Mca Iii Final: Shock

Front 1

describe shock (3)

Back 1

1. decreased tissue perfusion
2. impaired cellular metabolism (aerobic -> anaerobic)
3. imbalance btw. supply and demand of O2 and nutrients

Front 2

initial stage of shock (3)

Back 2

1. aerobic -> anaerobic metabolism
2. increase in lactic acid
3. no noticeable s/s

Front 3

what system will get initiated first and how will it respond

Back 3

SNS will be initiated first and it will increase the HR & RR

Front 4

what organ is the first to recognize a low fluid state

Back 4

the kidneys

Front 5

what will happen in response to a low fluid state

Back 5

1. low urine output
2. increased specific gravity b/c of the higher concentration (yellow -> tea color)
3. creatinine increases

Front 6

what is the best indicator of kidney dysfunction

Back 6

GFR/creatinine clearance. urine collected over a 24 hour period

Front 7

what medication may not allow you to rely on the SNS

Back 7

beta blockers b/c you will not see in the increase in HR

Front 8

compensatory stage of shock

Back 8

1. activation of SNS through baroreceptors and chemoreceptors
2. response of body system. renin-angiotensin increases BP and retains H20 (decrease in urine output)

Front 9

what happens to the GI system

Back 9

1. decrease in peristalsis. hypoactive/absent bowel sounds
2. decreased blood flow to stomach

Front 10

what happens to the skin

Back 10

decrease blood flow. bluish, cold, clammy

Front 11

what happens to the pulmonary system (3)

Back 11

1. increase in dead space ventilation
2. increase VQ mismatch
3. vasoconstriction in the lungs and bronchioles, will have to breath faster to get more O2 but will not work b/c of decrease circulating volume. decreased Hgl levels

Front 12

progressive stage of shock

Back 12

1. prolonged compensatory stage
2. results in end organ failre
failure or exhaustion of compensatory resonse

Front 13

what happens in end organ failure (7)

Back 13

the kidneys will shut down
- increase creatinine
- resp. failure
- liver producing increased glucose but not storing
- decrease HR
- dysrhythmias b/c of lack of O2 to cardiac muscle
- chest pain
- acidosis. lactic acid is produced supressing the contracitlity of the heart and CO is decreased

Front 14

what are different types of crystalloids

Back 14

NS, LR, D5

Front 15

what are different types of colloids

Back 15

hespan (made w/saline), hextend (made w/LR), Albumin

Front 16

what do you use in ARF

Back 16

NS

Front 17

why wouldn't you use LR or D5 in ARF

Back 17

LR b/c of the K component, and D5 b/c of the extra glucose. it will pull H2O into the intravascular space and it's not good on rapid infusion

Front 18

why are crystalloids preferred over colloids?

Back 18

you can not use colloids in large amts b/c of the coagulation problems.

Front 19

refractory stage of shock

Back 19

1. irreversible cellular death
2. death

Front 20

cardiogenic shock

Back 20

1. systolic or diastolic heart failure. systolic more common
2. decreased cardiac output

Front 21

cardiogenic shock s/s

Back 21

1. HR up
2. BP down
3. SVR up
4. CO/I down
5. RR up
6. CVP up
7. PAP, PAWP up

Front 22

cardiogenic shock will decrease urine output. should you use a fluid bolus?

Back 22

no b/c it will contribute to edema, fluid overload, increase PAWP and CVP

Front 23

cardiogenic shock Tx (meds)

Back 23

- Ibutamin. intotropic vasodilator to improve contractility
- dobutamine
- nipride to decrease SVR and decrease workload

Front 24

what is the problem with dopamine

Back 24

a chronotrope that increases HR. can be use doputamine but if HR exceeds 120 bpm, will need to DC

Front 25

cardiogenic shock Tx (non meds)

Back 25

O2, resting, IABP

Front 26

IABP

Back 26

inserted into femoral artery, sits in aorta. deflated during systole, inflated during diastole and vasodilates aorta

Front 27

hypovolemic shock

Back 27

low intravascular volume caused by fluid loss and third spacing

Front 28

hypovolemic shock s/s

Back 28

1. HR up
2. BP down
3. Preload down
4. SV, PAP, PAWP, CVP down
5. CO down

Front 29

explain the stages of hypovolemic shock

Back 29

stage I: no s/s
stage II: BP ok, increased HR, RR
stage III: obvious fluid loss.

Front 30

hypovolemic shock Tx

Back 30

fluid w/fluid. blood w/blood. then you can add meds (crystalloids) to tigten up the vessel tone

Front 31

what is the universal blood donor

Back 31

O negative

Front 32

neurogenic shock (4)

Back 32

1. spinal cord injury T5 or higher
2. massive vasodilation
3. SNS lost
4. no compensatory mechanism

Front 33

neurgenic shock s/s (2)

Back 33

hypotension, temp. dysregulation

Front 34

neurogenic shock Tx

Back 34

atropine to increase HR
vasopressors to reestablish vessel tone so blood gen back to circulatory system

Front 35

explain loss of SNS

Back 35

b/c of spinal cord injury there is no SNS response, there is no synapse that can travel to the brain

Front 36

neurogenic shock hemodynamics

Back 36

1. HR down
2. BP down
3. CVP down
4. PAP, PAWP down
5. CO/CI down

Front 37

what does neurogenic shock resemble

Back 37

fluid deficit b/c of the vasodilation and the lack of SNS

Front 38

anaphylactic shock (4)

Back 38

1. life threatening
2. release of vasoactive mediators
3. increase capillary permeability
4. can result in respiratory distress d/t edema and bronchoconstriction

Front 39

early s/s of anaphylactic shock

Back 39

lip swelling, wheezing, retlessness, anxiety, agitation, SOB (use of intercostal muscles), mucous

Front 40

2 types of vasoactive mediatros

Back 40

1. massive vasodialtion. BP drops and fluid goes into interstitial space d/tincrease capillary permeability
2. circulatory failure

Front 41

anaphylactic shock hemodynamics

Back 41

1. HR up
2. BP up
3. SVR down
4. PAP/PAWP down
5. CVP down

Front 42

anaphylactic shock Tx

Back 42

1. epi pen
2. corticosteroids -> benedryl

Front 43

sepsis

Back 43

1. systemic inflammatory (SIRS) response to an infectious process
2. common in critically ill pts
3. high mortality rate
4. one of the most common cuase of death in the ICU

Front 44

severe sepsis =

Back 44

sepsis plus (either)
evidence of hypoTN and end organ dysfuncion

Front 45

severe sepsis

Back 45

1. inflammation
2. coagulation
3. impairment of fibrolysis

Front 46

results of severe sepsis

Back 46

1. coagulopathy
2. microvascular thrombosis
3. MODS

Front 47

septic shock

Back 47

1. persistent hypotension despite fluid resuscitaiton
2. tissue perfusion abnormalities
3. bacterial infection

Front 48

septic shock s/s

Back 48

1. SNS response
2. hypotensive
3. decreased UO
4. alteration in neuro status
5. respiratory failure

Front 49

what is the #1 prevention of sepsis

Back 49

hand washing (& antibiotics)

Front 50

sepsis progressive stage hemodynamics

Back 50

1. CO/CI down
2. BP down
3. PAP/PAWP down
pretty much everything down

Front 51

why is MAP important

Back 51

norm of at least 60 b/c need enough pressure to send enough O2 and glcose to the brain

Front 52

shock management

Back 52

1. treat the cause
2. improve O2
3. restore tissue perfusion

Front 53

shock management is collaborative

Back 53

1. O2 and ventilation
2. fluid replacement (crystalloid, colloid, blood products)
3. vasopressors

Front 54

disseminated intravascular coagulation (DIC)

Back 54

1. microvascular coagulation
2. depletion of clotting factors
3. bleeding

Front 55

what can cause DIC?

Back 55

sepsis (most common), hypovolemic shock, and anaphylactic shock

Front 56

DIC can cause what type of shock

Back 56

hypovolemic shock

Front 57

why would a DIC be tachycardic

Back 57

b/c the blood loss w/in the intravascular space triggers the SNS which increases the HR

Front 58

why would a DIC pt. be cyanotic

Back 58

b/c of the loss volume and the lack of O2, clots get lodged in the fingers, toes, and pulmonary

Front 59

explain fibrinolysis

Back 59

- clot busting
- releases fibrin degradation products such as anticoagulants and RBC hemolysis
- clotting factors are used up and lead to hemorrhage

Front 60

DIC risk factors

Back 60

1. sepsis
2. multtrauma
3. burns
4. blood products or blood transfusions

Front 61

DIC CM (12)

Back 61

1. cyanosis
2. changes in LOC
3. angina
4. hypoxemia
5. oliguria/anuria (decreased urine)
6. stool occult positive
7. bloody emesis
8. hematuria (blood in urine)
9. oozing from IV sites
10. blood from body orifices
11. petechiae
12. ecchymosis

Front 62

what is the best coagulopathy test

Back 62

D Dimer. increase indicates DIC. will increase when there are lots of clots being broken up

Front 63

DIC hemodynamics

Back 63

1. d dimer up
2. PTT/PT INR up
3. wedge down
4. HH down
5. RBC down
6. fibrinogen & platelets down

Front 64

why are the PTT/PT and INR test down

Back 64

the clotting factors are being consumed

Front 65

blood products for intervention

Back 65

1. FFP for some fibrinogen replacement and correction of PT/PTT
2. cryprecipitate to place factor VIII and is specific to fibrinogen
3. vitamin K to correct coagulopathy
4. antithrombin II to inactivate thrombin and stop clotting
5. LMWH controversial b/c will prevent clot but will cause bleeding

Front 66

NTG in only for what type of shock

Back 66

cardiogenic

Front 67

NTG (4)

Back 67

1. vasodilates
2. more venous than arterial
3. aka Tridil
4. use special IV tubing and glass bottle

Front 68

Nitroprusside (Nipride)

Back 68

1. potent vasodilator
2. more arterial
3. protect from light w/foil or dark ba
4. used w/malignant hypothermia
5. short half life
6. cyanide poisening with large doses

Front 69

what type of shock do you use Nipride

Back 69

cardiogenic to lessen work load on the heart

Front 70

what do you need to remember when using Nipride

Back 70

always draw back and never flush or you will see a severe drop in BP

Front 71

Dopamine

Back 71

1. vasoconstrictor @ high doeses
2. inotropic and chornotropic

Front 72

what is a problem with dopamine

Back 72

chronotrope associated with tachycardia

Front 73

dobutamine (dobutrex) (4)

Back 73

1. inotrope
2. chronotrope
3. only use w/cardiac issues such as cardiogenic shock, s/p bypass surgery, MI
4. not so much for vasoconstriction

Front 74

newsynephrine (pnehylephrine) (3)

Back 74

1. vasopressor
2. sepsis, neurogenic, anaphylactic
3. doesn't contribute to increase HR or contractility

Front 75

epinephrine (5)

Back 75

1. alpha adrenergic stimulant
2. vasopressor
3. increases HR (chronotrope)
4. used in cardiac arrest
5. anaphylactic/septic shock

Front 76

norepinephrine (levophed) (5)

Back 76

1. potent vasopressor
2. increases HR and BP
3. chronotrope
4. titrate to effect
5. septic, neurogenic and anaphylactic shock

Front 77

SIRS caused by (5)

Back 77

1. infection
2. transfusion
3. ischemia
4. infarct
5. trauma

Front 78

SIRS triggers (6)

Back 78

1. tissue trauma
2. abscess formation
3. ischemic/necrotic tissue
4. microbial
5. gram negative
6. perfusion deficits

Front 79

SIRS patho

Back 79

inflammatory response -> vasodilation (decrease BP, CO), increase capillary permeability, release mediators and cyokines (tissue damage & hypoperfusion fo major organs), microvascular clotting

Front 80

SIRS early CM (6)

Back 80

1. hyperthermia or hypothermia
2. tachcardia
3. tachypnea
4. decrease UO
5. altered LOC
6. leukocytosis or leukopenia

Front 81

SIRS late CM

Back 81

altered organ perfusion
1. increased agitation and confusion
2. hypoxemia
3. oliguria or anuria
4. mottled skin/cyanotic

Front 82

MODS

Back 82

progresson of SIRS, high mortality rate

Front 83

primary MODS

Back 83

rapid, direct injury to organ can be d/t trauma

Front 84

secondary MODS

Back 84

from persistent or prolonged SIRS, 7-10 days

Front 85

MODS nursing management (7)

Back 85

1. treat the cause
2. promote tissue oxygenation
3. promote cardiac output
4. adequate hemoglobin
5. decrease O2 demand
6. nutritional and metabolic demands
7. support failing organs

Front 86

what can you provide to decrease metabolic demands

Back 86

neuromuscular blockades

Front 87

evidence based practice guidelines (12)

Back 87

1. CVP 8-12
2. MAP > 65
3. fluid resuscitation (measured with CVP, hydrate then meds)
4. tranfusion for decresed Hgb
5. vasopressors to maintain CO/BP
6. diagnose early
7. antibiotic therapy
8. low Vt mechanical ventilation
9. sedation
10. tight glycemic control
11. prophylaxis for stress ulcers/DVT
12. early enteral nutrition