Shock

Front 1

two types of shock due to low blood flow are...

Back 1

cardiogenic and hypovolemic

Front 2

three types of shock due to maldistribution of blood flow...

Back 2

septic, anaphylactic, neurogenic

Front 3

neurogenic shock

Back 3

occurs about 30 minutes after a spinal cord injury; blood pools in the spinal cord and doesn't move to tissues where it needs to be

Front 4

absolute hypovolemia vs. relative hypovolemia

Back 4

absolute: loss of intravascular fluid volume
relative: the fluid volume moves where it doesn't need to be, but isn't gone

Front 5

causes of absolute hypovolemia

Back 5

hemorrhage; GI loss; fistula drainage; diabetes insipidus; hyperglycemia; diuresis

Front 6

causes of relative hypovolemia

Back 6

3rd spacing (ascites, edema, etc)

Front 7

clinical manifestations of hypovolemic shock

Back 7

anxiety; tachypnea; increase in CO, HR; decrease in SV, PAWP, UO

Front 8

PAWP

Back 8

pulmonary arterial wedge pressure; measured with a catheter wedged into the distal pulmonary artery; used to measure mean left atrial pressure

Front 9

if loss is greater than __%, blood volume must be replaced

Back 9

30

Front 10

hypotension is defined as

Back 10

a SBP of less than 90 or a reduction of more than 40 from baseline and in which BP is not adequate for normal perfusion

Front 11

what are the 4 stages of shock?

Back 11

1. initial
2. compensatory
3. progressive
4. refractory

Front 12

initial stage of shock

Back 12

usually not clinically apparent; metabolism changes from aerobic to anaerobic-- lactic acid accumulates and must be removed by blood and broken down by liver; process requires O2 that is unavailable

Front 13

compensatory stage of shock

Back 13

clinically apparent; hopefully, patient's body is able to compensate on its own or clinically; if not, patient moves on to progressive stage.
Baroreceptors in carotid and aortic bodies activate SNS in response to lowered BP--vasoconstriction while blood to vital organs is maintained; the decrease of blood to kidneys activates the renin-angiotensin-aldosterone system to increase venous return to the heart, CO, BP; GI motility is impaired; cool, clammy skin (except septic patient who is warm and flushed); arterial O2 levels decrease, rate and depth of respirations are increased; the SNS stimulation increases myocardium O2 demands; if perfusion deficit is corrected, patient recovers with no residual sequelae

Front 14

progressive stage of shock

Back 14

begins when compensatory mechanisms fail; capillary permeability INCREASES and fluid leaks into places it shouldn't-- protein in particular, which leads to systemic interstitial edema (anasarca); blood flow to pulmonary capillaries DECREASES and to other solid organs/peripheral tissues; PULMONARY EDEMA; BRONCHOCONSTRICTION; fluid moves into alveoli, causing edema and decreased SURFACTANT; TACHYPNEA, CRACKLES, INCREASED WORK OF BREATHING; CO begins to fall, hypotension, weak peripheral pulses; ischemia of distal extremities; dysrhythmias, MI, complete deterioration of CV system; mucosal barrier of GI system becomes ischemic--ULCERS AND BLEEDING; risk of translocation of bacteria, decreased ability to absorb nutrients, "DEAD GUT"; liver fails to metabolize drugs and wastes----> JAUNDICE; elevated enzymes, loss of immune function, risk for significant bleeding---> acute tubular necrosis/ acute renal failure

Front 15

what happens to potassium levels during the progressive stage of shock?

Back 15

increases

Front 16

refractory stage of shock

Back 16

exacerbation of anaerobic metabolism; accumulation of lactic acid; increased capillary permeability; profound hypotension and hypoxemia; tachycardia worsens; decreased coronary blood flow; CEREBRAL ISCHEMIA; failure of one organ system affects others, and recovery is unlikely; severe hypotension (SBP < 80); very rapid, weak pulse; rapid, shallow respirations with crackles and wheezes; cool, pale skin, mottled with cyanosis; disoriented; lethargic; comatose; ANURIA; loss of reflexes; decreased or absent pulses

Front 17

what sort of therapy is used for septic, hypovolemic, and anaphylactic shock?

Back 17

volume expansion; isotonic crystalloids (ie normal saline) for initial resuscitation of shock

Front 18

what do you do if patient does not respond to 2 to 3 L of crystalloids?

Back 18

blood administration and central venous monitoring

Front 19

complications of fluid resuscitation

Back 19

hypothermia; coagulopathy

Front 20

nutrition that is given to decrease morbidity from shock

Back 20

initiate enteral nutrition within the first 24 hours; initiate parenteral nutrition if enteral feedings are contraindicated or fail to meet at least 80% of the caloric requirements

Front 21

what is normal urinary output in ml/kg/hr

Back 21

>0.5 ml/kg/hr

Front 22

hormones released in response to low BP

Back 22

ADH, renin, epinephrine, aldosterone

Front 23

how long can kidneys tolerate hypoxia and anoxia without damage?

Back 23

one hour

Front 24

cellular death liberates what ion

Back 24

potassium

Front 25

urine specific gravity remains at what level when kidneys fail

Back 25

1.010

Front 26

shock is characterized by

Back 26

impaired oxygen and nutrient exchange

Front 27

what is a common feature of various types of shock?

Back 27

physiologic response

Front 28

which lab result would you monitor while administering Ringer's Lactate intravenously during shock resuscitation?

Back 28

lactate, because the liver is unable to convert it

Front 29

which lab test reveals nutritional status accurately?

Back 29

serum protein

Front 30

what happens to blood glucose levels during the compensatory state of shock?

Back 30

increases due to SNS stimulation

Front 31

what happens to blood glucose levels during the refractory period of shock?

Back 31

decreases

Front 32

daily weights during shock management are done to measure what?

Back 32

fluid status

Front 33

nutritional therapy is begun early in shock management to...

Back 33

enhance GI perfusion

Front 34

more causes of relative hypovolemia

Back 34

bowel obstruction (thus pooling of blood or fluids); burns; internal bleeding (ie fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis; massive vasodilation (ie sepsis)

Front 35

what happens to urine specific gravity during hypovolemic shock?

Back 35

increases

Front 36

a patient may compensate himself/herself for up to how much of total blood volume?

Back 36

15%

Front 37

at what point of fluid loss do SNS changes begin to occur?

Back 37

15-30%

Front 38

at what point of fluid loss do the compensatory mechanisms begin to fail, causing the necessity for immediate replacement with blood or blood products?

Back 38

30% or more

Front 39

the rule for fluid resuscitation during hypovolemic shock?

Back 39

3:1 (3 ml of isotonic crystalloid for every 1 ml of estimated blood loss)

Front 40

overall goals for patient in shock

Back 40

1. assurance of adequate tissue perfusion
2. restoration of normal/baseline BP
3. return/recovery of organ function
4. avoidance of complications from prolonged states of hypoperfusion