Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pipi&pi3 > ARF and ARDS > Flashcards

ARF and ARDS Flashcards

1
Q

What is Acute Respiratory Failure (ARF)?

A
  • State of disturbed gas exchange resulting in abnormal ABG
  • Condition that develops rapidly with little time for physiologic compensation

PaCO2 is the most important criteria in labelling RF
- PaCO2 < 60 mmHg
~ Hypoxemia
- PaCO2 > 50 mmHg
~ Hypercapnia
- pH <7.35 when px is on room air

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the types of ARF?

A

Type I (Failure of oxygenation/perfusion)
- PaCO2 < 60 mmHg but PaCO2 is normal/low
~ Hypoxemia w/o hypercapnia

Type II (Failure of ventilation)
- PaCO2 < 60 mmHg + PaCO2 > 50 mmHg
~ Hypoxemia w hypercapnia

Type III (due to lung atelectasis)
- Common perioperatively
~ After GA, dec in functional capacity can lead to collapse of lung units

Type IV (due to hypoperfusion of resp. muscles in shock)
- Px in shock often experience resp. distress due to pulmonary edema, lactic acidosis and anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the pathophysiology of hypoxemia?

A

1) Diffusion limitation
- O2 con. is alveoli is unchanged/unaffected, but gas transfer ability is impaired

2) Alveolar hypoventilation
- Lungs do not adequately exchange gases due to insufficient ventilation of the alveoli

3) Low inspired oxygen
- eg in commercial flights

4) V/Q mismatch
- a) Impaired ventilation, preserved perfusion
~ Area of the lung can receive little ventilation in comparison to the amount that can be perfused
- b) Impaired perfusion, preserved ventilation
~ PE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the pathophysiology of hypercapnia?

A
  • Due to alveolar hypoventilation
  • If the capacity of muscle pump is slightly > load, uncomfortable compensation occurs
    ~ Dyspnoea
  • If capacity of pump < load, body is unable to compensate
    ~ Respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the common causes of Type I ARF?

A
  • V/Q mismatch
    ~ Imbalance between ventilation (V)—the air reaching the alveoli—and perfusion (Q)—the blood flow reaching the alveoli for gas exchange in the lungs
    ~ Eg PE
  • Alveolar hypoventilation
  • Diffusion problem
  • Shunt
  • Bronchial asthma
  • Emphysema
  • Bronchitis
  • Pneumonia
  • PE
  • HF
  • ARDS Type I/II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the common causes of Type II ARF?

A
  • ^ airway resistance
    ~ eg COPD
  • Reduced WOB
  • Dec in area of lung for gas exchange
    ~ eg bronchitis
  • Neuromuscular problems
    ~ Myasthenia gravis
    ~ GBS
    ~ Spinal cord trauma
  • CNS depression
    ~ Head injuries
    ~ Drug overdoes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the early clinical signs of ARF in general?

A
  • Restlessness, fatigue
  • Headache
  • Dyspnea, use of accessory muscles, paradoxical breathing
  • Tachypnea
  • ^ BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the late clinical signs of ARF in general?

A
  • Confusion
  • Central cyanosis
  • Diaphoresis
  • Tachycardia
  • Tachypnea, respiratory arrest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the complications of respiratory failure?

A
  • Chronic RF -> Pulmonary vasoconstriction -> Pulmonary arterial hypertension -> Right ventricular function impaired -> Right heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What investigations are done for respiratory failure?

A
  • ABG
  • FBC
  • U/E/Cr
  • CXR
  • Lung CT
  • Sputum, blood, urine c/s
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the treatment goals for RF?

A

1) Maintain adequate air patency
- Chest PT, brochodilators, NIV, intubation

2) Correct underlying cause
3) Optimizing oxygen delivery
- Supplemental O2, positioning, blood transfusion to ensure sufficient Hb

4) Minimizing oxygen demand
- Timing of ADLs, bed rest, addressing sepsis, restlessness & px-ventilator desynchrony

5) Preventing complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the treatment for hypoxemic RF?

A
  • Long-term O2 therapy >15 hrs/day
    ~ If PaO2 is <7.3 kPa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the treatment for hypercapnic RF?

A
  • Domiciliary (home) non-invasive ventilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the treatment for Type III RF?

A
  • Frequent changes in position, chest PT and control of pain
  • NIV to reduce regional atelectasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the treatment for Type IV RF?

A
  • Intubation
  • MV to redistribute CO away from respiratory muscles and back to vital organs while the shock is being treated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is acute respiratory distress syndrome (ARDS)?

A

Clinical syndrome of
- severe dyspnea of rapid onset
- hypoxemia
- diffuse pulmonary infiltrates

Subset of acute lung injury (ALI)
- Condition characterized by widespread inflammation and increased permeability of the alveolar-capillary barrier, leading to pulmonary edema, hypoxemia, and reduced lung compliance

17
Q

What are the 3 criteria to diagnose ARDS from ALI?

A

PaO2/FiO2 ratio:
- <200 (ARDS)
- <300 (ALI)

Bilateral infiltrates
- Present in ARDS

Pulmonary artery occlusion pressure (PAOP)
- <18 mmHg or no clinical evidence of left atrial hypertension in ARDS

18
Q

What are the causes of ARDS?

A
  • Bacteremia, sepsis
  • Trauma, fractures, burns
  • Massive transfusion
  • Pneumonia
  • Aspiration
  • Drug overdose
  • Pancreatitis
  • Fat embolism
19
Q

What is the pathophysiology of ARDS?

A

1) Injury to alveolar-capillary membrane
- Releases inflammatory mediators
~ Bronchoconstriction, vascular narrowing and obstruction, and pulmonary edema cause impairment in gas exchange

  • Damages type II alveolar cell
    ~ Dec surfactant production causes atelectasis which dec lung compliance and impairs gas exchange
20
Q

What are the complications of ARDS?

A
  • Impaired gas exchange
    ~ V/Q mismatching
  • Dec lung compliance due to lung stiffness
  • Pulmonary HTN
21
Q

What are the stages of ARDS?

A

Stage 1 (Injury)
- Within 24 hours
- ^ dyspnoea and RR
- Coarse bilateral crackles
- Patchy infiltrates on CXR

Stage 2 (Exudative)
- 1-7 days
- Mediator induced interstitial and alveolar edema
- Damage to hyaline membrane formatio
- Increased permeability to proteins
- Hypoxia is resistant to supplemental O2
~ Requires MV

Stage 3 (Proliferative)
- 1-2 weeks after injury
- Hemodynamic instability
- Evidence of systemic inflammatory response syndrome (SIRS)
~ < 36 or >38 deg C
~ HR > 90
~ RR > 20/min
~ WBC <4000 cells/mm^3 or >12000 cells/mm^3
- Generalised edema, with denser and more fibrous lungs
- Thickened alveolar membrane

Stage 4 (Fibrotic)
- 2-3 weeks after injury
- Lung is remodelled by collagenous and fibrous tissues
- Increased dead space -> poor ventilation -> increased alveolar pressure

22
Q

How to diagnose ARDS?

A
  • During the first few days, ARDS will resemble acute cardiogenic PE
  • Dx made on onset + additional tests
    ~ BNP (hormone released by heart failure or during ARDS)
    ~ Echo (can detect L ventricular dysfunction and valve abnormalities)
    ~ Pulmonary artery catheterisation (PAC) (only if there is pulmonary artery HTN)
23
Q

What is the treatment for ARDS?

A
  • Mainly supportive while waiting for lungs to heal
  • Constant monitoring
  • Treatment of underlying causes of ARDS

pipi&pi3 (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions