Circulatory

Shock

Dr Shikha Baisakhiya
Associate Professor
Department of Physiology
GMC Bhopal
 Definition
• Circulatory shock is a syndrome characterized by
serious reduction in tissue perfusion with absolute
or relative reduction in cardiac output
• In other words shock means inadequate delivery of
oxygen, nutrients to vital organs like heart ,brain and
kidneys
• Kumar and Parrillo (1995) - “The state in which
profound and widespread reduction of effective
tissue perfusion leads first to reversible, and then if
prolonged, to irreversible cellular injury.”
 Types of shock
• 1. Hypovolemic shock
• 2. Distributive /Low resistance shock
• 3. Cadiogenic shock
• 4. Obstructive shock
 Shock:
Hypovolemic shock -Classification
due to decreased circulating blood volume in
relation to the total vascular capacity and characterized by a reduction
of diastolic filling pressures
Cardiogenic shock - due to cardiac pump failure related to loss of
myocardial contractility/functional myocardium or
structural/mechanical failure of the cardiac anatomy and characterized
by elevations of diastolic filling pressures and volumes
Extra-cardiac obstructive shock - due to obstruction to flow in
the cardiovascular circuit and characterized by either
impairment of diastolic filling or excessive afterload
Distributive shock - caused by loss of vasomotor control resulting in
arteriolar/venular dilatation and characterized (after fluid
resuscitation) by increased cardiac output and decreased SVR
 Hypovolemic shock
• Also known as cold shock
• Caused by low blood volume resulting in
decreased cardiac output
• Causes :
• Hemorrhagic shock
• Dehydration shock : GIT/Kidney/skin burn
• Traumatic shock : (associated neurogenic
shock )
 Hypovolemic
Shock
Degree of volume loss response
• 10% well tolerated (tachycardia)
• 20 - 25% failure of compensatory mechanisms (hypotension,
orthostasis, decreased CO)
• > 40% loss associated with overt shock (marked hypotension, decreased CO,
lactic acidemia)
Low resistance or vasogenic shock
• This type of shock is also k/a as distributive shock
• It occurs when neural reflexes or toxic
substances cause excess vasodilatation due to
vasodilatation size of capacitance vessels
increase thus cardiac output is decreased in spite
of normal blood volume
• This type of shock is also known as warm shock
as skin is warm and not cold like in hypovolemic
shock
 Types of Low resistance shock
• Neurogenic shock
• Anaphylactic shock
• Septicaemic shock
• Endotoxic shock
 Neurogenic shock
• Marked reduction in vasomotor tone :
• Deep general anaesthesia
• Spinal anaesthesia
• Brain damage
• Antihypertensive drugs
• Postural syncope
• Profound increase in vagal tone :
• Vasovagal syncope
 Anaphylactic shock
• Acute allergic reaction
• Large quantity of histamine and histamine like
substances in allergic reaction causes
widespread vasodilatation reducing peripheral
resistance
• Increased in capillary permeability leads to
fluid loss adding hypovolemic element to low
resistance shock
 Septicemic shock
• Septicemia is a condition in which bacteria circulate and
multiply in blood and form toxic products and cause high
fever
• Septicemia occurs in conditions like acute
peritonitis ,perforation of bowel ,puerperal sepsis
• Septicaemic shock develops due to following effects of
bacteria and toxic products ;
• Marked vasodilatation
• Sludging of blood : RBC Aggutination in response to
degenerating tissue
• DIC
 Endotoxic shock
• Produced by endotoxins released by gram
negative bacteria
• Marked vasodilatation reducing peripheral
resistance
• Depressing myocardial contractility reducing
cardiac output
• Increased capillary permeability causing
hypovolemia
 Cardiogenic shock
• Occurs due to decreased pumping ability of
heart because of some cardiac abnormality
• Severe depression of systolic cardiac function
• Since heart is unable to pump all the venous
return so there occurs congestion in lungs and
viscera
• Also k/a congested shock
 Causes of cardiogenic shock
• Myocardial infarction
• Cardiac arrhythmia
• Congestive heart failure
• Valvular dysfunction
 Obstructive shock
• Occurs due to impairment of ventricular filling
during diastole due to some external pressure
on the heart
• Or impaired systolic contraction due to
increased ventricular afterload
 Classification of
ImpairedCirculatory Shock
EXTRACARDIAC OBSTRUCTIVE
diastolic filling (decreased ventricular preload)
• Direct venous obstruction (vena cava)
- intrathoracic obstructive tumors
• Increased intrathoracic pressure
- Tension pneumothorax
- Mechanical ventilation (with
excessive pressure or volume
depletion)
- Asthma
• Decreased cardiac compliance
- Constrictive pericarditis
- Cardiac tamponade

Impaired systolic
contraction (increased
ventricular afterload)
• Right ventricle
- Pulmonary embolus
(massive)
- Acute pulmonary
hypertension
MODS
 Stages of shock
• First stage :non progressive shock
• Second stage :progressive shock
• Third stage : refractory shock
 First stage
(Non progressive shock)
• Non progressive shock also known as
compensated shock or initial stage of shock
occurs when there is a moderate reduction in
cardiac output secondary to fluid loss or
venous pooling or negative ionotropic effect
on heart depending on type of shock
• Hypovolemic shock due to acute blood loss
occurs when 10-15% of total blood volume is
lost
 Compensatory mechanisms

• Rapid compensatory mechanisms (neural

mechanisms)
• Intermediate compensatory mechanisms
• Long term compensatory mechanisms
Rapid compensatory mechanisms (neural mechanisms)

• Baro receptor reflex

• Chemo receptor reflex
• CNS ischemic response
 Baro receptor reflex

• Decrease in BP
• Decreases baroreceptor discharge
• Generalized increase in sympathetic vasomotor discharge to
heart,arteries and veins
• Generalized vasoconstriction (sparing brain and heart)
• Decrease in cutaneous/splanchnic/skeletal blood flow
• Venoconstriction increases VR and hence CO
• Constriction of afferent and efferent arterioles of kidney decreases
GFR
• By these mechanismsBP is maintained at a level so that blood
flow to vital organs is not affected
• Although it occurs at a cost of other organs
 Chemoreceptor reflex
• Acute hemorrhage leads to loss of RBC leading
to decrease oxygen carrying capacity
• The resultant anemia and hypoxia as well as
acidosis stimulates chemoreceptors
• Activation of VMC
• Same effects as baroreceptor reflex
 CNS ischemic response
• When pressure fall below 50
• Powerful sympathetic discharge occurs due to
direct activation of VMC
 Sign and symptoms
• Rapid compensatory mechanisms account for following
• Pale ,cold, moist skin (due to cutaneous vasoconstriction
and increased sweating due to sympathetic activation )
• Cynotic tinge of skin (due to increased oxygen extraction
from blood)
• Tachycardia and fall in PP (Thready pulse)
• Increased rate and force of respiration (chemoreceptor)
• Oliguria (renal arteiolar constriction)
• Restlessness and apprehension (stimulation of brain stem
reticular formation by catecholamines from adrenal
medulla)
 Intermediate compensatory mechanisms

• Renin angiotensin vaso constrictor mechanism

• Reverse stress relaxation
• Capillary fluid shift mechanism
Long term compensatory mechanisms
• Restoration of plasma volume and proteins
• Restoration of red cell mass
 Restoration of plasma volume and proteins

• After a moderate hemorrhage the plasma volume is

restored to normal in 12 to 72 hours
• Improvement in blood volume is merely because of
increase in amount of plasma (fluid and electrolytes)
• The plasma protein concentration and hematocrit value
is reduced (hemodilution)
• There is rapid entry of preformed albumin from
extravascular stores
• After this initial influx of albumin rest of the plasma
protein loss are restored by hepatic synthesis in 3-4 days
 Restoration of red cell mass
• In mean time there occurs excess release of
erythropoeitin which increases the rate of cell
production in the bone marrow within 10 days
• Normal red cell mass is restored in 4-8 weeks
• Under normal circumstances the circulatory
compensatory mechanisms described above
cause full recovery without help of outside
therapy during the stage of non progressive
shock
• Timely outside therapy hastens the recovery
 Progressive shock
• It is second stage of shock
• It occurs after a 15to 25% loss of total blood volume
• In this stage compensatory mechanisms are not able to stop
progression of shock
• The intense arteriolar constriction in this stage is not adequate to
maintain normal BP
• in progressive shock structures of circulatory system begin to
detoriate and various positive feedback mechanisms develop
• Timely therapeutic intervention are essential at this stage
• Otherwise vicious cycle of positive feedback mechanisms will
cause progressive decrease in cardiac output and patient will go
into stage of refractory shock
 Positive feedback cycles
• Positive feedback cycles are responsible for
continuous progression of shock
• If not interrupted by timely therapeutic
intervention will lead into refractory shock
 Positive feedback cycles
• Cardiac failure
• Vasomotor failure
• Septicemia and toxaemia
 Cardiac failure

• Due to severe decrease in arterial pressure

particularly diastolic pressure the coronary
blood flow decreases leading to coronary
ischemia
• This weakens the myocardium
• Furthur decreases CO and BP
• Progressive cardiac detoriation leads to
complete heart failure
 Vasomotor failure

• Blood flow to heart and brain is usually

preseved when cardiac output is decreased
• However when there occurs severe fall in BP
there occurs cerebral ischemia and failure of
medullary VMC
• Failure of VMC results in vascular dilatation
causing venous pooling and decreased venous
return
• CO and BP are further reduced
 Septicemia and toxaemia

• Due to prolonged vasoconstriction there occurs hypoxia of GIT

• Hypoxic damage causes breakdown of normal protective
mucosal barrier in the gut leading to entry of intestinal
bacteria into portal circulation
• Simultaneous distruction of liver causes bacteria and bacterial
endotoxins to reach the systemic circulation leading to
Septicemia and toxaemia
• Leading to widespread vasodilatation and cardiac depression
• At this stage treatment wont be able to restore the circulatory
functions
Effect on body tissues in progressive shock
• Generalized cellular damage
• Liver/lung/heart damage
• Liver is first organ affected usually
• At cellular level
• Decrease in Na and K active transport through cell membrane leads to
accumulation of Na in the cells so cell begin to swell
• Mitochondrial activity decreases
• Lysosomes begin to split the tissues throughout the body
• Cellular metabolism is decreased
• Hypoxia of tissues lead the cells to switch to anaerobic metabolism leading
to accumulation of lactic acid and also sluggish flow leads to CO2
accumulation
• Acidosis and co2 both increase vasodilatation which further aggravates
shock
 Refractory shock
• Depletion of high energy phosphate compounds
• Mainly in liver and heart
• ATP—ADP—AMP—Adenosine
• Adenosine diffuses out of the cell and gets converted to
uric acid which cannot reenter the cell
• Adenosine synthesis in body occurs slowly hence once
depleted the high energy phosphate stores of the body are
difficult to replenish during shock and this contributes to
final stage of irreversibility
• Patchy necrosis of liver,kidney,lungs heart occurs
(MULTIORGAN FAILURE)
 A Clinical Approach to Shock
Diagnosis and Management
Immediate Goals in
Shock
Hemodynamic support MAP > 60mmHg
PAOP = 12 - 18
mmHg
Cardiac Index > 2.2
L/min/m2
Maintain oxygen
delivery Hemoglobin > 10 g/dL
Arterial saturation >
92% Supplemental
oxygen and mechanical
Reversal of oxygen ventilation
dysfunction Decreasing lactate (< 2.2
mM/L) Maintain urine output
` Reverse encephalopathy
Improving renal, liver function
tests
 General measures of shock

• Room temperature “should be kept cold”

• Raising foot end (Trendelenburg position)
 Replacement therapy

• In hemorrhagic shock
• Whole blood
• Plasma
• Plasma substitute dextran
• In Burn
• Plasma
• Dextran
• In Dehydration
• Infusion of balanced electrolyte solution (ringer lactate)
 Sympathomimetic drugs

• Not much useful in hemorrhagic shock as

sympathetic system is already active
• Useful in neurogenic and anaphylactic shock
(where cause of shock is vasodilatation /loss of
vasomotor tone)
• Dopamine is drug of choice as it causes renal
vasodilatation and vasoconstriction else where it
also has positive ionotropic effect
• Epi/norepi can be used if dopamine not available
 Glucocorticoids

• Useful in anaphylactic shock

• Increase strength of heart
• Stabilize lysosomal membranes prevent
release of enzymes of cells
• Help in glucose metabolism in damaged cells
 Hypovolemic Shock

•Rapid replacement of blood, colloid, or crystalloid

• Identify source of blood or fluid loss

• Cardiogenic Shock (infarction)

•Correction of cardiac cause

• Revascularization
- angioplasty
- coronary bypass
- Extra-cardiac Obstructive Shock
• Pericardial tamponade
• pericardiocentesis
• surgical drainage (if needed)

•Pulmonary embolism
• Heparin
- thrombolytic therapy
- Embolectom
- Distributive Shock
• Identify site of infection and drain, if possible
• Antimicrobial agents (key rules)
• ICU monitoring and support with fluids, vasopressors, and inotropic agents
• Thank you