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
2
Q
criteria for sepsis
A
2 SIRS and confirmed or suspected infection
3
Q
criteria for severe sepsis
A
sepsis + signs of end organ damage + hypotension (SBP <90) + lactate >4 mmol
4
Q
criteria for septic shock
A
severe sepsis with persistent hypotension, signs of end organ damage, lactate >4 mmol
5
Q
in septic shock, how much should the bolus be
A
30 mL/kg
6
Q
sepsis six
A
- give high flow oxygen (15 L NRB)
- give a fluid challenge
- take blood cultures
- give IV antibiotics
- measure lactate
- measure urine output
7
Q
hour 1 bundle for sepsis and septic shock
A
- measure lactate level
- obtain blood cultures before administering antibiotics
- administer broad-spectrum antibioics
- begin rapidly administering 30 mL/kg crystalloid for hypotension or lactate >= 4 mmol/l
8
Q
CO =
A
HR x SV
9
Q
BP
A
CO x PVR
10
Q
most deadly shock
A
neurogenic
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
12
Q
what is a critical urine output?
A
below 0.5 mL/kg/hr
13
Q
cardiogenic shock
A
- systolic or diastolic dysfunction
- compromised CO
14
Q
early manifestations of cardiogenic shock
A
- tachycardia
- hypotension
- narrowed pulse pressure
- increased myocardial O2 consumption
- heart’s inability to pump blood forward
15
Q
absolute hypovoemia
A
loss of intravascular fluid volume
16
Q
relative hypovolemia
A
results when fluid volume moves out of the vascular space in extravascular space
17
Q
how much can a patient compensate for fluid loss?
A
up to 15% of the total blood volume (approx. 750 mL)
18
Q
further volume loss (more than 15%-30%) will result in what?
A
sympathetic nervous system (SNS)-mediated response
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
20
Q
when do we usually transfuse patients?
A
8/28
21
Q
clinical manifestations of hypovolemic shock
A
- anxiety
- tachypnea
- increased CO and HR
- decreased SV, PAWP and urinary output
22
Q
common lab studies to test for hypovolemic shock
A
- H&H
- electrolytes
- lactate
- blood gases
- hourly urine output
23
Q
three types of distributive shock
A
- neurogenic shock
- anaphylactic shock
- septic shock
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
25
what happens in anaphylactic shock?
- 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
26
septic shock
- presence of sepsis with hypotension below 90/40 despite fluid restriction
- presence of inadequate tissue perfusion resulting in hypoxia
27
three major pathophysiologic effects of septic shock
- vasodilation
- maldistribution of blood flow
- myocardial depression
28
obstructive shock
develops when physical obstruction of blood flow occurs with decreased CO
29
clinical signs of obstructive shock
- decreased CO
- increased afterload
- variable left ventricular filling pressure
- JVD
- pulsus paradoxus
30
what is the final stage of shock and what occurs?
- the irreversible stage
- decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism
- accumulation of lactic acid occurs (metabolic acidosis)
- increased capillary permeability
31
what drug is given to patients in the irreversible stage of shock?
levophed - norepinephrine
32
who is critical in early recognition and successful management of shock?
nurses
33
collaborative care of cardiogenic shock
- 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
34
collaborative care of hypovolemic shock
- 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)
35
collaborative care of septic shock
- antibiotics after cultures (started within first hour)
- glucose levels <180 mg/dL
- stress ulcer prophylaxis
- DVT prophylaxis
36
collaborative care of neurogenic shock
- treatment of hypotension and bradycardia with vasopressors and atropine
- fluids used cautiously as hypotension generally is not related to fluid loss
- monitor for hypothermia
37
collaborative care of anaphylactic shock
- 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)
38
collaborative care of obstructive shock
- 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
39
when cells die, what is released?
K+
40
normal pH
7.35-7.45
41
acidodic pH
<7.35
42
alkalotic pH
>7.45
43
how do buffers maintain pH?
through adequate functioning of the respiratory and renal systems
44
where is the respiratory center located and what does it do?
in the medulla, it controls breathing
45
increased RR lead to
increased CO2 elimination and decreased CO2 in blood ~ losing CO2 = alkalotic
46
decreased RR lead to
CO2 retention
47
bicarbonate (HCO3) has to do with what system?
renal/metabolic
48
CO2 has to do with what system?
respiratory
49
how does the renal system work in regulation?
conserves bicarbonate and excretes acid
50
normal PaCO2
35-45 mm Hg
51
normal HCO3
22-26 mEq/L
52
normal PaO2
80-100 mm Hg
53
normal SaO2
>95%
54
ROME pneumonic
Respiratory
Opposite
Metabolic
Equal
55
respiratory acidosis
- carbonic acid excess caused by hypoventilation or respiratory failure
- low RR = more acid intake
- acidosis = sedated
- treatment: ambu bag, intubate
56
compensation of respiratory acidosis
kidneys conserve HCO3 and secrete H+ into urine
57
respiratory alkalosis
- 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
compensation of respiratory alkalosis
- rarely occurs when acute
- renal compensation if chronic (like in COPD)
59
metabolic acidosis
- excess carbonic acid or base bicarbonate deficit caused by ketoacidosis, lactic acid accumulation (shock), severe sepsis (loss of bicarbonate), kidney disease
- think DKA
60
compensation of metabolic acidosis
- increased CO2 excretion by lungs (kussmaul RR deep and rapid)
- kidneys excrete acid
61
what does the anion gap tell us?
- helps determine the source
- acid gain = anion gap
62
high acid gain means what is happening?
metabolic acidosis
63
metabolic alkalosis
base bicarbonate excess caused by prolonged vomiting or gastric suctioning (gain of HCO3)
64
compensation of metabolic alkalosis
- renal excretion of HCO3
- decreased RR to increase plasma CO2
65
how can we remember ARDS?
A = alveoli, atelectasis
R = refractory hypoxemia 60-80
D = decreased compliance of lungs
S = surfactant
*advanced directives
66
what occurs first: respiratory alkalosis or acidosis?
alkalosis first, then acidosis
67
when alveoli capillary membranes become damaged and more permeable what happens?
alveoli fill with fluid ~ pulmonary edema
68
results of ARDS
- severe dyspnea
- hypoxia
- decreased lung compliance
- diffuse pulmonary infiltrates
69
most common cause of ARDS
sepsis
70
in the fibrotic phase of ARDS, what can happen?
long-term ventilator support
71
early manifestations of ARDS
- dyspnea
- tachypnea
- cough
- restlessness
- chest auscultation may be normal or may reveal fine, scattered crackles
72
what would ABGs show in early stages of ARDS?
mild hypoxemia and respiratory alkalosis caused by hyperventilation
73
CO2 narcosis
too much CO2
74
late clinical manifestations of ARDS
- 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
how can we check to see if renal failure is occurring?
30 mL/hr
1-2 mL/kg/hr
creatinine <1
76
complications of treatment for ARDS
- VAP
- barotrauma
- volutrauma
- high risk for stress ulcers
- renal failure
77
how can we prevent VAP?
- strict infection control measures
- elevate HOB 30-45 to prevent aspiration
- daily "sedation holidays"
- venous thromboembolism prophylaxis
- daily oral care with chlorhexadine
78
what nephrotoxic drug used to treat ARDS related infections can cause renal failure?
vancomycin
79
nursing assessment for ARDS
- 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
PEEP
Positive End Expiratory Pressure
- can increase chest pressure, leading to decreased CO and BP, so you would need to bolus
- keeps alveoli open
81
what risk do we have when using PEEP?
pneumothorax
82
acute respiratory failure
- 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
2 classifications of acute respiratory failure
- hypoxemic respiratory failure
- hypercapnic respiratory failure
84
hallmark of hypoxemic respiratory failure according to labs
PaO2 <60 mm Hg on inspired O2 concentration >= 60%
85
dead space V/Q mismatch
occurs when you have ventilation, but no perfusion like with pulmonary embolism
86
intrapulmonary shunting V/Q mismatch
occurs when you have perfusion but no ventilation
87
hallmark of hypercapnic respiratory failure according to labs
- PaCO2 above normal (>45 mm Hg)
- acidemia (pH <7.35)
88
goal with oxygen levels in acute respiratory failure
- 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
what drug relieves bronchospasm?
albuterol
90
what drug reduces airway inflammation?
steroids
91
ventilator assessment acronym
DOPE
D - displacement
O - obstruction
P - pneumothorax
E - equipment
92
expected outcomes in respiratory failure
- 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
risk factors for pulmonary embolism
- oral contraceptive hormones
- a. fib.
- fractured long bones
- DVT
- immobility
- surgery
- malignancy
- obesity
- smoking
- HF
- pregnancy/delivery
- clotting disorders
- central venous catheters
94
clinical manifestations of PE
- dyspnea most common
- tachypnea, cough, chest pain, hemoptysis, crackles, wheezing, fever, tachycardia, syncope, change in LOC
95
two complications of PE
- pulmonary infarction
- pulmonary HTN (right ventricular hypertrophy)
96
main study used to diagnose PE
- spiral (helical) CT
- requires IV contrast
97
what do you want to make sure of if someone is having a dye injected?
- allergies
- kidney function
- creatinine <1
- no metformin for 48 hours
98
what study do we use to diagnose a PE if the patient cannot have dye?
V/Q scan
99
what kind of V/Q would be expected in a patient with PE?
high
100
how can we prevent a PE?
- sequential compression devices
- early ambulation
- prophylactic anticoagulation
101
what do anticoagulation agents do?
prevent new clots from forming
102
what do fibrinolytic agents do?
dissolve clots
103
what kind of test do you want ran on those on heparin?
aptt
104
reversal for heparin
protamine sulfate
105
reversal for warfarin
vit. k
106
spontaneous pneumothorax
rupture of blebs
107
risk factors for a spontaneous pneumothorax
smoking, tall/thin, male, family hx, hx of previous event, vaping
108
what occurs in a tension pneumothorax?
tracheal deviation
109
serous fluid color
yellow
110
serosanguinous fluid color
yellow/blood
111
sanguinous fluid color
blood
112
how to treat a tension pneumothorax
urgent needle decompression
113
emergency treatment for a penetrating chest wound
- a vent dressing
- occlusive dressing secured on 3 sides
114
signs of respiratory distress in a pneumothorax
- dyspnea
- cough with or without hemoptysis
- cyanosis
- tracheal deviation
- decreased breath sounds
- decreased O2 sat
- frothy secretions
115
signs of cardiovascular compromise in a pneumothorax
- rapid, thready pulse
- decreased BP with narrowed pulse pressure and/or asymmetric readings
- distended neck veins
- muffled heart sounds
- chest pain
- dysrhythmias
116
initial interventions for a pneumothorax
- 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
what does bubbling in a chest tube indicate?
- air leaks
- initially, it is expected but should disappear
- if new onset, notify MD
118
what does tidaling in a chest tube mean?
- reflects changes in pressure
- disappears as lung reexpands
- normal
119
water suction control on chest tube
- filled to -20cm of water
- adjust suction until gentle bubbling in third chamber
120
nursing management of chest tubes
- observe tidaling
- observe for air leak
- observe fluid levels in water-seal chamber
- observe and document drainage
121
when should you notify MD with chest tube issues?
- drainage >200 mL, 100 mL if pure blood
- subcutaneous emphysema
- respiratory distress
122
what should you never do with a chest tube?
- do not elevate it above chest
- do not clamp
- do not milk
