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ACS > Acute Respiratory Insufficiency > Flashcards

Acute Respiratory Insufficiency Flashcards

1
Q

What is the primary muscle involved in ventilation?

A

Diaphragm

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2
Q

What accessory muscles are used when experiencing difficulty breathing?

A

Sternocleidomastoids, trapezius, and pectoralis major

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3
Q

What is the parietal pleura? What is the visceral pleura?

A

Parietal pleura is a thin layer of tissue lining the thoracic cavity. Visceral pleura lines the outside of the lungs.

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4
Q

What is the mechanism of action of inspiration? Is it active or passive?

A

Diaphragm moves down - there is opposing pull between two pleura creating negative pressure - chest expands and pulls visceral pleura with it - there is negative space in the lungs - air rushes in
Active process

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5
Q

What is the process of expiration? Is it active or passive?

A

Diaphragm relaxes - chest wall relaxes - intrapulmonary pressure increases - air moves out
Passive process

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6
Q

What are the conducting airways?

A

Trachea, bronchi, non-respiratory bronchioles

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7
Q

What are the respiratory units?

A

Respiratory bronchioles, alveolar ducts

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8
Q

What bronchial main stem is more likely to experience an aspiration? Why?

A

Right. It branches off only at 25 degrees and is wider whereas the left branches off at 45 degrees and is more narrow.

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9
Q

Why would terminal bronchioles close?

A

They aren’t supported by cartilage or connective tissue. They are comprised of smooth muscle. If smooth muscle constricts, these airways close.

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10
Q

Describe type 1 cells in alveoli.

A

Make up 90% of SA in alveoli; very susceptible to injury. Chief structural cell.

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11
Q

Describe type 2 cells in alveoli.

A

Make up 10% of SA in alveoli but are greater in number than type 1 cells (VERY TINY). If alveoli is injured these cells divide and turn into type 1 cells. These cells produce surfactant.

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12
Q

What does surfactant do?

A

Helps keep alveoli open

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13
Q

What is the definition of resp insufficiency?

A

Inability or failure to perform normal or adequate resp function.

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14
Q

What three things are indicative of normal resp function?

A

Normal ABG, normal resp assessment/findings, effective ventilation/gas exchange (no support, on RA).

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15
Q

What are three things indicative of resp. insufficiency?

A

Normal ABG or minimal change. SOB and other abnormal cues. Starting to need some O2.

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16
Q

What are three things indicative of resp. failure?

A

Abn ABG, abn. assessment findings and SOB, need full support with NIV, mech vent, and O2.

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17
Q

What is the definition of pneumonia?

A

Acute inflammation of lung parenchyma that is caused by infectious agent that can lead to alveolar consolidation

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18
Q

How is community acquired pneumonia (CAP) described? What is a common organism? What might someones sputum look like?

A

Individual has never been hospitalized/hospitalized for LESS THAN 48 hours. It is not ususally polymicrobial. Streptococcus pneumonia is most common. Normally gram + bacteria. Sputum is thin and watery.

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19
Q

How is healthcare associated pneumonia (HCAP) described? Usually gram + or - bacteria?

A

Individual is in hospital for greater than 48 hours or receiving healthcare unit/hosp. based interventions (i.e. chemo, dialysis, wound care) or recent IV abx in past 90 days. Normally gram - bacteria.

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20
Q

Describe HAP. What does this type of pneumonia include? Describe the sections. Usually gram - or + bacteria?

A

Individual has been hospitalized >48 hours. Normally polymicrobial. Includes VAP. Copious secretions, tinted green-yellow. Usually gram -.

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21
Q

What is the criteria for VAP?

A

On mech vent for >48 hr.

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22
Q

Describe typical pneumonia. What is seen on CXR? What area of the lungs might this affect?

A

Infection from bacteria. Bacteria mutiply extracellularly in alveoli. Consolidation is seen on CXR.

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23
Q

Describe atypical pneumonia. What is seen on CXR? Where might this affect the lungs?

A

Viral, fungal, mycoplasmic infection. Inflammation in alveolar septum and interstitium of lung. On CXR seen as patchy infiltrated.

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24
Q

Fungal pneumonia is common in what type of person? What are some common causes?

A

Immunocompromised. Aspergillus and candidiasis.

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25
Q

Location of bronchopneumonia?

A

Affects clusters of alveoli in patches throughout lungs (a few alveolus affected within each bunch).

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26
Q

Location of lobar pneumonia?

A

Affects a whole lobe

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27
Q

Location of interstitial pneumonia?

A

Affects space in between alveoli, inflammation of respiratory airways

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28
Q

How can infectious agents enter the respiratory tract?

A

Inhalation, aspiration, bacteremia, translocation.

29
Q

What is translocation?

A

Gut flora mobilized via compromised gut mucosa, enters the body and leads to local and systemic infection.

30
Q

Why is aspiration a common cause of HAP (6)?

A
  1. Disrupted gag/cough reflex
  2. Alt LOC
  3. Abn swallowing
  4. Artificial airway
  5. Alt stomach pH (PPI, antacid, enteral feed all inc pH and promote bacterial growth)
  6. NG tube is a wick which allows bacteria to move from stomach to pharynx to be aspirated
31
Q

How might someone present with ARI? What might be seen in acute lung failure?

A

Inc RR, dec tidal volume, worsening ABG/O2 sats, inc HR, dec LOC, confusion, disorientation, adventitious breath sounds, cough, noisy breathing (wheeze, stridor, moaning, pleural rub), pursed-lip breathing, nasal flaring, accessory muscle use
Development of hypoxemia, hypercapnia, acidosis

32
Q

What are some diagnostics to rule out ARI?

A

Gram stain, C and S

CXR, SpO2

33
Q

How does gram + bacteria stain? Gram -? What about yeast and fungus? Do viruses stain?

A

Gram + = purple
Gram - = Pink
Yeast and fungus stains purple (+)
Viruses don’t stain as no cell wall

34
Q

What is the treatment for ARI?

A 
Primary = abx, antiviral, treat the underlying CAUSE 
Supportive = ventilation, gas exchange, maintain hemodynamic stability, decrease O2 demands
35
Q

What are things to consider with primary treatment of ARI?

A

Start ABX early if indicated. Obtain BCX first if at all possible, but if it will delay admin of abx then give abx. Start with broad spectrum abx and then narrow as results start to come in. Monitor the patient’s response to treatment. May need to change abx if not improving (persistent fevers, inc WBC, ongoing hemodynamic instability)

36
Q

What are things important to communicate in rounds when patient has an infection?

A

When Cx drawn, any new BW results, abx stop date, if pt has poor kidney fx or start dialysis (will need to change dosing)

37
Q

What is the max FiO2 someone would receive from O2 via NP at 5-6 lpm?

A

40-45%

38
Q

What is the FiO2 someone would receive via FM at 5 lpm, 10 lpm?

A

30%, 50%.

39
Q

What is the FiO2 someone would receive via FM with bag reservoir (non-rebreather) at 6, 7, 8, 9, 10 lpm?

A

60, 70, 80, 80-100%, 80-100%

40
Q

When might oxygen toxicity become a problem?

A

Breathing FiO2 >50% for >24 hours

41
Q

How does oxygen toxicity occur?

A

O2 is metabolized and free radicals are produced which are toxic. Normally lung enzymes would clear, but too much O2 metabolites overpower enzymes and begin to damage lung tissues and vasculature.

42
Q

What are symptoms of O2 toxicity in eyes, central, muscular, and respiratory?

A

Eyes: visual field loss, near sightedness, cataract formation, bleeding, fibrosis.
Central: seizures
Muscular: twitching
Resp: jerky breathing, irritation, coughing, pain, SOB, tracheobronchitis, ARDS

43
Q

If a patient has a pneumonia, how do we want to position them in bed? Why?

A

Good lung down. It is related to perfusion. Gravity will bring more perfusion down to the “good lung” that is down and the best ventilation will be maximized with perfusion to help oxygenation.

44
Q

What is the idea behind proning a patient?

A

Exudate tends to move to posterior side of lung. By proning, blood flow will move to area of lung (anterior) that is less affected by exudate which supports ventilation and oxygenation.

45
Q

What are PaO2 values of mild hypoxemia, moderate, and severe?

A

Mild: 60-80
Moderate: 40 - 59
Severe: <40

46
Q

What is something to consider in O2 therapy for a patient with COPD?

A

Ventilation can be suppressed by supplemental O2 (disrupts their dependence on “hypoxic drive” as a ventilatory regulator. BUT, it is not acceptable to withhold O2 from COPD pt when it is indicated particularly on a basis of small possibility it may suppress ventilation.

47
Q

What is resorption atelectatis?

A

Quick burst of high FiO2 washes out nitrogen which usually splints alveoli open (as it does not move into bloodstream well) without alveoli splinted open they collapse. This process accelerates as more atelectasis of alveoli occurs.

48
Q

What is the criteria for NIPPV?

A 
Mod-severe WOB
RR >24 in individuals who are hypercapnic, or >30 in individuals who are hypoxemic
Accessory muscle use
Paradoxical breathing 
ABG changes (pH <7.35, PaCO2 >45)
PaO2/FiO2 ratio <200
49
Q

What are absolute contraindications to NIPPV (5)?

A
  1. Resp arrest
  2. Hemodynamic instability (as will cause further instability)
  3. Frequent arrhythmias (hemodynamic instability)
  4. Uncontrolled ACS
  5. Uncontrolled GI bleed
50
Q

What are 8 relative contraindications to NIPPV?

A
  1. Unable to protect airway
  2. Inc aspiration risk
  3. Excessive secretions
  4. Agitation, lack of cooperation
  5. Unable to fit mask
  6. Facial hair
  7. Facial trauma or burns
  8. Recent UGI bleed or surgery on airway
51
Q

How are CPAP, PEEP, EPAP all similar? How do they support oxygenation (7)?

A

All provide CONSTANT positive pressure on airway during entire respiratory cycle.
Thin A-C membrane, prevent alveoli from collapsing, increase alveolar SA, open collapsed/underventilated alveoli, keep alveoli open so they can participate in gas exchange, increases FRC, support lung compliance

52
Q

IPAP supports _______ EPAP supports _____

A

Ventilation, oxygenation

53
Q

How does IPAP support ventilation? When is IPAP delivered? What would we want to monitor to ensure our IPAP is effective?

A

Increases TIDAL VOLUME, also dec WOB
Delivered for duration of inspiration
Want to monitor PaCO2 levels (indicator of ventilation)

54
Q

What are some key things about CPAP?

A

Patient sets own breathing rate (spontaneous) and depth, continuous PAP during entire resp. cycle, promotes gas exchange by thinning AC membrane

55
Q

What are some key things to remember about BiPAP?

A

Employs different pressure for inspiration and expiration
Can set minimum RR (backup rate) to give breaths if minimum rate not met. Will alarm if this occurs.
Can set FiO2

56
Q

How does EPAP support oxygenation? When is it triggered? What is the typical pressure started for EPAP? What do we want to monitor while someone receives EPAP?

A

Thins the AC membrane, supports lung compliance, and constantly applies pressure to alveoli to keep open and improve SA for gas exchange
Triggered by expiration. Pt can breathe out until preset pressure which will prevent alveoli from completely emptying
Usually 5 cm H20 to start
Monitor PaO2 levels (indicator of oxygenation)

57
Q

The difference between IPAP and EPAP is what?

A

The amount of INSPIRATORY SUPPORT we are providing

58
Q

How does BiPAP affect hemodynamics?

A

Postive pressure exerted - increases intrathoracic pressure - dec venous return - dec preload - dec contractility - dec CO - dec BP

59
Q

What can be done to prevent an affect on hemodynamics when starting BiPAP?

A

Fluid bolus

60
Q

Why is BiPAP beneficial for a patient with CHF?

A

Can help with fluid overload in lungs. Decreased preload will help improve contractility in the CHF patient. Will help offload fluid from lungs as blood is pumped more effectively throughout the body by the heart.

61
Q

What is something to consider before discontinuing BiPAP? Especially in someone who has CHF?

A

IV lasix to ensure there is no flash pulmonary edema from fluid rushing back into the lungs once the pressure is discontinued.

62
Q

What are some cautions with BiPAP/CPAP?

A

Pt must be able to remove own mask (in case of emesis) as is a large aspiration risk, be cautious with administration of sedation and narcotics as patient needs to be able to protect their own airway

63
Q

When might we consider weaning from BiPAP?

A

Underlying reason resolved or under control, ABG improved, accessory muscle use greatly diminished, CXR poss. improved, hemodynamics stable (BUT need to monitor for pulmonary edema once discontinuing - consider IV lasix 1 hour before d/c)

64
Q

What does the weaning process of BiPAP look like?

A

Switch to CPAP first then try sprints without/keep on at night to support rest

65
Q

Why might the individual feel worse when BiPAP comes off?

A

They will be working harder to breathe than with BiPAP on and will look like they’re working a bit harder. Need to reassure them. It may be uncomfortable.

66
Q

What might support external lung compliance, internal lung compliance, resp. muscle function? (all aspects of ventilation on O2 S and D)

A

External: PEEP/CPAP/EPAP
Internal: PEEP/CPAP/EPAP
Resp. muscle: PEEP/EPAP/CPAP (increased FRC) and IPAP

67
Q

If a patient is already on BiPAP, but based on their ABG, changes need to be made to support their oxygenation, why might you go up on both IPAP and EPAP, and not solely EPAP?

A

Because if going up solely on EPAP, the difference between IPAP and EPAP decreases, which means we have just decreased inspiratory support which would DECREASE ventilatory support and we would likely see negative impacts in their PaCO2 levels
Always increase the two together especially if we are worried about ventilation in our patient. If we are not concerned about ventilation at all in our patient we can consider increasing EPAP alone. If we are happy with our gap of 10 between the two, for example, increase both numbers to keep same amount of support, if we need more support, go up on gap (like increasing IPAP).

68
Q

What is something important to remember when making changes to BiPAP? Please provide examples.

A

Identify the problem on the ABG first (ventilation, oxygenation, or both) and then make changes to BiPAP settings based on our problem. If vent is an issue, we would want to increase IPAP or increase the gap between IPAP and EPAP. If oxygenation is an issue, we would want to increase EPAP or FiO2.
If at all possible, try to make changes ONE AT A TIME so we can see what the effect of each change is.

ACS (3 decks)

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