Emergency Treatment in Pediatric

Supraventricular Tachycardia in Pediatric

Supraventricular tachycardia will usually present with signs of congestive cardiac failure or shock, but will also depend on the age of the child. Sinus tachycardia can be up to about 200 beats per minute. Supraventricular tachycardia (SVT) is usually above 220 beats per minute.

Assessment

Symptoms

Infants usually present with pallor, dyspnea and poor feeding. Older children have palpitations and chest discomfort.

Signs

In SVT there is a regular tachycardia with a heart rate usually 180–300 per minute. Hypotension might be present but is often compensated early on in presentation. Heart failure with hepatomegaly with gallop rhythm occurs, especially in infants. Consult cardiology urgently if tachycardia is broad complex or irregular.

Management and Treatment

The child must be monitored with continuous ECG trace and frequent measurements of blood pressure. The options for treatment are listed below.

• If necessary apply oxygen 10 liter/min by facemask

• If child is shocked (i.e. hypotensive, poor peripheral perfusion, impaired mental state) proceed to direct current cardioversion (see below)

• If child is not shocked treat with intravenous adenosine

Shocked child

If the child is shocked, then direct current cardioversion is needed. You must:

• Call ICU. Ensure experienced staff and full resuscitative measures are present

• Ensure child is on oxygen, and has intravenous access

• Administer diazepam intravenously if there is any chance of awareness

• DC revert using a synchronised shock of 0.5 J/kg. If this is unsuccessful, increase

dose to 1 J/kg and then to 2 J/kg if still unsuccessful

• An unsynchronised shock is necessary for ventricular fibrillation or polymorphic ventricular tachycardia

Stable child

If the child is stable, vasovagal maneuvers and adenosine should be tried:

• Vagal maneuvers: use the Valsalva maneuver if child old enough, the gag or icepack/iced water for infants (apply to face for a maximum of 30 seconds). Do not use eyeball pressure.

• Intravenous adenosine

• Insert cannula into a large proximal peripheral vein (the cubital fossa is ideal) with a 3-way tap attached

• Draw up starting dose of adenosine 50 µg/kg. If necessary dilute to 1 ml with

normal saline

• Draw up 10 ml saline flush

• Turn on the ECG trace recorder

• Administer adenosine as a rapid i.v. push followed by the saline flush

• Repeat procedure at 2-minute intervals, until tachycardia terminated, increasing the dose of adenosine by 50 µg/kg to a total dose of 300 µgµg/kg for infants of less than 1 month, and to a total dose of 500 µg/kg1 to children between 1 month and 12

years.

• Perform 12-lead ECG postreversion

The recorded strip at the time of conversion to sinus rhythm should be inspected and saved, for concealed pre-excitation may only be revealed during the first few beats after conversion to sinus rhythm. After a patient has been reverted, a 12-lead ECG should be performed to look for pre-excitation and other abnormalities. Rapid re-initiation of tachycardia is not uncommon, mostly because of premature atrial contractions stimulated by the adenosine. If this occurs consider trying adenosine again. Side effects including flushing and chest tightness or discomfort are not uncommon but they are usually brief and transient. Rarely atrial fibrillation or prolonged pauses may occur. Adenosine is contraindicated in adenosine—deaminase deficiency (rare immune deficiency) and patients taking dipyridamole (Persantin). Care is required in asthma, as it may cause bronchospasm. If these measures fail to revert the SVT, consult a cardiology specialist.

Disposition

A follow-up plan should be made in consultation with cardiology. Some children may be started on beta blockers. There may be an underlying conduction abnormality such as Wolff-Parkinson-White syndrome.

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Management of Shock in Pediatric

Airway and breathing

The resuscitation mantra of Airway, Breathing, Circulation or ‘ABC’ remains the management priority in the shocked child as in any other. Before assessment of the nature or severity of shock can be made, the clinician must ensure that the airway is patent and that the patient is breathing adequately without assistance. If this is not so then appropriate steps should be taken to stabilise the airway and ensure adequate breathing.

Intubation and judicious positive pressure ventilation can benefit the shocked child when significant myocardial dysfunction exists and will reduce oxygen consumption caused by increased work of breathing. High flow oxygen should be administered via a facemask with a reservoir bag to maximise oxygen concentration. The shocked child must not be allowed to become hypoxic by the omission of a simple treatment such as oxygen therapy.

As the airway and breathing are being managed, the following monitoring should take place:

• Pulse oximetry

• 3 lead electrocardiogram monitoring

• Blood pressure

Circulation

The clinician should pay particular attention to:

• Pulse rate, rhythm and volume

• Peripheral skin color, temperature, capillary refill time, rashes

• Respiratory rate and work of breathing

• Signs of cardiac failure

• Neurological state

• Signs of injury that might have caused hemorrhage (limb fracture, abdominal trauma, head trauma)

• Urine output

Whilst relatively uncommon in children, the presence of cardiac dysrhythmia associated with shock will require immediate management. Vascular access should be achieved as quickly as possible. At least one, but preferably two, large-bore venous cannule should be sited. If poor perfusion makes this impossible then intraosseous, central venous (femoral or internal jugular vein) or peripheral venous cutdown are acceptable alternatives. At the time of vascular access appropriate blood samples should be taken:

• Full blood count and film

• Blood cross-match—in hemorrhage; most children with septic shock will require transfusion

• Coagulation screen—particularly in septic shock

• Plasma urea, creatinine and electrolytes

• Serum calcium

• Plasma glucose and lactate

• Blood gas estimation—arterial or central venous gases are most useful

• Blood culture and microbial sensitivities

A bedside blood glucose test should also be performed and hypoglycemia corrected promptly. Once assessment and monitoring have been completed (in the acutely sick child this should take no more than 1–2 minutes), the clinician then moves on to definitive management of the shock state. With reference to the three factors involved in the shocked heart there are three objectives of treatment:

1. Correction of hypovolemia (preload)

2. Optimising the cardiac pump (contractility)

3. Ensuring peripheral distribution of blood (afterload)

Following restoration of circulation, a secondary survey for organ specific signs should be carried out.

Correction of hypovolemia

The objective of volume replacement in shock is to optimise preload. The hypovolemic child should be managed initially with a rapid intravenous infusion of warmed fluid of 20 ml/kg. The approximate weight of a child can be calculated by using the formula:

WEIGH of CHILD (Kg) = 2 (Age in years + 4)

The selection of fluid is a matter of departmental policy and no little controversy in the literature. The author recommends 0.9% saline as the fluid of choice in volume resuscitation except in suspected meningococcemia and septic shock when 4.5% human albumin solution is preferred. This is because albumin offers a more logical approach and a theoretically longer duration of action in the presence of the profound capillary leak that occurs, particularly in meningococcal sepsis. Close attention should be made to the effect of the fluid bolus on heart rate, pulse volume and, to a lesser extent, blood pressure. A lack of or very transient fall in heart rate should be followed by a second similar fluid bolus. Further boluses of 10–20 ml/kg may be required depending on clinical response.

Prompt consideration of definitive airway support and intensive care unit admission will be required for these patients as the risk of pulmonary edema is very high. If available, reference to serial blood gas and plasma lactate measurements may aid assessment of progress and invasive monitoring of central venous pressure (CVP) is a marker of preload in the unobstructed heart. A CVP higher than that usually acceptable (i.e. >10mmHg) will be required to optimise cardiac performance in myocardial dysfunction which is universal in septic shock.

Important management notes

• When hemorrhage is suspected, no more than 40 ml/kg of crystalloid should be given before blood is used as the replacement fluid

• In meningococcemia and septic shock, 4.5% albumin is preferred to crystalloid

• In infants with gastroenteritis, 4.5% albumin should be used after 40 ml/kg crystalloid, and other diagnoses considered, e.g. volvulus, peritonitis

• Children with meningococcal sepsis often require up to and over 100 ml/kg fluid in resuscitation

Optimising the cardiac pump

Inotropic support may be required when shock persists despite significant fluid replacement. This may not apply when hemorrhage is the cause of hypovolemia. In this case surgical management of the bleed will be required whilst the child continues to receive blood as volume replacement. Patients in septic shock commonly demonstrate poor myocardial contractility and concurrent low SVR in the presence of metabolic acidosis and endothelial injury. These children benefit from agents producing strong inotropy and peripheral vasoconstriction. Table below lists commonly used inotropes, their principal actions and therapeutic dose ranges.

Inotropic drug in pediatric shock treatment

Inotropic drugs in pediatric shock treatment

Choice of inotropic agent is not without controversy and is an issue for departmental consideration. Dopamine is widely used as the first line inotrope in the shocked child, followed by epinephrine (adrenaline) if response to dopamine is inadequate. In cases of septic shock, where low SVR is likely, there is logic in choosing first an agent that produces vasoconstriction. Epinephrine (adrenaline) (often in conjunction with norepinephrine (noradrenaline) offers positive inotropy and peripheral vasoconstriction, and its early use in the septic shocked child can be very valuable. The dose of inotrope should be titrated according to clinical response. Once this level of cardiac support has been instituted, the patient is likely to have been intubated and ventilated and requires invasive blood pressure monitoring and definitive intensive care management.

Ensuring peripheral distribution of blood

Afterload can be too great or too low to allow normal delivery of blood to the tissues. In the vasodilated child, such as in sepsis, norepinephrine (noradrenaline) and epinephrine (adrenaline) provide vasoconstriction to improve SVR and reduce maldistribution. In the child with cardiogenic shock, such as in those following cardiac surgery, the afterload is relatively high as the injured heart struggles to pump efficiently. Vasodilators such as sodium nitroprusside can ‘off-load’ ventricular work improving cardiac output. More recently phosphodiesterase inhibitors, such as enoximone and milrinone, are increasingly used, as they provide low-level inotropy in conjunction with vasodilatation to enhance cardiac output.

Specific therapies

Individual problems require action in addition to the general principles of management employed in most cases of shock. The following are for consideration:

• Antimicrobial drugs as clinically indicated, e.g. in meningococcemia or the immunocompromised

• Coagulopathy—correct with fresh frozen plasma or cryoprecipitate

• Metabolic acidosis—can improve with volume replacement or might require alkalising agents

• Electrolyte disturbances—correct as necessary

Clinical Signs of Shock

Most physical signs are consistent regardless of the origin of shock; there are some exceptions. Table below presents the principal clinical findings in the shocked child.

Physical examination may give clues as to the etiology of shock, which may aid management, e.g.

• meningococcemia purpuric and petechial rash

• cardiac failure gallop rhythm/hepatomegaly

• dehydration dry mucous membranes, oliguria, reduced skin turgor

• anaphylaxis angioedema, pallor, urticaria, wheeze, stridor

Clinical Signs of Shock in Pediatric

Classification of shock

The diagnosis of shock is purely clinical. It is possible to classify shock into physiological categories but in reality there is usually overlap between these in individual patients. Classification may be useful in diagnosis since clinical signs may differ between types, as may treatment. Shock is most commonly classified by the anatomical site of the circulation failure.

1. Hypovolemic Shock

Hypovolemic shock results from a fall in actual circulating volume within the intravascular space. In children there are:

• Common causes

• dehydration, e.g. diarrhea and vomiting

• hemorrhage

• sepsis (due to fluid redistribution secondary to increased capillary permeability)

• Less common

•burns

• peritonitis

Compensatory mechanisms will be employed in response to a fall in circulating volume.

Cardiac output is maintained or augmented by tachycardia and peripheral vasoconstriction, the latter maintaining afterload. Renal perfusion is reduced as blood is diverted to the brain and heart, resulting in activation of the renin-angiotensin system and a subsequent increase in circulating volume by sodium and water reabsorption.

2. Cardiogenic shock

Cardiogenic shock refers to situations where myocardial contractility is compromised resulting in reduced cardiac output and tissue perfusion. It is less common than hypovolemia as the primary etiology in the shocked child but, since reduced perfusion will always eventually affect myocardial function, it is an inevitable consequence wherever shock is prolonged (see Figure 3.1). Causes are as follows:

• heart failure

• cardiac surgery

• intrinsic myocardial disease, e.g. acute viral myocarditis, cardiomyopathy

• drug toxicity

• electrolyte and acid-base disturbances

• dysrhythmias.

Reduction in cardiac output brings about compensatory manoeuvres as with hypovolemia.

3. Obstructive shock

Obstructive shock describes a scenario where despite adequate contractility the heart is unable to pump out an adequate volume of blood to be oxygenated and/or distributed to the tissues. Causes include:

• obstructive congenital cardiac lesion, e.g. aortic coarctation or critical aortic valve

stenosis

• tension pneumothorax

• cardiac tamponade.

4. Distributive shock

Distributive shock is usually a complication of severe infection. It is the principal pathophysiological process that defines septic shock. In the presence of overwhelming sepsis an unchecked, generalised inflamma-tory response develops. Inflammatory mediators such as TNFα, inter-leukin-1 and lipopolysaccharide endotoxin are produced causing local cell damage particularly to vascular endothelium. The vasoactive effects of these mediators on the endothelium produce variation in vascular tone. Whilst areas of vasoconstriction and vasodilatation may coexist side-by-side, the overall effect is that of peripheral vasodilatation and a fall in systemic vascular resistance (SVR). This means that blood is not distributed efficiently to the tissues despite a state of high cardiac output, which may exist in septic shock. Adults in septic shock secondary to Gram negative bacteremia classically present with this picture where good peripheral perfusion mediated by profound vasodilatation gives rise to the description of ‘warm shock’. In children, however, the more common presentation is that of cold peripheries, skin mottling and prolonged capillary refill time. Causes of distributive shock include:

• Septic

• meningococcemia

• Gram negative bacteremia

• streptococcal infection (group B streptococcus in neonates, pneumococcus in older children)

• Non-septic

• anaphylaxis

• neurogenic, e.g. following transection of the spinal cord

• drugs, e.g. vasodilators or anesthetics

5. Dissociative shock

Dissociative shock occurs when there is inadequate oxygen capacity. It occurs in:

• profound anemia

• methemoglobinemia

• carbon monoxide poisoning

Shock in Pediatric

Shock is most simply conceptualised as failure of the circulation to provide adequate delivery of oxygen and essential nutrients to the tissues to ensure normal cell respiration. The process leading to this state may be single or multifactorial. In the management of sick and injured children, the emphasis lies in swift recognition of shock followed by rapid assessment of the nature of the circulatory failure. The latter is essential because avoidance of significant morbidity and mortality relies on the clinician’s ability to determine the origin(s) of the shock accurately and initiate appropriate and specific management.

At a cellular level inadequate oxygen delivery leads to lactic acid formation and the development of metabolic acidosis. Up to a point the body compensates for this by redistributing blood flow away from non-essential tissues (e.g. mesenteric circulation, skin) to the vital organs (e.g. brain and heart). This state of compensated shock is completed by increased extraction of oxygen from the blood by these essential organs to maintain oxygen delivery. Uncompensated shock develops when despite these mechanisms the pathological insult makes it impossible for the body’s vital organs to overcome the inadequacy of oxygen delivery. Untreated, uncompensated shock will inevitably lead to a spiralling deterioration. An inflammatory cascade ensues at the endothelium causing cellular tissue damage. If prolonged, this damage becomes irreversible and indeed restoration of adequate circulation at this stage may lead to reperfusion injury, itself exacerbating the damage. Multi-organ failure will follow, which in many cases will be unrecoverable. However, compensated and early, uncompensated shock are treatable and so this chapter focuses on the clinician’s recognition, assessment and initial management of shock in the Pediatric Emergency Department.

Heart Condition During Shock

Shock can be thought of in terms of three key elements that affect the heart’s ability to provide an adequate circulation, namely preload, contractility and afterload.

Preload

Preload refers to the degree of tension placed upon the cardiac muscle as it begins to contract. It is usually considered to be the end-diastolic pressure at the completion of ventricular filling. A sufficient degree of stretch to the myocardium is required to produce a level of contraction as governed by the Frank-Starling mechanism. This stretch is produced by venous return, itself inherently linked to actual circulating volume. A fall in circulating volume will reduce venous return, myocardial stretch, force of myocardial contraction and cardiac output.

Contractility

The force generated during ventricular contraction defines ventricular contractility. Contractility is maximised in a neutral homeostatic environment when myocardial oxygen delivery is adequate, acidosis absent, electrolytes in balance, etc. Improvement in contractility increases cardiac output through improved stroke volume.

Afterload

Afterload may be thought of as the resistance against the heart as it exerts its force during contraction. It is actually the pressure created in the artery leading from the ventricle during ventricular systole. Whilst it is true that too high an afterload would result in a reduction in the output by the ventricle, too low an afterload itself poses significant problems since adequate organ perfusion relies on a finely balanced relationship between preload, contractility and afterload.

Management

Treatment of the victim of near-drowning can be attempted even before rescue from the water. Having said this, basic life support is difficult unless the rescuer has a firm foothold. Rescuers must always make a safe approach, otherwise further unnecessary deaths may occur.

Once on dry land the child’s airway should be opened and cleared but attempts at emptying the lungs of water are time wasting and fiitile. Fluid filled lungs have reduced compliance and so require higher inflation pressures. Resuscitation follows standard guidelines and most survivors will usually start to breathe after about 5 minutes.

The stomach is often full of water and vomiting often follows successful resuscitation attempts. Stomach decompression and intubation guards against this and both should be achieved once resuscitation has got underway. Once the child has been intubated, continuous positive airways pressure (CPAP) and positive end expiratory pressure (PEEP) are useful in ventilating stiff lungs.

Near-drowning can be complicated by a number of other factors, which must be borne in mind during resuscitation attempts. Many drowning incidents result from children falling or diving into water. In these circumstances the child could also have been injured and the rescuer should assume this until it can be ruled out. Particularly when there has been a diving accident in shallow water, there is significant risk of a cervical spine injury and the neck must be adequately immobilized until this possibility can be excluded.

The large surface area: volume ratio of children means that even during warm weather hypothermia is a common feature of near-drowning. A core temperature should be determined at an early stage during resuscitation using a low reading thermometer.

Hypothermia is a mixed blessing. Although its presence hampers resuscitation attempts, rapid cooling slows the metabolic rate and protects the vital organs. Children have survived long periods of submersion in cold water and resuscitation attempts should be equally prolonged. Survival has been recorded in children after an hour following submersion in cold water. Cardiac arrhythmias are frequently seen at low body temperatures, which also make them all the more difficult to treat. Ventricular fibrillation is often refractory at core temperatures below 30°C. Resuscitation should not be abandoned until the child has been rewarmed to at least 33°C. A child should not be declared dead until it is ‘warm and dead’.

Rewarming

The techniques used to rewarm a child depend on the degree of hypothermia. Methods are divided into external and core rewarming but must not hamper CPR.

External rewarming alone is usually adequate where core temperature is more than 32° C. Below 32°C, core warming is necessary. The means used depend on the skills of the rescuers and the facilities available

Means of external rewarming, temperature >32°C

• Remove wet clothing

• Dry child

• Wrap in warmed blankets

• Use radiant heat lamp

Means of core rewarming, temperature <32°C

• Infusion of warm intravenous fluids (at 43°C)

• Ventilation with warm gases (at 43°C)

• Instillation of warm fluids into body cavities (at 43°C)*

• Cardiac bypass

*Instillation of warm fluids into body cavities is used by some, but thought to

confer no advantage to others.

Indicators of outcome

Abandoning resuscitating is always a difficult decision and should ideally be made by a senior doctor. As already mentioned, despite an initially poor outlook, children have still survived. A number of factors may help when coming to a decision. The majority of successful resuscitations occur in children who have had submersion times of less than 10

minutes

Indicators of good outcome

• Submersion for <10 minutes

• Submersion in cold water

• Initial core temperature below 33°C preserves vital organ (especially brain)

function

• Initial spontaneous breath in first few minutes

Indicators of poor outcome

• No spontaneous respiratory attempt within 40 minutes

• Arterial pO2 less than 8.0 kPa (60 mmHg) despite resuscitation

• Blood pH below 7.0 despite resuscitation

• Persisting coma

Definition

Drowning is defined as death by asphyxiation following submersion in a fluid, which is usually water. During the initial resuscitation it does not seem to make any difference whether this is fresh or salt water. Near-drowning occurs when the victim recovers, however briefly, following submersion.

Epidemiology

Bodies of water act as a strong draw for children and are a favored play area. Every year hundreds of children drown and this is a significant cause of death particularly in the under 4–year-olds who are often oblivious to the potential dangers. Carers should be ever mindful of this and should never leave children unsupervised especially if they suffer with epilepsy. Whether it be the garden pond or the unattended bathtub, they are all potential death traps. Children should be encouraged to learn to swim from an early age.

Pathophysiology

In drowning accidents, the primary event is a respiratory arrest eventually leading to a secondary cardiac arrest. A child submerged in water will initially hold their breath and their heart rate slows as part of the diving reflex. If this process continues, hypoxia develops and the child then becomes tachycardic. Eventually the child will take a breath and inhale water, which on contact with the glottis results in laryngospasm and secondary apnoea. In about 10% of cases no water actually enters the lungs in what is known as ‘dry drowning’. In the remaining cases, secondary apnoea is followed by the disappearance of laryngeal spasm and the development of involuntary respiration. Water and debris are then drawn down into the lungs. The child becomes progressively more hypoxic and acidotic, with a terminal bradycardia or arrhythmia acting as the prelude to eventual cardiac arrest.