SHOCK:

Pathophysiology and Classification.

 Shock or Cardiovascular collapse, is

the final common pathway for a
number of potentially lethal clinical
events.
Regardless of the underlying
pathophysiology, Shock constitutes
systemic hypoperfusion owing to
reduction either in cardiac output or
in the effective circulating blood
volume.

Empiric Criteria for Shock

4 out of 6 criteria have to be met
Ill appearance or altered mental
status
Heart rate >100
Respiratory rate > 22 (or PaCO2 < 32
mmHg)
Urine output < 0.5 ml/kg/hr
Arterial hypotension > 20 minutes
duration

Stages of Shock
Insult
Pre shock
(compensation)
reduce

Early intervention
can arrest or
the damage.

Shock
(compensation overwhelmed)
End organ damage
Death

 Initial: state of hypoperfusion causes

hypoxia.

due to lack of oxygen cells

perform
lactic
acid fermentation.
Lactate accumulates causing lactic
acidosis.

Compensatory:
Blood loss/ trauma etc
Activation of sympathetic adrenal system
Vasoconstrictive substances
( catecholamines, angiotensin II, vasopressin, endothelin)
Activation of
a receptors
Constriction of micro angia
shunts

activation of
B receptors
opening of A V

Additional Compensatory
Mechanisms
Renin-Angiotensin-Aldosterone
Mechanism
AII components lead to vasoconstriction
Aldosterone leads to water conservation

ADH leads to water retention and

thirst
Inflammatory cascade

Compensatory significances
Venous constriction stored blood return to
circulation (self blood transfusion) (60~70%)
Capillary pressure fluid transfer from
interstitial arterial space to circulation (self fluid
infusion) (1500ml)
Catecholamines , AII cardiac contractility
peripheral vascular resistance
Redistribution of blood Decrease blood flow
to the skin, skeletal muscle, kidneys and
abdominal organs
maintain blood supplying to heart and brain

Progressive:
Should the cause of the crisis not be
successfully treated, shock will
proceed to the progressive stage and
compensatory mechanisms begin to
fail.

Effects of inadequate perfusion on

cell function

Microcirculation stasis

returned blood volume

BP

Brain ischemia

Dull/coma
cyanosis

CO
renal blood flow

oliguria

stasis in kidney stasis in skin

Refractory:
At this stage, the vital organs have
failed and the shock can no longer be
reversed.

Impairment of cell metabolism

(1) Oxygen deficiency and glycolysis
enhancement ATP, Lactic acid
(2) Energy deficient, sodium pump
dysfunction and Na+, H2O inflow
Cellular edema, Hyperkalemia
(3) Lactic acid and CO2 Local
acidosis

Definitions of Sepsis
Systemic Inflammatory Response
Syndrome (SIRS) 2 or > of:
-Temp > 38 or < 36
-RR > 20
-HR > 90/min
-WBC >12,000 or <6,000 or
more than 10%
immature bands

 Sepsis SIRS with proven or

suspected microbial source

Severe Sepsis sepsis with one or

more signs of organ dysfunction or
hypoperfusion.

Septic shock = Sepsis +

Refractory hypotension
-Unresponsive to initial fluids 2040cc/kg Vasopressor dependant

MODS multiple organ dysfunction

syndrome
-2 or more organs

Stages of Sepsis
SIRS

7%

Sepsis

16%

Severe sepsis

20%

Septic shock

70%

MODS/ Death

Pathophysiology
Inflammatory Cascade:

Humoral, cellular and Neuroendocrine

(TNF, IL etc)
Endothelial reaction

Endothelial permeability = leaking

vessels
Coagulation and complement systems

Microvascular flow impairment

End result = Global Cellular Hypoxia

Three Major types of Shock

Type of Shock

Clinical Examples

Principle
Mechanisms

Cardiogenic

MI
Ventricular rupture
Arrhythmia
Cardiac tamponade
Pulmonary Embolism

Failure of myocardial
pump owing to
intrinsic myocardial
damage, extrinsic
pressure or
obstruction to
outflow.

Hypovolemic

Hemorrhage
Fluid loss eg.
Vomiting, diarrhea,
burns or trauma.

Inadequate blood or
plasma volume.

Septic

Overwhelming
microbial infections
Endotoxic shock
Gram positive
septecemia

Peripheral
vasodilation and
pooling of blood;
leukocyte induced
damage; DIC;

ty
Cardiogeni
c

Heart fails
to pump
blood out

CO

BaroRc
SVR

Obstructive Heart
pumps
well, but
the outflow
is
obstructed

CO

BaroRc
SVR

Hemorrhagi Heart
c
pumps
well, but
not enough
blood
volume to
pump

CO

BaroRc
SVR

Distributive

SVR

CO

No
Change in
neurogeni
c shock

No
Change in
neurogeni
c shock

Heart
pumps
well, but
there is
peripheral
vasodilatio
n

Cardiogenic Shock: Causes

MAP =

CO (HR x Stroke Volume)

x SVR

Decreased Contractility (Myocardial Infarction, myocarditis,

cardiomypothy, Post resuscitation syndrome following
cardiac arrest)
Mechanical Dysfunction (Papillary muscle rupture post-MI,
Severe Aortic Stenosis, rupture of ventricular aneurysms etc)
Arrhythmia (Heart block, ventricular tachycardia, SVT, atrial
fibrillation etc.)
Cardiotoxicity (B blocker and Calcium Channel Blocker
Overdose)

Obstructive Shock: Causes

MAP =

SVR

Heart is working but there is a block to the outflow

CO (HR x Stroke Volume)

Massive pulmonary embolism

Aortic dissection
Cardiac tamponade
Tension pneumothorax

Obstruction of venous return to heart

Vena cava syndrome - eg. neoplasms, granulomatous disease
Sickle cell splenic sequestration

Hypovolemic Shock: Causes

MAP =

CO (HR x Stroke Volume)

SVR

Decreased Intravascular volume (Preload) leads to

Decreased Stroke Volume
Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic
pregnancy
Hypovolemic - burns, GI losses, dehydration, third spacing (e.g.
pancreatitis, bowel obstruction), Adesonian crisis, Diabetic
Ketoacidosis

Distributive Shock: Causes

MAP

CO (HR x SV) x

SVR

Loss of Vessel tone

Inflammatory cascade
Sepsis and Toxic Shock Syndrome
Anaphylaxis

Post resuscitation syndrome following cardiac arrest

Decreased sympathetic nervous system function
Neurogenic - C spine or upper thoracic cord injuries

Toxins
Due to cellular poisons -Carbon monoxide,
methemoglobinemia, cyanide
Drug overdose (a1 antagonists)