Categories: disorders

Hemodynamic Disorders: Pathology, Shock and Thrombosis

HEMODYNAMIC DISORDERS

Before discussing the hemodynamic disorders we must know “Hemostasis”.

Hemostasis

is defined as the capacity of living organisms to maintain vascular wall integrity as well as to maintain intra vascular pressure & osmolarity within physiologic ranges. When any injurious stimulus crosses over the limits of Hemostasis then the Hemodynamic disorders took place which are…

  • Edema
  • Thrombosis
  • Embolism
  • Infarction

Hemodynamic definition

Hemodynamic means disturbances in normal blood flow which are major causes of human morbidity and mortality resulting in…

  • Myocardial infarction
  • Pulmonary embolism
  • Cerebrovascular accident (CVA)

HEMODYNAMIC DISORDERS are a very silent killer that can attack the body.

HEMODYNAMIC DISORDERS

EDEMA

  • 60% of body weight is water.
  • 2/3 is intravascular & 1/3 is extravascular.
  • Edema is defined as significantly increased fluid in the interstitial tissue spaces.

Clinical category of edema

  • Hydorthroix (increased fluid collection in the thoracic cavity)
  • Hyropericardium (increased fluid collection in the pericardial cavity)
  • Hydroperitoneum (increased fluid collection in the peritoneal cavity)
  • Anasarca (generlize profound subcutaneous swelling)

PATHOPHYSIOLOGICAL CATEGORIES

Increase hydrostatic pressure.

Impaired venous return

  • Congestive cardiac failure
  • Constrictive pericarditis
  • Ascites (liver cirrhosis)
  • Venous obstruction or compression
  • Thrombosis
  • External pressure e.g. mass
  • Lower limb inactivity and prolong dependency.

Arteriolar dilation.

  • Heat
  • Neurohormonal dysregulation.

Reduced plasma osmotic pressure (hypoproteinemia)

  1. Protein-losing glomerulopathies
  2. (nephrotic syndrome)
  3. Liver cirrhosis
  4. Malnutrition
  5. Protein-losing gastro enteropathies.

Lymphatic obstruction.

  • Inflammatory
  • Neoplastic
  • Post-surgical
  • Post-irradiation.

Sodium retention.

  • Excessive salt intake with renal insufficiency
  • Increased tubular reabsorption of sodium.
  • Renal hypoperfusion
  • Increased renin-Angiotensin-Aldosterone secretion.

Inflammation

  • Acute inflammation
  • Chronic inflammation

HEMODYNAMIC DISORDERS can be fetal.

PATHOPHYSIOLOGY

  1. A) Increased hydrostatic pressure.

REDUCED PLASMA OSMOTIC PRESSURE

  • Protein-losing glomeropathies (nephrotic syndrome)
  • Cirrhosis of liver
  • Protein-losing gastroenteropahties.

HEMODYNAMIC DISORDERS

Edema

LYMPHATIC OBSTRUCTION

  • Local edema
  • Inflammation
  • Neoplastic
  • Post-surgical

INFLAMMATION

  • Acute.
  • Chronic.
  • Angiogenesis

MORPHOLOGY

  • Grossly it is easily recognizable.

Microscopy:-

  • Cells are swollen
  • Prominent intercellular spaces
  • Incase of CCF extremities shows an edematous picture.
  • In nephrotic syndrome, periorbital swelling is seen & depending parts show pitting edema.
  • In the case of left-sided heart failure, pulmonary edema is the presentation in which lung’s weight ranges 2/3 times more than normal.
  • Edema of the brain develops due to head injury, abscess & neoplasm. It may be local or generalized revealing narrow sulci & swollen gyri.
  • edema is one of the HEMODYNAMIC DISORDERS

HYPEREMIA AND CONGESTION

  • The Hyperemia congestion indicates the local increase volume of blood.
  • Hyperemia is an active process due to arteriolar dilation & congestion is a passive process due to impaired outflow of fluid from tissue.
  • Congestion & edema commonly occur

Morphology:

  • C/S revel hemorrhagic & wet.
  • Microscopically capillaries engorged with blood in acute pulmonary congestion with an area of hemorrhage.
  • In chronic pulmonary congestion thicken & fibrotic septa may contain numerous hemosiderin-laden macrophages (heart failure cells)
  • also in acute hepatic congestion, central vein and sinusoids are distended with blood leading to central hepatocyte degeneration.
  • In chronic passive congestion of liver central regions of hepatic lobules are grossly red-brown and slightly depress as compare to surrounding zones of the uncongested tan liver (nutmeg lover)
  • Microscopically there is evidence of centrilobular necrosis with loss of hepatocytes dropout and hemorrhage.
  • In severe long-standing conditions may lead to hepatic fibrosis (cardiac cirrhosis)
  • HEMODYNAMIC DISORDERS are explained here.

HEMORRHAGE

  • It indicates extravasation of blood due to vessel rupture which may be external or may be enclosed.
  • Minute 1- 2 mm hemorrhage into the skin, mucous membranes or serosal surfaces as called petechiae hemorrhages which are usually associated with increased local intravascular pressure, low platelet count, defective platelet function or clotting factor deficits.
  • > 3mm hemorrhages are called purpura which may be due to the same disorders of petechiae and secondary to trauma, vascular inflammation or increased vascular fragility (e.g. in amyloidosis).
  • > 1-2 cm subcutaneous hematoma (bruises) are called ecchymoses saw after trauma. RBCs are degraded and phagocytosed by macrophages.
  • A large accumulation of blood in body cavities is called hemothorax, hemopericardium, hemoperitoneum or hemarthrosis.
  • The clinical significance of hemorrhage is a hypovolemic shock.

HEMOSTASIS AND THROMBOSIS

  • Hemostasis is defined as the integrated functioning of body systems to keep the body in the ranges of normal physiological state.
  • Due to hemostasis blood is kept in a fluid, clot free state in normal vessels & provides rapid and localized hemostatic plug at the site of vascular injury.
  • The opposite state of hemostasis is called thrombosis which is characterized by activation of the normal hemostatic process e.g. formation of a clot in uninjured vessels and thrombotic occlusion of the vessel after miner injury.
  • Both hemostasis & thrombosis are being regulated by vascular wall, platelet & coagulation cascade.
  • maintenance of hemostasis is very important in HEMODYNAMIC DISORDERS.

NORMAL HEMOSTASIS

  • After the initial injury, a transient period of arteriolar vasoconstriction due to reflex neurogenic augmented by endothelin (endothelium-derived vasoconstrictor)
  • Endothelial extracellular matrix (ECM) is exposed which allows platelets to adhere and become activated. Within minutes recruited additional platelets to form a hemostatic plug (Primary hemostasis)
  • Tissue factor membrane-bound endothelium-derived procoagulant factor is exposed activate the coagulation cascade by activation of thrombin which converts fibrinogen to insoluble fibrin thrombin also induces platelet recruitment and granule release (secondary hemostasis)
  • Polymerized fibrin and platelet form the solid permanent plug. Counter regulatory mechanisms (tissue plasminogen activator (t-PA) get into action to limit the hemostatic plug.

ROLE OF ENDOTHELIUM

  • Flow to liquid blood is maintained by endothelial antiplatelet,
  • anticoagulants
  • & fibrinolytic properties.
  • Injury endothelium, infection agents, hemodynamic factors, plasma mediators & cytokines stimulate the endothelium which exhibits several procoagulant activities.
  • The balance between endothelial antithrombotic and prothrombotic activities determines whether thrombus formation, propagation, or dissolution occurs.
  • the endothelium is involved in HEMODYNAMIC DISORDERS

Antithrombotic properties:

  • Antiplatelet effect:
  • Intact endothelium prevents plasma coagulation factors from meeting the ECM.
  • Endothelial prostacyclin and nitric oxides are potent vasodilators and platelet aggregation.
  • Anticoagulant effects:
  • Membrane-associated heparin-like molecules and thrombomodulin act indirectly with antithrombin III to inactive thrombin factor Xa and several other coagulation factors.
  • Thrombomodulin indirectly with thrombin converting it from a procoagulant and anticoagulant activating protein C which inhibits clotting by proteolytic cleavage of factors Va & VIIa and requires protein S which is synthesized by endothelium.
  • The endothelium is a source for tissue factor pathway inhibitors which inhibits activated tissue factor VIIa & Xa molecules.
  • Fibrinolytic effects. Tissue type plasminogen activator (t-PA) promote fibrinolytic activity to clear fibrin deposits from endothelial surfaces

PROTHROMBOTIC PROPERTIES

  • Platelet effect;
  • Adhesion of platelets takes place after endothelial injury which is facilitated by the ECM von Willebrand factor (vWF).
  • Procoagulant effects;
  • It is reduced by bacterial end toxin, cytokines (TNF & IL-I). To synthesize tissue factor which activates the extrinsic clotting
  • Antifibrinolytic effects;
  • Endothelium secretes inhibitors of plasminogen activator (PAIs) which depress fibrinolysis.
  • In summary intact, endothelial cells serve primarily to inhibit platelet adherence and blood clotting injury or activation of endothelial cells however, results in a procoagulant phenotype that augments local clot formation.

PLATELETS

  • Platelets play a central role in normal hemostasis due to two specific types of granules.
  • Alpha granules express the adhesion molecule P-selectin and contain fibrinogen fibronectin, factors V and VIII, platelet factor IV, platelet growth factor & transforming growth factor β.
  • δ granules contain ADP, ATP, ionized calcium histamine, serotonin, and epinephrine.
  • After the vascular injury platelet encounter, ECM undergoes three reactions…

Adhesion:

It is mediated via vWF Which acts as a bridge between platelet surface receptors & exposed collagen.

Secretion

It is initiated by binding of agonists to platelet surface receptors followed by intracellular protein phosphorylation cascade which is calcium depended

ADP potent mediator of platelet aggregation leads to surface expression of phospholipids complexes  which provide critical nucleation and binding sites for calcium and coagulation factors in the intrinsic clotting pathway

Platelet Aggregation.

In Addition to ADP, the vasoconstrictor thromboxane A2 secreted by platelets is an important stimulus for platelet aggregation (This primary aggregation is reversible)

With the activation of the coagulation cascade, thrombin is generated which binds to platelet surface receptor leading to further aggregation leading to secondary hemostatic plug.

Thrombin converts fibrinogen to fibrin which is the central point of thrombi formation

RBCs & WBCs are also found in Hemostatic plug via adhesion molecules P-selection to endothelial thrombin stimulate neutrophil and monocyte adhesion & generate chemotactic fibrin split products from the cleavage of fibrinogen.

SUMMARY

  • Platelet adhere to ECM
  • On activation secrete ADP & TxA2
  • Platelet exposes phospholipids complexes which are important in the intrinsic coagulation pathway.
  • Injured or activated endothelial cells expose tissue factor which triggers extrinsic coagulation cascade.
  • ADP stimulates the primary hemostatic plug which is converted into secondary plug after interaction with thrombin and TxA2.
  • Fibrin deposition stabilized and anchors the aggregated platelets.
  • platelets are involved in HEMODYNAMIC DISORDERS

COAGULATION CASCADE

  • The coagulation cascade is essentially a series of enzymatic conversions turning inactive proenzymes into activated enzymes and culminating in the formation of thrombin. Thrombin then converts the soluble plasma protein fibrinogen precursor into the insoluble fibrous protein fibrin.
  • The intrinsic pathway may be initiated in vitriol by activation of Hageman factor (factor XII)
  • The extrinsic pathway is activated by tissue factor, a cellular lipoprotein exposed at sites of tissue injury.

COAGULATION CASCADE

  • Coagulation cascade must be restricted to the local site of vascular injury to prevent the clotting of the entire vascular tree.
  • At the same time clotting also regulated by three types of natural anticoagulants.
  • Antithrombins (antithrombin III). It is activated by binding to heparin-like molecules on endothelial cells. Then it inhibits the activation of thrombin.
  • Protein C & S: (Vitamin K dependent) these inactivate factors Va and VIIa.
  • Tissue factor pathway inhibitor: (TFPI) is secreted by endothelium & inactivate Xa and VIIa complex formation.

Fibrinolytic cascade:

  • Besides coagulation, this fibrinolytic cascade limits the size of the final clot.
  • It is accomplished by the generation of plasmin which is derived from the enzymatic breakdown of its inactive circulating precursor plasminogen either by factor XII dependent pathway or by two distinct types of plasminogen activators.
  • Urokinase like PA. it is present in plasma & capable of activating plasminogen which converts inactive pro-urokinase precursor to active u-PA.
  • Tissue type of PA. synthesized by endothelium & become active when attached to fibrin.
  • Plasminogen can also be activated by bacterial products.
  • Plasmin breaks down fibrin resulting in fibrin degradation products (FDPs) which also act as weak anticoagulants.
  • Elevated levels of FDPs/FSPs can be estimated in clinical lab separately & also as fibrin D-dimer especially in DIC, DVT, pulmonary thromboembolism.

THROMBOSIS

  • It is a dysregulated normal homeostasis mechanism leading to thrombus formation.

PATHOGENESIS:

  • Virchow triad. It leads to thrombus formation
  • Endothelial injury
  • Stasis or turbulence of blood flow
  • Blood hypercoagulability

Endothelial injury

  • Especially in heart & arterial circulation, ulcerated plaques in atherosclerotic arteries, sites of traumatic or inflammatory vascular injury.
  • After injury ECM is exposed, adhesion of platelet release of tissue factor, & local depletion of PGI2 & PAs take place.
  • The imbalance between pro-and antithrombotic defect of endothelium leads to the initiation of local clotting events.
  • Significant endothelial dysfunction may be seen due to hypertension, scarred valves or bacterial endotoxins, hypercholesterolemia & products absorbed from cigarette smoke.

Stasis or turbulence of blood flow

  • Stasis is a major factor in the development of venues thrombi.
  • Any alteration in normal blood flow brings.
  • Platelets into contact with the endothelium,
  • Prevents dilution of activated clotting factor by fresh flowing blood.
  • Retard the inflow of clotting factor inhibitor & permit the build-up thrombi.
  • Promote endothelial cell activation predisposing to local thrombosis leukocyte adhesion.
  • Ulcerated atherosclerotic plaques expose ECM.
  • Aneurysms cause local stasis & favored sites of thrombosis.
  • MI is a site of endothelial injury & with the element of stasis leading to the formation of mural thrombi.
  • Atrial fibrillation site of stasis & prime location for thrombus formation.
  • Hyperviscosity syndromes (polycythemia) & sickle cell anemia vascular occlusions resulting in stasis leading to thrombosis.

Blood hypercoagulability

  • It may be primary or secondary.
  • Primary: Mutation in factor V gene, Prothrombin gene & methyltetrahydrofolate gene.

Due to prolonged bed rest, MI, Atrial fibrillation tissue damage after surgery, fracture and burn.

  • DIC, heparin-induced thrombocytopenia antiphospholipid syndrome (SLE)
  • Cardiomyopathies,
  • Nephrotic syndrome.
  • Oral contraceptive use hyperestrogenic states (pregnancy)
  • sickle cell anemia & smoking.

MORPHOLOGY

  • Thrombus is attached with arterial wall cardiac chamber which may propagate toward the direction of flow & tail is prone to create an embolus.
  • Thrombus shows lines of Zahn produce by an alternating pale layer of platelet admixed with fibrin dark layer of RBCs. When thrombi arise in heart chambers or aortic lumen are termed mural thrombi.
  • Arterial thrombi are occlusive common sites are coronary cerebral and femoral arteries
  • Venous thrombi or invariably occlusive common sites or lower limb veins periprostatic plexus peri uterine veins dural sinuses portal vein & hepatic vein.
  • Bacterial & fungal blood-borne infections may lead to large thrombotic masses around the heart valves (vegetations which may be infective or nonbacterial).
  • Noninfective, verrucous (Libman-Sacks) endocarditis are due to elevated levels of circulating immune complexes usually seen in SLE

FATE OF THROMBUS.

  • Propagation: Leading to vessel obstruction
  • Embolization: Thrombi may dislodge and travel to other sites in the vasculature
  • Dissolution: Removed by fibrinolytic activity.
  • Organization and recanalization: It may induce inflammation and fibrosis and may recanalize to establish vascular flow

THROMBOSIS

CLINICAL FEATURES

  • Venous thrombosis: usually seen in a superficial and deep vein of legs (DVT). It causes local pain and distal edema leading to collateral bypass channels.
  • Usually seen with states & hypercoagulable.
  • The tumor-associated procoagulant release is responsible for increased risk of thromboembolic phenomena in disseminated cancers (migratory thrombophlebitis)
  • Arterial and cardiac thrombosis: Seen in atherosclerosis  MI, Rheumatic heart disease, atrial fibrillation, and mitral valve stenosis.

HEMODYNAMIC DISORDER EMBOLISM

  • An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin.
  • Embolism is a part of thrombus are droplets of fat bubbles of air or nitrogen atherosclerotic debris (cholesterol emboli), tumor fragments, bits of bone marrow foreign bodies such as bullets.
  • A consequence of embolism is ischemic necrosis leading to infarction after the involvement of pulmonary or systemic circulation.

PULMONARY THROMBOEMBOLISM

  • 20 to 25 per lac hospitalized patients.
  • 2% to 6% is fatal rate & still causing 2 lac deaths per year.
  • 95% venous emboli originate from a deep vein of leg & may get plugged in the main pulmonary artery (saddle embolus) are may involve small pulmonary arteries.
  • Rarely embolus may pass into the systemic circulation (paradoxical embolism).
  • 60% to 80% of pulmonary emboli are silent.
  • Sudden death due to cor pulmonale occurs when 60% are more pulmonary circulation is obstructed.
  • Embolic obstruction in medium-size arteries results in pulmonary hemorrhage without infarction due to dual blood flow.
  • Embolic obstruction of end arteriolar pulmonary branches leads to infarction.
  • Multiple emboli may cause pulmonary hypertension with right heart failure.

SYSTEMIC THROMBOEMBOLISM

  • 80% arise from intracardiac mural thrombi due to left ventricular wall infarcts and left atrial fibrillation.
  • Remaining originate from aortic aneurysms, ulcerated atherosclerotic plaques are valvular vegetation major site for arteriolar remobilization are the lower extremities 75% and brain 10%.
  • Consequences depend upon extent of collateral vascular supply & degree of occlusion.

FAT EMBOLISM

  • After a fracture of long bones (90% ), fat embolism takes place of clinically significant (10%).
  • Fat embolism syndrome is characterized by pulmonary insufficiency neurologic symptoms, anemia & thrombocytopenia.
  • Mechanical obstruction & biochemical injury are the main pathogenesis causes of a fat embolism which are aggravated by platelet & RBCs aggregation releasing free fatty acid from fat globules causing local toxic injury to endothelial which initiate further thrombosis.

AIR EMBOLISM

  • Gas bubbles can obstruct vascular flow.
  • Air may enter circulation during the obstructive procedure or chest wall injury.
  • 100 cc is required to have a clinical effect.
  • A special form of gas embolism (decompression sickness) occurs when individuals are exposed to sudden atmospheric changes.
  • Scuba and deep-sea divers take a breath under high pressure, an increase in the amount of gas (Nitrogen) gets dissolved in tissues.
  • When pressure is released, Nitrogen expands and bubble out of solution in the blood to form gas emboli.
  • Rapid formation of gas bubbles within skeletal muscles, supporting tissue and about joints is responsible for painful conditions called “the bends” (Grecian Bend) gas emboli may induce local ischemia, edema hemorrhages & focal atelectasis or emphysema leading to respiratory distress called chokes.
  • Treatment is to put the individuals in the compression chamber and slowly release pressure chronic form of decompression sickness is called caisson disease in which persistence of gas emboli in the skeletal system leads to multiple foci of ischemic necrosis involvement femurs, tibia, and humerus.

AMNIOTIC FLUID EMBOLISM

  • It is 1 in 50000 deliveries having a mortality rate of 20% to 40%.
  • It is characterized by dyspnea, cyanosis and hypotensive shock followed by seizures and coma may lead to pulmonary edema & DIC.
  • The cause is the infusion of amniotic fluid or fetal tissue into the maternal circulation via a tear in the central membranes or rupture of uterine veins.
  • The classical finding is the circulation of squamous cells shed from fetal skin, lanugo hair, fat from vernix and mucin from fetal respiratory or GIT leading to diffuse alveolar damage as well as DIC.

INFARCTION

  • An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in particular tissue.
  • Half of the deaths usually take place due to myocardial & cerebral infarction.
  • Pulmonary infarction is common complication.
  • Bowel infarction is fatal.
  • Ischemic necrosis of extremities (gangrene) is a serious problem of diabetes mellitus.
  • 99% of all infarct results from the thromboembolic phenomenon.
  • Other uncommon causes include twisting of vessels (testicular torsion or bowel volvulus)
  • Bypass channels rapidly open after the thrombosis providing some outflow from the area improving the arterial inflow.
  • Venus thrombus is seen in the organ by single venues outflow channel (testis & ovaries)

MORPHOLOGY

  • Red (hemorrhagic) & white (anemic) which may be either septic or bland.

Red Hemorrhagic Infarcts:

  • Ovarian torsion
  • Lungs
  • Small intestine
  • Previously congested organ due to impaired outflow.

White infarcts:

  • Arterial occultation in solid organ with end arterial circulation e.g. heart, spleen & kidney.
  • Infarcts are wedge-shaped having an apex at the sight of occlusion and periphery forming the base.
  • Initially, infarcts are poorly defined and partly hemorrhagic.
  • In solid organ, some areas of dark brown due to hemosiderin-laden macrophages.
  • The dominant histologic characteristic of infarction is ischemic coagulative necrosis.
  • Later on, the acute inflammatory reaction is seen around the infarcts followed by fibrosis and scar formation.
  • In case of brain liquefactive necrosis
  • Septic infarcts may emboli after bacterial vegetation and some time it may be to abscess formation.

CLINICAL FEATURES

  • It depends upon it…

Nature of vascular supply.

  • In the case of dual blood supply, small obstruction does not cause infarction e.g. liver. While in the case of renal and splenic circulation, end arteries lead to infarction.

Rate of development of the occlusion

  • If collateral circulation sufficient no infarction will be seen otherwise small areas of tissue will be ischemic if any vessel is partly occlusive.

Vulnerability to hypoxia:

  • Neurons undergo irreversible damage when deprived of blood supply for 3 to 4 minutes. Myocardial cells dye after 20 to 30 minutes of ischemia in contract fibroblasts within myocardial remains viable even after many hours of ischemia.

Blood oxygen content.

  • Partial flow obstructing of a small vessel in an anemic or cyanotic patient lead to infarction whereas it would be without any effect under normal oxygen tension e.g. CCF with compromised flow and ventilation caused infarction in mild blockage of the vessel.

SHOCK

  • Shock is a term used to describe acute circulatory failure with critical impairment of tissue perfusion resulting in generalized cellular hypoxia
  • Result is

– Hypotension

– Impaired tissue perfusion

– Cellular Hypoxia

shock is a type of HEMODYNAMIC DISORDERS

ETIOLOGY

  • There are three main causes
  • Hypovolemia
  • Peripheral vasodilation
  • Severe reduction in cardiac output
  • PERIPHERAL VASODILATION

PRIMARY CARDIAC DISEASES

  • Ac myocardial infarction
  • Ac myocarditis
  • Arrhythmias

TYPES OF SHOCK

  • Cardiogenic shock
  • Hypovolemic shock
  • Septic shock
  • Neurogenic shock
  • Anaphylactic shock

SEPTIC SHOCK.

  • Endotoxin – gram –ve bacteria.
  • Gram +ve bacterial infections.
  • Fungal sepsis.

PATHOGENESIS OF SEPTIC SHOCK

  • Endotoxins à bacterial wall LPS
  • Toxic fatty acid core
  • complex polysaccharide coat
  • TLR mediated activation.
  • Innate immune system.
  • Eradicate invading microbes.

Effects produced depend on LPS Dosage

AT LOW DOSES

LPS activates monocytes, macrophages & neutrophils.

  • Also directly activate complement.
  • Mononuclear phagocytes respond to LPS by producing TNF à IL -1.
  • NET EFFECT Ac inf. Response

MODERATE DOSES

  • augmentation of cytokine cascade
  • systemic effects of TNF & IL -1

At High doses

  • Systemic vasodilation
  • Diminished myocardial contractility
  • Widespread endothelial injury
  • Activation of coagulation system à DIC

Anaphylactic shock

  • IgE mediated type -1 hypersensitivity reaction

Neurogenic shock

  • Loss of vascular tone à peripheral pooling of blood
  • g. spinal cord injury

STAGES OF SHOCK

  • STAGE OF COMPENSATION
  • THE STAGE OF IMPAIRED TISSUE PERFUSION
  • STAGE OF DECOMPENSATION

STAGE OF COMPENSATION

  • Neurohormonal mechanisms
  • Baroreceptor reflexes
  • Release of catecholamines
  • Activation of the renin-angiotensin axis
  • ADH release
  • Generalized sympathetic stimulation

THE STAGE OF IMPAIRED TISSUE PERFUSION

Prolonged impaired tissue perfusion leads to…

  • Lactic acidosis
  • Cell necrosis

LACTIC ACIDOSIS

  • Hypoperfusion à anaerobic glycolysis à lactic acidosis

à vasodilation à hypotension

CELL NECROSIS 

Sustained hypoperfusion produces cell necrosis e.g. ;

  • ATN à Renal failure
  • ARDS à hypoxia à hypoperfusion à Alveolar damage à alveolar edema à hemorrhage à formation of the hyaline member. à impair oxygenation

LIVER NECROSIS 

ISCHAEMIC NECROSIS OF INTESTINES

  • STAGE OF DECOMPENSATION

MORPHOLOGY

ADRENAL CHANGES

  • Cortical cell lipid depletion due to the conversion of inactive vacuolated cells to metabolically active cells that use stored lipids for a synth. of steroids

KIDNEYS

  • ATN à oliguria à Anuria and electrolyte dist.

GIT

  • focal mucal hemorrhage à necrosis

LUNGS

ARDS à hypoxia à hypoperfusion à Alveolar damage à alveolar edema à hemorrhage à formation of the hyaline member. à impair oxygenation  shock lung

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