Respiratory failure Flashcards
Define respiratory failure
- failure of respiratory system to maintain normal blood gases
- hypoxemic (PaO2 50 mmHg)
• acute vs. chronic (compensatory mechanisms activated)
Px of hypoxemia
restlessness, confusion, cyanosis, coma, cor pulmonale
Px of hypercapnia
headache, dyspnea, drowsiness, asterixis, warm periphery, plethora, increased ICP (secondary to vasodilatation)
Define type 1 & type 2 RF
Type 1: hypoxaemic
PaO2 decreased, PaCO2 normal or decreased
V/Q mismatch problem & involves hyperventilation (hence normal/low CO2)
Type 2: hypercapnic
• PaCO2 increased, PaO2 decreased
Fatigue, lack of respiration problem. (hence low O2, high CO2)
Describe relationship b/w H+ & K+
Acidosis = hyperkalaemia Alkalosis = hypokalaemia
H+ and K+ swap places (H+ into cell, K+ out of cell if too much H+. hence more K+ detected)
Rx of T1 RF
- reverse the underlying pathology
- oxygen therapy: maintain oxygenation (if shunt present, supplemental O2 is less effective)
- ventilation, BiPAP and PEEP/CPAP: positive pressure can recruit alveoli and redistribute lung fluid
• improve cardiac output: ± hemodynamic support (fluids, vasopressors, inotropes), reduction of O2 requirements
Should you give O2 in RF?
Yes - T1 RF
No but Yes - T2 RF (decrease hypoxic drive to breathe but still need to give O2 if hypoxic)
Should you give O2 in COPD?
Yes - provide suppl O2 to achieve target SaO2 from 88-92%
Causes of hypercapnia
- high inspired CO2
- low total vent (e.g. brainstem stroke, myasthenia gravis, Guillain-Barre, muscle fatigue)
- high deadspace vent
- high CO2 production (e.g. fever, sepsis, seizure, acidosis)
Rx of T2 RF
• reverse the underlying pathology
• if PaCO2 >50 mmHg and pH is acidemic consider noninvasive or mechanical ventilation
• correct exacerbating factors
- NTT/ETT suction: clearance of secretions
- bronchodilators: reduction of airway resistance
- antibiotics: treatment of infections
• maintain oxygenation (see above)
• diet: increased carbohydrate can increase PaCO2 in those with mechanical or limited alveolar ventilation; high lipids decrease PaCO2
Define ARDS
clinical syndrome characterized by severe respiratory distress, hypoxemia, and noncardiogenic pulmonary edema
Defined by:
• Hypoxaemia PaO2/FiO2
What criteria do you use for ARDS and what does it consist of?
The Berlin criteria
- acute onset - within 7 d of a defined event, such as sepsis, pneumonia, or patient noticing worsening of respiratory symptoms – usually occurs within 72 h of presumed trigger - bilateral opacities consistent with pulmonary edema on either CT or CXR - not fully explained by cardiac failure/fluid overload, but patient may have concurrent heart failure - an objective assessment (e.g. echocardiogram) should be performed if no clear risk factors
What are the risk factors for ARDS?
• direct lung injury:
- airway: aspiration (gastric contents, drowning), pneumonia, inhalation injury (oxygen toxicity, nitrogen dioxide, smoke) - circulation: embolism (fat, amniotic fluid), reperfusion injury
• indirect lung injury
- circulation: sepsis, shock, trauma, blood transfusion, pancreatitis - neurogenic: head trauma, intracranial hemorrhage, drug overdose (narcotics, sedatives, TCAs)
What is the pathophysiology of ARDS?
• disruption of alveolar capillary membranes -> leaky capillaries -> interstitial and alveolar pulmonary edema -> reduced compliance, V/Q mismatch, shunt, hypoxemia, pulmonary HTN
Cx of ARDS
Fibrotic lung changes
• sequelae of ARDS include residual pulmonary impairment, severe debilitation, polyneuropathy and psychologic difficulties, which gradually improve over time