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Critical Care Test #3 > Shock/SIRS/MODS > Flashcards

Shock/SIRS/MODS Flashcards

1
Q

What are the four different stages of shock listed in order?

A

initial
compensatory
progressive
refractory

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2
Q

What occurs during the initial phase of shock?

A

decreased CO

ineffective tissue perfusion

lactic acidemia - anaerobic metabolism used due to lack of oxygen, causes more cellular damage when built up

USUALLY VITALS SIGNS ARE RELATIVELY NORMAL, HARD TO DIAGNOSE AT THIS STAGE

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3
Q

What are the compensatory mechanisms that our body has to fight against shock? 3 things.

A

SNS activation - increases CO and BP through adrenal medulla stimulation making norepinephrine entering the bloodstream causing vasoconstriction, increaseed myocardial contractility, and increased HR

Endocrine response -

    • ADH is secreted by posterior pituitary which increases venous return to heart and therefore preload
  • -ACTH increases secretion of glucocorticoids increases BG

Renin-angiotensin-aldosterone - renin stimulates angiotensin release, ACE converts to angiotensin II, which stimulates vasoconstriction and stimulates aldosterone release, which tells kidneys to conserve water and sodium and kick out potassium

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4
Q

What does our body initially do in the compensatory phase of shock to combat the lactic acidosis?

A

hyperventilation.

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5
Q

What does someone in compensatory shock look like clinically?

A

increased HR, BP, RR, normal CO

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6
Q

What is going on at a cellular level during the progressive stage of shock?

A

anaerobic metabolism proves ineffective for metabolic needs

sodium-potassium pumps begin to fail - cell swells

energy production stops

oxygen utilization fails

autodigestion occurs due to digestive enzymes leaking from swollen cell

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7
Q

What can happen when the CNS, hematologic, pulmonary, renal, and GI systems begin to fail through shock?

A

CNS - cardiac and respiratory depression, thermoregulatory failure, vasodilation if SNS fails

Hematologic - DIC in response the inflammation in system

pulmoary - ARF

Renal - ATN

GI - ischemia and failure due to vasoconstriction

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8
Q

Describe the refractory stage of shock, what can occur within it?

A

This is where the shock becomes unresponsive to therapy and eventually MODS develops.

This is the irreversible stage of shock, death occurs.

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9
Q

At least how many organs have to be failing to be considered MODS?

A

2

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10
Q

What are the different classifications of shock?

A

Hypovolemic

cardiogenic

Distributive: anaphylactic, neurogenic, and septic

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11
Q

What is the definition of hypovolemic shock, is this a common form of shock?

A

lack of circulating volume leads to decreased tissue perfusion

THIS IS THE MOST COMMON FORM OF SHOCK

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12
Q

What is the difference between absolute and relative hypovolemic shock?

A

absolute is the literal decrease in the amount of fluid available (blood loss & dehydration)

refractory is fluid shifting from intravascular to extravascular space (burns for example)

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13
Q

What are some hemodynamic changes that occur from hypovolemic shock?

A

decreased preload

decreased CO

decreased CI

SvO2 decreased (<60%)

increased SVR

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14
Q

In hypovolemic shock, there are four stages that are based on how much fluid loss has occured. What are the volumes that separate each phase? these correlate with the stages of shock.

A

1 - <500 - initial

2 - 500-1000 - compensatory

3 - 1000-2000 - progressive

4 - 2000-3000 - refractory

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15
Q

Describe the initial stage of hypovolemic shock, how much fluid has been lost?

A

<500 lost compensatory mechanisms being used and CO is normal, symptom free

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16
Q

Describe the compensatory stage of hypovolemic shock, how much fluid has been lost at this point?

A

500-1000ml lost

tachycardia, hypotension, decreased urine output, weak pulse, cool extremities, mild acidosis may be present, narrowed PP

increased SVR, CO REMAINS RELATIVELY NORMAL, BUT BEGINS TO FALL

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17
Q

Describe the progressive stage of hypovolemic shock, how much fluid has been lost at this point usuaully?

A

1000-2000 lost

same as compensatory, worsened.

include progressive acidosis, neuro symptoms like decreased LOC, tachypnea (acidosis), SvO2 <60, UOP <30ml/h, dysrhythmias may develop, decreased CO and increased SVR

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18
Q

Describe the refractory phase of hypovolemic shock, how much volume has been lost at this point?

A

2000-3000ml

same as progressive

ADD: decreased oxygen saturations, anuric, mental stupor and possible coma, extreme extremity signs of vasoconstriction, severe acidosis

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19
Q

What is the primary focus of management of hypovolemic shock?

A

identifying the cause of the fluid loss, stopping it, and increasing circulating volume

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20
Q

What is the first line fluid type used in treating hypovolemic shock?

A

crystalloid solutions, isotonic solutions are preferred (lactated ringers or 0.9% normal saline) NOT D5W

LR IS CONTRAINDICATED IN RENAL FAILURE CLIENTS

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21
Q

When are colloids and other volume expanders primarily used in the treatment of hypovolemic shock?

A

usually in the case of blood loss, this includes PRBCs to include the oxygen carry capacity

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22
Q

Are colloid solution recommended for early treatment of hypovolemic shock?

A

Not usually in the beginning of treatment, usually once stable, in the beginning of treatment the capillary permeability still may be high enough to allow the larger particles of colloid solution to escape the vascular space.

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23
Q

When is autotransfusion a good idea?

A

chest trauma hemorrhage

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24
Q

How do you mintor fluid replacement therapy?

A

CVP monitoring (0-8mmHg)

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25
Q

What size IV is preferred for fluid administration for hypovolemic shock, any preference where access is gained?

A

16 or larger in the AC or central

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26
Q

What are two possible complications of fluid volume replacement, especially if rapid?

A

hypothermia (fluids may be warmed)

pulmonary congestion (ensure administration is at rate that prevents this)

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27
Q

Nursing management for hypovolemic shock?

A

`monitor i/o

daily weights

limiting blood samples

maintin invasive lines

positioning

monitor for fluid overload

28
Q

What are some risk factors for the development of cardiogenic shock?

A

older age

LVEF <35%

large MI, left ventricular infarct is most common cause

history of DM

previous MI

septal ruptures of heart, papillary muscle rupture, cardiomyopathies, PE, myocarditis, cardiac tamponade

dysrhythmias - brady and tachy

open heart surgery

29
Q

What are the hemodynamic findings when it comes to cardogenic shock? (SBP, MAP, CI, PAOP, SVR)

A

SBP <90

MAP <70

CI <2.2L/min/m^2

PAWP >18mmhg

SVR > 1400

30
Q

What are the signs and symptoms of cardiogenic shock that the client will show that arre unique to this specifiic type of shock? radiography?

A

S3 S4, crackles, rhonchi, JVD, myocardial ischemia (troponin), respiratory alkalosis, decrease in PaO2 on ABG, rhonchi

Radiographic: enlarged heart, pulmonary congestion

THINK HEART FAILURE

31
Q

What are some ways the cardiogenic shock can be managed?

A

increasing contractility - dopamine, epinephrine, levophed, vasopressin

decreasing fluid overload - diuretics

vasodilate - nitro, ace inhibitors,

vasoconstrict - amrinone, mirinone, dobutamine

thrombolytics

cath lab

IABP

32
Q

What are the two ways anaphylactic shock can occur/?

A

IgE mediated (initial exposure creates it, then second exposure activates) and anaphylactoid (non IgE, first sures causes reaction)

33
Q

What are anaphylactoid reactions commonly associated with?

A

NSAIDS, and aspirin

34
Q

What is the dosage of epinephrine for anaphylaxis?

A

1:1000 (1mg/ml), 0.2-0.5ml im or subQ every 5 minutes

35
Q

What are some specific signs of anaphylaxis?

A

vasodilation, increased capillary permeability, peripheral vasodilation, excessive mucous secretion, coronary vasoconstriction, smooth muscle constriction in bladder and uterus, urticaria and pruritus

angioedema - face, oral cavity, lower pharynx

respiratory - laryngeal edema, wheezing, stridor, dysphagia, tightness in chest, vomiting, cramping

36
Q

Management of anaphylaxis?

A

Overview: remove offending antigen, reverse effects of biochemical mediators, promote adequate tissue perfusion

Mild: oxygen, antihistamine (IM or subQ) MAYBE epi

Severe:
manage AIRWAY AIRWAY AIRWAY

EPI, bronchodilator, corticosteroid, vasoconstrictors, positive inotropes

fluid replacement

37
Q

What is happening with neurogenic shock?

A

loss of suppression of sympathetic tone, onset occurs in minutes, can last for weeks

38
Q

What can cause neurogenic shock?

A

SPINAL CORD INJURY ABOVE LEVEL OF T6, SPINAL ANALGESIA, SEVERE EMOTIONAL DISTRESS, PAIN, DRUGS

39
Q

What are the signs and symptoms of neurogenic shock?

A

hypotension, bradycardia, HYPOTHERMIA (heat loss from excessive vasodilation, warm dry skin, motor/sensory dysfunctions (spinal shock)

decreased CO

duration depends on severity

40
Q

How do you manage neurogenic shock?

A

C-spine

Fluid resuscitation (if SBP <90) (UOP<30ml/h, changes in mental status)

vasoconstrictors

warmings/environmental control

pulmonary support

dysrhythmia treatment

41
Q

if spinal cord injuries require immobilization, what needs to be prevented? through what measures?

A

DVT

measure calf and thigh, passive rom, ted hose, scd, anticoagulant therapy

42
Q

why HOB slightly elevated after spinal anaesthesia?

A

so it doesnt travel up CNS to prevent systemic effects

43
Q

What are the differences between uncomplicated sepsis, severe sepsis, and septic shock? why are these categories made?

A

uncomplicated sepsis - SIRS resulting from an infection

Severe sepsis - sepsis associated with organ dysfunction, hypoperfusion, or hypotension

septic shock - sepsis accompanied with persistent hypotension despite adequate fluid resuscitation along with presence of perfusion abnormalities

THESE ARE IN ORDER OF PROGRESSION OF SEPSIS

44
Q

What are some things that increase the risk of developing septic shock?

A 
extreme of age
malnutrition
debilitation
chronic illness
drug or ETOH
neutropenia
splenectomy
multiple organ failure
45
Q

What are some risk factors for progression of sepsis to severe sepsis?

A 
SBP <110
temp more than 38.2 - 100.76
hypernatremia
platelets less than 150 x 10^9
bili more than 30
mechanical ventilation
infection present
46
Q

Does sepsis have a high mortality rate? septic shock?

A

20% sepsis

70% septic shock

47
Q

What is the primary cause of sepsis?

A

= uncontrolled inflammatory response

48
Q

What does sepsis do to coagulation?

A

causes clots to form throughout vasculature, eventually running them dry = DIC

impaired fibrinolysis leaves clots in microvasculature increasing ischemia

49
Q

Other than hypercoagulation, what else does sepsis do?

A

increased capillary permeability

myocardial depression - cytokines cause this

hypermetabolic state - increased energy consumption, no response to insulin, glycogen stores are used up, switch to anaerobic metabolism = aciosis, EFFECTS LIVER from triglyceride breakdown for ketones to be used in krebs cycle

maldistribution of blood - widespread vasodilation reduces return to heart, vasoconstriction of microcirculation decreased perfusion to vascular beds decreasing tissue perfusion

organ failure - due to ineffective energy sources and blood flow from above mechanisms

50
Q

What assessment finding might be present in a client experiencing initial sepsis? (hemodynamics included)

A

decreased RAP and PAOP, decreased SVR and PVR

Increased HR causes a normal CO/CI initially

hypoxemia due to pulmonary vasoconstriction and microemboli

increased immature neutophils (bands)

elevated BG

widened PP

warm,pink skin

bounding pulse

hypoxemia, respiratory alkalosis, metabolic acidosis, crackles

decreased LOC

decreased UOP

temp > 38 or < 36

51
Q

S/S of secondary stage of sepsis?

A

decreased CO, Hypotension, vasoconstriction

stupor or coma

skin is cold/clammy

mottling, cyanosis (peripheral)

pulses weak and rapid

shallow respirs abnormal pattern

anuria

52
Q

What are the goals of management for septic shock?

A

maximize oxygen delivery to meet demands

halt inflammatory response

prevent progression to MODS

53
Q

What are specific management techniques for patients experiencing sepsis?

A

identify the specimen through cultures

ABX therapy (may be hazardous)

vent - keep PaO2 > 70

diet high in protein

labs - WBCs, aPTT, PT, platelet

surgical debridement if wound present

fluids - crystalloid

vasoconstrictors - dobutamine

positive inotropes

temp control

CVP of 8-12 or 12-15 for vented with MAP of 65 or greater

no steroids,no protein C

bg less than 150

54
Q

Why might sepsis incidents be increasing?

A

increasing elderly population

increasing debilitated clients

increased patients with underlying disease

overuse of antibiotics

55
Q

What is SIRS?

A

systemic inflammatory response syndrom - systemic inflammation, precursor to septic shock

56
Q

What are the diagnostic criteria for SIRS?

A

temp >38 or < 36

HR > 90

RR > 20 or PaCO2 <32

WBC >12,000 or < 4,000

TWO OR MORE MUST BE PRESENT

57
Q

With a infection evident through a blood culture or tissue sample along with SIRS present is called what?

A

Sepsis

58
Q

What does the progression of sepsis result in?

A

MODS

59
Q

What is MODS?

A

presence of altered function in two or more organs in an acutely ill patient that requires intervention to maintain homeostasis

60
Q

What is the mortality rate of MODS?

A

75%

61
Q

What are some causes of MODS?

A

uncontrolled SIRS

prolonged release of inflammatory mediators

62
Q

Which organs are first to be affected by MODS?

A

lungs, heart, and kidneys

once the first is effected, the likelihood of another being effected increases dramatically

63
Q

What are some signs of MODS?

A

neuro: altered LOC, confusion, psychosis

Respir - tachypnea, PaO@ < 70, SaO2 < 90%,

renal - oliguria, anuria, increased CK

CV - tachycardia, hypotension, altered CVP & PAOP

hepatic (late: compensates well) - jaundice, increase enzymes, decreased albumin, increased PT, increased bilirubin, ammonia increase, DIC

hematologic - decreased platelets, increased PT, aPTT, decreased protein C, increased d-dimer, lactic acid elevation

HYPERGLYCEMIA

64
Q

How do you treat MODS?

A

hemodynamic support

nutrition

control BG

respiratory support - vent with high PEEP

conserve energy

manage fever

SIMILAR TO TREATMENT OF SEPSIS

65
Q

What is the resuscitation bundle for sepsis? What timeframe is this for?

A

lactate measurement

blood cultures from 2 sites prior to antibiotic administration

broad-spectrum antibiotics started

30ml/kg bolus of crystalloid

vasopressors for persistent hypotension

CVP >8

ScvO2 > 70%

THIS IS USED IN THE FIRST 6 HOURS

66
Q

following the lactate measure during the resuscitation bundle for sepsis, what is the bolus amount given for a value of >4 or for someone with hypotension?

A

30ml/kg ASAP

Critical Care Test #3 (6 decks)

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