Shock Flashcards
Shock
- A condition of profound hemodynamic and metabolic disturbance characterized by failure of the circulatory system to maintain an appropriate blood supply to the microcirculation with consequent inadequate perfusion of vital organs
- The final common pathway for a number of potentially lethal clinical events: massive hemorrhage, extensive trauma and burns, massive MI, massive PE, bacterial sepsis
- Hypoperfusion and cellular hypoxia result in injury that is initially reversible but eventually irreversible that often proves fatal
3 general categories of shock
- Cardiogenic shock
- Hypovolemic shock
- Septic shock
Cardiogenic shock
Decreased cardiac output due to pump failure
Hypovolemic shock
Decreased cardiac output due to loss of circulating volume
Less common categories of shock
- Anaphylactic shock
- Neurogenic shock
Anaphylactic shock
Widespread vasodilation and increased vascular permeability from IgE hypersensitivity reaction
Neurogenic shock
Follow anesthetic accident, acute brain, or spinal cord injury, neural control of vasomotor tone is lost resulting in generalized vasodilation
Systemic Inflammatory Response Syndrome (SIRS)
Exaggerated and systemic manifestation of a LOCAL inflammatory reaction, often fatal
Systemic Inflammatory Response Syndrome (SIRS) - Diagnosis
2 or more signs of systemic inflammation (fever, tachycardia, tachypnea, leukocytosis or leukopenia) in the setting of a known cause of inflammation:
- T > 100.4 F (38 C) or 90 bpm
- RR > 20 breaths per min
- WBC > 12,000 or 10% immature WBCs is also significant
Sepsis
SIRS with a culture-proven infection or obvious infection
Septic Shock
Clinical SIRS severe enough to lead to hypotension and organ dysfunction
Septic Shock - Epidemiology
- Mortality 20%
- 200,000 deaths per year in US
- # 1 cause of deaths in ICUs
Septic Shock - Triggers
- Gram negative bacterial infections
- Gram positive bacterial and fungal infections
Septic Shock - Inflammatory Mediators
TOLL-LIKE RECEPTORS (TLRs) on leukocytes
- Recognize microbial elements and trigger responses that start sepsis
TNF, IL-1, IFN-γ, IL-12, IL-18 + OTHERS are produced by inflammatory cells creating a PRO-INFLAMMATORY state
PROSTAGLANDINS and PAF
- Activate endothelial cells, causing adhesion molecule synthesis and pro-coagulant state
COMPLEMENT CASCADE
- Activated by microbial components
- Contributes to the hyperinflammatory states
Septic Shock - Endothelial Cell Activation and Injury
Activation is by microbial components and inflammatory mediators
Septic Shock - Endothelial Cell Activation and Injury - 3 major consequences of activation
THROMBOSIS - DIC (seen in up to 50% of patients with septic shock)
- Inflammatory mediators stimulate tissue factor and PAI-1 production
- Decreased production of tissue factor pathways inhibitor, thrombomodulin and protein C (anti-coagulant factors)
- Decreased blood flow produces stasis
INCREASED VASCULAR PERMEABILITY
- Causes 3rd spacing and edema which increases interstitial fluid pressure which impedes blood flow into the tissues = tissue hypoperfusion and stasis
VASODILATION
- Increased NO synthesis + vasoactive inflammatory mediators lead to vasodilation, hypotension and tissue hypoperfusion
Septic Shock - Metabolic Abnormalities
Hyperglycemia and Insulin resistance
- Cytokines, stress-induced hormones and catecholamines drive GLUCONEOGENESIS
- Pro-inflammatory cytokines SUPPRESS INSULIN RELEASE and promote INSULIN-RESISTANCE
- RESULTING HYPERGLYCEMIA DECREASES NEUTROPHIL FUNCTION
Septic Shock - Immune Suppression
- Hyperinflammatory state can activate counter-regulatory immunosuppressive mechanisms
- Whether immunosuppressive mediators are helpful or harmful in sepsis is UNCERTAIN
Septic Shock - Organ Dysfunction
- Tissue hypoperfusion (resulting from hypotension, edema and small vessel thrombosis) starves organs of oxygen and nutrients
- Changes in cellular metabolism interfere with tissues utilizing nutrients
- Myocardial contractility is weakened by cytokines and secondary mediators decreasing cardiac output
- Decreased cardiac output, increased vascular permeability and endothelial injury can damage the lungs resulting in adult respiratory distress syndrome
- Other organs are affected by changes that take place in septic shock, particularly KIDNEYS, LUNGS, LIVER AND HEART
Septic Shock - Stages
- Nonprogressive phase
- Progressive phase
- Irreversible state
Septic Shock - Stages - Nonprogressive phase
Reflex mechanisms compensate and tissue perfusion is maintained (SIRS)
Septic Shock - Stages - Progressive stage
Tissue hypoperfusion ensues with worsening circulatory and metabolic imbalances including acidosis
Septic Shock - Stages - Irreversible state
Such extensive cellular and tissue injury has occurred that even with infection control and hemodynamic correction, death is inevitable
Septic Shock - Treatment
- Control infection with antibiotics
- Fluid resuscitation and vasopressor drugs to maintain systemic pressures
- Insulin therapy for hyperglycemia
- Corticosteroids at physiologic doses
- ANTI-INFLAMMATORY TREATMENTS TO CONTROL THE INFLAMMATORY RESPONSE HAVE NOT BEEN VERY SUCCESSFUL THUS FAR
- ACTIVATED PROTEIN C TO REDUCE COAGULATION AND INFLAMMATION IS STILL CONTROVERSIAL
Septic Shock - Clinical outcome
- Initial threat of shock is from the underlying cause:MI, hemorrhage, sepsis, etc.
- Rapidly secondary complications of tissue hypoperfusion exacerbate the situation
- Prognosis varies with origin of shock, duration and underlying comorbidities of the patient
