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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_885_Библиотеки_им_академика_М_И_Перельмана.pdf
208 D. Burneikis and F. M. Pieracci
• For metabolic acidosis specifically, calculating the anion gap and the gap-gap
ratio (Table 2) can further aid in developing a differential diagnosis and is
discussed below.
• For metabolic alkalosis, measuring urine [Cl−] can help differentiate between
potential primary drivers of the acid-base disturbance.
• Primary respiratory acid-base disturbances must be broadly classified as acute
or chronic. This determination is made by clinical evaluation that takes into
account patient’s history (e.g. pre-existing COPD, acute lung injury, ventilatory support etc.)
• In respiratory acidosis and alkalosis, HCO3 will increase and decrease,
respectively, by the amount predicted in Table 1.
{ For primarily acute respiratory acid-base disturbance, if actual HCO
3
is
less than predicted, then a concomitant metabolic acidosis may be present.
Alternatively, if actual HCO3 is greater than predicted, then a coexisting
metabolic alkalosis must be considered.
{ For primarily chronic respiratory acid-base disturbance, compensatory
mechanisms are slower and can take up to three days to respond fully. Thus
if actual HCO3 is less than predicted, then the compensatory response is
considered to be incomplete, or a coexisting metabolic acidosis is present.
Similarly, if HCO3 is greater than predicted, the compensatory response is
incomplete or a coexisting metabolic alkalosis is present.
• Mixed acid-base disturbances can make ABGs a challenge to interpret, there-
fore therapy should be aimed at treating the underlying disease and not
chasing numbers.
Anion Gap
• Anion gap (AG) is calculated to estimate the amount of unmeasured anions (e.g.
lactic acid) present in blood. AG is derived from equation in Table 2, which uses
measured electrolyte concentrations obtained with a basic metabolic panel.
• AG can be used to further differentiate between “gap” and “non-gap”
metabolic acidosis.
• The principal unmeasured anion that determines AG is albumin. Thus in
patient’s with low albumin, AG should be corrected according to equation in
Table 2. Failing to correct for albumin may result in a falsely-normal AG and
concealed presence of an AG acidosis.
• It is possible to have a “gap” and “non-gap” metabolic acidosis occur simul-
taneously. Such a scenario can be unmasked by calculating the gap-gap ratio
(GGR) (Table 2).
Acid-Base Physiology 209
• GGR is a ratio of change in AG to change in HCO
. GGR less than 1 indicates
3
that the AG does not fully account for the decrease in HCO3, and thus a
“non-gap” metabolic acidosis must be present (e.g. coexisting hyperchloremic acidosis and lactic acidosis). Alternatively, GGR greater than 1
indicates that HCO3 is higher than would be expected for a given AG, and
thus a concomitant metabolic alkalosis should be suspected.
III. Common causes of acid base disturbances in the ICU
• Metabolic acidosis
{ Anion gap
Diabetic ketoacidosis
Alcoholic ketoacidosis
Lactic acidosis
Renal failure with accumulation of organic anions
Methanol and ethylene glycol intoxication
Salicylate overdose
{ Non- anion gap
Dilutional, resuscitation with HCO3-free fluids resulting in hyperchlo-
remia
Diarrhea, fistulas resulting in GI loss of HCO
Renal tubular acidoses (RTAs)
3
• Metabolic alkalosis
{ Chloride responsive
Vomiting, gastric suctioning resulting in GI loss of H
Diuretic use resulting in intravascular depletion
{ Chloride resistant
Hyperaldosteronism
Hypokalemia
Excess HCO
administration
3
• Respiratory acidosis
{ Airway obstruction
{ Asthma
{ COPD
{ Ventilatory restriction (rib fractures, flail chest)
+
210 D. Burneikis and F. M. Pieracci
{ Pneumonia
{ Pulmonary edema
{ CNS depression
• Respiratory alkalosis
{ Pregnancy
{ High-altitude residence
{ Salicylate overdose
{ Anxiety-hyperventilation syndrome
IV. Sample ABG analyses
Example 1: 7.62/20/20
1. acidosis or alkalosis? Æ alkalosis
2. primary respiratory or metabolic? Æ respiratory (PCO2 < 40 mm Hg)
3. secondary metabolic disturbance? Æ NO [predicted ΔHCO3 =
0.2 (40–20) = 4 mEq]. So, predicted HCO3 = 20 = actual HCO3.
4. diagnosis = pure respiratory alkalosis
Example 2: 7.28/33/18 Na = 135 Cl = 111 HCO3 = 18
1. acidosis or alkalosis? Æ acidosis
2. primary respiratory or metabolic? Æ metabolic (HCO3 < 24 mm Hg)
Anion gap? Æ NO {Na – (Cl + HCO3) = 135 – (111 + 18) = 6}
3. secondary metabolic disturbance? Æ NO [predicted ΔPCO2 =
1.2 × (24–18]. So, predicted PCO2 = 33 = actual PCO2.
4. diagnosis = non-AG metabolic acidosis, likely hyperchloremic
(Cl = 111)
Example 3: 7.26/32/14
1. acidosis or alkalosis? Æ acidosis
2. primary respiratory or metabolic? Æ metabolic (HCO3 < 24)
3. secondary metabolic disturbance? Æ YES [predicted ΔPCO2 =
1.2 × (24–10) = 12]. So, predicted PCO
actual PCO2 > predicted PCO2 additional respiratory acidosis
must be present.
4. diagnosis = primary metabolic acidosis with secondary respiratory
acidosis
Example 4: 7.34/30/16 Na = 133 Cl = 107 HCO3 = 16 Albumin = 1.7 g/dL
1. acidosis or alkalosis? Æ acidosis
= 40–12 = 28. Because
2
Acid-Base Physiology 211
2. primary respiratory or metabolic? Æ metabolic (HCO
Anion gap? Æ NO (Na – (Cl + HCO3) = 133 – (107 + 16) = 10
Corrected AG? Æ AG + 2.5 × (4.5 – Albumin) = 10 + 2.5 × (4.5 – 1.7)
AGc = 17
3. secondary metabolic disturbance? Æ NO [predicted ΔPCO2 =
1.2 × (24 – 16) = 9.6]. So, predicted PCO2 = 30 = actual PCO2.
4. diagnosis = pure AG acidosis
Example 5: 7.34/30/16 Na = 145 Cl = 115 HCO3 = 16
1. acidosis or alkalosis? Æ acidosis
2. primary respiratory or metabolic? Æ metabolic (HCO3 < 24)
Anion gap? Æ YES (Na – (Cl + HCO3) = 145 – (115 + 16) = 14
GGR? Æ (AG – 12)/(ΔHCO3) = (14 – 12)/(24 – 16) = 0.25.
Since GGR < 1, a concomitant non-AG metabolic acidosis
should be suspected
3. secondary metabolic disturbance? Æ NO [predicted ΔPCO2 =
1.2 × (24 – 16) = 9.6]. So, predicted PCO2 = 30 = actual PCO2.
4. diagnosis = combined AG metabolic acidosis and non-AG
metabolic acidosis
< 24)
3
Practical Algorithm(s)/Diagrams
212 D. Burneikis and F. M. Pieracci
Table 1. Equtions for calculating expected compensation to acute acid-base
disturbances.
Metabolic Acidosis ΔPCO2 = 1.2 × ΔHCO3PCO2 < predicated = resp. alkalosis
Metabolic Alkalosis ΔPCO
Acute Respiratory Acidosis ΔHCO
Acute Respiratory Alkalosis ΔHCO
Chronic Respiratory Acidosis ΔHCO
Chronic Respiratory Alkalosis ΔHCO
= 0.7 × ΔHCO3PCO2 > predicated = resp. acidosis
2
= 0.1 × ΔPCO2HCO3 < predicated = metab. acidosis
3
= 0.2 × ΔPCO2HCO3 > predicated = metab. alkalosis
3
= 0.4 × ΔPCO2HCO3 < predicated = incomp. response
3
> predicated = metab. alkalosis
HCO
= 0.4 × ΔPCO2HCO3 < predicated = metab. acidosis
3
3
> predicated = incomp. response
HCO
3
Table 2. Equations used to calculate the Gap-Gap Ratio.
AG = Na – (Cl + HCO3) [nl = 12 +/− 4] AG > 12 = gap acidosis
AGc = AG + 2.5 × (4.5 – albumin) for pts w/ hypoalbuminemia
Gap-Gap Ratio = (AG – 12) / ΔHCO
3
GGR < 1 = nl AG metab. acidosis
GGR > 1 = metab. alkalosis
Review of Current Literature with References
• An alternative, physiochemical approach to examine acid-base homeostasis
was proposed by Stewart in 1983 [Stewart et al. Can J Physiol Pharmacol
1983; 61(12): 1444–61]. The “Stewart Method” addressed many of the criticisms of the physiological approach. Specifically, it redefined H+ and HCO3
as dependent variables that change in response to acid-base derangements
rather than cause them. Stewart identified three independent variables responsible for acid-base homeostasis in the human body: PCO2, total weak acid
concentration (ATOT), and the strong ion difference (SID). SID is central to
the physiochemical approach and is defined as follows:
{ SID = (Na + K + Ca + Mg) – (Cl + Lactate) normal = 40–42 mEq/L
Because of the principle of electric neutrality, SID will change in the same
direction as pH. While the “Stewart Method” is more aligned with the laws
of physical chemistry, the physiological approach described in this chapter is
still the most commonly utilized approach clinically.
Chapter 6-(iii)
Mechanical Ventilation
James Haenel, RRT*
* Surgical Critical Care Specialist, Denver Health Medical Center
Take Home Points
clinical examination and assessment of gas exchange.
PCO2 or pH as indicators of respiratory failure may not be appropriate to all
patients.
functions to replace the patient’s intrinsic pump and as a supportive tool during lung failure.
,
2
combination of control, phase, and a variety of conditional variables that
permit either mandatory or spontaneous breaths.
on diagnosis, gas exchange abnormalities, hemodynamic status and various
extrinsic factors such as patient position and body habitus.
when acute lung injury is present.
Contact information: Denver Health Medical Center, 777 Bannock St., MC 0206, Denver,
CO 80204; Email: James.Haenel@dhha.org
213
214 J. Haenel
positive end expiratory pressure (PEEP), the value of recruitment maneuvers
or use of rescue modes of ventilation.
patient’s intrinsic pump (Pmus) and that of the mechanical ventilator pump
(Pvent). Additional patient factors that come into play include mechanical,
chemical, neuroreflexes and behavioral components that will alter demand for
ventilation.
necessitates an immediate and thorough evaluation to discriminate between
an emergent airway event versus an acute pulmonary decomposition.
setting of respiratory failure is to minimize the potential for side effects,
mainly hemodynamic compromise and ventilator-induce lung injury while
supporting gas exchange thus allowing the underlying disease process to
reverse.
Background
frequently not a “blood gas” decision. Assessment of vital signs in conjunction with evidence of tachypnea, use of accessory muscles, ability to protect
the airway, and worsening hypoxemia based on noninvasive monitoring all
validate the need for early intubation and mechanical support.
required:
(1) Inadequate respiratory drive i.e. immediate post-operative period, drug
overdose, brain injury.
(2) Inability to maintain adequate alveolar ventilation i.e. neuromuscular
disease, high cervical injury, chronic ventilatory failure.
(3) Hypoxia i.e. Acute lung injury, acute respiratory distress syndrome,
COPD.
of lung volumes.
At no time should MV be considered curative and in fact, it may potentially be responsible for ventilator induced lung injury (VILI). Pragmatically,
in the absence of an appropriate pressure generated by the patient’s own
respiratory muscles (Pmus), the conveyance of an external pressure by the
Mechanical Ventilation 215
MV (Pvent) will provide air flow and tidal volume according to the equation
of motion: Pvent + Pmus = RV′ + EV + Pi where RV′ is the resistive load
defined as the pressure required to deliver the flow of gas (resistance times
flow) and EV + Pi is the elastic load or the pressure required to deliver the
tidal volume (elastance or compliance times tidal volume). Simplistically, the
MV may be seen as a pump when the patient’s own intrinsic pump fails.
Conversely, during respiratory (lung) failure, the MV is utilized purely as a
supportive tool to enhance gas exchange.
modes of mechanical ventilation and this often contributes to the confusion
and unfamiliarity of clinicians when prescribing mechanical ventilation.
Compounding this, a significant amount of the published literature and by far
the most contentious debates surrounding mechanical ventilation apply to
only a small subset of patients intubated and ventilated in the ICU, i.e.
patients with acute respiratory distress syndrome (ARDS). The vast majority
of ventilated ICU patients actually spend an average of four days or less
receiving mechanical ventilation.
Full ventilator support (FVS) in order to optimize oxygenation and to eliminate PaCO
. Once hemodynamic stability has been achieved, the patient may
2
either be extubated or converted to a partial mode of ventilation (PVS), see
Fig. 1.
achieve ventilator synchrony. Ventilator breaths can either be controlled or
assisted. A controlled breath is a machine delivered breath where the rate, the
inspiratory time (I:E ratio) and tidal volume are clinician-determined so as to
relieve the patient of all work. An assisted breath consists of the same input
variables but it is essential that the ventilator flow as well as pressure delivery
are synchronized with the patients effort during all three breath phases: initiation or trigger, delivery of breath or target and termination or cycle.
, inspiratory:
2
expiratory ratio and PEEP selection will vary in different clinical circumstances. Appropriate settings will depend upon the patients clinical and
pulmonary status, i.e. does the patient have normal underlying lung function,
does the patient have obstructive lung disease such as COPD or asthma or
severe restrictive disease secondary to ARDS?
weight (IBW) has become clinically accepted for ARDS patients after the results
of the National Institutes of Health trial that compared 6–12 Ml/Kg/IBW.
216 J. Haenel
Controversy still remains regarding Vt selection in the patient who does not
exhibit acute lung injury but none the less remains at risk.
and pressure delivery must synchronize with the patient’s effort during all
three phases of breath delivery: breath initiation (trigger), peak flow delivery
and breath termination (cycling).
critically ill patient who has marginal cardiopulmonary reserves. J.S. Haldane
astutely pointed out in 1921 that “Anoxemia not only stops the machine but
wrecks the machinery.” Adequate oxygenation is crucial for survival. As little
as four minutes of cerebral hypoxia may cause irreversible brain injury.
Moreover, suboptimal peripheral oxygen delivery has been recognized as a
critical etiologic factor in multisystem organ injury.
Main Body
Initiation of ventilation: modes of ventilation and phase variables
Selection is dependent upon whether the patient or ventilator performs the
work and whether the ventilator or the patient initiates (triggers) the breath.
Initial choice of the mode of mechanical ventilation basically comes down to
choosing either a controlled or an assisted breath delivery. A controlled breath
means that the clinician sets the rate, the inspiratory time and the tidal volume
with the goal being that the patient will do no work of breathing. The term
“control” can be confusing. It does not refer to a machine setting but infers
that breath delivery is managed by either sedation or a combination of sedation and use of a neuromuscular blocking agent (NMB). Risks involved with
use of controlled breaths are diaphragmatic muscle weakness and atrophy,
impaired cough and secretion retention, and an array of sedation and NMB
drug complications. In contrast to controlled breaths is the assisted breath,
where the patient is permitted to interact with the ventilator on all or just an
occasional breath. The amount of work performed during an assisted breath
ideally will be shared by the ventilator; however if the patients respiratory
drive is increased (sepsis, fever, agitation or increased deadspace ventilation)
and the ventilators peak flow setting or set pressure is inadequate then the
patient may experience significant levels of work. Spontaneous breaths are
selected usually once the patient is ready to perform some or all of the work
for breathing. These breaths are triggered, limited and cycled by the patient.
Mechanical Ventilation 217
tilation following intubation until either gas exchange stabilizes or the NMB
associated with the intubation period is no longer present. At this point, use
of assisted breaths is the general rule. Since the patient is expected to interact with the ventilator, sedation must be titrated to minimize anxiety but
not suppress respiratory drive. Strict attention to the ventilators flow and
pressure settings is obligatory to allow the patient to synchronize their
inspiratory efforts during all three breath phases: initiation (triggering), flow
delivery and termination (cycling). Improper attention to any of the three
phases of breath delivery can result in increased effort to initiate breath
delivery, continued diaphragm contraction beyond the triggering of the
breath if flow is inadequate or mismatching of timing of end inspiration to
exhalation. Any one of these situations may lead to excessive work loads
imposed on the patient.
ing number of ways to provide mechanical ventilation. There is a popular
textbook of mechanical ventilation that describes over 62 modes! I will be
using the KISS principle (keep it simple) because that is what I am capable
of! Let us look at the phase variables because this incorporates 90% of what
you need to master. There are three phase variables that are used to begin one
of the three phrases (trigger, target and cycle) of the ventilator cycle.
{ Trigger: The trigger variable is clinician set and permits inspiration to
begin.
It may either be a preset pressure (generally –2 cm H2O), a preset
volume, a designated flow change (generally 3 L/M) or an elapsed
time period.
{ Target: The target variable is what governs gas flow during the breath.
The target variables may either be pressure, flow or volume and they
cannot be exceeded during inspiration. Inspiration is therefore limited
once a preset volume is delivered, a preset peak airway pressure is
reached or when a preset peak flow is attained.
{ Cycling: Cycling refers to the factors that terminate inspiration and lead
to exhalation.
A breath may be pressure, volume or flow cycled.
The definition of what constitutes a “mode of ventilation” then is the relationship between the breath types (Mandatory, Assisted and Spontaneous) and the
inspiratory phase variables just described.