2. What is Shock????
• Profound hemodyamic and metabolic
disturbance characterized by failure of the
circulatory system to maintain adequate
perfusion of vital organs.
• Normal relationship between oxygen demand
and oxygen supply is impaired.
3. Etiology of circulatory shock
Reduced cardiac output
Hypovolaemic shock
• Reduction in circulating volume causing a reduction in venous
return and consequential reduction in cardiac output
• haemorrhage
• Dehydration
Obstructive shock
• Mechanical obstruction to normal venous return or cardiac
output
• massive pulmonary embolism
• tension pneumothorax
• cardiac tamponade
5. Low peripheral resistance
Distributive shock
• Peripheral vasodilatation – may be associated with
inadequate increase in cardiac output
• septic shock
• anaphylaxis
• neurogenic
Endocrine shock
• Addisonian crisis
• Hyper/hypothyroid crisis
6. Stages of shock
• Nonprogressive stage (sometimes called the
compensated stage) - normal circulatory compensatory
mechanisms eventually cause full recovery without
help from outside therapy.
• Progressive stage - without therapy, the shock
becomes steadily worse until death.
• Irreversible stage - shock has progressed to such an
extent that all forms of known therapy are inadequate
to save the person’s life, even though, for the moment,
the person is still alive.
7. What makes the shock to go into compensated
or decompensated state???
• Depends on the feedback mechanism elicited by the
shock
• Can be negative feedback mechanism or positive
feedback mechanism.
• Negative feedback predominant – compensdated
stage of shock
• Termed negative because the direction of the
secondary change in response to shock is opposite to
the direction of the initiating change
8. • Positive feedback mechanisms exaggerate any
primary change initiated aggravating the hypotension
induced by shock and tend to initiate "vicious"
cycles, which may lead to decompensated or
irreversible stage.
• Whether a positive feedback mechanism will lead to
a vicious cycle depends on the gain of that
mechanism.
• Gain is defined as the ratio of the secondary change
evoked by a given mechanism to the initiating
change itself.
• A gain greater than 1 induces a vicious cycle; a gain
less than 1 does not
9. Non progressive or compensated shock
Negative feedback mechanism responsible for
non progression of shock includes:
Baroreceptor reflexes –
• elicit powerful sympathetic stimulation of the circulation.
• Generalized arteriolar constriction is a prominent response to the
diminished baroreceptor stimulation
• The reflex increase in peripheral resistance minimizes the fall in
arterial pressure caused by the reduction of cardiac output.
• Vasoconstriction most pronounced in the cutaneous, skeletal
muscle and splanchnic vascular beds, slight or absent in the
cerebral and coronary circulations.
• Renal vasoconstriction resisted by autoregulatory mechanism
initially but with severe shock there occurs intense renal and
splanchnic vasoconctriction.
10. Chemoreceptor reflexes.
• Reductions in arterial pressure below about 60 mm Hg do not evoke
any additional responses through the baroreceptor reflexes.
• Inadequate blood flow hypoxia in chemoreceptor tissues and
activation of chemoreceptor reflex.
CNS ischaemic response.
• Fall in Mean Arterial Pressure below 50 mm hg activates the response.
• The sympathetic nervous discharge is several times greater than the
maximal neural activity that occurs when the baroreceptors cease to be
stimulated.
• With more severe degrees of cerebral ischemia, however, the vagal
centers also become activated.
Reverse stress-relaxation of the circulatory system,
• causes the blood vessels to contract around the diminished blood
volume, so that the blood volume that is available more adequately fills
the circulation.
11. Formation of endogenous vasoconstrictors.
• Epinephrine from the adrenal medulla, whereas norepinephrine from both
the adrenal medulla and the peripheral sympathetic nerve endings
reinforce the effects of sympathetic nervous.
• Vasopressin , a potent vasoconstrictor, is actively secreted by the
posterior pituitary gland.
• The plasma concentration of vasopressin rises progressively as the
arterial blood pressure diminishes. The receptors responsible for the
augmented release of vasopressin are the sinoaortic baroreceptors and
stretch receptors in the left atrium.
12. • Diminished renal perfusion during shock secretion of renin from
the juxtaglomerular apparatus conversion of angiotensinogen to
angiotensin I ACE converts angiontensin I to angiotensin II.
• Angiotensin II is a powerfull vasoconstrictor.
Compensatory mechanisms that return the blood volume back
toward normal.
• Absorption of fluid into the blood capillaries from the interstitial spaces
of the body.
• conservation of water and salt by the kidney by release of aldosterone.
• increased thirst and increased appetite for salt, which make the person
drink water and eat salty foods if able.
13. Progressive stage of shock
• Caused by a vicious circle of cardiovascular
deterioration.
• Positive feedback mechanism evoked by
uncorrected shock results in the vicious progression.
• Requires prompt and aggressive intervention else
the shock enters the irreversible stage where death
is imminent
14. • Different types of “positive feedback” that can lead to progression of
shock. (courtesy- guyton n hall textbook of physiology 11th edition
15. Cardiac depression.
• blood pressure coronary blood flow hypoxia and decrease
nutrition of myocardium leading to diminshed contractility and reduced
cardiac output.
• The consequent reduction in cardiac output leads to a further decline in
arterial pressure, a classic example of a positive feedback mechanism
• The role of cardiac failure in the progression of shock during
hemorrhage is controversial.
• The reduced blood flow to the peripheral tissues leads to an
accumulation of vasodilator metabolites which decreases peripheral
resistance and therefore aggravates the fall in arterial pressure
• All investigators agree that the heart fails terminally, but opinions
differ about the importance of cardiac failure during earlier stages of
hemorrhagic hypotension.
• The heart has tremendous reserve capability that normally allows it to
pump 300 to 400 per cent more blood than is required by the body for
adequate bodywide tissue nutrition.
16. Ventricular function curve for the left ventricle during the course of hemorrhagic shock.
Curve A represents the control function curve; curve B, 117 min; curve C, 247 min; curve D,
280 min; curve E, 295 min; and curve F, 310 min after the initial hemorrhage. (Redrawn from
Crowell JW, Guyton AC: Am J Physiol 203:248, 1962.)
17. Vasomotor Failure.
• Diminished blood flow to the brain’s vasomotor center
depresses the center so much that it becomes progressively
less active and finally totally inactive.
• Complete circulatory arrest to the brain for 10 to 15 minutes,
depresses the vasomotor center such that no evidence of
sympathetic discharge can be demonstrated.
• The resulting loss of sympathetic tone then reduces cardiac
output and peripheral resistance which reduces mean arterial
pressure and intensifies the inadequate cerebral perfusion.
• Various endogenous opioids, such as enkephalins and β-
endorphin, may be released into the brain substance or into
the circulation in response circulatory shock, which further
depresses brainstem centres.
• Vasomotor center usually does not fail if the arterial
pressure remains above 30 mm Hg
18. Acidosis.
• The inadequate blood flow during shock affects the metabolism
of all cells in the body.
• Hypo-perfusion reduces adenosine triphosphate (ATP)
availability required for maintenance of transmembrane
potential. Leaky cell membranes cause interstitial fluid uptake
and massive cell oedema.
• This oedema obstructs adjacent capillaries reducing oxygen
delivery
• The decreased oxygen delivery to the cells accelerates the
production of lactic acid and other acid metabolites by the
tissues.
• Impaired kidney function prevents adequate excretion of the
excess H+, and generalized metabolic acidosis ensues .
• The resulting depressant effect of acidosis on the heart further
reduces tissue perfusion and thus aggravates the metabolic
acidosis
19. • Acidosis also diminishes the reactivity of the heart and
resistance vessels to neurally released and circulating
catecholamines, and thereby intensifies the hypotension.
Blockage of Very Small Vessels—“Sludged Blood.”
• sluggish blood flow in the microvessels due to decrease
arterial pressure leads to their blockage.
• Acidosis and deterioration products from the ischemic
tissues, causes local blood agglutination, resulting in minute
blood clots, leading to small plugs in the small vessels.
• an increased tendency for the blood cells to stick to one
another makes it more difficult for blood to flow through the
microvasculature, giving rise to the term sludged blood.
20. Aberrations of blood clotting.
• The alterations of blood clotting after hemorrhage are
typically biphasic. An initial phase of hypercoagulability is
followed by a secondary phase of hypocoagulability and
fibrinolysis.
• In the initial phase, platelets and leukocytes adhere to the
vascular endothelium, and intravascular clots, or thrombi,
develop few minutes of the onset of severe hemorrhage.
• Coagulation may be extensive throughout the small blood
vessels.
• The initial phase is further enhanced by the release of
thromboxane A2 from various ischemic tissues.
• Thromboxane A2 aggregates platelets. As more platelets
aggregate, more thromboxane A2 is released and more
platelets are trapped
21. • Later tisuue ischaemia activates endothelial plasminogen
activator whilst hypo-perfusion inhibits plasminogen
activator inhibitor, thus promoting hyperfibrinolysis.
• Acidosis inhibits the activity of coagulation factors and
leads to increased degradation of fibrinogen.
• systemic activation of the anticoagulant protein C pathway
also occurs in later stage of shock.
Increased Capillary Permeability.
• In prolonged shock due to capillary hypoxia and lack of
other nutrients, the permeability of the capillaries gradually
increases, and large quantities of fluid begin to transude into
the tissues.
• Further deteriorates blood volume and cardiac output.
22. Release of Toxins by Ischemic Tissue.
• shock causes tissues to release toxic substances, such as
histamine, serotonin, and tissue enzymes, that cause further
deterioration of the circulatory system.
• Endotoxin is released from the bodies of dead gram-
negative bacteria in the intestines.
• Diminished blood flow to the intestines often causes
enhanced formation and absorption of this toxin.
• The circulating toxin causes cardiac depression and further
decreases cardiac output.
23. Depression of Reticuloendothelial system.
• During the course of circulatory shock, reticuloendothelial
system (RES) function becomes depressed.
• The phagocytic activity of the RES is modulated by an
opsonic protein and the opsonic activity in plasma
diminishes during shock.
• When the RES is depressed, normal flora endotoxins
invade the general circulation. Endotoxins produce
profound, generalized vasodilation, mainly by inducing the
abundant synthesis of an isoform of nitric oxide synthase
in the smooth muscle of blood vessels throughout the
body.
• The profound vasodilation aggravates the hemodynamic
changes.
24. Vasopressin deficiency.
• posterior pituitary hormone released in response to increased
plasma osmolality or decreased intravascular volume.
• Plasma vasopressin levels subsequently decline, secondary
to depletion of the pituitary neurohypophyseal stores.
• Decrease vasopressin decreased vasoconstriction and
renal absorption of fluid decreased blood volume
decreased cardiac output.
Activation of ATP-sensitive potassium channels
(KATP)
• KATP channel opening allows an efflux of potassium ions
and results in membrane hyperpolarization and reduced
calcium ion movement into the cell.
25. • Under resting conditions, the KATP channels are closed.
• Altered tissue metabolism or hypoxia leads to channels
activation, causing vasodilatation.
• Vasodilation decreased peripheral resistance,
decreased venous return decreassed cardiac out put
Activation of the inducible form of nitric oxide
synthase enzyme.
• Nitric oxide is a vasodilator produced in vascular
endothelium.
• Production is controlled by a group of enzymes called nitric
oxide synthases.
• In shock, there is an increased expression of the inducible
form of nitric oxide synthase (NOS) due to circulating
cytokines
• Increase NOS increase NO increase vasodilation
26. Generalized Cellular Deterioration.
• Active transport of sodium and potassium through the
cell membrane is greatly diminished sodium and
chloride accumulate in the cells, and potassium is lost
from the cells the cells begin to swell.
• Mitochondrial activity in the tissues becomes severely
depressed.
• Lysosomes in the cells in widespread tissue areas begin
to break open, with release of hydrolases that cause
further intracellular deterioration.
• Cellular deterioration further leads to multiorgan
failure.
• Lobular necrosis begins to occur in liver.
27. • Necrosis of the central portion of a liver lobule in severe circulatory
• shock. (Courtesy Dr. J. W. Crowell.)
28. • Pulmonary failure “shock lung’’ ensues.
• Initial phase: intrapulmonary blood volume
ventilation-perfusion ratio.
• Late phase: fibrin and leucocytes in interstitial
and alveolar spaces.
• Accumulation of Neutrophill in pulmonary
circulation release of proteases
• permeability - surfactant, edema and hemorrhagies
• Adult respiratory distress syndrome:
29. • In kidney blood flow GF oliguria.
• Countercurrent mechanism failure isosthenuria
• Ischemia of renal tissue azotemia and acute
tubular necrosis
• Marked ischemia acute renal failure.
30. Interactions of Positive and Negative Feedback
Mechanisms
• The gain of any specific mechanism varies with the
severity of the shock .
• With only a slight loss of blood, mean arterial pressure is
within the normal range and the gain of the baroreceptor
reflexes is high.
• With greater losses of blood, when mean arterial pressure
is below 60 mm hg the baroreceptor reflex gain is zero or
near zero.
• a general rule, with minor degrees of blood loss, the gains
of the negative feedback mechanisms are high, whereas
those of the positive feedback mechanisms are low and
vice versa
31. Irreversible stage of shock
• Any therapeutic intervention ceases to be effective.
• Therapy can, on rare occasions, return the arterial pressure
and the cardiac output to normal or near normal for short
periods, but the circulatory system continues to deteriorate,
and death ensues in another few minutes to few hours.
32. Why no going back from irreversible
stage of shock??
• The high-energy phosphate reserves in the tissues of the
body, are greatly diminished in severe degrees of shock.
• All the adenosine triphosphate downgrades to adenosine
diphosphate, adenosine monophosphate, and, eventually,
adenosine.
• adenosine diffuses out of the cells into the circulating
blood and is converted into uric acid, a substance that
cannot re-enter the cells to reconstitute the adenosine
phosphate system.
• Adenosine depleted is difficult to replenish
• The cellular depletion of these high energy compounds
leads to no going back.
33. Monitoring CO, securing CV line Adequate volume correction,
inotropes and vasopressors
Early management – Recovery
Delayed care – Progression to
irreversible stage
Identifying and correcting the cause
of shock
