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PALS

HOME REVIEW PACKET

Prior to class, please complete ACLS self-assessment test by accessing the student

website: www.Heart.org/eccstudent and enter the code “PALS15”. Bring completed

pre-course material to class.

www.CPRguys.biz

Health & Safety Training Institute Office: (888) 679.5650 Fax: (888) 679.5650

3515 SW 12 ST MIAMI, FL 33135 Info@HealthandSafetyTrainingInstitute.com

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BLS Review

Unresponsiveness: After determining that the scene is

safe, check to see if victim is responsive and breathing

normal. If the infant or child victim is unresponsive

and NOT breathing normally, send someone to

activate the emergency response system (EMS) –

phone 911 and get the AED.

IF IN THE HOSPITAL, CALL A CODE BLUE.

For unwitnessed arrest, the rescuer will yell for

“HELP” and immediately begin CPR for 2 minutes d

then phone 911 for children and infants only. The goal

of this fast approach is to deliver oxygen quickly

because the most common cause of cardiac arrest in

infants and children is a severe airway breathing

problems, respiratory arrest, or shock.

Exception: for sudden, witnessed collapse of child or

infant, active EMS immediately after verifying that

victim is unresponsive and then begin CPR.

C-A-B and D

1ST

Circulation

2nd

Airway

3rd

Breathing

4th Defibrillation

Key points Circulation:

Check for pulse for 5 – 10 seconds.

Push Hard. Push Fast.

Allow for full chest recoil.

Minimize interruptions.

The best location for performing a pulse check for a child is the carotid artery of the neck. On an infant

up to the age of one year, check the brachial pulse.

You should start cycles of chest compression and breathing when the victim is unresponsive, is not

breathing adequately, and does not have a pulse or has a weak pulse with signs of poor perfusion (HR

>60 bpm)

The compression to ventilation ratio is 30:2 for single rescuer and 15:2 for multiple rescues.

Proper compression technique requires the right rate and depth of compression, as well as full chest

recoil.

Take your weight off your hands and allow the chest to come back to its normal position. Full chest

recoil maximizes the return of blood to the heart after each compression.

The rate of performing chest compression for a victim of any age (adult, child and infant) is at a rate of

at least 100 to 120 compressions per minute.

Compressions on the child, two hands are placed in the center of the chest between the nipples on the

lower half of the sternum.

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Compressions on an infant are performed by using the two finger technique (pressing two fingers along

the sternum, just below the nipple line, and the fingers of the hand wrap around the back and press in

with each compression)

Compression depth is about 2 inches on a child and about 1 ½ inches on an infant.

Rotation of 2 – person CPR is every 2 minutes (5 cycles of 30:2) or after 5 cycles of 15:2 for two person

CPR on infant and children.

Minimize interruptions in chest compression will increase the victim’s chance of survival.

Airway:

Open the Airway

The head tilt-chin lift is the best way to open unresponsive victim’s airway when you do NOT suspect

cervical spine injury.

The jaw-thrust with cervical spine immobilization is used for opening airway without tilting the head or

moving the neck if a neck injury is suspected (this includes drowning victims) – after two unsuccessful

attempts, use head tilt-chin lift.

Breathing:

Given two breaths

To give breaths, pinch the victim’s nose closed, or for an infant place your mouth over the infant’s nose

and mouth, and given 1 breath (blow for 1 second), watch for the chest to rise. If the chest does not rise,

make a second attempt to open the airway with a health tilt-chin lift. Then give 1 breath (blow over 1

second) and watch for the chest to rise. Of course, if using mask barrier device or bag mask ventilation,

there is no need to pinch the nose. Only provide enough air to see the chest rise and fall. If using a bag

mask, there is no need to compress the bag completely.

DO NOT over-inflate the lungs. The positive pressure in the chest that is created by rescue breaths will

decrease venous return to the heart. This limits the refilling of the heart, so it will reduce cardiac output

created by subsequent chest compressions.

Some victims may continue to demonstrate agonal or gasping breaths for several minutes after a cardiac

arrest, but these breaths are too slow or too shallow and will not maintain oxygenation. If there is a

pulse, perform rescue breathing.

Defibrillation:

Attach the Automated External Defibrillator (AED)

The probably of successful defibrillation diminishes rapidly over time. Immediate CPR and

defibrillation within no more than 3 to 5 minutes given a person in sudden cardiac arrest the best chance

of survival.

The AED is used on an adults, children and infants. If pediatric pads are unavailable, it is acceptable to

use adult pads on an infant in cardiac arrest

Adult or Child victim: place one pad on the victim’s upper right chest just below the collar bone and to

the right of the sternum and the other pad on the left side and below the nipple, being careful that the

pads do not touch. If the infant or child is small and the pads would touch, place the pads in an

anterior/posterior position.

Steps for defibrillation are: Power on the AED & Attach pads, clear the victim and allow the AED to

analyze the rhythm – make sure not to touch the victim during the analyze phase, clear the victim and

deliver shock, if advised.

Make sure to clear the victim before shocking so that you and others helping do not get shocked.

If not shock is advised, leave the AED pads on the victim and continue CPR, beginning with

compressions.

CPR alone may not save the life of sudden cardiac arrest victim. Early defibrillation is needed.

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Primary Assessment: ABCDE A – Airway

• Look for movement of the chest or abdomen

• Listen for air movement and breath sounds

B – Breathing

• Respiratory Rate

• Respiratory Effort

• Chest expansion and air movement

• Lung and airway sounds

• Oxygen saturation by pulse oximetry

• A consistent respiratory rate of less than 10 or more than 60 breaths/min in a child of any age is abnormal and

suggests the presence of a potentially serious problem.

Head Bobbing – often indicate that the child has increased risk for deterioration

• Caused by the use of neck muscles to assist breathing

• Most frequently seen in infants and can be a sign of respiratory failure

Pulse Oximetry Readings

• A child may be in respiratory distress yet maintain normal oxygen saturation by increasing respiratory rate

and effort, especially if supplementary oxygen is administered.

C – Circulation

• Heart rate and rhythm

• Pulses (both peripheral and central)

• Capillary refill time

• Skin color and temperature

• Blood Pressure

D – Disability

• Decrease level of consciousness

• Loss of muscular tone

• Generalized seizures

• Pupil dilation

E – Exposure

• Undress the seriously ill or injured child as necessary to perform a focused physical examination

• Maintain cervical spine precaution when turning any child with a suspected neck or spine injury.

• Look for evidence of trauma such as bleeding, burns, or unusual markings that suggest no accidental

trauma

Glasgow

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Coma

Scale

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Management of Respiratory Emergencies

Respiratory Problems can be categorized into two categories based upon severity

• Respiratory Distress: tachypnea, increased respiratory effort, grunting, stridor, wheezing, seesawing or

“abdominal” breathing, head bobbing

• Respiratory Failure: bradypnea, periodic apnea, falling heart rate/bradycardia, diminished air movement,

low oxyhemoglobin saturation, coma, poor muscle tone, cyanosis

Respiratory Problems are categorized into four categories based upon type: Evaluate by observing symmetric

chest expansion and by listening for bilateral breath sounds. Breath sounds should be auscultated over the

anterior and posterior chest wall and in the axillary areas. Listen for intensity and pitch of sounds.

Upper Airway obstruction:

Croup, anaphylaxis and foreign body airway obstruction are common causes

Inspiratory Stridor

Treatment – treat croup with modified oxygen and nebulized epinephrine, corticosteroids treat

anaphylaxis with IM epinephrine or auto injector, albuterol, antihistamines, corticosteroids, aspiration

foreign body by allowing position of comfort and specialty consultation.

Lower Airway obstruction:

Asthma and bronchiolitis are common causes.

Expiratory wheezes

Treatment – treat bronchiolitis with nasal suctioning and bronchodilator, treat asthma with

albuterol, corticosteroids, SQ epinephrine, magnesium sulfate, terbutaline

Lung Tissue (Parenchymal) disease

Pneumonia/Pneumonitis and pulmonary edema are common causes

Treatment – treat pneumonia/pneumonitis with albuterol and antibiotics, treat pulmonary edema

with ventilator and vasoactive support, and consider a diuretic

Disordered control of breathing:

Increase ICP, Poisoning/overdose, and neuromuscular disease are common causes

Irregular breathing pattern (“funny breathing”)

Treatment – treat increased ICP by avoiding hypoxemia, hypercarbia, and hyperthermia, treat

poisoning/overdose with antidote and call poison control center, treat neuromuscular disease with

ventilator support.

Respiratory Distress

o Tachypnea

o Increased respiratory efforts (eg, nasal flaring, retractions)

o Inadequate respiratory effort (eg, hypoventilation or bradypnea)

o Abnormal airway sounds (eg, stridor, wheezing, grunting)

o Tachycardia

o Pale, cool skin

o Changes in level of consciousness

Respiratory Failure

o Marked tachypnea (early)

o Bradypnea, apnea (late)

o Increased, decreased, or no respiratory efforts

o Poor or absent distal air movement

o Tachycardia (early)

o Bradycardia (late)

o Cyanosis

o Stupor, coma (late)

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Key points:

STRIDOR -Upper airway obstruction (Foreign body)

GRUNTING -Upper airway obstruction (Swollen airway). Pneumonia (grunting to recruit alveoli)

WHEEZING -Lower airway obstruction (Asthma)

CRACKLES -Fluid in lungs (Wet), Atelectasis (Dry)

ABSENT/DECREASED BREATH SOUNDS -Collapsed lung (Air, blood). Lung tissue disease (Pneumonia)

In some instances, breath sounds can provide information about the source of the breathing problem.

Airway Devices

Nasopharyngeal Airway – semi – conscious

o Choose size based upon the diameter of the nostril (a 12F or 3mm will generally fit a full

term infant)

o For proper length, measure from the nose to the ear

o A shortened E.T. tube may be used

Oral pharyngeal Airway – unconscious

o Choose correct size by measuring from the corner of the mouth to the angle of the jaw.

o Insert while using a tongue depressor to hold the tongue on the floor of the mouth

o It is still necessary to keep the head and neck in the sniffing position after the oral

pharyngeal airway is in place

o Do not suction for more than 10 seconds at a time

Endotracheal Tube – usually the ideal airway in hospitalized patients

o The E.T. tube is placed using a laryngoscope, looking for the triangular vocal cords, and

placing the E.T. tube through them.

o If bradycaria develops or the clinical condition of the child being intubated deteriorates, interrupt

the intubation attempt to provide bag-mask ventilation with 100% oxygen.

o Insertion of an advanced airway may be deferred until several minutes into the attempted

resuscitation, since airway insertion requires an interruption in chest compression for

longer than 10 seconds

Key Points:

• Always monitor a patient with pulse oximetry

• When possible, monitor with capnography.

• Maintain the arterial oxyhemoglobin saturation >94%. An Oxyhemoglobin saturation of 100% is

generally an indication to wean the FiO2

• Pulse oximetry evaluates oxygenation, but not effectiveness of ventilation (elimination of CO2)

• Determine effectiveness of bag-mask ventilation by observing for visible chest rise.

Confirming E.T. Tube placement:

• Mist in the tube

• Auscultation of lungs for bilateral breath sounds

• Auscultation of the gastric area – no gurgling should be heard that would indicate intubation of the

esophageal area

• Confirmation with CO2 detector changing color after six ventilation or Esophageal Detector (now

one or the other is required for primary confirmation). Do not use esophageal detector on children

less than 20Kg.

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Once an advanced airway is in place, there is no need to pause chest compression for ventilations.

Provide 100 compressions per minute and 1 breath every 6 – 8 seconds.

If deterioration in respiratory status occurs in an intubated child, use the DOPE mnemonic

D – Displacement – especially without cuffs, E.T. tubes in children can become displaced easily and should

correct placement should be confirmed each time a child is moved.

O – Obstruction – E.T. tube in children can be very small and easily become occluded

P – Pneumothorax – If breath sounds are diminished on one side, there may be tracheal deviation, O2

saturation remains low, tachycardia and tachypnea are present, perform immediate needle

decompression followed by chest/thoracotomy tube placement.

E – Equipment – always check to make sure that the equipment is functioning properly.

Key Points:

Capillary refill, if prolonged (>2 seconds), may indicate shock, measure blood pressure early. Shock is defined

as inadequate delivery of oxygen and nutrients to the tissues relative to tissue metabolic demand.

Shocks

Shock can be

categorized into

two categories

based upon

severity:

• Compensated

Shock: Normal

systolic BP,

decreased level of

consciousness,

cool extremities

with delayed

capillary refill,

and faint or non-

palpable distal

pulses

• Hypotensive

Shock:

Hypotension with

signs of shock

*** For children

ages 1 to 10 years

of age,

hypotension is

defined as

systolic BP <70

mm Hg + (child’s

age

in years x2) mm

Hg ***

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PHARMACOLOGY

Vasopressors vs. Anti-dysrhythmic

Vasopressors:

A vasopressor is a medication that produces vasoconstriction and a rise in blood pressure. The vasopressors

that can be used in the treatment of VF/Pulseless VT are epinephrine and/or vasopressin. Epinephrine is

primarily used for is vasoconstrictive effects. Vasoconstriction is important during CPR because it will help

increase blood flow to the brain and heart. Vasopressin is also used for its vasoconstrictive effects and has been

shown to have effects similar to those of epinephrine.

Anti-dysrhythmic:

Antiarrhythmic medication are a group of pharmaceuticals that are used to suppress abnormal rhythms of the heart

(cardiac arrhythmias), such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation. Drugs

such as Amiodarone, Lidocaine, Procainamide and Magnesium are antiarrhythmic medications that are used in the

pulseless arrest algorithm.

VASOPRESSORS

EPINEPHERINE

Classification: Catecholamine, vasopressor, inotrope

Indications: Cardiac Arrest, anaphylaxis, asthma, symptomatic bradycardia

Croup, hypotensive shock, toxins/overdose

Actions: Positive β effects (increased heart rate, contractility and automaticity)

Positive α effects (peripheral vasoconstriction)

Dosage: IVP IV every 3-5 minutes (see Broselow tape for exact weight based

doses)

Route: IV/IO push

Adverse Effects: Tachycardia

Hypertension

PVC’s

Palpitations

Increased myocardial O2 demand

The α-adrenergic-mediated vasoconstriction of epinephrine increases aortic diastolic pressure and thus

coronary perfusion pressure, a critical determinant of successful resuscitation. Although epinephrine has been

used universally in resuscitation, there is little evidence to show that it improves survival in humans. Both

beneficial and toxic physiologic effects of epinephrine administration during CPR have been shown in animal

and human studies. Current studies show no survival benefit from routine use of high dose epinephrine and it

may be harmful, particularly in asphyxia arrest. High dose epinephrine may be considered for special

resuscitation circumstances. (Chapter 9 PALS text)

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ANTIARRHYTHMICS

AMIODARONE

Indications: SVT, Ventricular tachycardia with pulses, Pulseless arrest (VF and

Pulseless V-Tach.

Actions: Prolongs the action potential duration and effective refractory period,

slows sinus rate, prolongs PR and QT intervals and noncompetitively

inhibits α-adrenergic and β-adrenergic receptors

Dosage: VF/VT= Cardiac arrest: 5mg/kg IVP for first dose and up to 15mg/kg

max dose (see Broselow tape for exact weight based doses) For SVT

and V-Tach with pulses 5mg/kg IV/IO over 20-60 minutes (max dose

300mg) Upon ROSC: See JHACO Guidelines for infusions

Route: IV/IO

Adverse effects Hypotension, Bradycardia, SA node dysfunction, sinus arrest,

CHF, torsades, pulmonary fibrosis, ARDS

Amiodarone may be considered as part of the treatment of shock-refractory or recurrent VF/VT. Amiodarone

has α-adrenergic and β-adrenergic blocking activity; affects sodium, potassium, and calcium channels; slows

AV conduction; prolongs the AV refractory period and QT interval; and slows ventricular conduction (widens

the QRS). Adult studies showed increased survival to hospital admission but not to hospital discharge when

amiodarone was used compared to lidocaine. One study in children demonstrated the effectiveness of

amiodarone for life-threatening ventricular arrhythmias, but there have been no published studies on the use of

amiodarone for pediatric cardiac arrest.

LIDOCAINE

Classification: Anti-arrhythmic

Indications: Ventricular Fibrillation, Pulseless Ventricular Tachycardia, Rapid

sequence intubation (RSI) i.e. ICP protection

Actions: Depresses ventricular irritability and automaticity

Increases fibrillation threshold

Dosage: V-Tach with a pulse or VF/Pulseless VT: see Broselow tape for

weight based doses. MAINTENANCE INFUSION upon ROSC: see

JHACO infusion protocol.

Route: IVP, IO or IV Infusion

Adverse Effects: Muscle tremors, heart block, myocardial depression, hypotension,

seizures, cardiac arrest in bradycardias.

Lidocaine continues on next page.

Lidocaine has long been recommended for the treatment of ventricular arrhythmias in infants and children

because it decrease automaticity and suppresses ventricular arrhythmias. Data from a study of shock-refractory

VT in adults showed that lidocaine was inferior to amiodarone, so lidocaine has been recommended as a second

line drug in shock-refractory cardiac arrest only when amiodarone is not available. Its indications in the

treatment of other ventricular arrhythmias are uncertain. There have been no published studies on the use of

lidocaine in pediatric cardiac arrest.

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MAGNESIUM SULFATE

Classification: Electrolyte, bronchodilator

Indications: Hypomagnesemia

Torsades de Pointes

Asthma (refractory status asthmaticus)

Actions: Smooth muscle relaxer

Exerts antiarrhythmic action

Dosage: Cardiac arrest due to torsades: IV/IO route 25-50mg/kg; 25-50

mg/kg over 10-20 minutes for VT with pulses associated with

torsades or hypomagnesemia; 25-50mg/kg by slower infusion (15-30

minutes) for treatment of status asthmaticus.

Adverse Effects: Mild bradycardia, hypotension, hypermagnesemia, respiratory

depression, weakness, heart block, and cardiac arrest may develop

with rapid administration. Contraindications: renal failure

Magnesium Sulfate should be administered for the treatment of torsades de pointes or hypomagnesemia. There

is insufficient evidence to recommend for or against the routine use of magnesium in pediatric cardiac arrest.

OTHER DRUGS

ATROPINE

Classification: Anticholinergic

Indications: Symptomatic bradycardia (usually secondary to vagal stimulation;

Toxins (organophosphate overdose, carbamate); rapid sequence

intubation (i.e. when using succinylcholine)

Actions: Increases heart rate and cardiac output by blocking vagal stimulation;

blocks acetylcholine and other muscarinic agonists

Dosage: 0.5 mg IVP in bradycardic patient. NOT TO EXCEED 3.0 mg

Route: IV or IO

Adverse Effects: Tachycardia, dilated pupils, blurred vision, headache, dysuria,

weakness, bradycardia if used in smaller than recommended doses.

**Document clearly if used for patients with head injury, because

atropine will distort pupillary exam by causing pupil dilation.

**Special considerations: Use drug in any child with bradycardia at time of endotracheal intubation. Consider

using drug to prevent bradycardia when succinylcholine is used in an infant or young child, especially in the

presence of hypoxia and acidosis.

Atropine is indicated for the treatment of bradyarrythmias. There are no published studies suggesting its

efficacy for treatment of cardiac arrest in pediatric patients. (See PALS text for complete discussion)

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CALCIUM CHLORIDE

Classification: Calcium ion (electrolyte)

Indications: Hypocalcaemia, hyperkalemia, consider for hypomagnesaemia and

treatment of calcium channel blocker overdose.

Actions: Needed for maintenance of nervous, muscular, skeletal systems,

enzyme reactions, normal cardiac contractility, and blood

coagulation.

Dosage: 20 mg/kg IO/IV slow push during cardiac arrest if hypocalcemia is

known or suspected; may repeat if documented or suspected clinical

indication persists. Infuse over 30-60 minutes for other indications

Adverse Effects: Hypotension, bradycardia, asystole, heart block, cardiac arrest,

arrhythmias, venous thrombosis, necrosis upon infiltration,

hypercalcemia

SODIUM BICARBONATE

Classification: Alkalinizing agent, electrolyte, buffer

Indications: Metabolic acidosis from an unknown cause or suspected acidosis

from confirmed prolonged down time, sodium channel blocker

overdose (e.g.Tricyclic antidepressant) Hyperkalemia

Actions: Increases plasma bicarbonate, which buffers H+ ion (reversing

metabolic acidosis) forming carbon dioxide; elimination of carbon

dioxide via the respiratory tract increases pH.

Dosage: 1mEq/kg IV push, can be repeated as ordered by clinician in cardiac

arrest

Route: IV/IO

**Special considerations: Do not administer via endotracheal route; Irrigate IV/IO tubing with NS before and

after infusions or use another line to administer.

Sodium bicarbonate is recommended for the treatment of symptomatic patients with hyperkalemia, Tricyclic

antidepressant overdose, or an overdose of other sodium channel blocking agents. Routine use of sodium

bicarbonate in cardiac arrest is not recommended. After you have provided effective ventilation and chest

compressions and administered epinephrine, you may consider sodium bicarbonate for prolonged cardiac arrest.

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ADENOCARD/ADENOSINE

Classification: Antiarrhythmic

Indications: SVT

Dose: IV/IO Rapidly: Exact weight based doses on Broselow tape

Actions Briefly blocks conduction through AV node and interrupts pathways through AV node.

Allows return of NSR in patients with SVT, including SVT associated with WPW.

Depresses sinus node automaticity.

******Note: This is NOT a complete list of drugs used in the PALS course. Please consult your PALS

textbook for a complete list of drugs including classifications, indications, doses and

actions of each drug.

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Pediatric Algorithm

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In contrast with cardiac arrest in adults, cardiopulmonary arrest in infants and children is rarely sudden and is

more often caused by progression respiratory distress and failure or shock than by primary cardiac arrhythmias.

Therefore, oxygen is the number one treatment of most pediatric conditions.

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H’s and T’s of ACLS

Knowing the H’s and T’s of ACLS will help prepare you for any ACLS scenario. Don’t forget your H’s and

T’s. The H’s and T’s of ACLS is a mnemonic used to help recall the major contributing factors to pulseless

arrest including PEA, Asystole, Ventricular Fibrillation, and Ventricular Tachycardia. These H’s and T’s will

most commonly be associated with PEA, but they will help direct your search for underlying causes to any of

arrhythmias associated with ACLS. Each is discussed more thoroughly below.

The H’s include: The T’s include

The H’s include:

Hypovolemia

Hypovolemia or the loss of fluid volume in the circulatory system can be a major contributing cause to cardiac

arrest. Looking for obvious blood loss in the patient with pusleless arrest is the first step in determining if the

arrest is related to hypovolemia. After CPR, the most import intervention is obtaining intravenous access/IO

access. A fluid challenge or fluid bolus may also help determine if the arrest is related to hypovolemia.

Hypoxia

Hypoxia or deprivation of adequate oxygen supply can be a significant contributing cause to cardiac arrest.

You must ensure that the patient’s airway is open, and that the patient has chest rise and fall and bilateral

breath sounds with ventilation. Also ensure that your oxygen source is connected properly.

Hydrogen ion (acidosis)

To determine if the patient is in respiratory acidosis, an arterial blood gas evaluation must be performed.

Prevent respiratory acidosis by providing adequate ventilation. Prevent metabolic acidosis by giving the patient

sodium bicarbonate.

Hyper-/hypokalemia

Both a high potassium level and a low potassium level can contribute to cardiac arrest. The major sign of

hyperkalemia or high serum potassium is taller and peaked T-waves. Also, a widening of the QRS-wave may be

seen. This can be treated in a number of ways which include sodium bicarbonate (IV), glucose insulin, calcium

chloride (IV), Kayexalate, dialysis, and possibly albuterol. All of these will help reduce serum potassium levels.

The major signs of hypokalemia or low serum potassium are flattened T-waves, prominent U-waves, and

possibly a widened QRS complex. Treatment of hypokalemia involves rapid but controlled infusion of

potassium. Giving IV potassium has risks. Always follow the appropriate infusion standards. Never give

undiluted intravenous potassium.

Hypoglycemia

Hypovolemia Toxins

Hypoxia Tamponade (cardiac)

Hypothermia Tension pneumothorax

Hydrogen ion (acidosis) Thrombosis (coronary and pulmonary)

Hyper-/hypokalemia Trauma

Hypoglycemia

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Hypoglycemia or low blood glucose can have many negative effects on the body, and it can be associated with

cardiac arrest. Treat hypoglycemia with IV dextrose to reverse low blood glucose. Hypoglycemia was removed

from the H’s but is still to be considered important during the assessment of any person in cardiac arrest.

Hypothermia

If a patient has been exposed to the cold, warming measures should be taken. The hypothermic patient may be

unresponsive to drug therapy and electrical therapy (defibrillation or pacing). Core temperature should be

raised above 86 F (30 C) as soon as possible.

The T’s include:

Toxins

Accidental overdose of a number of different kinds of medications can cause pulseless arrest. Some of the most

common include: tricyclics, digoxin, beta blockers, and calcium channel blockers). Street drugs and other

chemicals can precipitate pulseless arrest. Cocaine is the most common street drug that increases incidence of

pulseless arrest. ECG signs of toxicity include prolongation of the QT interval. Physical signs include

bradycardia, pupil symptoms, and other neurological changes. Support of circulation while an antidote or

reversing agent is obtained is of primary importance. Poison control can be utilized to obtain information about

toxins and reversing agents.

Tamponade

Cardiac tamponade is an emergency condition in which fluid accumulates in the pericardium (sac in which the

heart is enclosed). The buildup of fluid results in ineffective pumping of the blood which can lead to pulseless

arrest. ECG symptoms include narrow QRS complex and rapid heart rate. Physical signs include jugular vein

distention (JVD), no pulse or difficulty palpating a pulse, and muffled heart sounds due to fluid inside the

pericardium. The recommended treatment for cardiac tamponade is pericardiocentesis.

Tension Pneumothorax

Tension pneumothorax occurs when air is allowed to enter the plural space and is prevented from escaping

naturally. This leads to a buildup of tension that causes shifts in the intrathroacic structure that can rapidly

lead to cardiovascular collapse and death. ECG signs include narrow QRS complexes and slow heart rate.

Physical signs include JVD, tracheal deviation, unequal breath sounds, difficulty with ventilation, and no pulse

felt with CPR. Treatment of tension pneumothorax is needle decompression.

Thrombosis (heart: acute, massive MI)

Coronary thrombosis is an occlusion or blockage of blood flow within a coronary artery caused by blood that

has clotted within the vessel. The clotted blood causes an Acute Myocardial Infarction which destroys heart

muscle and can lead to sudden death depending on the location of the blockage.

ECG signs indicating coronary thrombosis are 12 lead ECG with ST-segment changes, T-wave inversions,

and/or Q waves. Physical signs include: elevated cardiac markers on lab tests, and chest pain/pressure.

Treatments for coronary thrombosis include use of fibrinolytic therapy, PCI (percutaneous coronary

intervention). The most common PCI procedure is coronary angioplasty with or without stent placement.

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Thrombosis (lungs: massive pulmonary embolism)

Pulmonary thrombus or pulmonary embolism (PE) is a blockage of the main artery of the lung which can

rapidly lead to respiratory collapse and sudden death. ECG signs of PE include narrow QRS Complex and

rapid heart rate. Physical signs include no pulse felt with CPR. Distended neck veins, positive d-dimer test,

prior positive test for DVT or PE. Treatment includes surgical intervention (pulmonary thrombectomy) and

fibrinolytic therapy.

Trauma

Trauma can be a cause of pulseless arrest, and a proper evaluation of the patients physical condition and

history should reveal any traumatic injuries. Treat each traumatic injury as needed to correct any reversible

cause or contributing factor to the pulseless arrest. Trauma was removed from the T’s but is still to be

considered important during the assessment of any person in cardiac arrest.