Shock

Xu Zhi-Yue

Hunan Provincial Children's Hospital

Emergency Center ICU-1

Definition
Refers to a variety of pathogenic factors causing sharp
reduction in effective circulating blood volume, leading to
organ and tissue microcirculation, hypoperfusion, resulting in
tissue hypoxia, cell metabolism and organ dysfunction
syndrome
Deterioration in shock from inadequate tissue
perfusion is a development of multiple organ
dysfunction to the failure of the pathological process

Pathophysiology

Clinical Features

Diagnosis
Differential diagnosis

Etiology

Shock

Laboratory assistant
examination

Treatment

Cardiac output
CO = Stroke volumeHeart rate

Preload

Afterload

Myocardial contractility

Question
Preload can be made infinitely increase?
Afterload increases will not reduce
stroke volume?
where is Myocardial contractility
confined ?
The faster heart rate, cardiac output,
the larger it?

Critical shock

Acute lack
of effective circulating blood volume

Blood volume

Cardiac pump
dysfunction

Vascular
volume

shock

Etiology
hypovolemic shock
hypovolemic shock
cardiogenic shock
septic shock
allergic shock
neurogenic shock

Etiology

Shoc
k

Maldistributive
shock
cardiogenic shock
Cardiac obstructive
shock

Hemodynamic classification

Pathophysiology
contraction

Release

congestion

Catecholami

Microthrom
bi and DIC

ne
Aldosterone
Vasoactive
peptide

Microcir
culation

Metabolic
changes in body
fluids

Inflammator
y mediators
Endothelial
cell injury
Reperfusion
injury

Release of
inflammatory
mediators

Pathophysiological changes

MODS
Myocardial
depression
Alveolar
collapse
cerebral
edema
oliguria

Secondary
damage to
vital organs

Pathophysiology Stage
Early shock(Phase )

(Period of ischemia and hypoxia)

Shock medium(Phase )

(congestive hypoxia period Decompensatory

stage)

Late shock(Phase )
(Micro-circulatory failure period)

Pathophysiology

Blood cell aggregation into clumps,

like mud-like,
swinging in the intravascular

Clinical features - clinical

stage
1. Decompensated shock
Sympathetic tone
increased catecholamines
heart and brain outside ischemia, hypoxia
heart and brain tissue compensation
Pale, clammy extremities, decreased urine output or
normal
blood pressure is not low or slightly elevated pulse
pressure, heart rate slightly faster
Normal blood lactate, pH value of gastrointestinal
mucosa decreased

2. Reversible decompensated
Catecholamine response to the small blood
vessels decreased
there microcirculation congestion
Pale or schungite, cold limbs, oliguria
Temperature did not rise, pulse rate, disturbance
of consciousness, low heart sound blunt, blood
pressure, or could not be check out
Acidosis obvious
There may be organ dysfunction or failure

3. Shock refractory period

Serious microcirculation stasis, DIC
Gastrointestinal mucosal barrier
damage, endotoxin into the blood and
endogenous infection
MODS/M0F
Death is inevitable

Laboratory tests
Blood
Blood

Urine,
Urine, stool
stool

RBC/Hb

Judge

haemorrhagic
shock

Renal
function

WBC count

gastrointesti
nal bleeding

septic shock

Coagulation
Coagulation

Blood
Blood
biochemistry
biochemistry

Determine the
coagulation

Organ

examinations
X ray
Hemodynamic
CO

ECG

PCWP
CVP
Microcirculation
inspection

General monitoring
Mental state
Skin temperature, color
Blood pressure
Pulse rate
Urine

Special monitoring
shock
shock
Central venous pressure

PCWP

5-10cmH2O

(6-15mmHg)

Special
monitoring

CI

Blood gas
analysis

Lac

DIC
Gastrointestinal
Mucosa ph

Diagnosis
1 The incentive of a shock
2 Disturbance of consciousness

Diagnostic

3 Puls 100 m
4 Crt 3s ,urine 0.5ml/(kgh)

criteria
5 BP 90mmHg
6 Vessel pressure 30mmHg
7 Systolic pressure decrease > 30

Differential diagnosis
Distinguish
various types

shock
Physical
hypotension

Orthostatic
hypotension

Treatment principles
Remove the causes, incentives

Shock
treatmeint

To restore an effective
circulating blood volume
Correct the microcirculation
Improve heart function
Return to normal metabolic

General treatment 1
1

Sedation

head-down

oxygen
fasting
to reduce
the move

ECG

legs levated

BP

20 -30
heart failure
or pulmonary
edema were
semi-supine

Keep warm

Breath
SPo2

General treatment 2
5

Indwelling
catheter
to monitor
urine output

To add
volume

Improve
hypoxemia

Correct
acidosis

Vasoactive drugs
Low-dose 10g/(kgmin)
Dopamine

Dobutamine

Isoproterenol

High-dose 15g/(kgmin)

cardiogenic shock 2.5-10g/(kgmin)

Bradycardia, atrioventricular block:

0.5-1mg 5%GS 200-300ml,2-4g/min

Vasoactive drugs
Norepin
ephrine

Adrenaline

Severe, very severe septic shock

4-8g/min

neurogenic shock 0.5-1mg,im

Other drugs
Other drugs

Glucocorticoid
septic shock

Naloxone

allergic shock

0.4 0.8mg ,iv

Hydrocortisone

1.6mg 500ml,ivgtt

300-500mg/d 3
5d

Prevent complications and MODS

1
Correcting water,
electrolyte and acidbase balance
disorders
to maintain effective

Additional capacity
should be only used
potent diuretics
cerebral edema:
dehydrating agent can
be used

renal perfusion

Acute renal failure

CRRT

Prevent complications and MODS

Keep the airway open

continuous oxygen

use respiratory stimulant

Mechanical ventilation

Acute
respiratory
failure

Prevent complications and MODS

Excited breathing

Reduce
intracranial
pressure

Cerebral
metabolic
activator

Treatment of
cerebral edema

Diazepam,
phenobarbital

support
treatment

Prevent complications and MODS

Heparin

Added
coagulation
factor

Anti-platelet
aggregation

DIC

.Improve

Management of

microcirculation

Thrombolytic
therapy

complications

Septic shock - cause

Virus

Gram-positive
bacterial
infections

Gram-negative
bacilli infection

Common
causes

Other pathogenic
microorganisms

Fungi

Diagnostic criteria of septic

shock State of consciousness:

the light case is irritability ,coma or convulsions

for severe case

kidney:

Oliguria or anuria, urine output <0.5ml / (kg.h)

pulse and heart change:

faster pulse, thin, faster heart rate, heart sounds

low blunt and other

skin changes:

The skin pattern, pale, cyanosis, clammy

extremities

CRT Extend
Hypoxic lactic acidosis 3mmol/l

6 hours of treatment of cluster recovery

lactic acidosis 4mmol/l has clinical significance
Timely and appropriate antibiotic treatment:
emergency three-hour period, ICU1 hours
Studies has shown that every delay in 1 hour, 7.6% lower
in survival rate

Early goal-directed fluid resuscitation, the goal

within 6 hours
CVP8-12mmHg MBP65mmHg urine0.15ml/
(Kkg.h),ScvO2 70%
If the CVP is not up to achieve our goals and ScvO2 is
not RBC transfusion need to 30%

24 hours cluster of recoveryoriented treatment

Low-dose glucocorticoid application.
Intensive insulin therapy, active control of
blood glucose.
Activated protein C in critically ill patients
to use.
the plateau pressure limit 30cmH2O for
Mechanical ventilation patients

Fluid resuscitation
Treatment of early target

1.Fluid infusion

2. Vasoactive drugs

To achieve CVP 812cmH2O

Dopamine

MAP65mmHg

Norepinephrine,

urine0.5ml/kgh

Dobutamine

CVP or SvO270%

Fluid resuscitation
Treatment of early target

3. Red blood cell transfusion

4. Added platelet

Fluid resuscitation to CVP

has reached the 8-12mmHg,
but SvO2 <65% or ScvO2
<70%, Hb <70g / L, red blood
cell transfusions should
make hematocrit> 30%, Hb
rose to 70 ~ 90g / L

pt 5109/L to treat platelet

suspension 1-2U
Pt 5-30109/L And there is
evidence of bleeding tendency,
platelet transfusion should be
considered