Shock
Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
Imbalance in supply and demand for oxygen and nutrients
Hypovolemic Shock
Total body fluid decreased (all fluid compartments)
Cause/Risk
Hemorrhage
Trauma, GI ulcer, surgery, inadequate clotting (hemophilia, liver disease, malnutrition, bone marrow suppression, cancer, anticoagulant therapy)
Dehydration
Vomiting, diarrhea, heavy diaphoresis, diuretic therapy, nasogastric suction, diabetes insipidus, hyperglycemia
Response to acute volume depends on: age, injury, health
If loss greater than 30%, blood volume must be replaced
Cardiogenic Shock
Direct pump failure (fluid volume not affected)
Cause/Risk
MI
Cardiac Arrest
Ventricular dysrhythmias
Fibrillation, tachycardia
Cardiac amyloidosis
Cardiomyopathies
Viral, toxic
Myocardial degeneration
Early Manifestations: Tachycardia, hypotension, narrowed pulse pressure, increased SVR, increased myocardial O2 consumption
PE Findings: Tachypnea, pulmonary congestion, crackles
Increase in pulmonary artery wedge pressure (PAWP) and pulmonary vascular resistance
Signs and Symptoms of peripheral hypoperfusion: Renal blood flow, urine output
Anxiety/delirium with impaired cerebral blood flow
Distributive Shock
Fluid shifted from central vascular space (total body fluid volume normal or increased)
Cause/Risk
Neural induced
Pain, anesthesia, stress, spinal cord injury, head trauma
Chemical-induced
Anaphylaxis, sepsis, capillary leak (burns, extensive trauma, liver impairment, hypoproteinemia)
Obstructive Shock Cardiac function decreased by noncardiac factor (indirect pump failure). Total body fluid is not affected although central volume is decreased. Pericarditis Cause/Risk
Cardiac tamponadeArterial stenosis
Pulmonary embolus
Pulmonary embolus
Constrictive pericarditis
Thoracic tumors
Tension pneumothorax
Stages of Shock
Initial stage (Early stage): May be clinically apparent, metabolism changes from aerobic to anaerobic (Lactic acid accumulates), lactic acid must be removed by blood and broken down by liver (Requires unavailable O2)
Compensatory stage (Nonprogressive stage): Attempt homeostasis, baroreceptors in carotid and aortic bodies activate SNS in response to decreased BP, decreased blood to kidneys activates renin-angiotensin system (RAAS).
Progressive stage (Intermediate stage): Begins when compensatory mechanisms fail, aggressive interventions to prevent multi-organ dysfunction syndrome, hallmarks of decreased cellular perfusion and altered capillary permeability, anasarca, movement of fluid from pulmonary vasculature to interstitium, fluid moves into alveoli, CO begins to fall, myocardial dysfunction results in: arrhythmias, ischemias, MI and end result is complete deterioration of cardiovascular system. Liver fails to metabolize drugs and waste
Refractory stage (Irreversible stage): Exacerbation of anaerobic metabolism, accumulation of lactic acid, increased capillary permeability, hypotension and tachycardia worsen, decreased coronary blood flow, cerebral ischemia, hypoxemia, failure of organ system affects others, RECOVERY unlikely

Neurogenic Shock Can begin 30 minutes after injury and last days to weeks
Occurs after spinal cord injury at T5 or above
Results in massive vasodilation leading to pooling of blood in vessels
Manifestations of hypotension and bradycardia
Hypothalamic dysfunction is characteristics (temperature dysregulation)