College of Health Sciences

Integrated Sciences Division

BMS Department

CHS
 Objectives
At the end of the Chapter, the student must be able to:
1. define circulatory shock.
2. discuss the three types of shock in detail
3. recognize the reflex compensatory mechanisms
activated during circulatory shock
4. explain the mechanisms behind the compensations
done by the body to restore normal blood pressure
5. cite the various systemic effects of circulatory shock
6. discuss in detail the systemic effects of shock in acute
renal failure.
 Objectives
7. compare and contrast the three main stages of
circulatory shock progression
8. discuss the therapy of shock
o Circulatory shock is a condition in which the
cardiovascular system fails to perfuse tissues
adequately.

o Inadequate tissue perfusion can result in:

– generalized cellular hypoxia
– widespread impairment of cellular
metabolism
– tissue damage  organ failure
– death
PATHOPHYSIOLOGY OF SHOCK

oImpaired tissue perfusion occurs when an

imbalance develops between cellular oxygen
supply and cellular oxygen demand.
oAdequate blood flow to microcirculation
depends on arterial blood pressure, which, in
turn depends on:

 Cardiac output
 Blood volume (plasma volume)
 Peripheral vascular resistance
Types of Shock
• Cardiogenic Shock
– PUMP problem

• Hypovolemic Shock
– VOLUME problem

• Vascular Shock (Septic, Anaphylactic)

– VESSEL problem
 A. Cardiogenic Shock

• The impaired ability of the heart to pump

blood
• Most common cause is LV Anterior MI
• Occurs when > 40% of ventricular mass is lost
• Mortality rate of 80 % or more.
 Ponder Point
List down other etiologies that produce a rapid
myocardial failure leading to cardiogenic shock

Refer to page 295 - 296

 Cardiogenic Shock
Impaired pumping ability of LV

Decreased SV

Decreased CO

Decreased BP

 Tissue perfusion
 Hypovolemic Shock

Inadequate circulating blood volume 

Decrease tissue perfusion  Shock

o ETIOLOGY:
 Internal fluid/blood loss
 External fluid/blood loss

o Most common causes:

 Hemorrhage
 Dehydration
Etiologies of Hypovolemic Shock:

1A.  Capillary hydrostatic pressure

Eg. Severe thromboembolism
1B ---Capillary damage (trauma,anoxia,immune)
2. Dehydration
• Diarrhea & vomiting
• Kidney disease (Protein loss & electrolyte
imbalance)
3. Hemmorhage
4. Third Degree burns
Pathophysiology of Hypovolemic Shock
Decreased intravascular volume

Decreased venous return

Decreased ventricular filling

Decreased stroke volume

Decreased CO

Inadequate tissue perfusion
• Compensatory / adjustment mechanisms can
restore BP to normal if there are only small
volume and pressure declines
 Vascular Shock
o Widespread vasodilation   BP

o Inadequate perfusion of tissues

o Intravascular volume is improperly distributed

because of alterations in blood vessels as a lot of
plasma goes into the interstitial spaces and leads to
decrease in blood volume

o Common types of vascular shock:

1. Septic shock (most common)
2. Anaphylactic shock
Septic shock
Initiated by severe gram-negative (most common) or gram
positive bacteria, fungi, or viruses

Massive phagocytosis of bacteria

Release of Endotoxins

 Monocytes & macrophages to release TNF-α and other
mediators

1. Systemic arteriolar
vasodilation
2. Endothelial damage

 Capillary permeability and movement of fluid into interstitial
spaces
Pathophysiology of Septic Shock
 Ponder Point
What is toxic shock?
What are the sources of toxins in toxic shock?

Refer to page 299

2. Anaphylactic Shock

 A type of vascular shock that results from

widespread systemic allergic reaction
following a 2nd exposure to an antigen

 This hypersensitive reaction is LIFE

THREATENING
Pathophysiology of Anaphylactic Shock
1st Antigen (allergen ) exposure

Body stimulated to produce IgE
antibodies specific to an antigen


Re-exposure to antigen causes IgE binding to mast

cells and basophils

Release of chemical mediators of inflammation
(eg. histamine and serotonin)

Anaphylactic response
Anaphylactic response:
o Vasodilatation
o Increased vascular permeability
o Bronchoconstriction
o Increased mucus production
o Increased inflammatory mediators
 Reflex Compensations In Shock
A. Baroreceptors & CV Centre (medulla)

B. CNS ischemic response

C. Interstitial fluid shift

D. Kidneys: RAAS
A. Baroreceptors
• These are pressure-sensitive receptors located
in the:
a. aortic arch
b. carotid sinus

• These send BP-related information to the

cardiovascular integrating center in the
medulla oblongata which, in turn, sends
responses to adjust BP.
Reflex Compensation in Shock

Reflex Control of Blood Pressure

• CVS reflexes function to adjust BP during normal
activities.

• Baroreceptos also stimulate the Sympathetic nervous

system (SNS), effects of which are:

a. increased heart rate

b. increased contractility
c. vasoconstriction (increased afterload)
d. increased preload
B. CNS Ischemic Response

Extreme decrease in BP


CV center neurons are directly affected by

ischemia and hypoxia


Intense Sympathetic stimulation

- purpose is to raise BP to avoid serious anoxic
damage to the CNS.
C. Interstitial Fluid Shift

BP

Blood Hydrostatic Shift of fluid from tissue to
pressure capillaries

Less tissue fluid formed 

Increase in plasma volume
BHP falls less rapidly and systemic arterial
 pressure is supported.
BP
 Ponder Point

Review and discuss the response of the kidney

to a decrease in renal perfusion
via the
Renin-Angiotensin-Aldosterone System

Refer to page 301

 Failure of Compensatory Response

o Decreased blood flow to the tissues causes

cellular hypoxia
o Anaerobic metabolism begins
o Cell swelling, mitochondrial disruption, and
eventual cell death
o If low perfusion states persist:

IRREVERSIBLE  DEATH IMMINENT!!

Systemic Effects of Shock
 Ponder Point
Enumerate the possible
systemic effects of circulatory shock
Refer to pages 302 - 303
Systemic Effects of Shock

Acute Renal Failure

 Stages of Shock
1. Non-Progressive Shock

o Compensatory mechanisms and therapy

succeed in reversing shock and may lead to
full recovery.

o Reflex compensatory mechanisms are

activated  BP and tissue perfusion
resorted to normal
2. Progressive Shock
o Characterised by tissue hypoperfusion and organ
damage

o Depression of cardiac function

o Pressure loss, inadequate compensation, lack of

therapy intervention  progressive decline of
tissue perfusion  hypoxic cell injury to vital
organs  Initiation of positive feedback cycling 
Rapid deterioration
Positive Feedback Cycling
 Ponder Point

Revise through Figure 11.12

page 304

Progressive Shock
3. Irreversible Shock
o Death occur due to severe organ damage
even if aggressive therapy restores blood
pressure.

o Since the point of irreversible damage is

difficult to determine, therapy is
maintained vigorously until shock
progression is arrested or death occurs.
Circulatory Shock Therapy
 Therapy in Shock
• First restore blood flow to dependent tissues
– Hypovolemic shock  fluid replacement

• Eliminate cause of shock

– May be difficult in cadiogenic shock (e.g. MI)

• Drug therapy:
– Neurogenic or Vascular  give vasoconstrictors
– Cardiogenic  Improve CO, reduce afterload
Eg. Isoproterenol

• Surgery eg. Cardiac tamponade

• Antibiotics eg. Septic shock

• Hypovolemic shock has a better prognosis as compared to cardiogenic

or septic shock because fluid replacement can easily be given.
 Reference
• Unless otherwise specified, all information and
multimedia in this presentation were obtained from:

Pathophysiology : Concepts and Applications for

Health Care Professionals , Third edition

By Thomas J. Nowak & A. Gordon Handford

Chapter 11 Circulatory Shock

Pages 294 - 305