Exam 3 Flashcards
(122 cards)
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