PALS Flashcards
In specific settings, when treating pediatric patients with febrile illnesses, the use of restrictive volumes of isotonic crystalloid leads to improved survival T/F
True
administration of IV fluid for children with septic shock
There is evidence that excessive fluid boluses given to febrile patients with shock can lead to complications, especially if there is no ICU unit ( mechanical vent,inotropic support)
There is no evidence to support the routine use of atropine as a premedication to prevent bradycardia in emergency pediatric intubations. T/F
TRUE, is controversial
It may be considered in situations where there is an increased risk of bradycardia.
There is no evidence to support a minimum dose of atropine when used as a premedication for emergency intubation.
If invasive hemodynamic monitoring is in place at the time of a cardiac arrest in a child, it is NOT reasonable to use it to guide CPR quality. T/F
False, it is reasonable!
Which is the recommended vasopressor in pediatric cardiac arrest?
Epi
In children with cardiac diagnoses and in-hospital arrest what do you consider?
If available, extracorporeal CPR
What is Extracorporeal cardiopulmonary resuscitation ?
method of cardiopulmonary resuscitation that passes the patient’s blood through a machine in a process to oxygenate the blood supply. A portable extracorporeal membrane oxygenation device is used as an adjunct to standard CPR
How is the management of fever in a comatose patient after cardiac arrest?
temperature should be monitored continuously and fever should be treated aggressively.
For comatose children resuscitated from OHCA,- maintain either 5 days of normothermia (36°C to 37.5°C) or 2 days of initial continuous hypothermia (32°C to 34°C) followed by 3 days of normothermia.
For children remaining comatose after IHCA, there are insufficient data to recommend hypothermia over normothermia.
IHCA- in hospital cardiac arrest
What do you do after return of spontaneous circulation (ROSC) after cardiac arrest, in terms of fluids/inotropes ?
fluids and inotropes/vasopressors should be used to maintain a systolic blood pressure above the fifth percentile for age.
Intra-arterial pressure monitoring should be used to continuously monitor blood pressure and identify and treat hypotension.
What is the goal of systolic BP after ROSC post arrest?
above the fifth percentile for age.
70 mmHg+ (Age in years x 2)
What do you do after return of spontaneous circulation (ROSC) after cardiac arrest, in terms of O2 ?
Target sat 94-99%
Hypoxemia should be strictly avoided
Targetin normoxemia improves outcomes
CAB sequence
compressions, airway and breathing
CPR- Rate of compressions?
100-120/min
CPR- how deep in chest?
~1/3 of the depth
In infants : 1.5in( 4cm)
In children: 2 in(5cm)
In children reached puberty at least 2 in but no more than 2.4 ( 6cm).
and allow complete chest recoil
compression ventilation ratio?
30: 2 for single
15: 2 for 2 or more rescuers
compression ventilation after an advanced airway is in place?
deliver 10 breaths per min ( 1 min every 6 seconds) while continuous chest compressions.
What is the drug of choice for treating shock refractory Vfib or pVT in children?
Amiodarone or Lidocaine. No benefit of one over the other.
BLS, where do you tap the children and infant to see if they are responsive?
Children: shoulder
Infant : heel
BLS algorithm
- Verify the scene is safe
- Check for responsiveness- “Are you OK”
- If unresponsive - shout for nearby help, ACTIVATE THE EMERGENCY RESPONSE SYSTEM VIA MOBILE IF POSSIBLE
- Assess the child breathing and pulse ( no more than 10 seconds)
breathing: scan victims chest for rise and fall.
if patient is breathing, monitor until additional help
arrives.
if patient is not breathing then he has respiratory or cardiac( .if no pulse) arrest.Check pulse:infant: brachial artery
children: carotid or femoral pulseIf you dont feel pulse within 10 seconds start CPR
Where do you check pulse in infants and children?
Check pulse:
infant: brachial artery -
children: carotid or femoral pulse
if you feel it, attempt to feel the pulse for at least 5 sec
If you dont feel pulse within 10 seconds start CPR
If patient is not breathing, but has a pulse whats next?
1 breath every 3-5 seconds or about 12-20 breaths/min
Add compressions if pulse =< 60/min with signs of poor perfusion
Activate emergency response system after 2 min if not done already
Continue rescue breathing, check pulse every 2 min
signs of poor perfusion
TAPS Temperature: cool extremities Altered mental status: decrease in responsiveness Pulses: weak pulses Skine: paleness, mottling, cyanosis
No breathing/ No pulse
Activate the emergency response system - 911
Get the AED equipment , if there is someone else send them to get it
CPR- remove or move the clothing and do CPR
CPR in children and infant
infant: 2 fingers
Child: 1-2 hands
Infant 2 finger technique ( 1 rescuer)
- Place the infant on a firm flat surface
- Place 2 fingers in the center of the chest, just below the nipple line
- compressions 100-120/min
- At the end of each compression allow recoil
- After every 30 compressions, open airway give 2 breaths, each over 1 second. the chest should rise with each breath.
- After 5 cycles or 2 min ask for AED
- continue compressions until AED
Why do you have to allow for chest recoil?
Allows blood to flow into the heart.
Incomplete recoil–> less filling between compressions and reduces the blood flow created by chest compressions.
Infant 2 thumb-encircling hands technique ( 2 rescuers preferred)
- Place the infant on a firm flat surface
- Place thumbs side by side in the center of infants chest, on lower half of breastbone. (thumbs may overlap in very small children)
- compressions 100-120/min
- At the end of each compression allow recoil
- After every 15 compressions, open airway give 2 breaths, each over 1 second. the chest should rise with each breath.
- After 5 cycles or 2 min ask for AED
- continue compressions until AED
Why is the 2 thumb encircling hand technique the preferred when 2 rescuers? (3)
- produces better blood supply to the heart
- Helps ensure consistent depth and force of chest compressions
- May generate higher BPs
Methods for opening airway
head tilt-chin lift
jaw thrust manuevers
KEEP HEAD IN NEUTRAL POSITION
When there are 2 rescuers- how often they should switch roles?
Every 5 cycles or 2 min
Attenuator in the AED for children , how much reduces the dose of the shock
2/3.
Child vs. Adult pads of AED cutoff age.
Child pads : for infants and children < 8 years. If not available use adult.
Children> 8: adult pads
Location of adult pads/child pads
Adult pads: in the upper right chest and in the left lateral part
Child: in front and back ( most commonly for infants)
In infants why a manual defibrillator is preferred over an AED?
More capabilities than AED, and can provide lower energy doses
if this is not available and nor is an AED with attenuator , use the regular AED as is better to shock than do nothing.
PAT triangle ( Pediatric Assessment triangle)
ABC
Appearance - consciousness, TICLS ( tone, interactiveness, consolability, look/gaze, speech/cry)
breathing -
look patients position ( tripod or sniffing position)
retractions
stridor, sonorous respirations
color
Evaluate-Identify-Intervene approach
If no life-threatening condition
Evaluate
Primary assessment: rapid ABCDE approach, VS, oximetry
Secondary assessment: focused medical history and PE
Diagnostic assessments
Identify
Type and severity of the problem
Intervente
This cycle should be repeated over and over,:
with every single intervention or with any change ( improvement or deterioration) until the child is stable.
ABCDE approach
Airway Breathing Circulation Disability Exposure
How do you determine airway patency ?
- Look for movement of the chest and abdomen
- Listen for air mov and breath sounds
- Feel for movement of air at the nose and mouth
Breathing should be assessed as the same time as you check pulse - T/F
tRUE
Upper Airway Status
- Clear
- Maintenable
- Non maintenable
Definition of clear, maintenable and non maintenable airway
Clear: airway is open and unobstructed for normal breathing
Maintenable: Airway is obstructive but can be maintaned by simple measures( e.g. head tilt chin lift)
Not-maintenable: Airway is obstructed and needs advanced intervations ( intubation)
Signs that suggest that the airway is obstructed?
- increased inspiratory effort with retractions
- Abnormal inspiratory sounds ( snoring, high-pitched stridor)
- Episodes where no airway or breath sounds are present despite respiratory efforts ( complete upper airway obstruction)
Simple measures to maintain airway
POSITIONING:
If responsive child- allow him to assume a position of comfort or elevate the head of the bed.
If unresponsive:
Turn the child on his side if you dont suspect cervical injury or head tilt chin lift or jaw thrust .
If unresponsive and the jaw thrust is not open, use head tilt chin lift or jaw thrust with jaw extension because open airway is a priority.
SUCTIONING-nose and oropharynx , avoid overextending head and neck
Relief techniques if foreign object
AIRWAY ADJUNCTS: eg. oropharyngeal aiway ( to avoid the tongue from falling back) - NEVER RELY ON THIS ALONE, ALWAYS DO SOMETHING ELSE
Simple measures to maintain airway
positioning
suctioning
relief techniques for foreign body airway obstruction
airway adjuncts
If child suspected of aspirating foreign body and has complete airway obstruction? responsive/unresposive
responsive:
< 1 year: give 5 back slaps and 5 chest thrusts
>=1 year: give abdominal thrust
If unresponsive: activate or send someone to activate the emergency response system and start CPR
Advanced interventions to maintain airway patency
Endotracheal intubation
Application of continuous positive airway pressure or non invasive ventilation
Removal of foreign body requires direct laryngoscopy
Cricothyrotomy
5 things to assess breathing
- Respiratory rate and pattern
- Respiratory effort
- Chest expansion and air movement
- Lung and airway sounds
- O2 Saturation by pulse oximeter
Normal respiratory rate in
infant
toodler
preschooler
school-age
30-53 22-37 20-28 18-25 12-20
Abnormal breathing is RR< 10 and more than 60 is abnormal in any child T/F
True
How to determine RR
count the number of times the chest rises in 30 seconds and multipy by 2
*Normal sleeping infants may have irregular( periodic) breathing pauses lasting up to 10 or even 15 seconds.
Normal sleeping infants may have irregular( periodic) breathing pauses lasting up to 10 or even 15 seconds.
True
Irregular respiratory pattern may be a sign of?
Neurological condition
Tachypnea causes
- respiratory distress ( particularly when accompanied of respiratory effort)
- no respiratory causes - when there is just fast RR but no effort:
- fever, pain, anemia, cyanotic heart disease, sepsis
- Dehydration
Causes of bradypnea ( 7)
- respiratory muscle fatigue
- CNS injury or any problem that affects the respiratory control center
- Severe hypoxia
- Severe shock
- Hypothermia
- Drugs that repress respiratory drive
- Muscle disease that causes resp muscle weakness
What does bradypnea or irregular respiratory rate mean in a critically ill child?
signals of impending arrest
Definition of apnea
Cessation of breathing longer than 15 seconds
Classification of apnea
Central : no respiratory effort- abnormality or supression of the brain or spinal cord
Obstructive: inspiratory effort present without airflow. -ventilation is impeded , resulting in hypoxemia, hypercapnia or both.
Mixed apnea: periods of obstructive and periods of central apnea.
Why does increased respiratory effort occur?
In conditions where there is increased resistance to airflow ( asthma, bronchiolitis), or that causes lungs to be stiffer and difficult to inflate (pneumonia, pulmonary edema, pleural effusion)
Non respiratory conditi
Non respiratory conditions that cause increased respiratory effort
whatever that causes severe metabolic acidosis: shock, DKA, salicylate ingestion, inborn errors of metabolism)
Signs of increased respiratory effort?
nasal flaring
retractions( inward mov of the chest wall or tissues or sternum during inspiration)
head bobbing or seesaw respirations
location of retractions correlates to severity?
Yes
Location of retractions if mild-moderate?
subcostal, substernal, intercostal
Location of retraction if severe?
( may include same retractions than in mild-moderate) and
supraclavicular
suprasternal
sternal
retractions accompanied by stridor or inspiratory sound suggest..
upper airway obstruction
retractions accompanied by expiratory wheezing suggest..
lower airway obstruction ie.asthma bronchiolitis
retractions accompanied by grunting or labored resp suggest..
lung tissue disease
why does Head bobbing occur and what does it mean?
use of neck muscles to assist breathing
sign of increased deterioration/ respiratory failure
what are seesaw respirations and what do they mean?
when chest retracts and the abdomen expands during inspiration. During expiration the mov reverses.
Usually indicate UPPER AIRWAY OBSTRUCTION
May also be obseverd in sever lower airway obstruction
Characteristic of infants and chilren with NM weakness.
What respiratory effort pattern is Characteristic of infants and chilren with NM weakness.
seesaw respirations
Cause of seesaw breathing
NM disease, weakness of the abdominal and chest wall muscles.
Strong contraction of diaphragm that dominates the weaker abdominal and chest muscles.
Definition of tidal volume and normal value
volume of air inspired with each breath
Normal: 5-7 mL/kg
Ausculation lungs
anterior ( left and right to the sternum)
under the armpits ( best location to assess lower airway)
posterior: both sides of the back
Where is the best place to assess distal air entry?
auscultate below the axillae
What is minute ventilation
The volume of air that moves into or out of the lungs each min
Vmin= RR X Tidal volume
Causes of Low minute ventilation ( hypovent)
Since Vmin= RR X Tidal volume
low RR
Low Tidal volume ( stiff lungs, airway resistance)
Extremely fast RR that leads to low tidal volume
What is a stridor and what does it indicate?
Coarse, high pitched breathing typically on inspiration but can be heard in both inspiration and expiration.
upper airway ( extrathoracic) obstruction
Stridor causes
foreign body
infection ( croup)
congenital airway abnormalities ( eg, laryngomalacia)
acquired airway abnoramlities( tumor or cyst)
edema of upper airway
Snoring causes besides sleep
soft tissue swelling or decreased level of consciousness
What is grunting and when does it occurs
short, low-pitched sound heard during EXPIRATION
Sometimes misinterpreted as soft cry
Occurs as child exhales against a partial closed glottis
SIGN OF LUNG TISSUE DISEASE- small airway collapse, alveolar collapse or both.
Causes of grunting
progression of respiratory distress to failure
pneumonia
pulmonary contusion
acute respiratory distress syndrome
CHF resulting en pulmonary edema
sign of PAIN ( abdominal pathology: bowel obstruction, perforated viscus, appendicits)
What is gurgling and when does it occur
bubbly sound heard during inspiration or expiration
upper airway obstruction due to airway secretions, vomit, blood
Wheezing and causes
high or low pitched whistling most often during expiration
Indicates lower airway obstruction, especially of smaller airways( asthma, bronchiolitis)
Isolated inspiratory wheezing: foreign body aspiration or partial obstruction of the trachea.
Crackles and rales are the same T/F
True! word embedded
rub several hairs together
Crackles
moist crackles: accumulation of alveolar fluids ( pneumonia and pulmonary edema)
dry crackles : atelectasis and interstitial lung disease
Crackles are always present in pulmonary edema T/F
False, they may not be present
How do you describe crackles?
Type: fine, medium, coarse
when: inspiratory or expiratory
where: bilateral, unilateral, upper lobe, lower lobe etc.
Pulse oxymeter
tool to monitor the percentage of hemoglobin that is fully saturated with oxygen
Does oxyhemoblogin saturation indicate the amount of O2 delivered to the tissues?
NO!
Delivery is the product of the arterial O2 content ( O2 bound to Hb+ Dissolved O2) and CO.
ie. in anemia there is decreased hb and saturation can be 100%- and the delivery is still low.
O2 does not provide information about the effectiveness of ventilation T/F
True
Sat % that indicates hypoxemia?
< 94%, needs additional vent.
How does a pulse oximeter works?
has two parts that must be placed opposite to the other.
Lights of different wavelenghts are produced from one side of the probe and the light is captured on the other side of the tissue by the other probe.
A processor in the oximeter calculates the percent of each light that has been absorbed by tissues.
Hemoglobin that is fully saturated absorbs light different than if its fully saturated.
So the pulseoximeter can estimate the percent of hemoglobin that is fully saturated
Situations to keep in mind with pulseoximeter
- Anemia - sat can be 100%, but O2 delivery is low
- Carboxyhemoglobin-Methemoglob- 100% Sat – obtain ABGs.
- If it cant detect a consistent pulse or there is an irregular or poor waveform, the child may have poor distal perfusion or the oximeter may not be accurate
Signs of probable respiratory failure 7
- Very rapid or inadequate respiratory rate; possible apnea
- Significant, inadequate, or absent respiratory effort
- Absent distal air movement
- Extreme tachycardia or bradycardia
- Low O2 sat despite high flow supplementary oxygen
- Decreased level of consciousness
- Cyanosis
Circulation assessment components (5)
Heart rate and rhythm Pulses ( both peripheral and central) Capillary refill time Skin color and temperature Blood pressure
Arrhythmia can result from shock or hypoxia T/F
True
Hypoxia ( delivery) is the most common cause of bradycardia in children
True
If you see sign of poor perfusion, support vent with bag and mask and give O2.
If patient is breathing and poor perfusion
check pulse, if =< 60 compressions despite good oxygenation and ventilation.
HR > 180 in infants and > 160 in toddlers/children is ABNORMAL.
Yes, require further assessment.
What do you consider in a kid with congenital heart disease, when evaluating the heart rate and rhythm?
consider its baseline, he may have conduction abnormalities.
Respiratory sinus arrythmia what is it?
HR increases with inspiration and slows with expiration
Central pulses-
Femoral
Brachial ( infants)
Carotid ( in older children)
Axillary
-felt stronger because of the increased vessel size and proximity to the heart
peripheral pulses
Radial
Dorsalis pedis
Posterior tibial
how do the pulses change in shock
peripheral vasoconstriction leads to exaggeration of the central pulses
pulsus paradoxus
is an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as pulsus paradoxus.
inspiration–> increased venous return–> increased blood in RV and leads to bulging towards the LV decreasing the size/volume.
asthma, pericardial tamponade
Capillary refill time definition and normal val
The time it takes for blood to return to tissue blanches by presssure
Normal: =< 2 seconds.
How do you evaluate capillary refill time?
lift the extremity slightly above the level of the heart, press and remove fast.
Causes of delayed capillary refill time
dehydration
shock
hypothermia
in septic shock it may be normal or even fast!
How do you measure temperature and why?
back of your hand, more sensitive.
palm has thicker layer of skin.
Acrocyanosis
hands, feet and around mouth- normal in newly born but not in older children
Causes of peripheral cyanosis
Shock
CHF
Peripheral vascular disease
Conditions causing venous stasis
Causes of central cyanosis
( lip or other mucous membranes)
Low ambient O2 tension
Alveolar hypoventilation ( TBI, drug overdose)
Diffusion defect ( pneumonia)
Ventilation/perfusion mismatch ( asthma, bronchiolitis, ARDS)
Intracardiac shunt
Central pallor suggests:
Anemia or poor perfusion
When does cyanosis occur?
is apparent when at least 5g/dl of Hb is desaturated.
The O2 saturation at which a child will appear cyanotic depends on the child hemoglobin concentration
Children with different hemoglobin levels will be cyanotic at different levels of O2 Sat.
True,
cyanosis may be detected at higher O2 sats if the Hb is high.
Accurate BP measurement
cuff bladder should cover about 40% of the mid-upper arm circumference. The BP cuff should cover 50-75% of the length of the upper arm.
Hypotension in term neonates, infants,children (1-10y), children(>10)
Is based on the SBP -- the tresholds approximate just above the 5th percentile for age-- term neonates < 60 infants < 70 children (1-10y) <70 +(age in years x 2) children(>10) < 90
What do you think when a patient with hemorrhage develops hypotension
~ has lost 20-25% of circulating volume
Hypotension in septic shock?
can occur due to loss of intravascular volume or
inappropriate vasodlation or severe vasoconstriction, or inadequate CO/CI
Why do we measure urine output?
Indirect measure of kidney perfusion- indicates blood flow and hydration
In critically ill children accurate measurement requires an indwelling catheter.
Normal value of urine output in infant and younger children
1.5 - 2 mL/kg per hour
Normal value of urine output in older children and adolescents
1 mL/kg per hour
Children with shock typically have decreased urine output. T/F
True
Disability assessment
AVPU ( Alert, responsive to voice, responsive to pain, unresponsive) Pediatric Response scale
GCS
Pupil response to light
Blood glucose test
AVPU Pediatric Response scale
To evaluate cerebral cortex function
Rates the level of consciousness in 4 states:
( Alert, responsive to voice, responsive to pain [sternal rub, pinching trapezius], unresponsive)
Causes of decreased level of consciousness
BRAIN: poor cerebral perfusion TBI Seizure activity Encephalitis/meningitis
OTHERS severe shock hypoglycemia hypoxemia hypercabnia drugs
GCS
EVM 456
Eye
Spontaneous, to voice, to pain, no eye opening
Verbal
Oriented, confused, inappropriate words, incomprehensible words, no response
Motor Obeys commands Localizes pain Withdraws from pain Abnormal flexion Abnormal extension No response
GCS classification
Mild head injury 13-15
Moderate 9-12
Severe < 9
Modified version of GCS for infants
see phone
When do you prefer AVPU vs. GCS
AVPU may be more appropriate in the pre-hospital setting
GCS in the hospital ED.
Correlation AVPU GCS
Alert 15
Response to verbal 13
Pain stimulation 8
Unresponsive to noxious stimuli 6
Pupil response to light should be done in any patient with altered mental status
True
useful indicator of brainstem status
Pinpoint pupils causes
narcotic ingestion - opioids
Dilated pupils causes
Predominant sympathetic activity Sympathomimetic ingestion ( cocaine) Anticholinergic ingestion ( atropine) Increased intracranial pressure
Unilaterally dilated pupils
Inadvertent topical absorption of a breathing treatment ( ipratropium)
Dilating eye drops
Unilaterally dilated pupils with altered mental status
IPSILATERAL uncal herniation
Description of pupils
PERRL
Pupils Equal, Round, Reactive to light.
Hypoglycemia values
In newborn =<45
In child=<60
Exposure is the last component of primary assessment:
Undress
Look for evidence of trauma ( bleeding, burns, abnormal markings)
petequia/purpura
deformities/bruises
Secondary assessment components
Focused history ( SAMPLE)
Focused PE
Ongoing reassessment
SAMPLE for focused history
Signs and Symptoms
Allergies - meds, food,latex/associated reaction
Medications- include overthecounter, vit, last dose and time of recent meds, meds that can be found in childs environment.
Past Medical History - born, Cxs/hospitalizations, illness, immunization
Last meal - time and nautre of last meal. elapsed time between last meal and presentation of current illness
Events - leading to current illness or injury ( sudden, gradual), hazards at scene, treatment during inteval from oset, time of onset.
Components of ongoing reassessment
PAT
ABCDE of primary approach with acquisition of VS and pulseoximetry
Assessment of abnormal anatomic and physiologic findings
Review the effectiveness of treatment interventions with each cycle
PaO2 indicates ..
O2 dissolved in plasma
PaO2 normal and Hb of 3, what can you say about the saturation and delivery to tissue
Saturation can be 100%, but due to the low Hb there is inadequate delivery to the tissues
Acid-Base algorithm
say it
serial ABGs are better than only once, because it just indicate a state in a time point.
true
What is hyperoxia
increased arterial O2 sat detected by direct measure in ABG .
what does increased base deficit means
accumulation of acid in the blood
When do you do venous blood gases, advantages/disadvantages
When there is no arterial sample available, usually not very useful for arterial oxygenation
there are differences based on where the same was taken from, so better central than peripheral.
There are some correlations of VBG to ABGs but not ideal.
Central venous O2 sat value and what does it reflect
indicator of the balance between delivery and O2 consumption
normal is 70-75%, considering an arterial Sat 100%
If sat is lower consider 30% less and that is the SVO2
Why does lactate is high in critically ill patients?
metabolic acidosis –> increase lactate
associated with tissue hypoxia and resultant anaerobic metabolism.
good prognostic indicator, and can be used to measure therapy response.
if no metabolic acidosis, some example of elevtion is stress hyperglycemia
Things to consider when measuring lactate
can be falsely elevated if not taken from a free flowing blood sample
Delayed testing of sample can affect accuracy
What is near infrared spectroscopy and how does it work?
non invasive optical technique to monitor tissue oxygenation in brain and other tissues
measures the concentration of oxyHb and desaturated Hb.
small heart in Xray causes
reduced cardiac preload, severe lung hyperinflation
large heart in Xray causes
normal or increased preload
pericardial effusion
CHF
or patient is unstable to take a deep breath
Heart size is different in the anteroposterior view compared to the posterior-anterior
Anteroposterior will look larger
Which are the most common scenarios of cardiac arrest in infants/children?
Usually result from progressive respiratory failure, shock or both. –HYPOXIC-ISCHEMIC ARREST
Less commonly result from an arrhythmia or ventricular tachycardia 5-15%
Respiratory failure without respiratory distress cant occur T/F
False
Respiratory failure without respiratory distress can occur
ASSOCIATED WITH DECREASED LEVEL OF CONSCIOUSNESS
The incidence of cardiac arrest from Vf/pVT increases with age and should be suspected in any patient with SUDDEN collapse T/F
TRUE
What is the rate of survival at hospital discharge if cardiac arrest occurs inhospital?
43%
What is the rate of survival at hospital discharge if cardiac arrest occurs out-of-hospital?
8%
Survival is higher if shockable rhythm vs. asystole
true
25-34% compared to 7-24%
What is cardiac arrest?
cessation of blood circulation resulting from absent or ineffective cardiac mechanical activity
no pulse, no breathing( cerebral hypoxia-> loss of consciousness-> stop breathing)
2 pathways for cardiac arrest in children
- Hypoxic ischemic- when there is respiratory failure or hypotensive shock there is progressive tissue hypoxia and acidosis
- Sudden cardiac arrest
Causes of sudden cardiac arrest, and predispositions
Vfib and pulseless Vtach
Predisposing conditions are:
- HCM
- anomalous coronary artery
- Long QT syndrome or other channelopathies
- Myocarditis
- Drug intox ( digoxin, ephedra, cocaine)
- Commotio cordis
Commotio cordis (Latin, “agitation of the heart”)
is an often lethal disruption of heart rhythm that occurs as a result of a blow ( chest impact) to the area directly over the heart (the precordial region), at a critical time during the cycle of a heart beat causing cardiac arrest.
Causes of cardiac arrest
< 6 months: SIDS
> 6 months: traumatic cardiac arrest- airway compromise, tension pneumothorax, brain injury
Reversible causes of cardiac arrests
6 Hs and 5 Ts
Hypoxia Hypothermia Hypovolemia Hypoglycemia H+ ( acidosis) hypo/HyperK
Toxins Thrombosis pulmonary Thrombosis coronary Tamponade Tension pneumothorax
Arrest rhythms
PEA
Asystole
pulseless Ventriculat Tachycardia, including torsaides de pointes
Vfib
Which are the most common arrest rhythms based on age
in younger than 12 is PEA, asystole
In older is Vfib, pVT and is associated to sudden cardiac arrest and/or predisposing conditions.
What is an agonal rhythm
Slow wide QRS complex that immediately precedes asystole
What is PEA
There is some sort of activity ( organized cardiac activity) in the ECG but there is no pulse.
pulsations may be detected by an arterial waveform or doppler, but no PULSE.
EKG may show different things:
- low or high amplitude T waves
- prolonged PR and QT intervals
- AV dissociation , complete heart block, ventricular complexes without p wave
Are there pulses in Vfib?
NO! Its a pattern of cardiac arrest.
Vfib- no organized rhythm and no coordinated contractions
electrical activity is chaotic
the heart is not able to pump blood– pulses are not palpable
Vfib may be preceded by a brief period of VT with or without pulses. T/F
True
Difference between Vfib and pulseless VTaq
Vfib- disorganized rhythm
pVT: organized, wide QRS complexes
Torsades de Pointes
polymorphic VT
seen in conditions with prolonged QT interval, including congential long QT syndrome, drug toxicity, hypomagnesemia
Causes of torsades des pointes
HypoMg, HypoK
Anti ABCDE+ opioids( methadone, oxycodone)+ HIV protease inhibitors
Arrhythmics ( IA,III)
Biotics (Macrolides, antimalarials, fluoroquinolones)
Cychotics ( haloperidol, risperidone)
Depressants ( SSRIs, TCAs)
Emetics ( ondansetron)
Congenital
Romano Ward- puRe heart
Jervell and Lange-Nielsen syndrome: cardiac + sensorineural deafness
Antiarrhythmics type I and subtypes
Na+ channel blockers ( slow or block conduction)
IA: The Queen Proclaims Disos pyramide ( Quinidine, Procainamide, Disopyramide)
IB: Lidia es Mexican, fea y toca en un restaurante ( Lidocaine, Mexiletine, phenytoin, tocamide
IC: Propon tener fleco
Propafenone, flecainamide
Antiarrhythmics type II
B blockers -lol
Prolong PR
Decrease SA and AV node activity
Antiarrhythmics type III
K channel blockers:
AIDS Amiodarone Ibutilide Dofetilide Sotalol
Prolong QT
Antiarrhythmics type IV
Ca channel blockers
Verapamil, diltiazem
Prolong PR
Although hands only CPR is an option, the ideal in hypoxic asphyxial arrest is CPR ( hands and ventilation)!!!!
True
Hands ony can be done if the rescuer has no expertise or doesnt want to give breath. Better this than nothing.
What is the difference of the Activation of emergency response system step between infants/children and adolescents/adults?
In infants and children:
If witnessed and no phone, leave the victim and get AED before CPR
If unwitnessed and single rescuer: give 2 min CPR, then go for AED and activation of emergency system, return to kid give CPR and use AED
In adolescents and adults:
If single rescuer: Activate emergency system and look for AED before starting compressions.
Otherwise send someone for AED and begin CPR.
How are the rate of compressions without advanced airway different between adolescents/adults and infants/children ?
adolescents/adults: if 1 or more rescuers 30:2
children/infants: 2 rescuers 15:2
1 rescuer 30:2
How are the rate of compressions with advanced airway different between adolescents/adults and infants/children ?
SAME
continuous compressions at a rate of 100-120/min
Give 1 breath every 10 seconds.
Hand placement for CPR in adults/adolescents, children ( 1 year-puberty), infants
adults/adolescents: 2 hands on the lower half of the breastbone
children ( 1 year-puberty): 2 hands or 1 hand ( rescuer can use either method on a small child) on the lower half of the breastbone ( sternum)
infants: 1 rescuer: 2 fingers in the center of the chest just below the nipple line
2 rescuers: 2 thumb encircling hand in the center of the chest just below the nipple line.
Breaths in CPR
Each rescue breath should be given over about 1 second
Each breast should result in visible chest rise
After an advanced airway is in place: 10 breaths per min ( 1 breath every 6 seconds).
After an advanced airway is in place how are the breaths in CPR
After an advanced airway is in place: 10 breaths per min ( 1 breath every 6 seconds).
What is PETCO2? Why is it useful?
measures ventilation
End tidal CO2 - seen in capnography
a measure of the amount of carbon dioxide present in the exhaled air.
Indirect evidence of que quality of the compressions.
Normal value is same as PaCO2: 35-45
What does a PETCO2 > 10-15mmHg mean?
CO during CPR is low and not much blood is being delivered to the lungs
Capnography
is the monitoring of the concentration or partial pressure of carbon dioxide (CO. 2) in the respiratory gases.
presented as a graph of expiratory CO
priority for drug delivery routes?
IV>IO>ET
Why is not very common to put a central venous access in cardiac arrest?
Although is the best option because of faster onset of meds and higher peak concentration of meds
Its placement requires interrumption of chest compressions
Complications: hematoma, vascular lacerations, pneumothorax, bleeding.
What is required when giving IV meds peripherally?
- Give them in boluses
- Give the drug while chest compressions are beign performed
- Follow with a 5 mL flush of normal saline to mode the drug from the peripheral to the central circulation.
IO access, why is a good option if the peripheral access doesnt work?
- BM provide access to a noncollapsible marrow venous plexus- so useful in profound shock, dehydration
- Followed by flush medications may reach central circulation
Contraindications and relative contraindications for IO access?
There are no absolute
Relative:
- trauma to the extremity- we dont know if there is damage of BM
-Overlying infection( cellulitis)
If an IO access stop working, change of bone. Its likely that if you try in same bone whatever you are inserting will leak through previous bone.
Osteogenesis imperfecta or congenital bone diseases are CI for IO access. T/F
False.
Equipment for IO access
Towel roll Gloves Antiseptic wipes IO needle/drill syringe/blood specimen containers for lab work connector tube saline flush
Location of IO access
In children: the proximal tibial site is approximately 2 cm below the tibial tuberosity and up to 1 cm medially on the tibial plateau
In skeletally mature adolescents and adults, the recommended site is 2 cm medial to and 1 cm above the tibial tuberosity.
Procedure of IO access
- Gloves
- place towel roll below the knee or straight knee
- Antiseptic wipes
- Lidocaine at the site and inside the periostium if conscious
- Insert the IO needle ( has a trocar/stylet to avoid the core bone to get inside the hollow needle)
- Aspirate
- Flush saline and see signs of infiltration anteriorly and posteriorly
- med
- flush with saline after med.
When does a IO access needs to be replaced
max 24 hrs
Alternative locations of the IO access?
distal femur ( needs a larger needle)
distal tibia, above medial maleolus
proximal humerus
always in the flat , tuberosities have growth plates.
Needles for the IO drill
3-39 kg: 15 gauge and 15 mm lenght
>40kg: 15 gauge and 25 mm lenght
obese: extralong
Drugs that can be given ET?
Lipid soluble drugs
LEAN and vasopressin Lidocaine Epinephrine Atropine Naloxone
What considerations exist when giving drugs by ET in cardiac arrest?
- Drug absorption in the endotracheal tree is unpredictable - drug dose/effects unpredictable
- optimal dose of most of the meds given by ET is unknown.
- Recommended drug doses by ET are higher than for IV/IO
- For epinephrine is 10x the dose given by IV/IO
- For other drugs ~2-3x
Technique for administering drugs via ET
- Instill the drug into the ET tube ( briefly pause compressions during instillation)
- Follow with a minimum of 5 mL normal saline flush, smaller volume may be needed for neonates
- Provide 5 rapid positive pressure breaths after drug is instilled
depolarizing myocytes with AED and return to organized cardiac activity doesn’t ensure survival T/F
True, the organized cardiac rhythm must produce ROSC (defined as palpable pulse) – can be assessed with PETCO2 or intra arterial pressure.
What do you do after AED shock?
resume compressions
Goal of meds during cardiac arrest
Increase coronary and cerebral perfusion and blood flow
Stimulate spontaneous and forceful myocardial contraction
Accelerate heart rate
Correct and treat the possible cause of cardiac arrest
Suppress or treat arrhythmias
Indication of epinephrine
cardiac arrest
high doses may be given for resuscitation in cases of B blocker overdose
MOA epinephrine
alpha adrenergic mediated vasoconstriction –> increased aortic diastolic pressure and coronary perfusion
Amiodarone indication
shock refractory Vfib or pVT
MOA amiodarone
alpha adrenergic and b adrenergic blocking activity
blocks K channel
prolongs AV refractory period and QT interval
slows ventricular conduction ( Widens the QRS)
Lidocaine indication
shock refractory Vfib or pVT
MOA Lidocaine
Class IB antiarrhythmic
Decreases automaticity and suppresses ventricular arrhythmias
Atropine indication
tto of bradycardia, especially if due to excessive vagal tone, organophosphates, complete AV block
MOA atropine
Increases HR
Calcium indication
not rutinely for cardiac arrest
indicated in :
- ionized hypoCa ( can be present during sepsis or after cardiopulmonary bypass)
- hyperkalemia, if hemodynamic compromise
- Ca channel blocker overdose
- hyperMg
MOA Calcium
Restores Ca
Helps maintain the cell membrane action potential treshold
helps maintain gradient between intracel K and extracellular Na.
Sodium bicarbonate indication
Not recommended in cardiac arrest
Recommended in:
hyperK
TCA overdose
Overdose with Na blocking channels
MOA Sodium bicarbonate
helpful in TCA overdose
Rapidly reduces K concentrations.
Why you have to avoid excessive ventilation during resucitation?
- impedes venous return and decreases CO
- increases intrathoracic pressure–RA pressure and decreases coronary perfussion
- causes gastric distention- impeding ventilation and increases the risk of regurgitation
How do you confirm and monitor ET tube placement?
capnography and clinical exam
What if capnography doesnt show CO2 but clinical examination shows adequate position of the ET tube?
use direct laryngoscopy
In the OHCA there was no difference in survival between ET tube and effective bag-mask ventilation.
True,
but this didnt address in-hospital, but suggest that immediate intubation may not be necessary.
shockable rhythms
Vfib/pVT
Non shockable rhythms
PEA/Asystole
Cardiac arrest algorithm for both shockable and non shockable rhythms
say it
Shock energy for defibrillator
First shock 2 J/kg
Second shock 4 J/kg
Subsequent shocks >= 4 J/kg, maximum of 10J/kg
Dose and freq of epinephrine IO/IV
0.01 mg/kg repeat every 3-5 min
ET: 0.1 mg/kg
Dose and freq of amiodarone IO/IV
5mg/kg bolus during cardiac arrrest max single dose of 300 mg. May repeat up to 2 times for refractory VF/pulseless VT
max 2.2g per 24 hrs.
Dose and freq of lidocaine IO/IV
initial: 1 mg/kg loading dose
Maintenance 20-50 mcg/kg/min ( repeat bolus dose if infusion initiated > 15 minutes after initial bolus)
Criteria for ROSC
Presence of pulse and BP
Spontaneous arterial pressure waves and intra-arterial monitoring
What is the size for uncuffed ET for children 2-10yr ?
(age in years/4)+4
What is the size for uncuffed ET for children 2-10yr?
(age in years/4)+3.5
What should be the cuffed inflation pressure in the ET?
<20-25 cmH20
Monophasic vs biphasic AED
monophasic - current delivered in one direction
biphasic- current delivered in both directions
monophasic:
has higher energeny use, higher risk of trauma, burns, myocytes damange
first success rate 60%
biphasic: less of all of the above, first success rate 90%.
what do you need to consider when using paddles for AED shock delivery?
put conducting gel! to decrease impedance
dont put saline soaked gauze pads, alcohol pads.
Paddle size for > 10 kg ( 1 year or older)
large adult paddles ( 8-13 cm)
Paddle size for <10 kg (< 1 year )
small infant paddle (4.5 cm)
Location of pad/paddle for DEA
1 electrode on the upper right side of chest below the right clavicle
the other to the left of the left nipple in the anterior axillary line directly over the heart.
they shouldnt touch! allow 3 cm between them
What do you do before delivering a shock?
Revise that no one is near the child,
high flow 02 is not directed to the chest
Shout a warning message. “clear for shock, deliverying at the count of 3)
Timing of epinephrine
There is no current recommendation for the adequate timing of epinephrine.
In a monitored setting it is reasonable to check the rhythm first before the second shock, to avoid unnecessary dose of epi.
When should the IV/IO meds be administered in CPR?
During chest compressions because blood flow generated by compressions help circulate the drugs. immediately before or after the shock.
Why epinephrine via ET is usually given like 10x the IV/IO dose?
low doses of epi ( because of not adequate absorption via ET) may cause B adrenergic effects –> hypotension, lower coronary artery perfusion pressure and flow
reduce the potential for ROSC
CPR with advanced airway
1st rescuer: continuous CPR
the other team member: 1 breath every 6 seconds ( ~10 breaths per min)
rotate every 2 min
Mg dose if torsades de pointes
25-50 mg/kg bolus IV/IO
max 2 g
Prepare each drug prior to rhythm check, so that can be given with CPR after shock
T
Management of traumatic cardiac arrest
CPR plus:
- control visible hemorrhage
- Suction airway
- Try not to movilize cervical spine, so airway with jaw thrust manuever
- Ventilate with bag mask device using 100%
- If advanced airway inserted stabilize head
- if tension pneumothorax- needle decompressions - thoracotomy
- FLUIDS- so peripheral access and fluids.
- vasopressor if spinal shock( loss of sympathetic innervation)
- NO PLACE OF IO IN A BONE WITH CONCERN OF FX.
Management of cardiac arrest due to drowning
CPR +ADE plus:
bag mask, suction airway
Evaluate core body temperature ( rewarming if < 30)– the heart may be unresponsive to resucitative efforts until this core temperature is achieved.
- Extracorporeal circulation is the most rapid and effective technique for rewarming severly hypothermic cardiac arrest after submersion in icy water.
When do you suspect spinal shock? What do you give?
-combination of areflexia/hyporeflexia and autonomic dysfunction that accompanies spinal cord injury.
loss of sympathetic outflow, resulting in refractory hypotension and bradycardia.
The initial hyporeflexia presents as a loss of both cutaneous and deep tendon reflexes below the level of injury
Give VASOPRESSOR
What is the most rapid and effective technique for rewarming severly hypothermic cardiac arrest after submersion in icy water.
Extracorporeal circulation.
What happens in anaphylaxis
airway edema and obstruction
profound vasodilation –> relative hypovol
bronchoconstriction –compromises oxygenation and O2 delivery
4 things that are needed in cardiac arrest due to anaphylaxis
CPR Establishment of adequate airway bolus fluid administration - Epinephrine every 3-5 min during cardiac arrest provide epi infusion as needed
Post-cardiac arrest period – give methylprednisolone 1-2 mg/kg IV/IO
What should you consider in ET intubation in anaphylaxis?
it is possible that due to airway edema you need to use a smaller ET tube than predicted by the child’s age or lenght.
What medication should be given in the post-cardiac arrest care after anaphylaxis?
steroids, methylprednisolone 1-2 mg/kg IV/IO
Cardiac arrest + hypoglycemic, what do you suspect?
B-blocker or alcohol overdose
normalize glucose
What are single ventricule defects? Which are these?
A heart that has only one ventricle large and strong enough to pump blood
- hypoplastic left heart syndrome
- pulmonary atresia
- tricuspid atresia
In which patients with single ventricle defect is indicated standard resucitation?
- single ventricular anatomy after stage I palliation ( Norwood)
- univentricular heart and aortopulmonary shunt.
Norwood Procedure
Treatment for hypoplastic left heart syndrome
three-step surgical procedure called staged palliation to create a new functional systemic circuit
Stage 1 of the Norwood procedure involves atrial septectomy and transection and ligation of the distal main pulmonary artery.
Stage 1
shortly after birth
It converts the right ventricle into the main ventricle pumping blood to both the lungs and the body. The main pulmonary artery and the aorta are connected and the main pulmonary artery is cut off from the two branching pulmonary arteries that direct blood to each side of the lungs.
Shunt between pulmonary arteries and the aorta to supply blood to the lungs.
Stage 2 (Bi-directional Glenn Operation) six months after the Norwood to divert half of the blood to the lungs when circulation through the lungs no longer needs as much pressure from the ventricle. The shunt to the pulmonary arteries is disconnected and the right pulmonary artery is connected directly to the superior vena cava, the vein that brings deoxygenated blood from the upper part of the body to the heart. This sends half of the deoxygenated blood directly to the lungs without going through the ventricle.
Stage 3 (Fontan Operation) This is the third stage, usually performed about 18 to 36 months after the Glenn. It connects the inferior vena cava, the blood vessel that drains deoxygenated blood from the lower part of the body into the heart, to the pulmonary artery by creating a channel through or just outside the heart to direct blood to the pulmonary artery. At this stage, all deoxygenated blood flows passively through the lungs.
Considerations for resucitation in single ventricular defects
standard CPR if indicated
Heparin in kids with aortopulmonary or right ventricular pulmonary shunt if the shunt patency is a concern.
PETCO2 may be not a reliable
ERCP may be considered.
Resuscitation in pulmonary HTN
- Correct hypercapnia/acidosis
- isotonic crystalloid to maintain preload
- if patient was receiving pulmonary vasodilator ( eg, NO, prostacyclin) continue giving
- Consider inhaled Nitric oxide or prostacyclin to reduce pulmonary resistance
- Consider ECPR
What is Respiratory distress
condition of abnormal respiratory rate or effort
What is the O2 consumption in infants vs. adults
infants 6-8mL/kg
adults: 3-4 mL/kg
Define hypoxemia?
Permissive hypoxemia?
decreased arterial oxygen SATURATION detected by pulse oximeter or direct measurement in ABG
Permissive hypoxemia is a pulseoximetry < 94% which may be appropriate in certain conditions ( eg, congenital heart disease)
Difference between hypoxemia and tissue hypoxia
hypoxemia: low arterial 02 saturation (Sat<94%)
hypoxia: body as a whole (generalized hypoxia) or a region of the body ( tissue hypoxia) is deprived of an adequate oxygen supply.
hypoxemia does not necessarily lead to tissue hypoxia T/F
True
tissue hypoxia may occur when arterial O2 sat is normal T/F
True , in chronic diseases like in cyanotic heart disease where compensatory mechanisms help maintain arterial O2 content near normal.
In tissue hypoxia, what is the responding mechanism
hyperventilation pCO2< 35. ( dont let it be < 30)
tachycardia
can be due to increased respiratory rate, increased tidal volume
What are the early and late signs of tissue hypoxia?
Early: Tachypnea Increased respiratory effort Tachycardia Pallor, mottling, Agitation, anxiety, irritable
Late:
bradypnea, inadequate respiratory effort, apnea
increased respiratory effort/: head bobbing, seesaw respirations, grunting.
Bradycardia
mottling/pallor,cyanosis
decreased level of consciousness
Arterial O2 content formula
[1.36 x Hb concentration x SaO2] + (0.003x PaO2)
Dissolved O2- (0.003 x PaO2)
Mechanism of hypoxia in alveolar hypoventilation
increased tension of CO2 displaces alveolar O2–> so if alveolar O2 is low–> arterial O2 is low–> PaO2 low.
Causes of alveolar hypoventilation
CNS lesion
TBI
NM disease
drug overdose/sedation/apnea
Mechanism of hypoxia in diffusion defect
no exchange between CO2 and O2.
examples: pulmonary edema, alveolar proteinosis, interstitial pneumonia
Mechanism of hypoxia in V/Q mismatch
blood flow through areas of the lung that are inadequately oxygenated -> incomplete oxygenation of the blood returning to the right heart.
There is decreased arterial O2 and Saturation , and to a lesser extent increased PaCO2.
causes of V/Q mismatch
pneumonia atelectasis ARDS Asthma Bronchiolitis Foreign Body
Mechanism of hypoxia in R to left shunt
shunting of unoxygenated blood from the R side of the heart to the left ( or from the pulmonary artery into the aorta)– results in low PaO2
Causes of R to left shunt causing hypoxia
Cyanotic congenital diseases
Extracardiac vascular shunt
PLUS SAME CAUSES OF V/Q MISMATCH
pneumonia atelectasis ARDS Asthma Bronchiolitis Foreign Body
Define Hypercabia and what does it mean
increased CO2 tension in the arterial blood ( PaCO2)
Means that ventilation is inadequate.
Causes of hypercabia
airway obstruction ( lower or upper)
Lung tissue disease
Decreased or inadequate respiratory effort ( central hypoventilation)
Best way to measure hypercapnia
ABG
Capnography showing the end tidal CO2 may be not identical to arterial CO2.
What clinical sign makes you think of hypercabia?
decreased level of consciousness
The Sat O2 can be normal in some cases with hypercabia T/F
True
What are the factors associated with increased work of breathing?
Increased airway resistance
Decreased lung compliance
Use of accessory muscles
Disorder in CNS control of breathing
Formula for resistance and meaning when airflow is laminar vs. turbulent
Normal breathing-> laminar flow ( organized,quiet)
Resistance is 1/r^4 ( means that small changes in diameter will increase significantly resistance and work of breathing.
Agitation, crying–> turbulent flow
Resistance is 1/r^5( meaning that in addition to small size this flow will increase the resistance .
So maintain patient calmed to decrease resistance.
Definition of compliance
change in lung volume produced by a change in driving pressure across the lung
Name the inspiratory muscles of respiration
diaphgram intercostal muscles accessory muscles( abdomen, neck)
How does Inspiration occurs:
inspiratory muscles ( mainly diaphgram) increases intrathoracic volume–> decreases pressure
When intrathoracic pressure is less than the atmopsheric. air flows into the lungs.
How does expiration occurs:
relaxation of inspiratory muscles and elastic recoil of the lung and the chest wall.
These changes increase intrathoracic pressure more than atmospheric leading to expiration.
How is diaphgram contraction different if dome shape and flattened?
dome shaped- more forceful
flattened ( ie. lung hyperinflation in asthma)-contraction is less forceful and ventilation is less efficient.
How is the control of breathing through central and peripheral chemoreceptors
centrally- respond to changes in H+ in CSF, PaCO2
peripherally (eg carotid body)- respong to decrease in PaO2 ; and some respond to increased PaCO2
Mechanisms involved in breathing control
Brainstem respiratory centers
Central and peripheral chemoreceptors
Voluntary control (cerebral cortex)
Mild vs. severe respiratory distress
Mild:
Tachypnea
Mild increase in respiratory effort ( eg.nasal flaring,retractions)
Abnormal airway sounds( strictor, wheezing, grunting)
Mottling
Severe or possible respiratory failure: Marked tachypnea, apnea hypoventilation or bradypnea abnormal airway sounds pale, cool skin, cyanosis DECREASED LEVEL OF CONSCIOUSNESS.
Respiratory failure
state of inadequate oxygenation, ventilation or both. abnormal appearance ( altered consciousness), poor color, and reduced responsiveness.
Where do you auscultate during respiratory physical exam?
Anterior ( on either side of the breastbone)
Posterior
Lateral ( under the axilla)
Which are the types of respiratory distress/failure?
Upper airway obstruction
Lower airway obstruction
Lung tissue disease
Disordered control of breathing
Causes of upper airway obstruction
foreign body
infection
swelling of airway ( anaphylaxis, tonsillar hyperthrophy, croup, epiglottitis)
mass ( pharyngeal or peritonsilar abscess)
thick secretions
congenital abnormalities ( congenital subglotic stenosis)
decreased level of consciousness- muscles relax, tongue falls back and obstruct the oropharynx
Common causes of lower airway obstruction
Asthma
Bronchiolitis
Presentation of upper airway obstruction
respiratory distress drooling, snoring, gargling sounds stridor poor air entry at auscultation poor chest rise
Presentation of low airway obstruction
increased RR, respiratory effort possible decreased air movement on auscultation Prolonged expiratory phase wheezing cough
Explain the mechanism of air trapping and lung hyperinflation
there is an increase in intrapleural pressure because of the forced expiration.
increased intrapleural pressure compresses airways proximal to the alveoli
So further expiratory obstruction.
- children tend to breath slower to increase tidal volume
- is different from infants ! (pg 125)
Why does grunting occurs?
grunting produces early glottic closure during expiration– compensatory mechanism to maintain positive airway pressure and prevent collapse of the alveoli and small airways.
In lung disease hypoxia occurs first than hypercapnia T/F
True, in lung tissue disease the kids have better ventilation than oxygenation.
Causes of disordered control of breathing
neurologic ( seizures, CNS infections, head injury, tumor)
metabolic abnormalities
drug overdose
Breath sounds in upper airway obstruction
stridor(typically inspiratory)
barking cough
hoarseness
Breath sounds in lower airway obstruction
wheezing (typically expiratory)
prolonged expiratory phase
Breath sounds in lung tissue disease
Grunting
Crackles
Decreased breath sounds.
Rescue breathing in respiratory arrest
- Give 12 to 20 breaths per min ( 1 breath every 3-5 seconds)
- Give each breath in one second
- Visible chest rise
- check pulse every 2 minutes, if pulseless CPR
- Use o2 as soon as possible
How to do you know the size of the oropharyngeal airway in children?
it should extend from the corner of the patients lips to the tragus or the angle of the jaw
How do you place an oropharnygeal airway?
use a tongue depressor and put the oropharyngeal airway in horizontal and then put it into place
check for adequate air exchange, place bag mask and see inflation
How to do you know the size of the nasoopharyngeal airway in children?
it should extend from the nare to the tragus or the angle of the jaw
How do you place a nasopharyngeal airway?
add lubricant and insert it into the patients nose
insert all the way into the disc
Mac vs Miller blade for intubation
Mac is curved
Miller is straight
When is Miller (straight) blade preferred over the Mac?
In children younger than 2 years
they have a floppy omega shaped epiglottis
with the miller you can put the blade on top of the epiglottis and facilitate view of vocal cords
In which situations is preferred cuffed and uncuffed ET tubes?
uncuffed:
- young children
cuffed ET:
- higher pressures
- mechanical ventilation for prolonged time
- aspiration concern
What do you do if a patient is with respiratory distress or failure? (heart ok)
Airway
- check patency- let children positioning or implement manuevers: head tilt chin lift, jaw thrust
- airway suctioning if indicated
- consider an oropharyngeal airway or nasopharyngeal to improve airway patency or openness ( usually in decreased consciousness, or patients with gag reflex loss)
Breathing
- monitor SaO2
- Provide O2. use a high concentration delivery device such as non rebreathing mask
- Administer inhaled medication( albuterol or epinephrine) if needed - reduce airway swelling
- Assist ventilation with bag mask device
- prepare for advanced airway
Circulation
-Check heart rate, rhythm, blood pressure
In which conditions of respiratory distress you have to be careful with suctioning?
in cases of upper airway edema from infection- this may lead to agitation in children and further respiratory distress.
CROUP what is it? organism?
layngotracheitis
common in winter,infectious
characterized by inspiratory stridor, barking cough, and hoarseness
Parainfluenza type 1 (MC)
VERY less common:
RSV
Mycoplasma pneumoniae
Classification of croup
Mild- occasional barking cough, little or no stridor at rest, absent or mild retractions.
Moderate- frequent barking cough, easily audible stridor at rest, retractions at rest, little or not agitation, good air entry by auscultation of the peripheral lung fields
Severe- frequent barking cough, prominent inspiratory and occasional expiratory stridor, marked retractions, significant agitation, decreased air entry by auscultation of the lungs
impending respiratory failure:
all of severe plus lethargy/decreased level of consciousness and pallor/cyanosis despite supplementary O2
Treatment of croup per severity degree
mild
dexamethasone
Moderate to severe:
- NPO
- Dexamethasone, humidified O2, NEBULIZED EPINEPHRINE
- Observe for at least 2 hours after giving nebulized epinephrine to ensure no recurrence of stridor
- consider heliox ( helium -oxygen mixture) for severe disease if the child requires no higher than 40% inspired O2 concentration
Impending respiratory failure
- high [O2]- non rebreathing mask
- assisted ventilation( bag masked ventilation timed to support child’s own inspiration) for peristent , severe hypoxemia despite O2 vent.
- Dexamethasone IV/IM
- Endotracheal intubation ( smaller ET tube than expected to reduce injury to subglottic area)
- prepare for surgical airway if needed
What ET tube size do you use in respiratory failure due to croup?
smaller ET tube than expected to reduce injury to subglottic area
Anaphylaxis measures if mild and moderate/severe
Mild
- remove offensive agent
- ask caregiver or patient about history of allergies, look bracelent
- consider antihistamine dose
Moderate/severe
-IM epinephrine each 15-20 minutes; repeated doses may be needed.
- Methylprednisolone or equivalent steroid IV
- If bronchospasm - give albuterol by meter dose inhaler or nebulized sln
- If severe bronchospasm, give nebulized solution
-Anticipate use of ET
- Anaphylaxis–>hypotension
Administer NSS or LR 20 ml/KG bolus ( repeat as needed)
- For hypotension unresponsive to fluids and iM epinephrine, administer an epinephrine infusion titrated to achieve adequate BP for age
What do you do in anaphylaxis if patient has refractory hypotension?- not responding to fluids/epinephrine boluses?
epinephrine infusion titrated to achieve adequate BP for age
Foreign body airway obstruction management in infants
If mild, do not intervene. Call for help and allow the infant to spill it out coughing
If severe:
- confirm airway obstruction
- Give up to 5 back slaps and up to 5 chest thrusts ( 2 fingers)
- repeat step 2 until objects comes out or kid unresponsive
If unresponsive activate emergency response system, CPR, and with each breath delivery check airway to see if object is there. NO blind FINGER
Foreign body airway obstruction management in >1 yr to puberty
If mild, do not intervene. Call for help and allow the infant to spill it out coughing
If severe:
- confirm airway obstruction , ask are you choking?
- Stand or kneel– Heimlich manuever
- repeat step 2 until objects comes out or kid unresponsive
If unresponsive activate emergency response system, CPR, and with each breath delivery check airway to see if object is there. NO blind FINGER
Complications of hyperventilation
-providing too many breaths or breaths with too much volume.
Complications:
- Gastric distention–>high risk of vomit/aspiration, can prevent adequate mov of diaphgram affecting ventilation
- pneumothorax: decreased blood return to heart, risk of lung collapse and complications ( hypoxemia, obstructive shock)
-severe air trapping - decrease oxygenation, decreased venous return to heart and CO.
What is bronchiolitis?
lower airway obstruction secondary to airway edema, mucous and cellular debris. Impaired gas exchange can occur as a result of airway obstruction and ventilation- perfusion inequalities.
< 2 years
current or antecedent upper respiratory tract infection symptoms
late fall or winter months.
What causes bronchiolitis?
MC- RSV
other viruses:
adenovirus, influenza, human metapneumovirus, and parainfluenza,
Bronchiolitis Dx?
Clinical:
< 2 years
current or antecedent upper respiratory tract infection symptoms
late fall or winter months.
respiratory distress, such as tachypnea, intercostal retractions, and wheezing, are not necessarily correlated with the level of hypoxemia.
Labs:
Often not done, but PCR is the most accurate
Chest X ray
ABGs
Treatment of bronchiolitis
Suctioning and supplemental oxygen
- if they persist with ss, trial with bronchodilators- if work they continue.
- Pts with bronchiolitis dont respond to steroids so dont give them!
Why pulsus paradoxus in severe asthma
airways start to tighten and swell. The lungs start to overinflate in response, which puts extra pressure on the veins carrying unoxygenated blood from the heart to the lungs.
As a result, blood backs up in the right ventricle which presses against the left side of the heart.
Management of acute asthma
- humidified O2 in high concentration via nasal cannula or O2 mask; titrate with pulseox > 94%
- Albuterol by meter-dose inhaler or nebulizer solution
- Oral corticosteroids
Management of moderate/severe asthma
- humidified O2 in high concentration to maintain SaO2 > 95%;use non-breathing mask if needed. If unsuccessful- noninvasive positive pressure ventilation or ET intubation
- Albuterol by meter-dose inhaler or nebulizer solution. If wheezing or aeration not alleviated– continuous albuterol
- Corticosteroids PO/IB
PLUS
- Ipratropium by nebulizer solution
- Magnesium sulfate by slow (15-30 min)IV bolus infusion , monitoring heart rate and BP
- Perform ABGs, Chest Xray
Peak expiratory flow in mild, moderate and severe asthma
mild: > 80%
moderate 60-80%
severe <60%
Why giving magnesium in asthma?
produces smooth muscle relaxation
thought to act by enhancing calcium uptake in the sarcoplasmic reticulum(3) and/or as a calcium antagonist
Management of impending respiratory failure in asthma?
- O2 via nonrebreathing mask
- Albuterol via continuous nebulizer
- Corticosteroid
- Terbutaline SC or IV infusion titrate but monitor for toxicity - b adrenergic so risk of seizures, angina, hypertension or hypotension, tachycardia with rates up to 200 beats per minute, arrhythmias, nervousness, headache,
- bilevel positive airway pressure
- Endotracheal intubation
Examples of lung tissue disease
Infectious pneumonia Chemical pneumonitis Aspiration pneumonitis Cardiogenic pulmonary edema Noncardiogenic pulmonary edema( ARDS)
What is chemical pneumonitis,
inflammation of the lung tissue caused by inhalation or aspiration of toxic liquids, gases or particulate matter such as dust or fumes.
-can lead to pulmonary edema and increased capillary permeabilty
Management of chemical pneumonitis
Albuterol
CPAP or noninvasive ventilation, potentially ET intubation
Management of aspiration pneumonia
Consider CPAP or noninvasive ventilation, potentially ET intubation
Abcs if fever + infiltrate on chest x ray
prophylaxis with Ab is indicated in aspiration pneumonia T/F
FALSE
Abcs only if fever + infiltrate on chest x ray
What is the most common cause of acute cardiogenic pulmonary edema in children?
Left ventricular myocardial dysfunction
can be congenital heart disease, myocarditis, cardiomyopathy, inflammatory processes..
Interventions besides airway, breathing and circulation for cardiogenic pulmonary edema
Ventilatory support ( noninvasive or mechanical ventilation with PEEP)
Diuretics
Normalize temperature.
Indications for ventilatory support ( noninvasive vent or ET intubation) in cardiogenic pulmonary edema
- Persistent hypoxemia despite oxygen administration and noninvasive ventilation
- Impending respiratory failure
- Hemodynamic compromise ( hypotension, severe tachycardia)
ARDS criteria
Acute onset ( within 7 days of insult) PaO2/FiO2 300 or less Oxygenation Index >=4 New infiltrate on chest xray No evidence for a cardiogenic or fluid overload cause of pulmonary edema
Oxygenation Index([FIO2 x mean airway pressure x100]/PaO2)
Oxygenation Index FORMULA
([FIO2 x mean airway pressure x100]/PaO2)
Medications to avoid in NM disease
syccynilcholine for intubation–> hyperK, malignant hyperthermia
amino glycosides: intrinsic neuromuscular activity that worsen respiratory muscle weakness.
self-inflating bags vs. free flow bag
constant concentration of oxygen
refill even if the seal is poor or ventilation is inadequate
resucitation scenario
not as experienced personnel
if o2 source is empty is not connected,
snesthesia, ICU care team
depends on adequate sealing, and rate of squeezing to deliver adequate vol.
Bag size
at least 450-500 mL or larger in infants and young child
in older children or adolescents 1000mL or larger
The bag mask ventilation is for scenario were there are two rescuers, if one it should be mouth to barrier device technique T/F
True
In case there are 2 , there can also be two ventilating the patient. one rescuer does the E-C clamp technique with both hands while the other delivers O2.
Situations in which 2 person bag mask ventilation may be necessary
- Difficulty making a seal
- providers hands are too small
- Significant airway resistance or poor lung compliance
- Spinal motion restriction is necesary
Once you are giving oxygen through bag mask, how do you check is correct?
- chest rise with each breath
- O2 saturation
- Exhaled CO2
- HR
- BP
- Distal air entry
- Signs of improvement of deterioration
What do you think of when there is sudden increase in lung stiffness during ventilation with bag mask?
May indicate:
airway obstruction
decreased lung compliance
development of a pneumothorax
also- if there is excessive ventilation which leads to lung distention
Types of suction devices
Portable suction devices (not very adequate force -80 to -120mmHg)
Bulb or syringe suction device ( no requirement of outside vacuum, but inadequate in large patients or copious secretions)
Wall mounted suction (higher suction force more than -300mmHg)
Complications of suctioning
hypoxia vagal stimulation resulting in bradycardia gagging,vomiting soft tissue injury agitation
use of soft vs rigid catheter for suctioning
soft- aspiration of thin secretions, suctioning in an advanced airway (ET tube)
rigid-suctioning of the oropharynx, particularly if thick secretions
Why suctioning attempts should be 10 seconds or less?
reduces risk of hypoxemia.
And you can give short periods of Oxygen 100% immediately before and after.
EXCEPT in patients who have really copius secretions needed to be removed for breathing
When do you use an oropharyngeal airway?
Unconscious child with no gag reflex
procedures to open airway didnt work
NEVER USE IN SEMICONSCIOUS OR CONSCIOUS- stimulates gagging reflex and vomit.
What is the FiO2 and flow of a low flow nasal cannula?
FiO2- 20-60%
Flow 0.5-4L/min
What is the FiO2 and flow of a low flow face mask?
FiO2- 35-60%
Flow 4-10 L/min
What is the FiO2 and flow of a high flow non rebreathing mask with reservoir?
FiO2- 60-95%
Flow 10-15 L/min
What is the FiO2 and flow of a high flow nasal cannula?
FiO2> 60%
Flow 4-40L/min
Name parts of the nebulizer
Mouthpiece or face mask T piece spacer nebulizer cup nebulizer reservoir tubing compressor
What is the gas flow you have to maintain for nebulizer
5-6 lts
How long should be the treatment with neulizer
8-10 minutes
For inhaled medications, why do you need a spacer?
to effectively deliver to the lungs. If no spacer, only 1/3 arrives to the lungs and the rest stays at the mouth
How do you use a Metered Dose Inhaler with spacer device?
While the child is exhaling, activate the MDI by pressuring down.
Tell the child to take 5 slow, deep, breaths through the mouth piece and hold the last breath for 10 seconds.
Pulse oximetry can accurately estimate oxygen saturation but does not provide evidence of oxygen delivery! It also doesnt directly evaluate the effectiveness of ventilation (CO2).
TRUE
Sudden deterioration in an intubated patient causes
DOPE mnemonic
Displacement of the tube - out of trachea or into the R/L trachea
Obstruction of the tube- secretions( blood, pus, foreign body), kinking of the body
Pneumothorax
simple: decreased SAO2, breath sounds and chest expansion decreased in the affected sides.
tension: same as simple plus hypotension and decreased CO. Trachea is shifted away from affected side.
Equipment failure
- disconnection of the O2 supply from ventilation system
- Leak in ventilator circuit
- failure of power supply to the ventilator
Presentation of simple vs. tension Pneumothorax
Pneumothorax
simple: decreased SAO2, breath sounds and chest expansion decreased in the affected sides.
tension: same as simple plus hypotension and decreased CO. Trachea is shifted away from affected side.
Management of intubated patient who has a sudden deterioration
In addition to DOPE
Observe for chest rise and symmetry auscultate check monitors (SaO2, HR, Capnography) Suction ET tube if secretions Use sedatives or analgesics to reduce agitation and control of ventilation; ONLY when you have ruled out a correctable cause
Definition of shock
physiologic state characterized by inadequate tissue perfusion to meet metabolic demands and tissue oxygenation.
- is often but NOT ALWAYS characterized by inadequate peripheral and end organ perfusion)
What are the consequences of inadequate tissue perfusion
tissue hypoxia anaerobic metabolism accumulation of lactic acid and CO2 irreversible cell damage organ damage
Goal for treating shock
improve systemic perfusion and O2 delivery
Explain utility of Central Venous Oxygen Saturation (ScvO2) in shock
normally, arterial blood contains MORE O2 than what tissues need.
If demands increase-tissues extract more leading to reduced O2 saturation in the Scvo2
so it helps us identify when there are increased demands in the body.
If O2 content is normal and metabolic demands normal, and Scvo2, think of decreased CO
Adequate tissue delivery depends on 3 things..
- Sufficient O2 content in the blood
- Adequate blood flow ( CO)
- Appropriate distribution of blood flow to tissues
Arterial oxygen content formula
Saturated + unsaturated
1.34xHb x SaO2)+(0.003 x PaO2
Oxygen delivery formula
CO + Arterial Oxygen content
CO X ( (1.34xHb x SaO2)+(0.003 x PaO2))
Formula for CO
HR X SVR
BP formula
CO x SVR
O2 delivery may be normal despite hypoxemia if the CO increases commesurate with the decrease in 02 content
true!
O2 delivery=CO + Arterial Oxygen content
Compensatory mechanisms for hypoxia
Increased CO initially
polycythemia if hypoxia is chronic
Which is the compensatory mechanism if CO decreases
CO= SVx HR
So either one, or both can increase
HR increases is LIMITED-Otherwise arrythmia and less time of diastole and filling ventricle.
How are the compensatory mechanisms for increasing CO different between infants and children/adolescents?
In infants, CO highly depends on HR. Their SV is small and has limited capacity to increase.
In child/adolescent is HR and SV but remember that HR is limited.
How is the appropriate distribution of blood determined?
by the size of the blood vessels supplying a specific organ. – vascular resistance.
- vessels large-> resistance is low
- vessel small-> resistance high
Vasconstriction = abnormally increased resistance
True
Determinants of Stroke volume
Preload, contractility, afterload
Indirect measure of preload?
Central venous pressure, but is partially true. Because this also depends on ventricle compliance and pressure and volume measures are different.
Compensatory mechanisms of shock
First: Increase HR
When O2 delivery to tissues is compromised BLOOD FLOW IS REDIRECTED to VITAL ORGANS–> occurs through selective increase in SVR:
reduced peripheral perfusion (delayed capillary refill,
cool extremities, less easily palpable peripheral pulses)
and reduced perfusion to gut and kidneys (decreased
urine output)
Increased contractility
Increase in venous smooth tone– improving venous return and preload.
As CO decreases in shock, BP can be normal or slighly elevated because increased SVR compensation
True
Pulse pressure
SBP-DBP
What happens with Pulse pressure in shock?
narrows, because an increased in SVR raises DBP.
In sepsis, SVR is low, so diastolic pressure decreases and pulse pressure widens.
Compensated vs. decompensated shock
depends on the SBP.
Compensated: signs of inadequate tissue perfusion but bp IS within nom al range. SPB above fifth percentile of age ( 70+(agex2))
Decompensated: hypotension
SHOCK CAN BE PRESENT EVEN IF THE BP IS NORMAL.
SHOCK CAN BE PRESENT EVEN IF THE BP IS NORMAL.
True, is a compensatory mechanism
Hypotensive shock is the new name for Decompensated shock
True
Hypotension is generally a late finding in most types of shock.
Partially true,
In sepsis can occur early because mediators of sepsis produce vasodilation and reduce SVR.
When SVR is decreased hypotension will be an early rather than a late sign of shock
True, septic shock.
Hypotension formula
SBP: 70 + [age in years x2]
compensated shock–> hypotensive shock–> cardiac arrest
True
warning signs: loss of peripheral pulses and decreased level of consciousness
Bradycardia and weak central pulses- omnious signs of impending cardiac arrest
What does third space mean
plasma loss into the interstitium or capillary leak
Goals of shock treatment
Improve O2 delivery Balance tissue perfusion and metabolic demand Reverse perfusion abnormalities support organ function prevent progression to cardiac arrest
Optimization of O2 content in shock
High flow O2 ( Nonrebreathing mask)
invasive or noninvasive ventilation to improve oxygenation
If Hb low, provide RBC
Ionized serum Ca changes with ph
Acidosis–> increased Ca
General management of shock
- Positioning
- Support airway, oxygenation and ventilation
- Establishing vascular access
- Provide fluid resuscitation
- Monitoring
- Performing frequent reassessment
- Obtaining labs
- Meds
- Consulting specialists.
Fluid resuscitation in shock
In general, isotonic crystalloids in a 20mL/kg bolus over 5-20 min.
In severe hypotension, hypovolemic shock: over 5-10 min
In cardiogenic shock-smaller bolus ( 5-10 mL/kg given over 10-20 min)
Overall, reassess and repeat boluses as needed.
Good urine output response after shock therapy in infants/young children, and older children and adolescents
infants and young children: 1.5-2 mL/kg/hr
older children and adolescents: 1 mL/kg/hr
Possible etiology and intervention for decreased Hb and Hcto in shock
Hemorrhage
Fluid resuscitation (dilution)
Hemolysis
Possible interventions:
Administer O2
Control bleeding, transfuse blood
Titrate fluid administration
Possible etiology and intervention for decreased or increased WBCs in shock
sepsis
obtain appropriate cultures
give Abcs
Possible etiology and intervention for decreased platelets in shock
DIC
Decreased platelet production
Transfuse platelets if has serious bleeding
ibtain PT,PTT, fibrinogen, D-dimers
Possible etiology and intervention for increased or decreased glucose in shock
stress
sepsis
decreased production ( liver failure)
adrenal insufficiency
give dextrose bolus and start infusion of dextrose-containing solution if needed.
Possible etiology and intervention for increased or decreased K in shock
Renal dysfunction Acidosis (increases K) Diuresis ( decreased) Adrenal insufficiency (increased)
correct acidosis
treat hypo or hyperK
Possible etiology and intervention for decreased ionized [Ca] in shock
Sepsis
Transfusion of blood preserved with citrate phosphate dextran
Colloid administration
Buffering agents ( Sodium bicarbonate)
Give Ca.
Possible etiology and intervention for increased Lactate in shock
increased as product of anaerobic metabolism from tissue hypoperfusion
- tissue hypoxia
- increased glucose production
- Decreased metabolism( liver failure)
Increase tissue perfusion
Treat acidosis if end-organ dysfunction is impaired.
Inotropes examples and MOA
- Dopamine
- Epinephrine
- Dobutamine
MOA
Increase cardiac contractility, HR
Variable effect on SVR
-includes agents with both adrenergic and B adrenergic effects.
PDE examples and MOA
Milrinone
Decrease SVR
Improve coronary artery blood flow
improve contractility
Vasodilators examples and MOA
Nitroglycerin
Nitroprusside
Decrease SVR and venous tone
Vasopressors examples and MOA
Epi ( doses>0.3 mcg/kg/min)
NE
Dopamine ( >10mcg/kg/min)
Vasopressin
Increase SVR
Increase myocardial contractility ( except vasopressin)
Examples of isotonic crystalloid solutions
NS and lactate ringer
isotonic crystalloid solutions are the first choice of resucitation fluid
True
advantages isotonic crystalloid solutions
inexpensive, readily available, no sensitivity reactions
disadvantages colloid solutions
not readily available, may cause sensitivity reactions,
use limmited to 20-40mL/kg
Volume of fluid and rate for hypovolemic/distributive shock
20mL/kg bolus over 5-10 min ( repeat as needed)
Volume of fluid and rate for Cardiogenic shock( non-poisoning)
5-10 mL/kg bolus over 10-20 min ( repeat as needed)
Volume of fluid and rate for poisoning ( Ca channel blockers, B adrenergic blockers
same as cardiogenic shock,
5-10 mL/kg bolus over 10-20 min ( repeat as needed)
Volume of fluid and rate for DKA with compensated shock
10-20 mL/kg PER LOCAL PROTOCOL~ 1-2 HRS
Rapid fluid delivery system
2 large IV catheters
Place an in line 3 way stopcock
deliver fluid by using a 30- to 60 mL syringe to push fluids throught the stopcock
Indication for blood product administration
Inadequate perfusion despite 2-3 boluses of 20 mL/kg OF isotonic crystalloid. administer 10 mL/kg of blood product.
crossmatching meaning
is testing before a blood transfusion to determine if the donor’s blood is compatible with the blood of an intended recipient
Priority for the blood type or blood products
Crossmatched
Type specific
Type O negative ( O negative preferred in females, O+/- in males)
*predered for females of childbearing age to avoid Rh sensitization
Rapid infusion of cold blood or blood products, mparticularly in large vol, may lead to
hypothermia
myocardial dysfunction
ionized hypoCa
To minimize: warm blood and blood products
and if hypoCa is anticipated with a specific product administer Ca empirically
Clinical signs of hypoglycemia
poor perfusion diaphoresis tachycardia hypothermia irritability or lethargy hypotension
Definition of. hypoglycemia
preterm/term neonates < 45
infants/children/adolescents < 60
Management of hypoglycemia
minimal ss and normal mental status: oral glucose( eg,orange juice)
symptomatic- IV glucose 0.5-1 g/kg.
IV dextrose D25W(2-4mL/kg) OR D10W(5-10 mL/kg)
IV dextrose solutions
IV dextrose D25W(2-4mL/kg) OR D10W(5-10 mL/kg)
Why not routinely infuse dextrose containing fluids for volume resucitation -
hyperglycemia–> osmotic diuresis–> exacerbation of hypovolemia
Children with hypovolemic shock who receive fluids within the first hour have better chance of recovery and survival.
True! Adequate timing is very important!
Dehydration definition
loss of water with varying loss of electrolytes leading to a hypertonic ( hypernatremic) , isotonic, hypotonic ( hyponatremic) state.
Clinically significant dehydration in children
at least 5% of volume depletion- corresponding to a fluid deficit of 50 mL/kg or greater.
Degrees of dehydration and %(mL/kg)
Mild - 5% (50)
Moderate 10% (100)
Severe 15%(150)
Failure to improve hypovolemic shock with at least 3 boluses of isotonic crystalloid solution indicates..
o The extent of fluid losses may be underestimated
oThe type of fluid replacement may need to be altered (eg, need for colloid or blood)
oThere are ongoing fluid lossess( occult bleeding)
oInitial assumption about the etiology may be incorrect
Classification of blood loss
mild -< 30%
moderate 30-45%
Severe > 45%
Management of hypovolemic shock
- Rapidly infuse 20 mL/kg boluses of isotonic crystalloid
- May repeat up to 3 boluses
- If pt continues unstable consider transfusion of RBCs if hemorrhagic, or consider re-evaluate what is going on.
3 mL to 1 mL route
In hemorrhagic shock, give about 3 mL of isotonic crystalloid for every 1 mL of blood lost.
blood replacement in hemorrhagic shock
use PRBCs in 10mL/kg
Indications for transfusion in hemorrhagic shock
Crystalloid refractory hypotension or poor perfusion
Known significant blood loss
Any medication that can be administered IV can be given IO route T/F
True
Contraindications to IO access
Fractures and crush injuries near the access site
Conditions withf fragile bones ( osteogenesis imperfecta)
Previous attempts to establish IO access in the same bone.
Avoid IO cannulation if infection is present in the overlying tissues
Symptomatic bradycardia
bradycardia ( usually < 60/min) + cardiopulmonary compromise
cardiopulmonary compromise: hypotension, altered mental status, signs of shock
Primary vs. Secondary Bradycardia
Primary: congenital or acquired heart conditions that slow the spontaneous depolarization rate of the hearts normal pacemaker cells or slow conduction through system
Secondary: result fo noncardiac conditions affecting the heart
Causes of primary bradycardia
Congenital abnormality of the heart pacemaker or conduction system
Surgical injury to the pacemaker or conduction system
Cardiomyopathy
myocarditis
Causes of secondary bradycardia
hypoxia acidosis hypotension hypothermia drug effects
ECG characteristics of bradycardia
HR- slow
P waves- may or not be visible
QRS narrow or wide ( depending on the origin of the rhythm and/or location of injury to the conduction system)
Conditions in which bradycardia may be normal
- healthy children when metabolic demands are relatively low( ie sleep)
- athletes
why athletes have lower HR- Sinus bradycardia?
they have high SV and increased vagal tone
AV block
disturbance of electrical conduction through the AV nose
First degree AV block
Prolonged PR
asymptomatic
Causes of First degree AV block
- May be present in normal children
- Increased vagal tone
- myocarditis
- MI
- cardiac surgery
- electrolytes( hyperK)
- hypoxemia
- acute rheumatic fever
- intrinsic AV nodal disease
- Drugs ( Ca channel blockers,digoxin, B adrenergic blockers)
Second Degree AV block, Mobitz I
Occurs at the level of AV node
progressive prolongation of the PR interval until an atrial impulse is not conducted to the ventricles.
So until a p wave is not followed by a QRS
presyncope
Causes Second Degree AV block, Mobitz I
- Note: may be present in healthy children
- Any condition that stimulates vasovagal tone
- MI
- Drugs ( Ca channel blockers,digoxin, B adrenergic blockers)
Second Degree AV block, Mobitz II
Occurs below the AV node
Non-conduction of some atrial impulses to the ventricle without any change in the PR.
Often consistent ratio of atrial to ventricular depolarizations~ 2pwaves :1QRS
palpitations, syncope, pre-syncope
Causes Second Degree AV block, Mobitz II
- Intrinsic conduction normal abnormalities
- Cardiac surgery
- Myocardial infarction
Third degree AV block (aka complete AV block)
None of the atrial pulses conduct to the ventricles
No relationship between P waves and QRS complexes
No atrial impulse reaches the ventricle
Ventricular rhythm maintained by a slower pacemaker.
fatigue, syncope, pre-syncope
Causes Third degree AV block (aka complete AV block)
- Extensive conduction system disease or injury, myocarditis
- Cardiac surgery
- Congenital complete heart block
- MI
- Increased parasympathetic tone, toxic drug effects or severe hypoxia/acidosis.
Signs of hemodynamic instability associated with tachyarrythmias
hypotension
altered mental status
signs of shock
others: sudden collapse with rapid, weak pulses
respiratory distress/failure
How tachyarrhythmia affects cardiac output and coronary perfusion?
decreased SV due to insufficient time of filling during diastole
no diastole–poor perfusion
Tachyarrhythmia increases myocardial O2 demand leading to myocardial dysfunction.
Inadequate CO–> cardiogenic shock
What is sinus tachycardia
a sinus node depolarization rate faster than normal for the childs age.
in response to need for increased CO or O2 delivery.
Narrow tachycarida (=<0.09)- is not a tachyarrythmia.
Causes of sinus tachycardia
- exercise
- fever
- pain
- anxiety
- tissue hypoxia
- hypovolemia
- shock
- fever
- metabolic stress
- injury
- toxins/poisons/drugs
- anemia
Characteristics of sinus tachycardia
usually < 220 in infants
<180 in children
R-R variable
QRS narrow
P waves and PR normal
Cause of SVT
Reentry mechanism through accessory pathway or within AV node
Other mechanisms that can cause SVT:
Atrial flutter
Ectopic atrial focus
In infants SVT is often diagnosed when CHF develops
True,
common signs of CHF includes irritability, poor feeding, rapid breathing, unusual sleepiness, vomiting, pale
In order children signs may be shortness of breath, palpitations, chest pain, light headedness
ECG characteristics SVT
infants > 220
children > 180
P waves may be absent or abnormal ( after P wave)
RR constant
QRS narrow
Which is the most common type of SVT in children
Narrow QRS complex SVT , IN> 90%
What are the types of SVT?
Narrow QRS complex SVT ( MC in ediatrics)
Wide QRS complex SVT
What is Wide QRS complex SVT
SVT with aberrant intraventricular conduction ( uncommon in peds) produces a wide complex QRS
Occurs as a result of rate-related bundle branch block within the ventricles or pre-existing bundle branch block
-Can be also caused by accessory pathway ( different from AV node) from atria to ventricle, and then return through AV node or another accessory pathway
Sinus tach vs. SVT
Sinus tach
- Gradual onset
- Hx compatible with ST- fever, pain, dehydration
- PE: Signs of underlying condition( crackles, fever, hypovol)
- HR in infants < 220/min, children< 180/min
SVT:
-Abrupt onset or termination, or both
Infant: symptoms of CHF ( rales, hepatomegaly)
CHild: sudden onset of palpitations
- HR in infants >=220/min, children>= 180/min
Signs of instability in patient with arrhythmia
- Respiratory distress or failure
- Shock with poor end organ perfusion, which may occur with or without hypotension
- Irritability or a decreased level of consciousness
- Chest pain or vague feeling of discomfort in older children
- Sudden collapse
Algorithm for pediatric bradycardia with pulse and poor signs of perfusion
all.
MOA epinephrine
b adrenergic activity: increases heart rate and cardiac contractility
alpha adrenergic: causes vasoconstriction
In bradycardia, when do you prefer atropine over epinephrine
in bradycardia caused by increased vagal tone, cholinergic drug toxicity ( organophosphates) or complete AV bloc
why do you use atropine over epi in AV block due to primary bradycardia?
epi can cause ventricular arryhtmias if the myocardium is abnormal or hypoxic/ischemic.
So first atropine, if not working then give epi
synchronized vs unsynchronized cardioversion
synchronized: shock delivery is timed to coincide with the R wave of the patient QRS complex
Unsynchronized: delivered at any time in the cardiac cycle, used for cardiac arrest rhythms that have no QRS.
When to you use synchronized vs. unsynchronized cardioversion
synchronized: in SVT and Vtaq with pulse
Unsynchronized: in cardiac arrest rhythm
Defibrillation vs. Cardioversion
Defibrillation - is the treatment for immediately life-threatening arrhythmias with which the patient does not have a pulse, ie ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT).
Cardioversion - is any process that aims to convert an arrhythmia back to sinus rhythm.
Indications for synchronized cardioversion
unstable patients ( poor perfusion, hypotension, or heart failure) with tachyarrthythmias (SVT, atrial flutter, VT) , but palpable pulses
Elective cardioversion, under direction of pediatric cardiologist, for children STABLE with SVT, Atrial flutter, VT with a pulse.
Energy dose for cardioversion
less than defibrillation dose
Start with 0.5-1 J/kg for cardioversion of SVT or VT with pulse
If inefective, 2 J/kg
Drug of choice for SVT
Adenosine
Indications adenosine
SVT
adenosine MOA and precautions
Blocks conduction through the AV node temporarily ( ~10 seconds)
a cause of failure is if its given too slowly or with inadequate IV flush.
A brief period of bradycardia ( asystole or complete AV block) may ensue, so warn the pt.
Amiodarone MOA
Inhibits alpha and B adrenergic receptors, producing vasodilation and AV nodal suppression
Inhibits outward potassium current, prolonging the QT duration
Inhibits Na channels, slowing conduction in the ventricles and prolongs QRS.
Amiodarone SE
are rare
bradycardia
hypotension
polymorphic VT
Precautions of Amiodarone
be careful in prolonged QT conditions as it prolongs further the QT.
hepatic patients.
Procainamide indications
SVT, atrial flutter, VT with pulse
MOA Procainamide
Blocks Na channels so prolongs the effective refractory period of both atria and ventricles and depresses conduction within system
So by slowing intraventricular conduction, prolongs QT, QRS, PR intervals.
