infarction to shock

7/30/2019 infarction to shock

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Infarction


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Infarct

An area of ischemic necrosis caused by

occlusion of either the arterial supply or the

venous drainage in a particular tissue


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Infarct

Nearly 99% of all infarcts result from

thrombotic or embolic events, and almost all

result from arterial occlusion

Infarcts caused by venous thrombosis are

more likely in organs with a single venous

outflow channel, such as the testis and ovary.


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Red infarcts occur

(1)With venous occlusions(2)In loose tissues

(3) In tissues with dual

circulations

(4) In tissues that werepreviously congested

because of sluggish venous

outflow

(5) When flow isreestablished to a site of

previous arterial occlusion

and necrosis


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solid organs

Arterial insufficiency


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All infarcts tend to be wedge-

shaped, with the occluded

vessel at the apex and theperiphery of the organ

forming the base

The lateral margins may be

irregular, reflecting the

pattern of vascular supply

from adjacent vessels


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Initially

all infarcts are poorly definedand slightly hemorrhagic

Eventually

the margins of both types ofinfarcts tend to become

better defined by a narrowrim of hyperemia attributableto inflammation at the edgeof the lesion


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In solid organs

the relatively fewextravasated red cells are

lysed, with the releasedhemoglobin remaining in theform of hemosiderin.

white infarcts typicallybecome progressively morepale and sharply defined withtime


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In spongy organs

Over the course of a few

days

become more firm and

brown, reflecting the

development of

hemosiderin pigment


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The dominant histologic characteristic of

infarction is ischemic coagulative necrosis

Ischemic injury in the central nervous system

results in liquefactive necrosis


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Factors That Influence Development of

an Infarct

Nature of the vascular supply:

The availability of an alternative blood supply

Rate of development of occlusion:

Slowly developing occlusions are less likely to

cause infarction since they provide time for the

development of alternative perfusion pathways


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Factors That Influence Development of

an Infarct

Vulnerability to hypoxia: The susceptibility of a tissue to hypoxia influences the

likelihood of infarction

Neurons: 3 to 4 minutes

Myocardial cells: 20 to 30 minutes of ischemia

Oxygen content of blood: The partial pressure of oxygen in blood

Partial flow obstruction of a small vessel in an anemicor cyanotic patient might lead to tissue infarction,whereas it would be without effect under conditionsof normal oxygen tension


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Shock

Cardiovascular collapse

Systemic hypoperfusion

Reduction either in cardiac output or in theeffective circulating blood volume

hypotension impaired tissue

perfusion and cellular hypoxia tissueinjury death


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Cardiogenic shock

low cardiac output


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Cardiogenic shock

Myocardial pump failure

Intrinsic myocardial damage (infarction)

Ventricular arrhythmias

Extrinsic compression (cardiac tamponade)

Outflow obstruction (e.g., pulmonary embolism)

Rupture of aortic aneurysm


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Hypovolemic shock

low cardiac output


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BURNS


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Septic shock

Septic shock results from spread and

expansion of an initially localized infection

Endotoxins

bacterial wall lipopolysaccharides (LPS) released

when the cell walls are degraded

lipid A core and a complex polysaccharide coat

unique to each bacterial species


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Systemic microbial infection

Gram-negative infections (endotoxic shock)

Also occur with gram-positive and fungal infections


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Neurogenic shock

Loss of vascular tone and peripheral pooling

of blood due to peripheral or central

vasomotor injury

Anesthetic accident

Spinal cord injury


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Episode: Nine Inch Nailed


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Anaphylactic shock


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Generalized IgE-mediated hypersensitivity response Associated with systemic vasodilation and increased

vascular permeability


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Endocrine shock

Total pituitary and adrenal failure

Insulin shock (insulin overdose)

causes metabolic disruption and hypovolemia that

in turn lead to a compensatory adrenergic

vasomotor response

Adrenalin shock in pheochromocytoma

causes massive vasoconstriction


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STAGES OF SHOCK

INITIAL NON-

PROGRESSIVEPHASE

Reflexcompensatorymechanism

Vital organs aremaintained

PROGRESSIVE

PHASE Tissue

hypoperfusion

Worseningcirculatory and

metabolicimbalance

IRREVERSIBLE

PHASE Severe cellular and

tissue injury

Survival is notpossible


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Nonprogressive phase of shock

A variety of neurohumoral mechanisms help

maintain cardiac output and blood pressure

baroreceptor reflexes

release of catecholamines

activation of the renin-angiotensin axis

antidiuretic hormone release

generalized sympathetic stimulation


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Nonprogressive phase of shock

Net effect:

Tachycardia, peripheral vasoconstriction, and

renal conservation of fluid

Cutaneous vasoconstriction

Coronary and cerebral vessels

less sensitive to this compensatory sympathetic

response and thus maintain relatively normal caliber,

blood flow, and oxygen delivery to their respective vital

organs

Progressive Phase Widespread tissue


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Progressive Phase: Widespread tissue

hypoxia

Intracellular aerobic respiration is replaced by

anaerobic glycolysis with excessive production

of lactic acid

Blunts the vasomotor response

Arterioles dilate

Blood pools in the microcirculation

worsens cardiac output organ

failure px is confused, u/o is dec

Irreversible stage: Widespread cell


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Irreversible stage: Widespread cell

injury

Lysosomal enzyme leakage

Myocardial contractile function worsens

If ischemic bowel allows intestinal flora to enter

the circulation endotoxic shock

Complete renal shutdown due to acute tubular

necrosis

Death is inevitable


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Morphology

The cellular and tissue changes induced by

shock are essentially those ofhypoxic injury

Since shock is characterized by failure of

multiple organ systems, the cellular changes

may appear in any tissue

Particularly evident in brain, heart, lungs, kidneys,

adrenals, and gastrointestinal tract


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Brain ischemic encephalopathy

Heart

focal or widespread coagulation necrosis subendocardial hemorrhage or contraction band

necrosis

Kidneys typically exhibit extensive tubularischemic injury

oliguria, anuria, and electrolyte disturbances


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Lungs seldom affected in pure hypovolemic shock because they are

resistant to hypoxic injury

Shock lung When shock is caused by bacterial sepsis or trauma, however, changes

of diffuse alveolar damage


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Adrenal glands cortical cell lipid depletion

conversion of the relatively inactive vacuolated

cells to metabolically active cells that use storedlipids for the synthesis of steroids

Gastrointestinal tract

Hemorrhagic enteropathy patchy mucosal hemorrhages and necroses


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Liver

Fatty change

Central hemorrhagic necrosis


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With the exception of neuronal and myocyte

loss, virtually all of these tissue changes may

revert to normal if the patient survives.

Most patients with irreversible changes owing

to severe shock succumb before the tissues

can recover.


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Clinical course

The prognosis varies with the origin of shock

and its duration.

Hypovolemic shock

80 to 90% of young, otherwise healthy patients survivewith appropriate management

Cardiogenic shock associated with extensive

myocardial infarction and gram-negative shock

mortality rates of up to 75%, even with the best care


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Fever


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infarction to shock