Shock - Haemodynamics PDF

SHOCK Dr. Saima Irum Assistant professor of pathology  LEARNING OBJECTIVES Define shock Enlist different categories of shock with causes of each Explain physiological consequences Correlate the physiological and pathophysiological consequences of Shock. Outline management...

SHOCK Dr. Saima Irum Assistant professor of pathology  LEARNING OBJECTIVES Define shock Enlist different categories of shock with causes of each Explain physiological consequences Correlate the physiological and pathophysiological consequences of Shock. Outline management options  SHOCK characterized by systemic hypotension due either reduced cardiac output or due to reduced effective circulating blood volume.  WHAT WILL BE CONSEQUENCE….? leads to impaired tissue perfusion and cellular hypoxia. Initially the cellular injury is reversible; however, prolonged shock eventually leads to irreversible tissue injury that often proves fatal PATHOPHYSIOLOGY  TYPES OF SHOCK General categories: 1) Cardiogenic shock 2) Hypovolemic shock 3) Neurogenic shock 4) Septic shock 5) Anaphylactic shock MAJOR TYPES OF SHOCK  CLINICAL FEATURES Clinical manifestation of shock depends on precipitating insult. In hypovolemic and cardiogenic shock patients exhibit hypotension, weak rapid pulse, tachycardia, cool clammy and cyanotic skin. In septic shock skin may be warm and flushed owing to peripheral vasodilatation Prognosis varies with origin of shock and its duration.90% of hypovolemic shock in young and otherwise healthy patients survive. Septic and cardiogenic shock is associated with worse outcome. CLINICAL PRESENTATION  MORPHOLOGY The cellular and tissue changes induced by cardiogenic or hypovolemic shock are essentially those of hypoxic injury changes can manifest in any tissue although they are particularly evident in brain, heart, lungs, kidneys, adrenals, and gastrointestinal tract. The kidneys typically exhibit acute tubular necrosis..  The lungs are seldom affected in pure hypovolemic shock, because they are somewhat resistant to hypoxic injury. However, when shock is caused by bacterial sepsis or trauma, changes of diffuse alveolar damage may develop, the so- called shock lung. In septic shock, the development of DIC leads to widespread deposition of fibrin-rich micro thrombi, particularly in the brain, heart, lungs, kidney, adrenal glands, and gastrointestinal tract. The consumption of platelets and coagulation factors also often leads to the appearance of petechial hemorrhages on serosal surface and the skin  CARDIOGENIC SHOCK Results from low cardiac output due to myocardial pump failure. MECHANISM: Failure of myocardial pump resulting from intrinsic myocardial damage, extrinsic pressure, or obstruction to outflow  CAUSES CLINICAL EXAMPLES 1) Myocardial infarction 2) Ventricular rupture 3) Arrythmias 4) Cardiac temponade 5) Pulmonary embolism  HYPOVOLEMIC SHOCK Results from low cardiac output due to the loss of blood or plasma volume CLINICAL EXAMPLE: Fluid loss….may be blood, may be plasma 1) Massive hemorrhage(GI bleed, aortic aneurysm, PPH, ectopic pregnancy) 2) fluid loss from diarrhea, vomiting or severe(3rd degree burns)  SEPTIC SHOCK Results from vasodilation and peripheral pooling of blood d/t endothelial activation/injury; leukocyte-induced damage, disseminated intravascular coagulation, activation of cytokine cascades. CAUSES  PATHOGENESIS OF SEPTIC SHOCK Septic shock is associated with severe hemodynamic and hemostatic derangements. With a mortality rate near 20%, septic shock ranks first among the causes of death in intensive care units systemic vasodilation and pooling of blood in the periphery leads to tissue hypo perfusion.  MAJOR FACTORS IN PATHOPHYSIOLOGY Inflammatory mediators Endothelial cell activation and injury Metabolic abnormalities Immune suppression Organ dysfunction  changes in widespread metabolism endothelial that directly cell activation suppress and injury, cellular often leading function to DIC. hypo perfusion and dysfunction of multiple organs failure  PATHOGENESIS Inflammatory cells Macrophages, Neutrophils, and other cells of the innate immune system express a number of receptors that respond to a variety of substances derived from microorganisms. Once activated, these cells release inflammatory mediators, as well as a variety of immunosuppressive factors that modify the host response. microbial constituents also activate humoral elements of innate immunity, particularly the complement and coagulation pathways. PATHOGENIC PATHWAY  INFLAMMATORY MEDIATORS cytokines inflammatory cells produce TNF, IL-1, IFN-γ, IL-12, and IL-18, as well as other inflammatory mediators such as high mobility group box 1 protein (HMGB1) Reactive oxygen species and lipid mediators such as prostaglandins and platelet activating factor (PAF) are also elaborated  INFLAMMATORY MEDIATORS The complement cascade is also activated by microbial components, both directly and through the proteolytic activity of plasmin resulting in the production of anaphylotoxins (C3a, C5a), chemotactic fragments (C5a), and opsonins (C3b) that contribute to the pro-inflammatory state. microbial components such as endotoxin can activate coagulation directly through factor XII and indirectly through altered endothelial function.  Coagulation and inflammation are interlinked The systemic procoagulant state induced by sepsis not only leads to thrombosis, but also augments inflammation through effects mediated by protease-activated receptors (PARs) found on inflammatory cells.  ENDOTHELIALCELL ACTIVATION & INJURY Endothelial cell activation by microbial constituents or inflammatory mediators produced by leukocytes has three major sequelae: (1) thrombosis (2) increased vascular permeability and (3) vasodilation. ENDOTHELIAL CELL ACTIVATION & INJURY Increase pro coagulants and decreased anticoagulants Pro-inflammatory cytokines result in increased tissue factor production by endothelial cells (and monocytes as well), while at the same time decrease in fibrinolysis by increasing PAI-1 expression The production of other endothelial anti-coagulant factors, such as tissue factor pathway inhibitor, thrombomodulin, and protein C are diminished.  ENDO.CELL ACTIVATION & INJURY The procoagulant tendency is further exacerbated by decreased blood flow at the level of small vessels, producing stasis and diminishing the washout of activated coagulation factors. these effects promote the deposition of fibrin-rich thrombi in small vessels, often throughout the body, which also contributes to the hypoperfusion of tissues.  METABOLIC ABNORMALITY Septic patients exhibit insulin resistance and hyperglycemia. Cytokines such as TNF and IL-1, stress-induced hormones (such as glucagon, growth hormone, and glucocorticoids), and catecholamines all drive gluconeogenesis. the pro-inflammatory cytokines suppress insulin release while simultaneously promoting insulin resistance in the liver and other tissues, likely by impairing the surface expression of GLUT-4  IMMUNOSUPRESSION The hyperinflammatory state initiated by sepsis can activate counter-regulatory immunosuppressive mechanisms, which may involve both innate and adaptive immunity. Proposed mechanisms for the immune suppression include a shift from pro-inflammatory (TH1) to anti- inflammatory (TH2)  ORGAN DYSFUNCTION Systemic hypotension, interstitial edema, and small vessel thrombosis all decrease the delivery of oxygen and nutrients to the tissues, which fail to properly utilize those nutrients that are delivered due to changes in cellular metabolism.  High levels of cytokines and secondary mediators may diminish myocardial contractility and cardiac output, and increased vascular permeability and endothelial injury can lead to the adult respiratory distress syndrome COMPARISON OF DIFFERENT TYPES