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Pathology 301. Awatif Jamal, MD, MSc, FRCPC, FIAC Consultant & Associate Professor Department of Pathology King Abdulaziz University Hospital. Hemodynamic Disorders Thrombosis & Shock. Shock. Shock. Shock or cardiovascular collapse. Shock constitutes systemic hypo perfusion due to
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Pathology 301 • Awatif Jamal, MD, MSc, FRCPC, FIAC • Consultant & Associate Professor • Department of Pathology • King Abdulaziz University Hospital
Hemodynamic Disorders Thrombosis & Shock • Shock Shock
Shock or cardiovascular collapse Shock constitutes systemic hypo perfusiondue to reduction either in : --cardiac output --or in the effective circulating blood volume. It is the common final pathway for a number of potentially lethal events including ; severe hemorrhage Extensive trauma Severe burns Large myocardial infarction Massive pulmonary embolism Massive microbial sepsis.
Shock or cardiovascular collapse The end results are: • 1.Hypotension, followed by • 2.Impaired Tissue Perfusion • 3.Cellular Hypoxia • 4. Hypoxic and metabolic effects of hypoperfusion causes initially reversible cell injury. • 5. Persistence of shock causes irreversible cell injury, even to death of patient.
Shock • Shock or “cardiovascular collapse” could be grouped into three Main Categories: • Cardiogenic shock • Hypovolemic shock • Septic shock • Others: • Neurogenic Shock (spinal cord injury) • Anaphylactic Shock
Cardiogenic Shock Results From Severe Myocardial Pump Failure Due to: Myocardial Infarction Ventricular Arrhythmia Extrinsic Compression (Cardiac Tamponade) Outflow Obstruction (Pulmonary Embolism)
Hypovolemic Shock • Results From Loss of Blood or Plasma Volume: • Hemorrhage • Fluid loss from severe burns or trauma
NEUROGENIC SHOCK • In case of spinal cord injury or anesthetic accident which can lead to; • Loss of vascular tone • And peripheral pooling of blood
ANAPHYLACTIC SHOCK • Initiated by generalized Ig E-mediated hypersensitivity reaction associated with systemic vasodilatation and increased vascular permeability.
Septic Shock Most common cause of death in ICU’s in the US • The incidence is increasing due to; • Improved life support for high-risk patients • Increased invasive procedures • Increasing number of immunocompromized cases as HIV infection, secondary to chemotherapy, and immunosuppression. • Caused by systemic microbial infection; most often by endotoxins-producing gram-negative bacilli infection (endotoxic shock) [in 70% of cases], but can also occur with gram-positive and fungal infections
Pathogenesis Of Endotoxic [Septic] Shock Endotoxins are bacterial wall lipopolysaccharides (LPS) which consists of ; --a toxic fatty acid (lipid A) core and --a complex polysaccharide coat. LPS are released when the cell walls are degraded in an inflammatory response.
Pathogenesis Of Endotoxic [Septic] Shock • Free LPS attaches to circulating LPS- binding proteins, • It will then bind to a receptor ( CD14) in macrophages , monocytes, and neutrophils leading to their activation and production of TNF, and IL-1. • Depending on the dose and number of macrophages that are activated ,the secondary effects of LPS release can cause severe pathologic changes including the fatal shock.
Pathogenesis Of Septic Shock • High quantities of LPS • systemic vasodilatation (hypotension) • diminished cardiac contractility (low cardiac output) • endothelial injury and activation leukocyte adhesion • activation of coagulation system ( Disseminated Intravascular Coagulopathy) • adult respiratory distress syndrome ( ARDS) • multiorgan system failure and death
Shock Stages of Shock: Shock is a progressive disorder that evolves through 3 stages, and if uncorrected will lead to death. • Initial “Non-progressive stage”: • Reflex compensatory mechanism activation maintain perfusion of vital organs through maintenance of cardiac output and blood pressure. • C/P; tachycardia, • peripheral vasoconstriction ,cold skin, pallor (although septic shock may be associated with inflammation and hotness)
Stages of Shock • Irreversible stage: • Severe cellular and tissue injury thus survival is not possible • Acute renal tubular necrosis • Adult respiratory distress syndrome ( ARDS ) • Bowel ischemia and release of its flora. • Disseminated Intravascular Coagulopathy • “Progressive stage: • tissue hypo perfusion with widespread hypoxia circulatory & metabolic imbalance. • C/P: patient is confused • Reduced urine output.
Disseminated Intravascular Coagulation (DIC) • Sudden widespread fibrin deposition in microcirculation • Rapid consumption of platelets and coagulation proteins (consumption coagulopathy) • Secondary massive fibrinolysis, all the little thrombi dissolve • Clotting disorder turns into a Bleeding Disaster