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Vichram S Paulraj
Medical Student
OBJECTIVES
Definition
Physiology
Classification of Shock
Common Etiologies
Recognition and Assessment
Management
DEFINITION
An acute, complex state of circulatory
dysfunction that results in failure to deliver
sufficient amount of oxygen and nutrients to
meet tissue metabolic demands.
Therefore, basically DO2 < VO2.
If prolonged and left untreated- Can lead to
multiple organ failure and eventually death.
igure 1.
Hgb
CaO2
A-a gradient
DPG
Acid-Base Balance
Blockers
Competitors
Temperature
Influenced By
Oxygenation
DO2
Influenced By
Drugs
Conduction System
HR
CO
EDV
SV
CVP
Venous Volume
Venous Tone
Ventricular
Compliance
Influenced By
ESV
Contractility
Influenced By
Afterload
Temperature
Drugs
Metabolic Milieu
Ions
Acid Base
Temperature
Drugs
Toxins
Blockers
Competitors
Autonomic Tone
Heart
Vessels
Blood
Inadequate Pump
Inadequate preload
Poor contractility
Excessive Afterload
Inadequate HR
PHASES OF SHOCK
Compensated Shock
- Intrinsic regulatory mechanisms
- Vital organ function is maintained
Uncompensated Shock
- Compromise of microvascular perfusion
- Deterioration of organ function
- Hypotension develops
Irreversible Shock
- Damage to key organs
.
RECOGNITION &
ASSESSMENT
Respiratory
- Quality of Respirations
- Auscultatory Findings
Cardiovascular
- Pulse
- Blood Pressure, Pulse pressure
Skin
-Color
-Capillary Refill
-Temperature
-Moist/ Dry
SIGNS OF SHOCK
1.
2.
3.
4.
Early Signs
Tachycardia
Normal blood pressure
Mildly delayed capillary refill
Fussy child
Signs of Shock..
Late Signs
1.
2.
3.
4.
5.
6.
7.
FUNCTIONAL CLASSIFICATION
OF SHOCK
Distributive
Cardiogenic
Obstructive
Infectious
Pericardial
tamponade
CMP
Plasma loss
Fluid/
electrolyte
losses
Spinal
anesthesia
Septic
Carditis
Metabolic
Arrythmia
Tension
Pneumothorax
Pulmonary
HTN
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Hypovolemic
HYPOVOLEMIC SHOCK
MCC of shock in children
Decrease in the intravascular blood volume to
such an extent that effective tissue perfusion
cannot be maintained.
Preload decrease
Decreased Stroke Volume
Decreased C.O.
Management of
Hypovolemic Shock
Establishment of adequate oxygenation and ventilation
O2- ALWAYS the first drug administered.
Adequate IV or IO
Early correction of hypovolemia
-Crystalloids: Readily available, safe, least expensive
-First bolus 20cc/kg- ASAP
-Continuous monitoring of vitals
-Monitoring of CVP: Maintain > 10mmHg
-Identify causes of ongoing losses
- Blood available: if hemorrhagic shock.
Solution makeup
Osmol Glucose
5% D/W
10%D/W
.45% NS
.9% NS
LR
278
556
154
308
274
50g/l
0
0
100g/l
0
0
0
77
77
0
154 154
0
130 109
0
0
0
0
0
0
0
0
4
1.5
0
0
0
0
28
HR maintains CO
CARDIOGENIC SHOCK
1. a. Toxic substances released during
course of shock.
b. Myocardial Edema
c. Adrenergic receptor dysfunction
d. Impaired sarcolemmic Calcium flux
e. Reduced coronary blood flow
2. Diastolic Dysfunction
Pathophysiology
LV able to eject less volume of bld/ beat
Dec. Stroke Volume
Increased Venous Return
Increased EDV
Dec.C.O
Increased O2
extraction by
tissues
Etiology of Cardiogenic
Shock
Dysrrhythmias
Cardiomyopathies
Hypoxic-Ischemic event
Infectious
Metabolic
Connective Tissue Disorder
NM disorders
Toxins
Others
Excessive Resp
effort
Prolonged
feeding time
Poor weight
gain
Excessive
sweating
Frequent resp.
tract infections
Physical Examination
CXR
Cardiomegaly
Pulm
venous
congestion
Hyperinflation
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History
Correct
Dysrhythmias
Exclude
traumatic or
CHD
normothermia
Optimize
Preload
Explore
Provide
sedation
Improve
Contractility
Correct
anemia
Reduce
Afterload
surgical options
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Maintain
OBSTRUCTIVE SHOCK
Normal Preload
Normal myocardial function
Inadequate C.O.
Ac. Pericardial Tamponade
Etiology
Tension Pneumothorax
Pulmonary/ Systemic HTN
Congenital/ Acquired outflow
obstructions
DISTRIBUTIVE SHOCK
PathoPhysiology:
a. Maldistribution of blood flow to tissue due to abnormal
vasomotor tone.
b. Profound inadequate tissue oxygenation.
c. Normal or High C.O.
Etiology
Anaphylaxis
Spinal or Epidural anesthesia
Disruption of spinal cord
Iatrogenic
SEPTIC SHOCK
SIRS/Sepsis/Septic shock
Mediator release:
exogenous & endogenous
Cardiac
of blood flow
dysfunction
Imbalance of
oxygen
supply and
demand
Alterations in
metabolism
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Maldistribution
SEPSIS
ACUTE ORGAN
DYSFUNCTION
(Severe Sepsis)
DEATH
Sepsis
Severe Sepsis
Systemic inflammatory
response to variety of severe
clinical insults indicated by 2 or
more of the following:
Temp > 38 or < 36
HR > 90bpm (adults)/
>2SD(ped)
RR > 20/min (adults)/>2SD(ped)
OR PACO2 <32mmhg
WBC>12000, <4000 or > 10%
bands
Systemic response to
infection manifested by
2 or more of the
following as a result of
infection:
Temp > 38 or < 36
HR>90
RR>20 or PaCO2 < 32
WBC>12000. <4000 or
>10% bands
Sepsis associated
with:
Organ dysfunction
Hypoperfusion (Lactic
acidosis, oliguria,
altered mental status)
Hypotension
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SIRS
Warm Shock
Cold Shock
Fluid-Refractory/
Dopamine resistant
Catecholamine
Resistant
Refractory Shock
Early,
Late,
Persistance of shock
despite > 60cc/kg
fluid resuscitation
Persistance of shock
despite administration of
direct acting
catecholamines
Epinephrine/
Nor-Epinephrine
Persistance of shock
despite:
-Goal direct inotropic/
pressor therapy
-Use of vasodilators
-Maintenance of
metabolic and
hormonal homeostasis
Clinical
Signs
-Inc.HR
-Warm
extremities,
bounding pulses
Physiologic
Parameters
-Wide PP
-Inc. C.O.
-Inc. MvO2
-Dec.SVR
Lab
Data
-Hypocardia
-Inc. Lactate
-Inc.Glucose
Uncompensated
Clinical Signs
-Cold, clammy extremities
-Rapid, thready pulses
-Shallow breathing
Physiologic
Parameters
-Narrow PP
-Dec.CVP, C.O
-Dec. MvO2 sat
-Inc. SVR
-Oliguria
-Capillary Leak
Data
-Metab. Acidosis
-Hypoxia
-Coagulopathy
-Hypoglycemia
Persistance of shock
despite Dopamine at
>10mcg/kg/mn
Lab
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compensated
Community-Acquired Sepsis
References