Mass Spectrometers Respiratory

Mass Spectrometers Respiratory MASS SPECTROMETERS

and APPLICATION IN RESPIRATORY THERAPY

by

Raymond Clay, RRT (C) 1989 Raymond Clay and Med Ed Online, Inc Fort Worth, Texas 4th Revision All Rights Reserved Electronic Distribution Only permitted so long as Copyright Notice accompanies text. For permission to reprint on paper contact: Raymond Clay : <Banquos Ghost> CIS : 74730,1344 GE : R.CLAY1 AppleLink : Raymond6 StarText : 209287 817-534-4026

Introduction

The SARA [System for Analysis of Respiratory and Anesthetic Gases] mass spectrometer has been in use for several years now. It is in continual use by anesthesia but only sporadically by Respiratory Care departments. The primary reason for this is a general lack of understanding about what SARA is for and/or how to use it. This paper is intended to correct this problem.

Although the conditions discussed apply to both spontaneously breathing, non-entubated patients, this paper addresses entubated patients.

What’s SARA for, anyway?

SARA will monitor your patients inspired and endtidal gas.

And? So? Just What does that mean?

One thing this means is that, if your patient is on SARA, you can turn off your O2 analyzer . A mass spectrometer is more accurate [by several orders of magnitude] and far more stable than any regular O2 analyzer.

Of course, SARA is a general hassle while an O2 analyzer is only an occasional one. There must be something else.

There is.

When using SARA you can monitor changes in: Dead Space Shunt Fraction And by monitoring these values you can also assess: Cardiovascular and pulmonary response to Ventilator Changes. Cardiovascular and Pulmonary response to other therapies. Efficacy of the Cardiovascular system. Perhaps most clinicaly important is the ability to monitor CPR for: Efficacy of circulation or cardiac compressions. ET tube placement. All of these things may be easily estimated at the bedside. The

setup procedures, while easy, take several minutes. However, in most instances the data SARA provides are of greatest utility only when tracked over time, either on a graphic display, a flowsheet, or in the therapists memory.

The data provided by SARA that is most useful are the Endtidal CO2 [PetCO2], the Inspired O2 [FiO2 or PiO2], the Endtidal O2 [FetO2 or PetO2], and the Inspired minus Expired O2 [delta I-E O2].

The change in FiO2, or in CO2 clearance, will be reflected in the change in FetO2 or PetCO2. This change is in the form of a curve.

If the FiO2 is altered SARA will reflect this change in the next analysis. The change in FetO2 and delta I-E O2 will be more gradual and will graph as a curve known as the Washin or Washout curve (also called a log-dose response curve). FetO2 will change on the next analysis, but it will continually change in a decelerating fashion until a new stability is reached. This phenomena is caused by the removal of Nitrogen or Oxygen from the circulating blood volume and the alveoli.

If there is a low cardiac output, or if the patient has a large degree of airway obstruction, Washin/Washout will take longer and show a flatter curve. In cases where there are non-communicating, air filled alveoli and/or airways the curve will be even longer and flatter, although this is significant only in the most extreme cases. Finally, static bowel gas or interstitial gas will slow Washin/Washout even further, but once again only the most extreme cases will have a visible effect.

PetCO2 will show the same characteristics when ventilation changes are made if extreme obstructive pulmonary disease is present. In most cases the PetCO2 will stabilize over ten to twenty breaths. This difference in Washin/Washout is due to the physical properties of oxygen and carbon dioxide and the diffusion pressures across the alveolar membrane.

Using SARA to monitor Washin/Washout is useful for two reasons. First, you can tell when it is time for another ABG instead of waiting a predetermined time that may be too long or too short. Second, you can assess the level of airway obstruction present. Third, you have a relative index of the effectiveness of Cardiac Output [Q] (ie; if Q is low but Washin/Washout is normal then the Q is still adequate). Fourth, immediately post-operatively you may monitor the clearance of anesthetic agents.

Endtidal CO2

Endtidal CO2 is the level of CO2 measured at the end of expiration. In practice this is the highest PCO2 detected during a measurement. In the normal lung this will be almost entirely alveolar gas. In many disease states, and in the presence of high rates or high levels of PEEP, this gas will be mixed with greater quantities of Dead Space gas and therefore be lower.

Dead Space [Vds] is that portion of a lung volume [tidal, minute or total lung volume] that does not exchange gas in the alveoli. This volume is made up of two components:

1. Anatomic Dead Space [Vd-ant] – the volume of the conducting airways, including the oropharnyx, the trachea, the bronchous, and the bronchioles. This does not include the respiratory, or terminal, bronchioles.

Vd-ant can be decreased by the presence of an artificial airway, bronchoconstriction or brochial edema. Vd-ant can be increased by the application of PEEP/CPAP or breath stacking. The effect of both actions is to distend the airways and increase the Functional Residual Capacity [FRC]. At normal levels of PEEP/CPAP [< 10cmH2O] there is rarely a significant change in Vd-ant. 2. Physiological Dead Space [Vd-phy] – the volume of gas in the alveoli, and terminal bronchioles, that does not exchange with the pulmonary blood flow. Vd-phy can be increased by a loss of blood flow to the alveoli or a diminishment in the diffusion capacity of the alveolar membranes, or by a pulmonary embolism, or by hypoventilation. Blood flow may be decreased by cardiac arrest, or by a fall in cardiac output due to volume depletion or right heart failure, or by loss of vascular tone [shock], or by excessive ventilating pressures or PEEP levels [high transpulmonary pressure inhibiting blood flow into the pulmonary capillaries]. Vd-phy can be decreased by an increase in alveolar blood flow or an increase in the diffusion capacity of the alveolar membranes. Blood flow may be increased by increased cardiac output, increased blood volume, increasing vascular tone, decreasing transpulmonary pressures.

Another factor affecting PetCO2 is hypo- or hyper- ventilation. This can be caused by inadequate or excessive Respiratory Frequency [f] or Tidal Volume [Vt]. Most significant (other than inappropriate ventilator settings) is the effect of Pulmonary Compliance [C] and Airway Resistance [Raw] changes. A decreasing C will decrease alveolar ventilation secondary to pressure limiting or lost volume in the ventilator circuit or overdistension of the airways. In the spontaneously breathing patient a falling C will increase the work of breathing to the point that the patient cannot adequately clear CO2.

In a ‘perfect’ lung the PetCO2 will equal the arterial carbon dioxide pressure [PaCO2]. Due to the normal Vd fraction the PetCO2 will be 4 – 6 mmHg lower than the PaCO2 in a patient with normal lungs. If a patients hemodynamics and ventilation are stable, the PetCO2 will always track the PaCO2 regardless of dead space. If there is an increase in Vds the difference between PetCO2 and PaCO2 is increased, a decrease in Vds will cause a decrease in this difference. If you can track PetCO2 over time, you can observe your patient for changes in Vds, and so observe changes in circulatory or airway status.

If the PetCO2 changes in the absence of ventilation changes then the patients Vds is changing, due to changes in perfusion or C, and a blood gas should be obtained and the ventilator adjusted accordingly.

A decrease in rate, where the patient does not significantly increase spontaneous respiration, should show an increase in PetCO2. If this is not the case then the patient is being underventilated. A blood gas should be obtained immediately and the ventilator adjusted accordingly.

If the PetCO2 falls in the absence of ventilation changes then the patients Vds is increasing. In this case there is trouble ahead. A fall in PetCO2 without an increase in ventilation indicates a decrease in pulmonary perfusion. This may be due to fluid depletion, pulmonary embolus, loss of vascular tone, or right heart failure. Immediate investigation and treatment are required.

Changes in Vt and/or rate should cause changes in PetCO2. By observing the trend in PetCO2 following such a change you can determine when equilibration has occurred. When the PetCO2 has ceased to change, or [in the case of increasing spontaneous respirations] a new average PetCO2 is achieved, it is time for a blood gas.

Changes in I:E ratios can also have an effect on Vds. As an I:E approaches 1:1 a point will be reached where there is insufficient time for expiration (dependent on C and Raw). At this point, Vds will begin to rise (due to the unexpired gas). As the E portion of the I:E increases Vds will diminish. This phenomena can sometimes be detected by an increase in Inspired CO2, since alveolar air is still being expired at start inspiration.

A pulmonary embolism, which stops or radically diminishes blood flow to part or all of one or both lungs, will suddenly create new dead space units. A sudden fall in PetCO2 to a new level suggests a pulmonary embolism. The absence of such a change cannot rule out a pulmonary embolus since collateral circulation may provide blood flow to the affected areas.

Endtidal CO2 Response to Ventilator Changes

Expected changes in PetCO2 with alteration of Ventilation Parameters : Change in Change in Ventilation PetCO2 PaCO2 ——————— —— —– Increase f falls falls * Decrease f rises rises Increase Vt rises falls Decrease Vt falls rises Increase Flow [decrease It] rises * falls * Decrease Flow [increase It] falls * rises * Increase PEEP may fall may rise Decrease PEEP may rise may fall Change in Hemodynamics ———————- Increase CO rises falls Decrease CO falls rises

• Dependent on I:E Ratio. If Breath Stacking does not occur, or stops, with stated change, then indicated change in gas should result.

In general, if the expected change does not occur, a blood gas should be drawn immediately.

Changes in spontaneous respiration should give the same results as above except for extreme increases in work of breathing. Such a case will result in heavy respiratory workloads (especially in conditions of decreasing C and/or rising Raw such as ARDS, status asthmaticus; etc), causing increased CO2 production, causing increased respiratory drive, causing increased respiratory workloads, etc; etc.

Endtidal CO2 Response to Non-Ventilator Changes

In the Absence of Ventilation changes: Change in PetCO2 Possible Cause —————- ————– Increasing Resolving pulmonary disease (ie; increasing C and/or decreasing Vd) Increase in Q Increase in pulmonary capillary perfusion Increasing blood volume Increasing temperature Decreasing Worsening pulmonary disease (ie; decreasing C and/or increasing Raw) Decrease in Q Decrease in blood volume Decrease in pulmonary capillary perfusion Possible pulmonary embolus Leaking air (via bad cuff or chest tube) Decreasing temperature Loss of PetCO2 Loss of pulmonary perfusion (ie; cardiac arrest, shock, exsanguination) Artificial airway misplaced

Endtidal Oxygen Fraction

The Endtidal Oxygen Fraction [FetO2] is the measured expired O2 at the time of the peak expired CO2, or the PetCO2 point. This value is most useful for detecting O2 equilibrium following an FiO2 change, although its scale makes it less sensitive than the dI-EO2. It is also helpful in assessing the amount of airway obstruction present.

Inspired Oxygen Fraction

The Inspired Oxygen Fraction [FiO2] is the highest detected oxygen concentration during a SARA sampling period. This value is useful for calibrating or verifying oxygen analyzers.

Difference in Inspired to Expired O2

The Delta (or change) Inspired-Expired Oxygen [dI-EO2] is the difference in inspired and endtidal O2. This value is a rough indicator of O2 consumption. By tracking this value you can indirectly monitor your patients O2 consumption and Shunt Ratio.

1. Shunted Blood Flow [Qs] – Blood flow in the lung that does not exchange gas in the alveoli. This is primarily the result of alveoli that are perfused but not ventilated, such as in ARDS or atelectasis. This also occurs when there is inadequate alveolar surface area, such as in COPD. A small, normal shunt exists as a result of anastomosis in the lung and due to the nature of venous drainage from the heart.
2. Shunt Ratio [Qs/Qt] – The ratio of Shunted blood flow to Total blood flow [Qt].

The Qs/Qt will rise in cases of alveolar collapse, airway obstruction, or hypoventilation. The Qs/Qt will fall following the correction of any of these conditions. 3. O2 Consumption [VO2] – the volume of O2 consumed over time, usually expressed as a minute volume [ml/minute]. VO2 may decrease in the presence of an increased Qs/Qt, severe hypoperfusion [low Qt or loss of vascular tone], or to a small degree in the case of a pulmonary embolism. VO2 may increase in the presence of a decreased Qs/Qt or when metabolic demand or cardiac output increase. Metabolic demand will increase in the patient recovering from anesthesia or neuromuscular blockade, the agitated and active patient, or the tachypnic patient.

An increase in dI-EO2 may be caused by a decrease in the Qs/Qt, or an increase in metabolic activity, temperature or Qt.

A decrease in dI-EO2 may be caused by an increase in the Qs/Qt, a decrease in metabolic activity, temperature or Qt.

A sudden fall of the dI-EO2 to or near zero indicates either a sampling error or an imminent cardiac arrest.

Observing the dI-EO2 following a change in Fio2 can detect equilibrium conditions. When the dI-EO2 is stable it is time for a blood gas.

Airway obstruction will cause prolonged equilibrium times following a change in FiO2. To assess this condition you should place a patient on 100% O2 and monitor the dI-EO2 for equilibrium. Note this time. Now return the patient to the previous FiO2. Observe the dI-EO2 for equilibrium. If this is done on a daily or shift basis this time value becomes useful for tracking airway obstruction. Evaluation of bronchodilator therapy may also be done by such a maneuver before and after a treatment, preferably to start with the initial treatment.

Oxygen Response to Ventilator Changes

Expected Changes in dI-EO2 from changes in Ventilation/ Oxygenation and Hemodynamic Parameters : WI = Wash In WO = Wash Out nc = No Change inc = Increase dec = Decrease Change in Change in Parameters dI-EO2 FetO2 PaO2 ——————– —— —– —- Increase FiO2 WI nc/inc WI inc inc Decrease FiO2 WO nc/inc WO dec dec Increase PEEP inc/nc dec/nc inc/nc Decrease PEEP dec/nc inc/nc dec/nc Increase f inc/nc dec/nc inc/nc Decrease f dec/nc inc/nc dec/nc Increase Vt inc/nc dec/nc inc/nc Decrease Vt dec/nc inc/nc dec/nc Increase Flow [decrease It] dec/nc inc/nc dec/nc Decrease Flow [increase It] inc/nc dec/nc inc/nc Change in Hemodynamics ———————- Increase CO inc dec inc Decrease CO dec inc dec

Oxygen Response to Non-Ventilator Changes

Change in Oxygen Probable Cause —————- ————– Increasing FetO2 Worsening pulmonary disease (ie; or increasing airway obstruction) Decreasing dI-EO2 Decreasing Q Decrease in blood volume Possible pulmonary embolus Decreasing temperature Decreasing Metabolism (sedation, seizure control, loss of consciousness) Decreasing pulmonary capillary perfusion Decreasing FetO2 Resolving pulmonary disease or Increasing Q Increasing dI-EO2 Increase in blood volume Increasing temperature Increasing Metabolism (activity, seizures, regaining consciousness) Increasing pulmonary capillary perfusion dI-EO2 equals Zero Loss of pulmonary perfusion (ie; cardiac arrest, shock, exsanguination) Artificial airway misplaced

Case Histories

Case 1

45 yo W/M; Post Op Day 3; Sepsis – [Alcoholic Liver Disease]

Perotinitis/Pancreatitis/ARDS

Vent Vt-1000 f-12 FiO2-0.4 PEEP-5 PS-30

no spont resp

ABGs 7.33 48 78

PetCO2 has been stable at 30 mmHg
dI-EO2 has been stable at 4.0%

An order is received to decrease the rate to 8 to begin weaning the patient. After 2 or 3 minutes the patient began breathing spontaneously at a rate of 40-50 with a spontaneous tidal volume of 400.

The PetCO2 initially rises, after the change in rate, but falls after the patient begins to breath spontaneously. After several minutes the PetCO2 is back to 30. The PetCO2, over the next 30 minutes, rises and falls but the average is still about 30. The PaCO2 does not change significantly.

The dI-EO2 is very erratic but is trending upwards (approx 5.0%). The arterial PO2 is 88

The patient is diaphoretic, confused and agitated and is using his accessory muscles. Pulse has increased from 130 to 160. BP increased from 140/95 to 180/110.

What’s wrong with this picture?

This patient has inadequate muscular tone to maintain an increase in spontaneous ventilation. The PetCO2 rose initially since the rate was decreased and the patient did not immediately begin to breath. The fall after the patient began spontaneous breathing is what was expected to happen. The rise back to previous levels after that was due to the tremendous effort the patient was putting forth to breath, and the corresponding increase in CO2 production. His work of breathing was too great for his status and he had to be placed back on a higher rate for several more days before being weaned successfully.

Case 2

20 yo W/M; Post Op Day 0; CHI – [MVA]

evacuation of hematoma

Vent Vt-1000 f-14 FiO2-0.4

no spont resp

ABGs 7.44 33 66

PetCO2 stable at 27
dI-EO2 stable at 3.5%

The rate was increased to 16 and 5 cmH2O PEEP were added. There are still no spontaneous respirations.

The PetCO2 decreased to 18, the PaCO2 to 28 and the PaO2 increased to 88.

Why did the difference between the PetCO2 and the PaCO2 increase from 6 to 10?

The addition of PEEP increased the patients anatomical Vds by distending his airways at end expiration. The rate of 16 may have contributed by stacking breaths and further increasing the Vds. When the PEEP was removed several days later the difference fell to 7 mMhg.

Case 3

32 yo B/F; Post Op Day 3; Blunt Trauma – [MVA] Pulmonary Contusion/Hemo-Pneumothorax/ Multiple Fractures/ARDS

Vent Vt-900 f-15 FiO2-0.5 PEEP-8

no spont resp

ABGs 7.33 55 71

PetCO2 is stable at 26
dI-EO2 is stable at 3.5%

The SARA limits have been set manually to close tolerances. SARA gives an alarm over a High PetCO2 [31]. Several minutes later SARA alarms for a Low PetCO2 [21]. Trends of PetCO2 and PAP show that the changes in PetCO2 followed changes in PAP. An ABG returns 7.38 49 99. The physician declines to make any adjustments. Several hours later SARA gives an alarm for a low FetO2 [34.5%], the dI-EO2 is now 5%. ABGs return 7.38 48 144. The FiO2 is decreased to 0.4. SARA still indicates a high FetO2 [35%] and ABGs return 7.38 49 140. The PEEP is decreased to 4 over the next two hours. The PetCO2 is now 31, the dI-EO2 is 4% and the ABGs are 7.47 39 95. The next day ABGs return 7.43 32 112 with a PetCO2 of 27 and a dI-EO2 of 4%. The PEEP is discontinued and ABGs return 7.45 30 105 with a PetCO2 of 25. The rate is progressively decreased through the day with spontaneous respirations of 400- 500 mls at a rate 16. On a f-4 ABGs return 7.43 36 98 with a PetCO2 of 30. The patient is placed on CPAP of 0 and FiO2 of 0.4. Spontaneous respirations remain the same. ABGs return 7.40 39 88 with a PetCO2 of 34. Two hours later similar results are obtained and the patient is extubated without difficulty.

What caused the changes in PetCO2 that seemed to follow changes in PAP? The patients ARDS was resolving, as this occurs the ventilating pressures will be increasingly transmitted to the pulmonary vasculature. An increase in pulmonary perfusion, caused by a rise in PAP (in response to increased trans-pulmonary pressures), decreased Vd-phy and increased the PetCO2. The increasing transmission of pressures to the vasculature made this a short lived phenomena. It is likely that the patient was on excessive levels of PEEP from that point on.

As the patient was progressively weaned over two days the difference between the PaCO2 and PetCO2 closed and the dI-EO2 increased. This data, in conjunction with timely ABGs, guided the weaning progress in a real time, primarily non-invasive, manner.

Case 4

3 yo W/F; Post Op Day 2; Blunt Abdominal Trauma – [Child Abuse] Ruptured Spleen, Gall Bladder, Large and Small Bowel/Lacerated Liver

Vent Vt-200 f-24 FiO2-0.35 PEEP-5

no spont resp

ABGs 7.36 30 104

PetCO2 stable at 22
dI-EO2 stable at 3%

SARA alarms and gives a NO BREATH indication, the PetCO2 is 0 and the dI-EO2 is 0%. The patient is dusky but not frankly cyanotic and the heart rate and invasive blood pressure are unchanged. Breath sounds are diminished but present. The resident on call insists that the tube is in place but that the ventilator is malfunctioning. The therapist changes the SARA filter and removes the child from the ventilator and bags her with the SARA fitting in place. SARA still says NO BREATH. A CRNA arrives and, at the insistence of the therapist and the nurse, checks for tube placement. The tube is in the esophagus. At this point the patients heart rate and BP are rising and she is now frankly cyanotic. Another tube is passed and the patient is bagged via this tube. SARA returns a PetCO2 of 55 and a dI-EO2 of 5%. The child is placed back on the ventilator and the PetCO2 falls back to the low 20’s after several minutes. A CXR verifies placement.

Note that the first indication that the tube was out, and the first verification of placement of the new tube, came from SARA.

Case 5

24 yo B/M; Post Op Day 0 – [GSW abdomen and chest]

Hemo-Pneumothorax

Vent VT-1000 f-10 FiO2-0.5 PEEP-5

ABGs 7.43 38 113

PetCO2 is stable at 33
dI-EO2 is stable at 4.5%

The SARA monitor has the Smart Alarms on which set the limits tightly. A nurse approaches the therapist about SARA alarming for the last 5 minutes. The PetCO2 is now 17. The graphic screen shows that the PetCO2 and the dI-EO2 have been falling steadily for 10 minutes. The therapist advises the nurse to call the physicians. Before they arrive SARA returns a PetCO2 of 2 which is immediately followed by a precipitous drop in heart rate and invasive blood pressure. CPR is initiated with SARA still attached to the patient. Initially the PetCO2 remains below 5, fluids and drugs are administered and the PetCO2 rises to 15. A pulse is obtained and the PetCO2 is now 23. The patient is returned to the ventilator and ABGs are obtained where the PetCO2 is 29, the PaCO2 is 34.

This patient had bleed out in his abdomen and the blood loss had caused a fall in pulmonary perfusion that was detected by SARA 10 minutes before any other signs appeared. During resuscitation SARA advised of the efficacy of CPR.

Case 6

58 yo B/M; CHF, COPD, Hypertension

Vent Vt-800, f-16, FiO2-0.6

ABGs 7.28 34 88
PetCO2 stable at 18
dI-EO2 stable at 3.5%

The patient arrested in the step down unit and was brought to MICU and placed on a Ventilator. The conditions above existed at 6 hours after admission to MICU. The patient was hypotensive at this time – 95/50, maximum dopamine was onboard.

The PetCO2 began a gradual downward trend, followed by an upward trend in the FetO2. The PetCO2 alarm was set to 7.5mmHg. SARA began alarming as the PetCO2 reached this point. The patients nurse put SARA on standby to silence the alarm. Five minutes later the patients heart rate fell to 40 and BP to 50/25. Within another minute the patient was in a full arrest. CPR commenced with SARA back on and attached to the Bag. Compressions continued for 10 minutes until a pulse was obtained. During this time the therapist observed SARA for any return of CO2 or removal of O2. This was observed to be sporadic in nature and somewhat dependent on who was doing compressions. At nine minutes into CPR the PetCO2 rose to 26 and stabilized. After the return of a pulse the PetCO2 rose to 51 and the dI-EO2 to 5%. The values then fell and stabilized in 5 minutes to PetCO2 of 17 and a dI-EO2 of 3.5%. These values then began a gradual fall until the patient arrested again.

This scenario was repeated 6 more times. In each case the first sign of impending arrest was a fall in PetCO2 and the first indication of successful resucitation was an increase in both PetCO2 and dI-EO2.

Case 7

55 yo W/F; CVA – [Metastatic Ca] Seizure Disorder; COPD; Ventilator

Dependent

Vent Vt-900 f-12 FiO2-0.35 PS-17

ABGs 7.35 44 76
FetCO2 steady at 31 at time of last ABG dI-EO2 3.2%

This patient had been ventilator dependent for several months. Weaning had been attempted on several occasions without success. The patient had been on a Bear I Ventilator until four days earlier when a PB 7200 Ventilator was placed for the purpose of Pressure Support. Weaning was to commence in the AM and SARA was initiated at 0730 after a 0600 ABG on the above settings. At 0800 the patient began to seize continuously. The FetCO2 promptly rose to 48 followed shortly by a rise in dI-EO2 to 6.5%. Valium, Phenobarbital and Dilantin were administered in increasing dosages but seizures continued until 1030. During this time the FetCO2 rose to 63 and the dI-EO2 to 8.8%. After control of the seizures was obtained both values returned to their previous levels. No spontaneous ventilation was noted.

ABGs were not obtained during this period, although they were requested by the therapist repeatedly.

This case is an extreme example of the effects of metabolic changes on FetCO2 and dI-EO2. Such large changes should only be seen in extreme hyper- or hypothermia, uncontrolled seizure and extreme agitation. More often we will see smaller, sometimes subtle, changes reflecting variation in metabolism. This needs to be remembered when interpreting changes in SARA readings.

References:

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3. Kalenda Z; Capnography during anesthesia and intensive care. ACTA ANAESTHESIOL BELG 1978; 29(3):201-28
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