HEMODYNAMIC DYSFUNCTION May 19, 2008 Pathophysiology Premed 2 Dr. ROOPA
Dec 26, 2015
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