SHOCK AND ITS MANAGEMENT

Presented By

Dr. Jobaida Parvin

&
Dr. Ismat Jahan Shimi
Dept of Paediatrics, DMCH
 Objectives
• What is shock
• Types and etiology of shock
• Pathophsiology of shock
• Signs of shock
• Management of different types of shock
 DEFINITION

Shock is an acute, dramatic syndrome,

characterized by inadequate circulatory
provision of oxygen, so that the metabolic
demands of vital organs or tissues are not met.
 CLINICAL CLASSIFICATION OF SHOCK

• HYPOVOLEMIC
• Water Loss (diarrhea, vomiting with poor PO
intake, diabetes, major burns)
• Blood Loss (obvious trauma; occult bleeding
from pelvic fractures, blunt abdominal trauma)

• SEPTIC
Bacterial, viral, fungal.
 Clinical classification of shock

CARDIOGENIC
Cardiogenic shock may occur
as a complication of—
• Severe cardiac dysfunction
before or after cardiac surgery
• Congenital heart disease
• Severe burn
• Arrhythmia
• Cardiomyopathy
• Myocarditis
• Myocardial infarction
• Acute central nervous system
disoder
• DISTRIBUTIVE- Etiologies
• Anaphylaxis
• Anaphylactoid reactions
• Spinal cord injury/spinal
shock
• Head injury
• Early sepsis
• Drug intoxication--
Barbiturates,
Phenothiazines,
Antihypertensives
• OBSTRUCTIVE
Causes:
•Pericardial tamponade
•Tension pneumothorax
•Critical coarctation of
the aorta
•Aortic stenosis
•Hypoplastic left heart
syndrome
 PATHOPHYSIOLOGY
Extracorporeal fluid Hypovolemic shock may be due to direct blood
loss loss through hge or abnormal loss of body fluids

Hypovolemic shock may also result

Lowering plasma oncotic from hypoprotinaemia
forces
Distributive shock occurs when there is loss of
Abnormal vasodilatation vascular tone( venous, arterial or both)

Sepsis may change vascular

permeability in the absence of any
Increased vascular permeability change in capillary hydrostatic
pressure( endotoxin from sepsis,
histamine release in anaphylaxis

Peripheral hypoperfusion may result from

Cardiac dysfunction any condition that affects hearts pumping
action (ischemia, acidosis, drugs, sepsis,
constrictive pericarditis)
 Stages of shock
•Initial nonprogressive
•Progressive stage
•Irreversible stage
 Compensatory mechanism
• Baroreceptor reflexes
• Release of catecholamine
• Activation of renin-angiotensin axis
• Antidiuretics hormone release
• Generalized sympathetic stimulation
• Renal conversion of fluid
• Peripheral vasoconstriction
• Maintenance of blood flow in vital organ
 Events in non progressive stage
• Widespread tissue hypoxia
• Anaerobic glycolysis with excessive production of
lactic acid
• Metabolic latic acidosis lowers tissue pH & blunts
vasomotor response
• Arteriols dilatation causes peripheral pooling of blood
• Decreased CO
• Endothelial injury with subsequent DIC
 Events in irreversible shock
• Widespread cell injury is reflected in lysosomal
enzyme leakage
• Profound decrease in effective circulation
• Multi organ failure
• Myocardial contractile function worsens due
to nitric oxide synthesis
• Superimposed endotoxic shock
• Acute renal shutdown due to renal tubular
necrosis
 Signs of Decreased Perfusion

Organ System Perfusion Perfusion Perfusion

CNS ------- Restless, Apathetic, Agitated, Stuporous,

Anxious Coma

Resp ------- Ventilation Ventilation

Metabolism ------- Compensated Met Uncompensated Met

Acidosis Acidosis

Gut -------- Motility Ileus

Kidney Urine Volume Oliguria(<0.5ml/Kg/Hr) Oliguria/Anuria

Urinary Sp Gravity

Skin Delayed Capillary Refill Cool Extremities Mottled, Cyanosis, Cold

Extremities

CVS Heart Rate Heart Rate

Heart Rate Hypotension
Peripheral Pulse Central Pulses Only
 Evaluation
• Regardless of the cause: ABC’s
– First assess airway patency, ventilation, then
circulatory system
• Respiratory Performance
– Respiratory rate and pattern, work of breathing,
oxygenation (color), level of alertness
• Circulation
– Heart rate, BP, perfusion, and pulses, liver size
– CVP monitoring may be helpful
 Evaluation Continued

• Early signs of shock

– Sinus tachycardia
– Delayed capillary refill
– Fussy, irritable
• Late signs of shock
– Bradycardia
– Altered mental status (lethargy, coma)
– Hypotonia
– Cheyne-stokes breathing
– Hypotension is a very late sign
– Lower limit of SBP = 70 + (2 X age in years)
In addition to these sign skin(temp, color, turgor, presence of
rash), mucus membrane(color, moistness), urine output should
be evaluated.
Treatment
Airway management
– Always provide supplemental oxygen
– Endotracheal intubation and controlled
ventilation is suggested if respiratory failure or
airway compromise is likely
• Elective is safer and less difficult
• Decrease negative intrathoracic pressure
• Improved oxygenation and O2 delivery and
decreased O2 consumption
• Can hyperventilate if necessary
 Treatment Continued

Circulation
– Based on presumed etiology
– Rapid restoration of intravascular volume
• PIV-if unstable you have 60-90 seconds
• I.O. if less than 4-6 years old
• Central venous catheter
• Use isotonic fluid: NS, LR, or 5% albumin
• PRBC’s to replace blood loss or if still unstable after
60cc/kg of crystalloid
– anemia is poorly tolerated in the stressed, hypoxic,
hemodynamically unstable patient
GENERAL MANAGEMENT OF
SHOCK
 Sign of hypoperfusion Airway, ventilation,IV access.
Send blood for investigations

Assess volume status.periphery cool or warm

Hypovolemia,cool Hypovolemia, warm Hypervolemia, history

periphery,obvious loss periphery, signs of sugesstive of cardiac disease
infection

Hypovolemic shock Cardiogenic or obstructive shock

Septic shock

Control ongoing loss Correct volume status

Replace volume Replace volume
Antibiotic adm Relieve obstruction
Consider blood trans

If signs of hypoperfusion persist, reasses the patient for further evaluation and
management
 Assess and maintain ABC within 5 min

Start fluid therapy 20ml/kg over 15-20 min

If no improvement
2nd bolus 20 ml/kg over 15-20 min
3rd bolus 20ml/kg over 15-20 min

Dopamin and or Dobutamin @ 10mcg/kg/min

within 60 min

Fluid refractory and Dopamin/ Dobutamin resistant

shock

Shift to PICU Reassess and further Mx according

to cause
 Treatment Continued

• Volume resuscitation is of paramount

importance in supporting the child with
shock. At least two separate intravenous
(IV) lines are required to administer fluids
and necessary medications. Intraosseous
infusion may be used when peripheral
vascular access cannot be obtained rapidly.
 Treatment Continued

• An intraosseous needle or bone marrow

aspiration needle is inserted into the lower
extremity on the flat surface of tibia 1-3cm below
the tibial tubersity until a fall in resistance is felt.
Frequently a small amount of bone marrow can
be aspirated to confirm placement, and fluid
should infuse easily without evidence of soft-
tissue swelling. The technique is most successful
in children younger than age 6, but it may be
employed in older children.
 Treatment Continued

Sites of intraosseous infusion

 Drugs used in Shock
DOSE
DRUG
Dopamine 5 to 10 mcg/kg per minute (inotropic dose)
10 to 20 mcg/kg per minute (vasopressor dose)

Dobutamine 2 to 20 mcg/kg per minute

Epinephrine 0.1 to 0.3 mcg/kg per minute (inotropic dose)
0.3 to 2 mcg/kg per minute (vasotropic dose)

Norepinephrine 0.05 to 1 mcg/kg per minute

Milrinone 50 to 75 mcg/kg loading dose over 10 to 60 minutes,

followed by infusion of 0.5 to 1 mcg/kg per minute
 Drugs used in Shock
DRUG INFUSION INFUSION RATE
PREPARATION
Dopamine Body weight in kg x 6 = 1 mL/h = 1 mcg/kg per minute
Dobutamine Amount of drug (mg) to be (Example: to deliver 10 mcg/kg
added to total volume of per minute, run infusion at 10
100 mL IV fluid mL/h)
Epinephrine Body weight in kg x 0.6 = 1 mL/h = 0.1 mcg/kg per minute
Norepinephrine Amount of drug (mg) to be (Example: to deliver 0.3 mcg/kg
Milrinone added to total volume of per minute, run infusion at 3
100 mL IV fluid mL/h)
Newer agent
Dopexamine increase CO and reduces
afterload.
Dose 0.5-6 mcg/kg/min
 Metabolic Issues
Electrolytes
• Electrolytes
– Calcium is important for cardiac function and
for the pressor effect of catecholamines
– Hypoglycemia can lead to CNS damage and is
needed for proper cardiovascular function
– Check the BUN and creatinine to evaluate
renal function
– Hyperkalemia can occur from renal
dysfunction and/or acidosis
 Metabolic Issues
Acid-Base
• Metabolic acidosis develops secondary to tissue
hypoperfusion
• Profound acidosis depresses myocardial contractility and
impairs the effectiveness of catecholamines
• Treatment:
o Fluid administration and controlled ventilation
o Treatment of underlying cause
o Bicarbonate should be given only for severe acidosis that
fails to respond to adequate resuscitation.
 Monitoring of a Patient with
Shock
• Hourly temperature recording
• Blood pressure measurement
• Volume and character of pulses
• Respiration
• Pulse oximetry
• Hourly urine output
• Measurement of ongoing loss
• Strict fluid balance monitoring
• Central venous pressure
• Frequent blood glucose monitoring (younger infants)
• Arterial blood gas monitoring

Ref: Hand book of PICU Protocols

 Laboratory evaluation
• Investigation to find out etiology of shock
• Evaluate hemoglobin, hematocrit, and platelet count
– Should be followed as these values may drop after
fluid resuscitation
• Shock from any etiology can lead to DIC and end organ
damage
– CBC, PT, INR, PTT, Fibrinogen, Factor V, Factor VIII, D-
dimer, and/or FDPs
– Check LFT’s, follow CNS and pulmonary status
 HYPOVOLEMIC SHOCK

Most common cause of shock in children

• Low preload leads to decreased SV and
decreased CO.
• Compensation occurs with increased HR and
SVR

• Supine hypotension and tachycardia are the

hallmark of hypovolemic shock
 Hypovolemic Shock

BLOOD
PRESSURE

PERIPHERAL VASCULAR
CARDIAC OUTPUT RESISTANCE

HEART RATE STROKE VOLUME

PRELOAD CONTRACTILITY AFTERLOAD

 Internal or external fluid loss

What happens in Decreased intravascular fluid volume

hypovolemic
shock ? Diminished venous return

Reduced preload(filling pressure)

Decreased stroke volume

Lowered cardiac output

Reduced mean arterial blood pressure

Decreased tissue perfusion

Reduced oxygen and nutrient delivery to cells

Multiple organ dysfunction syndrome

 TREATMENT
• Mainstay of therapy is fluid
• Goals
– Restore intravascular volume
– Correct metabolic acidosis
– Treat the cause
• Degree of dehydration
– Reassess perfusion, urine output, vital signs
• Isotonic crystalloid
– 20 to 60 ml/kg rapidly if cardiac function is normal
 Inotropic and vasoactive drugs are not a substitute for fluid.
Pt with hypovolemic shock may occasionally have poor cardiac output despite
appropriate preload if myocardium is ischemic, in such situation Dopamine is required.
– Can have various combinations of hypovolemic and septic and cardiogenic
shock

Hemorrhagic Shock
Treatment is PRBCs or whole blood
– Treat the cause if able (stop the bleeding)
– Transfuse if significant blood loss is known or if patient
unstable after 60ml/kg crystalloid
 Special situation
Heamorrhagic shock encephalopathy
syndrome
• Unusual form of shock initially look similar to heat stroke
• Seen in children younger than 3 yr old
• Characterized by encephalopathy, fever, shock, watery
diarrhoea, DIC and renal and hepatic dysfunction
• May develop seizure and other severe neurologic finding
due to cerebral edema
• Treatment- fluid therapy and supportive care for renal and
hepatic function
• Mortality high and survivors have high incidence of
neurologic problems.
 SEPTIC SHOCK
Septic shock is defined as sepsis plus
cardiovascular organ dysfunction
manifested by the persistence of
hypoperfusion or hypotension for > 1 hr
despite adequate fluid resuscitation or a
requirement for inotropic agents or
vasopressors.
 infants and
children children with
3 mo to 3 yr serious injuries

children on
chronic anti- Who malnourishedc
hildren
bacterial therapy
are at
risk ?

children with Children who are

chronic medical immune
problem suppressed
 Causative organisms
In neonate -- group B strept
Escherichia coli
Listeria monocytogenes
enterovirus
herpes simplex virus

In older children
Streptococcus pneumoniae
Neisseria meningitidis
Staph aureus(methicillin sens or resistant)

In immunocompromised and hospitalized pt- Escherichia coli,

pseudomonas
klebsiella,
Acinetobacter
Enterobacter
Serratia
 PATHOGENESIS

Septic shock

Hypovolemic Cardiogenic Distributive

Intravascular fluid
losses occurs Myocardial- Result of decreased
through capillary depressant effect systemic vascular
leak of sepsis resistance
 PATHOGENESIS
• It is important to distinguish between the infection and host
response to the infection, the inflammatory process.
• This host immune response produces an inflammatory cascade of
highly toxic mediators, including hormones, cytokines, and
enzymes.
• If this inflammatory cascade is uncontrolled, SIRS occures with
subsequent organ and cellular dysfunction from derangement of
microcirculatory system
PATHOPHYSIOLOGY OF SEPTIC
PROCESS
 Superantigens and
Focus of infection
endotoxin

Activated inflammatory cell Activation of host defence

Activation of Activation of
complement system coagulation system
Activated endothelium-increased
expression of endo derived adhesion
molecule
Decreased thrombomodulin, increased
plasminogen activator inhibitor
Thrombosis and antifibrinolysis
Endogenous mediator release
Pro-inflammatory cytokines
Anti-inflammatory cytokines
Platelet activating factors
Arachidonic acid metabolite
Myocardial depressant
substance
Endogenous opiates

Hypovol, cardiac and vascular failure,

capillary leak, ARDS, DIC, decreased steroid
synthesis
DEATH
SHOCK MODS
 Clinical Features
Initial sign symptoms-
-alteration in temp regulation
- tachycardia
- tacypnea
Hypotension(sys art pressure <2 SD below the mean for age).
Signs of poor cardiac output-
-delayed capillary refill
-diminished peripheral and central pulses
-cool extremities
-decreased urine output
-alteration in mental status( confusion, agitation, lethargy,
anxiety, coma.
 Cutaneous lesions- petechiae, diffuse erythema,
ecchymoses, ecthyma gangrenosum and
symmetric peripheral gangrene
Jaundice can be seen either as a sign of
infection or as a result of MODS.
Patient may also have evidence of focal
infection such as meningitis, pneumonia,
arthritis, cellulitis or pyelonephritis.
 Septic shock

Septic shock has 2 phases:

Early or Warm shock- occurs in some patients with
- increased hyperdynamic cardiac output and
- decreased systemic vascular resistance.
- manifested by bounding pulse, widened pulse pressure

Late or Cold shock- occurs in other patients with

-decreased cardiac output
-elevated systemic vascular resistance.
-manifested by poor peripheral perfusion(prolonged capillary
refill)
In both cases ,perfusion to major organ systems may be compromised.
 MANAGEMENT
RECOMMENDED STEPWISE SUPPORTIVE CARE AND CLINICAL
PARAMETERS FOR THE HEMODYNAMIC SUPPORT OF PEDIATRIC
PATIENTS WITH SEPTIC SHOCK—

Designed by American College of Critical

Medicine and American heart association.
 First 5 min
Recognition: altered mental status and perfusion
Treatment: maintain airway and establish vascular access

5-15 minutes
Push 20ml/kg isotonic crystalloid or colloid up to and over 60ml/kg
Correct hypoglycemia and hypocalcemia

Fluid refractory
Fluid responsive Establish central venous pressure, start dopamin10-
shock -observe 20µgm/kg /min, establish arterial monitoring

Fluid refractory, dopamin resistant

shock
Dopamin
responsive-
observe Cold shock Warm shock
Titrate epinephrine Titrate norepinephrine
0.1-1μgm/kg/min 0.1-2 μgm/kg/min
 Cold shock
Titrate epinephrine 0.1-1μgm/kg/min

60 min
Catecholamine responsive-observe Catecholamine resistant shock
At risk for adrenal insufficiency?
Normal blood
pressure, cold Yes No
shock, SVC sat Give hydrocortisone 50 mg/kg/day
<70%
Low blood pressure, cold Low blood pressure warm shock
shock, SVC SO2< 70%
Add vasoilatory or
type III Titrate volume and
phosphodiesterase Titrate volume and norepinephrine
inhibitor, plus epinephrine-observe Low dose vasopressin
volume observe observe

Persistant catecholamine resistant shock

Place pulm art cath
Direct therapy:fluid, vasopressor, vasodilator and
inotropeic support to attain normal MAP, CVP and CI>3.3
and <6 L/min/m2 Consider ECMO
• Antibiotic therapy
• Anemia should be treated in the setting of
septic shock to improve delivery of oxygen
to the tissues.
• Treatment of hypoglycaemia and
hypocalcemia
•Immunomodulator soluble TNF receptors, IL-1
receptor antagonists, bactericidal permeability-
increasing protein, and endogenous anti-endotoxin
antibody.
•Another approach has been to modify the cellular
effects of the cytokines, most notably through
inhibition of nitric oxide. No large pediatric studies
have been performed, but preliminary data are
encouraging. Until more data become available, the
cornerstone of management remains aggressive
supportive care.
 CARDIOGENIC SHOCK
• It is characterized low cardiac output and
hypotension and therefore results in inadequate
tissue perfusion.
• The pump fails.
• Cardiac output decreases.
• Hypotension ensues.
• Heart rate increases to compensate for hypotension.
• Oxygen demand exceeds supply.
• Peripheral vasoconstriction occurs.
 Cardiogenic Shock

BLOOD PRESSURE

CARDIAC OUTPUT PERIPHERAL VASCULAR

RESISTANCE

HEART RATE STROKE VOLUME

PRELOAD CONTRACTILITY AFTERLOAD

 Management

•Patient with cardiogenic shock presents with cool

extremities, delayed CRT, poor peripheral and central
pulses, tachypnoea, increased obtundation, decreased
urine output.

•Treatment is aimed at reinstitution of adequate cardiac

output and peripheral perfusion

• management of the underlying cause.

• The ideal agents optimize Cardiac output while

decreasing SVR.
• Administration of oxygen
• Administration of inotropes
Dopamine is the 1st line agent.
Dobutamine improves systolic function and
decreases SVR without a significant increase in
heart rate.
MiIrinone provide diastolic relaxation and
improve ventricular preload
Epinephrine- in pt with persistant, profound
hypotension.
• Administration of vasodilator-(Nitroprusside, Nitroglycerine, PGE1)
Some pt may show signs of high SVR(diagnosed by poor peripheral perfusion and
acidosis) despite adequate CO with the support of inotropes.
• The use of cardiac glycoside to treat acute low cardiac output states should be
avoided.
-Digoxin has a slower effect than catecholamine, even with IV administration.
- in cardiovascular shock pt usually have compromised renal perfusion, so adm
of digoxin may result in high persistant blood level.

When digoxin is required for these pt, a lower and less frequent dosage should be
used and S. digoxin level must be monitored frequently.
• Pt with deteriorating cardiogenic shock may
benefit from
-Left ventricular assist device(LVAD)
- Right and left ventricular assist
device(BiVAD)
- Extracorporeal membrane
oxygeation(ECMO)
- Heart transplantation
 Obstructive Shock
• Low CO secondary to a physical
obstruction to flow
• Compensatory increased in SVR
• Initial clinical presentation can be identical
to hypovolemic shock
• Initial therapy is a fluid challenge.
•Initial therapy is a fluid challenge
•Treatment of underlying cause
-pericardial drain, chest tube, surgical
intervention
-if the patient is a neonate with a ductal
dependent lesion then give PGE
•Further evaluation, invasive monitoring,
pharmacologic therapy, appropriate consultation to
be done according to cause
 Distributive Shock
• It is characterized by high CO and low SVR (opposite
of hypovolemic, cardiogenic, and obstructive)
• Maldistribution of blood flow causing inadequate
tissue perfusion
• Due to release of endotoxin, vasoactive substances,
complement cascade activation, and microcirculation
thrombosis
• Early septic shock is the most common form
 Distributive Shock

BLOOD
PRESSURE

PERIPHERAL VASCULAR
CARDIAC OUTPUT RESISTANCE

HEART RATE STROKE VOLUME

PRELOAD CONTRACTILITY AFTERLOAD

• Treatment- initial fluid therapy.
• Epinephrine is the treatment of choice for pt
with anaphylactic shock
• Phenylephrine and vasopressin causes
vasoconstriction and may be considered in the
treatment for pt with spinal cord injury
 Shock in neonate

Etiology of shock in neonate

A. Hypovolemic shock (may be secondary to antepartum or
postpartum blood loss):
Antepartum blood loss(Associated very often with asphyxia)
-Abruptio placentae
-placenta previa
- twin-twin transfusion
-Fetomaternal hge
Postpartum blood loss:
-Coagulation disorder
-Vitamin K deficiency
- Iatrogenic causes(loss of an art catheter)
-Birth trauma
B. Septic shock –usually involves gram-
negative organism
C. Cardiogenic shock:
Birth asphyxia
Metabolic problems
Congenital heart disease
Arrhythmias
D. Neurogenic shock:
birth asphyxia
Intracranial hge
E. Drug induced hypotension
F. Endocrine disorder
G. Extreme prematurity
 management

A. Hypovolemic shock
-volume expansion using intravenous
crytalloid.Colloids are to be used with caution.
-Blood replacement therapy
B. Septic shock
-obtain blood culture
- give empiric antibiotic therapy
-volume expansion and inotropic agent
-Use of steroid is controversial
C. Cardiogenic shock:
-Treat arrhythmia if present
-correct metabolic causes
- Give inotropes: Dopamine is drug of first choice. If
dopamine fails to improve BP, Dobutamine is
recommended as second line drug. In neonates, it is usually
given together with dopamine infusion.
- Epinephrine and isoproterenol are sometimes used.
D. Neurogenic shock:
- volume expansion and inotropic agents
E. Drug induced hypotension:
-volume expansion
- discontinuation of offending drugs
F. Endocrine disorder:
- Adrenal hge is treated with volume
expansion, blood replacement and corticosteroids
- Congenital adrenal hyperplasia is treated with
corticosteroid.
G. Hypotension of ELBW infants
- antenatal steroid
-physiologic doses of hydrocortisone
- dopamine
 PEM with shock

How to give IV fluids for shock in a child with

severe malnutrition?
• Insert an IV line (and draw blood for
emergency laboratory investigations)

• Give IV fluid 15 ml/kg over 1 hour.

• Check pulse and R/R every 5-10minutes
If there are signs of improvement (pulse and
respiratory rates fall):
• repeat IV 15 ml/kg over 1 hour; then
• switch to oral or nasogastric rehydration
with ReSoMal 10 ml/kg/h up to 10 hours;
• initiate feeding with F-75
If the child fails to improve after the first 15ml/kg
IV, assume the
• child has septic shock:
• give maintenance IV fluid (4 ml/kg/h)
• blood transfusion10 ml/kg slowly over 3 hours
(use packed cells if in cardiac failure)
• start antibiotic treatment
If the child deteriorates during the IV rehydration (R/R increases
by 5 breaths/min or pulse by 15 beats/min), stop the infusion
because IV fluid can worsen the child’s condition.
 TAKE HOME MESSAGE
• Goal of therapy is identification, evaluation, and treatment of
shock in its earliest stage
• Initial priorities are for the ABC’s
• Fluid resuscitation begins with 20cc/kg of crystalloid or
10cc/kg of colloid
• Subsequent treatment depends on the etiology of shock and
the patient’s hemodynamic condition
• Successful resuscitation depends on early and judicious
intervention
• Aggressive resuscitation except if cardiogenic
• Consider Vasopressors if hypotensive despite fluids
TH

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