shocky Flashcards

1
Q

hypotension
bradycardia
warm, dry skin

classic signs of

A

neurogenic shock

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2
Q

clinical hallmark of neurogenic shock

A

very ↓ SVR + signs of excessive PS activity (ex: bradycardia)

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3
Q

every shock needs

A
  • find and treat cause
  • maximize O2 support
  • fluid resuscitation (except cardiogenic - diurese to decrease preload first)
  • glucose control = good outcomes
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4
Q

why epinephrine for anaphylaxis?

A

decreases basophil and mast cell degranulation

vasoconstricts

reverses airway constriction

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5
Q

anaphylaxis: volume results x3

A

vasodilation
peripheral pooling
relative hypovolemia

(d/t increase capillary permeability)

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6
Q

four systems activated with septic shock

A

complement, coagulation, kinin systems, cellular immunity

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7
Q

hypovolemic shock class I

A

0-15% loss

minimal tachycardia (usually no Δ in BP, RR, pulse pressure)
delayed cap refill (loss of 10%)
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8
Q

hypovolemic shock class II

A

15-30% loss

tachycardia, tachypnea, pulse pressure
cool/clammy, delayed cap refill
slight anxiety

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9
Q

hypovolemic shock class III

A

30-40% loss

significant tachycardia, tachypnea, SBP
oliguria
confusion or agitation

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10
Q

hypovolemic shock class IV

A

greater than 40% loss

significant tachycardia, tachypnea, BP, pulse pressure (or no DBP)
oliguria/anuria
LOC
cold & pale

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11
Q

these patients may not have tachycardia in response to hypovolemia

A

BB, CCB, or pacemakers

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12
Q

plasma cascades activated in MODS

A

complement, kallikrein‐kinin, coagulation, fibrinolytic

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13
Q

reperfusion injury

A

organ damage occurring after reestablishment of blood flow post-ischemia

O2 radicals attack already damaged tissues

seen in MODS

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14
Q

myocardial depression in MODS d/t

A

caused by: myocardial depressant factor (MDF), TNF, IL‐1 → cardiac contractility

alterations: α‐adrenergic receptors (heart)

myocardial hypoxia

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15
Q

primary MODS

A

initial organ insult (usually d/t ischemia, impaired perfusion) results in inflammatory response / ex: shock, trauma, thermal injury, soft tissue necrosis, invasive infection

hypoperfusion both local (in organs) & generalized (gen not always seen)

stress response initiated, not usually as exaggerated as secondary - neutrophils primed can lead to secondary

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16
Q

secondary MODS

A

results from another insult (often mild), NOT primary MODS, but after latent period since primary - organs different from primary site

primed neutrophils go bananas disproportional to insult = inflammation self-perpetuates

primed macrophages release mediators to further damage endothelium

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17
Q

MODS monitoring consideration

A

primary hard to monitor, secondary has an established pattern

18
Q

secondary MODS phase: approximately 24 hours post-event

A

low‐grade fever, tachycardia, tachypnea, dyspnea, altered mental status, general hyperdynamic and hypermetabolic state

19
Q

secondary MODS phase: 24 to 72 hours

A

lung failure begins; ARDS possible

20
Q

secondary MODS phase: 7 - 10 days

A

intensification of hypermetabolic/hyperdynamic state; bacteremia w enteric organisms common; development of hepatic, intestinal, and renal failure

21
Q

secondary MODS phase: 14 - 21 days

A

↑ severity of renal & liver failure; encephalopathy w AMS (confusion - deep coma); hematologic & myocardial failure = late manifestations; death

22
Q

secondary MODS phases x4

A

24ish - fever, tachy, AMS, general hyperdynamic/hypermetabolic

24-72 lung failure begins, possible ARDS

7-10 worsened hyper state, gut bacteremia common, development of hepatic, intestinal, renal failure

14-21 worsened renal/liver failure (liver develops early but not detectable until late), encephalopathy = AMS (coma possible), heme & myocardial failure = late manifestation, death

23
Q

late manifestation of secondary MODS

A

hematologic & myocardial failure

24
Q

major burn injury when and what it involves

A

burn greater than 20% BSA in adults

associated with massive evaporative H2O losses & flux of large amounts of fluid/electrolytes in tissues

manifestations: generalized edema & circulatory hypovolemia

25
major burn injury manifestations x2
generalized edema & circulatory hypovolemia
26
burn shock
phenomenon consisting of both hypovolemic cardiovascular component & cellular component
27
burn shock: immediate (acute) phase
hypovolemia - massive losses d/t ↑ cap permeability persisting ~24hr after injury loss of electrolyte homeostasis contribute to shock
28
burn shock: ebb phase
cardiac contractility diminished during initial 24‐hr resuscitation period → blood shunting away from liver, kidney, gut hallmark of burn shock: CO w precipitous ↓ often result in inadequate perfusion of most tissues at capillary level normal blood vol doesn’t result in restoration of normal CO d/t phenomenon called myocardial depression ↓ viscera perfusion = ↓ viscera function; ↓ gut barrier function
29
burn shock: end point
state in which individual able to maintain adequate UOP for 2hr w IVF admin rate equal to individual’s calculated maintenance rate; “capillary seal”
30
capillary seal
term describing vascular status of patient at burn shock endpoint
31
hallmark of burn shock
CO w precipitous ↓ often result in inadequate perfusion of most tissues at capillary level
32
myocardial depression in burn shock
phenomenon during ebb phase - normal blood vol doesn’t result in restoration of normal CO
33
burn + fluid resuscitation = inevitable
massive edema developing in burned and unburned areas - can result in airway obstruction (requiring intubation) - can result in increased pulmonary edema (already there d/t inhalation injury)
34
fluid resuscitation in burn
(ex: LR) involves infusion of fluid at rate faster than the loss of circulating volume; eventually results in improved outcome of massively burned patients - hallmark (precipitous CO decrease) - massive edema (inevitable) first 24 hours crucial
35
3 critical elements of major burn injury survival
- meticulous wound management - adequate fluids/nutrition (massive amounts IVF required) - early surgical excision/grafting (autograft)
36
first degree burn
involve the superficial skin without loss of protective function - partial-thickness injury involving only epidermis, without injury to underlying dermal/subcutaneous tissue
37
second-degree burn
superficial (blister formation) or superficial involving partial skin thickness with a waxy white appearance and no involvement of dermal appendages - superficial-partial thickness injury vs deep-partial thickness injury
38
third-degree burn
involve full skin thickness + often underlying tissues - painless - can be life threatening d/t hypovolemic shock + metabolic + immunologic responses - full-thickness injury involving destruction of entire epidermis, dermis, often underlying SQ tissue; bone/muscle can be involved
39
partial‐thickness burn manifestations
- local pain, erythema - no blisters until ~ 24 hrs after injury - skin peeling 24-48 hours or slightly red heals 3-5 hours
40
superficial partial‐thickness burn manifestations
- painful - thin‐walled, fluid‐filled blisters develop w/in MINUTES of injury heals 21-28 days
41
deep partial‐thickness burn manifestations
- waxy white skin surrounded by margins of superficial partial-thickness injury - skin may peel off in sheets - indistinguishable from full‐thickness injury until 7 - 10 days when skin buds & hair appear heals 30 days to months
42
full thickness burn manifestations
- white, cherry red, or black - delineation between normal & burned skin not accompanied by significant color change - blisters rare, wound dry/leathery won't heal, needs skin graft