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Critical Care > Acute Respiratory Distress > Flashcards

Acute Respiratory Distress Flashcards

1
Q

Acute Respiratory Failure

A

defined by physiologic criteria

sudden onset of one or more of the following:

  • PaO2 less than or equal to 50 mmHg (on room air)
  • PaCO2 more than or equal to 50 mmHg.
  • pH is 7.35 or less

a medical diagnosis not a disease (caused by some other issue - like exacerbation of chronic COPD/asthma, a PE > V/Q mismatch)

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2
Q

Two Types of Respiratory Failure

A

Hypoxemic = PaO2 is 50 mmHg or less

Hypercapnic = PaCO2 is 50 mmHg or greater

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3
Q

Hypoxemic Respiratory Failure: Causes

A

respiratory issue

cardiac issue

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4
Q

Hypercapnia Respiratory Failure: Causes

A
  • respiratory issue
  • CNS issue (such as decrease in ventilation. When ventilatory rate decreases, causes CO2 to rise. Could be caused by something wrong with nervous system like spinal chord injury, drugs like opioids that have caused decrease in respiratory rise in pt > RR to decrease > build up of CO2)
  • Chest Wall injury (pneumothorax, chest trauma injury, flail chest > pt is not able to increase ventilatory rate or breaths are shallow > can’t open alveoli > build up of CO2 b/c pt is not taking deep enough breaths and exhaling enough CO2 > hypercapnia)
  • Neuromuscular System (Guillain-barre syndrome, MS, lou gehrig’s disease > decrease in pt’s ability to maintain RR so they can expel CO2)
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5
Q

Causes of ARF

A

Direct:

  • smoking inhalation
  • near drowning
  • aspiration (of one’s own secretion, or aspiration that occurs in drowning)

Indirect:

  • toxins
  • ischemia
  • sepsis
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6
Q

Signs of ARF

A

Neuro signs first (pt is not getting enough O2 to brain):

  • HA
  • irritability
  • confusion
  • increasing somnolence, coma

then:

  • cyanosis
  • dyspnea
  • exhaustion
  • tachycardia
  • hypotension
  • cardiac dysrhythmias

Seen in those w/ right or left HF:

  • peripheral edema
  • neck vein distention
  • hepatomegaly
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7
Q

Major Lung Sounds Heard

A
  • wheezing: caused by constriction or inflammation of the bronchial tree itself
  • rhonchi: caused by mucus accumulating in bronchial tree, may clear with cough
  • rales/crackles: caused by fluid in alveoli or in the interstitium of alveoli
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8
Q

ARF/ARDS Leads to:

A
  • organ failure
  • MODS (multi-organ system disorder syndrom)
  • 50% mortality rate
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9
Q

ARF/ARDS: Tx

A

diuretics - to pull fluid out of interstitium and out of alveoli themselves

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10
Q

V/Q Mismatch: Causes

A
  • absolute shunt, no ventilation d/t fluid (or secretions) filling the alveoli
  • V/Q mismatch: ventilation partially compromised by secretions in the airway (small mucus plug > partial compromise (some cells can pick up O2 and some cannot))
  • V/Q mismatch: perfusion partially compromised by emboli obstructing blood flow (perfusion issue, clot in pulmonary capillary bed itself > perfusion isn’t going to occur)
  • Dead space, no perfusion d/t obstruction of the pulmonary capillary (PE > no perfusion getting to alveoli at all)
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11
Q

Two Types of Shunting

A

Anatomic Shunt

Intrapulmonary/Absolute Shunt

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12
Q

Anatomic Shunt

A

blood passes through an anatomic channel in the heart and bypasses the lungs

  • blood cells not picking up O2 on the way
  • no perfusion, ventilation
  • something is causing shunt
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13
Q

Intrapulmonary/Absolute Shunt

A
  • anatomical issue
  • blood flows through the pulmonary capillaries without participating in gas exchange
  • it is seen in conditions in which the alveoli fill with fluid
  • when O2 is given, you do not see improvement in pulse ox or blood gases

*hallmark of shunting is a hypoxemic patient who does not improve with oxygen

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14
Q

ARF: Tx

A

tx underlying cause (like bronchodilators for asthmatic)

goal:
- maintain adequate CO
- SBP > 90 and MAP > 65
- stable lab values

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15
Q

ARF: Ventilation Problem

A

secretion or fluid in alveoli or vasoconstriction

pt is unable to ventilate d/t tightly constricted bronchial tree

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16
Q

ARF: Perfusion Problem

A

pulmonary embolism, or small mini clots in the capillary bed of the pulmonary bed

happens frequently in pts w/ sickle cell anemia

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17
Q

Sepsis

A

a life-threatening organ dysfunction caused by dysregulated host response to infection

sepsis starts somewhere locally (pneumonia, wound infection, UTI, etc)

result of sepsis = ARF

underlying cause of a lot of ARDS = sepsis (usually from pneumonia)

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18
Q

Septic Shock

A

subset of sepsis-induced in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality

persisting hypotension requiring vasopressors to maintain MAP > 65 mmHg and serum lactate > 2 mmol/L despite adequate volume resuscitation

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19
Q

Uses for an Arterial Line?

A
  • put them in pts who are ventilated and want to get serial ABGs (better to do this in existing arterial line rather than continuing to stick pts radial artery)
  • titrate vasoactive drugs, treating and titrating drugs according to arterial BP from beat to beat, instead of consistently cycling BP cuff
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20
Q

Goals for Treating Patients w/ ARF

A
  • maintain a patent airway (ET Tube)
  • optimize O2 delivery (ET tube and ventilator)
  • minimize O2 demand (by breathing for pt, give pain and sedation meds so they aren’t working against vent)
  • prevent complications
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21
Q

Meds for ARF

A
  • bronchodilators (if needed)
  • corticosteroids (to decrease inflammation of lungs)
  • antibiotics (for pneumonia - draw blood and sputum cultures first)
  • expectorants (loosen mucus especially w/ pneumonia)
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22
Q

Predisposing Conditions to ARDS

A

direct: pneumonia (could be aspiration pneumonia)

indirect: sepsis or TRALIs (transfusion related acute lung injuries)
* pt can go into acute respiratory failure b/c of blood transfusion reaction

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23
Q

Types of Pneumonia

A

CAP: community acquired
HAP: hospital acquired
VAP: ventilator associated

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24
Q

Primary Preventions in the Community to Prevent Pneumonia

A 
flu shot
pneumonia vaccine (if they are over 65)
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25
Q

Biggest Pesonnel-Related RF for VAP Development

A

Handwashing

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26
Q

Nursing Diagnosis w/ ARDS

A
  1. impaired gas exchange
  2. ineffective airway clearance (pts inability to expectorate their secretions)
  3. ineffective breathing patter (RR is labored)
  4. dysfunctional ventilator weaning response
  5. alteration in nutrition
    - risk for imbalance fluid volume r/t sodium and water retention
27
Q

NIPPV

A
  • used in tx of pts w/ acute or chronic respiratory failure
  • pt doing work of breathing
  • mask placed tightly over the pts nose or nose and mouth (if not intubated) and the pt breathes spontaneously while positive pressure is delivered

-if intubated, pt breathes through ET tube while on NIPPV mode

CPAP or biPAP

28
Q

Positive Pressure Ventilation

A

BiPAP: bilevel positive airway pressure (different pressure level for inspiration and expiration

CPAP: continuous positive airway pressure (same pressure that is being delivered on inspiration and expiration - no change in pressure)

29
Q

Contraindications of NIPPV

A
  1. absent respirations (pt has to be initiating breathing)
  2. excessive secretions (secretions would fill up in mask and removing it would cause loss of pressure and then O2 will drop)
  3. decrease LOC (unless they are on palliative comfort care)
  4. increased O2 requirements (it can only go up to 42% FiO2, if pt requires more than this then they need to be intubated)
  5. facial trauma (b/c of mask and how tightly it has to be against the face so it’s not leaking)
  6. hemodynamically unstable
30
Q

High Flow Nasal Cannula

A
  • heated and humidified O2
  • high flow rates of gas delivered to match pt’s inspiratory flow demands.
  • pt preferred b/c it’s less invasive compared to CPAP or BiPAP
31
Q

Drug Therapy for ARDS

A
  • albuterol (bronchospasms)
  • corticosteroids (airway inflammation)
  • antibiotics (pulmonary infection)
  • meds to reduce anxiety, pain, and agitation
32
Q

When would a Pt need Intubation:

A
  • has airway obstruction
  • lacks protective reflexes
  • needs suctioning
  • needs ventilation assistance
33
Q

What can you use to maintain airway patency?

A
  • oral airway (only on pt’s who are unconcious)
  • nasal trumpet for pts who are concious
  • then bag for pt until advanced airway can be placed
34
Q

What is needed in a pt’s room to manage airway?

A

O2

suction and suctioning equipment

35
Q

Intubation: Definition

A

used for absence of respiratory effort or when apnea is anticipated

ET tube (ETT): control airway

  • size of tube is based on pt size
  • men = 8-9
  • women = 7.5-8
36
Q

Medication used for Intubation

A

neuromuscular blocking agent (block acetylcholine):

  • Succinylcholine chloride “sux”
  • Pancuronium bromide
  • Vecuronium bromide
  • Atracurium
  • can be given by RN under direction of provider
  • *Pt must be sedated prior to admin

Sedative agents:

  • etomidate
  • ketamine
  • versed
37
Q

How do you secure the ETT?

A
  • shave skin if necessary
  • apply barrier cream to protect skin and help device stick to skin
  • inflate lungs and listen to ensure both lungs are being properly inflated
  • look for color change on CO2 detector
  • tape down or use commercial device to secure
  • chest x-ray to verify placement
38
Q

What info do you want as the critical care nurse regarding the pt’s airway and ventilation?

A

ETT:

  • size
  • location (the measurement of how deep it is and where that measurement was taken at - lips? teeth?)

Ventilator:

  • mode
  • rate
  • FiO2
  • Tidal Volume
  • PEEP
39
Q

Complications of Mechanical Ventilation

A
  • plugged or kinked tubing
  • ETT/trach cuff rupture
  • decreased CO (b/c we are giving pt positive pressure, we are pushing ventilation in them > extra pressure in chest wall that presses on superior vena cava > decrease venous return to heart > decreased CO)
  • VAP
  • barotrauma/ pneumothorax
  • Stress ulcer and GI bleed
  • Na and H20 retention
  • nutrition problems
  • failure to wean
40
Q

Goals of Mechanical Ventilation

A
  • correct potentially life-threatening ABGs and acid-base abnormalities
  • provide support during Broncho-active pharmacologic therapy
  • rest respiratory muscles, allowing recovery from fatigue
  • use sedation only if necessary (if fighting the ventilator, pts withdrawing from alcohol/narcotics/other substances will fight ventilator)
41
Q

Ventilator Settings

A

FiO2 = concentration of O2 delivered (30%-100%)

PEEP = positive end expiratory pressure

  • restores functional residual volume to allow for diffusion of gases
  • can effect CO and lower BP

Tidal Volume = amount of gas delivered with each breath (avg = 5-7 mL/kg)

Rate = breaths per minute delivered to the pt

  • mode is dependent on pt condition/desired volume
  • ordered by provider and monitored by RT
42
Q

Ventilator Volume Modes

A

Principle: delivers a preset volume with every breath

Disadvantage: volume is delivered regardless of the pressure required

  • could be a reason why the pt is fighting the ventilator
  • pt may require volume but pt may fight volume even though they need it, therefore they may be heavily sedated

Normal Tidal Volume (Vt)

  • 8-12 mL/kg
  • 6mL/kg in ARDS - lower volumes for critically ill pts b/c we don’t want to hyperinflate their lungs
43
Q

Positive Pressure Mode of Ventilation

A

Volume Control:

  • Assist Control (AC): volume set on all breaths
  • Spontaneous Intermittent Mode of Ventilation (SIMV): volume set on ventilator breaths, but if pt generates volume on spontaneous breaths, it won’t give them more than that set breath

Pressure Control:

  • Pressure Control ventilations: RR is set, Pt is going to breathe on their own and if pt breathes over set rate, that’s fine
  • Pressure Support Ventilation: no RR is set, pt is doing all breathing on their own, only getting pressure (this mode is used for weaning)
44
Q

Oxygen Toxicity

A

risk for oxygen toxicity increases when FiO2 is greater than 60% for more than 48 hours

  • which is why we are always checking PaO2 via ABGs
  • nitrogen gas keeps alveoli open
  • no NO > alveolar instability and atelectasis

leads to:

  • increased pulmonary microvasculature permeability
  • decreased surfactant production and surfactant inactivation
  • fibrotic changes in alveoli
45
Q

PEEP

A
  • amount of pressure in our alveoli after we fully exhale
  • applies positive pressure at the end of expiration
  • decreases intra-pulmonic shunting
  • 5cm = “physiologic”
  • allows for decrease in FiO2 (opens the alveoli)
  • allows for gas exchange to occur between CO2 and O2
  • increased in 5-10cm increments in adults
  • wean slowly so lungs don’t collapse when pressure is suddenly gone
46
Q

Disadvantages of PEEP

A

may cause:

  • barotrauma
  • pneumothorax
  • decrease venous return to the heart & CO

if breaths are stacked (pt is unable to completely exhale before ventilator delivers another breath) > increase in pressure in chest wall > barotrauma and pneumothorax

47
Q

What to do when ventilator alarm is going off?

A
  • assess pt regularly and anytime the ventilator alarm sounds
  • cause of alarm can be dysfunction anywhere from lungs to the machine
  • troubleshooting is carried out in systemic manner, starting with pt and moving towards the ventilator
  • if alarm continues to sound and cause cannot be determined, or if pt is in respiratory distress, assumes it’s ventilator issue and disconnect pt from ventilator and manually ventilate w/ BVM until RT can replace the ventilator
48
Q

High-Pressure Alarm

A

increased resistance somewhere in the system
-check from lungs to the ventilator

caused by:

  1. secretions (suction w/ closed tracheal suction system)
  2. pt biting on ET tube (no bite block so ventilation can’t reach pt lungs)
  3. Pneumothorax: ventilator can’t deliver ventilation to pt lung if it’s collapsed
  4. Condensation in tubing (need to remove this, DO NOT empty water back into humidifier reservoir, reservoir has sterile water in it, condensation is not sterile)
49
Q

Low-Pressure Alarm

A

the system is not reaching minimal pressure required for ventilation
-check from lungs to the ventilator

caused by:

  1. tubing disconnection (ET tube is not connected to ventilator)
  2. Extubation (ventilator is trying to administer O2 but it’s not getting to pt)
  3. Air leak (ET tube cuff leak, O2 is not reaching lungs and leaking out of cuff)
50
Q

Dyspnea Causes, Assessment, and Preventions

A
  • cause = most common is dysynchrony > respiratory distress and dyspnea
  • assess: is it pain/anxiety causing the asynchrony? are they short of breath?
  • preventions: adjust machine to the pt, opioids, mind-body interventions
51
Q

Ventilator Principles to Reduce Risk of Complications

A
  • suction only when needed to keep the number of passes at a minimum
  • aseptic technique
  • never enter the trachea w/ catheter that has been contaminated w/ oropharyngeal secretions
  • hyperoxygenate w/ 100% FiO2 before and after suctioning
  • limit suction time to 10-15 seconds
  • always observe for any adverse affects during suctioning
  • stop immediately if there is change in cardiac rate, rhythm, or pt color
  • observe pulse ox and use it as guide for oxygenating during passes
52
Q

Complications of ETT Suctioning

A 
tissue trauma
hypoxemia
cardiac dysrhythmias
atelectasis
pneumonia
bronchoconstriction
tracheitis
53
Q

Weaning Parameters

A
  • acceptable ABGs
  • tidal volume > 10mL/kg
  • VC > 15 mL/kg
  • FiO2 requirement is less than 0.5
  • max inspiratory pressure > 220cm H2O
  • resolution of underlying disease process
  • able to follow commands
  • secretions under control
  • pt is able to protect airway
  • hemodynamically stable
  • normal Hct (>30%)
  • weaning trials may consist of PS trials, T-piece, or trach collar trials
  • observe pt closely for signs of respiratory distress and increased effort to breathe
54
Q

Goal of NMBAs

A

administer the lowest dose for the shortest time

Peripheral nerve stimulator (Train of Four): goal = 2-1 twitches

  • 0 twitches = 100% blockade
  • 1 twitch = 90% blockade
  • 2 twitches = 75-80% blockade
  • 3 twitches = 75% blockade
  • 4 twitches = <75% blockade
  • don’t want 0 twitches b/c that means too much blockade on board
  • don’t want 3-4 twitches b/c that means not enough blockade on board and need to titrate up
55
Q

Nursing Management during NMBA Administration

A
  • airway management and adequate ventilation
  • monitor for dysrhythmias
  • pain and anxiety (keep them well sedated during this process, if they wake up and can’t move > anxiety increases > delirium)
  • communication (they can’t communicate w/ us)
  • ROM frequently
  • eye care (lubricate w/ artificial tears and tape eyes shut to prevent corneal ulcers b/c they can’t blink)
  • extubate only w/ full recovery from NMBAs (need to be able to follow commands so we know all NMBA is out of system before extubating)
56
Q

Pulmonary Function Tests for Weaning

A

when we believe pt is ready to be disconnected from ventilator and have ET tube removed, we look at:

  • minute ventilation = VT x RR
  • alveolar ventilation
  • anatomic dead space (150mL)
  • inspiratory force (done at bedside)
57
Q

How to Prevent VAP

A
  • head of bed up at 30 degrees or higher
  • mobility (every even hour, can ambulate pts on vents in some cases)
  • oral care (brush teeth/gums/tongue 2x/day using soft toothbrush, moisturizing oral and lip mucosa every 2-4 hours, perform oral care with chlorhexidine daily)
  • PUD prophylaxis (PPIs and H2 blockers)
  • DVT prophylaxis (SCDs, lovenox, heparin)
58
Q

Two Processes Crucial to VAP Development

A
  • bacterial colonization of oral cavity

- aspiration of contaminated secretions into lower respiratory tract

59
Q

Prone Positioning

A
  • redistributes opacities from the dorsal to the ventral regions
  • ventilation is improved d/t changes in pleural pressure
  • dorsal lung is no longer subject to high pulmonary pressure and dorsal atelectasis
60
Q

Hypoxemic Respiratory Failure

A

PaO2 < 60 when the pt is receiving an FiO2 >60%

cause: acute lung injury = 300 or ARDS = 200

hallmark sign of shunting is when we are giving pt O2, but PaO2 and pulse ox don’t improve

61
Q

Lactate

A

released by cells that are going through anaerobic metabolism (not enough circulating O2 anymore > cells turning to anaerobic metabolism > lactic acid release as result of this)

-increased levels seen in pts going through sepsis

62
Q

Hypoventilation

A

increases CO2

63
Q

Hyperventilation

A

decreases CO2

64
Q

ETCO2

A

end title CO2

reading like pulse ox but it looks at end title CO2

higher it is, we know pt is hypercapnic

Critical Care (14 decks)

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