Shock is a condition of profound haemodynamic and
metabolic disturbance characterised by failure of the
circulatory system to maintain an appropriate blood
supply to the microcirculation, with consequent
inadequate perfusion of vital organs.
OR
inadequate tissue perfusion
Etiology / classification
• Loss of blood or fluid
• Trauma
• Infection
• Anaphylaxis
• Heart failure
• Strong stimulation of nervous system
Effective perfusion depends on
• Sufficient blood volume
• Normal vasoconstriction / dilation
• Normal function of heart pump
3 stages
• Ischemic hypoxia
• Stagnant hypoxia
• Refractory shock
Ischemic hypoxia
• Altered microcirculation and tissue
perfusion
– Arteriolar and pre-capillary sphincter
constriction, AV shunt
• Underlying mechanisms - varied
Compensatory mechanisms
• Increased heart rate / contractility
• Renin Angiotensin system
• Arteriole constriction
• Venous constriction – auto blood transfusion
• Reduced pressure in capillaries – auto fluid transfusion
• Redistribution of blood flow
Early shock (non-progressive)
activation of renin-alodsterone-angiotensin system ADH secretion - conservation of fluid by kidneys
catecholamine secretion - tachycardia - peripheral
vasoconstriction (except for shock caused by
abnormal vasodilatation)
cold limbs
limited urine output
Significance
Reversible compensatory stage
Stagnant hypoxia stage
• Altered microcirculation and tissue perfusion
• Decompensated stage
– Vessel dilatation
– Blood flow is true capillary
– Stasis of blood
Mechanisms of stasis
• Hypoxia – anaerobic glycolysis – low pH – blunts
vasomotor response to catecholamines – peripheral
pooling of blood
1. Acidosis
2. Local accumulation of metabolic
products:histamine,adenosine, K,kinin etc
3. Altered blood flow:↑ viscosity blood,↓.Perfusion
pressure →RBC & platelet aggregation.↑adhesion
molecules →WBC adhesion and FR production and
lysosomal enzymes →endothelial damage
4. Endotoxins bind TLR → ↑IL-1/TNF
5. Effect of humoral factors: histamine, NO cause
vasodil’n. Endorphin nulls constriction response by
inhibiting vasomotor centr. TXA 2 .→ platelet
aggregationTNF, IL-1 .→ WBC adhesion
BP falls
patient is confused
blood diverted to heart and brain
urine output falls
systemic acidosis
Refractory Stage
• Cardiac depression
• Failure of vasoconstriction responses
• Damage of vessels
• Deficiency of oxygen and nutrients
• DIC, MODS
Irreversible shock
lysosomal enzymes released from damaged cells
skin = cyanosed
kidneys = necrosis of tubular epithelium
gut = necrosis of tubular epithelium (causes sepsis)
lung = necrosis of alveolar epithelium
liver = necrosis of centrilobular cells
brain = necrosis of neurons, coma
heart = myocardial necrosis
death due to multiple organ failure
Multiple Organ Dysfunction
Syndrome (MODS)
Presence of altered organ function
in an acutely ill patient such that
homeostasis cannot be
maintained without intervention
Cellular and molecular mechanisms
• Alteration of cell metabolism
– Acidosis
– Lack of ATP
• Cell injury / apoptosis
• Humoral factors
– Vasoactive amines
– Endothelium derived vasoactive mediators
– Regulated peptides
• Catecholamines:prolonged
vasoconstricn →tissue ischemia &
hypoxia
• Histamine and 5 HT: arteriole & venule
relaxation.
• ↑capillary permeability→plasma
exudation, viscous blood.
• Nitric Oxide: activates guanylate cyclasein
smooth muscle to form cyclic GMP
• Endothelin: increased levels in hypoxia,
ischemia, platelet aggregation and adrenalin.
• Also induce intracellular Ca overload and
direct toxicity to myocardium
Regulated peptides
• Angiotensin
• Vasopressin
• Kinin: bradkykinin from kininogen by action of
kallikrein.dilation of arteriole and venule, increase
microvascular permeability and promote tissue
edema
• Endogenous opiod peptide:Endorphins blunts
constriction response by inhibiting vasomotor center.
Inappropriate inflammatory response
• Vascular endothelial damage
• Permeability – edema
• Impaired oxygen utilization
Metabolic derangements
• Decreased oxygen consumption
• Enhanced glycolysis
• Increased catabolism of fat
• Negative nitrogen balance
Water, electrolyte and acid base disturbance
• Na – K pump dysfunction – increased
intracellular sodium and water
• Anaerobic metabolism, impaired renal
excretion – acidosis
• Initial hyperventilation in compensatory stage
– respiratory alkalosis
• Shock lung in late stage – respiratory acidosis
Types of Shock
Hypovolemic shock
• Acute loss of 15-20% circulating blood volume
• Loss of blood, plasma or fluid, internal hemorrhage, redistribution
• Usually complicated by acute renal failure and endotoxemia
Cardiogenic shock
• myocardial infarction including complications of
myocardial infarction (eg acute mitral regurgitation,
VSD, free wall rupture, LV aneurysm)
• end-stage cardiomyopathy
• myocarditis
• LV outflow obstruction (HOCM, aortic stenosis)
• LV inflow obstruction (mitral stenosis, LA myxoma)
• sequela of cardiopulmonary bypass
Cardiogenic shock
• Compensatory mechanisms such as salt & water
retention and peripheral vasoconstriction tend to
exacerbate LV dysfunction.
• Also decreased perfusion pressure, especially in the
presence of multi-vessel coronary disease leads to
further depression of myocardial contractility.
Septic Shock
Spread and expansion of an initially
localised infection into the bloodstream
70% - endotoxin producing gram-ve bacilli
Escherichia coli, Klebsiella, Enterobacter, Proteus
Pseudomonas aeruginosa - associated with antibiotic
therapy and burn wounds; has very high mortality rate.
"Bacteroides fragilis" - most common cause of anaerobic
septicemias
• Cytokines TNF/IL-1 , stress hormones:
glucagon, GH, glucocorticoids, and
catecholamines →gluconeogenesis.
• Pro inflamatory cytokines suppress insulin
release and also cause insulin resistance in
liver and other tissues.
• Hyperglycemia decreases neutrofil function
→supressing bactericidal activity and cuase
incr. adhesion molecule expression on
endothelial cells. Though sepsis →initial rise
in glucocorticoid production , frequently
followed by adrenal insufficiency probably due
to adrenal necrosis
• Immune suppression: hypeinflammatory state
also activate counter regulatory
immunosuppressive mechanisms. TH2
cytokines increase , lymphocyte apoptosis,
imunosuppressive effect of apoptotic cells.
• MODS: systemic hypotension, interstitial
edema, small vessel thrombosis, decrease
delivery of O2 and nutrients to tissues.
Signs & Symptoms
similar to hypovolaemic shock except in the first stages:
• Pyrexia and fever, or hyperthermia, due to
overwhelming bacterial infection.
• Vasodilation and increased cardiac output due
to sepsis.
Anaphylactic shock
• Antigen antibody reaction – release of histamine by
mast cells
• Venous dilatation
• Arteriole dilatation
• Increased capillary permeability
Signs & Symptoms
• Blood vessels dilate,
producing red, blotchy skin
• Face and neck may swell
• Localised edema, especially
around the face.
• Weak and rapid pulse.
• Breathlessness and cough
due to narrowing of airways
and swelling of the throat.
Neurogenic shock
• Decreased sympathetic control of blood vessel
tone
– Brain / spinal cord injury
– Deep general anaesthesia
Prevention and treatment
• Hemodynamic monitoring
• Basic life support
• Cardiopulmonary resuscitation
• Airway maintenance
• Intravenous access
Improve microcirculation
• Volume replacement
• Acidosis correction
• Vasoactive drugs application
• Treatment of DIC
Block humoral factors
• TNF a monoclonal antibody
• Diphenhydramine
• Glucocorticoids
Cell Protection
• Membrane stabilizer, energy mixture and
free radical scavenger
• Myocyte protection by nicorandil,
glucose/insulin/potassium infusions, direct
inhibition of Na/H exchanger
Organ Protection
• General treatment
• Eliminating free radicals, stabilizing lysosome and supplying
nutrition
• Diuresis and dialysis for shock kidney
• Oxygen therapy and improving ventilation for shock lung
• Reducing pre-load and after-load for heart failure