2. Objectives
• By the end of this workshop, the learner will be
able to:
• Differentiate between septic and cardiogenic
shock states according to clinical assessment
and evaluation
• Generate a therapeutic/diagnostic plan
according to institutional and SCCM guidelines
where applicable
3. What is shock?
a. BP less than 5th percentile of age normal
b. Uncontrolled fluid loss/blood loss
c. Tachycardia and hypotension
d. Acidosis and increased lactate
e. Signs of organ dysfunction with decreased
UOP, altered mental status, etc.
4. Pediatric Shock
• Definition – what it is and what it is not
• Pathophysiology
• Recognition – early is key!
• Management- guidelines
• Case scenarios
• Ask for references, and you shall receive
6. Pediatric shock
• Cellular pathology
• Has nothing to do with blood pressure (until very late),
cardiac output, heart rate
• Inability to meet the metabolic demands (=oxygen) of the
tissue – or inability of the cell to use oxygen
• Supply-demand imbalance
7. What is shock?
• A hemodynamic abnormality that leads to inability to meet
tissue metabolic demands.
• Dynamic, progressive.
• A systemic reduction in tissue perfusion decreased
tissue O2 delivery.
• A shift to anaerobic metabolism
• Less efficient – 20-fold less ATP generated
• Leads to lactic acidosis
• Over time, progresses to,
• Cell membrane ion pump dysfunction
• Cellular edema, leakage of cells’ contents
• Inadequate regulation of intracellular pH
• Cell death, organ failure, cardiac arrest, and death.
9. Vocabulary
• CO –cardiac output
• CI cardiac index – CO indexed to BSA
• SVR, SVRI - systemic vascular resistance
• PVR,PVRI – pulmonary vascular resistance
• MAP – mean arterial pressure
• CVP – central venous pressure
• SV – stroke volume
• PAP – pulmonary artery pressure
• DO2 – oxygen delivery
• VO2 – oxygen consumption
10. Vocabulary - II
• CO – cardiac output: volume of blood ejected by the heart
in one minute 4-8 L/min
• Heart rate
• Stroke volume
• Contractility
• Afterload
• Preload
• SVR = MAP – CVP / CO
11. Oxygen Delivery – DO2
• Oxygen delivery= CO X CaO2 (Arterial oxygen content)
• CO=Heart rate X Stroke volume
• Stroke volume depends on preload, afterload and
contractility
•Arterial Oxygen content (CaO2) =
Hb x Sa02 x 1.34 +(0.003 x Pa02)
12. Oxygen Consumption – VO2
• VO2 = CO x (CaO2 – CvO2)
• Under normal conditions DO2 >> VO2 (physiological
reserve) – this is why you can exercise and don’t die
18. Shock – signs and symptoms
• Evidence of end organ hypoperfusion
• Decreased urine output
• Altered mental status
• Poor peripheral perfusion
• Metabolic dysfunction
• Lactic acidosis
• Altered metabolic demands
19. Shock: Feel the feet, look at the neck
• Tachycardia? - Non-specific, but early
• Skin changes? - Prolonged cap refill (vasoconstriction) with
compensated shock. Flash refill with early distributive shock and with
irreversible shock.
• Pallor? – If Hb is fine, is your patient acidotic
• Impaired mental status? – Fussy, irritable? Sleepy?
• Oliguria? – When was the last diaper?
• Hypotension? – You have missed the ball
• Widened pulse pressure (>40 mmHg)? - distributive shock, aortic
insufficiency, AVMs?
20. Compensatory Mechanisms
• Baroreceptors-In aortic arch and carotid sinus, low MAP
cause vasoconstriction, increases BP, CO and HR
• Chemoreceptors- Respond to cellular acidosis, results in
vasoconstriction and respiratory stimulation
• Renin Angiotensin Aldosterone - Decreased renal
perfusion leads to angiotensin causing vasoconstriction
and aldosterone causing salt and water retentions
• Humoral Responses-Catecholamines
• Autotransfusion-Reorientation of extravascular fluid
21.
22. Stages of Shock
• Compensated Shock:
• Cardiac output (HR x SV) and systemic vascular resistance (peripheral
vasoconstriction) work to keep BP within normal limits.
• Tachycardia; decreased pulses & cool extremities in cold shock; flushing
and bounding pulses in warm shock; oliguria; may have mild lactic acidosis
• Uncompensated Shock:
• Compensatory mechanisms are overwhelmed.
• Hypotension, altered mental status; increased lactic acidosis
• Generally quick progression to cardiac arrest.
• Irreversible Shock:
• Irreversible organ damage, cardiac arrest, death.
26. Classifications of Shock
• Hypovolemic Shock
• Decreased preload due to
internal or external losses.
• Distributive Shock
• Decrease in SVR, with
abnormal distribution of
blood flow functional
hypovolemia, decreased
preload.
• Typically, NL or CO.
• Cardiogenic Shock
• “Pump failure.” CO,
systolic function.
• Obstructive Shock
• Outflow from left or
right side of heart
physically obstructed.
30. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE
31. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Distributive
Anaphylactic
Neurogenic
CO ↑, then ↓, SVR
↓↓
Angioedema,
respiratory distress,
stridor, wheezing,
early hypotension
Start adrenergic
support while giving
fluids, obtain
vascular access
early,
supratherapeutic
doses of inotropes
might be required
CO normal, SVR ↓ Hypotension in the
absence of
tachycardia
Support SVR with
vasopressors,
phenylephrine might
be required, give
fluids as necessary
Obstructive Preload ↓, CO ↓,
SVR normal to ↑
Tachycardia,
hypotension, JVD,
tracheal deviation if
pneumothorax,
equalization of
pressures with
elevated CVP if
invasive monitoring
in place
Rapidly fatal if
underlying process
not recognized and
reversed, fluid
boluses should be
given while
preparation is made
for emergent
drainage
32. Type of shock Mechanism of circulatory
failure
Signs and symptoms Interventions
Septic “Warm shock”
CO ↑, SVR↓
Tachycardia, bounding
pulses, warm extremities with
hypotension, hyperpnoea,
altered mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, first
choice agents vasopressors
(dopamine or norepinephrine)
“Cold shock”
CO ↓, SVR ↑
(60% of pediatric cases)
Tachycardia, poor peripheral
perfusion, diminished pulses,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg, repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy
CO ↓, SVR ↓ Tachycardia, diminished
pulses, with hypotension,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy
34. What is the goal of shock treatment ?
•Optimizing oxygen content of the
blood
•Improving volume and distribution of
cardiac output
•Reducing oxygen demand
•Correcting metabolic derangements
35. Treatment
• Overall goal: Normalization of tissue perfusion and
homeostasis
• A - airway
• Secure, patent
• Oxygen administration – 100% FiO2 (except in some cases of
cardiogenic shock)
• B - breathing
• Decrease WOB, intubation-mechanical ventilation may be
necessary (decrease oxygen consumption)
• C - circulation
• Improve cardiac output
• Ensure adequate preload – FLUIDS!!!
36. Treatment - II
• Have I mentioned fluids?
• Give lots of fluids – fast!
• Then – give some more –up to 200 ml/kg may be required
• REASSESS! (After every step/intervention)
• Pay attention to hepatomegaly, JVD, rales, worsening
respiratory distress – if your patient is not responding to
the fluids, reconsider your diagnosis
• Once you reach 60 ml/kg, consider starting vasoactive
infusions –more on this later
37. Treatment - III
• D – “derangements”
• Correct metabolic abnormalities – hypoglycemia, hypocalcemia, etc
• Etiology specific treatment
•DO NOT DELAY ANTIBIOTICS FOR
ANY REASON IF YOU SUSPECT
SEPTIC SHOCK !
• Source control
• Consider transfusion of PRBCs
38. Assessing efficacy of treatment
• Blood pressure: Normal *
• Quality of central and peripheral pulses: Strong, distal
pulses equal to central pulses.
• Skin perfusion: Warm, with capillary refill 1-2 seconds.
• Mental status: Normal.
Urine output: >1 mL/kg per hour, once effective
circulating volume is restored.
39. Sepsis
• High mortality despite improvements
• KID database : 4.2% in all-comers, 2.3% in previously
healthy, 7.8% in chronically ill
• Guidelines are not effective unless protocol driven
• Early intervention is critical – no delay is acceptable.
• Every hour spent without reversing shock increases OR of
mortality
40.
41. SIRS SEPSIS SEVERE
SEPSIS
SEPTIC SHOCK
T > 38.5 or < 36
Tachycardia
Tachypnea
WBC
SIRS +
Infection
(suspected or
proven)
SEPSIS +
CV dysfunction or
ARDS or
≥ 2 organ failures
SEPSIS +
CV dysfunction
despite >40 ml/kg
in 1 hr
2 of the above 4
66. Ischemic Heart Disease in Children
• ALCAPA
• Anomalous Left Coronary Artery arising from the Pulmonary
Artery
• Kawasaki Disease
• Aneurysms
• Other vasculitis
67.
68.
69.
70. Treatment
• Support the failing pump
• Decrease oxygen consumption/metabolic demand
• Intubation*, mechanical ventilation
• Sedation, NMB
• Prevention of fever, stress
• Consider bolus 5-10 ml/kg
• Consider PGE
• Echo early
71. Treatment - II
• Optimize contractility
• Correct metabolic derangements
• Inotropic support
• Afterload reduction
• Decongestion
• Address the underlying cause – surgery?
• Mechanical support
• ECMO
• Implantable devices, VAD, EXCOR, etc
72.
73.
74. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE
75. Question
• 13 month old patient with DCM, HR 180 (sinus), CVP 25
mm Hg, BP 55/24, lactate 4->8, SvO2 50%, cap refill of 5
seconds, best choice of action is:
a. Epinephrine gtt
b. Milrinone gtt
c. Phenylephrine gtt
d. NS bolus 20 ml/kg
e. Esmolol (B-blocker) for HR control
76. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 155,
RR 35, BP 124/73, T 102. She is somnolent. Working
diagnosis is sepsis secondary to pyelonephritis. What is
the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis
77. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 110,
RR 25, BP 124/83, T 102. She is AAO x 3 and is .
Working diagnosis is sepsis secondary to pyelonephritis.
What is the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis
78. Case 1
• 15-year-old male is just transferred to 11 WT from PICU, POD #3
from partial small bowel resection after multiple gunshot wounds
to the abdomen. The nurse calls an RRT because his HR has
increased in the last hour from 90 to 130, despite pain score of
1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP
80/50. Cap refill is >3 seconds in his cool extremities and pulses
are 1+.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your initial management?
79. Case 2
• 6-year-old previously healthy girl is transferred from West
Campus ER with fever, bloody diarrhea x 1 day. She’s had no
urine x 24 hrs and is becoming harder to awaken. On exam, her
HR is 152, BP 72/32, temp 103. She’s sleepy but arousable.
She’s flushed with capillary refill <1 second.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management? If a higher level of care is needed,
how would you obtain it?
80. Case 3
• 4-month-old boy former premie, presents to ED with decreased po
x 2 days with 2 times daily emesis, following what sounds like viral
URI. Urine output has been 3 wet diapers daily. He is afebrile
with HR 180; BP has not been obtained. He has a weak cry, is
mottled with 3-second capillary refill, pulses 1+ in all extremities.
Liver is palpable 4 cm below RCM. S4 is present without murmur.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management?
81. What is the end goal for resuscitation ?
• Mixed venous sats
• Lactate clearance
• Traditional clinical variables –
UOP, perfusion, pulses, CVP
• Combination of all three with common sense
Teacher’s GuideReferenced above: Watson RS et al. The epidemiology of severe sepsis in children in the United States, Am J Respir Crit Care Med 2003; 167:695. Bone, RC. Toward an epidemiology and natural history of SIRS (systemic inflammatory response syndrome). JAMA 1992: 268:3452.
Teachers’ Guide:(This represents hypovolemic shock.)Example questions and examples of acceptable answers: What is your assessment?15 year-old post-operative patient with sudden tachycardia and borderline low blood pressure with impaired peripheral perfusion. Suggests hypovolemic shock.2) What stage of shock? Compensated … for now, given his lack of hypotension by strict definition. Given rapidity of onset, be extremely cautious for rapid decline.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Hypovolemic shock, likely due to blood loss related to surgery; less likely septic shock (though you would be suspicious of this given the nature of his wounds) due to his physical exam findings. What is your initial management.Again, ABCDs, fluid resuscitation with 20 ml/kg crystalloid as needed to restore perfusion and blood pressure. Ensure a type and screen/cross match has been done and order PRBCs to the bedside in the event that bleeding continues. Stat baseline hemoglobin/hematocrit with repeat every 4 hrs until stable.MAIN TEACHING POINT: Hypovolemic shock is often first manifest by tachycardia and decreased peripheral perfusion. Hypotension is a late finding and indicates uncompensated shock.
Teachers’ Guide:(This represents cardiogenic shock.)Example questions and examples of acceptable answers: What is your assessment? 4 mo old with subacute onset of decreased desire to feed, emesis in setting of viral symptoms and possibly decreased urine output. Afebrile on exam with tachycardia and signs of hypoperfusion and liver distension and gallop. Suggests cardiogenic shock.2) What stage of shock? Answer is unclear given lack of available BP reading, but exam with impaired perfusion (and weak cry possibly indicating altered mental status) would suggest progression toward uncompensated shock.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Likely cardiogenic, given decreased desire to feed, emesis, impaired perfusion, distended liver, and S4. Additional information could be gained through CXR looking for cardiac enlargement and pulmonary edema, stat echo, lactate, possibly chemistry looking for acidosis due to hypoperfusion and electrolyte imbalances due to emesis, +/- BNP. What leads your differential for the etiology?Given recent viral illness, viral cardiomyopathy possible cause. What is your initial management?ABCDs, continuing to monitor blood pressure closely and ensuring sufficient access, 10 ml/kg bolus (repeated with caution and constant monitoring for worsening heart failure, as needed) to restore perfusion if altered mental status or other signs of end organ dysfunction. Stat cardiac echo (or at least bedside ultrasound). Dopamine stat to the bedside. Stat cardiology consultation.MAIN TEACHING POINT: Cardiogenic shock is marked by decreased peripheral perfusion due to decreased cardiac output. Despite increased preload in cardiogenic and obstructive shocks, fluid boluses may be needed to restore perfusion if signs of end organ dysfunction. Howerver, because patient may worsen with these boluses the volume should be small and re-evaluation should occur after each intervention.