DEPARTMENT OF PATHOLOGY
BANGLADESH MEDICAL COLLEGE
DEFINATIONShock give rise to systemic hypoperfusion caused by reduction either in cardiac
output or in effective circulatory blood volume.
End results are : Hypotension
Irreversible injury with persistent of shock
End organ dysfunction
Hypovolumic shock occurs due to rapid reduction in blood
volume or plasma volume.
Causes of hypovlumic shock :
2. Severe dehydration-severe vomiting, severe diarrhea
3. Severe burn
4. Abdominal ascities
5. Acute pancreatitis
6. Diabetes mellitus
7. Over use of Diuretics
Pathophysiology of hypovolumic shock :
Reduction in intravascular blood volume
Decreased stroke volume & CO
Tissue ischemia, hypoxia
Cellular & organ dysfunction
Cardiogenic shock is characterized by reduced pumping
ability of heart due to intrinsic myocardial damage or
extrinsic or obstruction to out flow. It is most commonly
occurs in association with and as a direct result of acute
-Cardiogenic shock occurs in 8.6% of patient with ST
-Myocardial ischemia with 29% of those presenting to the
hospital already in shock.
-2% of non ST segment elevation MI.
Risk factor :
-Pre existing myocardial damage
Pathophysiology of cardiogenic shock :
Myocardial ischemia or injury Myocardial dysfunction
Systemic inflammatory response Decreased CO & stroke volume
Increased NO synthesis Systemic hypoperfusion Hypotension
Vasodilatation Decreased coronary perfusion
Compensatory vasoconstriction Cardiac & other end organ damage
Progressive myocardial dysfunction
Sepsis is a clinical state that accompanies infection either
confined to a local site from which toxin are absored or
associated with invasion of organism in to the blood
Causes of septic shock:
-Overhelming microbial infection
-Gram +ve septicemia
-Endotoxic shock (Gram –ve septicemia)
Pathophysiology of septic shock :
Endotxin ( LPS ) & other microbial products
Binds to LPS binding protein in serum
Binds to CD14 receptors on mononeuclear cells
CD14 binds to TLR4
Release of chemical mediators
Pathophysiology of septic shock :
Patho-physiology of septic shock :
In septic shock systemic vasodilatation and pooling
of blood in the periphery leads to tissue hypo
perfusion and though the cardiac out put is preserved
this is accompanying widespread endothelial cell
activation and often leads to hablypercoagulable state
that can manifest DIC.Septic shock is associated with
change in metabolism that can directly suppress
cellular function. The net effect is hypo perfusion and
dysfunction of multi-organ.
Major factors contributing to the pathophysiology of septic shock are
Various microbial cell wall contains lipopolysaccaride are
released when the cell wall are degraded. Free LPS bind to circulatory
LPS.This complex then binds to a cell surface receptor CD14 on
macrophage, mononuclear paghocytic cell, endothelial cell.CD14
binds to the signal transducing protein TLR-4.Upon activation
cascade of cytokines mediators TNF,TL-1,IL-8,INF- .The compliment
cascade are activated directly or through proteolytic activity of
plasmin resulting in production of anaphylotoxins
C3a&C5a,chemotatctic factor C5a causes vasodilatation & increases
vascular permeability.Activated endothelial cell and macrophage
release NO contribute to pro-inflammatory state.
Endothelial cell activation and injury:
Endothelial cell activation by microbial products or
inflammatory mediators produced by leukocytes. Has 3
major sequele-thrombosis,increase vascular
Pro-inflammatory cytokines result in increased tissue
factor production by endothelial cell and monocyte.The
production of endothelial anti-coagulant factor-tissue
factor pathway inhibator,thrombomodulin and protein-C
reduced.Reduced blood flow at the level of small vessels'
produce stasis that reduce the wash out of activated
coagulation factor results in deposition of fibrin rich
thrombi in small vessels, that lead to tissue
In DIC increase consumption of coagulation factor &
platelet leads to bleeding & hage.
Increase vascular permiability leads exudation of
fluid in to interstitum causing oedema.
Endothelium increase the relase of NO.
Metabolic abnormalities:Septis patient exhibit insulin
resistance and hypoglycemia. Cytokines such as TNF
& IL-1,stress induced
gluconeogenesis.At the same time the pro-
inflammatory cytokines suppress insulin release while
simultaneously promoting insulin resistance in the
liver & other tissue, by surface expression of glucose
transporter. Hyperglycemia reduced neutrophil
function & bactericidal activity. Sepsis also related
with adrenal insufficiency & factional deficency of
hyper inflammatory state activate immuno-
suprssion mechanism which involve both innate &
adaptive immunity by production of anti-
inflammatory mediators(soluable TNF receptors,IL-
recepor antagonist& IL-10).
Systemic hypotension, interstitial edema, small
vessels thrombosis reduce the delivery of oxygen &to
High level of cytokines, secondary mediators reduces
myocardial contractility & CO. Increase vascular
permeability & endothelial injury acute respiratory
distress syndrome ultimately cause multiple organ
Toxic shock syndrome:
Toxic shock syndrome is a potentially fatal illness
caused by bacterial toxin(super antigen) released by –
Staphylococcus aureus & Streptococcus pyogens.
Streptococcal TSS associated with recent soft tissue
injury like surgery,pharyngitis,NSAID drug use.
Staphylococcal TSS observe mostly among
menstruating women, but also associated with cutaneous
infection, post-partum & C/S wound infection & focal
staphylococcal infection like abscess,empyma,pneumonia.
Neurogenic shock occurs in the setting of anesthetic
accident or spinal cord injury causes loss of vascular
tone and peripheral pulling of blood.
In Anaphylactic shock,decreased systemic vascular
resistance due primarily to massive histamine release
from mast cell after activation of IgE mediated
hypersensitivity reaction as well as increase synthesis
of prostaglandin. That leads to vasodilatation and
increase vascular permiability.Ultimate results are
systemic hypotension, tissue perfusion and cellular
Causes of anaphylactic shock:
2.Accidental exposure to an allergen and co-exiting
respiratory complaints(wheezing & dyspnea)& or
Systemic inflammatory response in anaphylactic shock:
STAGES OF SHOCK
1.An initial non progressive phage
2.A progressive stage
3.An irreversible stage
An initial non progressive phage:
In this phage a varieties of neuro-hormonal &
haemostatic mechanism helps to maintain cardiac
out-put & blood pressure. These includes:
- Baro-receptor reflex mechanism
- Release of catecholamine's
- Activation of Renin-angiotension axis
- Anti-diuretic hormone release
-Generalized sympathetic activation
Net effects are- 1.Tachycardia
3.Renal conservation of fluid
Resulting in restoration of circulation and tissue
If the compensatory mechanism fails to restore
circulation, vital organ shows the effects of
hypoxia.Persistant oxygen deficiency leads to intra
cellular anaerobic glycolysis with lactic acidosis,thus
reduce tissue pH and vasomotor response. Resulting
reduce cardiac output and anoxic injury to
endothelial cell leads to DIC.
When there is failure to restore circulation either
by compensatory mechanism or by therapeutic
intervention,the process of shock enters the
irreversible stage. Wide spread cell injury is reflected
in lysosomal enzyme lekage,nitric oxide reduced
myocardial contractility,acute tubular necrosis
MORPHOLOGY OF SHOCK
Since shock is characterized by failure of multi-organ
systems, the cellular changes may appear in any tissue.
Brain: ischemic encephalopathy.
Heart: coagulative necrosis or subendocardial hemorrhage
or contraction band necrosis.
Kidney: acute tubular necrosis.
Lung: diffuse alveolar damage develop shock lung.
Gastrointestinal tract: Hemorrhagic enteropathy.
Adrenal gland: cortical cell lipid depletion may occur.
Liver: fatty change, central hemorrhagic necrosis.
CLINICAL PRESENTATION OF
Altered mental status-
Patient may unconscious or semi-conscious
Cold clammy skin. Warm in septic shock
Pulse-Tachycardia, rapid weak thready pulse
Respiration-Tachypnia, slow and regular
Blood pressure-low blood pressure
Temperature may or may not be raised
Reduce urine output
DIAGNOSIS OF SHOCK
General and physical examination
Vital sign assessment
MANAGEMAENT OF SHOCK
Admitted in intensive care unit
Clear airway, adequate breathing, assessment of circulation-
Position of the patient
Trendelenburg or supine position to increase cerebral blood
Oxygenation-High flow oxygen should be delivered.
Establish IV access
Restore circulatory blood volume-blood in case of
bleeding,crystalioid(n/s,ringer’ s lactate )
Dopamine with or with out dobutamine provide
ionotropic support increasing perfusion of the ischemic
myocardium &all body tissue.
Surgical intervention if needed.
Insulin therapy in case of hyperglycemia
Treatment of underlying cause:
Broad spectrum antibiotic coverage in case of infection.
Cardiogenic shock-treatment according to cause such as
MI or left ventricular failure.
Hypovolumic shock-adrenalin I/m Hydrocortisone
In acute adrenal insufficiency-Corticosteroid use as
life saving drug.
Activated protein-C can be use in severe sepsis.
The prognosis varies with the origin of shock and its
80%-90% of young with hypovolumic shock survive
with appropiate management.
Cardiogenic shock associated with extensive
myocardial infraction mortality rate up to 75%
Septic shock -mortality rate up to 75%
PROGNOSIS OF SHOCK