Chapter 20 Flashcards
Tissue Perfusion
- tissue not being oxygenated
Causes of Shock
- cardiogenic (inadequate cardiac output despite sufficient vascular volume)
- obstructive (circulatory blockage, such as a large pulmonary embolus or cardiac tamponade, disrupts cardiac output)
- hypovolemic (loss of blood volume as a result of hemorrhage or excessive loss of extracellular fluids) (dehydration or blood loss from trauma)
- distributive (greatly expanded vascular space because of inappropriate vasodilation) (anaphylaxis)
Pathogenesis of Shock
- common factor among all types of shock is hypoperfusion amd impaired cellular oxygen utilization
- inadequate cellular oxygenation may result from decreased cardiac output, maldistribution of blood flow, and reduced blood oxygen content
Impaired tissue oxygenation
impaired oxygen utilization by cells
- disrupts function and, if ongoing or severe, may lead to cell death, organ dysfunction, and stimulation of inflammatory reactions
Impaired tissue oxygenation (outcomes of lack of oxygen)
- product of lactate
- failure of ion pumps leads to sodium and water accumulation in the cell (hydropic swelling which leads to tissue necrosis or any shock)
- formation of oxygen radicals
- induction of inflammatory cytokines
- cellular hypoxia, which causes anaerobic metabolism, free radical production, and macrophage induction
Reperfusion Injury
- ischemic cells may produce oxygen-free radicals when oxygen supplies are restored, causing cells to die
Impaired Tissue Oxygenation (TNF-alpha, IL-1, and failure of microcirculaiton)
- Tumor necrosis factor alpha and interlukin 1 cytokines increase during septic shock and are thought to be important mediators of vascular failure and progressive organ damage
- increased activity of inducible nitric oxide (NO) synthase leading to excess NO (is a massive vasodilator that causes vasodilation of brain)
- failure of microcirculation to autoregulate (tissue adjusts for BP change) bloodflow leads to activation of coagulation (leads to oxygen debt in tissues)
Compensatory Mechanisms and Stages of Shock
- three clinical stages including compensated shock, progressive shock, and refactory shock
Compensatory Stage of Shock
- homeostatic mechanisms are sufficient to maintain adequate tissue perfusion despite a reducction in CO, happens initially (good vital signs)
- SNS activation attempts to maintatin blood pressure even though CO has fallen, increased CO and vascular resistance (result of release of dopamine, etc.)
Progressive Stage of Shock
- marked by hypotension and marked tissue hypoxia
- lactate production increases with anaerobic metabolism
- lack of ATP leads to cellular swelling, dysfunction, and death
- cellular and organ dysfunction result from oxygen free radicals, release of inflammatory cytokines, and activation of the clotting cascade (can get organ failure)
Clinical Manifestations of Shock
- decreased levels of consciousness
- Thirst
- restlessness
- dilated pupils
- release of ADH
- Increased Heart Rate
- Increased Respiratory Rate
- decreased urine output
- increased specific gravity
- cool, clammy, blush, or gray color in the legs
- decreased capillary refill
- constriction of splanchnic vessels
- release of aldosterone and cortisol
- Hypotension
- Decreased pulse pressure
Clinical Manifestations of Cardiogenic Shock
- Hypotension
- High systemic vascular resistance
- low cardiac output
- High Cardiac Preload
- Low Venous ocygen saturation
- low urine output
- cool skin temp
Clinical manifestations of Hypovolemic Shock
- hypotension
- High systemic vascular resistance
- Low cardiac output
- Low cardiac preload
- Low venous oxygen saturation
- low urine output
- cool temp
Clinical Manifestations of Septic Shock
- Hypotension
- Low systemic vascular resistance
- High Cardiac Output
- Low cardiac preload
- High venous oxygen saturation
- low urine output
- warm temp
Cardiogenic Shock
- usually result of a severe ventricular dysfunction associated with MI
- Diagnostic features include decreased CO, Elevated left ventricular end-diastolic pressure (preload), S3 heart sounds (indication of volume overload), Pulmonary edema, Narrow pulse pressure
Results of Cardiogenic Shock
- Low CO = reduced oxygen delivery to tissues = higher oxygen extraction = low SvO2
Cardiogenic Shock Treatments
- therapy is aimed at improving CO and myocardial oxygen delivery, decreasing workload
- inotropic (gives heart nice squeez), preload reducing, and afterload reducing agents
- intraaortic balloon conterpulsation (catheter is threaded through groin to aorta)
- ventricular assist devices
- heart transplantation (only after many times)
Obstructive Shock
- results from mechanical obstructions that prevent effective cardiac filling and stroke volume
- common causes include pulmonary embolism, cardiac tamponade, and tension pneumothorax
- manifests as right sided heart failure
- rapid management of underlying obstruction is required to prevent cardiovascular collapse
Hypovolemic Shock
- Results from inadequate circulation blood volume precipitated by hemorrhage, burns, dehydration, or leakage of fluid into interstitial spaces (external hemorrhage is most common cause)
- Low CO and intracardiac pressures (low preload) lead to SNS activation = elevated HR (tachycardia), vasoconstriction, and increased contractility
- result of epinephrine & dopamine
- Severity of symptoms correlates with amt of blood loss
Treatment of Hypovolemic Shock
- Therapy is aimed at fluid replacements and controlling the source of volume loss
- Colloids: increase serum colloid osmotic pressure (RBC)
- Crystalloids: solutions that contain elecctrolytes (IV fluids, Saline, dextrose)
- Blood products
Distributive Shock
- characterized by excessive vasodialtion and peripheral pooling of blood
- CO inadequate due to reduced preload
- Types include anaphylactic shock, neurogenic shock (bad communication between CNS and receptors), and septic shock
Anaphylactic Shock
- result of excessive mast cell degranulation mediated by IgE antibodies in response to antigen
- Mast cells release vasodilatory mediators (histamine) resulting in severe hypotension
- causes include antibiotic therapy, in particular Beta lactams, peanuts and tree nuts, insect stings, and snake bites
Clinical Symptoms and treatment of Anaphylactic shock
- symptoms include urticaria (hives), bronchoconstriction, stridor (noise made from air trying to escape from lungs), Angioedema (subcutaneous swelling in the lips), wheezing (air trying to move through constricted airways), and itching (prutitis)
- Treatment includes maintenance of airway patency, , use of epinephrine (causes bronchodilation), bronchodilators, antihistamines, vasorepressors, and IV fluids
Neurogenic Shock
- results from loss of sympathetic activation of arteriolar smooth muscle
- causes include medullary depression (brain injury, drug overdose), or lesions of sympathetic nerve fibers (spinal cord injury)
- treatment includes vasorepressors, fluids, elevation of the legs, slow position changes, and the use of pressure stockings on the legs