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critical care > test 2 > Flashcards

test 2 Flashcards

1
Q

PaO2

A

partial pressure of o2

Normal level is 80-100

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2
Q

PaCO2

A

partial pressure of CO 2

normal level is 35-45

lower is basic, higher is acidic

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3
Q

hypoxemic failure

A

problem with oxygenation. o2 is low

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4
Q

hypercapnic failure

A

problem with ventilation, leads to acidosis. CO2 will be high, pH will be low

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5
Q

pulmonary causes of hypoxemia

A

hypoventilation
collapsed alveolus
blood clot
interstitial fluid

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6
Q

hypoventilation

A

occurs when alveoli don’t receive O2, and cannot participate in gas exchange. Air movement lacks but bloodflow is fine

clinical presentations- OD/sedation, shallow respirations, decreased rest rate, pain on inspiration

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7
Q

intrapulmonary shunting

A

alveoli not open, gas exchange can’t occur

maybe from pneumonia, atelactis

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8
Q

VQ mismatch

A

problem with o2 or perfusion. if O2 can’t get in, CO2 can’t get out

may be from pulm embolism

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9
Q

normal VQ ratio

A

0.8
rate at which O2 move in and out of the alveoli compared to rate of perfusion of blood through pulmonary capillaries

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10
Q

diffusion defect

A

diffusion of gas is slow due to increased space between alveolar membrane and cap beds

caused by COPD, and interstitial fluid

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11
Q

how does cardiac output and hgb affect tissue oxygenation

A

decreased cardio output leads to decreased hgb causing lower tissue oxygenation

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12
Q

what is resp failure

A

lack of O2 or increase In CO2

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13
Q

Neuro assessment findings in resp failure

A

first sign- confusion, restlessness, agitation

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14
Q

Resp assessment findings in resp failure

A

tachypnea at first - trying to blow off CO2 and bring in O2.
Later on we will see decreased shallow respirations,

auscultation will show coarse, wheezes
edema in alveoli will cause increased peak inspiratory pressure

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15
Q

Cardio assessment findings in resp failure

A

tachycardia initially as its trying to increase cardiac output.
Later we will see decreased BP, HR, chest pain, and dysthymia’s

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16
Q

goals for ARF

A
  1. maintain patent airway (bronchodilators, suction, sitting up)
  2. optimize o2 delivery (limit secretions, right o2 mask)
  3. minimize o2 demand (rest periods, meds)
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17
Q

acute resp failure patho

A

lung injury characterized by inflammation, edema, and loss of compliance. Damage to alv-cap membrane

2 phases: acute exudation and fibroproliferation

NONCARDIOGENIC pulmonary edema

caused by flu, pneumonia, aspiration of gastric contents chest trauma

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18
Q

criteria for ARDS

A

acute onset - within a week of insult
bilateral pulmonary opacities
altered PaO2/FiO2 ratio- O2 continuously goes down no matter how much o2 we give them

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19
Q

ARDS acute exudation

A

systemic inflammation. alveoli fill with exudate, protein and blood. Pulmonary Htn occurs

Can lead to platelet aggregation and thrombus formation
Ultimately leads to VQ mismatch

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20
Q

ARDS Fibroproliferation

A

fibrin matrix begins forming after 48 hours, fibrosis destroys alveoli and bronchioles

leads to decreased function and inflammation

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21
Q

ARDS interventions/treatments

A

we want a low tidal volume and low end inspiratory pressure because pressure is already high.

we want the FiO2 at about 60% or lower (<.60)

PEEP of 5 or less to recruit more alveoli to participate in oxygenation.

sedation- so they don’t exert energy

prone positioning

be conservative with fluids

nutrition and psychosocial support

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22
Q

ARF in COPD

A

we need to correct hypoxemia with supplemental o2. Ventilator is last resort for these patients. Try NPPV first (a mask)

COPD is chronic obstruction of airways. poor gas exchange and decreased ability to clear airway

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23
Q

ARF in asthma

A

Chronic inflammatory disorder of airways – causes bronchoconstriction, edema, increased mucous production, prolonged exhalation

Status asthmaticus – fails to respond to bronchodilators

try Bronchodilators/anticholinergics, and Steroids. Intubation may be needed if they don’t work.

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24
Q

Ventilator associated pneumonia (VAP) bundle- prevention

A

HOB 30-45
Sedation vacation to assess readiness to wean
DVT prophylaxis
PUD prophylaxis
Daily oral care

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25
Q

ARF with PE

A

Etiology – venous stasis, altered coagulability, damage to vessel walls

Pathophysiology – clot reaches pulmonary vasculatoure – leads to VQ mismatch because it stops perfusion = no gas exchange

Diagnostics – D dimer (positive means possible PE, negative means no PE), VQ scan, CT

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26
Q

Normal pH

A

7.35 - 7.45

lower is acidic, higher is basic

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27
Q

HCO3

A

bicarbonate

normal level is 22-26

lower is acidic, higher is basic

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28
Q

blood pH level that is deadly

A

acidic is 6.90 or below
basic is 7.80 and above

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29
Q

causes of resp acidosis- retention of co2

A

hypoventilation
CNS depression
restrictive lung issue
COPD
trauma

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30
Q

causes of resp alkalosis- loss of co2

A

hyperventilation
anxiety
pain
fever

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31
Q

causes of metabolic acidosis- increased blood acid

A

DKA
renal failure
Lactic acidosis
OD (salicylates)

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32
Q

causes of metabolic acidosis- too much acid loss or too much base

A

ingestion of antacids
admin of HCO3
blood transfusion
vomiting
NG suction
Diuretics

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33
Q

Tidal Volume

A

volume of normal breath

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34
Q

inspiratory reserve volume (IRV)

A

Max amount of gas that can be inspired at the end of a normal breath - deep breath - over and above the tidal volume

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35
Q

expiratory volume reserve (ERV)

A

Max amount of gas that can be forcefully expired at the end of a normal breath - extra pushed out

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36
Q

residual volume (RV)

A

Amount of air remaining in the lungs after max expiration - the air in luns at all times

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37
Q

inspiratory capacity (IC)

A

max volume of gas that can be inspired at normal resting expiration. this distends the lungs to the max amount

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38
Q

functional residual capacity (FRC)

A

volume of gas remaining in the lungs at normal resting expiration

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39
Q

vital capacity (VC)

A

Max volume of gas that can be forcefully expired after max inspiration

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40
Q

total lung capacity (TLC)

A

volume of gas in the lungs at the end of max inspiration

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41
Q

when to treat PaO2

A

if the value is less than 60

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42
Q

hypoxemia vs hypoxia

A

hypoxemia- decreased o2 of arterial blood

hypoxia- decreased o2 at tissue level

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43
Q

oxyhemoglobin dissociation left curve

A

Hgb clings to oxygen. o2 sat increases. we want this if pt is hyperthermic

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44
Q

oxyhemoglobin dissociation right curve

A

releases o2 from hgb to tissues. o2 sat decreases.
we want this for burn patients so they can heal their tissues

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45
Q

how does oxyhemoglobin dissociation occur

A

when the PaO2 falls below 60 mmhg, changes reflect in the oxygen saturation

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46
Q

intubation position

A

sniffing position- high shoulders, head back

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47
Q

airway management position

A

high fowlers

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48
Q

devices for airway management

A

oral airway
nasopharyngeal airway
endotracheal intubation

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49
Q

endotracheal suction uses

A

maintain a airway
remove secretions
prevent aspirations (cuff pressure 20-30)
provide mechanical ventilation

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50
Q

steps to verify placement of endotracheal intubation

A
  1. Auscultate the lungs- bilateral equal breath sounds
  2. Auscultate stomach
  3. ETCOx detector
  4. Chest x-ray

record cm ay lip line
secure tube once verified

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51
Q

what to do if pt desats with endotracheal intubation

A

**Immediately notify RT to obtain a vent

**Bedside suction

**Vitals signs

**Hyperoxygenating client with 100% oxygen

**Ensuring bedside access to a rigid tonsil tip suction cathether

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52
Q

how to tell if ET tube is in the right mainstream bronchus

A

we would only hear right breath sounds

this placement is wrong, it should be in the middle 2-3 inches above carina

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53
Q

what to do if ET tube is in the esophagus

A

take it out and redo it

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54
Q

tracheostomy indications

A

long term mechanical ventilation
frequent suctioning
protecting the airway
bypass an airway obstruction
reduce work of breathing

55
Q

cuffed vs uncuffed trach

A

Mechanical ventilation will always be cuffed.
Uncuffed is if you are trying to wean the patient, or if they are speaking

56
Q

when to suction ET tube

A

visible secretions
coughing
rhonchi
high PIP
ventilator alarm

don’t use saline

57
Q

indications for ventilation

A

hypoxemia
hypercapnia
progressive deterioration

58
Q

positive pressure ventilation

A

movement of gases into lungs through positive pressure.

we are shoving air into the lungs

59
Q

positive end expiratory pressure (PEEP)

A

keeps the alveoli open, reducing need for FiO2.

Can cause reduced cardiac output, hypotension and impede venous return if too high

60
Q

vent settings

A

FiO2 (0.21-1.0)
tidal volume 6-8 mL/kg
PIP less than 40 cm
resp rate 14-20 (look at ABG- pH, CO2)

61
Q

why may peep be above 40

A

Vent circuit disconnection, suction, bronchospasm, biting tube, kink

61
Q

what should the exhaled tidal volume not be more than

A

50 mL

62
Q

2 types volume ventilation

A

volume assist/control (V-A/C)

synchronized intermittent mandatory ventilation (SIMV)

63
Q

volume assist/control (V-A/C)

A

Assist control always gets set tidal volume. Spontaneous breathing may be there too but it doesn’t have to be. Risk for hyperventilation is present with assist- resp alkalosis

Ventilator performs most of work of breathing still even if person has spontaneous breaths

64
Q

synchronized intermittent mandatory ventilation (SIMV)

A

vent delivers a mandatory set rate, but spontaneous breaths may occur in between. the ventilator attempt to synchronize the spontaneous breaths with the preset rate.

this is used to wean patients from mechanical ventilation because patient contributes more to work of breathing.

65
Q

pressure ventilation types

A

CPAP, Pressure support (PSV), Pressure A/C, inverse ratio ventilation, airway pressure release (APRV)

66
Q

pressure A/C

A

Vent pressure will always be there, spontaneous breaths may or may not be there. You will always get the set pressure no matter what because vent kicks in

67
Q

Pressure support

A

spontaneous effort is assisted by preset of positive pressure.

This is the most common mode when pt is going to get extubated to wean them. You must be able to spontaneously breathe with this, but if you don’t the vent will alarm and you will be switched to a different setting

68
Q

CPAP

A

continuous positive airway pressure throughout resp cycle to pt who is spontaneously breathing

can be used to prevent re-intubation

The patient performs all the WOB. CPAP provides pressure at end-expiration, which prevents alveolar collapse and improves the functional residual capacity and oxygenation

69
Q

noninvasive positive pressure ventilation (NPPV)

A

he delivery of mechanical ventilation without an ETT or tracheostomy tube

Delivers via face mask, nasal pillow/mask

***Pt must be able to spontaneously breathe for this

People with this can eat and not be in discomfort

this is only intended for acute exacerbations

70
Q

types of vent alarms

A

high peek pressure
low pressure; low PEEP/CPAP
low exhaled tidal volume
low minute ventilation
high exhaled tidal volume
high minute ventilation
apnea

71
Q

barotrauma

A

trauma with pressure

could cause pneumothorax

monitor for subcutaneous crepitus, high PAP, tracheal shift, hypoxemia

72
Q

volutrauma

A

trauma from volume- overexpanding alveoli

damages the lung similar to early ARDS

73
Q

vent bundle

A

HOB at 30 degrees
awaken daily and assess readiness to wean
stress ulcer prophylaxis
DVT prophylaxis
oral care

74
Q

how to know when a vent pt is ready to wean

A

Stable, alert and oriented, not resp distressed.

IF NEGATIVE SYMPTOMS OCCUR WHEN WEANING STOP THE PROCESS AND PUT BACK ON VENT

75
Q

extubation

A

removing the ET tube

76
Q

functions of the kidney

A

regulation of:
Fluid volume
electrolyte balance
acid base balance
BP
erythropoiesis

excretion of nitrogenous waste
metabolism of vitamin D

77
Q

What is considered oliguria

A

urine output less than 0.5 ml/kg/hr

78
Q

what is azotemia

A

accumulation of nitrogenous wastes (bun and creatine)

79
Q

pre renal AKI

A

low bp, hypovolemia, dehydration like symptoms

ex that may cause- hemorrhage, sepsis, heart failure, DI, burns, diuretics, etc

80
Q

meds for prerenal AKI

A

norepinephrine- helps BP go up

81
Q

intrarenal AKI

A

acute tubular necrosis- lack of blood flow and o2 to the kidneys

examples that may cause this- ischemia, DM, htn, glomerulonephritis, thrombosis, etc

82
Q

post renal AKI

A

obstruction of urine flow

ex caused by- BPH, clots, renal stones, meds, foley Cath obstruction, etc

83
Q

initiation phase of AKI

A

phase spans several hours to 2 days, during which time the normal renal processes begin to deteriorate, but kidney cell death has not yet occurred.
The patient is unable to compensate for the diminished renal function and exhibits clinical signs and symptoms of AKI.
Kidney injury is potentially reversible during the initiation phase.

84
Q

maintenance phase AKI

A

phase last 1-2 weeks, but could last months

renal damage occurs in this stage
complications can be uremia, hyperkalemia and infection

85
Q

recovery phase AKI

A

recovery may take as long as 4-6 months

this is when renal tissue recovers and repairs itself

86
Q

normal creatine

A

around 1.0

87
Q

normal BUN

A

Around 20

88
Q

AKI diagnostics

A

KUB xray
renal ultrasound
MRI

IV pyelogram
computed tomography
renal angiography
renal scan
renal biopsy

89
Q

AKI interventions

A

I/o
daily weights
IV fluids
prevent infection
monitor electrolytes

90
Q

pre renal AKI med management

A

volume replacement
maintain perfusion

early recognition=better outcome

91
Q

intrarenal AKI med management

A

drug therapy
diet restriction
manage f&e
CRRT/dialysis

92
Q

post renal AKI med management

A

alleviate obstruction

93
Q

what does decreased GFR lead to

A

hyperkalemia

94
Q

treating elevated potassium

A

meds to lower- kayaxelate (sodium poly sulfonate)

shift potassium from outside cell to inside- insulin. must also give dextrose

calcium given to help protect the cardiac cell membrane - it doesn’t lower k

95
Q

potassium 6-7 EKG change

A

peaked T wave

96
Q

potassium 7-8 EKG change

A

peaked T wave
flattened p wave
prolonged PR interval
depressed ST segment

97
Q

potassium 8-9 EKG

A

atrial standstill
prolonged QRS duration
further peaking T wave

98
Q

potassium above 9 ekg changes

A

wave pattern. possible vtach

99
Q

why does hyponatremia happen in AKI

A

nephrons are damaged, they can’t conserve sodium

100
Q

types of dialysis

A

hemodialysis
continuous renal replacement therapy- CRRT
Peritoneal

101
Q

Interventions for patients with dialysis graft/shunt

A

monitor labs
weight pt daily
don’t admin water soluble meds
avoid antihyp before hand
assess bruit and thrill

102
Q

CRRT

A

like hemodialysis but slower

these pts need to be on bed rest

103
Q

4 types of CRRT

A

Slow continuous ultrafiltration (SCUF)- Used to remove plasma / water in case of fluid overload.

Continuous venovenous hemofiltration (CVVH)-Removes fluids and solutes across a hemofilter.

Continuous venonvenous hemodialysis (CVVHD)- Similar to CVVH except that instead of replacement fluid, dialysate is added around then hemofilter and causes increased removal of solutes and fluid.

Continuous venovenous hemodiafiltration (CVVHDF)- Maximum removal of fluid and uremic wastes

ASSESS HEMOFILTER every 2-4 hours for clotting

104
Q

normal output ml/kg/hr

A

0.5-1 ml/kg/hr

105
Q

where does acid base regulation occur

A

proximal and distal tubules in nephron

106
Q

what influences glomerular filt rate

A

mean arterial pressure

107
Q

if potassium is high and EKG shows abnormal rhythm what is the priority first step

A

calcium chloride- it will protect heart

after this give kayexelate to lower k

108
Q

Hematopoiesis

A

formation and maturation of RBC

109
Q

primary site of hematopoietic production

A

bone marrow

110
Q

secondary hematopoietic organs

A

spleen, liver, thymus, lymphatic system, lymphoid tissue

111
Q

erythrocytes

A

RBC- function to deliver hemoglobin throughout the body

112
Q

platelets

A

first responders for clotting

113
Q

granulocytes

A

neutrophils, basophils, and eosinophils, all of which function in phagocytosis

114
Q

agranulocytes

A

monocytes and lymphocytes

115
Q

function of neutrophils

A

bacterial infection

116
Q

function of eosinophils

A

parasites
skin, lung, GI tract

117
Q

basophils function

A

inflammatory/allergic response

118
Q

monocyte function

A

mature into macrophage then do phagocytosis- attack foreign bodies and remove dead cells

119
Q

lymphocyte function

A

humoral immunity- B lymphocytes (antibody prod)

cellular immunity- T lymphocytes (long term immunity)

120
Q

what mechanisms trigger clotting

A

tissue injury
vessel injury
foreign body in the bloodstream

121
Q

symptoms of all anemia types

A

fatigue, weakness, short of breath

122
Q

aplastic anemia s/s

A

bruising
nosebleeds
petechiae

123
Q

hemolytic anemia s/s

A

jaundice, abd pain, liver/spleen enlargement

124
Q

sickle cell anemia s/s

A

joint swelling, pain

125
Q

How does HIV lead to AIDS

A

by depleting helper T cells, CD4 cells, and macrophages

126
Q

AIDS CD4 count

A

less than 200/microliter and presence of indicator of condition

127
Q

HIV treatment

A

antiretroviral therapy

128
Q

thrombocytopenia

A

low platelets under 150k

risk for bleeding

treated by platelets (depending on type)

129
Q

heparin induced thrombocytopenia (HIT)

A

Adverse reaction to heparin

it causes hypercoagulability and thrombus

treatment- stop heparin, admin drugs that inhibit thrombin (bivalirudin)

130
Q

Disseminated intravascular coagulation (DIC)

A

Increased microvascular clotting, depletion of clotting factors and subsequent bleeding

most common cause is sepsis.

after thrombotic phase, clots begin to lyse and excessive bleeding occurs

131
Q

DIC diagnosis

A

elevated fibrin degradation products
increased d-dimer
decreased antithrombin III

132
Q

treatment of DIC

A

treat underlying cause
platelet transfusion
FFP transfusion
RBC for hemorrhage
heparin
cryoprecipitate

critical care (4 decks)

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