Shock SIRS MODS (5)_d6b37b93ec5992d227abb3d3520a005b.PDF

Shock, Systemic Inflammatory Response Syndrome (SIRS), and Multiple Organ Dysfunction Syndrome (MODS)  Shock Shock states have different causes and different clinical presentations Some features are common to all shock states: Hypoperfusion Hypercoa...

Shock, Systemic Inflammatory Response Syndrome (SIRS), and Multiple Organ Dysfunction Syndrome (MODS)  Shock Shock states have different causes and different clinical presentations Some features are common to all shock states: Hypoperfusion Hypercoagulability & Activation of the inflammatory response  Pathophysiology of Shock State of hypoperfusion Activation of the sympathetic nervous system, inflammatory response, & the immune system Derangement of compensatory mechanisms Further circulatory and respiratory dysfunction Multiple organ damage  Pathophysiology of Shock Imbalance of oxygen Oxygen is consumed at a much greater rate than it is delivered Cellular hypoxia and dysfunction Compensatory mechanisms result in increase in: Heart rate Systemic vascular resistance (SVR) Preload & Cardiac contractility Compensatory Mechanisms  SIRS Shock activates the inflammatory response SIRS indicates activation of inflammatory response Inflammation is normal, essential response May be caused by any type of shock Other insults: massive blood transfusion, traumatic injury, brain injury, surgery, burns, and pancreatitis and typically precedes septic shock  SIRS Local inflammation leads to systemic response Ultimately leads to generalized activation of inflammation and coagulation Marked release of various inflammatory mediators Cytokines (e.g tumor necrosis factor alpha (TNFα) and interleukin-1 (IL-1)  SIRS Criteria Should be evaluated in any patient with shock or any condition that might lead to shock SIRS & MODS  Stages of Shock Shock stages overlap Stage 1 (non-progressive) Compensatory mechanisms are effective in maintaining relatively normal vital signs and tissue perfusion Commonly goes unrecognized Stage I: non -progressive  Stages of Shock Stage 2 (progressive) Compensatory mechanisms begin to fail Metabolic and circulatory derangements become more pronounced Signs of failure in one or more organs Stage 3 (irreversible) Severe cellular and tissue injury Correction of metabolic, circulatory, and inflammatory derangements is difficult Cellular hypoxia and death ensue Stage 2  Classification of Shock Three (or 4) main types: Hypovolemic Cardiogenic Distributive Obstructive  Hypovolemic Shock Inadequate circulating volume Caused by sudden blood loss or severe dehydration, burns Decreased CO Blood shunted to vital organs (heart, lungs, and brain) Other organs suffer  Hypovolemic Shock Hypotension, electrolyte, and acid–base disturbances, and organ dysfunction resulting from hypoperfusion anaerobic metabolism → accumulation of acid Failed compensatory mechanisms cause the myocardial fatigue Hypovolemic Shock  Hypovolemic Shock: Assessment Altered mentation (lethargy/unresponsiveness) Rapid and deep respirations, then labored and shallower Cool and clammy skin Weak and thready pulses Tachycardia Hypotension Decreased urine output Darker and more concentrated  Hypovolemic Shock: Assessment Labs: Lactate ABG’s CBC (H&H) Electrolytes Coagulation panels U.O.  Hypovolemic Shock: Managment Management Restore circulating volume with crystalloids first LR’s Blood products Oxygen, monitor VS, Labs, respiratory status, mentation, UO Have 2 large-bore IV’s Monitor for IV replacement complications: Hypervolemia (pulmonary congestion) Hypothermia  Cardiogenic Shock Loss of critical contractile function of the heart Extensive left ventricular myocardial infarction (LAD) Compensation: neuroendocrine mechanism Vasoconstriction to increase BP But, cardiac workload increases  Cardiogenic Shock Assessment findings are similar to HF but are more severe Conduct thorough Hx Chest pain, hypotension, cool skin, oliguria, decreased mentation, dyspnea, crackles Labs: elevated myocardial tissue markers (Tbn), Brain natriuretic peptide (BNP) Cardiogenic Shock  Cardiogenic Shock: Management Goals: increase myocardial oxygen delivery, maximize cardiac output, decrease left ventricular workload Correct reversible problems intra-aortic balloon pump Fluids, diuresis, or nitrates To decrease left ventricular filling pressures Analgesia, sedatives Inhibit sympathetic nervous system response  Cardiogenic Shock: Management Periods of rest Monitor for dysrhythmias and hemodynamic status Monitor respiratory status Correct any electrolyte imbalance Augmentation of CO thru using meds should be used cautiously  Distributive Shocks Loss of blood vessel tone Loss of sympathetic innervation: Neurogenic shock Vasodilating substances in the blood Anaphylactic & Septic shock Distributive Shocks  Neurogenic Shock Loss or disruption of sympathetic tone causes peripheral vasodilation and subsequent decreased tissue perfusion SCI above T6, spinal analgesia, emotional stress, pain, drugs, CNS problems Circulating volume is decreased because of venous pooling Characterized by hypotension, bradycardia, and hypothermia Manage with fluids and vasopressors  Anaphylactic Shock Allergic reaction to a specific antigen (food, insect stings, medications) Life-threatening hypersensitivity reaction Decreased venous return resulting from displacement of blood volume away from the heart Assess for known allergens  Anaphylactic Shock Obtain a thorough history PE findings: generalized erythema, urticaria, and pruritus, anxiety and restlessness, dyspnea, wheezing, chest tightness, a warm feeling, nausea and vomiting, angioedema, and abdominal pain, laryngeal edema, and severe bronchoconstriction Sense of impending doom  Anaphylactic Shock: Management Early recognition Remove offending antigen Mild symptoms: oxygen, subcutaneous or IV diphenhydramine Life-threatening: epinephrine, fluids, steroids, bronchodilators, vasopressors Airway management, VS, and hemodynamic status  Septic Shock Generalized process that involves all organ systems Initiated by an infection gram-negative or -positive bacteria, fungi, and viruses Resp. infections, UTI’s, GI infections, infected wounds, or through invasive devices Proinflammatory and hypercoagulable state  Septic Shock Cardiovascular alterations Vasodilation, maldistribution of blood flow, and myocardial depression Pulmonary alterations Capillary leak in the pulmonary interstitium: ARDS Hematologic alterations DIC Metabolic alterations Severe metabolic dysfunction  Septic Shock Infection & Bacteremia SIRS: ≥ 2 out of the 5 criteria Sepsis: SIRS + known or suspected infection Severe sepsis: Sepsis associated with organ dysfunction, hypoperfusion, or hypotension Septic shock: Severe sepsis with hypotension, despite adequate fluid resuscitation MODS: Presence of altered organ function in an acutely ill patient such that homeostasis cannot be maintained without intervention  Septic Shock Signs of septic shock: Tachycardia Increased respiratory rate as compensation for the metabolic acidosis Either fever or hypothermia Abnormal WBC count Pt edematous yet intravascularly depleted Ischemia  Septic Shock: Management Treat underlying infection Use of sepsis protocol or sepsis bundles Restoring intravascular volume Maintaining an adequate cardiac output Ensuring adequate ventilation and oxygenation Restoring balance between coagulation and anticoagulation Providing an appropriate metabolic environment  MODS The exact cause of MODS is unknown Release of systemic inflammatory mediators found in SIRS may play a role in the etiology of MODS Translocation: loss of integrity of mucosal barrier function may liberate bacterial toxins from the gut causing damage to multiple organs Tissue hypoxia caused by microvascular thromboses Hypotension, tachycardia, tachypnea, hypothermia, and hyperthermia  MODS: Management Prevent nosocomial infections Treat hemodynamic and metabolic derangements Supportive measures for organ systems CRRT, low tidal volume ventilation Normalize ScvO2, arterial lactate, base deficit, and pH Questions?