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High Acuity > Shock > Flashcards

Shock Flashcards

1
Q

MODs Early Pulm failure

A

(Alveolar capillary injury)

Hypoxia, disruption in surfactant (vent 3-5 days)

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2
Q

MODs Late Pulm failure

A

ARDs

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3
Q

MODs Early Renal failure

A

(Renal ischemia)
Oliguria < 480 cc/day
riding creatinine . 2-3 mg/dl
increased urine osmolaity

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4
Q

MODs Late Renal failure

A 
Anuric < 50 cc/day
continuous dialysis (unable to handle massive fluid shifts)
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5
Q

MODs Early Intestinal failure

A 
(Bacerial translocation and abd HTN, Impair blood flow to the gut)
Ileus (enteral intolerant) > 5 day
decreased bowel sounds and hypoactive
decreased peristalsis and absorption
diarrhea
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6
Q

MODs Late intestinal failure

A

stress ulcers
GI bleed
Cholecystitis w/o stones
abd compartment syndrome

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7
Q

MODs Early Hepatic failure

A

Bilirubin > 2 mg/dl
LFT 2x normal values
decreased albumin
decreased clotting factors

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8
Q

MODs Late Hepatic failure

A

Jaundice with bilirubin > 8-10

Coagulopathy

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9
Q

MODs Early Cardio failure

A

(decreased perfusion, MDF production)
Ejection fraction < 65%
Capillary leak syndrome (IV fluids leak into tissue)
Loss of capillary seal (r/t nitric oxide)

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10
Q

MODs Late Cardio failure

A 
Decreased contractility (MDF)
Decreased CO
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11
Q

MODs Early Hematologic failure

A

(clotting mechanisms > fibrinolytic system = procoagulant state)
PT and PTT > 25%
Platelets < 80000
Decreased fibtinogen

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12
Q

MODs Late Hematologic failure

A

DIC

increased FSP and D-dimer titers

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13
Q

MODs Early Neuro failure

A

confusion and disorientation

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14
Q

MODs Late Neuro failure

A

LOC and irreversible coma

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15
Q

MODs Hct and Hbg

A

Decreased (anemia)

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16
Q

MODs WBC

A

increased (infection and inflammation)

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17
Q

MODs Platelets

A

Decreased

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18
Q

MODs Lactate

A

Increased (latic (meta) acidosis)

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19
Q

MODs BUN and Creatinine

A

Increased renal failure

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20
Q

MODs Interventions

A

Increase oxygen delivery
decrease oxygen consumption
decrease tissue injury and infection risk
Improve nutrition status
prompt, rapid and adequate fluid resuscitation
restoration of bowel blood supply
Use of oxygen free radical scavengers (mannitol, vit C and E, reduce reperfusion injury)
extensive escharectomy
support organ function that begins to fail

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21
Q

How to maximize oxygen delivery

A 
Supplemental Oxygen (intubation and vent may be required)
Fluids (crystalloids, colloids, PRBC, and whole blood)
Inotropes- increase contractility (dopamine, dobutamine, Milrinone)
Vasopressors - vasoconstrict - (Epi, Norepi, dopamine and vasopressin)
Afterload reduction - Vasodilator (doputamine, milrinone, nitro)
Trendelenburg
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22
Q

How to Minimize oxygen consumption

A

paralytics, sedatives, hypothermic therapy, management of pain and anxiety,

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23
Q

How to decrease tissue injury and infection risk

A

reticuloendothelial dysfunction, hand hygiene, especially art lines

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24
Q

How to improve nutrition status

A

enteral feedings are perferred to maintain gut

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25
Q

Things that increase O2 consumption

A 
Hyperventilation (pain and anxiety)
Hyperthermia
Trauma (inflammation/healing)
Sepsis
Anxiety (propofol or ativan to decrease stimulation
Stress (SNS response)
Hyperthyroidism
Increased muscle activity (seizure, shivering/fever)
Head trauma and burns
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26
Q

Things the decreased O2 consumption

A 
Hypoventilation
Hypothermia (w/o shivering)
Sedation
Anesthesia
Neuromuscular blocking agents
Hypothyroidism
inactivity
Oxyhemoglobin dissociation curve
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27
Q

Functional classifications of shock

A

Hypovolemic
Transport
Obstructive
Cardiogenic

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28
Q

Hypovolemic shock

A

impaired oxygenation because of inadequate CO as a result of decreased intravascular volume. Volume loss or volume maldistribtion

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29
Q

Transport shock

A

Impaired oxygenation because of a diminished supply of Hbg in which to carry O2 to tissues. Decreased oxygen carrying capacity.

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30
Q

Obstructive shock

A

impaired oxygenation because of a mechanical barrier to outflow of blood. Shifting the medistinal content creates an obstruction.

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31
Q

Cardiogenic shock

A

Impaired oxygenation because the heart fails to function as a pump to deliver oxygenated blood. pump failure.

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32
Q

Hypovolemic shock - Abosolute Volume loss

A

Whole blood (hemorrhage, GI bleed, surgery) Plasma (burns)

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33
Q

Hypovolemic shock - Relative Volume loss

A

Blood/plasma loss to interstitial space (sepsis capillary permeability

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34
Q

Hypovolemic shock - Volume maldistribution - Neurogenic

A

loss of sympathetic tone, head trauma, SCI, Vasodilation from injury down.

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35
Q

Hypovolemic shock - Volume maldistribution - Anaphylactic

A

Massive histamine release, Type 1 hypersensitivity inflammatory mediators released

36
Q

Hypovolemic shock - Volume maldistribution - Septic

A

Vasoactive endotoxin released; gram - bacteria, toxins are released as antibiotic destroy cells. Initially symptoms are blunted.

37
Q

2 causes of hypovolemic shock

A

Loss of intravascular volume

Increase in intravascular compartment

38
Q

Loss of intravascular volume

A

loss of blood (hemorrhage)
Loss of fluid from persistant diarrhea, vomiting, massive diuresis
Loss of fluid from the intravascular compartment to the interstital space (third spacing)

39
Q

Increase in intravascular compartment

A

Vasodilatation (neurogenic, Anaphylactic and septic shock)

40
Q

Transport shock - decreased Hbg volume

A

Anemia
hemorrhage
Hemodilution (crystalloid) (fluid therapy causes a thinning of Hbg in the blood.

41
Q

Transport shock - inappropriate Hbg binding

A 
Carbon monoxide (200 x affinity)
Heavy metal poisoning
42
Q

Obstructive shock - Cardiac tamponade

A

Bleeding into pericardial sac
The pressure around the heart impairs vent filing and decreases CO
May also be cardiogenic

43
Q

Obstructive shock - Pulm Embolus

A

Increases in alveolar dead space and a V/Q mismatch.

Inpaired gas exchange and increased pulm vascular resistance.

44
Q

Obstructive shock - Tension pneunothorax

A

as it proceeds to mediastinal shift.
Air enters pleural space but cant leave during expiration.
Mediastinal shift compresses other lung.
Kinks aorta and vena cava –> cardiopulmonary arrest

45
Q

Cardiogenic shock - MI

A

Dysfunction of left vent (impairs contractility and CO, bllod backs up in pulm system causing pulm congestion)
Dysfunction of right vent (Back up in to systemic circ)

46
Q

Cardiogenic shock - Cardiac structural defect/damage

A

Chest trauma - damage to myocardium which becomes unable to eject content

47
Q

Cardiogenic shock - Dysrythmias

A

increased HR = decreased CO and decreased perfusion to coronary arteries leads to MI
Dissociation of contraction decreases filing time
Torsade de pointe and V-fib

48
Q

The stages of shock

A

Initial
Compensatory
Progressive
Refactory

49
Q

Initial stage

A 
Cellular anaerobic metabolism
- Decreased CO and tissue perfusion
- Decreased O2 delivery to cells
S/S LOC and mentation changes, decreased urine output, no SNS stimulation.
- Best stage to catch and treat shock.
50
Q

Compensatory stage

A

SNS stimulated (fight or flight)

  • Augment cardiac output
  • Redistribute blood flow - shunting occurs (to vital organs)
  • Restore blood volume - activation of the SNS
  • Neuroendocrine responses are activated to restore CO and O2 delivery
  • S/S diaphoresis and cool skin, decrease urine output, decreased peristalsis, increased HR and Resp, increased glycolysis.
  • BP may drop and then rise.
51
Q

Progressive stage

A

Failure of compensatory mechanisms

  • Major dysfunction of many organs
  • The continued low blood flow, poor perfusion, inadequate O2 delivery, and build up of metabolic wastes over time lead to MODs
  • S/S HR erratic, no urine output, confused, low BP as a compensatory mechanism begins to fail.
52
Q

Refractory stage

A

Unresponsive to therapy (death is inevitable)

  • Profound hypotension
  • Remains hypoxemic despite O2 therapy
  • Swelling at capillary-alveolar membrane
  • Resistant to vasoactive meds and O2
53
Q

Compensatory mech

A
  • Complex neuroendocrine responses are triggered to over come ineffective circulating BV
  • The hormones ACTH, aldosterone, and ADH are released to increase CO
  • SNS releases massive amount of Norepinephrine, which produces multiorgan responses in an effort to sustain a life threatening situation.
54
Q

Assessment of shock

A

BP, HR, mentation, and UO

55
Q

Hypovolemic shock S/S

A

Vasoconstriction (high SVR and HR)
- cool skin, poor cap refill
Decreased output (low CO, BP, PAP)
-Tachycardiais evident and urine output is low
Decreased filling pressures (CVP and PCWP)

56
Q

Hypovolemia treatment

A

2-3 L crystalloid until blood replacement is available. caution because too much could lead to transport shock

57
Q

Neurogenic S/S

A 
Vasodilation (warm, low SVR) - below level of injury
Decreased output (CO and BP)
- lowers RAP, PAP, PCWP and CO
Decreased sympathetic response (low HR)
- parasympathetic
58
Q

Neurogenic treatment

A

Treat bradycardia w/ atropine

Fluid resuscitation

59
Q

Anaphylactic S/S

A

Resp Distress
Vasodilation (warm, low SVR)
Decreased output (edema, CO and BP)
HR increases in a normal sympathetic response

60
Q

Anaphylactic treatment

A

Airway management
Epinephrine and antihistamine
Fluid resuscitation - for BP maintainance to avoid renal failure
Steroid given for capillary seal - leaky membrane

61
Q

Septic S/S - Early

A

WARM
Febrile - warm to hot skin - 100.3
Increased output - HR, BP, CO
CO is increased to 9-14 L/min d/t rapid HR leads to increased O2 demand
BP may be normal even if it should be low d/t vasodilation

62
Q

Septic S/S- Late

A 
COLD
Classic shock (variable HR, Swelling and decreased BP)
63
Q

Septic treatment

A

Antibiotic therapy (usually Gm-) and fluid reuscitation

  • first dose antibiotics should be given w/in 1 hr of physician order or w/in 1-3 hrs of admission
  • Fluid resuscitation of 8-12 L/24hr
  • Xygris - activated protein C; interferes with inflammation and clotting
  • Tight blood glucose control 80-150 to decreases mortality
  • steroids - immunocompromised and increase BG
64
Q

Transport S/S

A

Decresed Hct/Hgb
- shock caused by anemia or hemorrhage
-RAR and PCWP may be normal, depending on volume status
Increased Carboxyhemoglobin
- Common symptoms HA, malaise, nausea, difficulties with memory and personality changes

65
Q

Transport Treatment

A

Blood replacement and hyperbaric therapy

66
Q

Obstructive S/S

A

Tamponade
- Pulsus paradoxus - classic sign of cardiac tamponade
- Beck’s triad - elevated RAP, decreased BP and muffled heart sounds. widening pulse pressure
PE - SOB, Hypoxia and Hypotension
Pneumothorax - absent breaths sounds

67
Q

Obstructive treatment

A

Tamponade - remove fluid, pericardicentesis
PE - Thrombolytics, med management
Pneumothorax - chest tube

68
Q

Cardiogenic S/S

A 
Vasoconstriction (cool, increased SVR and HR)
Decreased Output (CO, BP, PAP)
Increased filling pressure (CVP, PCWP)
- Left vent
* Dyspnea
* Bilateral crackles
* Distant heart sounds, S3 and S4
* Elevated PCWP
* Low CI
- Right vent
* Peripheral edema
* clear lung sounds
69
Q

Cardiogenic treatment

A 
Support myocardium (IABP, VAD)
Revascularization - stent
70
Q

General therapy for shock

A

Maximize O2 delivery

Minimize O2 consumption

71
Q

Reversal of shock states

A 
Small changes are most significant
ALL
- BP +/- 20 mm/Hg of pre shock state
- Temp - WNL
HR - 60 - 100 beat per min
Alert and oriented - Glasgow to pre-shock state
Urine output - > 30 cc/hr
72
Q

Hypovolemic goal

A

Restore fluid volume

73
Q

Neurogenic goal

A

maintain stability of spine and optimize O2 delivery

74
Q

Anaphylactic goal

A

AIRWAY

support BP

75
Q

Septic goal

A

Antibiotics within 1 hr of dr order

Maintain fluid

76
Q

Transport goal

A

restore O2 carrying capacity
O2 or blood transfusing
Hyperbaric

77
Q

Obstructive goal

A

Remove barrier to blood flow

78
Q

Cardiogenic goal

A

Fluid

Med management and IABP or VAD

79
Q

Transition from SIRS to MODS

A
  1. failure to control the source of infection or inflammation
  2. persistent hypo-perfusion
  3. Presence of necrotic tissue
  4. Altered (increased) cellular oxygen consumption
80
Q

Primary MODs

A
  • Organ failure is related to the initial injury/insult (original)
  • It occurs early
    Tramua, aspiration, near drowning. Pneumonia or PE.
81
Q

Secondary MODs

A
  • As a result of SIRS
  • Occurs later (7-10 days)
  • Occurs in organs distant from original injury
82
Q

Risk factors for sepsis

A

Diabetes
Diseases of the genitourinary system, biliary system, or intestinal system
Diseases that weaken the immune system such as AIDS
Indwelling catheters (those that remain in place for extended periods, especially intravenous lines and urinary catheters and plastic and metal stents used for drainage)
Leukemia
Long-term use of antibiotics
Lymphoma
Recent infection
Recent surgery or medical procedure
Recent use of steroid medications

83
Q

SIRS is indicated by the presence of two or more of the following symptoms:

A
  • temperature higher than 38°C or lower than 36°C
  • heart rate greater than 90 beats per minute
  • respiratory rate greater than 20 breaths per minute or a partial pressure of arterial carbon dioxide level less than 32 mm Hg
  • abnormal white blood cell count (greater than 12,000/mm3 or less than 4,000/mm3 or greater than 10% bands).
84
Q

SIRS test

A

Increased Interleukin-6

Increased Lactate

85
Q

Inflammation = Clots

A

Inflammation = Clots

High Acuity (2 decks)

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