Exam 3 Flashcards
stages of shock
1- compensatory “non-progressive”, reversible, switches from aerobic to anaerobic (lactate greater than 1); 2- decompensated “progressive”, compensation failing, extreme cardiovascular support takes place; 3- refractory, irreversible, severe tissue hypoxia, ischemia and necrosis occur
basic patho of shock
hypoxia -> reversible cell injury -> aerobic to anaerobic metabolism -> depletion of ATP -> lactic acidosis (metabolic) -> irreversible cell injury -> multiple organ dysfunction -> death
patho of stage 1 aka compensatory
no drop in BP; baroreceptors detect low perfusion and low O2; compensation mechanisms working; sympathetic response d/t release of epi and norepi causing increase HR and peripheral vasoconstriction (cool clammy pallor skin); endocrine system releases aldosterone, release renin, release ADH; hyperventilate; paralytic ileus
organs affected from stage 2 shock
brain- decreased CPP causing AMS and confusion; heart- cell death resulting in acute MI and dysrhythmia; kidney- acute tubular necrosis resulting in renal failure; lungs- increased capillary permeability causing pulmonary edema and ARDS; liver- acute failure; gut- decreased peristalsis in ileus and GI bleed; vessels use all clotting factors leading to DIC
patho of stage 2
drop in BP, persistent hypoperfusion; hypoxic injury d/t decreased perfusion and O2, increased capillary permeability (protein and fluids leaking); multiple organ failure
Patho stage 3
multiple organ dysfunction syndrome (MODS); end of septic continuum when tissue perfusion cannot be restored; fist occurs in lungs and heart then hepatic, GI, renal, Immune, CNS; patient cannot be saved
3 main types of shock
hypovolemic, cardiogenic, distributive
hypovolemic shock
decreased blood volume, decreased venous return (preload), decreased stroke volume; decreased cardiac output (CO = HR x SV); decreased tissue perfusion- tries to compensate with increasing HR and increasing vascular tone
signs and symptoms of hypovolemic shock
weak thready pulse, decreased cardiac output, tachycardia, hypotension, cyanosis, decreased capillary refill, cool pale skin, decreased central venous pressure, increased vasoconstriction, decreased O2 sat, tachypnea
labs associated with hypovolemic shock
lactic acid, CBC, ABGs, urine output (decreased)
treatment of hypovolemic shock
need two large bore IVs; stop bleeding or fluid loss; treat underlying cause; replace volume with crystalloids, blood products, or albumin; support BP with vasopressors; if >30% loss then need to replace blood volume
if administering vasopressors such as levophed…
need to give via central line; need A-line for monitoring
nursing management of hypovolemic shock
vitals q15; monitor cardiac and respiratory status; trendelenburg positioning; monitor temp for hypothermia; glucose <150; type and screen, get consent, and admin blood; meds like fluids and pressors
cardiogenic shock
pump failure; d/t problem with filling such as diastolic HF; contraction issues such as cardiomyopathy, HF, MI; d/t arrythmias causing conduction issues; structural issues like valvular diseases (regurgitation)
s/s of cardiogenic shock
weak peripheral pulse, decreased CO, increased HR, decreased BP, cool clammy skin, decreased capillary refill (>3sec), increased CVP, increased SVR from vasoconstriction, decreased O2 sat. JVD, chest pain, oliguria, confusion and agitation, dyspnea, pulmonary edema
labs associated with cardiogenic shock
lactate, troponin, ABG, CXR, EKG, echo, CRP, PCWP, CO, CI
management of cardiogenic
monitor O2 with ABGs and pulse ox; pain control via fentanyl and morphine; fluid control with diuretics; cardiovascular support with hemodynamic monitoring (increase SVR, increase contraction, fix arrhythmias, temporary assist device with intra-aortic balloon pump or ECMO; repair heart
how to increase SVR
vasopressors
how to increase contraction
inotropes
how to fix arrhythmias
Pacers, anti-arrhythmias, cardioversion
procedures to repair heart for cardiogenic shock
surgery, catheterization, LVAD, transplant
types of distributive shock
anaphylactic shock, neurogenic shock, septic shock; different reactions but all cause massive vasodilation
anaphylactic shock
massive release of histamine; allergen is entered into blood stream and interacts with B cells to produce antibodies (IgE); release H1 and H2 histamines
H1 histamine
bad one; increase capillary dilation (systemically) decreasing BP; increase capillary permeability systemically causing fluid shifts; bronchoconstriction of lungs; decrease conduction of AV node
H2 histamine
increase gastric acid production and can cause N/V and increase risk of aspiration; vascular smooth muscle relaxation causing decrease in BP
Type 1 vs Type 2 allergic reaction/anaphylaxis
type 1 needs sensitization and is IgE mediated; type 2 does not need sensitization and usually occurs with bee stings and IV contrast
signs of anaphylactic shock
rapid weak pulse, decreased CO, increased HR, decreased BP, generalized flushing of skin, decreased CVP, decreased SVP, decreased O2 sat, cardiac dysrhythmias/arrest, N/V, acute abdomen, wheezing/coughing, bronchoconstriction, itching, urticaria, flushing from massive vasodilation
nursing management of anaphylaxis
ABCs, Epinephrine to increase sympathetic response, intubate/ventilate, albuterol admin, IV fluids, H1 antihistamine (benadryl) and H2 antihistamine (zantac), corticosteroids to prevent rebound
Neurogenic shock
distributive shock caused from CNS injury; cervical or high thoracic injury (T6 and above); loss of sympathetic response and preserved parasympathetic activity, causes body to slow down (bradycardia)ca
causes of neurogenic shock
spinal cord injury, spinal anesthesia, nervous system damage, hypoglycemia, drug voerdose
patho of neurogenic shock
coronary vessels are impacted via decrease in afterload (SVR) and decrease in preload; loss of catecholamine response leading to decreased vascular tone and decreased BP; heart decreased in cardiac contraction and low heart rate; hypothermia from dysregulation in hypothalamus and no vasoconstriction
manifestations of neurogenic shock
decreased afterload (SVR), hypotension, bradycardia, decreased CO hypothermia (warm dry extrem.)
treatment of neurogenic shock
immobilize/protect spine; assess vitals and admin IV fluids, pressors, inotropes, increase HR (give epi); protect airway
septic shock stages
systemic inflammatory response (SIRS)- temp > 100.4F, respiration > 20, HR >90, WBC > 12000 or < 4000; sepsis- two or more of these conditions; severe sepsis- organ dysfunction hypotension, hypoperfusion; septic shock- symptoms despite adequate fluid resus, unable to fix
1 hour sepsis bundle
used to rapidly diagnose and provide immediate intervention; lactic acid draw > 2, cultures prior to antibx, broad spectrum antibiotics at first then narrow, Iv fluids like crystalloids, vasopressors to maintain map > 65 (levo), oxygenation, support failing organs
patho of septic shock
infection with bacteria, virus, or fungi in blood causing WBC to respond; result in pro-inflammatory mediators and nitric oxide that dilate blood vessels and decrease BP (drop SVR), leaky capillaries causing fluid shifts, less O2 and more fluid causes difficulty perfusing, lytic enzymes damage blood vessels and use up clotting factors (DIC), fluid accumulates in lungs (ARDS)
early clinical manifestations of septic shock
aka “warm”/compensated; fever, warm skin, increased RR, restless, anxious, glucose abnormalities (hyperglycemia d/t gluconeogenesis), elevated HR
late signs of septic shock
aka “cold”/uncompensated; cold clammy skin, respiratory distress/failure/ARDS, AMS/coma, glucose abnormalities (hypoglycemia), decrease in HR and BP
septic shock affects
heart, lungs, kidneys, GI, liver
septic shock affects on heart
stunned myocardium, HF; use IV fluids, vasopressors, blood products; DVT prohylaxis with lovenox
septic shock affects lunga
cyanosis, acidosis, ARDS; treat with BiPap and mechanical ventilation; sedate and neuromuscular blockade
septic shock affecting kidneys
oliguria, anuria, tubular necrosis, place on CRRT
septic shock affects liver
jaundice, glucose problems, liver failure; treat with IV insulin d/t TPN increasing BGL
septic shock affects GI
N/V, diarrhea, ileus; treat with parenteral or enteral nutrition; prophylaxis to prevent stress ulcer
Summary of hypovolemic shock symptoms
elevated HR, elevated SVR, decreased CO, decreased CVP, decreased O2, cold clammy skin
summary of cardiogenic shock symptoms
elevated HR, increased SVR, decreased CO, increased CVP, decreased O2 sat, cold clammy skin
summary of neurogenic shock symptoms
decreased HR, decreased SVR, decreased CO, decreased CVP, decreased O2, warm dry skin
summary of septic shock symptoms
increased then decreased HR, decreased SVR, increased Co then decreased, decreased CVP, decreased O2 sat the increased, warm hot dry skin then cold clammy skin