Acute Respiratory Failure

Question 1

respiratory failure is PaO2__ mmhg

Answer 1

PaO2<60mmhg and PaCo2>45 mmhg

Question 2

Respiratory Failure definition

Answer 2

• failure to provide sufficient oxygen in the blood
• failure to ventilate
• immunent threat to life.

Question 3

Type I resp railure. cause?

Answer 3

type I; acute hypoxemic respiratory failure.

• could be due to shunt. Hole in th eheart, or an AVM in the lung. or that the airspace is flooded– pus, water, cancer, protein– ARDS.

Question 4

cardiovascular causes of acute dyspnea

Answer 4

• acute myocardial infarction
• tamponade
• CHF

Question 5

rspiratory causes of acute dyspnea

Answer 5

Pleura: pneumothorax

Upper airway: aspiration, anaphylaxis
Lower airway: asthma, COPD, CHF

Parenchyma: Pneumonia, PE

Question 7

for O2 therapy: outline some eservoir systems

Answer 7

non rebreather, oxymizer

Question 8

note this scheme

Question 10

Berlin Definition of Adult Respiratory Distress Syndrome

Answer 10

1. Timing: within 1 week of a known clinical insult or a worsening respiratory symtpm
2. chest imaging: bilateral opacities
3. Origin of Edema: respiratory failure not fully explained by cardiac failure or fluid overlad. Need objective assessment to exclude hydrostatic edema if no risk factor present.
4. Oxygen: can be mild to severe.

Question 11

direct and indirect causes of acute lung injury

Answer 11

direct; gastric aspiraiton, pneumonia, inhalations, drowning, pulmonary contusion, fat and amniotic fluid embolism, inhalation injury.

indirect: sepsis, trauma, blood transfusion, pancreatitis, reperfusion injury (cardiopulmonary bypass), drug overdose.

Question 12

pathogenesis of ARDS

Answer 12

Blood and fluid and white cells and red cells leak out of the alveolus– there’s tons of cellular debris, fluid, and LOSS OF SURFACTANT in the interstiitum– the surface tension increase because of loss of surfactant. Causes alveolus to retract and get inflamed.

Question 13

Stages of ARDS

Answer 13

1. exudative stage: edema, hyaline membranes incresae
2. proliferative stage; interstitial inflammation
3. interstitial fibrosis; repair phase that causes degrees of permanent fibrosis.

Question 14

4 aspects of the exudative (early phase) of ards

Answer 14

• edema (both interstitial and intra-alverolar)
• cellular damage
• inflammation
• hyaline membranes

Question 15

in the fibroporliferative phase of ARDS, there is a proliferation of ____ ___, and ___ cells. There is phagocytsos of ___ and ____ debris

Answer 15

in the fibroporliferative phase of ARDS, there is a proliferation of FIBROBLAST , and TYPE II cells. There is phagocytsos of HYALINE MEMBRANES and CELLULAR debris

Question 16

in ards, there is a ___ problem resulting in significant hypoxemia. As you destroy blood vessels through inflammation, there are problems of __ ___ additionally.

there is low perfusion and there is a low amount of ___ which causes reduced compliance and a stiffer lung and reduced residual capacity.

• pulmonary hypertension because of diseased lungs causes increased ____ and thus ____ hypertension

Answer 16

in ards, there is a SHUNT problem resulting in significant hypoxemia. As you destroy blood vessels through inflammation, there are problems of DEAD SPACE additionally.

there is low perfusion and there is a low amount of SURFACTANT which causes reduced compliance and a stiffer lung and reduced residual capacity.

• pulmonary hypertension because of diseased lungs causes increased PERIPHERAL RESISTANCE and thus PULMONARY hypertension

Question 17

treatment of ARDS

Answer 17

• treat underlying disorder- might need antibiotics
• alter inflammatory cascade
• physiological supprt; gas exchange
• prevent complications: DVT and stress ulcers due to

Question 18

note :positive pressure (ventilation) is good cause it can re-puff up collapsed alveoli but you gotta be careful so the noraml alveoli don’t pop.

Answer 18

Question 19

characteristic CT findings in ARDS

Answer 19

ground glass opacities

• lung consolidation
• normal lung

Question 20

tidal volume strategites in ARDS (low stretch approach)

Answer 20

prior, there was a high priority to goals of restoring the acid-base balance, with lower priortty given to lung protection. now the opposite is choice. we have a higher priorty to lung protection.

Biologics, steroids don’t work. Gotta have “low stretch approach”– lower O2ml/kg amount from 15 to 8ml/kg or sometimes 4 ml/kg. Might get some acidosis but better than destroying the lungs.

Question 22

best positioning for ventilation (therapy for ARDS)

Answer 22

prone positioning when ventilated. prone positioning is ideal because less gravity.

Question 23

pulmonary function test abnoramlities after someone recovers from ARDS

Answer 23

doesn’t usually get quite back to normal. Often have a reduced QOL because of PTSD.

• reduced total lung capacity.
• reduction in diffusion capacity.
• possibly due to neuromuscular abnormalities.

Question 24

Type II respiratory failure

Answer 24

ventilatory failure. usually because of decreased alveolar ventilation (decreased drive, neuromuscular abnormalities, dead space (Vd)

-ex/ overdose, asthma, myasthenia gravis

Question 25

structures that play a role of neuro-muscular competence

Answer 25

1. medulla respiratory center
2. bulbospinal tract
3. anterior horn
4. phrenic nerve
5. neuromuscular junction
6. muscle

Question 26

Specific examples of diseases that affect
N-M competence

Answer 26

Question 27

Signs of CO2
Retention

Answer 27

• Decreased
LOC

• Asterixis

• Conjunctival
Edema

• Papilledema
• Flushing

Question 28

How to differentiate between Type II vs Mixed respiratory failure

Answer 28

type II often gives a normal A-a gradient

Question 29

indications and contraindications of non-invasive ventilation

Answer 29

Question 30

CO2 retention in COPD:

1. increase dead space ventilation- oxygen alters V/q relationship
2. haldane effect
3. hypoxemic drive reduction: if you beocme insenstiive to CO2, you can’t reduce the Co2 or else they will forget to breath. They need to have higher CO2 levels to keep up the respiratory drive.

Question 31

intrinsic and extrinsic causes of stridor

Answer 31

Question 32

therapies for stridor

Answer 32

• humidified o2
• heliox
• underlying pathology

PLUS: guided by underlying diagnosis

• • Antibiotics
  • Racemic Epinephrine
  • Steroids
  • Surgery
  • Radiotherapy
  • Chemotherapy

Question 34

3 physiologic causes of hypercapnia

Answer 34

1. “won’t breath”: decrease in neuromuscular competence
2. respiratory system load issues– bronchospasm, kyphosis, effusion, massive ascites
3. increased CO2 in minute ventilation loads; increased production (ex/ hyperthermic syndromes) or increased dead space (COPD, pulmonary embolism)