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NSG 420 Caring for Adult II > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

criteria for SIRS

A
  • temp: >100.4 or <96.8
  • RR: >20
  • HR: >90
  • WBC: >12,000 or <4,000 or >10% bands
  • PCO2: <32 mm Hg
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2
Q

criteria for sepsis

A

2 SIRS and confirmed or suspected infection

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3
Q

criteria for severe sepsis

A

sepsis + signs of end organ damage + hypotension (SBP <90) + lactate >4 mmol

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4
Q

criteria for septic shock

A

severe sepsis with persistent hypotension, signs of end organ damage, lactate >4 mmol

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5
Q

in septic shock, how much should the bolus be

A

30 mL/kg

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6
Q

sepsis six

A
  1. give high flow oxygen (15 L NRB)
  2. give a fluid challenge
  3. take blood cultures
  4. give IV antibiotics
  5. measure lactate
  6. measure urine output
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7
Q

hour 1 bundle for sepsis and septic shock

A
  1. measure lactate level
  2. obtain blood cultures before administering antibiotics
  3. administer broad-spectrum antibioics
  4. begin rapidly administering 30 mL/kg crystalloid for hypotension or lactate >= 4 mmol/l
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8
Q

CO =

A

HR x SV

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9
Q

BP

A

CO x PVR

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10
Q

most deadly shock

A

neurogenic

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11
Q

shock at the cellular level

A

when a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the microcirculatory level **hypoxia at the cellular level

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12
Q

what is a critical urine output?

A

below 0.5 mL/kg/hr

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13
Q

cardiogenic shock

A
  • systolic or diastolic dysfunction
  • compromised CO
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14
Q

early manifestations of cardiogenic shock

A
  • tachycardia
  • hypotension
  • narrowed pulse pressure
  • increased myocardial O2 consumption
  • heart’s inability to pump blood forward
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15
Q

absolute hypovoemia

A

loss of intravascular fluid volume

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16
Q

relative hypovolemia

A

results when fluid volume moves out of the vascular space in extravascular space

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17
Q

how much can a patient compensate for fluid loss?

A

up to 15% of the total blood volume (approx. 750 mL)

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18
Q

further volume loss (more than 15%-30%) will result in what?

A

sympathetic nervous system (SNS)-mediated response

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19
Q

SNS mediated response

A
  • results in increased HR, CO, RR, and depth
  • results in decreased SV, CVP, because of the decreased circulating blood volume
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20
Q

when do we usually transfuse patients?

A

8/28

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21
Q

clinical manifestations of hypovolemic shock

A
  • anxiety
  • tachypnea
  • increased CO and HR
  • decreased SV, PAWP and urinary output
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22
Q

common lab studies to test for hypovolemic shock

A
  • H&H
  • electrolytes
  • lactate
  • blood gases
  • hourly urine output
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23
Q

three types of distributive shock

A
  • neurogenic shock
  • anaphylactic shock
  • septic shock
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24
Q

what does neurogenic shock result in?

A

massive vasodilation, leading to pooling of blood in vessels (clots), tissue hypoperfusion, and ultimately impaired cellular metabolism

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25
Q

what happens in anaphylactic shock?

A
  • massive vasodilation
  • capillary permeability increases, fluid leaks from the vascular space into the interstitial space
  • can lead to respiratory distress due to laryngeal edema or severe bronchospasm and circulatory failure from massive vasodilation
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26
Q

septic shock

A
  • presence of sepsis with hypotension below 90/40 despite fluid restriction
  • presence of inadequate tissue perfusion resulting in hypoxia
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27
Q

three major pathophysiologic effects of septic shock

A
  • vasodilation
  • maldistribution of blood flow
  • myocardial depression
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28
Q

obstructive shock

A

develops when physical obstruction of blood flow occurs with decreased CO

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29
Q

clinical signs of obstructive shock

A
  • decreased CO
  • increased afterload
  • variable left ventricular filling pressure
  • JVD
  • pulsus paradoxus
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30
Q

what is the final stage of shock and what occurs?

A
  • the irreversible stage
  • decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism
  • accumulation of lactic acid occurs (metabolic acidosis)
  • increased capillary permeability
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31
Q

what drug is given to patients in the irreversible stage of shock?

A

levophed - norepinephrine

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32
Q

who is critical in early recognition and successful management of shock?

A

nurses

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33
Q

collaborative care of cardiogenic shock

A
  • restore blood flow to the myocardium by restoring the balance between O2 supply and demand
  • thrombolytic therapy
  • cardiac cath. is performed ASAP. angioplasty with stenting
  • CABG
  • drug therapy (diuretics to reduce preload) and positive inotropic agents to increase CO
  • circulatory assist devices
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34
Q

collaborative care of hypovolemic shock

A
  • stop the loss of fluid and restore the circulating volume
  • fluid replacement is calculated using a 3:1 rule (3 mL isotonic crystalloid for 1 mL of estimated blood loss)
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35
Q

collaborative care of septic shock

A
  • antibiotics after cultures (started within first hour)
  • glucose levels <180 mg/dL
  • stress ulcer prophylaxis
  • DVT prophylaxis
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36
Q

collaborative care of neurogenic shock

A
  • treatment of hypotension and bradycardia with vasopressors and atropine
  • fluids used cautiously as hypotension generally is not related to fluid loss
  • monitor for hypothermia
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37
Q

collaborative care of anaphylactic shock

A
  • prevention, then ABCs
  • epinephrine (it causes peripheral vasoconstriction an d bronchodilation and opposes the effect of histamine
  • maintain airway (nebulized bronchodilators, aerosolized epinephrine, diphenhydramine, intubation, fluid replacement to maintain BP, histamine receptor blockers, steroids)
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38
Q

collaborative care of obstructive shock

A
  • mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax ay be done
  • if PE, may require thrombolytic therapy
  • SVC syndrome treatment is radiation or removal of mass
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39
Q

when cells die, what is released?

A

K+

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40
Q

normal pH

A

7.35-7.45

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41
Q

acidodic pH

A

<7.35

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42
Q

alkalotic pH

A

> 7.45

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43
Q

how do buffers maintain pH?

A

through adequate functioning of the respiratory and renal systems

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44
Q

where is the respiratory center located and what does it do?

A

in the medulla, it controls breathing

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45
Q

increased RR lead to

A

increased CO2 elimination and decreased CO2 in blood ~ losing CO2 = alkalotic

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46
Q

decreased RR lead to

A

CO2 retention

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47
Q

bicarbonate (HCO3) has to do with what system?

A

renal/metabolic

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48
Q

CO2 has to do with what system?

A

respiratory

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49
Q

how does the renal system work in regulation?

A

conserves bicarbonate and excretes acid

50
Q

normal PaCO2

A

35-45 mm Hg

51
Q

normal HCO3

A

22-26 mEq/L

52
Q

normal PaO2

A

80-100 mm Hg

53
Q

normal SaO2

A

> 95%

54
Q

ROME pneumonic

A

Respiratory
Opposite
Metabolic
Equal

55
Q

respiratory acidosis

A
  • carbonic acid excess caused by hypoventilation or respiratory failure
  • low RR = more acid intake
  • acidosis = sedated
  • treatment: ambu bag, intubate
56
Q

compensation of respiratory acidosis

A

kidneys conserve HCO3 and secrete H+ into urine

57
Q

respiratory alkalosis

A
  • carbonic acid deficit caused by hypoxemia from acute pulmonary disorders or hyperventilation
  • can happen from a vent.
  • treatment: turn down vent. settings, breathe into a bag; give lorazepam to calm anxiety
58
Q

compensation of respiratory alkalosis

A
  • rarely occurs when acute
  • renal compensation if chronic (like in COPD)
59
Q

metabolic acidosis

A
  • excess carbonic acid or base bicarbonate deficit caused by ketoacidosis, lactic acid accumulation (shock), severe sepsis (loss of bicarbonate), kidney disease
  • think DKA
60
Q

compensation of metabolic acidosis

A
  • increased CO2 excretion by lungs (kussmaul RR deep and rapid)
  • kidneys excrete acid
61
Q

what does the anion gap tell us?

A
  • helps determine the source
  • acid gain = anion gap
62
Q

high acid gain means what is happening?

A

metabolic acidosis

63
Q

metabolic alkalosis

A

base bicarbonate excess caused by prolonged vomiting or gastric suctioning (gain of HCO3)

64
Q

compensation of metabolic alkalosis

A
  • renal excretion of HCO3
  • decreased RR to increase plasma CO2
65
Q

how can we remember ARDS?

A

A = alveoli, atelectasis
R = refractory hypoxemia 60-80
D = decreased compliance of lungs
S = surfactant

*advanced directives

66
Q

what occurs first: respiratory alkalosis or acidosis?

A

alkalosis first, then acidosis

67
Q

when alveoli capillary membranes become damaged and more permeable what happens?

A

alveoli fill with fluid ~ pulmonary edema

68
Q

results of ARDS

A
  • severe dyspnea
  • hypoxia
  • decreased lung compliance
  • diffuse pulmonary infiltrates
69
Q

most common cause of ARDS

A

sepsis

70
Q

in the fibrotic phase of ARDS, what can happen?

A

long-term ventilator support

71
Q

early manifestations of ARDS

A
  • dyspnea
  • tachypnea
  • cough
  • restlessness
  • chest auscultation may be normal or may reveal fine, scattered crackles
72
Q

what would ABGs show in early stages of ARDS?

A

mild hypoxemia and respiratory alkalosis caused by hyperventilation

73
Q

CO2 narcosis

A

too much CO2

74
Q

late clinical manifestations of ARDS

A
  • tachycardia
  • diaphoresis
  • change in mental status
  • cyanosis
  • pallor
  • diffuse crackles and coarse crackles
  • hypoxemia despite increased FiO2
  • increased WOB despite initial findings of PaO2 or SaO2
75
Q

how can we check to see if renal failure is occurring?

A

30 mL/hr
1-2 mL/kg/hr
creatinine <1

76
Q

complications of treatment for ARDS

A
  • VAP
  • barotrauma
  • volutrauma
  • high risk for stress ulcers
  • renal failure
77
Q

how can we prevent VAP?

A
  • strict infection control measures
  • elevate HOB 30-45 to prevent aspiration
  • daily “sedation holidays”
  • venous thromboembolism prophylaxis
  • daily oral care with chlorhexadine
78
Q

what nephrotoxic drug used to treat ARDS related infections can cause renal failure?

A

vancomycin

79
Q

nursing assessment for ARDS

A
  • tachycardia progressing to bradycardia
  • hypertension progressing to hypotension
  • pulsus paradoxus, JVD, pedal edema
  • abdominal distention, ascites
  • somnolence, confusion, delirium
  • changes in pH, PaCO2, PaO2, SaO2
  • decreased tidal volume
  • abnormal x-ray
  • abnormal central venous or pulmonary artery pressures
  • initial increased CO
  • as hypoxemia, hypercapnia, and acidosis become more severe, CO will decrease
80
Q

PEEP

A

Positive End Expiratory Pressure
- can increase chest pressure, leading to decreased CO and BP, so you would need to bolus
- keeps alveoli open

81
Q

what risk do we have when using PEEP?

A

pneumothorax

82
Q

acute respiratory failure

A
  • results from inadequate gas exchange
  • insufficient O2 transferred to blood: hypoxemia
  • inadequate CO2 removal: hypercapnia
  • not a disease but a symptom
  • result of one or more disorders involving lungs or other body systems
83
Q

2 classifications of acute respiratory failure

A
  • hypoxemic respiratory failure
  • hypercapnic respiratory failure
84
Q

hallmark of hypoxemic respiratory failure according to labs

A

PaO2 <60 mm Hg on inspired O2 concentration >= 60%

85
Q

dead space V/Q mismatch

A

occurs when you have ventilation, but no perfusion like with pulmonary embolism

86
Q

intrapulmonary shunting V/Q mismatch

A

occurs when you have perfusion but no ventilation

87
Q

hallmark of hypercapnic respiratory failure according to labs

A
  • PaCO2 above normal (>45 mm Hg)
  • acidemia (pH <7.35)
88
Q

goal with oxygen levels in acute respiratory failure

A
  • maintain PaO2 at 55-60 mm Hg or more and SaO2 at 90% or more at the lowest O2 concentration possible
  • mobilization of secretions
89
Q

what drug relieves bronchospasm?

A

albuterol

90
Q

what drug reduces airway inflammation?

A

steroids

91
Q

ventilator assessment acronym

A

DOPE
D - displacement
O - obstruction
P - pneumothorax
E - equipment

92
Q

expected outcomes in respiratory failure

A
  • maintain a patent airway with effective removal of secretions
  • achieve normal or baseline RR and rhythm, and breath sounds
  • maintain adequate oxygenation as indicated by normal or baseline ABGs
  • experience normal hemodynamic status
93
Q

risk factors for pulmonary embolism

A
  • oral contraceptive hormones
  • a. fib.
  • fractured long bones
  • DVT
  • immobility
  • surgery
  • malignancy
  • obesity
  • smoking
  • HF
  • pregnancy/delivery
  • clotting disorders
  • central venous catheters
94
Q

clinical manifestations of PE

A
  • dyspnea most common
  • tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, change in LOC
95
Q

two complications of PE

A
  • pulmonary infarction
  • pulmonary HTN (right ventricular hypertrophy)
96
Q

main study used to diagnose PE

A
  • spiral (helical) CT
  • requires IV contrast
97
Q

what do you want to make sure of if someone is having a dye injected?

A
  • allergies
  • kidney function
  • creatinine <1
  • no metformin for 48 hours
98
Q

what study do we use to diagnose a PE if the patient cannot have dye?

A

V/Q scan

99
Q

what kind of V/Q would be expected in a patient with PE?

A

high

100
Q

how can we prevent a PE?

A
  • sequential compression devices
  • early ambulation
  • prophylactic anticoagulation
101
Q

what do anticoagulation agents do?

A

prevent new clots from forming

102
Q

what do fibrinolytic agents do?

A

dissolve clots

103
Q

what kind of test do you want ran on those on heparin?

A

aptt

104
Q

reversal for heparin

A

protamine sulfate

105
Q

reversal for warfarin

A

vit. k

106
Q

spontaneous pneumothorax

A

rupture of blebs

107
Q

risk factors for a spontaneous pneumothorax

A

smoking, tall/thin, male, family hx, hx of previous event, vaping

108
Q

what occurs in a tension pneumothorax?

A

tracheal deviation

109
Q

serous fluid color

A

yellow

110
Q

serosanguinous fluid color

A

yellow/blood

111
Q

sanguinous fluid color

A

blood

112
Q

how to treat a tension pneumothorax

A

urgent needle decompression

113
Q

emergency treatment for a penetrating chest wound

A
  • a vent dressing
  • occlusive dressing secured on 3 sides
114
Q

signs of respiratory distress in a pneumothorax

A
  • dyspnea
  • cough with or without hemoptysis
  • cyanosis
  • tracheal deviation
  • decreased breath sounds
  • decreased O2 sat
  • frothy secretions
115
Q

signs of cardiovascular compromise in a pneumothorax

A
  • rapid, thready pulse
  • decreased BP with narrowed pulse pressure and/or asymmetric readings
  • distended neck veins
  • muffled heart sounds
  • chest pain
  • dysrhythmias
116
Q

initial interventions for a pneumothorax

A
  • ABCs
  • administer O2 to keep sat >90%
  • establish IV access with 2 large-bore catheters and begin fluid resuscitation as appropriate
  • remove clothing to assess injury
  • cover sucking chest wound with nonporous dressing taped on 3 sides
117
Q

what does bubbling in a chest tube indicate?

A
  • air leaks
  • initially, it is expected but should disappear
  • if new onset, notify MD
118
Q

what does tidaling in a chest tube mean?

A
  • reflects changes in pressure
  • disappears as lung reexpands
  • normal
119
Q

water suction control on chest tube

A
  • filled to -20cm of water
  • adjust suction until gentle bubbling in third chamber
120
Q

nursing management of chest tubes

A
  • observe tidaling
  • observe for air leak
  • observe fluid levels in water-seal chamber
  • observe and document drainage
121
Q

when should you notify MD with chest tube issues?

A
  • drainage >200 mL, 100 mL if pure blood
  • subcutaneous emphysema
  • respiratory distress
122
Q

what should you never do with a chest tube?

A
  • do not elevate it above chest
  • do not clamp
  • do not milk

NSG 420 Caring for Adult II (4 decks)

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