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What patients are at risk for desaturation in the immediate post-op period?
- 1) Atelectasis due to decreased FRC (diaphragm relaxes with anes)
- 2) Decreased mucociliary clearance (anes gases are drying)
- 3) Increased O2 consumption due to shivering (anes affects hypothalamus which controls temp reg)
- 4)Inhibition of HPV (anes gases vasodilate)
- 5) Hypoventilation due to residual anes effects
What factors would predispose someone to hypoxemia post-op?
Obesity, smoking, heart and lung disease (less reserve), extremes of age (increased closing capacity), thoracic and high abd surgery
What are examples of low flow O2 delivery? What makes them low flow?
- NC, simple face masks, partial and non rebreathers
- Part of inspired air comes from RA (entrainment)
- Poor control over precise FiO2
What are examples of high flow O2 delivery? What makes them high flow?
- Venturi mask, CPAP
- Allow more precision over FiO2
What is the difference between a partial rebreather and a non rebreather?
- The flow!
- Partial rebreather- lower liter flow (>8), dead space air is caught in reservoir bag and rebreather
- Non rebreather- higher liter flow (>10), gas takes path of least resistance, so dead space air is not rebreathed, breath in delivered O2
What type of oxygen delivery device would be ideal for a patient with COPD?
A high flow device as it allows precise control over Fi02. COPD pts depend on hypoxic drive (not CO2 levels) to breath
What happens to capillaries as PEEP is increased?
They get squished, BP and CO can decrease, usually with levels >10 cm H20
What are PEEP benefits?
- Recruit alveoli and expand alveoli
- Redistribution of extravascular lung water (moves away from blood gas barrier)
- Low CO or BP
- Can cause barotrauma in fragile lungs
What is auto-PEEP? When is it likely to occur?
- Airway pressure that exists in the body at end exhalation
- Can occur with high RR (alveoli can't fully empty), pts with obstructive lung disease
- Small amount of auto-PEEP can be helpful as it increases FRC and keeps airways open
What are the most common causes of hypercapnea?
Hypoventilation and COPD
What vent settings (TV and RR) should be used in patients with normal or mildly diseased lungs?
- Large TV (10-15 ml / kg) over 1 second
- RR 8-12 breaths/ min
These settings are better tolerated in awake or mildly sedated patients
What is an inflation hold and what does it do (hopefully)?
- End-inspiratory pause
- Exhalation is delayed to try to recruit alveoli
What's the difference between PIP and plateau pressure?
PIP is the peak pressure and can be elevated due to coughing, biting, or kinking of the tube, it does not have a predictable relationship to airway pressure
Plateau pressure (mean airway pressure) is the pressure felt by all alveoli
What is the goal plateau pressure for us as anesthetists?
<30 cm H2O
What are risks and benefits of extending inspiratory time?
Benefit- opening alveoli
Risk- decreased CO and BP due to high intrathoracic pressure
If a patient has an altered time constant would VC or PC ventilation be preferred? Why?
PC is better as the alveoli have more time at plateau pressure (no peak pressure, just plateau pressure)
A pt has stiff non compliant lungs, would PC or VC be better?
- Pressure Control
- watch tidal volume to make sure pt is getting adequate volumes
What is a normal I:E ratio?
1:1.5 - 1:3
What type of I:E ratio would be best for a patient with non-compliant lungs?
Lower I:E ratio, patients need more time to inhale due to non-compliance
When might you use reverse I:E?
Pt with ARDS, severe restrictive lung disease
Can you do reverse I:E in VC ventilation?
NO! Only with PC
Other than lowering I:E ratio how else could you lengthen plateau time in VC ventilation?
Can decrease Ti (insp time) so volume is delivered over shorter time, but lengthening plateau time
What is high freq ventilation?
Give very small TV (less than anatomic dead space) at very high frequency (60 - 100 / min), inspiration takes up 20-30% of the cycle
What is a major risk of HFV?
What mode of ventilation is least likely to cause barotrauma?
What are manifestations of pulmonary barotrauma?
- SQ emphysema
- Pneumo peritoneum / pericardium / mediastinum
- Venous and arterial air embolism
- Bronchopleural fistula
What types of patients might require a longer I:E ratio?
- Non-compliant, stiff lungs
- Trendelenburg position
What factors should be considered prior to extubation?
- Underlying indication for ventilatory support is reversed or improved (surgery over and paralytics reversed)
- Cardiopulmonary reserve is sufficient for spont vent
- General clinical state and labs do not indicate factors that would increase vent demand (shivering or hypothermic)
What inspiratory pressure should you have prior to extubation?
< -25 cm water
What tidal volume should you have prior to extubation?
> 5 ml / kg
What is RSBI? What value should it be prior to extubation?
- RSBI = rapid shallow breathing index
- RSBI = RR (breaths per minute) / TV
- Should be <100 to extubate
When assessing cardiopulmonary reserve what are you looking at?
- Vital Capacity
- Tidal Volume
- Respiratory Rate
- Heart Rate
- Hgb level
- Ventilatory demand
What is Virchows Triad?
- Risk factors for PE
- 1) venous stasis
- 2) hypercoagulability
- 3) vascular wall injury
PE is always due to a blood clot, T or F?
F! Can be due to lipids, air, or tissue fragments
What are s/sx of PE?
- Tachypnea, dyspnea, chest pain, V/Q imbalance, decreased PaO2, pulmonary infarction,
- pulmonary HTN, decreased CO, hypotension, shock
How could a PE cause hypotension?
A massive PE can reduce LA preload which reduces CO, causes hypotension
What ABG values might you see with a PE?
- Unexplained hypoxemia, normal or decreased CO2
During anesthesia what changes might be indicative of PE?
- Arterial hypoxemia, hypotension, tachycardia, bronchospasm (lung tissue damage releases cytokines and histamine)
- Decreased ETCO with a wide gradient!
- Normal is less than or equal to 5, due to dead space ventilation
What is cor pulmonale?
- Right heart failure secondary to PH
- High pressure in the pulmonary arteries is transmitted to RV causing it to fail
What is pulmonary hypertension?
Rise in PA pressure of 5 to 10 mmHg above normal (15 mmHg)
What is primary pulmonary hypertension?
- Small pulm arteries become narrowed due to hypertrophy of smooth muscle in the vessel walls
- Cause of these changes is unknown, may be due to endothelial dysfunction
What is secondary pulmonary hypertension?
- More common cause of PH
- Due to any respiratory or CV disorder that:
- 1) increases volume or pressure of blood entering pulmonary arteries
- 2) narrows or obstructs pulmonary arteries (chronic hypoxemia that causes HPV)
4 causes of pulmonary hypertension
- 1) elevated LV filling pressure (CAD and MV disease)
- 2) increased blood flow thru pulmonary circ (L to R shunt) in VSD or PDA
- 3) obliteration or destruction of pulmonary vasc bed (by PE) or by chronic destruction of alveolar wall (emphysema)
- 4) vasoconstriction of vasc bed due to hypoxemia, acidosis, or both
T or F?
The hypertrophy of the smooth muscle in the vessels is reversible.
Why would someone with chronic untreated OSA be at risk for PH?
hypoxemia can cause HPV which can cause PH