Infarction

Infarct
An area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue

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.

Red infarcts occur

(1)With venous occlusions (2)In loose tissues (3) In tissues with dual circulations (4) In tissues that were previously congested because of sluggish venous outflow (5) When flow is reestablished to a site of previous arterial occlusion and necrosis

solid organs

Arterial insufficiency

 All infarcts tend to be wedgeshaped, with the occluded vessel at the apex and the periphery of the organ forming the base The lateral margins may be irregular, reflecting the pattern of vascular supply from adjacent vessels

 Initially
all infarcts are poorly defined and slightly hemorrhagic

Eventually
the margins of both types of infarcts tend to become better defined by a narrow rim of hyperemia attributable to inflammation at the edge of the lesion

 In solid organs
the relatively few extravasated red cells are lysed, with the released hemoglobin remaining in the form of hemosiderin. white infarcts typically become progressively more pale and sharply defined with time

 In spongy organs
Over the course of a few days
become more firm and brown, reflecting the development of hemosiderin pigment

 The dominant histologic characteristic of infarction is ischemic coagulative necrosis Ischemic injury in the central nervous system results in liquefactive necrosis

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

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 anemic or cyanotic patient might lead to tissue infarction, whereas it would be without effect under conditions of normal oxygen tension

Shock
Cardiovascular collapse Systemic hypoperfusion
Reduction either in cardiac output or in the effective circulating blood volume hypotension impaired tissue perfusion and cellular hypoxia tissue injury death

Cardiogenic shock

low cardiac output

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

Hypovolemic shock

low cardiac output

BURNS

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

 Systemic microbial infection

Gram-negative infections (endotoxic shock) Also occur with gram-positive and fungal infections

Neurogenic shock

Loss of vascular tone and peripheral pooling of blood due to peripheral or central vasomotor injury

Anesthetic accident Spinal cord injury

 Episode: Nine Inch Nailed

Anaphylactic shock

 Generalized IgE-mediated hypersensitivity response

Associated with systemic vasodilation and increased vascular permeability

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

STAGES OF SHOCK

INITIAL NONPROGRESSIVE PHASE

Reflex compensatory mechanism Vital organs are maintained

PROGRESSIVE PHASE
Tissue hypoperfusion Worsening circulatory and metabolic imbalance

IRREVERSIBLE PHASE
Severe cellular and tissue injury Survival is not possible

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

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 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 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

Morphology
The cellular and tissue changes induced by shock are essentially those of hypoxic 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

 Brain
ischemic encephalopathy

Heart
focal or widespread coagulation necrosis subendocardial hemorrhage or contraction band necrosis

Kidneys typically exhibit extensive tubular ischemic injury

oliguria, anuria, and electrolyte disturbances

 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

 Adrenal glands
cortical cell lipid depletion conversion of the relatively inactive vacuolated cells to metabolically active cells that use stored lipids for the synthesis of steroids

Gastrointestinal tract
Hemorrhagic enteropathy
patchy mucosal hemorrhages and necroses

 Liver
Fatty change Central hemorrhagic necrosis

 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.

Clinical course
The prognosis varies with the origin of shock and its duration.
Hypovolemic shock
80 to 90% of young, otherwise healthy patients survive with appropriate management

Cardiogenic shock associated with extensive myocardial infarction and gram-negative shock
mortality rates of up to 75%, even with the best care

Fever