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Phases Shock
Question | Answer |
---|---|
Shock | The whole body’s response to poor (impaired) tissue oxygenation, a) any situation that affects oxygen to tissues and organs can precipitate shock |
All of your patients are at risk for shock | a) a drug allergy: anaphylactic shockb) an infection from a catheter, wound, IV: septic shockc) trauma/surgeryd) burns/stabbing: hypovolemic shock |
Shock Syndrome | Decreased blood flow to the tissues causes, Decreased oxygen to tissues which causes, Anaerobic cellular metabolism (metabolism without adequate oxygenation; inadequate metabolism: damaging to cells tissue & organs) which causes, Cellular dysfunction whi |
Adequate tissue/organ perfusion | requires adequate oxygenated arterial blood (has to get to the area) |
Perfusion is directly related to | Mean Arterial Pressure MAP |
Factors that affect MAP | Blood Volume: how much blood, plasma, platelets (all the components) is circulatingb) Cardiac Output: amount of volume in liters of blood ejected by the heart each minutec) Size of Vascular Bed: changes depending on vasodilatation/vasoconstricti |
Direct Relationship | Total blood volume and CO are directly related to MAP, If blood volume increased, MAP increases, If CO increased, MAP increases…and vice versa |
Inverse Relationship | The size of the vascular bed is inversely related to MAP, If the vascular bed increases (vasodilatation), than MAP decreases, If the vascular bed decreases (vasoconstriction), then MAP increases |
Compensatory Mechanisms (All kinds of shock when there is a decrease in MAP) | 1. A sustained decrease in MAP is sensed in the BARORECEPTORS (located in the carotid sinus and the aortic arch) which then transmit information to the brain (to increase MAP; body’s way of compensating for the decrease in MAP) |
Neural Compensation | 1. Activation of the Sympathetic Nervous System comes first causes:2. Blood vessels in the skin, GI tract and kidneys to constrict (preserving blood flow centrally, to more essential organs: brain, heart)3. Heart rate, blood pressure, CO, respiration |
Hormonal/Chemical Compensation | 1. Underlying cause of shock must be treated!!!!!!!!!!!!!!!!!!2. If underlying cause of shock is not corrected and MAP decreases even further…3. Decreased renal blood flow causes increased renin (vasoconstrictor) aldosterone, and ADH production4. Th |
Stages of Shock | 1. Initial Stage2. Non-progressive Stage3. Progressive Stage4. Refractory Stage (despite therapy ca be deadly)5. Shock progresses in a predictable outcome, if not treated, patient despite compensatory mechanisms will progress along and eventually |
Initial Stage | 1. Mild decrease of baseline MAP of 10mmHg or less a) important to know pt baseline2. Early compensatory mechanisms are working effectively, causing mild vasoconstriction and an increased heart rate. There may also be a slight increase in diasto |
Non-Progressive (Compensatory) Stage | 1. When all compensatory mechanisms have kicked in2. Conditions cause a decrease in MAP 10-15mmHg from baseline (more of a decrease despite early compensatory mechanisms)3. Neural compensation increases but is inadequate4. Hormonal/chemical compensa |
Progressive Stage | 1. This results when there is sustained, continued decrease in MAP of more than 20mmHg despite compensatory mechanisms2. Vital organs experience hypoxia (esp. w/ underlying CAD pt may have chest pain, +CIEs and decreased mental status)a) vital organs |
Refractory Stage | 1. Severe tissue hypoxia2. Release of myocardial depressant factor from the pancreas (depressed CO further)3. Build-up of toxic metabolites4. MODs (Multi Organ Dysfunction)5. Death is inevitable (“circling the drain”) |
Factors that Affect Stages of Shock | 1. There is no specific timeline (every pt responds differently)2. Pts agea) the older the pt the less able to handle shockb) pt gets sicker quicker3. Prior health a)pt with hx of CAD, renal failure, peripheral vascular disease will not b |
Causes of shock | 1. Insufficient quantity of blood (decreased blood volume)2. Failing pump (heart is failing)3. Abnormal distribution of blood volume in the vascular bed (due 2 vasoconstriction or vasodilatation) |
Shock Classifications | According to what function is affected by the shock1. Hypovolemic Shock2. Cardiogenic Shock3. Obstructive Shock4. Distributive Shock |
Hypovolemic Shock | 1. Insufficient blood volume2. MAP decreases3. Tissue oxygenation decreases (because blood carries O2)4. Most common type of shock in the ED or in pt who are post surgery or invasive procedure |
Causes of Hypovolemic Shock | 1. Hemorrhage 2. Dehydration (can occur quickly) |
Hemorrhage | a) external: trauma, wound, surgery (you will see; obvious to you) b) internal: blunt trauma, GI bleed, internal surgical sites (harder to see and dx; may take longer for you to notice s/s occur later; monitor CBC, H&H) * Inadeq |
Dehydration | a) due to decreased fluid intake or increased fluid losses b) profound dehydration can be caused by: *viruses *anorexia with use of diuretics (over diuresised) *DI *NG tube without adequate IV fluid replacement |
Cardiogenic Shock | 1. Not only infarcted or have a weak heart, but the heart is failing2. Direct failure of the heart as a pump3. CO, afterload and MAP are all decreased4. The most common complication of MI in pt who have had greater than 40% of their myocardium affec |
Causes of Cardiogenic Shock | 1. MI 2. Cardiac arresta) due to profound hypothermia, toxins, drugsb) heart stops working, pumping3. Ventricular arrhythmiasa) V tach can lead to V fibb) there is not adequate pumping of the heart 4. Cardiomyopathya) cause heart to weaken |
Obstructive Shock | 1. Not the heart itself, something else indirectly affects the heart’s ability to pump effectively |
Obstructive Shock Causes | a) cardiac tamponade: fluid and blood accumulate in the pericardium which cause inability of heart to pump effectivelyb) massive pulmonary embolusc) severe pulmonary HTNd) constrictive pericarditis: infection or inflammation that causes constricti |
Distributive Shock | 1. Profound blood vessel dilation2. Pooling of blood in the veins and capillaries causes increased blood vessel permeability3. 3rd spacing of fluid out of the vascular space occurs4. Can be Neural or Chemical |
Neural-Induced Distributive Shock | 1. Loss of sympathetic tone occurs2. Massive, widespread vasodilatation occurs3. Causesa) anesthesiab) spinal cord injuryc) head trauma |
Chemical-Induced Distributive Shock | 1. Chemicals or foreign substances start the diffuse changes in the blood vessel walls2. Circulating problem causes the vasodilatation to begin3. Three most common origins:a) anaphylaxis: response to and antigen (have been exposed to it before) whe |
Anaphylactic Shock | 1. Type of chemical induced distributive shock2. Do to an antigen antibody responsea) exposure to PCN may have had no problem the 1st time (or slight rash) but the body builds up antibodies3. Not likely to occur on the 1st exposure to and antigen |
Causes of Anaphylactic Shock | 1. Drugs (antibiotics, sulfa drugs etc.)2. Contrast media (question shellfish/iodine allergy)a) if needed pt premedicated with:Benadryl, corticosteroids, tagamet/pepcid3. Blood transfusions4. Insect bites (bee)5. Food allergy ( egg, peanut, she |
Septic Shock | 1. Most common form of distributive shock2. Had 40-85% mortality rate3. Microorganisms enter the vascular systema) sepsis more common in G- bacterial infections4. These organisms produce endotoxins this causes:5. A whole body inflammatory respo |
Risk Factors for Septic Shock | 1. > 85 years old2. Malnutrition3. Immunocompromised (steroid use, chemo, HIV, transplant pt be cause on chronic immunosuppressive tx 4. Pregnant 5. Hx of infection with resistant organisms (MRSA, VRE)6. Treatment related factors: open wounds, |
CARDIOGENIC SHOCK | An inadequate pumping of the heart, resulting in decreased systemic blood flow and inadequate tissue perfusion. Causes include: Myocardial infarction, dysrhythmias, severe congestive hear failure, cardiac tamponde. |
CARDIOGENIC SHOCK Key Assessment Findings | Elevated CVP with JVD, elevated PCWP, decreased CO, elevated systemic vascular resistance. |
CARDIOGENIC SHOCK Management | Administer beta-adrenergic meds (dopamine, dobutamine) and afterload reducers (Nipride, Tridil) IABP, oxygen, decreasing work load of the heart. |
SEPTIC SHOCK | Massive infection causing vasodilation and inadequate tissue perfusion, usually following endotoxemia due to gram negative bacilli (gram postitive cocci, infrequent). Causes include: Septicemia, localized infection from urinary tract procedures, indwellin |
SEPTIC SHOCK Key Assessment Findings | Hyperdynamic (WARM) Stage: SVR decreased due to peripheral vasodilation, CO increases, tachycardia, tachypnea, confusion.Hypodynamic (COLD) Stage: Low CO, elevated systemic vascular resistance, hypotension, cold clammy and pale skin, hypothermia, multip |
SEPTIC SHOCK Management | Antibiotics, Beta receptor stimulants which have a positive inotropic effect on the hear and vasodialate microcirculation, steroids |
ANAPHYLACTIC SHOCK | Histamine is released into the blood stream following an allergic antigen antibody reaction. There is a subsequent increase in capillary permeability and widespread dilation of arterioles and capillary beds. Causes included: contrast media, penicillins, f |
ANAPHYLACTIC SHOCK Key Assessment Findings | Urticaria, laryngeal edema, bronchospasm, hypotension, confusion, warm moist skin |
ANAPHYLACTIC SHOCK Management | Sympathomimetic (epinephrine) which will stimulate alpha receptors causing vasoconstriction of blood vessels, stimulate beta 1 receptors produciong positive inotropic effects stimulated beta2 receptors which induces bronchodialation, antihistamines and st |
Cardiogenic | PRELOAD - IncreasedAFTERLOAD - IncreasedCARDIAC OUTPUT - Decreased |
Hypovolemic | PRELOAD - DecreasedAFTERLOAD - IncreasedCARDIAC OUTPUT - Decreased |
Septic (WARM) | PRELOAD - WNL/lowAFTERLOAD - DecreasedCARDIAC OUTPUT - Increased |
Septic (COLD) | PRELOAD - DecreasedAFTERLOAD - IncreasedCARDIAC OUTPUT - Decreased |
Anaphylactic | PRELOAD - DecreasedAFTERLOAD - DecreasedCARDIAC OUTPUT - Decreased |