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Lecture # 39 HEMODYNAMICS - 7 Dr. Iram Sohail Assistant Professor Pathology College Of Medicine Majmaah University.

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Presentation on theme: "Lecture # 39 HEMODYNAMICS - 7 Dr. Iram Sohail Assistant Professor Pathology College Of Medicine Majmaah University."— Presentation transcript:

1 Lecture # 39 HEMODYNAMICS - 7 Dr. Iram Sohail Assistant Professor Pathology College Of Medicine Majmaah University

2 OBJECTIVES Discuss shock Correlate in explaining shock with hemodynamic mechanism

3 SHOCK Shock is a final & common pathway after hemorrhage, trauma, burn, myocardial infarction (heart attack), pulmonary embolism & microbial sepsis.

4 Shock gives rise to hypoperfusion, caused by reduced cardiac output or reduced blood volume. End results are – Hypotension – Impaired tissue perfusion – Cellular hypoxia

5 3 Main types 1.Cardiogenic shock – It results from failure of cardiac pump.

6 2.Hypovolemic shock – It is caused by loss of blood or plasma.

7 3.Septic shock – It results from microbial infections.

8 (Less common types/causes of shock) 4.Anesthetic shock 5.Neurogenic shock (spinal cord injury) 6.Anaphylactic shock (severe hypersensitivity reactions)

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10 Pathogenesis of septic shock Most of the septic shock caused by endotoxin released by gram negative bacilli. These endotoxins are called LPS (lipopolysaccharides)

11 These LPS will bind with proteins in circulation. This complex will bind to the macrophages monocytes and neutrophils. Cytokines (TNF, IL-1) will release from WBCs.

12 These cytokine release will result in – Vasodilation (hypotension) – Decreased myocardial contractility – Endothelial cell injury – Lung damage – Activation of coagulation system

13 These all things will result in DIC (disseminated intravascular coagulation) and multi organ failure. If untreated, shock can result in death.

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15 Stages of shock 1.Non-progressive stage Some neurohumoral mechanisms work like – Baroreceptor reflexes – Release of catecholamine – Activation of renin angiotensin mechanism – Release of ADH (antidiuretic hormone) – Sympathetic stimulation

16 The net effects are – Tachycardia – Peripheral vasoconstriction – Renal conservation of fluid

17 2.Progressive stage If the underlying cause in not corrected, the shock will pass to progressive Tissue hypoxia will occur. Decrease oxygen ----- anaerobic glycolysis ---- lactic acid accumulation ---- low PH ----- dilation of arterioles ---- pooling of blood in microcirculation ----- decrease cardiac out put

18 3.Irreversible stage Without any treatment, the shock will go into irreversible stage. Lysosomal enzymes leakage, worsen cardiac function, renal shut down and death.

19 Morphology Hypoxic injury & failure to many organs Fibrin thrombi in tissues In adrenal gland, cortical cell lipid depletion In kidney, ATN (acute tubular necrosis) In GIT, mucosal hemorrhage & necrosis In lungs, diffuse alveolar damage

20 Clinical course In cardiogenic & hypovolemic shock Hypotension Weak and rapid pulse Tachypnea (increased respiratory rate) Cold, clammy, cyanotic skin

21 In septic shock Warm skin Decrease renal out put Fluid & electrolyte imbalance

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