Hemodynaic Disorders- Ii

Hemodynamic disordersThrombosis, Embolism and Shock Dr. Mehzabin Ahmed

Thrombosis 

An intravascular mass of clotted blood formed in the circulation is called a thrombus

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Thrombus is composed of blood constituents (Platelets, WBCs and RBCs and fibrin)

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Fibrinolytic systems are activated to remove a thrombus once it is

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formed Thrombosis can occur at any place in the circulatory system in

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Arteries  Atheroma, aneurysm Veins  Compression, changes in coagulability of blood

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Heart valves  Vegetations Ventricles  Mural thrombus in MI Atrium  Atrial fibrillation, mitral stenosis

Pathogenesis of thrombus formation Clinical effects of thrombi Three main factors

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predispose to thrombus formation- the Virchow triad 

Endothelial dysfunction 

In direct injury and inflammation

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Change in flow pattern of blood 

Hypertension, aneurysms

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Change in blood coagulability

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Arterial thrombi cause  loss of pulses distal to the thrombus,  signs of impaired blood supply like cold, pale, painful and eventual tissues death or infarction and gangrene formation. Venous thrombosis  most commonly occurs in the leg veins  the area becomes tender, swollen and reddened.  Superficial as well as the deep veins of the legs may be involved.  Varicosity in the superficial veins ( saphenous veins) are prone for thrombosis.  The popliteal, femoral and iliac veins can be involved by thrombosis.  DVT is an important source of thromboembolism to the pulmonary

The hypercoagulabilty states that predispose to deep vein thrombosis (DVT)   

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Advanced age, prolonged bed rest or immobilization- causes stasis Cardiac failure Trauma, surgery, burns- result in vessel injury and causes release of coagulation promoting factors. Puerperal and postpartum states Disseminated cancers- due to release of procoagulant states.

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There are four main outcomes following thrombus formation: 

Propagation- enlarge and occlude blood vessel

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Organization- replaced by granulation tissue and fibrosis

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Recanalization – breakdown and form holes which allow blood to flow through it

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Embolization- break off and the fragments travel to distant organs and obstruct arterial supply

DIC- disseminated intravascular coagulation 

There is widespread formation of fibrin microthrombi throughout the circulation due to circulating procoagulant substances triggered by endothelial injury. Endothelial injury

Circulating procoagulant substances

Formation of fibrin microthrombi 

The thrombi occlude the microvasculature causing ischemia of the tissues and results in multiple organ failure

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It results in consumption or use up of the coagulation factors ultimately resulting in a bleeding disorder.

Thrombo-Embolism 

Occlusion of a blood vessel by material traveling in the blood is termed “embolism”. The mass is called an embolus

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Thrombo-emboli originating in 

systemic veins travel to the heart and impact in the pulmonary arterial system

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the heart (mural/ vegetations) travel via the aorta to systemic arterial circulation and impact in arteries leading to the brain, kidneys, spleen, gut, lower limbs

Pulmonary embolism 

Pulmonary thrombo-embolism is extremely common and arise in the deep veins of the leg  Depending on the size of the embolus it may cause major, minor and minor recurrent pulmonary embolism

Other types of emboli 

Tumor emboli give rise to metastatic tumors

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Fat and bone marrow embolism are seen in severe fracture trauma

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Nitrogen gas emboli form in Caisson Disease

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Amniotic fluid embolism may occur during child birth

Gangrene of toes due to emboli from aortic aneurysm

Infarction An infarct is an area of ischemic necrosis within a tissue or organ, produced by occlusion of either its arterial supply or its venous drainage Causes: 

Thrombotic or embolic obstruction

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Extrinsic compression of a vessel

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Twisting of the vessels

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Compression of the blood supply of a loop of bowel in a hernial sac

Types of infarcts Infarcts are divided into various groups on the basis of their color and presence or absence of microbial contamination. 

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Based on their color infarcts are called as 

Red or hemorrhagic infarcts- occur with venous occlusions and are common in organs, which have loose connective tissue and dual blood supply like lungs, liver and Testis

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White or anemic infarcts- occur due to arterial occlusion and are seen in solid organs like heart, spleen and kidney

Based on microbial contamination  

Septic infarcts- presence of microbial contamination

Infarction 

Lack of blood supply to an organ leads to infarction  Blockage of an artery generally leads to coagulative necrosis in the organs supplied by the blood vessel  Blockage of veins causes hemorrhagic infarcts

Shock 

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Shock is the result of collapse of the circulatory system. The cardiac output is reduced and enough blood does not reach the vital organs like the brain and kidneys. It may be classified as 

Cardiogenic shock 

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Hypovolemic shock 

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due to failure of the pump due to loss of blood volume in severe hemorrhage, diarrheas and vomiting

Septic shock 

due to pooling of the blood in the systemic circulation in gram negative infections due to peripheral vasodilatation and decreased venous return

Types of shock

Clinical Examples

Principal Mechanisms

Cardiogenic

Myocardial infarction Ventricular rupture Arrhythmia Cardiac tamponade Pulmonary embolism

Failure of myocardial pump owing to intrinsic myocardial damage, or obstruction to outflow

Hypovolemic

Hemorrhage Fluid loss Vomiting, Diarrheas Burns

Inadequate blood or plasma volume

Septic

Overwhelming microbial infections Endotoxic shock Gram-positive septicemia Fungal sepsis Superantigens

Peripheral vasodilatation and pooling of blood, endothelial activation / injury Leukocyte-induced damage Disseminated intravascular coagulation Activation of cytokine cascade

Neurogenic

Anaesthetic accident Spinal cord injury

Loss of vascular tone and increased vascular permeability

Anaphylactic

IgE- mediated hypersensitivity response

Systemic vasodilatation and increased vascular permeability

Pathogenesis of Septic Shock ( Bacterial lipopolysaccharide ) ( Tumor Necrosis Factor ) ( Interleukin – 1 ) ( Interleukin - 6 & 8 ) ( Nitric oxide, Platelet activating factor )

Clinical Manifestations of Shock

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Hypotension

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Weak rapid pulse

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Tachypnea (rapid breathing)

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Cool, clammy, cyanotic skin

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In septic shock the skin may initially be warm and flushed because of peripheral vasodilation