SHOCK

Dr Anuj Raj
Bijukchhe
 Introduction

Definition of shock
Types of shock
Causes of shock
Signs and symptoms of shock
Body’s response to shock
Treatment of shock
 Definition of Shock

In 1852, shock was defined as “a

rude unhinging of the machinery of
life.” Probably no better definition
exists to describe the devastating
effects of this process on a patient,
but a more recent definition calls
shock “the collapse and progressive
failure of the cardiovascular system.”
• Shock left untreated may be fatal. It
must be recognized and treated
immediately, or the patient may die
• The definition of shock does not
involve low blood pressure, rapid pulse
or cool clammy skin - these are merely
the signs.
• Simply stated, shock results from
inadequate perfusion of the body’s
cells with oxygenated blood.
• Circulatory shock, commonly known as just shock, is a
serious, life-threatening medical condition characterized by a
decrease in tissue perfusion to a point at which it is
inadequate to meet cellular metabolic needs.
• As the blood carries oxygen and nutrients around the body,
reduced flow hinders the delivery of these components to the
tissues, and can stop the tissues from functioning
properly. The process of blood entering the tissues is called
perfusion , so when perfusion is not occurring properly this is
called a hypoperfusional (hypo = below) state.
 Circulatory shock should not be confused
with the emotional state of shock , as the
two are not related. Medical shock is a life-
threatening medical emergency and one
of the most common causes of death for
critically-ill people. Shock can have a
variety of effects, all with similar
outcomes, but all relate to a problem with
the body's circulatory system. For
example, shock may lead to hypoxemia
 (a lack of oxygen in arterial blood)
 4 Stages of Shock

• 1. Initial
• 2. Compensatory.
• 3. Progressive
• 4. Refractory
• An initial non progressive stage- during which
reflex compensatory mechanisms are activated
and perfusion of vital organ is maintained.
• A progressive stage - characterized by
tissue hypo perfusion and onset of worsening
circulatory and metabolic imbalance.
• An irreversible stage - that sets in after the
body has incurred cellular & tissue injury so
severe that even if the hemodynamic defect are
corrected , survival is not possible.
 Mechanism of
microcirculatory disorder
of shock

9
 The stages and mechanisms of
microcirculatory disorder of shock

Ischemic hypoxia stage

Stagnant hypoxia
stage

Microcirculation failure
stage

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 Ischemic hypoxia stage
• Compensatory mechanism
Blood pressure Pulse pressure Blood flow Blood volume

angiotensinogen
Baroreceptors
chemoreceptors

Adrenal cortex
Vasomotor centre Adrenal medulla

Angiotensin ı

Sympathetic noradrenaline aldosterone

nervous adrenaline
activity Angiotensin Ⅱ

Venous
capacitance Circulating systemic
Volume resistance

Heart rate
Myocardial contractility Maintain venous return

Maintain cardiac output

Maintain blood pressure 11
Stagnant hypoxic stage
Ischemic hypoxia
Of microcirculation

Anaerobic metabolism
lactate

Dilation of precapillary sphincter constriction of postcapillary sphincter

In>out

Stagnation of blood

Capillary pressure

Capilary leak

Effctive circulatory blood volume

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Blood pressure
 microcirculation
Arteriolar and precapillary Precapillary sphincter constrict
sphincter

constrict Pressure of capillary

Microcirculatio
n Fluid from outer to vascular compartment
perfusion

Ischemic hypoxia Arteriovenous shunt

Of microcirculation

Ischemic hypoxia
Of microcirculation

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 DIC and MODS
Stagnation of blood

Ischemic hypoxia
of
microcirculatio
n

Injury of endothelium

Microembolism Release of cytokine

DIC

SIRS

MODS

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 Classification by causes
• Hypovolemic shock
• Traumatic shock
• Burn shock
• septic shock
• Cardiogenic shock
• Anaphylactic shock
• Neurogenic shock

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 Classification by
pathophysiological changes

• Hypovolemic shock
• Cardiogenic shock
• Obstructive shock
• Distributive shock

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 Hypovolemic shock

• Hemorrhage
• Burns
• Diarrhea
• Vomiting
• Peritonitis
 Cardiogenic

• Pulmonary Embolism
• Cardiomyopathy
• Heart Disease
• Cardiac Contusion
• Cardiac Tamponade
• Myocardial Infarction Arrhythmia
• Aortic Aneurys
 Vasogenic

• Psychogenic
• Anaphylactic
• Septic
 Hypovolemic Shock

Hypovolemic shock refers to a medical

or surgical condition in which rapid fluid
loss results in multiple organ failure due
to inadequate perfusion.
Trauma
Hemorrhage
Vomiting / diarrhea
Burns
 The human body responds to acute
hemorrhage by activating 4 major
physiologic systems: the hematologic
system, the cardiovascular system,
the renal system, and the
neuroendocrine system.
Hypovolemic Shock:Hematologic
System
Activating the coagulation cascade and
contracting the bleeding vessels (via local
thromboxane A2 release).
Platelets are activated which form an
immature clot on the bleeding source.
The damaged vessel exposes collagen,
which subsequently causes fibrin
deposition and stabilization of the clot.
 Hypovolemic Shock:
Cardiovascular
System
Increases the heart rate, increasing
myocardial contractility, and constricting
peripheral blood vessels.
This response occurs secondary to an
increase in release of nor epinephrine and
a decrease in baseline vagal tone (regulated
by the baroreceptors in the carotid arch,
aortic arch, left atrium, and pulmonary
vessels).
The cardiovascular system also responds by
redistributing blood to the brain, heart, and
kidneys and away from skin, muscle, and GI
tract.
 Renal System

The kidneys respond to hemorrhagic

shock by stimulating an increase in
renin secretion from the juxta
glomerular apparatus.
 Angiotensin II has 2 main effects,
both of which help reverse
hypovolemic shock,
vasoconstriction of arteriolar smooth
muscle and stimulation of
aldosterone secretion by the adrenal
cortex.
 Hypovolemic Shock:
Neuro endocrine System
• Causes an increase in circulating
antidiuretic hormone (ADH).
• ADH is released from the posterior
pituitary gland in response to a decrease
in blood pressure (as detected by
baroreceptors) and a decrease in sodium
concentration.
• ADH indirectly leads to an increase in
reabsorption of water and salt (NaCl) by
the distal tubule, the collecting ducts, and
the loop of Henle.
 Signs and symptoms
Hypovolemic shock
• Anxiety, restlessness, altered mental state  due to decreased
cerebral perfusion and subsequent hypoxia.
• Hypotension due to decrease in circulatory volume.
• A rapid, weak, thready pulse due to decreased blood flow combined
with tachycardia.
• Cool, clammy skin due to vasoconstriction and stimulation of
vasoconstriction.
• Rapid and shallow respirations due to sympathetic nervous system
stimulation and acidosis.
• Hypothermia due to decreased perfusion and evaporation of sweat.
• Thirst and dry mouth, due to fluid depletion.
• Fatigue due to inadequate oxygenation.
• Cold and mottled skin , especially extremities, due to insufficient
perfusion of the skin.
• Distracted look in the eyes or staring into space, often with pupils
dilated.
 Cardiogenic Shock

• Cardiogenic shock is characterized by

a decreased pumping ability of the
heart causing a shock-like state with
inadequate perfusion to the tissues.
• It occurs most commonly in
association with, and as a direct result
of, acute ischemic damage to the
myocardium.
 Cause
Intrinsic
Myocardial injury
Tachycardia
Bradycardia
Valvular defect
Extrinsic
Pericardial tamponade
Tension pneumothorax
Large pulmonary emblous
 Cardiogenic Shock: History

Most patients presenting with cardiogenic

shock do so in conjunction with an AMI and
therefore, present with the constellation of
symptoms of acute cardiac ischemia (e.g.
Chest pain, shortness of breath, diaphoresis,
nausea and vomiting).
Patients experiencing cardiogenic shock may
also present with pulmonary edema and
presyncopal or syncopal symptoms.
Cardiogenic Shock: Physical

Physical examination will often reveal

a patient in the middle of an AMI.
Patients appear in frank extremis,
profoundly diaphoretic and
complaining of severe shortness of
breath and chest pain.
Clinical assessment begins with
attention to the ABCs and vital signs.
Neck examination may reveal jugular venous
distention. This is evidence of right ventricular
failure and may be prominent.
With increasing degrees of ventricular dysfunction,
pulmonary edema and severe hypotension may
develop.
Auscultation of the chest may reveal varying
degrees of congestive heart failure (CHF).
• Cardiogenic shock, similar to
hypovolemic shock but in addition :
Distended jugular veins due to
increased jugular venous pressure
• Weak or absent pulse
• Arrhythmia, often tachycardia
 Vasogenic Shock

• Septic Shock
Hyperdynamic
Hypodynamic
• Toxic Shock
• Neurogenic Shock
• Psychogenic Shock
 Septic Shock vs. SIRS

Systemic Inflammatory Response

Syndrome (SIRS)
Physiologic alternations and organ
dysfunction seen with bacterial infections.
2 or more changes in these 4 factors, as
follows: body temperature, heart rate,
respiratory function, and peripheral
leukocyte count.
 Terms
Sepsis
Systemic host response to infection
with SIRS plus a documented infection
Severe Sepsis
Sepsis plus end-organ dysfunction or
hypoperfusion
Septic Shock
Sepsis with hypotension, despite fluid
resuscitation with evidence of
inadequate tissue perfusion
Septic Shock: Pathophysiology

In septic shock due to bacterial infection, circulatory

insufficiency occurs when bacterial products interact with
host cells and serum proteins to initiate a series of
reactions that may ultimately lead to cell injury and
death.
Not only are these bacterial products harmful
themselves, but the widespread and unregulated
host response to these substances also results in
the elaboration or an extensive array of chemical
mediators that lead to further cell damage.
Septic shock develops in less than
one half of patients with bacteremia.
It occurs in about 40% of those
patients with gram negative
bacteremia and about 20% of those
patients with Staphylococcus aureus
bacteremia.
 Septic Shock: History

• Fever
• Chills
• Sweating
• Altered mental status
Apprehension
Anxiety
Agitation
• Some localizing symptoms
Head and neck infections - earache, sore throat,
sinus pain or congestion, nasal congestion or exudate,
swollen lymph glands
• Chest and pulmonary infections - cough (especially if
productive), pleuritic chest pain, dyspnea
• Abdominal and GI infections - abdominal pain,
nausea, vomiting, diarrhea
• Pelvic and genitourinary infections - pelvic or flank
pain,
vaginal or urethral discharge, dysuria, frequency,
urgency
• Bone and soft tissue infections - focal pain or
tenderness, focal erythema , edema
 Septic shock
Similar to hypovolaemic shock except in the first
stages Pyrexia , due to increased level
of cytokines
• Systemic vasodilation resulting in hypotension
• Warm and sweaty skin due to vasodilation
• Systemic leukocyte adhesion to endothelial tissue
• Reduced contractility of the heart
• Diffuse capillary damage in the lung
• Activation of the coagulation pathways, resulting
in disseminated intravascular coagulation
• Increased levels of neutrophils
 Neurogenic shock
•  Neurogenic shock is the rarest form of shock.
It is caused by trauma  to the spinal cord
 resulting in the sudden loss
of autonomic and motor  reflexes below the
injury level. Without stimulation
by sympathetic nervous system the vessel
walls relax uncontrolled, resulting in a sudden
decrease in peripheral vascular resistance ,
leading to vasodilation  and hypotension .
 Neurogenic shock,

• similar to hypovolemic shock except in

the skin's characteristics. In neurogenic
shock, the skin is warm and dry or a
clear sweat line exists, above which the
skin is diaphoretic
 Anaphylactic shock
• Caused by a severe anaphylactic
reaction to
an allergen , antigen , drug or
foreign protein causing the release
of histamine  which causes
widespread vasodilation, leading to
hypotension and increased capillary
permeability.
 Psychogenic Shock

Also known as “fainting spells”

Caused by sudden dilation of blood

vessels which temporarily halts blood
flow to the brain
 Obstructive shock 
• In this situation the flow of blood is obstructed which
impedes circulation and can result in circulatory arrest .
Several conditions result in this form of shock.Cardiac
tamponade in which fluid in the pericardium prevents inflow
of blood into the heart (venous return). Constrictive
pericarditis , in which the pericardium  shrinks and hardens,
is similar in presentation.
• Tension pneumothorax . Through increased intrathoracic
pressure, bloodflow to the heart is prevented (venous
return).
• Massive pulmonary embolism is the result of a
thromboembolic incident in the bloodvessels of the lungs
and hinders the return of blood to the heart.
• Aortic stenosis hinders circulation by obstructing
the ventricular outflow tract .
• Obstructive shock, similar to
hypovolaemic shock but in
addition:Distended jugular veins due
to increased jugular venous pressure
• Pulsus paradoxus  in case of
tamponade
 Clinical manifestations

• The clinical syndrome of shock can

develop over the course of a few
minutes or several hours, depending
on the cause;all systems may be
affected.

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 Common manifestations
• Tachycardia, oliguria, a clouded
sensorium, cool mottled extremities
indicative of reduced blood flow to
the organ.
• Metabolic acidosis ,often due to
elevated blood lactate levels, reflects
prolonged inadequate blood flow to
tissues.

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 Specific manifestations
• Hypovolemic shock:have a history of
gastrointestinal bleeding
,hemorrhage,or diarrhea,vomitting
• Cardiogenic shock ： have signs of
heart disease,gallop rhythms
• Distributive shock: localized infection
as well as fever and chills

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 Manifestations
Cardiovascular system
Early Lately
•
Blood pressure N or ↓ ↓↓
• Heart rate N or ↑ ↑↑
• Cardiac output N or min↑ ↓↓

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 Manifestations
Cardiovascular system

 The ECG frequently shows signs of

ischemia, ST depression and
flattening of the T waves.
 The CVP can initially be high in
cardiogenic and obstructive
shock,low in hypovolemic shock,
and normal or low in septic shock.

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 Manifestations
renal system

 Reduction of hourly urinary output to less

than 0.5ml/kg occurs early in shock,
initially because of prerenal insufficiency.
 Without treatment,there may be rapid
progression to acute tubular necrosis .

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 Manifestations
repiratory system

• Early Lately

• Tachypnoea Tachypnoea
• Laboured breathing
• Central cyanosis

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 Manifestations
Gastrointestinal system

• There may be vomiting or diarrhea,

hepatic failure ,stress ulcer. Late in shock.
bowel sounds are infrequent or absent.
• Peritonitis is a common source of septic
shock and is accompanied by abdominal
pain and board-like rigidity.

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 Organ dysfunction

• Heart mechanism

• Blood volume of myocardium

• Oxygen consumption of myocardium
• Acidosis myocardial
contractility
• DIC in myocardium
• endotoxin
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 Organ dysfunction

• Respiratory failure
 Acute lung injury and acute respiratory distress
syndrome(ARDS) are menifested as non cardiogenic
pulmonary edema resulted from diffuse pulmonary
capillary endothelial and alveolar epithelial
injury,hypoxia,and bilateral diffuse pulmonary
infiltrates.

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 Organ dysfunction

• Impairment of digestive system

 stress ulcer, erosive gastritis, pancreatitis,
submucosal hemorrhage
 enteric Ischemia-reperfusion injury induced
enteric bacteria and endotoxin translocate
from gut lumen to the systemic circulation

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 Organ dysfunction
• Acute renal failure early stage

Renal perfusion GFR oliguria

Acute renal failure

(prerenal failure)
Functional renal failure

GFR- glomerular filtration rate

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 Organ dysfunction
• Acute renal failure late stage

Ischemia and microembolism

Acute tubular necrosis oliguria
of renal

Acute renal fuailure

Parenchymal renal failure

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 Diagonsis of shock
• Step 1 look: investigating the patient’s
skin and facial expression;
• Step 2 inquire: inquiring the history and
know if his/her sense is clear;
• Step 3 touching: touching the patient’s
pulse to know its intensity 、 speed and
rhythm, and touching the temperature and
humidity of the skin;
• Step 4 listen: listening to the heart sound
and measuring the blood pressure.

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 Diagonsis
• Manifestation: Dysfunctional signs of
each organ,
BP increase ,heart rate increase

compensatory stage
BP decrease, heart rate increase
decompensatory stage

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 Diagnostic standard by
stages
• Early stage:
Mechanism:Activation of sympathetic nerve
and release of catecholamine.
Symptom: Pale ,cool and damp extremities;
normal consciousness with agitation ,decreased
urine output ,normal or a little decreased BP,
Pulse pressure <20mmHg,SBP decreased more
than 40mmHg if the patient has hypertension
before.

64
 Diagnostic standard by
stages
• Middle stage:
Symptom: Normal consciousness
but with a slow response, thirsty for
water , thready pulse, Trachypnoea ，
urine output<20ml/h ， SBP 60~80mmHg.

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 Diagnostic standard by
stages
• End stage:
Symptom: Confusion or coma , cool
mottled or pale skins or cyanotic
extremities, peripheral pulses become
thready or may be absent;SBP <60mmHg or
can not be measured, anuria ， Tachypnoea,
tendency of DIC, manifestation of acidosis.

66
 Shock monitoring
1. Normal index
2. Invasive hemodynamic monitoring
3. Function of oxidative metabolism
4. Laboratory monitoring

67
 Normal index

• Mental status:
• Vital signs: Temperature, heart rate ,
breath rate, blood pressure
• Colour and temperature of the skin
• Shock index: pulse rate/SBP
> 1.0-1.5 indicate shock;
>2.0 severe shock
• Urine output <25ml/h indicate inadequate tissue
perfusion;
>30ml/h indicate shock corrected 68
 Invasive hemodynamic
monitoring

• MAP: DBP ＋ 1/3pulse pressure

≥80mmHg good perfusion
≤65mmHg poor perfusion
• CVP: Signs of blood volume ,pressure of right
heart
5 ～ 10cmH2O indicate normal;
<5cmH2O indicate hypovolemia;
>15cmH2O indicate heart failure or
high pressure of pulmonary circulation.

69
 Invasive hemodynamic monitoring

• By Swan-Ganz catheter
• PCWP :(pulmonary capillary wedge
pressure) PCWP is similar to the pressure
of left atria
PCWP<12mmHg indicate hypovolemia,
12 － 15mmHg indicate normal,
>15mmHg indicate hypervolemia or left
heart failure
• CO and CI :CO 4 ～ 6L/min, CI 2.5~3.5L/
(min.m2) CO=heart rate ×stroke
volume ,CI=CO/body area
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 Function of oxidative metabolism
• Sp02 ＞ 90% simple and noninvasive
• Arterial blood gas analysis
• PaO2 80 ～ 100mmHg;
 PaCO2 35 ～ 45mmHg ；
 PH 7.35 ～ 7.45;
 HCO3- 22-27mmol/L
● Lactic acid monitoring
lactic acid >2mmol/L

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 Laboratory monitoring
• Blood routine :Red blood cell count,
hemoglobin, and Hematocrit
• Electrolyte and renal function :K ,Na,Ca,
Serum creatinine
• DIC:
 Tendency of bleeding clinically
 APTT>normal index +3 seconds
 Number of platelet < 80×109/L or decline
gradually
 Fg<1.5g/L or gradually decreased

APTT --activated partial thromboplastin time

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 Differential diagnose

 Cardiogenic shock:History,ECG, cardiac

enzymes,cTnT,cTnI
 Gastrointestinal bleeding: Shock with
hematemesis and melena.
 Hemorrhage in abdomen: Rupture of spleen ,liver,
kidney ， tumor,and other kinds of hemorrhage.
 Hemorrhage of fracture:The volume of bleeding
amount to 1000-2000ml

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 Treatment
The aim of therapy is to improve the
supply of oxygenated blood to the
tissues.

74
 Principle of treatment
1. Normal treatment
2. Aetiology treatment
3. Restore normal blood volume
4. Provision of adequate oxygenation
5. vasoactive drugs
6. Correct acidosis, electrolyte disturbance
7. Glucocorticoids therapy
8. Prevention of DIC
9. Protect function of organs,prevention of
MODS

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 Normal treatment
• Body posture: lay flat or the legs are elevated by 30 。
Keep body calm and warm
• Keep the respiratory tract smoothly ， clear away
respiratory secretions in time. supply oxygen by nasal
catheter, mask, mechanical ventilation or endotracheal
intubation. oxygen flow
• Set up Venous access as early as possible. subclavian
vein, Jugular vein, Femoral vein catheterization for the
purpose of fluid infusion .CVP
• conscious-sedation ， alleviate pain ： if the patient is
agitated. proper treatment.
• Shock monitoring.

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 Restore normal blood
volume
• Restoration of optimal circulating blood volume
• Fluid infusion is a most important therapeutic measure
in the treatment of shock, whether it is the initial cause
of shock ,or a complication of cardiogenic , distributive
or obstructive shock. the velocity of liquid can be very
fast , the kind of liquid can be colloids or crystalloids
.But The volume and speed of administration depends
on the patient’s cardiac competence and must be
considered carefully if acute left ventricular failure and
the resultant pulmonary edema are to be avoided.

77
 Treatment

• Shock requires immediate interventions to preserve

life. Therefore, the early recognition and treatment
is essential even before a specific diagnosis is
made. Most forms of shock seen in trauma or sepsis
respond initially to aggressive intravenous fluids (ie.
1 liter normal saline bolus over 10 minutes).
Therefore this treatment is usually instituted as the
person is being further evaluated.
• Re-establishing perfusion to the organs is the
primary goal through restoring and maintaining the
blood circulating volume ensuring oxygenation and
blood pressure are adequate, achieving and
maintaining effective cardiac function, and
preventing complications .
 Hypovolemic shock

• In hypovolemic shock, usually hemorrhagic

shock caused by traumatic injury , it is necessary
to immediately control the bleeding and restore
the casualty's blood volume by giving infusions of
isotonic crystalloid solutions. 
• Blood transfusions , packed red blood cells (RBCs
),Albumin  (or other colloid solutions), or fresh-
frozen plasma are necessary for loss of large
amounts of blood , but can be avoided in smaller
and slower losses. 
• Hypovolemia due to burns, diarrhea, vomiting,
etc. is treated with infusions of electrolyte
solutions that balance the nature of the fluid lost.
 Type of fluid used in shock.
• Crystalloids – Such as sodium chloride (0.9%), or Lactated Ringer's solution
 (Hartmann's solution). Dextrose solutions which contain free water are less
effective at re-establishing circulating volume, and promote hyperglycaemia.
• Colloids – For example, polysaccharide (Dextran), polygeline (Haemaccel),
succinylated gelatin (Gelofusine) and hetastarch (Hespan). Colloids are, in
general, much more expensive than crystalloid solutions and have not
conclusively been shown to be of any benefit in the initial treatment of shock.
• Combination – Some clinicians argue that individually, colloids and crystalloids
can further exacerbate the problem and suggest the combination of crystalloid
and colloid solutions.
• Blood – Essential in severe hemorrhagic shock, often pre-warmed and rapidly
infused.
• It is to be noted that NO plain water should be given to the patient at any
point, as the patient's low electrolyte levels would easily cause water
intoxication , leading to premature death.
 Cardiogenic shock
• In cardiogenic shock, depending on the
type of myocardal infarction, one can
infuse fluids such as or in shock refractory
to infusing fluids, normal saline would be
an example of said fluids .
• Inotropic agents, which enhance the
heart's pumping capabilities, are used to
improve the contractility and correct the
hypotension.
• The main goals of the treatment of
cardiogenic shock are the re-establishment of
circulation to the myocardium, menimising
heart muscle damage and improving the
heart's effectiveness as a pump. This is most
often performed by percutaneous coronary
intervention and insertion of a stent in the
culprit coronary lesion or sometimes by
cardiac bypass.
 Blood transfusion
• Packed red cells ： Haematoglobin
concertration ≤ 70g ／ L 。 patient with no
active bleeding ,1 unit infusion can increase
heamatoglobin concertration
10g/L,hematocrit increase 3%.
• Platelet: <50×109 ／ L or hypofunction
• Fresh frozen plasma: Increase colloid osmotic
pressure , supply blood coagulation factor ，
massive haemorrhage 。
• the whole blood and plasma are better than
colloids in order to increase blood volume.

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 Provision of adequate
oxygenation
• All patients who are clinically shocked
should be given supplementary oxygen.
• Lung is an organ injured most easily in
shock,manifested as respiratory failure ,or
with shock goes on ,patient lay in coma.
we can take endotracheal intubation to
maintain the respiratory function by
mechanical ventilation.

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 Provision of adequate
oxygenation
• Mechanical ventilation is required if
oxygenation remains
inadequate,i.e.a PaO2 ＜ 60mmHg or
if respiratory acidosis develops,i.e. a
PaCO2 ＞ 60mmHg.

85
86
 To prevent the risks of oxygen toxicity , the
inspired oxygen concentration should be
limited to 60% or less.The PaO2 should be
kept at about 100mmHg and PaCO2 about
40mmHg. The addition of positive end
expiratory pressure(peep),up to 15
cmH2O,should be used if higher
concentrations of oxygen appear to be
necessary 。

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 vasoactive drugs
• vasoconstrictor :High-output and low-resistance
 Dopamine
 Dobutamine
 Noradrenaline
 Adrenaline
 Cardiac stimulant
• Vasodilatator :Low-output and high-resistance
 Nitroprusside sodium
 Phentolamine
 Glycerol trinitrate

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 Correct acidosis,electrolyte
disturbance
• lactic acidosis is most common in metabolic acidosis
.metabolic acidosis decrease the myocardial
contractility,increase the resistance of pulmonary and
renal circulation,decrease the affinity of Hb for O2
• cardiogenic shock and hypovolemic acidosis :deal
with etiological factor and volume resuscitation;
5%sodium bicarbonate ivgtt by ABGA
pH<7 ． 20 。
• Septic shock:deal with acidosis actively.

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 Glucocorticocids therapy
Glucocorticocids :
 Mechanism ：
 Anti-shock ,anti-toxin ,anti-
inflammatory response, anti-
anaphylaxis,stabilize cell membrane .
Inhibit release of inflammatory
mediators.It can be used in all kinds of
shock.

90
Prevention of DIC give heparin in early
stage.
Protect function of organs,
prevention of MODS.especially
acute renal failure.

91
 Distributive shock

• In distributive shock  caused by sepsis the infection

is treated with antibiotics  and supportive care is
given (i.e. inotropica , mechanical ventilation , renal
function replacement ). 
• Anaphylaxis is treated with adrenaline  to stimulate
cardiac performance and corticosteroids to reduce
the inflammatory response .
• In neurogenic shock because of vasodilation in the
legs, one of the most suggested treatments is
placing the patient in the Trendelenburg position,
thereby elevating the legs and shunting blood back
from the periphery to the body's core.
 Obstructive shock

• In obstructive shock , the only therapy consists of

removing the obstruction. 
• Pneumothorax  or hemothorax  is treated by
inserting a chest tube , pulmonary embolism
requires thrombolysis (to reduce the size of the
clot), or embolectomy(removal of the thrombus ).
• Tamponade is treated by draining fluid from
the pericardial space through pericardiocentesis .
 Prognosis

• The prognosis of shock depends on the

underlying cause and the nature and extent of
concurrent problems.
• Hypovolemic, anaphylactic and neurogenic
shock are readily treatable and respond well to
medical therapy.
• Septic shock however, is a grave condition and
with a mortality rate between 30% and 50%.
• The prognosis of cardiogenic shock is even
worse.
 Conclusion
• The ultimate outcome in the
treatment of shock depends on the
reversibility of the underlying
cause,the early recognition and
aggressive treatment of
complications.

95