Acute Respiratory Failure Flashcards
respiratory failure is PaO2__ mmhg
PaO2<60mmhg and PaCo2>45 mmhg
Respiratory Failure definition
- failure to provide sufficient oxygen in the blood
- failure to ventilate
- immunent threat to life.
Type I resp railure. cause?
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.
cardiovascular causes of acute dyspnea
- acute myocardial infarction
- tamponade
- CHF
rspiratory causes of acute dyspnea
Pleura: pneumothorax
Upper airway: aspiration, anaphylaxis
Lower airway: asthma, COPD, CHF
Parenchyma: Pneumonia, PE
for O2 therapy: outline some eservoir systems
non rebreather, oxymizer
note this scheme
Berlin Definition of Adult Respiratory Distress Syndrome
- Timing: within 1 week of a known clinical insult or a worsening respiratory symtpm
- chest imaging: bilateral opacities
- 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.
- Oxygen: can be mild to severe.
direct and indirect causes of acute lung injury
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.
pathogenesis of ARDS
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.
Stages of ARDS
- exudative stage: edema, hyaline membranes incresae
- proliferative stage; interstitial inflammation
- interstitial fibrosis; repair phase that causes degrees of permanent fibrosis.
4 aspects of the exudative (early phase) of ards
- edema (both interstitial and intra-alverolar)
- cellular damage
- inflammation
- hyaline membranes
in the fibroporliferative phase of ARDS, there is a proliferation of ____ ___, and ___ cells. There is phagocytsos of ___ and ____ debris
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
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
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
treatment of ARDS
- treat underlying disorder- might need antibiotics
- alter inflammatory cascade
- physiological supprt; gas exchange
- prevent complications: DVT and stress ulcers due to
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.
characteristic CT findings in ARDS
ground glass opacities
- lung consolidation
- normal lung
tidal volume strategites in ARDS (low stretch approach)
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.
best positioning for ventilation (therapy for ARDS)
prone positioning when ventilated. prone positioning is ideal because less gravity.
pulmonary function test abnoramlities after someone recovers from ARDS
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.
Type II respiratory failure
ventilatory failure. usually because of decreased alveolar ventilation (decreased drive, neuromuscular abnormalities, dead space (Vd)
-ex/ overdose, asthma, myasthenia gravis
structures that play a role of neuro-muscular competence
- medulla respiratory center
- bulbospinal tract
- anterior horn
- phrenic nerve
- neuromuscular junction
- muscle
Specific examples of diseases that affect
N-M competence
Signs of CO2
Retention
• Decreased
LOC
• Asterixis
• Conjunctival
Edema
- Papilledema
- Flushing
How to differentiate between Type II vs Mixed respiratory failure
type II often gives a normal A-a gradient
indications and contraindications of non-invasive ventilation
CO2 retention in COPD:
- increase dead space ventilation- oxygen alters V/q relationship
- haldane effect
- 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.
intrinsic and extrinsic causes of stridor
therapies for stridor
- humidified o2
- heliox
- underlying pathology
PLUS: guided by underlying diagnosis
- • Antibiotics
• Racemic Epinephrine
• Steroids
• Surgery
• Radiotherapy
• Chemotherapy
3 physiologic causes of hypercapnia
- “won’t breath”: decrease in neuromuscular competence
- respiratory system load issues– bronchospasm, kyphosis, effusion, massive ascites
- increased CO2 in minute ventilation loads; increased production (ex/ hyperthermic syndromes) or increased dead space (COPD, pulmonary embolism)
