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NRS G270 Exam #4 > Shock/Mods > Flashcards

Shock/Mods Flashcards

1
Q

Adequate blood flow to tissues and cells requires: (3)

A
  • effective cardiac pump
  • adequate vasculature/circulatory system
  • sufficient blood volume
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2
Q

shock is essentially…….

A

decreased tissue perfusion

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3
Q

4 types of shock

A
  • hypovolemic
  • cardiogenic
  • obstructive
  • distributive
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4
Q

examples of causes of hypovolemic shock. (3)

A

bleeding, dehydration, diarrhea

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5
Q

examples of causes of cardiogenic shock.(2)

A

MI,HF

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6
Q

examples of causes of distributive shock.(3)

A

-septic, neurogenic, anaphylactic

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7
Q

examples of causes of obstructive shock. (3)

A
  • PE
  • tension pneumothorax
  • cardiac tamponade
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8
Q

What are the three stages of shock?

A
  • compensatory
  • progressive
  • irreversible
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9
Q

Acid Base Balance for each stage of shock

A
  • Compensatory –> respiratory alkalosis
  • progressive –> metabolic acidosis
  • irreversible –> profound acidosis
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10
Q

Compensatory stage clinical manifestations (6)

A
  • normal BP
  • increased lactic acid (metabolic acidosis)
  • increased RR, deep respirations (compensatory respiratory alkalosis)
  • anxious/confused
  • skin is cool/clammy
  • decreased UO
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11
Q

Progressive stage Clinical Manifestations: respiratory decompensation (4)

A
  • rapid, shallow breaths, crackles
  • pulmonary hypoperfusion and hypoxemia
  • pulmonary capillaries leak: pulmonary edema and diffusion abnormalities, alveolar collapse
  • can progress to ARDS
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12
Q

Progressive stage Clinical Manifestations: cardiovascular decompensation IMPAIRED PUMP!!! (3)

A
  • tachycardia
  • low co
  • MI
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13
Q

Progressive stage Clinical Manifestations: Neurological decompensation (3)

A
  • decreased cerebral perfusion, hypoxia
  • mental status changes
  • lethargy –> loss of consciousness
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14
Q

Progressive stage Clinical Manifestations: renal decompensation (3)

A
  • MAP < 65; decreased GFR
  • AKI
  • oliguira
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15
Q

Progressive stage Clinical Manifestations: hepatic decompensation (3)

A
  • decreased blood flow to liver: impaired liver metabolism
  • increased lactic acid and ammonia
  • increased billirubin: jaundice
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16
Q

Progressive stage Clinical Manifestations: GI decompensation and ischemia (3)

A
  • stress ulcer; risk for GI bleed
  • GI necrosis: bloody diarrhea
  • bacteria toxins enter blood stream: sepsis
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17
Q

Progressive stage Clinical Manifestations: hematologic decompensation (2)

A
  • cytokines activate clotting cascade

- DIC

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18
Q

Irreversible or Refractory stage clinical manifestations (6)

A
  • severe organ damage: no response to treatment
  • acute metabolic acidosis
  • reserves of ATP depleted –> no cell metabolism causing cell damage
  • respiratory system damage: no adequate oxygenation/ventilation despite vent support
  • CV system damage: no adequate MAP despite vasopressors
  • multiple organ dysfunction progressing to complete organ failure
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19
Q

Shock Assessment: CNS early and late stages

A
  • Early –> anxiety/restlessness

- Late –> coma

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20
Q

Shock assessment: CV system early and late (BP, HR)

A

Early BP and HR–> BP is normal or slightly elevated and HR is > 100

Late BP and HR –> BP is < 90 and HR < 60

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21
Q

BP and SHOCK (3)

A

hypotension: SBP less than 90 mmHg

if hypertensive: decrease of more than 40 mmHg from baseline

Map < 65

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22
Q

Shock assessment: respiratory early and late

A

early –> rapid, deep respirations, hyperventilation (RR > 20), respiratory alkalosis (compensating for metabolic acidosis)

Late –> shallow respirations, poor gas exchange

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23
Q

Shock assessment: renal system (early and late)

A

Early –> sodium retention, water reabsorption, Oliguria < 0.5 ml/kg/hr, increased BUN, creatinine WNL

Late –> AKI with decreased GFR

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24
Q

Shock Assessment: GI system (early and late)

A

early –> decreased bowel sounds, distention, Nausea, constipation

late –> damage to microvilli causing bacteria translocation increasing risk of infection

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25
Q

Shock assessment: Hepatic (4)

A
  • altered liver enzymes
  • clotting disorders
  • inability to metabolize meds
  • increased susceptibility to infection
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26
Q

Shock assessment: hematological

A

DIC

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27
Q

Shock assessment: integumentary.

A

-skin color, temp, texture, and turgor –> central/peripheral cyanosis (late/unreliable sign)

28
Q

General management (4)

A
  • identify and treat underlying cause
  • restore optimum circulation (fluid replacement to restore intravascular volume, vasoactive meds: restore vasomotor tone and improve cardiac function)
  • minimize O2 consumption and enhance oxygen delivery to tissues
  • supplemental O2, mechanical vent
  • nutritional support for increased metabolic requirements during shock
29
Q

Fluid resuscitation: (4)

A
  • rapid infusion of crystalloid and colloid solutions (NS or LR) –> 30ml/kg NS
  • blood products
  • insufficient fluid causes an increased incidence of morbidity and mortality from lack of tissue perfusion
  • excessive fluid: systemic and pulmonary edema, ARDS, abdominal compartment syndrome, MODS
30
Q

Pharmacological Support (5)

A
  • vasoactive meds: improve hemodynamics
  • given when fluid therapy cannot maintain MAP
  • Regulate CO, HR, preload, afterload, and contractility
  • vasoactive meds require frequent VS monitoring
  • use central line to prevent infiltration
31
Q

Medications that improve contractility. (4)

A

-dopamine, dobutamine, epinephrine, milrinone

32
Q

Vasodilators (2)

A
  • nitroglycerin

- nitroprusside.

33
Q

vasopressor agents (5)

A
  • norepinephirine (levophed)
  • dopamine (intropin)
  • phenylephrine. (neosynephrine)
  • vasopressin
  • epinephrine
34
Q

Other pharmacological agents besides vasoactive (7)

A
  • sedatives: propofol, Verced, precedex
  • analgesics: fentanyl, morphine
  • insulin: increased glucose metabolism
  • corticosteroids: hydrocortisone, methylprednisone
  • Antibiotics
  • low-molecular weight heparin to prevent DVT
  • h2-receptor antogonist (famotidine) or PPI. (pantoprazole) to prevent gastric stress ulcer
35
Q

body temp regulation (4)

A
  • rapid administration of IV fluids may reduce temp
  • hypothermia (decreased cardiac contractility, impairs CO, impairs oxygenation)
  • fluid warmer
  • warm blankets
36
Q

nutritional support (3)

A
  • increased metabolic rate, increased energy requirements
  • enteral nutrition (within 24-48 hours of admission, preferred route, not for paralytic ileus)
  • parenteral nutrition (given if enteral nutrition not tolerated)
37
Q

most common cause of hypovolemic shock

A

decreased intravascular volume

38
Q

Clinical manifestations of hypovolemic shock (5)

A
  • increased HR
  • increased RR
  • decreased BP
  • Decreased SV
  • decreased CO. (skin pale)
39
Q

treatment for hypovolemic shock (9)

A
  • restore volume: MAP> 65, UO > 0.5ml/kg/hr, CVP WNL, HR WNL
  • restore gas exchange: O2 sat, RR, PaO2 and PaCO2 WNL
40
Q

Causes of cardiogenic shock (common (2) and noncoronary (5) )

A
  • most common: MI, HR

- non-coronary: hypoxemia, acidosis, hypoglycemia, hypocalcemia, K imbalances

41
Q

Cardiogenic shock clinical manifestations (7)

A
  • dysrhythmias
  • angina
  • tachycardia, decreased BP
  • increased preload: increased CVP
  • pulmonary congestion: dyspnea, SOB, coughing up pink-tinged, foamy sputum
  • decreased CO: oliguria (impaired organ perfusion)
  • anxiety
42
Q

Cardiogenic shock management (4)

A
  • correct underlying cause
  • promote contractility: dopamine, dobutamine
  • decrease myocardial oxygen demand: bed rest, ventricular assist device, reduce preload and afterload
  • increase oxygen supply to tissues
43
Q

Cardiogenic shock management: procedures

A
  • thrombolytics
  • PCI
  • CABG
  • intra-aortic balloon pump
  • VAD
44
Q

Cardiogenic Shock management: pharmacology (4)

A
  • fluids: monitor for overload
  • decrease preload: diuretics, venous vasodilators
  • increase CO: dopamine, dobutamine
  • decrease afterload: hydralazine
45
Q

obstructive shock clinical manifestations (4)

A
  • chest pain
  • dyspnea, hypoxia
  • JVD
  • cause-dependent findings
46
Q

Management of obstructive shock: treat cause

A
  • cardiac tamponade (pericardiocentesis)
  • tension pneumothorax (thoraacentesis and chest tube)
  • pulmonary embolism (fibrinolytic and anticoagulant)
  • aortic stenosis, dissection: emergency surgery
47
Q

Distributive Shock: what happens in the body (4)

A
  • loss of sympathetic tone or release of biochemical mediators
  • intravascular volume pooling in peripheral blood vessels
  • abnormal displacement of intravascular volume: relative hypovolemia
  • Widespread vasodilation. and decreased SVR
48
Q

Sepsis: response to microbial invasion (5)

A
  • systemic inflammatory and immune response: organ injury
  • gram (-) bacteria: most common microorganisms in sepsis
  • increase in gram (+), viral, fungal infections causing sepsis
  • increased capillary permeability results in fluid seeping from capillaries
  • systemic injury leads to SIRS
49
Q

Septic shock criteria (2016)

A

-post fluid resuscitation (bolus) hypoperfusion requiring vasopressors to maintain MAP > 65 or serum lactate > 2

50
Q

septic shock general overview (5)

A
  • impaired tissue perfusion
  • metabolic acidosis
  • failed compensatory mechanisms
  • major vasodilation
  • organ dysfunction
51
Q

septic shock clinical manifestations (16)

A
  • hypotensive, decreased CVP, decreased CO
  • tachycardia –> bounding pulses
  • increased RR
  • hyperthermia: fever with warm, flushed skin
  • decreased UO
  • N/V/D, decreased GI motility
  • hypermetabolism causing increased blood glucose and insulin resistance
  • decreased platelets
  • increased WBC, lactic acid, CRP, and procalcitonin (if bacterial origin)
52
Q

septic shock 3 hour bundle

A
  • blood cultures (if it doesn’t interfere with starting abx)
  • start ABX
  • Bolus
53
Q

Septic shock 6 hour bundle

A

-vasopressors to maintain MAP if bolus does not work

54
Q

Neurogenic shock causes (3)

A
  • spinal cord injury
  • spinal anesthesia
  • nervous system damage
55
Q

neurogenic shock clinical manifestations (5)

A
  • bradycardia
  • hypotension
  • warm, dry, flushed skin
  • hypothermia
  • increased risk of VTE
56
Q

neurogenic shock management (5)

A
  • stabilize spinal cord injury
  • proper positioning spinal block patients
  • HOB 30
  • fluid resuscitation
  • slow rewarming
57
Q

Anaphylactic shock clinical manifestations- 3 defining characteristics

A
  • acute onset of symptoms
  • presence of 2 or more signs and symptoms
  • CV compromise minutes to hours after exposure to antigen
58
Q

anaphylactic shock clinical manifestations (10)

A
  • headache, lightheadedness
  • difficulty breathing (laryngeal edema)
  • bronchospasm
  • dysrthymias
  • tachycardia and decreased BP
  • angioedema
  • diffuse erythema/generalized flushing
  • N/V, abdominal pain
  • pruritus
  • feeling of impending doom
59
Q

Anaphylactic shock management (4)

A
  • remove causative agent
  • protect and stabilize airway
  • fluid resuscitation
  • pharmacology (epinephrine, diphenhydramine, albuterol, corticosteroids)
60
Q

Anaphylactic shock: epinephrine side effects

A
  • tachycardia
  • angina for at risk patients
  • hypertension
  • decreased UO
  • bronchodilation
  • administer albuterol
61
Q

Most common cause of MODS

A

sepsis/septic shock

62
Q

which organs are severely affected in MODS? (4)

A
  • lungs
  • splanchnic bed
  • liver
  • kidneys
63
Q

MODS clinical manifestations (10)

  • cardiac
  • respiratory
  • vascular
  • neuro
  • hematologic
  • GI
  • GU
  • endocrine
  • pH
A
  • damage by inflammatory mediators, tissue hypoxia, and hypermetabolism
  • cardiac: tachycardia, MI, HF
  • Respiratory: tachypnea/hypoxemia, ARDS
  • vascular: decreased BP greater than 40 mmHg from baseline, MAP < 65 mmHg
  • neurological: change in LOC, severe –> coma with brain damage
  • hematologic: coagulopathy, petechiae/bleeding, DIC
  • GI: liver dysfunction, jaundice, abdominal distention –> necrosis
  • GU: AKI, oliguria –> anuria
  • endocrine: hyperglycemia
  • metablic acidosis
64
Q

Management of MODS patient (4)

A
  • support patient and monitor organ perfusion until organ insults are halted
  • control infection (abx)
  • provide adequate ventilation, tissue oxygenation and perfusion (maintain 88-92% O2 sat, maintain hemoglobin above 7-9)
  • restore intravascular volume (aggressive fluid resuscitation, isotonic crystalloids)
65
Q

end of life communication (4)

A
  • priority: family communication, inclusion on decision-making
  • contract organ procurement organization
  • follow hospital and organ procurement policies and procedures
  • CARE NURSE WILL NOT INITIATE DISCUSSION ON ORGAN DONATION

NRS G270 Exam #4 (3 decks)

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