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MEDI > CR IV - Shock Block > Flashcards

CR IV - Shock Block Flashcards

1
Q

What is the definition of shock?

A

The cardiovascular system cannot effectively regulate arterial pressue

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2
Q

What are the 4 main classifications of shock?

A

Hypovolemic
Obstructive
Cardiogenic
Distributive

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3
Q

What are 4 main causes of hypovolemic shock? What specific problems cause each?

A

Hemorrhagic - trauma, GI, retroperitoneal
Increase vascular capacitance - sepsis, anaphylaxis, toxin/drugs
Fluid depletion - External fluid loss - dehydration, vomiting, diarrhea, polyuria
Interstitial fluid redistribution - thermal injury, trauma, anaphylaxis

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4
Q

If volume loss is 10%, what clinical sign do you typically see? 20-25%? >40%?

A

10% - tachycardia
20-25% - failure to compensate - hypotension, orthostasis, decreased CO
>40% - overt shock, pass out and cannot waken up

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5
Q

What can cause left heart obstructive shock? Right heart? Another main cause?

A

LH - aortic disection
RH - PE
Increased intrathoracic - tension pnemothorax

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6
Q

What should be done in all pregnant women presenting with shock symptoms?

A

Roll onto left side to open up IVC

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7
Q

What is obstructive shock? How does that differ from cardiogenic shock?

A

Obstructive - impaired filling/preload, low CO

Cardiogenic - cardiac pumping failure due to muscle issue

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8
Q

What are some major causes of cardiogenic shock?

A 
MI (or hibernating)
Myocardial contusion
Septic myocardial depression
Cardiac tamponage
Arrythmias
Pharmogenic
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9
Q

What is distributive shock? What are 4 majors causes?

A 
Inappropriate peripheral vasodilation
Septic
Toxic Shock
Anaphylaxis
Neurogenic toxic shock - injury to spinal cord decreases sympathetic outflow
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10
Q

What do all types of shock lead to?

A

Decreased CO

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11
Q

Define sepsis

A

The body’s disregulated response to in infection or superantigen

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12
Q

Are all infections sepsis?

A

No

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13
Q

What is the most common cause of sepsis?

A

Bacterial

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14
Q

What do gram negatives have that are considered triggers for sepsis? Gram positives (more than 1)?

A

Gram negatives - LPS (endotoxin)

Gram positives - exotoxin, superantigen and TSST for S. Aureua, superantigen Spe A for S Pyogenes

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15
Q

What are 5 main pro inflammatory cytokines released during septic shock?

A

IL 1,2,6, TNFalpha, and IFN gamma

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16
Q

What two factors in the body rapidly decline in sepsis? What does this cause?

A

Antithrombin and aPC (activated protein C)

Causes hypercoaguable state

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17
Q

What does an increased S1P3:S1P1 ratio indicate?

A

Fluid is able to leak out of the endothelium between tight junctions - sepsis

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18
Q

What is the definition of Sepsis under the updated SIRS? What are the clinical criteria?

A

Life-threatening organ dysfunction caused by disregulated host response to infection
Clinical - suspected or documented inffection + acute increase of >=2 SOFA Points

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19
Q

What is the quick SOFA score? What does it tell you at 0, 1, and >= 2 points?

A

SOFA - RR>22, sBP<100, Altered GCS
0 points - mortality <1%
1 point = mortality 2-3%
>=2 points - mortality >10%

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20
Q

What is the definition of Septic Shock in the 2015 updated SIRS?

A

Subset of sepsis in which underlying circulatorya nd cellular/metabolic abnormalities are profound enough to substantially increase mortality (aka don’t respond to fluids)

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21
Q

What clinically will be seen in someone with septic shock?

A

Sepsis + vasopressor therapy needed to evaluate

MAP < 65 + lactate > 2 despite adequate fluid resuscitation

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22
Q

What are 3 places that must be checked for source of infection for sepsis?

A

Lung, abdomen, urinary tract

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23
Q

What is the most common cause of adult community acquired pneumonia? Neonate? In hospital?

A

Adult - s. pneumoniae
Neonate - group B strep, E. Coli
Hospital - S. Aureua, gram-, pseudomonas

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24
Q

What are two main causes of abdomen initiated sepsis?

A

E. COli or bacteroides fragilis

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25
Q

What is the main cause of urinary tract initiated sepsis?

A

E. Coli

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26
Q

What are thee main causes of sepsis in children?

A

S. pneumonia
N. meningitis
S. Aureus

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27
Q

What are the 5 clinical manefestation (stages) of sepsis?

A 
Stage 1 - introduction of a pathogen
Stage 2 - preliminary host response
Stage 3 - overwhelming systemic response
Stage 4 - Compensatory anti-inflammatory reaction
Stage 5 - immunomodulatory failure
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28
Q

When should IV polyclonal immunoglobulin be given to a patient?

A

When they have TSS or if they are IC

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29
Q

Wht 4 things must be done within the first 3 hours of presentation of sepsis?

A

Measure lactate
Obtain blood cultures prior to antibiotics
Administer broad spectrum antibiotics
Administer crystalloid 30ml/kg for hypotension or lactate >4 mmol/L

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30
Q

What should be done within 6 hours of presentation if no improvement in lactate or MAP?

A 
Vasopressors given (minimal dose possible)
MAP<65 or initial lactate >4
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31
Q

What should be done to reassess volume status?

A 
Focused PE orr two of following:
Measure CVP
Measure SvO2
Bedside cardiovascular ultrasound
Dynamic assessment of fluid with passive leg raise
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32
Q

What death percentage is associated with the following initial lactate levels: 0-2.5, 2.5-4, >4?

A 
0-2.5 = 2.5-5% death
2.5-4 = 5-9% death
>4 = 28% death
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33
Q

If you guess the cause of sepsis wrong, what is the change your patient will die? If you guess right?

A

Wrong - 62% chance

Right - 28% chance

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34
Q

What type of feeding should be done in a patient with sepsis?

A

Enteral, no parenteral

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35
Q

When should a low dose steroid be added to the sepsis regimen?

A

Only in shock if vasopressors are needing to be increased

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36
Q

What are 4 other beneficial measures to do in sepsis?

A

Optimize glycemic control
Limit transfusions
DVT prophylaxis
Stress ulcer prophylaxis - if GI bleed risk

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37
Q

What are 3rd generation cephalosporins good at treating?

A

Gram -, particularly pseudomonas and enterobacter

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38
Q

What is the MOA of Vancomycin? What does it cover? How is it not absorbed well? What is one main adverse effect?

A

Cell-wall synthesis inhibitor
Gram +
Poor oral absorption
Red man syndrome - flushing

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39
Q

What is the MOA of aminoglycosides? What group do they cover? How are they given? What are two adverse effects?

A

Protein synthesis inhibitors - interrupt mRNA coding
Gram -
Parenteral
Ototoxicity and renal toxicity

40
Q

What is the MOA of tetracyclines? What groups(s) do they cover? If given orally, what can they bind with that inhibits their absorption? What are AE in children?

A

Protein synthesis inhibitor - interupt bind of tRNA to mRNA
Gram +,-, atypical
Incomplete oral absorption what given with di/trivalent cations
AE in children inhibit bone and teeth structure
CI in pregnant women

41
Q

What is the MOA of fluroquiolones? How to bacteria gain resistance? Do they react with cations? What AE is prevalent after 60?

A

DNA gyrase inhibitor - bind to protein structure, slowign growth and replication
Gain resistance through gene mutations
Chelated when taken with cations
Tendonitis after 60

42
Q

What is the MOA of isoniazid?

A

Inhibits incorporation of mycolic acid into cell wall

43
Q

What is the MOA of rifampin? What is a pt alarming side effect?

A

Inhibits RNA polymerase

Body fluids turn orange

44
Q

What is the MOA of ethambutol?

A

Inhibits cell wall synthesis by inhibiting polymerization reactions

45
Q

What is the main anti-septic used? MOA?

A

chlorohexidine

Causes leakage of small molecules and precipitation of cytoplasmic proteins

46
Q

What three antimycobacterial drugs cause liver toxicity? What can be given to help this?

A

Isoniazid
Rifampin
Pyrazinamide
Give vit B6

47
Q

What antimycobacterial drug has the unique side effects of visual disturbances of acuity and red-green color blindness?

A

Ethambutol

48
Q

What should be followed in sepsis if you can’t get a positive culture? How do you know when the sepsis is under control?

A

Follow procalcitonin

Reduce it by 90%

49
Q

What happens in shock when ECBV is reduced by the following: <10%, 10-20%, >20%?

A

<10% - no change in pressure of CO
20% - arterial pressure maintained, but CO begins to fall
>20% - arterial pressure fails

50
Q

What are 5 compensatory mechanisms of shock? How long after sepsis begins can they compensate for?

A 
Baroreceptors
Chemoreceptors
Cerebral ischemia
Reabsorption of fluids
Endogenous vasoconstrictors
Can compensate if problem addressed within 1-2 hours
51
Q

What compensatory mechanism kicks in when MAP is <60? What happens?

A

Chemoreceptor
Hypoexmia and acidosis stimualte chemoreceptors to carotid sinus to increase ventilation to blow of pCO2
Respiration stimulation enhaves venous return and lymph flow

52
Q

What compensatory response happens when MAP<40? What happens in both the sympathetic and parasympathetic system?

A

Massive sympathetic and adrenal output cause vasoconstriction and increased myocardial contractility
Increase parasympathetic to heart decreases HR

53
Q

How does vasoconstriction and low ECBV cause reabsorption of fluids?

A

By decreasing hydrostatic pressure so net hydrostatic pressure < net oncotic pressure

54
Q

What 4 endogenous vasoconstrictors are released when MAP drops significantly?

A

Norepi - nerve release
Epi -adrenal medulla release
RAAS
Vasopressin - ADH (only affects constriction when ECBV drops by >10%)

55
Q

If shock persists for more than 2 hours, what are the 6 decompensation mechanisms that can occur?

A 
Cardiac failure
Vascular failure
Metabolic acidosis
CNS depression
Inappropriate clotting
Inactivation of Mononuclear Phagocytic system
56
Q

What is sympathetic escape? How does this cause the vascular system to fail?

A

Peripheral vasoconstriction fails probably due to desensitization due to depletion of alpha 1 receptors in the periphery

57
Q

How does metabolic acidosis occur in shock? How does low renal flow play a role? What happens to cardiac function?

A

Poor CO and tissue perfusion lead to glycolitic metabolism and a build up of lactate
Lactic acidosis ensues
Low renal blood flow inhibits ability to reabsorb bicarb
Acidosis further depresses cardiac output

58
Q

How does CNS depression occur in shock?

A

Initial massive sympathetic outflow however MAP unable to respond
Sympathetic then decreases, causing CNS depression

59
Q

Does a person remain hypercoaguable throughout shock?

A

No, hypercoagulation devolves into hypocoagulation

60
Q

What happens to the mononuclear phagocytic system during hemorrhagic hypotension? What two things does this cause?

A

MPS is depressed
Impairs antibacterial and antitoxin defense mechanisms
Endotoxins from gut (usually inactivated by MPS) increase causing vasodialtion, exacerbating shock

61
Q

What are 7 clinical presentation signs of shock?

A 
Hypotension
MAP<60
Tachy
Cool extremities
Olguria
Clouded sensorium (confusion)
Elevated lactate
62
Q

Should a patient in shock be assessed slowly?

A

No

63
Q

What should be examined when someone presents in shock? What should be done simultaneously?

A 
Simultaneously initiate fluid resuscitation
Foley cath
Assess conciousness (via gag reflex)
Systolic BP
MAP
PE: heart tones, breath sounds, mottling
Arterial line placement
Monitor response to fluids
64
Q

If a person in shock does not respond to fluids, what should be done?

A

Give vasopressin

65
Q

What labs should be ordered when someone is in shock?

A 
ABG (for metabolic acidosis)
CBC
CMP
coagulation parammeters
Cardiac enzymes
Lactate
Blood cultures
66
Q

What two goals should tried and be achieved in a shock patient? Which is more important?

A

MAP > 60

Improve clinical criteria - mental status number (most important)

67
Q

What equation can be used to calculate oxygen delivery?

A

DO2 = CO = HRSV = 10(1.34[HgB]*SaO2)

68
Q

What is the goal of fluid resuscitation? Vasopressor therapy? Inotropic therapy?

A

Fluid resuscitation - increase SV
Vasopressor therapy - increase perfusion and contractility
Inotropic therapy - increase contractility

69
Q

What volume expansion per liter is achieved with crystalloids? With colloids? Why are crystalloids used more?

A

Crystalloids - 100/200ml expansion per 1L
Colloids - 500-1000mll expansion pr 1L
Crystalloids are cheaper

70
Q

What three things should be treated in early goal directed therapy of shock? What order?

A

CVP - crystalloid or colloid
MAP - vasoactive agents
ScvO2 - transfusion of RBC until hematocrit > 30

71
Q

What are 7 vasopressors typically given? According to guidelines, what should be given 1st, 2nd, 3rd?

A 
Norepi #1
Epi #2
Vasopressin #3
Dopamine
Phenylephrine
Dobutamine
Phosphodiesterase inhibitor
72
Q

What receptors does norepi affect? What does it cause?

A

a1, a2, B1
Increases BP w/o adverse organ effects
Increases CO by increasing inotropic more than chronotropic

73
Q

What receptors does Epi affect? Why can the gut be less perfused with this drug? What is a major AE seen?

A

a1, a2, B1, B2
a1 more potent than norepi
Increases DO2, increasing O2 consumption
Decreases SVR so gut less perfused…can see ischemia

74
Q

What does vasopressin cause in relation to catecholamines? What risk decreases in likelihood when this is given? Is it taken off first or last?

A

Sensitizes system to catecholamines
May improve renal blood flow
Can decrease risk of a fib
Taken off last

75
Q

What must be present with shock for dopamine to now be used? What receptors does it affect? What is the major AE than causes it to not be used that often anymore?

A

Brady and shock
DA1 & DA2 (dilation) > B1 (contractility) > a (vasoconstriction)
Machy, decreased splanchnic perfusion, increase PAOP

76
Q

When should phenylephrine be used? For what type of shock? Which type of shock should it not be used for?

A

a1 agonist
Good choice when tachya rrythmias present
Use in drug induced shock
Do not use in septic shock

77
Q

What should be used if cardiogenic shock is present with no sepsis? Why?

A

Dobutamine

Increases contractility and CO

78
Q

What drug should really only be used in a cardiac transplant patient? What does it cause to increase in the cells?

A

Milrinone - phosphodiesterase inhibitor
Increases CAMP
AE: hypotension and tachy (less than dobutamine)

79
Q

Should fluids be given pre-hospital in hemorrhagic shock? When is acceptable?

A

Delay resuscitation and focus on stopping bleeding

Give fluids to maintain mental status and palpable radial pulse

80
Q

What is an unreliable indicator of shock in a young person? Why? Instead, what two indicators can be used?

A

Hypotension
young people have good control
Anxiety and tachypenea

81
Q

What is the gold standard for determining where bleeding is coming from?

A

CT

82
Q

What should be the primary focus is resusciation?

A

Stop bleeding

83
Q

What is massive transfusion?

A

1:1:1 ration RBC:Platelets:FFP

84
Q

If a person is in liver failure, what should be given to negate the preservatives in the blood?

A

Calcium choloride

85
Q

What 4 progoagulants can be given to a person in hemorragic shock?

A

TXA
Activaqted FVII
Prothrombin complex (PCC)
Fibrinogen concentrate

86
Q

What are Dr. Dank’s 4 alphabets of adjuncts to resuscitation?

A

FAST
REBOA
ROTEM/TEG - to determine what products they need
ECHO - best to eval MI and venacava

87
Q

What should be ordered first in a trauma patient? Drawn from where?

A

Lactate
From non-tourniquet arm
Taken to lab on ice

88
Q

What increases in trauma? What decreases?

A

Lactate increases

Base deficient decreases (becomes negative)

89
Q

What is PAOP suppose to reflect?

A

EDLV filling pressure

90
Q

In regards to distributive shock, how does CO, SVR, and PAOP present?

A

CO up
SVR down
PAOP normal

91
Q

In regards to cardiogenic shock, how does CO, SVR, and PAOP present?

A

CO down
SVR up
PAOP up

92
Q

In regards to hypovolemic shock, how does CO, SVR, and PAOP present?

A

CO down
SVR up
PAOP down

93
Q

In regards to obstructive shock, how does CO, SVR, and PAOP present?

A

CO down
SVR up
PAOP up/normal

94
Q

What should be given in cardiogenic shock to increase CO and decrease SVR?

A

Dobutamine

95
Q

What two things increase with breathing? When what?

A

Arterial line and sat problem (both increase) when volume is down

MEDI (11 decks)

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