Shock Flashcards
shock definition
a syndrome due to impaired tissue perfusion resulting in cellular hypoxia and build up of toxic metabolites
pathophysiology of shock
a trigger decreases blood flow to organs, compensatory mechanisms initiate (HR increase, aldosterone released, vasoconstriction), metabolic acidosis occurs (lactic acid released r/t anaerobic metabolism), leading to organ failure if continues to progress
s/s of shock
tachycardia, tachypnea, hypotension, thready pulse, decreased peripheral pulses, cyanosis, neurological symptoms, decreased UOP and absent bowel sounds; neurogenic would have a slow bounding pulse and cardiogenic would have bradycardia
distributive shock (vasogenic)
severe peripheral vasodilation; technically enough blood in the vessels but it can’t be distributed properly - vessels are too dilated
cardiogenic shock
heart can’t consistently pump out enough blood to meet needs of the body; low CO with hypotension; caused by MI* (cardiomyopathic), arrhythmias (arrhythmogenic), or valve issues (mechanical)
hypovolemic shock
most common type; reduced intravascular volume which reduces CO; hemorrhagic (some source of bleeding) or non-hemorrhagic (diarrhea, excessive diuresis, third-spacing)
obstructive shock
causes outside of the heart that cause pump failure, often associated with poor R ventricular output; causes could be PE, pulmonary HTN, tension pneumothorax, pericardial tamponade, or cardiomyopathy
absolute hypotension
SBP less than 90 or MAP less than 65
relative hypotension
drop in SBP of 40 or more
initial stage
narrowing pulse pressure; decreasing CO, tissue perfusion, and aerobic metabolism; increase in anaerobic metabolism and lactic acid production
later changes with shock
DBP decreases then the SBP decreases
compensatory stage
body attempting to preserve vital organs; sympathetic nervous system response: hormonal, neurological, and chemical
hormonal compensation
renin-angiotensin and antidiuretic hormone release, and an intracellular fluid shift; goal to increase intravascular volume
sympathetic nervous system
releases epinephrine and norepinephrine –> vasoconstriction; increases HR, cardiac output, and bp
progressive stage
compensatory mechanisms beginning to fail, anaerobic metabolism continues, more lactic acid is produced
refractory stage
shock undetected or unresponsive to therapy; cells are dying r/t apoptosis and Na-K+ pumps fail; MODS; death
effects on heart
decreased coronary artery perfusion, SV, CO, and bp
effects on lungs
increased pulmonary capillary membrane permeability, decreased gas exchange –> hypoxia, possibly ARDS
effects on brain
decreased function r/t hypoxia, unconsiousness, further impairment of cardiac and respiratory function, impaired thermoregulation
effects on liver
glycogen stores are depleted by excess circulatory epinephrine, coagulation factors, metabolic acids are NOT detoxified by liver –> metabolic acidosis; recovers fairly well when blood flow is restored
effects on kidneys
AKI and decreased UOP
ABCDE assessment
airway, breathing, circulation, disability (alert/responsive), exposure (looking over physically)
additional assessments
capillary perfusion: skin color, temperature, moisture; JVD: distended w/ cardiogenic shock or pulmonary congestion; flattened w/ hypovolemic or distrubritive shock
ABGs
early: respiratory alkalosis r/t tachypnea; pt will fatigue and RR decreases –> CO2 buildup –> respiratory acidosis; anaerobic metabolism continues and metabolic acidosis worsens
CVP less than or equal to 4
hypovolemia or vasodilation
CVP b/t 12-14
tamponade, volume overload, or pulmonary edema
lab monitoring
serum lactate greater than 2-4, base deficit +2 to -2, SVO2 (normal = 65-77%, critically ill = 60-80%)
management options
fluids, vasoconstrictors, vasodilators, inotropes, or anti-dysrrhthmics
causes of hypovolemic shock
whole blood loss (hemorrhagic shock), loss of fluids (n/v/d, massive diuresis), cirrhosis or severe sodium depletion
s/s hypovolemic shock
dependent on severity of volume loss; hypothermia is common (can cause clotting, acidosis, dysrhythmias, and decreased liver metabolism)
hypovolemic initial management
ABCDE, hemorrhage control, fluid therapy; large gauge bilateral (14-18) with short length and macro tubing; crystalloids, either LR or NS (LR preferred); colloids (albumin, hetastarch); blood replacement; warmed fluids
class 1 shock
less than 750ml lost (15%), normal vitals but anxious
class 2 shock
750-1500ml lost (15-30%), HR above 100, decreased pulse pressure, RR 20-30, anxious (start to see compensatory response)
class 3 shock
1500-2000ml lost (30-40%), HR above 120, decreased SBP and pulse pressure, RR 30-40 and confused (compensatory mechanisms failing)
class 4 shock
over 2000ml lost (over 40%), HR above 140, decreased SBP and pulse pressure, RR over 35 and lethargic
hemorrhagic shock
SBP doesnt decrease until 30% of blood volume lost for adults, and 40-45% for kiddos
trauma lethal triad
hypothermia, acidosis, coagulopathy
transfusion considerations
hyperkalemia (every unit of blood has around 60meq of K+) and hypocalcemia (citrate added to banked blood to prevent coagulation, after transfused the citrate will bind with calcium and decrease blood calcium levels), acidosis (banked blood pH 7.1), alkalosis (liver metabolizes citrate into HCO3), hypothermia (warm the blood, need core temp above 35C), coagulopathy
humerus fracture
500-1500ml blood loss
elbow fracture
250-750ml blood loss
rad/ulna fracture
250-500ml blood loss
pelvis fracture
750-6000ml blood loss
femur fracture
500-3000ml blood loss
tib/fib fracture
250-2000ml blood loss
ankle fracture
250-1000ml blood loss
priority nursing dx with hypovolemic shock
deficient fluid volume r/t active blood loss; decreased CO r/t alterations in preload; anxiety r/t threat to biologic, psychologic, or social integrity
classifications of distributive shock
septic, anaphylactic, and neurogenic shock
anaphylactic shock pathophysiology
life-threatening..duh, intervention needed w/i MINUTES; exposed to antigen and sensitized, body develops antibodies and reacts the next time they’re exposed to that antigen; histamine released–> vasodilation; acute changes in vascular permeability (can lose up to 35% of fluid volume in less than 10 min) and bronchial constriction
anaphylaxis & cardiovascular system
hypotension, HR usually goes up but sometimes decreases
anaphylaxis & respiratory
bronchoconstriction, laryngeal edema (obstructing airway), stridor/wheezing, dyspnea
anaphylaxis & skin
angioedema, redness, itching, urticaria
anaphylaxis & CNS
restless and confused
causes of anaphylaxis
medications, insect bites, food, contrast, etc
treatment of anaphylaxis
ABC, O2, IM epinephrine, fluid resuscitation; epi can be repeat q5 min; antihistamines, albuterol, steroids; maybe glucagon, beta blockers
anaphylactic shock nursing dx
ineffective breathing pattern, deficient fluid volume r/t relative loss, decreased CO r/t alterations in preload, decreased CO r/t alterations in afterload, impaired gas exchange r/t VQ mismatch or intrapulmonary shunting
Neurogenic shock
disruption of sympathetic nervous system; most uncommon; cause: spinal cord injury (not the same as spinal shock); loss/decreases sympathetic tone, decreased tissue perfusion, initiated general shock response
spinal shock
loss of activity below level of SCI and might not cause ineffective tissue perfusion
neurogenic shock progression
loss of sympathetic tone –> massive vasodilation –> blood pooling (relative hypovolemia) –> decreased preload –> decreased CO –> inadequate tissue perfusion
s/s of neurogenic shock
hypotension, bradycardia, peripheral vasodilation, warm and dry skin but progresses to hypothermia; pt dependent on environment to regulate temperature
neurogenic shock nursing dx
deficient fluid volume r/t relative loss; decreased CO r/t sympathetic blockade; hypothermia r/t exposure to cold environment, trauma, or damage to the hypothalamus
s/s of cardiogenic shock
EKG changes, dysrhythmias and HR increasing OR decreasing, hypertrophy of atrium or ventricles, tachypnea, hypoxemia, decreased bp, CO and CI, decreased LOC anxious–>confused–>lethargic–> unconscious; skin cool, pale and moist, long capillary refill; decreased UOP (less than 0.5ml/kg/hr), metabolic acidosis, peripheral pulses become thready
treatment goal for cardiogenic shock
correcting either.. preload, afterload, or contractility; L vent. HF would want to decrease afterload; R vent. HF would want to increase preload; might need IABP/LVAD, heart cath/stenting, give supplemental O2, give antiarrhythmics PRN
cardiogenic shock nursing dx
cardiogenic shock.. decreased CO r/t alterations in contractility and decreased CO r/t alterations in HR
