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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)

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

33
Q

Tidal Volume

A

volume of normal breath

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

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

36
Q

residual volume (RV)

A

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

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

38
Q

functional residual capacity (FRC)

A

volume of gas remaining in the lungs at normal resting expiration

39
Q

vital capacity (VC)

A

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

40
Q

total lung capacity (TLC)

A

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

41
Q

when to treat PaO2

A

if the value is less than 60

42
Q

hypoxemia vs hypoxia

A

hypoxemia- decreased o2 of arterial blood

hypoxia- decreased o2 at tissue level

43
Q

oxyhemoglobin dissociation left curve

A

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

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

45
Q

how does oxyhemoglobin dissociation occur

A

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

46
Q

intubation position

A

sniffing position- high shoulders, head back

47
Q

airway management position

A

high fowlers

48
Q

devices for airway management

A

oral airway
nasopharyngeal airway
endotracheal intubation

49
Q

endotracheal suction uses

A

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

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

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

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

53
Q

what to do if ET tube is in the esophagus

A

take it out and redo it

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

critical care (2 decks)

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