Deep Venous Thrombosis
CODES
ICD9
- 453.40 Acute venous embolism and thrombosis of unspecified deep vessels of lower extremity
- 454.9 Asymptomatic varicose veins
- 459.81 Venous (peripheral) insufficiency, unspecified
ICD10
- I82.409 Acute embolism and thrombosis of unspecified deep veins of unspecified lower extremity
- I83.90 Asymptomatic varicose veins of unspecified lower extremity
- I87.2 Venous insufficiency (chronic) (peripheral)
VENTILATOR MANAGEMENT
Ruth L. Lamm
BASICS
DESCRIPTION
- Mechanical ventilation is machine generated flow of gas into and out of the lungs that acts as a substitute for normal respiratory function
Basic Concepts: Physiology and Pulmonary Mechanics
- Mechanical ventilation is
positive pressure ventilation
indicating that forced gas delivery generates positive pressure during inspiration
- Negative pressure ventilation:
- Natural respiratory pattern
- At rest (functional residual capacity) surface tension of alveoli is balanced by elastic recoil of chest wall; alveoli pressure equals atmospheric pressure at this point
- In inspiration, lungs expand causing alveolar pressure to become negative compared with atmospheric pressure and air travels down pressure gradient into lungs
- Exhalation is normally passive, but can be made active with the use of accessory muscles in the setting of airway obstruction/increased airway resistance
- Minute ventilation (MV):
- Total volume of breaths in 1 min
- Breaths in 1 min is respiratory rate (RR)
- Standard breath is called tidal volume (TV)
- MV = TV × RR: Each component can be adjusted to control ventilation
- Oxygenation is controlled with adjusting fraction of inspired oxygen (FiO
2
) and positive end-expiratory pressure (PEEP)
- Compliance:
- Describes lung distensibility
- Defined as change in volume with given change in pressure
- Decreased lung compliance can be caused by problems with the lung parenchyma (i.e., pneumonia, ARDS) or problems with the chest wall/pleura (i.e., abdominal distension)
- Lung compliance determines
plateau pressure
:
- Plateau pressure is the steady state pressure; represents the attenuated pressure that is distributed to the small airways and alveoli during positive pressure ventilation
- Goal ≤30 mm Hg
- Resistance:
- Defined as change in pressure with given flow
- Main determinant is airway radius
- Increased resistance can be caused by problems with the airways (i.e., bronchospasm), problems with the endotracheal tube (i.e., secretions), or problems with ventilator tubing
- Resistance determines
peak pressure
:
- Peak pressure is the pressure seen in the larger airways before delivered volume is distributed to smaller airways and alveoli
- Also determined by TV delivered
- Goal ≤40 mm Hg
DIAGNOSIS
SIGNS AND SYMPTOMS
- Indications for mechanical ventilation:
- Failure to oxygenate:
- Diffusion defect (i.e., pulmonary edema, pneumonitis, pneumonia)
- Severe ventilation/perfusion mismatch (i.e., PE, severe hypoventilation)
- Severe shock:
- Shock = oxygen supply does not meet oxygen demand by tissues
- Mechanical ventilation can help improve shock states in 2 ways:
- Increased oxygen delivery
- Reducing overall oxygen demand by replacing organ system with high oxygen requirement
- Failure to ventilate:
- Obtundation/sedation
- Loss of ability to control diaphragm or intercostals (i.e., high spinal cord injury)
- Severe myopathy
- Dysfunctional chest wall (i.e., flail chest, increased abdominal pressures leading to decreased chest wall excursion, obesity)
- Increased dead space (large PE, airway obstruction)
- Metabolic acidosis (creates need for higher MV to compensate)
- Other:
- Patient safety/need for evaluation
- Predicted deterioration in clinical course
- Ventilation strategy should specifically address the indication for mechanical ventilation!
- Example: In the setting of severe acidosis a preferred mode would be one where you could control MV closely
- Example: In severe pulmonary edema controlling the MV is not as important as ensuring oxygen delivery
Incidence and Prevalence Estimates
HISTORY & PHYSICAL EXAM
- Focus on underlying etiology for respiratory failure
- Exam on mechanical ventilation should include assessing oxygen saturation, evaluating end-tidal CO
2
(ETCO
2
) with capnometry and capnography (see below), auscultating lung sounds/air movement, observing chest wall rise, palpating for abdominal distension
- ETCO
2
:
- Capnometry is the quantitative partial pressure of ETCO
2
.
- Capnography is the graphic representation of the changes in ETCO
2
with respiratory cycle
- Normal lungs have a small degree of ventilation/perfusion mismatch as well as anatomic dead space. As a result, ETCO
2
is usually around 2–5 mm Hg lower than PaCO
2
- Capnometry will be affected by: Amount of dead space or ventilation/perfusion mismatch; changes in metabolic CO
2
production (although ratio between PaCO
2
and ETCO
2
will not change); venous return (also will not affect ratio)
- Evaluation of the ETCO
2
waveform can be very useful:
- Can help assess response to bronchodilator therapy as waveform in airway obstruction has a steeper upslope instead of a plateau given the prolonged expiratory phase
- Can help assess adequacy of CPR (will see return of waveform with good compressions)
- Can help assess cause of tachypnea or dyssynchrony
- Monitor hemodynamic status closely with mechanical ventilation
DIAGNOSIS TESTS & NTERPRETATION
Lab
- Arterial blood gas (ABG):
- Should be checked within 15–30 min of initiation of mechanical ventilation and repeated with any change in clinical status
- pH and PaCO
2
will help assess ventilation
- PaO
2
will assess oxygenation
- With ability to assess continuous oxygen saturation and ETCO
2
need for frequent ABGs, even after change in ventilator settings, may be eliminated or reduced
- Serum chemistries including basic electrolytes with bicarbonate, liver function, renal function may help assess acid/base status which will affect ventilation strategy
- Hemoglobin/hematocrit will help describe state of oxygen delivery
Imaging
Imaging may include beside US, chest x-ray, and chest CT to assess for endotracheal tube placement and pathophysiology of the lung and chest wall
DIFFERENTIAL DIAGNOSIS
See indications for mechanical ventilation above
TREATMENT
PRE HOSPITAL
Respiratory support per local EMS protocol
INITIAL STABILIZATION/THERAPY
- Cardiac monitor
- BP monitoring
- Pulse oximetry
- End-tidal CO
2
monitoring when available
ED TREATMENT/PROCEDURES
Critical actions include: Choosing appropriate ventilatory mode; assessing and adjusting ventilator settings; standard postintubation care; treatment of the underlying process.
- Postintubation care is of utmost importance. Includes: Sedation and/or analgesia; confirmation of tube placement; adjustment of ventilator settings based on clinical condition and ABG; establishing ETCO
2
gradient if using capnometry; elevating head of bed; placement of NG or OG tube.
- Settings common to most modes include:
- RR:
- In all modes, but will be set by patient in more spontaneous modes
- Normal starting rates can vary from 12–20
- Consider underlying pathophysiology before arbitrarily setting rate (i.e., elevated ICP, severe asthma)
- Fraction of inspired oxygen (FiO
2
):
- Oxygen concentration in gas mixture
- Usually start out with FiO
2
of 1 (100%) but wean down quickly after confirmation of stable oxygenation with prompt ABG
- PEEP:
- Pressure that is applied to end expiration to maintain alveolar recruitment
- Significant increase in work of breathing is required to open up collapsed alveoli
- Collapsed alveoli do not participate in gas exchange, creating ventilation/perfusion (V/Q) mismatch and difficulty oxygenating and ventilating
- By stenting open more alveoli, increased PEEP can improve oxygenation, especially at lower TVs (although be careful of high PEEP and overdistension which can lead to significant alveolar injury)
- With normal chest wall compliance, basic starting PEEP will be 5–10 mm Hg
- In setting of low chest wall compliance (obesity, anasarca, abdominal distension) may need to start with higher PEEP, around 10–15 mm Hg
- Inspiratory:expiratory ratio (I:E): Will alter flow rates. Allows for optimal mechanics in disease specific situations: E.g., increase E fraction in obstructive airway disease to prevent “breath stacking.” Normal ratio ∼1:2.