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Resuscitation Sequence Intubation
Critical Care Updates
Pit Falls :
Dr Altaf Ahmad Bhat
Asistant consultatnt Pediatric emergency
King Fahd medical city , Riyadh
• Physiological killers during pre and peri intubation
• Epinephrine push dose
• Apnea oxygentation
• Brief NIPPV
• Approach to the Critically Ill Child: Shock
• Adverse Event Mitigation Strategy while RSI
Resuscitate Before You Intubate
• IN ADULTS :-
• Hefner AC et al and Kim WY et al evaluated over 2800 patients
requiring emergency intubation. In both trials the rate of cardiac
arrest (CA) within 10 minutes of intubation ranged from 1.7% –
2.4%. Both trials listed pre-intubation hypotension (SBP ≤90mmHg)
as a risk factor for cardiac arrest. Hefner et al also mentioned
hypoxemia as an important risk factor.
• IN KIDS :-
Physiologic killers during preintubation and
perintubation.
• Hypotension
• Hypoxemia,
• Metabolic Acidosis (pH)
• Reduce Mortality as well as morbidity
Hypotension Can kill
• Schwartz DE et al published a prospective study in
Anesthesiology 1995 which stated that pre-intubation hypotension
was the biggest predictor of CA.
• Basic Strategies:
• At secure peripheral IVs (PIVs)
• If unable to get PIVs, IO can be used as well for RSI
• Crystalloid IVF wide open
• Shoot for a higher than normal BP before intubating if possible
• In adults (SBP ≥140mmHg)
• In pediatric above 5th percentile for age and sex, after iv fluids
PUSH DOSE EPINephrine
• Systemic review of cohort studies 2a
• Both an alpha and beta agonist, increases vascular resistance and
blood pressure, but through its beta agonist effect also increases
cardiac output.
• Mixing and Dosing of Push Dose Epinephrine:
• Take a 10cc syringe of NS and get rid of 1cc (9cc left in
syringe)
• Draw up 1cc of Code Dose Epinephrine (100mcg/mL)
• This gives you 10mcg/mL of Epinephrine
• Dosing: 0.5 – 2mL (5 – 20mcg) q2 – 5minutes
• Pediatric dosing 1ug/kg
Sedatives Low & Paralytics High
• Doses of induction agents and paralytics should be adjusted according to
pre-RSI physiology.
• This means reducing the dose of your induction agent and increasing the
dose of your paralytic agent :
• Induction agents can drop BP in shock patients by decreasing vascular tone and
reducing venous return
• Some induction agents will decrease sympathetic tone (i.e. Benzodiazepines,
Propofol)
• Paralytics take longer to work in a shock state (cardiac output dependent)
• Shock by itself is a powerful anesthetic
ROCKETAMINE
• Ketamine agent of choice in shock patients
• Shock patients reduce this dose to 0.5mg/kg IV. Patients may
require subsequent doses of of 0.5mg/kg prior to paralytics being
given (be sure patient is completely sedated before pushing
paralytic).
• Succinylcholine possesses the fastest onset (45sec) and produces
the shortest period of muscle relaxation (6 – 10min) compared to
all other paralytic agents at standard doses.
• Rocuronium dosed at 1.6mg/kg IV , gives the same onset of
muscle relaxation as succinylcholine and gives a longer safe apnea
time making it the preferred paralytic of choice in the critically
ill.
Key message
• In the critically ill patient and shock state, another option to
improve hemodynamics both pre-intubation and peri-intubation
is push dose epinephrine
• In the critically ill patient and shock state, a physiologically
sound combination for induction and paralysis in RSI is
ROCKETamine (Ketamine 0.5mg/kg IV + additional doses of
0.5mg/kg until pt is fully sedated + Rocuronium 1.6mg/kg IV)
Awake Intubation
• By keeping the patient awake, they maintain their endogenous
catecholamines that may be suppressed by induction agents, thus allowing
for increased cardiac output and maintenance of vascular tone, ultimately
helping increase venous return
• How is an Awake Intubation Done:
• Spray 10cc of 4% lidocaine into the oropharynx with an EZ-Atomizer
• Apply at least 2 – 4% Topical Lidocaine to the posterior tongue with a tongue
depressor
• Spray another 5cc of 4% lidocaine just past the vocal cords
Clinical Bottom Line:
• Pre-Intubation Hypotension in adults (SBP ≤90mmHg) and pediatric
< 5th percentile for age and sex is a risk factor for Peri-Intubation
Cardiac Arrest:
• Options to Improve Hemodynamics:
• Don’t Forget the Basics (i.e. IVF)
• Use ROCKETamine, Dose Induction Agents Low and Paralytic Agents High
• Use Push Dose Epinephrine
• Use Peripheral Vasopressors Prior to Intubation
• If Time Permits, Perform the Awake Intubation
Hypoxemia can kill
• Adequate pre-oxygenation is typically defined as 8 vital capacity
breaths in a patient that can comply or 3 uninterrupted minutes of
administration of the highest achievable fraction of inspired
oxygen (FIO2).
• The purpose of preoxygenation is to provide an oxygen reservoir
from which the patient can draw once the apneic period ensues
following administration of the NMB.
• This is accomplished through the process of nitrogen washout,
(denitrogenation)which is repletion of the functional residual
capacity of the lungs with the highest possible oxygen
concentration.
• In hypoventilation or Apnea
• Tidal volume is inadequate, the proportion of dead space
ventilation increases, thereby limiting the effectiveness of
preoxygenation and placing the patient at risk for rapid
oxyhemoglobin desaturation once the NMB is administered.
• Pre oxygenation with BMV with 100% FiO2
Apneic Oxygenation
• Apneic oxygenation represents supplemental oxygen administered
via a nasal cannula that is thought to passively diffuse through the
large airways to the alveoli to supplement the oxygen reservoir
during the apneic period with a goal of prolonging the time before
oxyhemoglobin desaturation occurs
• 2 L/min for patients younger than 3 years, 4 L/min for those 3 to 8
years of age, and 6 L/min for those older than 8 years
“A Modern and Practical Review of RapidSequence Intubation in Pediatric Emergencies Matthew R. Mittiga,
MD, Andrea S. Rinderknecht, MD, Department of Pediatrics, University of Cincinnati College of Medicine,
Division of Emergency Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati”
• If you cannot get the O2 Saturation ≥95%, then consider the following:
• Lung Shunt Physiology (i.e. Pulmonary Edema, Pneumonia, )
These patients still need oxygen, but also need PEEP to recruit atelectatic
alveoli to overcome the shunt
• Intervention 1: HHFNC
• You don’t need to bag these patients,
• Bottom Line: In critically ill patients in which you cannot get O2 Sats
≥95%, consider shunt physiology and use Apneic CPAP Recruitment
Delayed Sequence Intubation (DSI)
• Procedural sedation for the procedure of preoxygenation
• Give 1mg/kg IV Ketamine -> Preoxygenate -> Paralyze the Patient -> Apneic
Oxygenation -> Intubate
• Evidence: Weingart et al Ann Emerg Med 2015
• Observational trial with >150 intubations -> 62 patients
uncooperative/combative
• Mean O2 Saturation increased from 89.9% unto 98.8%
• No Complications
• Bottom Line: In critically ill, agitated patients, who are
hypoxemic, that need to be intubated, consider using DSI, which is
procedural sedation for preoxygenation
Back Up Head Elevated (BUHE) Intubation
• Level of evidence 3:
• 528 Intubations
• Primary Outcome: Composite of Any Intubation-Related Complication
(Difficult Intubation ≥3 Attempts or > 10 min, Hypoxemia <90% O2 Sat,
Esophageal Intubation, or Esophageal Aspiration
• Primary Outcome Results:
• Standard Supine Intubation: 22.6%
• BUHE Intubation 9.3%
• Bottom Line: BUHE still needs prospective external validation in an ED
setting, but seems to decrease intubation-related complications in
comparison to standard supine intubation
pH Kills
• Try and avoid intubation in these patients if at all possible.
• Even consider a short trial of NIPPV while you try and correct the
cause of metabolic acidosis
Bicarbonate Therapy
• Forsythe et al wrote a review article on Bicarbonate Therapy in Lactic
Acidosis .
• Against the use of bicarbonate due to the fact that when giving bicarbonate
it eventually gets turned into CO2. Patients in severe metabolic acidosis
are already tachypneic in an effort to blow off CO2, so any further CO2
could make them more acidotic and lead to cardiac dysrhythmias. He lists
studies to support this contention:
• 18 Animal Studies: Increase serum pH, but Decrease Intracellular pH
• 2 Human Studies: Increase serum pH, but no improvement in hemodynamics or
catecholamine responsiveness
• Bottom Line: No controlled studies have shown improved
hemodynamics or catecholamine responsiveness due to sodium
bicarbonate infusion
Ventilator-Assisted Pre-OXygenation (VAPOX)
• If intubation does become necessary maintaining spontaneous
respirations is a critical action because maintenance of acid-
base homeostasis is dependent on a respiratory alkalosis (i.e.
hyperventilation). Even a brief apneic period can lead to
worsening metabolic acidosis leading to cardiac dysrhythmias.
• Although VAPOX is primarily used for pre-oxygenation ,helps
spontaneous respirations to avoid increase in CO2 and
worsening metabolic acidosis.
• Grant S et al, and Scott Weingart reported and have
discussed use of VAPOX in patients requiring intubation in
adults
• There are 6 settings that you need to setup
• (Before Induction Medications):
• Respiratory Rate = 0 (This lets the patient breath at their own rate)
• Tidal Volume = (6-8cc/kg of Ideal Body Weight)
• Fraction of Inspired O2 = 100%
• Pressure Support = 5 – 10cmH20 (Its hard to breath through a straw)
• PEEP = 5cmH20 (This can be titrated up to 15cmH20 if O2 sats ≥95%)
• HHFNC
• Inspiratory Flow Rate = as per weight of child (Normal ventilator
set at 60LPM; We want a slow breath so we don’t insufflate the
stomach
• Induction of Patient with RSI Meds
• Ensure the airway is open
• Turn the respiratory rate up to 12 BPM (This ensures the patient is still
blowing off CO2)
• Intubation of Patient
• The most experienced person in the room should do the intubation (We
want to ensure our best chance at 1st pass intubation)
• Attach the ventilator
• Turn the respiratory rate as required
Bottom line
• Severe Metabolic Acidosis in patients requiring intubation, if done
incorrectly can lead to severe cardiac dysrhythmias and cardiac
arrest
• The possibilities to ensure this doesn’t happen include:
• Intervention 1: Bicarbonate Therapy – This is a very controversial topic, but
no controlled studies to date have shown hemodynamic improvements or
improved catecholamine responsiveness
• Intervention 2: Ventilator-Assisted Pre-OXygenation (VAPOX) – This should
only be performed if there is someone who can use a ventilator and change
settings
Physiological understanding, Critically Ill
Child with Shock
• Shock is simply a state where tissue/organ blood flow is inadequate
to meet tissue/organ metabolic demands.
• To understand how kids with shock present differently , few basic
differences regarding intravascular volume and cardiovascular
system in children.
Physiological understanding, Critically Ill
Child with Shock
• Immature myocardial calcium regulation
• Dependent on extracellular calcium for adequate myocardial
contractility.
• Newborns and infants also have limited ability to increase
inotropic function and stroke volume and operate at a higher
baseline contractile state
• Type I collagen in myocardium less elastic .
• Rise in SVR allows the child to redistribute and preserve blood
flow to these vulnerable circulations.
• Blood pressure (diastolic more so than systolic) can be maintained
because of this compensation.
• As shock progresses, The elevated SVR presents an additional
stress on the LV in the form of increased afterload.
• Sustained tachycardia prevents diastolic filling and further
reduces preload. When these compensatory mechanisms are
exhausted, children develop hypotension.
• Therefore, hypotension, is always a late finding in pediatric shock.
• Systolic blood pressure correlating with a patient’s stroke volume
• However, as they compensate they will increase their diastolic blood
pressure, which reflects a patient’s systemic vascular resistance
(vascular tone).
• As systolic blood pressure or stroke volume is compromised, patient will
increase their diastolic blood pressure as systemic vascular resistance
increases. As their stroke volume drops and systolic blood pressure
decreases, diastolic blood pressure rises as SVR increase
• We may actually see a child with other evidence of poor perfusion
(delayed capillary refill, weak pulse strength, cold to touch), narrowed
pulse pressure with a normal overall normal blood pressure, but they are
in compensated shock. So pulse pressure represents stroke volume,
and a narrow pulse pressure should indicate to the us that our patients
stroke volume is compromised.
Adverse Event Mitigation Strategy while RSI
• Desaturation
• Adequate preoxygenation
• Minimum 3 min of 100% FIO2
Uninterrupted
• Apneic oxygenation
• Limit laryngoscopy attempt duration
based on time elapsed,
• Remove ETT if placement not confirmed
immediately with capnography (do not
wait for desaturation)
• Adequate reoxygenation between failed
attempt
• BVM with oral airway
Adverse Event Mitigation Strategy
• Bradycardia • Premedication with atropine
when indicated
1.Age <12 mo
2. Age <5 y and receiving
succinylcholine
• Any patient receiving a 2nd
dose of succinylcholine ]
• Any patient experiencing
bradycardia during
resuscitation before RSI
Adverse Event Mitigation Strategy
• Hypotention
• Inadequate paralysis
• Assess for risk and treat
preexisting hypotension
• with fluid administration
• Push dose epinephrine
• Inotropes
• Wait 45 s after NMB before
attempting laryngoscopy Careful
consideration of need to redose
sedative and NMB after failed
attempt
Adverse Event Mitigation Strategy
• Esophageal intubation
• Right main stem bronchus
intubation
• Unanticipated extubation
• Immediate capnography with
removal of ETT before
desaturation if capnography does
not confirm tracheal placement.
• Discussion of appropriate ETT
depth before placement
Auscultation to assess equality of
breath sounds Attention to
postintubation chest radiograph
• Immediate and careful attention
to postintubation sedation
•Thank You

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RSI in kids update and pitfalls

  • 1. Resuscitation Sequence Intubation Critical Care Updates Pit Falls : Dr Altaf Ahmad Bhat Asistant consultatnt Pediatric emergency King Fahd medical city , Riyadh
  • 2. • Physiological killers during pre and peri intubation • Epinephrine push dose • Apnea oxygentation • Brief NIPPV • Approach to the Critically Ill Child: Shock • Adverse Event Mitigation Strategy while RSI
  • 3. Resuscitate Before You Intubate • IN ADULTS :- • Hefner AC et al and Kim WY et al evaluated over 2800 patients requiring emergency intubation. In both trials the rate of cardiac arrest (CA) within 10 minutes of intubation ranged from 1.7% – 2.4%. Both trials listed pre-intubation hypotension (SBP ≤90mmHg) as a risk factor for cardiac arrest. Hefner et al also mentioned hypoxemia as an important risk factor. • IN KIDS :-
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  • 5. Physiologic killers during preintubation and perintubation. • Hypotension • Hypoxemia, • Metabolic Acidosis (pH) • Reduce Mortality as well as morbidity
  • 6. Hypotension Can kill • Schwartz DE et al published a prospective study in Anesthesiology 1995 which stated that pre-intubation hypotension was the biggest predictor of CA. • Basic Strategies: • At secure peripheral IVs (PIVs) • If unable to get PIVs, IO can be used as well for RSI • Crystalloid IVF wide open • Shoot for a higher than normal BP before intubating if possible • In adults (SBP ≥140mmHg) • In pediatric above 5th percentile for age and sex, after iv fluids
  • 7. PUSH DOSE EPINephrine • Systemic review of cohort studies 2a • Both an alpha and beta agonist, increases vascular resistance and blood pressure, but through its beta agonist effect also increases cardiac output. • Mixing and Dosing of Push Dose Epinephrine: • Take a 10cc syringe of NS and get rid of 1cc (9cc left in syringe) • Draw up 1cc of Code Dose Epinephrine (100mcg/mL) • This gives you 10mcg/mL of Epinephrine • Dosing: 0.5 – 2mL (5 – 20mcg) q2 – 5minutes • Pediatric dosing 1ug/kg
  • 8. Sedatives Low & Paralytics High • Doses of induction agents and paralytics should be adjusted according to pre-RSI physiology. • This means reducing the dose of your induction agent and increasing the dose of your paralytic agent : • Induction agents can drop BP in shock patients by decreasing vascular tone and reducing venous return • Some induction agents will decrease sympathetic tone (i.e. Benzodiazepines, Propofol) • Paralytics take longer to work in a shock state (cardiac output dependent) • Shock by itself is a powerful anesthetic
  • 9. ROCKETAMINE • Ketamine agent of choice in shock patients • Shock patients reduce this dose to 0.5mg/kg IV. Patients may require subsequent doses of of 0.5mg/kg prior to paralytics being given (be sure patient is completely sedated before pushing paralytic). • Succinylcholine possesses the fastest onset (45sec) and produces the shortest period of muscle relaxation (6 – 10min) compared to all other paralytic agents at standard doses. • Rocuronium dosed at 1.6mg/kg IV , gives the same onset of muscle relaxation as succinylcholine and gives a longer safe apnea time making it the preferred paralytic of choice in the critically ill.
  • 10. Key message • In the critically ill patient and shock state, another option to improve hemodynamics both pre-intubation and peri-intubation is push dose epinephrine • In the critically ill patient and shock state, a physiologically sound combination for induction and paralysis in RSI is ROCKETamine (Ketamine 0.5mg/kg IV + additional doses of 0.5mg/kg until pt is fully sedated + Rocuronium 1.6mg/kg IV)
  • 11. Awake Intubation • By keeping the patient awake, they maintain their endogenous catecholamines that may be suppressed by induction agents, thus allowing for increased cardiac output and maintenance of vascular tone, ultimately helping increase venous return • How is an Awake Intubation Done: • Spray 10cc of 4% lidocaine into the oropharynx with an EZ-Atomizer • Apply at least 2 – 4% Topical Lidocaine to the posterior tongue with a tongue depressor • Spray another 5cc of 4% lidocaine just past the vocal cords
  • 12. Clinical Bottom Line: • Pre-Intubation Hypotension in adults (SBP ≤90mmHg) and pediatric < 5th percentile for age and sex is a risk factor for Peri-Intubation Cardiac Arrest: • Options to Improve Hemodynamics: • Don’t Forget the Basics (i.e. IVF) • Use ROCKETamine, Dose Induction Agents Low and Paralytic Agents High • Use Push Dose Epinephrine • Use Peripheral Vasopressors Prior to Intubation • If Time Permits, Perform the Awake Intubation
  • 13. Hypoxemia can kill • Adequate pre-oxygenation is typically defined as 8 vital capacity breaths in a patient that can comply or 3 uninterrupted minutes of administration of the highest achievable fraction of inspired oxygen (FIO2). • The purpose of preoxygenation is to provide an oxygen reservoir from which the patient can draw once the apneic period ensues following administration of the NMB. • This is accomplished through the process of nitrogen washout, (denitrogenation)which is repletion of the functional residual capacity of the lungs with the highest possible oxygen concentration.
  • 14. • In hypoventilation or Apnea • Tidal volume is inadequate, the proportion of dead space ventilation increases, thereby limiting the effectiveness of preoxygenation and placing the patient at risk for rapid oxyhemoglobin desaturation once the NMB is administered. • Pre oxygenation with BMV with 100% FiO2
  • 15. Apneic Oxygenation • Apneic oxygenation represents supplemental oxygen administered via a nasal cannula that is thought to passively diffuse through the large airways to the alveoli to supplement the oxygen reservoir during the apneic period with a goal of prolonging the time before oxyhemoglobin desaturation occurs • 2 L/min for patients younger than 3 years, 4 L/min for those 3 to 8 years of age, and 6 L/min for those older than 8 years “A Modern and Practical Review of RapidSequence Intubation in Pediatric Emergencies Matthew R. Mittiga, MD, Andrea S. Rinderknecht, MD, Department of Pediatrics, University of Cincinnati College of Medicine, Division of Emergency Medicine, Cincinnati Children’s Hospital Medical Center, Cincinnati”
  • 16. • If you cannot get the O2 Saturation ≥95%, then consider the following: • Lung Shunt Physiology (i.e. Pulmonary Edema, Pneumonia, ) These patients still need oxygen, but also need PEEP to recruit atelectatic alveoli to overcome the shunt • Intervention 1: HHFNC • You don’t need to bag these patients, • Bottom Line: In critically ill patients in which you cannot get O2 Sats ≥95%, consider shunt physiology and use Apneic CPAP Recruitment
  • 17. Delayed Sequence Intubation (DSI) • Procedural sedation for the procedure of preoxygenation • Give 1mg/kg IV Ketamine -> Preoxygenate -> Paralyze the Patient -> Apneic Oxygenation -> Intubate • Evidence: Weingart et al Ann Emerg Med 2015 • Observational trial with >150 intubations -> 62 patients uncooperative/combative • Mean O2 Saturation increased from 89.9% unto 98.8% • No Complications • Bottom Line: In critically ill, agitated patients, who are hypoxemic, that need to be intubated, consider using DSI, which is procedural sedation for preoxygenation
  • 18. Back Up Head Elevated (BUHE) Intubation • Level of evidence 3: • 528 Intubations • Primary Outcome: Composite of Any Intubation-Related Complication (Difficult Intubation ≥3 Attempts or > 10 min, Hypoxemia <90% O2 Sat, Esophageal Intubation, or Esophageal Aspiration • Primary Outcome Results: • Standard Supine Intubation: 22.6% • BUHE Intubation 9.3% • Bottom Line: BUHE still needs prospective external validation in an ED setting, but seems to decrease intubation-related complications in comparison to standard supine intubation
  • 19. pH Kills • Try and avoid intubation in these patients if at all possible. • Even consider a short trial of NIPPV while you try and correct the cause of metabolic acidosis
  • 20. Bicarbonate Therapy • Forsythe et al wrote a review article on Bicarbonate Therapy in Lactic Acidosis . • Against the use of bicarbonate due to the fact that when giving bicarbonate it eventually gets turned into CO2. Patients in severe metabolic acidosis are already tachypneic in an effort to blow off CO2, so any further CO2 could make them more acidotic and lead to cardiac dysrhythmias. He lists studies to support this contention: • 18 Animal Studies: Increase serum pH, but Decrease Intracellular pH • 2 Human Studies: Increase serum pH, but no improvement in hemodynamics or catecholamine responsiveness • Bottom Line: No controlled studies have shown improved hemodynamics or catecholamine responsiveness due to sodium bicarbonate infusion
  • 21. Ventilator-Assisted Pre-OXygenation (VAPOX) • If intubation does become necessary maintaining spontaneous respirations is a critical action because maintenance of acid- base homeostasis is dependent on a respiratory alkalosis (i.e. hyperventilation). Even a brief apneic period can lead to worsening metabolic acidosis leading to cardiac dysrhythmias. • Although VAPOX is primarily used for pre-oxygenation ,helps spontaneous respirations to avoid increase in CO2 and worsening metabolic acidosis. • Grant S et al, and Scott Weingart reported and have discussed use of VAPOX in patients requiring intubation in adults
  • 22. • There are 6 settings that you need to setup • (Before Induction Medications): • Respiratory Rate = 0 (This lets the patient breath at their own rate) • Tidal Volume = (6-8cc/kg of Ideal Body Weight) • Fraction of Inspired O2 = 100% • Pressure Support = 5 – 10cmH20 (Its hard to breath through a straw) • PEEP = 5cmH20 (This can be titrated up to 15cmH20 if O2 sats ≥95%) • HHFNC • Inspiratory Flow Rate = as per weight of child (Normal ventilator set at 60LPM; We want a slow breath so we don’t insufflate the stomach
  • 23. • Induction of Patient with RSI Meds • Ensure the airway is open • Turn the respiratory rate up to 12 BPM (This ensures the patient is still blowing off CO2) • Intubation of Patient • The most experienced person in the room should do the intubation (We want to ensure our best chance at 1st pass intubation) • Attach the ventilator • Turn the respiratory rate as required
  • 24. Bottom line • Severe Metabolic Acidosis in patients requiring intubation, if done incorrectly can lead to severe cardiac dysrhythmias and cardiac arrest • The possibilities to ensure this doesn’t happen include: • Intervention 1: Bicarbonate Therapy – This is a very controversial topic, but no controlled studies to date have shown hemodynamic improvements or improved catecholamine responsiveness • Intervention 2: Ventilator-Assisted Pre-OXygenation (VAPOX) – This should only be performed if there is someone who can use a ventilator and change settings
  • 25. Physiological understanding, Critically Ill Child with Shock • Shock is simply a state where tissue/organ blood flow is inadequate to meet tissue/organ metabolic demands. • To understand how kids with shock present differently , few basic differences regarding intravascular volume and cardiovascular system in children.
  • 26. Physiological understanding, Critically Ill Child with Shock • Immature myocardial calcium regulation • Dependent on extracellular calcium for adequate myocardial contractility. • Newborns and infants also have limited ability to increase inotropic function and stroke volume and operate at a higher baseline contractile state • Type I collagen in myocardium less elastic .
  • 27. • Rise in SVR allows the child to redistribute and preserve blood flow to these vulnerable circulations. • Blood pressure (diastolic more so than systolic) can be maintained because of this compensation. • As shock progresses, The elevated SVR presents an additional stress on the LV in the form of increased afterload. • Sustained tachycardia prevents diastolic filling and further reduces preload. When these compensatory mechanisms are exhausted, children develop hypotension. • Therefore, hypotension, is always a late finding in pediatric shock.
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  • 29. • Systolic blood pressure correlating with a patient’s stroke volume • However, as they compensate they will increase their diastolic blood pressure, which reflects a patient’s systemic vascular resistance (vascular tone). • As systolic blood pressure or stroke volume is compromised, patient will increase their diastolic blood pressure as systemic vascular resistance increases. As their stroke volume drops and systolic blood pressure decreases, diastolic blood pressure rises as SVR increase • We may actually see a child with other evidence of poor perfusion (delayed capillary refill, weak pulse strength, cold to touch), narrowed pulse pressure with a normal overall normal blood pressure, but they are in compensated shock. So pulse pressure represents stroke volume, and a narrow pulse pressure should indicate to the us that our patients stroke volume is compromised.
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  • 34. Adverse Event Mitigation Strategy while RSI • Desaturation • Adequate preoxygenation • Minimum 3 min of 100% FIO2 Uninterrupted • Apneic oxygenation • Limit laryngoscopy attempt duration based on time elapsed, • Remove ETT if placement not confirmed immediately with capnography (do not wait for desaturation) • Adequate reoxygenation between failed attempt • BVM with oral airway
  • 35. Adverse Event Mitigation Strategy • Bradycardia • Premedication with atropine when indicated 1.Age <12 mo 2. Age <5 y and receiving succinylcholine • Any patient receiving a 2nd dose of succinylcholine ] • Any patient experiencing bradycardia during resuscitation before RSI
  • 36. Adverse Event Mitigation Strategy • Hypotention • Inadequate paralysis • Assess for risk and treat preexisting hypotension • with fluid administration • Push dose epinephrine • Inotropes • Wait 45 s after NMB before attempting laryngoscopy Careful consideration of need to redose sedative and NMB after failed attempt
  • 37. Adverse Event Mitigation Strategy • Esophageal intubation • Right main stem bronchus intubation • Unanticipated extubation • Immediate capnography with removal of ETT before desaturation if capnography does not confirm tracheal placement. • Discussion of appropriate ETT depth before placement Auscultation to assess equality of breath sounds Attention to postintubation chest radiograph • Immediate and careful attention to postintubation sedation

Editor's Notes

  1. This is the reason why the uses of Calcium Channel Blockers (ie Diltiazem, Verapamil) are contraindicated in pediatric tachydysrhythmia’s (3). Their use in the young child with a tachydysrhythmia can precipitate severe myocardial depression and even cardiac arrest. It is also a reason that the pediatric sepsis guidelines (as we will review in a later article) recommend checking ionized calcium levels and repleting calcium early. Intravenous calcium can have significant inotropic effects and may restore myocardial function and hemodynamic stability especially when ionized calcium levels are low. This is the reason why the uses of Calcium Channel Blockers (ie Diltiazem, Verapamil) are contraindicated in pediatric tachydysrhythmia’s (3). Their use in the young child with a tachydysrhythmia can precipitate severe myocardial depression and even cardiac arrest.. It is also a reason that the pediatric sepsis guidelines (as we will review in a later article) recommend checking ionized calcium levels and repleting calcium early. Intravenous calcium can have significant inotropic effects and may restore myocardial function and hemodynamic stability especially when ionized calcium levels are low.