hemodynamic dysfunction may 19, 2008 pathophysiology premed 2 dr. roopa

HEMODYNAMIC DYSFUNCTIONMay 19, 2008PathophysiologyPremed 2Dr. ROOPA

FLUID DISTRIBUTION

60% of lean body weight is water -2/3 is intracellular -1/3 is extracellular 5% of total body water is in blood plasma

DEFINITION OF TERMS

Hemmorhage: escape of blood from the vessels

-surrounding tissues-body cavity-outside of the body

HEMATOMA: BLOOD TRAPPED WITHIN THE TISSUE

Hemopericardium

Hemoperitoneum

Petechiae Purpura

Ecchymosis

A petechia (pronounced plural petechiae is a small (1-2mm) red or purple spot on the body, caused by a minor hemorrhage (broken capillary blood vessels

Purpura (from the Latin, purpura, meaning "purple") is the appearance of red or purple discolorations on the skin that do not blanch on applying pressure. They are caused by bleeding underneath the skin. Purpura measure 0.3-1 cm, whereas petechiae measure less than 3 mm, and ecchymoses greater than 1 cm.[1]

An ecchymosis is a spot caused by loss of blood from a vessel.

It implies a larger size than a petechia.[1]

It has a more diffuse border than purpura.[2]

It can be caused by a bruise (which implies trauma), but can also be caused by bleeding diathesis.[

Ecchymosis: The skin discoloration caused by the escape of blood into the tissues from ruptured blood vessels. Ecchymoses can similarly occur in mucous membranes as, for example, in the mouth.

INFARCTION An infarction is the process of tissue death

caused by blockage of the tissues blood supply.The supplying artery may be blocked by an obstruction.

Types:1. anemic/ white/ pale infarcts

- arterial occlusion- heart, spleen and kidney

2. hemorrhagic / red infarct- venous occlusion-intestines and lungs-areas with redundant blood supply

NORMAL HEMOSTASIS

A well regulated process maintains blood in a fluid, clot free state in

normal vessels induces the rapid formation of a localized

hemostatic plug at the site of vascular injury

NORMAL SEQUENCES OF HEMOSTASIS

1. Arteriolar vasoconstriction 2. Exposure of subendothelial ECM when

there is endothelial injury 3. Tissue factor released at site of injury 4. Formation of permanent plug

THROMBOSIS Blood coagulates inside the blood

vessels Interruption of blood flow Predisposing factors:

smokingOCPimmobilizationsickle cell diseasepolycythemiacancercongestive heart failure

THROMBOGENESIS

Formation of a thrombus Depends on: 1. platelets 2. endothelial cells 3. coagulation cascade

PLATELET PLUG Injury to the blood vessel exposes collagen in

the vessel wall Von Willebrand factor allows the platelets to

adhere Conformational change in the platelets Activation of the coagulation cascade Also, formation of TxA2: constricts blood

vessels, platelets aggregate

Von Willebrand factor (vWF) is a blood glycoprotein involved in hemostasis.

PLATELET PLUG

Fibrinogen links strengthen the plug Fibrin formation occurs Prostacyclin is secreted by endothelial cells;

limit the plug

COAGULATION CASCADE

2 pathways. Intrinsic pathway(contact activation pathway)

Extrinsic pathway(tissue factor pathway) Lead to fibrin formation Extrinsic pathway

-initiated by tissue factor-final product: formation of fibrin-prothrombin time-factors II, V, VII and X-fibrinogen

COAGULATION CASCADE

Intrinsic pathway Involves all the clotting factors except

VII and XIII Involves contact activation with:

-Hageman factor (factor XII)-prekallikrein-high molecular weight kininogen(HMWK)-factor XI

THROMBOTIC DISORDERS

Hereditary thrombophilia Antiphospholipid antibody syndrome Disseminated intravascular coagulopathy

HEREDITARY THROMBOPHILIA

Adolescents, young women Recurrent venous thrombosis Thromboembolism Deficiency: antithrombin III

protein S protein C

Most frequent cause: Factor V Leiden

DISSEMINATED INTRAVASCULAR COAGULATION Is a pathological activation of coagulation

mechanisms that happens in response to a variety of diseases.

Consumption of platelets and coagulation factors

Widespread thrombosis and hemorrhage

Disseminated intravascular coagulation (DIC), is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. As its name suggests, it leads to the formation of small blood clots inside the blood vessels throughout the body.[1] As the small clots consume all the available coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin critically ill, and may participate in the development of multiple organ failure, which may lead to death.[4]

KINDS OF THROMBI

Arterial thrombi-areas with active blood flow-lines of Zahn

Lines of Zahn are a characteristic of thrombi[1] that appear when formed in the heart or aorta. They have visible and microscopic laminations produced by alternating pale layers of platelets mixed with fibrin and darker layer containing red blood cells. Their presence implies thrombosis at a site of rapid blood flow. In veins or smaller arteries, where flow is not as constant, they are less apparent

VENOUS THROMBI

Areas with less blood flow Veins of lower extremities Venous stasis Dark red; no lines of Zahn

EMBOLISM

In medicine, an embolism (plural embolisms) occurs when an object migrates from one part of the body (through circulation) and causes a blockage (occlusion) of a blood vessel in another part of the body.

PULMONARY EMBOLISM

Sudden death Immobilized patients, heart disease (CHF) Saddle emboli: bifurcation of the pulmonary

artery Leads to pulmonary infarcts

ARTERIAL EMBOLI Originates from a mural thrombus Left atrium: mitral stenosis Left ventricle: Myocardial infarction Sites of arrest:1. Middle cerebral artery: most common2. Mesenteric arteries3. Renal arteries

PARADOXICAL EMBOLI

Emboli comes from venous side Passes though right-to –left shunt

atrial septal defectpatent foramen ovale

Reaches arterial circulation

OTHER FORMS OF EMBOLI

Fat emboli: bone marrow particles; fractures-go to brain, lungs, kidney-fat embolism syndrome:

difficulty breathingpetechiaeneurologic manifestations

Air emboli: air goes into the blood vessels-trauma to the chest; abortion-decompression sickness: “the bends”or muscle pains-caissons disease: infarcts in the CNS, bones, tissues-due to nitrogen bubbles in the blood

Amniotic fluid embolism: amniotic fluid in the blood-can lead to DIC, death

EDEMA

Abnormal fluid in the interstitial tissues spaces or body cavities

Caused by:-increased hydrostatic pressure

right sided heart failure: peripheral edema

left sided heart failure: pulmonary edema

EDEMA

Causes:-increased capilary permeability-decreased oncotic pressure-increased sodium retention-blocked lymphatics

TYPES OF EDEMA

Anasarca: generalized form Hydrothorax Hydropericardium Hydroperitoneum (ascites)

Transudate-non inflammatory-abnormal hyrdostatic

or osmotic pressure-low protein-sp.gr. < 1.012-high glucose

Exudate-inflammation-increased vascular

permeability-high protein content-sp.gr. >1.020-many WBC-low glucose

SHOCK Circulatory collapse Hypoperfusion Decreased oxygenation of tissues Caused by:-decreased cardiac output-widespread peripheral vasodilatation Organ most affected: kidney-acute tubular necrosis

TYPES OF SHOCK

Hypovolemic shock-loss in blood volume-massive hemorrhage-burns-vomiting, diarrhea

Cardiogenic shock-massive MI-pump failure of the left ventricle Septic shock-bacterial infections; endotexemia

Neurogenic shock-severe trauma-peripheral vasodilatation

STAGES OF SHOCK

1. nonprogressive (early stage)-compensatory mechanisms-increased heart rate; increased

peripheral resistance2. progressive stage

-compensatory mechanisms not adequate

-tissue hypoperfusion-circulatory and metabolic

imbalance

3. Irreversible stage-organ damage-metabolic imbalance -death