs Supraventricular Tachycardia
Sinus Tachycardia
Supraventricular Tachycardia
History
Physical exam
ECG Rate
P waves
QRS
Chest x-ray
fluid/blood loss (diarrhea, vomiting), anxiety, pain, hyperthyroidism,
fever, illness
dehydration, fever, pallor
< 220 bpm, fluctuating rate appropriate
for precipitating cause
present (may be difficult to see when superimposed on the preceding T wave)
narrow
normal to small heart
nonspecific, irritability, poor feeding, vomiting, sweating, cyanosis, pallor
Increased signs of CHF
( respiratory rate and work of breathing, rales, edema, hepatomegaly)
> 220 bpm, regular
may be absent
narrow
normal or enlarged heart
3. Atrial Flutter is a tachycardia originating in the atria, with an atrial rate of 230-300 bpm. Some heart block may be present, so the ventricular rate may be less than the atrial rate. The ECG appearance of atrial flutter (Figure 6) is often described as resembling a "saw tooth" or "picket fence". Atrial flutter is usually associated with congenital heart disease, especially mitral or tricuspid valvular heart disease.
Figure 6: Atrial flutter
Medical management of acute atrial flutter is rarely successful. The combination of digoxin and propranol may be effective. Cardioversion and overdrive pacing may also convert atrial flutter to normal sinus rhythm.
4. Ventricular Tachycardia (VT) is present when three or more consecutive premature ventricular contractions (PVCs) occur. This arrhythmia originates in the ventricles, so QRS complexes are wide. However, infant ventricular tachycardia may present with "narrow" QRS complexes because conduction through the ventricles is so rapid (see Figure 7).
Etiology includes congenital heart disease; metabolic/electrolyte abnormalities (acidemia, hypoxemia, hyperkalemia, hypokalemia, hypercalcemia and hypoglycemia); hypothermia; and drug toxicity (digoxin, cocaine and tricyclic antidepressants). A chemstrip and toxicology screen should be ordered on all children with unexplained ventricular tachycardia. VT is a dangerous rhythm that indicates ventricular irritability, and it may deteriorate into ventricular fibrillation.
VT with pulse is treated with oxygen. Also there should be treatment of any reversible causes, such as correcting potassium, glucose, calcium; lidocaine; and synchronized cardioversion if the rhythm persists. VT without a pulse is treated as cardiopulmonary arrest, with cardiac compressions and defibrillation rather than cardioversion.
Lidocaine is useful in the child with ventricular tachycardia because it suppresses discharge from ectopic foci, increases the fibrillation threshold and inhibits the formation of reentrant circuits that can lead to ventricular fibrillation.
E. Bradyarrhythmias are the most common terminal rhythms (prior to asystole) in children.
Bradycardia - Bradycardia is a decrease in the rate of atrial depolarization subsequent to slowing of the sinus node (sinus bradycardia), or absence of sinus discharge with emergence of pacing from another atrial focus. It is important to interpret heart rate in the context of normal range for the child's age. It is also important to assess the child's clinical status; a child who is pink and playing happily does not need acute therapy regardless of his/her heart rate.
Nonetheless, bradycardia is usually a very grave sign and should be treated aggressively in an unstable child. This rhythm is the most common terminal rhythm, so be prepared for cardiopulmonary arrest. Bradycardia can be classified as either primary or secondary. Primary bradycardia implies heart block or sinus node dysfunction caused by structural heart disease.
Secondary bradycardia implies a slow HR due to non-cardiac causes. Hypoxemia is the most common cause of secondary bradycardia in children. Secondary bradycardia also occurs with vagal stimulation (e.g. intubation and suctioning). The management of primary bradycardia can be found in the American Heart Association's Pediatric Advanced Life Support manual.
The correction of bradycardic rates includes administering oxygen, measuring a blood glucose and temperature, since an alteration in these may contribute to a slow heart rate.
F. Absent/Collapse Rhythms
Asystole is clinically diagnosed in a non-breathing child by the absence of a palpable pulse and no organized ECG waveform. Asystole generally reflects such profound hypoxia and acidosis that CNS survival is unlikely, unless a perfusing rhythm is rapidly restored. In pediatrics, respiratory failure is usually the precipitating cause of asystole and prompt restoration of adequate ventilation is more critical to success than pharmacological intervention. .
Since severe hypoglycemia may cause asystole, glucose administration (2-4 cc/kg D25W IV) should be considered in the asystolic child.
*Asystole will not respond to defibrillation.
Cardiac compressions, oxygenation, ventilation, and epinephrine are the treatments of choice.
2. Ventricular Fibrillation (VF) is a chaotic, disorganized series of depolarizations that result in a quivering myocardium without an organized contraction (Figure 8). There is, therefore, no detectable pulse. It is an uncommon terminal event in the pediatric age group. Underlying causes include hypoxemia, acidosis, hypothermia, drug intoxication and metabolic abnormalities.
Figure 8: Ventricular Fibrillation
Ventricular fibrillation is a medical emergency. It is important to remember that there is no blood flow during ventricular fibrillation unless cardiac compressions are performed. Therefore, the first step in the child with ventricular fibrillation is to begin cardiopulmonary resuscitation (CPR) while the defibrillator is being prepared. Conversely, defibrillation is the most effective treatment for ventricular fibrillation and should be used as soon as it is available.
If multiple defibrillations are unsuccessful, epinephrine (0.01 mg/kg of 1:10,000), initially is administered, followed by epinephrine (0.1 mg/kg of 1:1000). Epinephrine increases coronary perfusion pressure, and, therefore, myocardial blood flow. This helps restore myocardial cellular function and makes the heart more responsive to defibrillation. In addition, lidocaine (1 mg/kg) may be helpful in the treatment of ventricular fibrillation. If the child does not respond to defibrillation, epinephrine or lidocaine, then bretylium (5 mg/kg) should be used. The dose of bretylium may be doubled (10mg/kg) if a second dose is required. It is important to consider the correctable causes of ventricular fibrillation; these include hypoxia, acidosis, hypothermia, drug intoxication (e.g. tricyclic antidepressants) and metabolic abnormalities (e.g. hyperkalemia).
3. Pulseless Electrical Activity (PEA) is a clinical state characterized by organized cardiac electrical activity on ECG, but without a detectable pulse. PEA is most often seen as a wide complex bradycardia. If PEA is caused by hypovolemia, a narrow complex tachycardia or a normal heart rate is seen in the early stages. These rhythms are treated as collapse rhythms, but the cause must be identified and treated. Reversible causes include severe hypoxemia, severe acidosis, severe hypovolemia, tension pneumothorax, profound hypothermia, and cardiac tamponade. The cause should be identified and corrected. Note that three of the four causes are most often produced by trauma.
III. DEFIBRILLATION/SYNCHRONIZED CARDIOVERSION
A. Defibrillation is the delivery of electrical energy to the myocardium without an attempt to synchronize the delivery with cardiac depolarization (an unsynchronized shock). Defibrillation should depolarize the entire myocardium and return the myocardium to a normal rhythm.
Indications - ventricular fibrillation and pulseless ventricular tachycardia.
Procedure
Determine the need for defibrillation and set the defibrillator to the defibrillation (non-synchronized) mode. Be sure to continue CPR with as little interruption as possible.
Select paddle size - The largest size that allows good chest contact and good separation between the 2 paddles is preferred. There are several different sizes of paddles available. The 4.5 cm diameter paddle or INFANT paddle is adequate for infants up to 10 kg. The ADULT paddle (8.0 to 13.0cm)is generally used for pediatric patients weighing more that 10 kg.
Select the energy dose and charge the paddles. Two J/kg is used on the first attempt. If unsuccessful, 4 J/kg may be used subsequently. Increasing the energy dose is not necessary if the first attempt did succeed, but the dysrhythmia recurred afterward. If the defibrillator's lowest dose exceeds the calculated dose, use the lowest dose available. When the calculated dose is between two available energy levels, choose the higher level.
Apply the paddles to the skin surface to establish electrical contact using electrode gel or cream saline gel pads or self-adhesive defibrillation pads. Sonographic gels are unacceptable since they are poor electrical conductors and saline soaked pads may be an electrical hazard if the solution runs between the two pads during the electrical shock. Alcohol pads are a fire hazard and can produce serious chest burns. The paddles must be placed so that the heart is situated between them. The paddles should be far enough apart to prevent an arc of current between them. The usual placement is one paddle below the right clavicle and the other to the left of the left nipple in the anterior axillary line. Anterior/posterior positioning of self-adhesive defibrillation pads, with one electrode on the anterior chest over the heart and the other on the back, is acceptable.
Recheck the rhythm on the monitor before discharging the paddles.
Clear the area to make sure that no personnel are in contact with the child or the bed.
Discharge the paddles while applying firm pressure to the paddles.
Reassess ECG/pulse and treat accordingly.
Repeat the countershock using twice the energy as needed.
3. Problems
Failure of the machine to discharge usually means that it is in the synchronous mode or that it has not been charged.
Reliable delivery of low energy doses may be difficult to achieve; defibrillators should be checked periodically by the Biomedical Department in your hospital for satisfactory delivery of pediatric energy doses.
B. Cardioversion is the delivery of electrical activity to the heart that is synchronized (timed) to produce depolarization that coincides with the patient's R-wave (and avoids the T-wave). This is necessary in order to minimize the risk of producing ventricular fibrillation while restoring a normal sinus rhythm.
Indications - symptomatic supraventricular tachycardia, atrial flutter, atrial fibrillation, and ventricular tachycardia with a pulse
2) Procedure - identical to defibrillation, except:
Energy dose is lower (0.5 - 1.0 J/kg)
Defibrillator is set on the synchronous mode so that discharge does not occur during the T-wave
If the paddles are not capable of monitoring, the ECG cable must be connected to the defibrillator.
The discharge buttons must be pressed and held down until the countershock is delivered.
SHOCK
Definition - Shock is a clinical state characterized by inadequate delivery of oxygen and nutrients to meet the needs of the tissues; it is not related to specific hemodynamic changes, such as a decrease in BP or cardiac output. Second only to respiratory failure, shock is the most frequent causative factor of cardiopulmonary arrest in the pediatric patient. The child in shock requires immediate therapy.
Shock may occur with a normal or decreased blood pressure, or with normal, decreased or increased cardiac output.
Shock may be divided into three phases:
Compensated - Vital organ perfusion is maintained by intrinsic compensatory mechanisms, which maintain blood pressure in the normal range.
Decompensated - Despite shunting blood to vital organs, ischemia, acidosis secondary to anaerobic metabolism and cell injury occur. The compensatory mechanisms fail to maintain BP in the normal range and hypotension ensues.
Irreversible - The child progresses to this stage if the second phase is not effectively treated. This is a retrospective diagnosis.
B. Pathophysiology
Shock is a manifestation of circulatory compromise. When cardiac output is inadequate to meet tissue needs, the sympathetic nervous system shunts blood from non-vital tissues to the heart and brain. As a result, organ perfusion and oxygenation diminish in non-vital organs, such as the skeletal muscle and vascular beds. Anaerobic metabolism from inadequate tissue oxygenation reduces the production of adenosine triphosphate (ATP) and increases lactic acid production. Poor blood flow permits the buildup of CO2 and carbonic acid, and metabolic acidosis results.
C. Clinical findings - In the healthy child, the cardiovascular system exhibits effective compensatory capability, so that generally there is a stability of blood pressure until the child suddenly decompensates. Early signs of shock may be subtle and are usually those of sympathetic nervous system stimulation (tachycardia, peripheral vasoconstriction and decreased urine output). Signs and symptoms of shock include:
Tachycardia is an early finding in shock, although it may be difficult to distinguish from tachycardia due to pain or fear in a conscious child.
Tachypnea is an attempt to compensate for hypoxia-induced anaerobic metabolism and metabolic acidosis ( CO2).
Decreased peripheral pulses and delayed capillary refill - With significant reduction in circulation, the body will shunt blood flow to the central organs, therefore decreasing the perfusion to the periphery; this causes cool, pale extremities, mottled skin and decreased peripheral pulses. Children may occassionally appear mottled as a response to a cold environment or during the course of a mounting fever.
Changes in mental status or level of consciousness - anxious, irritable, lethargic or comatose
Decreased urine output - This is a sensitive indicator of cardiac output in the absence of primary renal disease.
Hypotension (a late sign!) - Blood pressure is maintained until relatively late in the course of shock. In general, children can tolerate acute losses of 25% of total blood volume without a change in blood pressure.
*Children in septic shock may not demonstrate pallor, cool extremities, or have diminished peripheral pulses.
D. Laboratory Findings
Hyperkalemia may be seen with metabolic acidosis resulting from the movement of potassium out of cells in exchange for protons (H+) moving into cells.
Metabolic acidosis is typical. pH may be normal if respiratory compensation is adequate.
Hyperglycemia is more common than hypoglycemia in the initial stages of cardiovascular compromise, and reflects the stress hormone response.
Hypoglycemia - Because infants have high glucose needs and low glucose stores, the development of low cardiac output may rapidly deplete glycogen stores, producing hypoglycemia.
E. Classification
Shock may be classified by etiologic mechanism into hypovolemic, cardiogenic, and distributive or septic shock. Although this oversimplifies shock, it does indicate the initial type of therapy required. Note that children with severe or long-standing shock typically require extensive support of cardiovascular function; this includes heart rate, preload or intravascular volume, myocardial contractility and vascular resistance.
Hypovolemic shock is a state of inadequate intravascular volume relative to vascular space. It is the most common cause of shock in the pediatric patient. When the intravascular volume falls, inadequate volume remains to fill the circulatory network. Return of venous blood to the heart falls and the ventricular chambers do not completely fill with blood. As a result of decreased filling during diastole, the volume ejected during systole is decreased. As stroke volume decreases, heart rate increases to compensate, but as volume loss continues cardiac output (CO) falls. As CO falls, BP is maintained by increased vascular resistance. With further compromise of tissue perfusion, local acidosis leads to vasodilation and pooling of blood in ischemic tissues. BP compensation then fails and the child rapidly deteriorates.
Etiology - hemorrhage (external or internal bleeding; e.g. GI bleeding, hepatic or splenic rupture, or major vessel injury), burns, capillary leak syndromes (e.g. sepsis or anaphylaxis), and fluid and electrolyte loss (e.g. dehydration, vomiting, diarrhea, diabetes insipidus, burns, or diabetic ketoacidosis).
Signs - Symptoms include signs of adrenergic stimulation with attempt to redistribute blood volume away from non-essential tissue (skin, gut, kidney) and preserve blood flow to the heart and brain. This includes tachycardia, cool pale extremities, delayed capillary refill, thready weak pulse, narrow pulse pressure, Æ urine output, and an altered sensorium. Hypotension may or may not be present. In children, hypotension may not be noted until the child has lost approximately 25% of the circulatory blood volume (all blood drawn for lab analysis should be considered when calculating blood loss). Normal circulating blood volume is 75-80 cc/kg.
Management - Therapy is directed toward expansion of vascular volume. A secure and reliable IV line should be established; alternately, an IO line may be established in children less than six years of age.
Crystalloids- A bolus of 20 cc/kg of isotonic crystalloid (NS or LR) should be given IV or IO as fast as possible and repeated as necessary until systemic perfusion improves. The components of Ringer's Lactate closely approximate the electrolyte concentration of blood. Large volumes of dextrose-containing solutions should not be given since resulting hyperglycemia may induce osmotic diuresis. Twenty ml/kg of 5% dextrose provides 1 g/kg of glucose, this will acutely increase glucose concentration by about 150 mg/dl. If hypoglycemia is documented (£ 40-60 mg/dL), give 2-4 cc/kg of 25% Dextrose and monitor serum glucose. Fluid boluses (10-20 cc/kg) should be repeated if systemic perfusion does not improve. A child with hypovolemic shock may require 60-80 cc/kg of a crystalloid solution in the first hour of resuscitation. Occasionally, up to 100-200 cc/kg may be needed during the first few hours. Due to the normal distribution of sodium in the extracellular space, only approximately one-fourth of the infused crystalloid solution remains in the plasma compartment; therefore, often 4-5 times the deficit must be infused to restore plasma volume. After 40-60 cc/kg, if the child remains poorly perfused, it is often helpful to change the resuscitation fluid to a colloid.
Colloids are substances that exert oncotic pressure similar to plasma proteins. By increasing colloidal oncotic pressure in the vascular bed, fluid is pulled from the interstitial compartment, and the total blood volume is increased. In general, colloids expand the plasma volume more effectively than crystalloid solutions; for each cc of colloid given, you achieve almost one cc of intravascular volume expansion. Colloids are more expensive and less readily available. Colloidal agents include albumin, synthetic colloids (Hetastarch, Dextran 40 and Dextran 60), fresh frozen plasma and packed red blood cells. Albumin and the synthetic colloids do not transmit the hepatitis virus nor the human immunodeficiency virus, but are capable of causing an anaphylactic reaction. These products do not have oxygen-carrying capacity, nor do they contain clotting factors. They are not meant to be a substitute for blood or plasma.
External bleeding should be controlled with direct manual pressure over the bleeding site and a sterile pressure dressing is applied. Tourniquets should be avoided.
Hypovolemic shock is not treated with inotropes; fluid resuscitation with frequent patient assessment is the key to successful treatment.
2. Cardiogenic shock occurs when abnormalities in cardiac pumping are responsible for failure in the cardiovascular system to meet the metabolic needs of the tissues. It is the final common pathway of all forms of advanced shock, and in most instances it is the result of decreased myocardial contractility. As the heart's pumping ability decreases, a decrease in ventricular emptying results. Consequently, ventricular filling pressures rise while stroke volume and cardiac output fall. Since the heart cannot pump blood effectively, tissue perfusion declines, with hypotension representing a late, decompensated state. In addition, pulmonary congestion develops from an increase in left atrial pressure and results in increased pulmonary vascular pressure. Oxygenation of circulating blood decreases with lung congestion. Thus, in cardiogenic shock, the body not only receives less blood but the blood contains less oxygen.
a. Etiology - prolonged shock, myocardial insult, dysrhythmias, drug intoxication, hypoxic/ischemic episodes (e.g. near-drowning, asphyxia and near-miss SIDS), acidosis, hypothermia, electrolyte or metabolic derangements, myocarditis, cardiac surgery, and congenital heart disease. Children with ductal dependent lesions will often present in cardiogenic shock during the first two weeks of life. Prostin (PGE1) should be administered to these children. Early consultation with a Pediatric Cardiology Referral Center is recommended.
b. Signs - Symptoms will be those of adrenergic stimulation, with an attempt to redistribute blood volume away from non-essential tissue (skin, gut, kidney) and preserve blood flow to the heart and brain. However, these compensatory mechanisms may actually become destructive. Severe peripheral vasoconstriction may increase impedance to left ventricular ejection and increase the work of the myocardium. These signs may include diminished systemic perfusion in the absence of hypovolemia, tachycardia, narrow pulse pressure, tachypnea, diaphoresis, evidence of high central venous pressure including periorbital edema and hepatomegly. Pulmonary edema may also be present if left ventricular dysfunction is severe.
c. Management- The child in cardiogenic shock requires careful maintenance of the airway, oxygenation and ventilation. Oxygen requirements must be mimimized. Cardiac preload must be optimal when cardiac dysfunction is present. The ventricles are impaired and require filling pressures that are higher than normal; therefore, small quantities of fluid may produce sharp rises in ventricular end diastolic pressure. Initial treatment with a small, isotonic fluid bolus (5-10 cc/kg of LR or NS) is preferred, watching carefully for increased work of breathing, rales, and hepatomegaly. The fluid bolus can be repeated based on assessment of the child's response. If the child fails to improve, inotropes may then be needed to maximize contractility. In the hypotensive child with cardiogenic shock, an epinephrine infusion is indicated. Restoration of normal blood pressure with a potent vasoactive agent is important in hypotensive children, because coronary perfusion is dependent on an adequate systemic perfusion pressure. In the normotensive child, dobutamine is the drug of choice. Other inotropes with vasodilatory actions, such as amrinone lactate, may also be used. Volume should be administered only if needed and drugs should be titrated carefully.
3. Distributive shock is a state in which abnormalities in the distribution of blood flow lead to profound inadequacies in tissue perfusion and oxygenation in selected vascular beds. The most frequent causes of distributive shock are infection (septic shock), drug reaction (anaphylaxis), CNS injury (spinal shock), and reactions to anesthesia or drugs that cause myocardial depression and peripheral vasodilation.
4. Septic Shock is a compromise in cardiovascular function, systemic perfusion, and tissue oxygen utilization secondary to the host's response to an infectious organism. Infants and children are at risk for septic shock because of their immature immune systems. Septic shock is associated with high mortality rates (20-50%) in children, as well as adults. Because of the multiple factors involved, the clinical pattern and presentation of septic shock varies, and depends on the dynamic interplay of the invading organisms, elapsing time, and host status. Septic shock is characterized by a loss of peripheral vascular resistance, initially producing a wide pulse pressure due to the fall in diastolic blood pressure. Hypotension usually occurs when the child develops excessive vasodilation and leakage of plasma through the capillary walls into the interstitial space. Hypotension may also result from poor cardiac contractility.
Etiology - The most common organisms causing septic shock in children are S. pneumonae, staph epidermidus, gram negative bacilli and N. meningitidus.
Signs - The clinical manifestations of septic shock are dependent upon which phase of septic shock the child is in.
1. Early, Warm or Hyperdynamic phase:
O2 consumption and cellular energy utilization
Early inflammatory response
Vasodilation and diastolic pressure - vasodilation causes a decrease in diastolic pressures and therefore a wide pulse pressure results.
Warm and flushed skin secondary to vasodilation
Tachycardia
Tachypnea - There is both sepsis-induced central hyperventilation and a compensatory mechanism for tissue hypoxemia and acidosis. Eventually this mechanism fails, as worsening hypoxia and acidosis depresses the respiratory drive center; at this time hypoventilation, agonal gasping and apnea supervene.
Bounding pulses are due to the hyperdynamic state, sympathetic stimulation and a wide pulse pressure from a low systemic vascular resistance.
Normal urine output
Normal to delayed capillary refill
Normal or increased cardiac output
Normal systolic blood pressure
WBC may be low, high or normal - Initially the child with bacteremia may have marked leukopenia.
Hyperglycemia is secondary to increased epinephrine release and a decrease in insulin release; it may also be seen in infants and chronically ill children with depleted glycogen stores.
2. Late stage:
edema - Edema is due to changes at the microcirculatory level. The cellular membrane is damaged and no longer acts as a selective barrier to sodium and H2O. Therefore, edema occurs.
metabolic acidosis - Anaerobic metabolism from inadequate tissue oxygenation reduces the production of adenosine triphosphate (ATP, which fuels most cellular activities) and increases lactic acid production. Decreased blood flow also leads to a buildup of tissue CO2.
hypotension
poor systemic perfusion - cold, clammy skin; prolonged capillary refill; thready pulse; mental status changes
oliguria secondary to poor contractility and vasoconstriction.
increased core temperature - Leukocyte activation results in the release of large quantities of endogenous pyrogen, which increases the body's temperature. In addition, peripheral perfusion is decreased; therefore, less heat is lost from the body, further increasing the body's temperature.
tachycardia - Tachycardia is due to the release of endogenous catecholamines in response to a decrease in circulatory blood volume.
tachypnea - Efforts may become labored as acidosis increases, muscle fatigue develops, and pulmonary edema develops.
Disseminated intravascular coagulation (DIC) - Endotoxins initiate the clotting cascade by activating Factor XII. Bacterial endotoxins also affect the fibrinolytic systems. Collections of thrombi in the microcirculation contribute to tissue ischemia.
hypoglycemia - Decreased glucose production is present.
*With aggressive fluid resuscitation and appropriate vasopressor use, most septic children remain in a compensated state.
c. Interventions - Rapid management when septic shock is suspected is necessary for a positive outcome. If health care providers wait for positive blood culture results, it will be too late.
Support the ABCs. Care must first be directed toward the maintenance of oxygenation, ventilation, and tissue perfusion. All children in shock should be given supplemental oxygen. In septic shock, there may be an impairment of oxygen extraction at the cellular level. Because of this, the septic child may require higher than normal PaO2s. Reversal of hypoxia and acidosis in uncompensated shock is imperative. Ventilatory assistance may be beneficial in the child, as detailed below. In addition, oxygenation is monitored via pulse oximetry if available
Place the child on a cardiorespiratory monitor. The child's heart rate should be monitored and maintained at a rate that is appropriate for the child's clinical condition. Specific dysrhythmias are treated. Perform cardiac compressions if the pulse is absent or the child is bradycardic and poorly perfused.
Control any obvious source of hemorrhage.
Establish vascular access (IV/IO).
Administer isotonic IV/IO fluids as needed. Fluid replacement is generally accepted as the most important therapeutic goal in shock. Early correction of the volume deficit is necessary to increase cardiac output and to re-establish the even distribution of microcirculatory flow. Twenty cc/kg of LR or NS given rapidly is the usual dose. If the child remains hypotensive or hypoperfused, follow with a second 10-20 cc/kg bolus. If additional volume is needed to maintain perfusion after 40-60 cc/kg, the fluid may be changed to a colloid if available.
All children should have frequent reassessment of heart rate, quality of pulses, capillary refill, and color during fluid challenges. Children receiving fluid boluses are monitored closely for positive response to the treatment. Volume overload usually is not a problem in children who have normal cardiac, pulmonary and renal function. Infrequently signs of volume overload such as rales, tachypnea, a cardiac gallop, hepatomegaly, and frothy secretions may occur in the already chronically compromised child. If volume overload occurs, diuresis may be necessary. A dose of furosemide (Lasix®; 1 mg/kg/dose) usually provides prompt diuresis. An inadequate diuretic effect may indicate that renal perfusion is severely compromised.
Inotropic support - Because of vasodilation and myocardial depression, pharmacologic agents such as epinephrine, norepinephrine, dopamine or dobutamine may be needed to enhance myocardial contractility and increase systemic vascular resistance. Once the infusion has begun, it is preferable not to interrupt the infusion or flush the line containing the solution; for practical purposes, this means that other medications are best given via another IV site.
Check glucose. Some children in shock are hypoglycemic due to rapidly depleted carbohydrate stores. If serum glucose is < 60 mg/dL, administer 2-4 cc/kg 25% Dextrose IV.
Restore normal body temperature - Temperature regulation is important in the balance of oxygen supply and demand. Extremes in body temperature will increase oxygen demand. Rapid external cooling will cause shivering and increased core temperature.
Obtain a history. Use the AMPLE mneumonic (A-allergies, M-meds, P-past medical history/prior surgery, L-last meal, E-evaluation). The history should be obtained as soon as possible from the parent or caregiver. Additional history should be directed toward identifying the etiology of shock; usually the parents will volunteer information which points to a diagnosis; but if not, the following general questions may be helpful:
Was there known trauma or a source of blood loss?
Has the child had symptoms of gastroenteritis (i.e. diarrhea, vomiting)?
Is the child a known diabetic or were there symptoms suggestive of diabetes?
Have there been symptoms compatible with sepsis (fever, chills, URI, UTI)?
Does the child have a known heart disorder?
What medications does the child take? Is there any chance of toxic ingestion?
How frequently has the child been voiding?
11. Obtain the following labs:
ABG - This is the most useful laboratory test in the child in shock. By definition, inadequate perfusion exists in the child in shock, and it should lead to anaerobic metabolism and metabolic acidosis. When arterial pH < 7.20, and adequate ventilation has been established, correction with sodium bicarbonate (1 mEq/kg) is usually indicated.
Electrolytes - In septic shock, children have altered calcium metabolism and serum ionized calcium concentration falls. BUN and creatinine will help determine the extent of dehydration.
Glucose - Carbohydrate stores are rapidly depleted in septic shock.
blood culture
urine culture/urinalysis
CBC with differential - hemoglobin is helpful to determine O2 carrying capacity. The WBC is non-specific; it may be high or low in septic shock. Platelets are often decreased in septic shock.
coagulation studies - Disseminated intravascular coagulation (DIC) is a hematologic complication of shock. It is characterized by increased partial thromboplastin time (PTT), and increased prothrombin time (PT), decreased fibrinogen concentration, low platelets, and bleeding from orifices and previous vascular puncture sites. DIC should be treated with fresh frozen plasma and/or platelets.
CSF studies as indicated for suspected meningitis, once the child is stabilized.
12. Obtain a chest x-ray. It can provide evidence of primary pulmonary infection. It may also demonstrate the presence of septic pulmonary emboli, cardiomegaly, pulmonary edema and evolving adult respiratory distress syndrome (ARDS). It helps differentiate cardiogenic from non-cardiogenic shock, and provides a valuable guide to initial volume administration by noting heart size.
13. Administer antibiotics to children in suspected septic shock. Loading patients with potent antibiotics may cause the release of large amounts of endotoxins from lysed bacteria. Therefore, children may initially appear worse after the administration of antibiotics.
14. Insert a foley catheter. Urine output is a sensitive measure of perfusion status and adequacy of therapy.
15. Insert a nasogastric/orogastric tube to decompress the stomach.
16. Hemodynamically unstable children should be initially managed by aggressive fluid resuscitation. Because of massive vasodilation and capillary leakage, parenteral fluid administration may be up to 60-80 cc/kg during the first hour.
If poor perfusion persists despite adequate ventilation, oxygenation and volume expansion, inotropic support is indicated.
Drug therapy should be initiated in normotensive children only after adequate fluid resuscitation. If the child is hypotensive, an epinephrine or norepinephrine drip should be started. In the hypotensive septic child, large doses (up to 1.0 -1.5 µg/kg/minute) may be needed.
If the septic child is normotensive but poorly perfused, a dopamine infusion is indicated. Dopamine is a less potent peripheral vasoconstrictive agent and is helpful in less severely ill children with sepsis. The initial infusion rate is 5-10 µg/kg/minute. If the infusion rate exceeds 20 µg/kg/minute, a more potent agent (epinephrine or norepinephrine) is indicated. Drugs used to improve cardiovascular stability are potent, and often have significant side-effects.
Antibiotic administration - Antibiotics should be given after blood, urine, and CSF cultures are drawn. They should have a wide spectrum and be effective against both gram-positive and gram-negative organisms.
The recent emergence of penicillin-resistant streptococcus pneumonae necessitates the addition of vancomycin. Vancomycin is not indicated in a child being treated for occult bacteremia.
Initial antibiotic coverage is dependent upon the age of the child. The following loading doses are recommended:
<1 months of age - ampicillin 200 mg/kg + cefotaxime (Claforan®) 100 mg/kg
OR
ampicillin 200 mg/kg + gentamycin 2.5 mg/kg
>1 months of age - vancomycin 10-15 mg/kg + ceftriaxone (Rocephin®) 50-75 mg/kg
OR
+ cefotaxime (Claforan®) 100 mg/kg
If the child has an indwelling invasive catheter (or VP shunt), the following antibiotics should be administered:
vancomycin (Vancocin®) 10 mg/kg
+ cefotaxime (Claforan®) 100 mg/kg
The septic child may initially get worse after antibiotics have been administered because endotoxins are released into the circulation when bacteria die.
The value of corticosteroids in the treatment of septic shock is unproven. In meningitis, data suggest a benefit, but decadron is no longer recommended unless the child is suspected to have H influenza meningitis.
Reduce fever - Fever should be treated with acetaminophen, ibuprofen and/or cooling blankets or a fan.
d. Summary
Recognition of shock by health care providers is the key to patient survival. Once decompensation and significant hypotension develop, the probability of mortality is high. In addition, frequent reassessments are necessary to ensure a good outcome. In pediatric patients with shock, the most common mistake that is made is not giving enough fluids. The key is to continue to reassess and administer fluid until perfusion returns to normal or the child becomes fluid overloaded.
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