1.

Anasarca -severe systemic edema

2. Noninflammatory
(protein poor
transudates) causes of
edema
1) Increased hydrostatic pressure
-systemic edema is most commonly due to CONGESTIVE HEART FAILURE (CHF)
2) Reduced plasma osmotic pressure
-occurs with ALBUMIN LOSS
-the reduced plasma volume --> diminished renal perfusion and resultant renin production (and
downstream effects on angiotensin and aldosterone), but the subsequent salt and water retention cannot
correct the plasma volume due to the underlying protein deficit
3) Sodium and water retention
-primary salt retention with obligatory associated water retention, causes BOTH increased hydrostatic
pressure and reduced osmotic pressure
-sodium retention can occur with any renal dysfunction
-PRIMARY water retention can occur with release of ADH either due to increased plasma osmolarity,
diminished plasma volume, or inappropriately in the setting of malignancy; lung or pituitary pathology can
also cause inappropriate ADH secretion
4) Lymphatic obstruction
-blocks removal of interstitial fluid
-obstruction is usually localized and related to inflammation or neoplastic processes
3. Morphology -edema is most easily appreciated grossly
-Micro: only as subtle cell swelling and separation of the extracellular matrix
*Subcutaneous edema
-may be diffuse or occur where hydrostatic pressures are greatest (e.g. influenced by gravity, called
DEPENDENT EDEMA [legs when standing, sacrum when recumbent]
-Finger pressure over substantial subcutaneous edema typically leaves and imprint, called PITTING
EDEMA
*Edema resulting from hypoproteinemia is GENERALLY MORE SEVERE and DIFFUSE. It is most evident
in loss connective tissue (e.g. eyelids, causing periorbital edema)
*Pulmonary edema - can result in lungs that are 2-3 times their normal weight. Sectioning reveals a frothy,
blood-tinged mixture of air, edema fluid, and erythrocytosis
*Brain edema - may be localized to sites of injury or may be generalized (e.g. encephalitis, hypertensive
crises, or obstruction of venous outflow)
-when generalized, the brain is grossly swollen with narrowed sulci and distended gyri flattened against the
skull
4. Clinical consequences -Subcutaneous edema - can IMPAIR WOUND HEALING or INFECTION CLEARANCE
-Pulmonary edema IMPEDES GAS EXCHANGE and INCREASES THE RISK OF INFECTION
-brain edema within the confined space of the skull can impede cerebral blood flow or cause HERNIATION,
compromising critical medullary centers
5. Hyperemia -an active process due to augmented blood inflow from arteriolar dilation (e.g. skeletal muscle during
exercise or at sites of inflammation).
-Tissues are red (erythema) owing to engorgement with oxygenated blood
6. Congestion -a PASSIVE PROCESS
-caused by impaired outflow from a tissue; it can be systemic (e.g. CHF) or local (e.g. an isolated venous
obstruction)
-tissues are blue-red (cyanosis) as worsening congestion leads to an accumulation of deoxyhemoglobin
-long standing stasis of deoxygenated blood can result in hypoxia severe enough to cause ischemic tissue
injury and fibrosis
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7. Morphology *Acute Congestion - vessels are distended, and organs are grossly HYPEREMIC
-capillary bed congestion is also commonly associated with interstitial edema
*In CHRONIC CONGESTION - capillary rupture may cause focal hemorrhage. Subsequent erythrocyte breakdown
results in HEMOSIDERIN-LADEN MACROPHAGES
-Parenchymal cell atrophy or death (with fibrosis) may also be present
-Grossly tissues appear BROWN, CONTRACTED, and FIBROTIC
-lungs and liver are commonly affected
*IN LUNGS - capillary engorgement is associated with interstitial edema and airspace transudates
-chronic manifestations = hemosiderin-laden macrophages (heart failure cells) and fibrotic septa
*IN LIVER - acute congestion manifests as central vein and sinusoidal distention and occasionally with central
hepatocyte degeneration
-in chronic congestion, the central regions of the hepatic lobules are grossly RED-BROWN and slightly depressed
(loss of cells) relative to surrounding uncongested tan liver (called nutmeg liver)
-Micro: there is CENTRILOBULAR NECROSIS with heptatocyte dropout and hemorrhage, including hemosiderin-
laden macrophages
-Since the centrilobular area is at the distal end of the hepatic blood supply, it is most subject to necrosis whenever
liver perfusion is compromised
8. Hemorrhage -a release of blood into the extravascular space
-rupture of a large artery or vein is usually due to vascular injury
-capillary bleeding can occur with chronic congestion
-a tendency to hemorrhage from insignificant injury is seen in a variety of disorders called HEMORRHAGIC
DIATHESES
9. Hemorrhage
classifications
*can be external or ENCLOSED WITHIN A TISSUE (=HEMATOMA)
*Petechiae - are minute, 1-2 mm hemorrhages in skin, mucous membranes, or serosal surfaces. These occur with
increased intravascular pressure, low platelet counts (thrombocytopenia), or defective platelet function
*Purpura - are greater than or equal to 3 mm hemorrhages. These occur for the same reasons as petechiae, as well
as with trauma, local vascular inflammation (vasculitis), or increased vascular fragility (e.g. amyloidosis)
*Ecchymoses - are greater than or equal to 1-2 cm subcutaneous hematomas (i.e. bruises). Typically associated
with trauma but are also exacerbated by other bleeding disorders. The characteristic color changes in a bruise are
due to progressive metabolism of extravasated hemoglobin by tissue macrophages
*Large accumulations of blood in body cavities are called HEMOTHORAX, HEMIPERICARDIUM,
HEMOPERITONEUM, or HEMARTHROSIS (joint), depending upon the location. Patients with extensive
hemorrhage occasionally develop jaundice from massive erythrocyte breakdown and systemic bilirubin release
10. Clinical
significance of
hemorrhage
depends on ____
-the volume and rate of blood loss
*rapid loss of less than 20%, or slow losses of even larger amounts, may have little impact
*Greater losses --> hemorrhagic (hypovolemic) shock
11. Hemostasis vs.
Thrombosis
*Hemostasis - normal, physiologic process maintaining blood in a fluid, clot-free state within normal vessels
while inducing a rapid, localized hemostatic plug at sites of vascular injury
*Thrombosis - represents a pathologic state - it is the inappropriate activation of hemostatic mechanisms in
uninjured vessels or thrombotic occlusion after relatively minor injury
12. Normal
Hemostasis
*After injury there is a characteristic hemostatic response
-transient reflex neurogenic arteriolar vasoconstriction augmented by endothelin (a potent endothelial-derived
vasoconstrictor)
-platelet adhesion and activation (i.e., shape change and secretory granule release) by binding to exposed
subendothelial ECM. Secreted products (ADP, TxA2) recruit other platelets to form a temporary hemostatic plug
(primary hemostasis)
-Activation of the COAGULATION CASCADE by release of TISSUE FACTOR (aka THROMBOPLASTIN or FACTOR
III), a membrane-bound lipoprotein procoagulant factor synthesized by endothelium; coagulation culminates in
THROMBIN GENERATION and conversion of CIRCULATING FIBRINOGEN TO INSOLUBLE FIBRIN; thrombin
also induces additional platelet recruitment and granule release
-Polymerized fibrin and platelet aggregates together form a solid, permanent plug (secondary hemostasis)
-Activation of counter-regulatory mechanisms (e.g. tissue plasminogen activator [t-PA] restricts the hemostatic plug to
the site of injury
13. Endothelium
(EC)
antithrombotic
properties
-intact endothelium blocks platelet access to thrombogenic subendothelial ECM
-Prostacyclin (PGI2) and nitric oxide (NO) inhibit platelet binding
-Adenosinediphosphatase degrades adenosine diphosphate (ADP), and inducer of platelet aggregation
-membrane-associated thrombomodulin converts thrombin to an anticoagulant protein
-tissue factor pathway inhibitor (TFPI) blocks intermediates in the coagulation cascade
-Heparin-like surface molecules facilitate plasma antithrombin III inactivation of thrombin
-t-PA cleaves plasminogen to form plasmin, which, in turn, degrades fibrin
14. Endothelium
prothrombotic
properties
-EC produce von Willebrand factor (vWF); EC damage allows platelet to bind the underlying ECM through interaction
with vWF
-TISSUE FACTOR production is the major activator of the extrinsic clotting cascade
-Plasminogen activator inhibitors (PAIs) limit fibrinolysis and favor thrombosis
15. Platelets -after vascular injury, platelets encounter ECM constituents (collagen, proteoglycans, fibronectin, and other adhesive
glycoproteins), which are normally sequestered beneath an intact endothelium. Then, platelets undergo ACTIVATION
involving adhesion and shape change, secretion (release reaction), and aggregation
*Platelet-ECM adhesion is mediated through vWF, thereby acting as a bridge between platelet receptors (mostly
glycoprotein Ib) and exposed collagen.
-Genetic deficiencies of vWF or glycoprotein-Ib (i.e. Bernard-Soulier syndrome) result in bleeding disorders
*Platelet granule secretion (release reaction) -occurs shortly after adhesion. ALPHA GRANULES express P-selectin
adhesion molecules and contain coagulation and growth factors; dense bodies or delta granules contain ADP,
calcium, and vasoactive amines (e.g. histamine)
-ADP is a potent mediator of PLATELET AGGREGATION, and calcium is important for the coagulation cascade
-The release reaction also results in surface expression of PHOSPHOLIPID COMPLEX, providing a locus for calcium
and coagulation factor interactions in the CLOTTING CASCADE
*Platelet aggregation
-platelets adhering to other platelets is promoted by ADP and thromboxane A2
-ADP activation changes platelet GpIIb-IIIa receptor conformation to allow FIBRINOGEN BINDING. FIBRINOGEN
bridges multiple platelets, forming large aggregates (GpIIb-IIIa deficiencies result in GLANZMANN
THROMBASTHENIA bleeding disorder)
-platelet derived TxA2 activates platelet aggregation and is a potent vasoconstrictor (recall that EC-derived PGI2
inhibits platelet aggregation and is a potent vasodilator)
16. Coagulation
Cascade
*Intrinsic Pathway
-classically initiated by activation of HAGEMAN FACTOR (factor XII)
*Extrinsic cascade
-activated by TISSUE FACTOR
17. Prothrombin
time (PT)
-screens for the function of the proteins in the extrinsic pathway (VII, X, II, V, and fibrinogen)
18. Partial
thromboplastin
time (PTT)
-screens for the function of the proteins in the intrinsic pathway (XII, XI, IX, VIII, X, V, II, and fibrinogen)
19. Control
mechanisms
*factor activation can only occur at sites of exposed phospholipids. Also, activated clotting factors are diluted by flow
an are cleared by the liver and tissue macrophages
*Antithrombins (e.g. antithrombin III), complexed with heparin-like cofactors on endothelium, inhibit thrombin and
other serine proteases - factors IXa, Xa, XIa, and XIIa
*Endothelial THROMBOMODULIN modifies thrombin so that it can cleave PROTEINS C and S; these, in turn,
inactivate factors Va and VIIIa
*TFPI (Tissue factor pathway inhibitor) inactivates tissue factor-factor VIIa complexes
*Thrombin induces endothelial t-PA release; t-PA generates active PLASMIN from circulating PLASMINOGEN
-Plasmin can also be generated by a factor XII-dependent pathway. Plasmin cleaves fibrin and interferes with its
polymerization; the resulting FIBRIN SPLIT PRODUCTS also act as weak anticoagulants
*Functional plasmin activity is restricted to sites of thrombosis
-t-PA activates plasminogen most effectively when bound to fibrin meshwork
-Free plasmin is rapidly neutralized by serum a2-plasmin inhibitor
*Endothelium modulates anticoagulation by releasing PLASMINOGEN ACTIVATOR INHIBITORS (PAIs), which
inhibit t-PA binding to fibrin. Thrombin and certain cytokines increase PAI production; cytokines released in the
setting of severe inflammation can therefore cause intravascular thrombosis
20. Virchow's triad *3 primary influences on thrombus fomation
1) Endothelial injury - is dominant and can independently cause thrombosis (e.g. endocarditis or ulcerated
atherosclerotic plaque). Injury can be due to hemodynamic stresses (e.g. HT or turbulent), endotoxin, radiation, or
noxious agents. thrombosis results from exposed subendothelial ECM, increased platelet adhesion or procoagulant
production (i.e. tissue factor, PAI) or reduced anticoagulant activity
2) Alterations in normal blood flow -can promote thrombosis. normal blood flow is LAMINAR (i.e. cellular elements
flow centrally in the vessel lumen, separated from endothelium by a plasma clear zone).
*Stasis and turbulence (the latter forms eddy currents with local pockets of stasis):
-disrupt laminar flow and bring platelets into contact with the endothelium
-prevent dilution of activated clotting factors by flowing blood
-retard the inflow of clotting inhibitors
-promote endothelial cell activation
3) Hypercoagulanility
*Heritable hypercoagulable states
-Factor V gene mutations = most common; 2-15% of caucasians (and 60% of patients with recurrent DVT) carry the
so-called LEIDEN MUTATION, thereby rendering factor V resistant to protein C inactivation
-Deficiencies of ANTITHROMBIN III, protein C, or protein S
*Acquired hypercoagulable states
-oral contraceptives or the hyperestrogenic state of pregnancy may cause hypercoagulability by increasing hepatic
synthesis of coagulation factors and reduced synthesis of antithrombin III
-Certain malignancies can release procoagulant tumor products
*Heparin-induced thrombocytopenia syndrome -occurs when heparin products (unfractioned more commonly than
low molecular weight heparin) induces circulating antibodies that activate platelets and injure ECs
*Antiphospholipid antibody syndrome - occurs in patients with antibodies against anionic phospholipids that
activate platelets or interfere with protein C activity
21. Morphology
of
Thrombosis
*Venous thrombi characteristically OCCUR IN SITES OF STASIS and are OCCLUSIVE
*Arterial or cardiac thrombi usually begin at sites of endothelial injury (e.g. atherosclerotic plaque, endocarditis) or
turbulence (vessel bifurcation)
-Aortic or cardiac thrombi- these thrombi are typically NONOCCLUSIVE (mural) as a result of rapid and high volume
flow
-smaller arterial thrombi can be OCCLUSIVE
*Thrombi are generally FIRMLY ATTACHED at their site of origin and typically PROPAGATE TOWARD THE HEART
-thus arterial thrombi extend RETROGRADE from the attachment point, whereas venous thrombi extend in the
direction of blood flow
*Arterial and cardiac mural thrombi have gross and microscopic laminations (lines of Zahn) produced by pale layers of
platelets and fibrin alternating with darker erythrocyte-rich layers
*Venous thrombi (phlebothrombosis) -typically occur in a relatively static environment, resulting in a fairly uniform cast
containing abundant erythrocytes among sparse fibrin strands (red or stasis thrombi). Phlebothrombosis most
commonly affects the veins of the lower extremities (more than 90% of cases)
*Valve thrombosis
-infectious endocarditis - organisms form large, infected thrombotic masses (vegetations) with associated valve damage
and systemic infections
-Nonbacterial thrombotic endocarditis: non-infected, sterile vegetations develop in hypercoagulable states, typically
without valve damage
-Verrucous (Libman-Sacks) endocarditis (sterile vegetations) - this occurs in SLE due to immune complex deposition;
inflammation can cause valve scarring
22. Fate of
Thrombus
*Propagation
*Embolization: thrombi dislodge an travel to other sites
*Dissolution - by fibrinolytic activity
*Organization and recanalization - ingrowth of endothelial cells, smooth muscle cells, and fibroblasts to create vascular
channels, or incorporate the thrombus into the vessel wall
*Mycotic aneurysm - rarely, microbial seeding of a thrombus leads to a mycotic aneurysm
23. Clinical
consequences
*Thrombi can:
1) obstruct vessels
2) embolize
24. Venous thrombosis
(Phlebothrombosis)
-occurs most commonly in deep or superficial leg veins
*superficial thrombi usually occur in varicose saphenous veins, causing local congestion and pain but rarely
embolizing. Local edema and impaired venous drainage predispose to skin infections and VARICOSE ULCERS
*DEEP THROMBI in larger leg veins above the knee (e.g. popliteal, femoral, and iliac veins) can result in pain
and edema, as well as increased risk for embolization. Venous obstruction is usually offset by collateral flow, and
deep vein thromboses are asymptomatic in approximately 50% of patients, being recognized only after
embolization
*DVT occurs in multiple clinical settings
-advanced age, bed rest, immobilization, thereby diminishing the milking action of muscles in the lower leg and
slowing venous return
-CHF
-trauma, surgery, and burns --> reduced physical activity, injury to vessels, release of procoagulant substances
for tissues, and reduced tPA
-The puerperal (period of 6 weeks after childbirth) and postpartum states are associated with amniotic fluid
embolization and hypercoagulability
-tumor-associated procoagulant release (migratory thrombophlebitis or Trousseau syndrome)
25. Arterial and
Cardiac
Thrombosis
-Atherosclerosis is the major cause of arterial thrombi due to abnormal and endothelial damage
-MI with dyskinesis and endocardial damage can cause mural thrombi
-RHEUMATIC VALVULAR DISEASE resulting in mitral valve scarring and stenosis, with left atrial dilation,
predisposes to atrial thrombus formation; concurrent atrial fibrillation augments the blood stasis and propensity
to thrombose
-cardiac and aortic mural thrombi can embolize peripherally; brain, kidneys, and spleen are prime targets
26. DIC -reflected by widespread fibrin microthrombi in the microcirculation
-caused by disorders ranging from obstetric complications to advanced malignancy
-DIC is not a primary disease, but rather it is a complication of any diffuse thrombin activation
*Microthrombi can cause diffuse circulatory insufficiency, particularly in the brain, lungs, heart and kidneys
-there is also concurrent consumption of platelets and coagulation factors (consumption coagulopathy), with
fibrinolytic pathway activation, thereby leading to uncontrollable bleeding
27. Pulmonary
embolism
-greater than 95% come from DVT
-PE can occlude the main pulmonary artery, impact across the bifurcation (saddle embolus), or pass into smaller
arterioles
*In general, ONE PE PUTS A PATIENT AT RISK FOR MORE
*Rarely, emboli pass through atrial or ventricular defects into the systemic circulation (PARADOXICAL
EMBOLISM)
-Most PE (60-80%) are small and clinically silent. They eventually organize and get incorporated into the vessel
wall or leave a delicate, bridging fibrous WEB
-Sudden death, right sided heart failure (cor pulmonale), or CV collapse occur when 60% or more of the
pulmonary circulation is obstructed with emboli
-PE in medium-sized arteries can cause pulmonary hemorrhage but usually not pulmonary infarction due to
collateral bronchial artery flow; however, with left-sided cardiac failure, infarcts can result
-PE in SMALL END-ARTERIOLAR vessels typically cause hemorrhage or infarction
-MULTIPLE EMBOLI over time can cause pulmonary hypertension and right ventricular failure
28. Systemic
Thromboembolism
-refers to emboli in the arterial circulation
~80% arise from intracardiac mural thrombi
-2/3 are secondary to myocardial infarcts, and 25% arise in the setting of dilated left atria and fibrillation
-can also originate from AORTIC ANEURYSMS, THROMBI ON ULCERATED ATHEROSCLEROTIC PLAQUES,
OR VALVULAR VEGETATIONS
-they rarely originate from PARADOXICAL EMBOLI
-10-15% are unknown origin
*Major sites for arteriolar embolization are the LOWER EXTREMITIES (75%) and brain (10%)
-consequences depend on collateral circulation, tissue vulnerability to ischemia, and vessel caliber
-most arterial emboli cause tissue infarction
29. Fat and Marrow
embolism
*PE of microscopic fat globules
-occurs after FRACTURES of long bones or, rarely, after burns or soft tissue trauma
-occur in 90% of severe skeletal injuries; less than 10% have any clinical findings
*FAT EMBOLISM SYNDROME
-fatal in 10%
-heralded by sudden pulmonary insufficiency 1-3 days after injury
-20-50% of patients have a diffuse petechial rash and may have neurologic symptoms (irritability and
restlessness) that progress to delirium or coma
-thrombocytopenia and anemia can also occur
-fatty acid release --> toxic injury
-edema and hemorrhage can be seen micro
30. Air embolism -gas bubbles within the circulation
-obstruct vascular flow and cause ischemia
*small amounts in the coronary or cerebral circulation (introduced following surgery) can be catastrophic
-100 cc required
*DECOMPRESSION SICKNESS
-special form of air embolism caused by sudden changes in atmospheric pressure; deep-sea divers and individuals
in unpressurized aircraft during rapid ascent are at risk
-Air breathed at high pressure causes increasing amounts of gas (particularly nitrogen) to be dissolved in blood
and tissues
-Subsequent rapid ascent (depressurization) allows the dissolved gases to expand and bubble out of solution to
form gas emboli
-formation of gas bubbles in skeletal muscles and joints causes painful BENDS
-In lungs and, edema, hemorrhage, and focal emphysema --> resp distress, or CHOKES. Has emboli may also
cause focal ischemia in a number of tissues, including brain and heart
-a more chronic form of decompression sickness is CAISSON DISEASE; persistent gas emboli in poorly
vascularized portions of the skeleton (heads of the femurs, tibia, and humeri) lead to ischemic necrosis
31. Amniotic fluid
embolism
-embolization of amniotic fluid into the maternal pulmonary circulation is a serious (80% mortality) but
uncommon (1 in 40,000 deliveries) complication of labor and postpartum period
*syndrome = sudden severe dyspnea, cyanosis, and hypotensive shock, followed by seizures and coma. Pulmonary
edema, DIFFUSE ALVEOLAR DAMAGE, and DIC ensue from release of toxic (fatty acid) and thrombogenic
substances in amniotic fluid
-Classic histologic findings include fetal squamous cells, mucin, lanugo hair, and fat from vernix caseosa in the
maternal pulmonary microcirculation
32. Red Infarct *occur in:
-venous occlusions (e.g. ovarian torsion)
-loose tissues
-tissues with dual circulations
-tissues previously congested b/c of sluggish venous outflow
-site of previous occlusion and necrosis when flow is reestablished
33. White
infarcts
-occur in SOLID ORGANS with end arterial circulations (i.e. few collaterals)
-i.e. spleen, kidney
34. Infarction -all tend to be WEDGE-SHAPED; the occluded vessel marks the apex, and the organ periphery forms the base. Lateral
margins may be irregular, reflecting the pattern of adjacent vascular supply
-dominant histo feature: COAGULATIVE NECROSIS followed temporally by an inflammatory response (hours to days)
and by a reparative response (days to weeks) beginning in the preserved margins
-most infarcts are ultimately replaced by scar tissue
*Infarction in the CNS --> LIQUEFACTIVE NECROSIS
35. Shock *systemic HYPOPERFUSION resulting from reduction in either CARDIAC OUTPUT of the effective circulating blood
volume
1) Cardiogenic shock -low cardiac output due to outflow obstruction (i.e. PE) or myocardial pump failure (arrythmia,
tamponade, MI)
2) hypovolemic shock - low cardiac output due to hemorrhage or fluid loss (e.g. burn)
3) Septic shock - results from vasodilation and peripheral blood loss pooling caused by microbial infection
*rarer - neurogenic (loss of vascular tone and peripheral pooling (anesthetic accident or spinal cord injury), and
ANAPHYLACTIC
36. Septic
shock
-most commonly caused by gram-positive bacteria - gram neg - bacteria - fungi
-procoagulant EC phenotype develops (DIC in up to 50% of cases)
-Metabolic abnormalities - insulin resistance and hyperglycemia are characteristic of the septic state, attributable to
inflammatory cytokines and the early production of stress-induced hormones such as glucagon, GH, and cortisol. With
time, adrenal insufficiency may supervene
-Immune suppression
-Organ dysfunction - reduced perfusion to tissues; myocardial contractility may be directly impacted, and endothelial
damage underlies the dev. of ACUTE RESP DISTRESS SYNDROME
37. Stages of
Shock
1) Nonprogressive phase - phase during which reflex neurohumoral compensatory mechanisms are activated and
perfusion of vital organs is maintained
2) Progressive phase - tissue HYPOPERFUSION and worsening circulatory and metabolic abnormalities including lactic
acidosis due to anaerobic glycolysis. The acidosis also blunts the vasomotor response, causing vasodilation
3) Irreversible phase
-damage is so severe that, even if perfusion is restored, survival is not possible
-Renal shutdown due to ACUTE TUBULAR NECROSIS and ischemic bowel leaking microbes into the bloodstream
(sepsis) can be terminal events
38. Morphology
of shock
*acute tubular necrosis --> oliguria, anuria, and electrolyte disturbances
*lungs are seldom affected in hypovolemic shock but can be and lead to DAD in septic or traumatic shock
*brain, heart, lungs, kidneys, adrenals, and GI tract are particularly affected
39. Clinical
consequences
*Hypovolemic and cardiogenic shock - there is hypotension with a weak, rapid pulse; tachypnea; and cool, clammy,
cyanotic skin
*Septic shock - skin may be initially warm and flushed owing to peripheral vasodilation
*pts. surviving the initial complications enter a SECOND PHASE DOMINATED BY RENAL INSUFFICIENCY and
marked by a progressive fall in urine output, as well as severe fluid and electrolyte imbalances
*prognosis: varies with the origin and duration of shock: cardiogenic and septic shock carry worse mortality rates than
hypovolemic shock