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Respiratory Failure Flashcards

1
Q

Acute PE is a condition of impaired:

A

Perfusin

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2
Q

4 Components of Pathophysiology of PE

A
  1. large thrombi obstruct perfusion in the pulmonary artery or its branches
  2. blockage
  3. increased neutrophils due to the inflammatory response lead to increased platelet activating factor
  4. increased intrapulmonary shunting
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2
Q

Pulmonary Pressure

A

type of high blood pressure that affects the arteries in the lungs and the right side of the heart

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2
Q

Virchow’s Triad

A
  1. Hypercoaguable State: increased ability to clot
  2. Venous Stasis: pooling of blood/low flow rate
  3. Vessel injury: inflammatory response at that site
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2
Q

D-Dimer Lab for PE dx

A
  • Indicative of fibrin (holds clot together) degradation (fibrinolysis= thrombolysis)
  • Non-specific – indicates clot; not location
  • Lab indicates body trying to get rid of a certain clot
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2
Q

5 PE Symptoms

A
  1. dyspnea/SOB
  2. VQ mismatch
  3. tachycardia
  4. pleuritic chest pain
  5. pleural friction rub
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3
Q

The blockage that occurs in PE leads to what 5 things:

A
  1. increased pulmonary pressure (pressure on right side of heart)
  2. increase resistance to blood flow in right ventricle
  3. increased right ventricle workload
  4. decreased lung perfusion
  5. RSHF if right ventricle cannot pump against the pressure
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4
Q

Intrapulmonary shunting

A

Occurs in PE

develops when blood passes through the lungs but fails to take part in gas exchange. Goes from right side of the heart to the left side of the heart without being oxygenated

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5
Q

Gold Standard for PE dx

A

CT PE (with contrast)– Pulmonary angio

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6
Q

What would you expect in initial v. later on ABG of patient with PE?

A

Initially: blowing off CO2 with increased RR to compensate– respiratory alkalosis

Long-term: likely will enter respiratory acidosis

PaO2: low/hypoxemic

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7
Q

Interventions for massive PE that treat ventilation/diffusion vs. perfusion

A

ventilation/diffusion: high flow O2 and mechanical ventilation

perfusion: anticoagulants and thrombolytics

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8
Q

True or False; every PE patient will receive thrombolytic therapy

A

False: risk for bleed is too great; body cannot clot at all on this medication. Stable patients will only receive anticoagulants

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9
Q

Complications of PE

A
  1. Cor Pulmonale/RSHF
  2. Shock
  3. Pleural Effusion
  4. Respiratory Failure
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10
Q

Why is shock seen as complication of PE?

A

Increased right sided workload can lead to obstructive shock

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11
Q

Why is pleural effusion seen as complication of PE?

A

Area of lung is not getting oxygen (ischemic portion) induces inflammatory response (increased permeability and fluid)

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12
Q

Why does respiratory failure occur as a complication of PE?

A

VQ mismatch

  • well ventilated portion of the lung is not getting perfused because of blockage in PA
    > failure to oxygenate blood (type 1 hypoexemic)
    > if massive - increased alveolar deadspace/failure to ventilate = type 2 (hypercapnic)
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13
Q

How does respiratory distress/insufficiency differ from acute respiratory distress?

A

Body has used up its ability to compensate; bradycardia may begin

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14
Q

Type 1 Respiratory Failure

A

Oxygenation/Hypoxemic Resp Failure

PaO2 < 60mmHg

Pneumonia, ARDS, restrictive

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15
Q

Type 2 Respiratory Failure

A

Ventilation Failure/Hypercapnia

PCO2 > 50
pH < 7.35
Obstructive disorders

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16
Q

4 Points of Pathophysiology of Respiratory Failure

A
  1. Some disease process (can be any) alters lung function
  2. V/Q mismatch leads to decreased PaO2
  3. Body increased RR/depth to compensate, increasing PaO2 and decreasing PaCO2
  4. As a result of compensation, metabolic rate increases- - more oxygen consumption by tissues and more CO2 produced - leads to failure of compensatory mechanism as we are already trying to remove CO2
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17
Q

3 Points of Clinical Criteria to be diagnosed respiratory failure

A

PaCO2 > 50mmHg

pH <7.30

PaO2 <60mmHg

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18
Q

Identify the 3 primary organs and describe the overall effects of respiratory failure on them

A

Primary Organs: lungs, heart, brain

Usually, body shunts oxygen to just these organs

Are prioritized but still NOT getting oxygen they need

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19
Q

Effects of oxygenation (T1RF) failure on pulmonary system

A

o Dyspnea
o Tachypnea
o Increased pulmonary vascular resistance

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20
Q

Effects of oxygenation (T1RF) on CVS

A

o Increased BP
o Increased HR
o Dysrhythmias
o Weak thready pulse
o Cyanosis

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21
Q

Effects of oxygenation failure (T1RF) on CNS

A

o Altered LOC
o Restlessness
o Confusion

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22
Q

Effects of ventilation failure (T2RF) on pulmonary system

A

tachypnea or bradypnea

23
Q

Effects of ventilation failure (T2RF) on CVS

A

o Bounding pulse
o Increased BP
o Increased HR

24
Q

Effect of ventilation failure (T2RF) on vascular

A

o Headache
o Flushed, wet skin

25
Q

Effect of ventilation failure (T2RF) on CNS

A

CO2 Narcosis !! Buildup on CO2 in brain

CO2 major vasodilator leading to hypoperfusion worsening hypoxia)
o Lethargy
o Drowsiness
o Coma

26
Q

Interventions for Respiratory Failure

A

EMERGENT - ABC

  1. maintain/establish airway (GCS < 8 = intubate)
  2. oxygenate
  3. Correct A/B balance
  4. Support the systems (CV with fluids)
  5. Treat cause of failure
  6. Prevent and control complications
27
Q

How would you oxygenate a patient in respiratory failure?

A

FiO2 to increase PaO2 - DIFFUSION

Add pressure to fully VENTILATE more areas of the lung

28
Q

ARDS is a type of acute respiratory failure with these 5 features:

A
  1. persistent hypoxemia even with 100% oxygen
  2. decreased pulmonary compliance
  3. dyspnea
  4. bilateral pulmonary edema
  5. dense pulmonary infiltrates on x-ray.
29
Q

ARDS often occurs after:

A

an acute lung injury related to other conditions,

30
Q

ARDS is severe, often fatal, _________ of the lung

A

inflammation

31
Q

How does inflammation in ARDS (caused by other conditions) worsen the condition?

A

Inflammation = cytokine release = increased permeability = fluid leakage in to interstitial space

32
Q

How does the fluid leakage in interstitial spaces in ARDS affect oxygenation?

A

Fluid in interstitial space not allowing for adequate diffusion across membrane

33
Q

ARDS is sudden onset of __________ and _________ not due to _____

A
  1. pulmonary edema
  2. respiratory failure
  3. heart failure
34
Q

4 Components of Berlin Definition of ARDS

A
  1. timing
  2. chest imaging
  3. origin of edema
  4. oxygenation
35
Q

Describe the timing to be diagnosed with ARDS

A

Within 1 week of known clinical insult or worsening resp symptoms

36
Q

Describe the chest imaging to be diagnosed with ARDS

A

Bilateral opacities- not fully explained by effusions, collapse, or nodules. Happening throughout entire lung fields, not contained patho. It is everywhere!!!

37
Q

Describe the origin of edema to be diagnosed with ARDS

A

Resp failure NOT fully explained by cardiac or fluid overload

Widespread inflammatory response causing fluid all over the lungs; no other cause

38
Q

Describe the oxygenation to be diagnosed with ARDS

A

Hypoxemia even with 100% FiO2 (refractory hypoxemia)

39
Q

Direct Risks for ARDS

A

(in lungs)
* Pneumonia
* Aspiration of gastric contents
* Inhalation injury
* Pulmonary contusion
* Pulmonary vasculitis
* Drowning

40
Q

Indirect Risks for ARDS

A

(outside lung – usually systemic inflammatory responses)
* Non-pulmonary sepsis
* Major trauma
* Pancreatitis
* Severe burns
* Non-cardiogenic shock
* Drug overdose
* Multiple transfusions

41
Q

The direct and indirect risks for ARDS lead to

A

Lung Inflammation in 3 Phases: exudative, proliferative, and fibrotic

42
Q

Exudative Phase of ARDS

A

Neutrophils migrate into the alveoli in response to inflammatory stimulus, interfering with surfactant production (causing alveoli collapse), tissue edema/destruction (impairing gas exchange), inability of capillaries to absorb fluid (pulmonary edema), and thickening of alveoli in body’s attempt to heal (impairing diffusion)

43
Q

Proliferative Phase of ARDS

A

Body attempts to heal damage. If it is not successful, the tissue transitions to the fibrotic phase

44
Q

Fibrotic Phase of ARDS

A

Inadequate healing results in long term pulmonary damage

45
Q

ARDS can affect affect all organ systems because of

A

Hypoxemia

46
Q

If ARDS is accompanied by decreased CO, you can expect:

A

Hypo-Perfusion/Shock

47
Q

What oxygenation and ventilation support occur for ARDS

A
  1. POSITIVE PRESSURE - PEEP/intubation/CPAP
  2. Prone positioning
  3. ECMO
48
Q

How do you support the rest of the systems in ARDS management?

A
  1. assure hemodynamic stability: vasopressors, diuretics & conservative IV fluids– negative or neutral
  2. decrease O2 consumption
  3. fever/pain control
  4. nutrition
  5. prevention complications such as DVT or VAP
49
Q

How do you increase supply in a patient’s oxygenation status

A
  • Supplemental oxygen
  • Invasive or non-invasive mechanical ventilation when necessary
  • Suction tracheal secretions
  • Monitor for and correct acidosis
  • Positioning
50
Q

How do you decrease demand in a patients oxygenation status

A
  • Minimize O2 consumption
  • Limit physical activity and nursing interruptions, provide adequate time for rest
  • Administer sedation – decrease response/stimulation for less energy utilization
  • Control fever
  • Reduce anxiety
51
Q

Why is prone positioning used to increase oxygenation?

A
  • Alveoli recruitment (pops them back open) of posterior lungs
  • Heart and abdominal organs shift off lung tissue
  • Indicated EARLY in ARDS
52
Q

What is BiPAP?

A

(Bilevel positive airway pressure) – non invasive

Non-invasive mechanical positive pressure ventilation - 2 settings

53
Q

Describe the 2 pressure settings on BiPAP

A

1 setting for inhalation (high pressure/ipap) giving more pressure to help person breathing

1 setting for exhalation (lower pressure/epap) less pressure but still keeps alveoli open

54
Q

What is CPAP?

A

Provides a continuous level of positive airway pressure for a spontaneously breathing person

Continuous state of blowing to keep airways open
* 1 pressure setting

55
Q

When is mechanical ventilation used and what are the settings on the device?

A
  • When we can no longer maintain airway or gas exchange
  • Highly invasive
  • Many settings, including FiO2, PEEP, RR, tidal volume
56
Q

What is PEEP?

A

Positive end-expiratory pressure (PEEP)

The positive pressure that will remain in the airways at the end of exhalation that is greater than the atmospheric pressure in mechanically ventilated patients

57
Q

What does PEEP do?

A

Prevents collapse of alveoli (key issue with ARDS) and recruits alveoli “pops them back open”

58
Q

A patient on PEEP likely has problems with:

A

In problems with surfactant – without surfactant cannot stay open

59
Q

What happens when PEEP is low?

A

Alveoli collapse/atelectasis

Decreases oxygen diffusion due to less surface area and more pressure will be needed to re-expand alveoli leading to atelectotrauma

60
Q

5 Points on Preventing Ventilator-Acquired Pneumonia

A
  1. elevate HOB 30-45
  2. daily assessment of readiness to extubate/sedation vacation
  3. oral care with chlorhexidine
  4. DVT prophylaxis
  5. peptic ulcer prophlyaxis

High Acuity (20 decks)

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