PALS Part 2.1 (7-10) (Respiratory & Shock) Flashcards

1
Q

Hypoxemia VS Hypoxia

A

Hypoxemia is when there is lower O2/hemoglobin saturation (below 94%)

Hypoxia (generalized = whole body ; tissue = specific region) is when there is inadequate O2 being delivered to the body

They do not happen at the same time in all instances

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2
Q

Early Vs Late signs of tissue hypoxia

A

Early Signs:

  • Tachypnea
  • Tachycardia
  • Increased resp effort: nasal flaring, retractions
  • Pallor, mottling, cyanosis
  • Agitation, anxiety, irritability

Late Signs:

  • Bradypnea, inadequate resp effort, apnea
  • Increased resp effort: head bobbing, seesaw resps, grunting
  • Bradycardia
  • Pallor, mottling, cyanosis
  • Decreased LOC
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3
Q

What exactly is Arterial O2 content and what is the formula for calculating it?

A

Arterial O2 Content = the total amount of O2 carried in the blood. It consists of the sum of O2 bound to hemoglobin AND the amount dissolved into arterial blood plasma.

Arterial O2 Content = (1.36 X Hgb concentration X SaO2) + (0.003 x PaO2)

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4
Q

Review the 5 different mechanisms of Hypoxia on page 111-112

A

Seriously review it, they’re not the normal causes of respiratory distress you think of!!!

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5
Q

When should you begin to suspect hypercarbia as the cause of respiratory distress instead of hypoxia/hypoxemia?

A

When the pt further deteriorates despite adequate O2, which is typically a sign that ventilations are inadequate whether spontaneous via pt or artificial via BVM

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6
Q

Stopped at Airway resistance

A

Stopped at Airway resistance

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7
Q

What are the 4 major factors associated with increased work of breathing?

A

AIRWAY RESISTANCE:
- the impedance to airflow within the airways, which is primarily changed by the size of the airway. Larger airways have less resistance than smaller airways. Obviously if there is a blockage or space taken up then the airway will be smaller and thus resistance increased.

LUNG COMPLIANCE:
- The change in lung volume produced by a change in driving pressure across the lung, this is done with the lungs and chest wall/diaphragm expand and relax. There are several conditions that decrease lung compliance such as a pneumo, pneumonia, ARDS, Inflammation, and pulmonary edema; but the root cause of decrease compliance is the increased presence of water/fluids in the interstitial spaces. This acts like a sponge filled with water which decreases its natural elasticity b/c of the extra water weight.

USE OF ACCESSORY MUSCLES:
- The muscles of inspiration are the diaphragm, intercostal muscles, and accessory muscles (mainly the neck and abdomen). The diaphragm creates he most change in pressure by contracting downward in a dome shape, however the range of motion of the diaphragm contraction can be decreased my things like intraabdominal pressure or abdominal distention. In young children and infants the intercostal muscles serve mainly to stabilize the chest and cannot effectively lift the chest wall to increase intrathoracic volume to compensate for a loss of diaphragm motion.

CNS DISORDER OF THE BREATHING CONTROL SYSTEMS:
- Includes brainstem respiratory centers, central/peripheral chemoreceptors, and voluntary control (via the cerebral cortex). Things like an infection of the CNS, traumatic brain injury, and drug overdose can impair these systems.
- NOTE: Central Chemoreceptors are responsive to the hydrogen ion content in the cerebrospinal fluid which is largely determined by the arterial CO2 tension.
Peripheral Chemoreceptors are responsive to a decrease in arterial O2 (though a few also response to CO2 levels)

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8
Q

Laminar Airflow Vs Turbulent Airflow?

A

Laminar Airflow = quite, smooth, and orderly

Turbulent Airflow = irregular

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9
Q

How is lung and chest wall compliance different for infants and small children?

A

B/c the infant and smaller children chest wall has not become rigid yet like in older children and adolescents and is still very flexible (i.e. very compliant), when a child changes intrathoracic pressures very quickly and forcefully as in labored breathing, it will bring in the chest wall during a forceful inspiration causing the retractions of the chest wall between the ribs seen during labored breathing.

This actually limits lung expansion and is not useful. Once the chest wall becomes rigid in older kids, the forceful inspiration can be helpful

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10
Q

How is airway swelling different in infants and children than adults?

A

Obviously the airways are going to be smaller which is fine with their comparatively smaller bodies. However, b/c swelling is circumferential in the airways, the same amount of swelling causes a MUCH smaller airway in infants. Pg 114 has a good picture example.

A crying infants creating turbulent airflow can reduce lumen size causing an increase in airway resistance and cause a 16-32x increase in work of breathing.

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11
Q

Respiratory Distress VS Failure

A

Respiratory Distress:
- This is when there is an increase in respiratory rate and effort. Typically assessment for includes looking at rate, effort, quality of breath sounds, and mental status (typical an AMS indicated more failure than distress)

Respiratory Failure:
- occurs when the pt can no longer maintain adequate oxygenation, ventilation, or both. Typically this is identified by an “abnormal appearance” aka AMS or decreased LOC or cyanotic.

NOTE: When respiratory effort is inadequate, respiratory failure can occur without typical signs of respiratory distress.
For instance if a pt OD’d on an opioid, they may not go through the phase of respiratory distress before reaching failure b/c they are already in a depressed state/LOC before respiratory depression and thus may not fight for air the normal way.

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12
Q

Where should you auscultate lung sounds when doing a respiratory exam?

A
  • Anterior (either side of the chest wall)
  • Posterior
  • Lateral (under the axillae)

NOTE: remember though that due to small chest cavity space, sometimes the lung on the opposite side can be heard while auscultating the other side and mask problems. So listening under the armpit where you are the furthest away from the opposite lung may yield the most accurate sounds

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13
Q

What are the 4 types of respiratory problem types?

more like locations of cause

A

UPPER AIRWAY OBSTRUCTION:

  • Nose, pharynx, larynx (airways above the thorax)
  • Typically from some sort of obstruction (Ex. FBAO), inflammation (Ex. Epiglottitis), or infection (Croup)
  • Most common signs are stridor, hoarseness, change in voice/cry, typically during inspiration. Other signs could be increased resp rate/effort, drooling, snoring, gurgling, poor chest rise, poor air entry sounds on auscultation

LOWER AIRWAY OBSTRUCTION:

  • Lower trachea, bronchi, bronchioles (airway within the thorax)
  • Commonly caused by asthma and bronchiolitis.
  • Typically signs are seen during inspiration where there is a wheeze and prolonged expiratory phase the requires increased expiratory effort.

LUNG TISSUE DISEASE:
- Disease of the lung tissues/substances
- This causes stiff lungs b/c of the increase in fluids accumulated in the alveoli, interstitium, or both. This causes severe respiratory effort seen by accessory muscle use/retractions and marked hypoxia (from alveolar collapse or pulmonary edema and/or inflammation debris in the alveoli
- The disease can be caused by a ton of things including, pulmonary contusion, allergic reaction, toxins, CHF, ARDS, pneumonia, ect.
- Often signs and symptoms will include, crackles/rales, decreased air movement, decreased breath sounds, tachypnea, increased effort, tachycardia, and hypoxemia despite O2 supp).
(EARLY SIGN = hypoxemia b/c of damaged alveoli, low oxygenation ; LATE SIGN = grunting and hypercarbia b/c of decreased ventilation and hypercarbia)

DISORDERED CONTROL OF BREATHING:

  • in this state there is inadequate respiratory effort (often the parent will say the child is “breathing funny”) which leads to hypoventilation and hypercarbia. Typically the LOC will be decreased as a result of the other two.
  • Can be caused by neurologic disorders, metabolic abnormalities, and drug overdose.
  • Signs often include, variable/irregular breathing patterns and effort, shallow breathing with inadequate effort, central apnea, normal or decreased air movement
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14
Q

Specific Management for Different Types of Upper Airway Obstructions

A

ALL Emergencies Get the Basic:

  • airway positioning
  • suction as needed
  • oxygen
  • Pulse Ox
  • ECG Monitoring as needed
  • BLS as indicated

UPPER AIRWAY OBSTRUCTION

  • Croup:
    a) nebulized epi
    b) corticosteroids (dexamethasone)
  • Anaphylaxis
    a) IM Epi:
    b) albuterol
    c) antihistamine
    d) corticosteroids
  • FBAO:
    a) position of comfort
    b) specialty consulation
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15
Q

Specific Management for Different Types of Lower Airway Obstructions

A

ALL Emergencies Get the Basic:

  • airway positioning
  • suction as needed
  • oxygen
  • Pulse Ox
  • ECG Monitoring as needed
  • BLS as indicated

LOWER AIRWAY OBSTRUCTION

  • Bronchiolitis:
    a) nasal suctioning
    b) consider bronchodilator trial
  • Asthma:
    a) albuterol + ipratropium
    b) corticosteroids
    c) magnesium sulfate (for status asthmaticus)
    d) IM epi (if severe)
    e) Terbutaline
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16
Q

Specific Management for Different Types of Lung Tissue Disease

A

ALL Emergencies Get the Basic:

  • airway positioning
  • suction as needed
  • oxygen
  • Pulse Ox
  • ECG Monitoring as needed
  • BLS as indicated

LUNG TISSUE DISEASE

  • Pneumonia, Infectious/Chemical/Aspiration Pneumonitis
    a) albuterol
    b) antibiotics as needed
    c) consider non invasive or invasive ventilatory support with PEEP
  • Pulmonary Edema, Cardiogenic/NonCardio (ARDS):
    a) consider non invasive or invasive ventilatory support with PEEP
    b) consider vasoactive support
    c) consider diuretic
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17
Q

Specific Management for Different Types of Disordered Control of Breathing

A

ALL Emergencies Get the Basic:

  • airway positioning
  • suction as needed
  • oxygen
  • Pulse Ox
  • ECG Monitoring as needed
  • BLS as indicated

DISORDERED CONTROL OF BREATHING

  • Increased ICP:
    a) avoid hypoxemia
    b) avoid hypercarbia
    c) avoid hyperthermia
    d) avoid hypotension
  • Poisoning/Overdose:
    a) antidote as indicated
    b) contact poison control
  • Neuromuscular Disease:
    a) consider non invasive or invasive ventilatory support with PEEP
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18
Q

Why might you not want to use succinylcholine in a ped pt with a neuromuscular disease?

A

It can trigger hyperkalemia or malignant hyperthermia

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19
Q

What is a pop off valve and when should it not be used?

A

A pop off valve is a pressure limited valve on a BVM that prevents excessive airway pressure above 35-45 cm H2O being vented into the patient.

When you are doing CPR on a ped patient who with poor lung compliance, has airway resistance, or needs CPR the automatic pop-off valve may prevent sufficient tidal volume from being delivered. Therefore when doing CPR you should TAKE OR TURN OFF THE POP OFF VALVE

SIDE NOTE*** even with O2 supp ventilations using a reservoir and secondary 100% O2 source, the O2 concentration can vary from 30-80%. So do make sure you deliver high O2 concentration (60-95%) you must make sure you are using a reservoir and supp O2 flow of at least 15L/min

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20
Q

What is a fish-mouth or leaf-flap operated nonrebreathing outlet valve?

A

They are adult specific non rebreathing valves that DO NOT provide a continuous flow of O2 to the mask. They only open when the bag is squeezed or enough inspiratory pressure forces the valve to open (when spontaneous breaths are present). However, kids cannot generate enough inspiratory force to open these valves so DO NOT USE ON CHILDREN.

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21
Q

What size volume self-inflating bags should be used for infants/children and which for adolescents?

A

For infants and small children used a 450-500mL bag

For adolescents use a 1000mL (adult) bag

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22
Q

What steps should you take when equipment testing your BVM?

A
  • Check bag for leaks by placing finger on outlet valve and squeezing bag
  • Check gas flow control valves to verify function
  • Check the pop-off valve to ensure it can be closed/taken off
  • Check that the O2 tubing is securely connected to the device and O2 source
  • Listen for the sound of O2 flowing into the bag
  • Ensure that the cuff of the mask is adequately inflated
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23
Q

What is the ideal position for infants and toddlers to make an open/patent airway through positioning?

A

The “sniffing” position

Aim to place the external ear canal in line with the anterior of the top of the shoulder by flexing the neck forward and extending the head.

For children OLDER than 2 you may need to put padding under the occiput and for children YOUNGER than 2 you may need to pad under the shoulder blades.

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24
Q

How many rescuers are recommended in order to use a BVM?

How does the technique change when there is 1 vs 2 rescuers?

When might a 2 person rescuer control over the BVM be necessary?

A

AHA says 2, and if there is only 1 they recommend the mouth-to-barrier technique

A 1 rescuer using a BVM should use the E-C clamp technique (the normal one; thumb & pointer make a C holding the mask secure to face, the other 3 fingers go under chin to hold the head back)

A 2 rescuer using a BVM should have one rescuer doing essentially an E-C clamp with both hands while the other squeezes the bag

Time when a 2 rescuer team may be necessary is if:

  • making a seal is difficult
  • one provider’s hands are too small
  • significant airway resistance
  • restricting spinal motion is necessary
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25
Q

What are 3 reasons to avoid over ventilation?

A
  • Increases intrathoracic pressure and impedes venous return, thus reducing filling of the heart between compressions, reducing blood flow generated by the next compression, and reducing coronary perfusion and cerebral blood flow
  • Causes air trapping and barotrauma in children with small airway obstruction
  • Increases risk of regurgitation and aspiration in children without an advanced airway
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26
Q

When is a low flow-inflating bag (anesthesia bag) more beneficial than a self-inflating bag?

A

When a child has spontaneous breathing is can be difficult to time the compression of a self inflating bag with the child’s breaths and miss-timing it can cause regurgitation, coughing, laryngospasm, or gastric inflation.

Therefore a low flow-inflating bag may be more beneficial b/c they can provide CPAP and the flow can be manipulated to the needs of the child.

These bags are typically used in the intensive care unit, delivery room, and operating room.

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27
Q

Causes of gastric inflation during artificial ventilations

A
  • partial airway obstruction
  • high airway pressures are needed, such as in a child with poor lung compliance
  • the BVM rate is too fast
  • the tidal volume is too much
  • the Peak inspiratory pressure created is excessive (more than 30 cm H20)
  • the child is unconscious or is in cardiac arrest (b/c the gastro-esophageal sphincter opens at a lower than normal pressure)
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28
Q

How much suction is provided with a wall mounted VS portable suction device?

How much force is typically needed to remove secretions?

A

Wall Mounted = more than -300 mmHg

Portable = varies by machine but is definitely way less than 300 and may not be adequate when patient is large or secretions are thick/copious

Typically at least a suction power of -80 to -120 mmHg is needed to remove secretions

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29
Q

When should you use soft vs rigid catheters for suctioning?

A

Use a soft catheter when secretions are thin or for suctioning an ET or trach tube.

Use a rigid catheter when suctioning THICK secretions

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30
Q

What things should you be sure to monitor while suctioning?

A
  • Heart rate
  • O2 Sat
  • clinical appearance

You may need to give O2 and ventilations before and after secretions to avoid hypoxia.

Typically you should not suction for longer than 10 seconds but when secretions are blocking an airway so bad you may need to go over as you wont be able to give vents and O2 without the removal of large amounts of fluids

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31
Q

Where should the tip of the OPA land when placed and sized correctly?

How should you size the OPA and what can happen if it is too large or too small?

A

A correctly sized and placed OPA should land the tip at the angle of the jaw which should align with the glottis opening.

To size an OPA the tip should extend from the corner of the mouth to the angle of the jaw

If it is too LARGE it can block the airway or cause trauma to the laryngeal structures (& soft tissue)

If is is too SMALL it can push the tongue into the back of the throat

(Remember they recommend to use a tongue depressor to push the tongue down before inserting, this replaces the need to insert at a 45 or 90 degree angle and then twisting into place)

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32
Q

What 3 clinical situations should you automatically think to give a child O2 supp?

A
  • resp compromise (distress/failure/arrest)
  • Shock
  • AMS

REMEMBER to try to get a humidifier attached asap to prevent airway dryness (don’t think this is on truck)

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33
Q

What considerations should you have when it comes to giving O2 to a conscious child or infant?

A

Sometimes giving O2 supp can freak the child out more b/c the equipment can be scary, this will cause an increase in O2 consumption secondary to agitation.

Weigh the risk vs reward/need and consider letting the parent introduce the O2 equipment or if one method agitates the child try a different less aggressive one like nasal cannula or blow by technique

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34
Q

What are considered low-flow O2 delivery systems vs high-flow O2 delivery systems?

A

LOW-FLOW O2 DELIVERY SYSTEMS: (22-60% O2, typically used when child is relatively stable and require minimal aid)

  • NASAL CANNULA:
    a) offers O2 concentration of 22%-60%
    b) Recommended flow rate is 0.25 to 4Lpm
    c) the exact inspired O2 concentration cannot be determined alone by the flow rate b/c other conditions affect it such as the child’s size, inspiratory flow rate, volume inspired, Naso or Oro volume, Nasal or Oro resistance.
  • SIMPLE OXYGEN MASK
    a) offers O2 concentration of 35%-60%
    b) recommended flow rate is 6 to 10 Lpm
    c) this does not offer as much O2 concentration as a non-rebreather b/c there are not ports that close off when the pt is breathing in to prevent room air from entering. I.E. this will deliver mixed room air and O2 line the nasal cannula

HIGH_FLOW O2 DELIVERY SYSTEMS: (O2 concentration delivery of over 60% at a minimum of 10 Lpm, typically given to critical pts in shock or resp distress)

  • NON-REBREATHER:
    a) an O2 concentration of 95% can be reached with a flow rate of 10-15Lpm and a tight seal on face
  • HIGH FLOW NASAL CANNULA:
    a) for adolescents and older the 4Lpm can be turned up to 40+ Lpm titrated to effect
    b) keep in mind though that this will still deliver mixed room air and O2 from the compressed source
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35
Q

At what flow rate should a nebulizer be set at?

A

5-6 Lpm

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36
Q

How should you tell the child to breath when administering a MDI with a spacer device?

A

After pressing on the inhaler to release the medicine, have the child breath normally for 3-5 breaths and then hold their breath for 10 seconds on the last breath

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37
Q

What are 2 things you should look at for discrepancies in what the Pulse Ox may be reading at?

A

There may be a malfunction if the heart rate the pulse ox is saying does not match the actual pts heart rate

There may be a malfunction if the O2 sat does not match the presentation of the child

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38
Q

What are 6 situations when the Pulse Ox reading may be inaccurate?

A
  • cardiac arrest
  • shock or hypovolemia
  • motion, shivering, or bright overhead light
  • problem with the skin probe interface
  • misaligning the sensor with light source
  • cardiac arrhythmias with low cardiac output
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39
Q

The definition of shock does not require the presence of ______?

A

Hypotension!

The definition of shock does not require the presence of HYPOTENSION, shock can be present with a normal, increased, or decreased systolic blood pressure.

(this is b/c by definition it is when tissue perfusion does not meet metabolic demands and tissue oxygenation)

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40
Q

What are two of the first effected organs (besides the heart) in the presence of shock and can be big clues to shock being present?

A

THE BRAIN AND KIDNEYS

The brain will develop a decreased level of consciousness, and the kidneys will have a decreased or no urine output

(obviously the heart will also be affected quickly)

41
Q

What are 4 main causes/types of shock?

What can make shock worse or progress faster?

A

HYPOVOLEMIC SHOCK
- Inadequate blood volume or oxygen-carrying capacity - Caused by gastroenteritis, burns, hemorrhage, dehydration, sepsis, or osmotic diuresis

DISTRIBUTIVE SHOCK

  • Poor distribution of blood volume and flow
  • Caused by sepsis, anaphylaxis, or spinal cord injury

CARDIOGENIC SHOCK

  • Impaired cardiac contractility
  • Caused by congenital heart disease, myocarditis, cardiomyopathy, or arrhythmia

OBSTRUCTIVE SHOCK

  • Obstructed blood flow
  • Caused by tension pneumo, cardiac tamponade, PE, or constriction of the ductus arteriosus in infants with ductal-dependent congenital heart lesions

Anything that increases O2 demand will make shock worse or progress faster. These include things like fever, infection, injury, resp distress, and pain.

42
Q

What is the main goal in treating shock?

A

To increase systemic perfusion and O2 delivery to help prevent end-organ injury and stop the progression to cardiopulmonary failure and cardiac arrest

43
Q

What is produced by anaerobic metabolism?

A

Lactic Acid

44
Q

What 3 things does adequate tissue O2 delivery depend on?

What primarily determines blood O2 content?

A

Adequate tissue O2 delivery depends on:

  • Sufficient O2 content in the blood
  • Adequate blood flow to the tissues (cardiac output)
  • Appropriate distribution of blood flow to the tissues

The hemoglobin concentration and % of saturated hemoglobin determine blood O2 content. (plasma carries only a small amount of O2)

45
Q

Does the presence of hypoxemia automatically mean there is tissue hypoxia?

A

NO

Hypoxemia is when there is an overall low O2 count bound to hemoglobin (low O2 sats) but hypoxia is when there is inadequate tissue perfusion or inadequate O2 delivery to the systems.

So if there is hypoxemia present, the heart can increase cardiac output as a compensatory mechanism which will offset the low O2 sats by pumping more blood to the tissues and thus delivery a semi normal amount of O2.

46
Q

Cardiac output = ? x ?

A

Cardiac output = heart rate X stroke volume

***NOTE: remember that infants and young children have a harder time changing stroke volume and therefore depend on their heart rate for compensatory mechanisms. This is why bradycardia is so bad b/c they cannot compensate like an adult by changing their stroke volume

47
Q

What 2 things determine adequate blood flow to the tissues?

A

Cardiac output and vascular resistance

CO = HR X SV

48
Q

What is Stroke Volume?

What 3 things determine stroke volume?

A

Stroke volume is the amount of blood ejected by the ventricles with each contraction and is determined by:

  • Preload
  • Contractility
  • Afterload
49
Q

Increased Vascular Resistance = ?

Decreased Vascular Resistance = ?

A

Increased Vascular Resistance = Vasoconstriction

Decreased Vascular Resistance = Vasodilation

(obviously things like an emboli or plaque build up will also increase vascular resistance)

50
Q

What is the most common cause of low stroke volume and therefore low cardiac output?

A

Inadequate Preload!

This is typically caused by hemorrhaging, severe dehydration, and vasodilation

THIS RESULTS IN HYPOVOLEMIC SHOCK

(i.e. hypovolemic shock is related to inadequate preload!!!)

51
Q

At a steady state, where does most of the blood reside?

A

In the VEINS, about 70%

52
Q

How can you assess the right ventricular preload?

A

By measuring the Central Venous Pressure in the superior vena cava or the right atrium!

53
Q

Poor cardiac contractility is related to what type of shock?

What are some things that can cause poor contractility?

A

Poor cardiac contractility is related to Cardiogenic Shock, this is b/c it directly impairs cardiac output via decreased stoke volume.

This is also considered to be “myocardial dysfunction” and can be caused by inflamed heart muscle (myocarditis), metabolic problems like hypoglycemia, or toxic ingestions like calcium channel blockers.

54
Q

What is the bodies normal response to a decrease in cardiac output and how does that further hurt the body?

A

When the body experiences a decrease in cardiac output it maintains tissue perfusion by vasoconstriction. This further hurts the cardiac output however b/c it increases AFTERLOAD, so the heart is having a harder time ejecting blood out of the left ventricle, decreasing stroke volume and cardiac output further still

55
Q

What are the 4 main compensatory mechanisms the body does to compensate for shock?

A
  • Increased Heart Rate (Tachycardia) (First sign to occur)
  • Increased systemic vascular resistance (SVR) (vasoconstriction)
    (this is seen by selectively causing peripheral vasoconstriction to shunt blood towards the core organs. This shunting is seen through delayed cap refill, cold extremities, weaker peripheral pulses, and reduced perfusion to the gut and kidneys which produces a low urine output (oliguria))
  • Increased Cardiac Contractility
  • Increase in Venous Smooth Muscle Tone
56
Q

What 2 things determine blood pressure?

A

Cardiac Output and SVR (Systemic Vascular Resistance)

57
Q

Compensated Shock VS Hypotensive Shock

A

COMPENSATED SHOCK:

  • Clinical state where there are signs of inadequate tissue perfusion but the pts blood pressure is in the normal range.
  • Clinical findings include tachycardia, delayed cap refill, mental status changes, and decreased urine output. (recall the 4 main comp mechanisms on the other note card; tachy offsets the low stroke volume, delayed cap refill, cool extremities, weak peripheral pulses and low urine output (oliguria) are all signs of blood shunting to core)

HYPOTENSIVE SHOCK:

  • THIS IS THE NEW NAME FOR DECOMP SHOCK
  • This is when blood pressure has dropped below normal b/c the vasoconstriction is no longer able to offset the low cardiac output.
  • Clinical findings include weak peripheral AND central pulses, mottling, cool extremities, and altered LOC.

WHEN YOU FIND SIGNS OF SHOCK, DO NOT WAIT FOR BLOOD PRESSURE BEFORE YOU START TREATING!

58
Q

In what ways does septic shock not follow the normal path of Comp shock to Decomp shock to Arrest?

What is the Hypotension Formula for pts 1-10yo?

A

Septic shock can skin right to decomp shock because it will quickly cause vasodilation, taking away the main pathway for the heart to attempt to compensate for shock.

Therefore, hypotension can be an early or late sign of septic shock. Often if it is an early sign you will have hypotension but still warm extremities, brisk or flash capillary refill, and full peripheral pulses.

HYPOTENSION FORMULA FOR AGES 1-10yo:
If the BP is LESS than the below formula then the pt is Hypotensive :
(Child’s age x 2)mmHg + 70 mmHg

59
Q

What is the relationship between shock and the term “Accelerating Process”?

A

It is referring to the fact that shock progression is UNPREDICTBLE.

It may take HOURS for compensated shock to develop into hypotensive shock, but only MINUTES for hypotensive shock to develop into cardiac arrest

60
Q

What is a special aspect of septic and anaphylactic shock that increases severity outside of their vasodilatory effects causing distributive shock?

What is a late sign of distributive shock?

A

B/c of their added effects to the permeability of capillaries (it increases it), there is also loss of fluids from the intravascular space to the extravascular space, causing increased loss of circulating fluids.

Also b/c of the fast progression of vasodilation that leads to fast blood flow to tissue beds but not away from them, once the metabolic processes switch to anaerobic it causes a pooling of lactic acid at the tissue beds, this combo of blood not being shunted away and build up of lactic acid is why the extremities stay warm and in fact WHEN THEY GO COLD IS A LATE SIGN OF DISTRIBUTIVE SHOCK

61
Q

How does neurologic injury cause distributive shock?

What are the main three signs?

A

An injury that causes neurological damage such as to the upper cervical spine, can cause a loss of vascular tone via a disruption in nervous system signal reaching the smooth muscle; which in effects results in severe vasodilation like in sepsis and anaphylaxis which all three cause distributive shock.

The main three signs of neurologic distributive shock are:

  • hypotension with wide pulse pressure
  • normal heart rate or bradycardia (the loss of NS signals to the smooth muscle also prevents tachycardia
  • Hypothermia
62
Q

What is the most common form of distributive shock?

A

Septic Shock - an abnormal host immune response to infectious organisms or their by-products (endotoxins) that lead to small blood vessels dilating and leaking fluids into tissues.

63
Q

What are the 5 steps to the Systemic Inflammatory Cascade leading to Septic shock?

A
  • Infectious organism or its by products activates the immune system including neutrophils, monocytes, and macrophages
  • These cells stimulate release or activation of inflammatory mediators (cytokines) that perpetuate inflammatory response
  • Cytokines produce vasodilation and damage to the lining of the blood vessels (endothelium), causing increased capillary permeability
  • Cytokines activate the coagulation cascade and may result in microvascular thrombosis and disseminated intravascular coagulation
  • Specific inflammatory mediators can impair cardiac contractility and cause myocardial dysfunction
64
Q

What makes treating sepsis so hard?

A

B/c the inadequate perfusion combined with possible microvascular thrombosis leads to ischemia that is diffuse and patchy so the individual organs get varying degrees of hypoxia and ischemia.

65
Q

How are the Adrenal Glands effected by sepsis?

A

The Adrenal Glands are especially prone to microvascular thrombosis and hemorrhage in septic shock; and since the adrenal glands produce cortisol (which is an important hormone in the body’s stress response), the lowered levels of cortisol that may be present as a result contributes to low SVR (systemic vascular resistance) and myocardial dysfunction

66
Q

What is microvascular thrombosis?

A

I LOOKED THIS UP, THIS IS NOT FROM AHA

I think it is when fibrin and other clotting factors close off small vessels in the presence of a septic infection to try to prevent the infection from spreading. The end result is it blocks off small vessels. Later, leukocytes will eliminate the infection and repair the damaged vessels

67
Q

REVIEW DIFFERENT SIGNS AND SYMPTOMS ASSOCIATED WITH DIFFERENT TYPES OF SHOCKS IN THE SECOND HALF OF PART 9, LOOK FOR ONES THAT ARE SPECIFIC TO EACH TYPE

A

REVIEW DIFFERENT SIGNS AND SYMPTOMS ASSOCIATED WITH DIFFERENT TYPES OF SHOCKS IN THE SECOND HALF OF PART 9, LOOK FOR ONES THAT ARE SPECIFIC TO EACH TYPE

68
Q

What is angioedema?

A

Swelling of the face, lips, and tongue (common in anaphylaxis)

69
Q

What are going to be your main clues that differentiate Neurogenic Shock and Hypovolemic Shock?

A

Hypovolemic Shock is typically associated with:

  • hypotension
  • NARROW pulse pressure (from compensatory vasoconstriction)
  • Tachycardia (from compensatory mechanism)

Neurogenic shock the compensatory mechanisms above, vasoconstriction and tachycardia, do not occur because of interruption between the sympathetic nervous system and the heart and blood vessels (neuro will have hypotension with a WIDE pulse pressure and no tachy)

70
Q

DEFINITELY LOOK AT THE COMPARISON CHART OF THE DIFFERENT SIGNS AND SYMPTOMS PRESENT WITH THE 4 DIFFERENT TYPES OF SHOCK ON PAGE 188!!!!!

A

DEFINITELY LOOK AT THE COMPARISON CHART OF THE DIFFERENT SIGNS AND SYMPTOMS PRESENT WITH THE 4 DIFFERENT TYPES OF SHOCK ON PAGE 188!!!!!

71
Q

What are the 3 main characteristics of Cardiogenic shock?

What are the 6 main pathological reactions occurring in the presence of cardiogenic shock?

A

The 3 main characteristics are tachycardia, high SVR, and decreased cardiac output (remember this is pump failure).

  • Increased heart rate and left Vent afterload, which increases vent work and myocardial O2 demand
  • Compensatory increase in SVR to redirect blood from peripheral and splanchnic tissues to the heart and brain.
    (remember that this increase in SVR actually helps in hypovolemic ​shock to shunt peripheral blood to core, but in cardiogenic shock it also makes the failing left vent work harder and increase O2 demand which can be detrimental to the heart)
  • Decreased stroke volume due to decreased myocardial contractility and increased afterload
  • Increased venous tone, which increases central venous (right atrial) and pulmonary capillary (left atrial) pressures
  • Diminished renal blood flow resulting in fluid retention
  • Pulmonary Edema resulting in myocardial failure and high left ventricular end-diastolic, left atrial, and pulmonary venous pressures, and from increased venous tone and fluid retention
72
Q

What is the main distinguishing S&S between hypovolemic and cardiogenic shock?

A

Increased Resp Effort (secondary to pulmonary edema)

Remember that in cardiogenic shock, the decreased contractility is causing left vent pump failure, and that fluid is going to back up into the lungs as end-diastolic volume in the L and R vents rise.

73
Q

What are some way to distinguish that Cardiac Tamponade is the cause of obstructive shock?

A

The ECG will have small QRS complexes showing low voltage

There may be the presence of pulsus paradoxus, a drop of more than 10mmHg on inspiration

74
Q

How do you use a manual BP cuff to assess the presence of Pulsus Pardoxus?

A

Inflate the cuff as normal, as you slowly decrease the pressure note wen you hear the initial KOROKOFF SOUNDS, which will be when the child is exhaling. Continue to deflate the cuff and note when you consistently hear the Korotkoff sounds throughout the respiratory cycle. If the difference between these 2 points is greater than 10 mmHg, the child has pulsus paradoxus

75
Q

What is a major difference noted between hypovolemic shock and obstructive shock?

A

Time of Onset!

Obstructive shock from a PE, cardiac tamponade, or tension pneumo will be an ACUTE ONSET

76
Q

What is the end result of cardiac tamponade and tension pneumo if left untreated?

A

They will develop into cardiac arrest with PEA

77
Q

What are the 4 main goals in treating shock?

What are the 4 main treatment plans to achieve these goals?

A

Shock Treatment Goals:

  • improve O2 delivery
  • balance tissue perfusion and metabolic demand
  • support organ function
  • prevent progression to cardiac arrest

Shock Treatment Interventions:

  • Optimize O2 content of blood: this is done by;
    a) admin high flow O2
    b) use invasive or noninvasive mechanical vents
    c) if hemoglobin is low, admin blood transfusion
  • Improve Volume and Distribution of Cardiac Output:
    a) fluid boluses/drips (for most not all)
    b) vasopressors
  • Reducing O2 Demand:
    a) reduce work of breathing, pain, anxiety, and fear
  • Correct Metabolic Derangements:
    a) these include hypoglycemia, hypocalcemia, hyperkalemia, metabolic acidosis (lactic acid levels), all affect heart contractility
    b) correct this with things like oral glucose, D50W, sodium bi carb, etc.
78
Q

Overview of fluid resuscitation guidelines

A

In general all should be given as a bolus of 20mL/Kg over 5-20 minutes:

  • 10-20mL/kg for septic patients over 5-10min
  • 20mL/kg over 5-10 minutes for ALL other forms of shock unless specified (like cardiogenic)
  • In cardiogenic shock when pulmonary edema is likely, reduce the bolus to 5-10mL and increase the time given to 10-20min
79
Q

REVIEW TABLE 51 ON PAGE 197 GOING OVER VASOACTIVE DRUGS AND WHAT CLASS AND EFFECT THEY HAVE
(it goes over which drugs are inotropes, vasodilators, ect)

A

REVIEW TABLE 51 ON PAGE 197 GOING OVER VASOACTIVE DRUGS AND WHAT CLASS AND EFFECT THEY HAVE
(it goes over which drugs are inotropes, vasodilators, ect)

80
Q

When are vasoactive drugs indicated for a shock pt?

A

When shock persists despite adequate volume resuscitation to optimize preload.

Ex. If a septic pt is still hypotension after fluid boluses, they may greatly benefit from a vasoconstrictor

81
Q

REVIEW SUMMARY OF INITIAL MANAGEMENT PRINCIPALS OF SHOCK MANAGEMENT ON PG 198.
(it has the general overview of what to do early and for all forms of shock)

A

REVIEW SUMMARY OF INITIAL MANAGEMENT PRINCIPALS OF SHOCK MANAGEMENT ON PG 198.
(it has the general overview of what to do early and for all forms of shock)

82
Q

What is the goal of fluid therapy in shock?
Which types of shock benefit the most from fluid therapy?
What is the preferred fluid and why?

A

The primary objective of fluid resuscitation is to restore intravascular volume and tissue perfusion.

Hypovolemic and Distributive shock benefit the MOST from fluid therapy

Isotonic Crystalloid Solutions such as normal saline or lactated ringer’s are preferred because they are widely available, inexpensive, and do NOT cause many sensitivity reactions.

(Colloid Solutions are not widely available, may take time to prepare, may cause sensitivity reactions, and synthetic versions may cause coagulopathies.

83
Q

LOOK AT TABLE OF EXACT FLOW RATES AND VOLUMES OF FLUID RESUSCITATION FOR EACH TYPE OF SHOCK ON PAGE 201

A

LOOK AT TABLE OF EXACT FLOW RATES AND VOLUMES OF FLUID RESUSCITATION FOR EACH TYPE OF SHOCK ON PAGE 201

84
Q

What is considered hypoglycemic for pre-term and term neonates Vs infants, children, and adolescents?

How should you treat it?

A

Pre-term and Term Neonates are hypoglycemic if they are below: 40 mg/dL

Infants, Children, & Adolescents are hypoglycemic if they are below : 60 mg/dL

If they are normal mental status and minimal symptoms then give oral glucose

If they are AMS or critically symptomatic then give:

  • IV Glucose at a dose of 0.5-1 g/kg
  • D25W at 2-4mL/kg
  • D10W at 5-10mL/kg

(All three are separate options)
(Dextrose is the SAME SUBSTANCE as glucose)

85
Q

Can a pt have only 1 type of shock at a time?

A

NO

A pt can have several different types of shock, for example a septic pt will start off as distributive shock but may develop into cardiogenic shock as the myocardium begins to become ischemic and as contractility fails, it becomes cardiogenic shock. But septic shock is still the MAIN source

86
Q

What is the primary therapy for hypovolemic shock?

A

Rapid Fluid Administration!

Other components include:

  • identifying type of volume loss (hemorrhagic or not)
  • replacing volume deficit
  • preventing and replacing ongoing losses
  • restoring acid-base balance
  • correcting metabolic derangements
87
Q

How much fluid loss constitutes clinical dehydration?

A

After a pt has lost at least 5% volume, is equates to about 50mL/kg or more, the pt is clinically dehydrated.

B/c of this giving the initial fluid bolus of 20mL/kg may be insufficient to completely correct dehydration. Conversely, it is not really necessary to replenish ALL lost fluids within the first hour; the total fluid deficit can be corrected over the next 24-48 hours.

Basically so long as the pt receives the initial 20mL/kg fluid bolus WITHIN THE FIRST HOUR then pt outcome is much better

88
Q

Hemorrhagic VS Nonhemorrhagic Hypovolemic Shock

A

NONHEMORRHAGIC volume loss contains electrolyte containing fluids through things like diarrhea, vomiting, and osmotic diuresis; as well as protein & electrolyte containing fluids from things like burns and peritonitis.

89
Q

LOOK AT STAGES OF DEHYDRATION ON PGS 206 AND 207, IT GIVES RANGES OF FLUID LOSS ASSOCIATED TO WHAT S&Ss YOU MAY SEE

A

LOOK AT STAGES OF DEHYDRATION ON PGS 206 AND 207, IT GIVES RANGES OF FLUID LOSS ASSOCIATED TO WHAT S&Ss YOU MAY SEE

90
Q

What is the 3mL to 1mL rule?

A

It relates to HEMORRHAGIC SHOCK in that for every 1mL of blood lost from bleeding, administer 3mL of isotonic crystalloid

IT MAY BE NECESSARY TO GIVE 3 BOLUSES OF 20ml/kg TO FIGHT HEMORRHAGIC SHOCK, THIS MEANS UP TO 60 ml/kg
(I believe this is similar to the recommendation for septic shock as needed)

91
Q

What is Crystalloid-refractory hemorrhagic shock?

A

Hypotension that persists despite the admin of 40-60ml/kg of a crystalloid solution

92
Q

When is sodium bicarb indicated and not indicated when metabolic acidosis is present?

A

Sodium Bicarb is NOT INDICATED when the metabolic acidosis is caused by hypovolemic shock, this is because so long as fluid resuscitation is administered and improves end-organ function, then metabolic acidosis will be well tolerated as it is gradually corrected.

Sodium Bicarb IS INDICATED when metabolic acidosis is caused by significant bicarbonate loss from renal or gastrointestinal losses (a non-anion gap metabolic acidosis)

93
Q

What are the 3 primary goals of the initial management of septic shock? Anaphylactic shock? Cardiogenic Shock?

A

Septic Shock Goals:

  • restoration of hemodynamic stability
  • support of organ function
  • identification and control of infection

Anaphylactic Shock Primary Goal:
- Treating life threatening cardiopulmonary problems and reversing or blocking the mediators released as part of the uncontrolled allergic response

Cardiogenic Shock Primary Goal:
- improve the effectiveness of cardiac function and cardiac output by increasing the efficiency of ventricular ejection.

94
Q

When dealing with a distributive shock pt, the first thing to do is to give fluid resuscitation. But what is the next step if the BP stays low despite fluids or if the diastolic pressure remains low with a wide pulse pressure?

A

Give Vasoactive agents!

95
Q

For a fluid refractory septic shock pt, which vasoactive med is preferable as a next step: epinephrine, norepinephrine, or dopamine?

A

Epinephrine and Norepinephrine are considered to be equally sufficient but both are better than dopamine.

The book says that epi is preferred for ped with septic shock and cold extremities

96
Q

What may be wrong if the septic child is fluid refractory and epi/norepi resistant?

A

They probably have an Adrenal insufficiency, especially if they have a history of it (like prolonged steroid users)

If this is suspected administer 1-2mg/kg of Hydrocortisone IV bolus early.

97
Q

What is a main concern in forming a treatment plan for a patient with cardiogenic shock?

A

The regular amount of fluids given in other forms of shock may WORSEN the patient.

Only give small fluid boluses (5-10ml/kg) over longer periods of time 10-20min and monitor frequently!

98
Q

Specific management recommendations for the different causes of obstructive shock`

A

Ductal Dependent:

  • prostaglandin E1
  • Expert Consultation

Tension Pneumo:

  • Needle Decompression
  • Tube Thoracostomy

Cardiac Tamponade:

  • Pericardiocentesis
  • 20mL/kg NS/LR bolus

PE:

  • 20mL/kg NS/LR bolus repeat PRN
  • Consider thrombolytics, anticoagulants
  • Expert Consultation
99
Q

What are acceptable sites for IO access?

What are 3 contraindications for IO access?

A
  • Proximal Tibia (just below the growth plate)
  • Distal Tibia (just above the medial malleolus)
  • Distal Femur
  • Anterior-Superior iliac spine
  • New drills allows for Proximal Humerus in older children, adolescents, and adults

Contraindications:

  • fractures or crush injury near the site
  • conditions with fragile bones
  • previous attempts to establish access in the same bone

REVIEW IO ACCESS PROCEDURE ON PG 223 (main take away is for the normal spot at proximal tibia, place insertion 1-3cm or 1 finger width below the tibial tuberosity)