Research paper published in “Advance for Respiratory Care Practitioners.“ Vol 4, NO 10, Mar 11, 1991: pp.14-15.
Often go Undetected in the Critically Ill.
by Desmond Allen, PhD, RCP
Original Research by Michael Burt and Desmond Allen
There are essentially three types of abnormalities that result in respiratory insufficiency: those disorders that cause inadequate ventilation of the alveoli; those that decrease oxygen transport to the tissues; and those that reduce the diffusion of gases through the respiratory membrane.
We are especially interested in the third type. These diffusion abnormalities may be further divided into three subcategories: those that decrease the area of respiratory membrane; those that increase the thickness of the respiratory membrane; and those that cause an abnormal ventilation/perfusion ratio in some areas of the lung; and it is this third category with which we are primarily concerned.
Despite the knowledge and experience of even the best physician, the clinical diagnosis of certain life threatening ventilation/perfusion disorders can go undetermined, and thereby go untreated. Unfortunately, these abnormalities appear to be more widespread than most suspect.
“Ventilation/perfusion mismatch is considered the most common cause of hypoxia. Any disease process that interferes with either side of the equation upsets the physiologic balance and can lead to respiratory failure as a result of reduction in arterial oxygenation levels.” Pulmonary thromboembolism (PTE) is one such illness. “PTE is a leading cause of morbidity, and can appear in many clinical contexts. . . . Available information suggests that an antemortem diagnosis has been made in only 10 to 30 percent of all cases in which old or recent embolism is demonstrated at autopsy.”
Obviously, in the treatment of the critically ill patient with ventilation/perfusion abnormalities, knowing the etiology of the disorder is imperative if the appropriate therapy is to be administered. Fortunately, special physiological tests are able to distinguish between pulmonary shunting and increased physiological dead space. Thus, one can determine whether the abnormality is in the airways and pulmonary tissue or in the vascular distribution system.
In March 1999, Hewlett Packard installed "Merlin" Model 66 M1176A bedside monitoring in the Medical Intensive Care Unit of East Alabama Medical Center (EAMC). Merlin is a sophisticated computerized monitor which has the capacity to perform numerous calculations. Three of these calculations (oxygen, ventilation, and homodynamics) may be useful in immediate differential diagnosis of ventilation/perfusion abnormalities.
Respiratory physiology studies utilize values from the ventilation parameters, cardiac output (CO), arterial blood gases (ABGs), mixed venous blood gases (MVBG's), and partial pressure of exhaled carbon dioxide (Pc02) to calculate shunt fraction (Qs\Qt) and dad space to tidal volume ratio (Vd/Vt).
EAMC respiratory therapists began studies in conjunction with a representative of Hewlett Packard to determine the accuracy, reproducibility, and clinical correlation of these calculations. Therapists devised a system to collect the patient's expired gases from the mechanical ventilator. Using the analyzed Pc02 value as an input factor for Merlin, it performs ventilation calculations to yield the Vd/Vt ratio. An existing central venous catheter (preferably a Swann Ganz, which gives pulmonary artery access) is used to collect MVBG samples. These, as well as ABGs and the current CO provide the information for several oxygenation calculations.
Due to the difference in the solubility or dissociation of carbon dioxide (C02) and oxygen (02) at a ratio of twenty to one, a distinction can be made between a primary ventilation and primary perfusion abnormality. “When the ventilation/perfusion ratio is abnormal because of poor ventilation of many alveoli, the blood perfusing these alveoli does not become aerated. Therefore, the blood is said to be shunted through the lungs -- that is, it passes through the lungs without being exposed to functional alveoli. When the abnormality is caused by poor blood flow to alveoli that are normally ventilated, the ventilation of these alveoli is wasted. Therefore, the physiological dead space of the lungs increases.”
For instance, the physiologic hallmark of pulmonary vascular occlusion (a perfusion problem) is the development of an increase in dead space, or wasted ventilation. "In the diseased lung, the effects of ventilation/perfusion ratio inequality of gas transfer may be very severe because the degree of uneven ventilation and blood flow is far greater than in the normal lung. The arterial P02 may be depressed by 50 mmHg or more, and in practice no amount of increased ventilation unable to return it to its normal level." The PC02 however, due to its greater dissociation properties, is often maintained at or near the normal level by the increased ventilation.
Such clinical situations are reflected in the Qs\Qt fraction and the Vd/Vt ratio. If the Qs\Qt fraction is markedly increased and the Vd/Vt ratio is near normal or moderately elevated, the abnormality lies in ventilation, not perfusion. This would include such disorders as pneumonia, atelectasis, pulmonary edema, viscid secretions, bronchospasms and ARDS. Therapy would therefore be directed at correcting the ventilation abnormality via vigorous pulmonary toilet such as chest physiotherapy, suctioning, bronchodilators and aerosol.
Calculations showing a near normal or moderately elevated Qs\Qt fraction and a drastically increased Vd/Vt ratio would indicate a perfusion abnormality in the pulmonary vasculature. Classically, this is observed in abnormalities such as pulmonary thromboembolus, vascular obliteration (as seen in late ARDS and DIC), or cardiogenic shock. In the case of PTE, therapy would be directed toward correcting the perfusion abnormality with anticoagulant thrombolytic. If the problem is cardiogenic shock, the CO must be increased.
Yet in some illnesses, such as COPD and interstitial disease of the lung, both the Qs\Qt fraction and the Vd/Vt ratio are elevated. Guyton observes: "in lung disease the ventilation/perfusion ratio can become so severely abnormal in different parts of the lung that the diffusing capability for this reason alone may be reduced to as little as one-fifth normal, this reduction often occurring even though both total ventilation and total perfusion of the lungs are entirely normal."
Ultimately, of course, these figures cannot in and of themselves diagnose a given situation. They do, however, provide the physician with a valuable diagnostic tool.
Respiratory physiology studies also contribute significant weaning criteria. We are all familiar with standard weaning parameters; that is, a PH of 7.35 – 7.45, a PaC02 of 35 – 45, a Po2 of at least 80 mmHg on 40 % Fio2, a spontaneous tidal volume (Vt) of at least 5 ml/kg, a forced vital capacity (FVC) of at least 10 ml/kg, and a negative inspiratory force (NIF) equal to or greater than -20. The Qs\Qt fraction, the Vd/Vt ratio, and the AaDO2 (alveolar-arterial oxygenation difference), give additional information to the clinician.
The normal Vd/Vt ratio ranges from 25% to 40%. Values between 60% usually indicate that weaning will be unsuccessful. The Qs\Qt fraction normal range is 3% to 5%. In general, the Qs\Qt fraction should be less than 20% before ventilatory support is discontinued.
The normal range of the AaDO2 is from 10 to 15 mmHg on 100% oxygen. Assuming a normal CO, an AaDO2 below 350 mmHg corresponds to a Qs\Qt fraction less than 15% to 20%.
This test, however, requires at least 20 minutes of ventilation on 100% oxygen. On the other hand, a pulmonary artery catheter is not necessary (as it is for Qs\Qt fraction calculations).
The case studies which follow have been provided to illustrate the importance of respiratory physiology calculations as both weaning parameters and diagnostic tool for the immediate differential diagnosis between ventilation and perfusion abnormalities.
There studies were performed on mechanically ventilated patients from March to July 1990, in EAMC.
PECO2 Collection Method
1. “Merlin” Model 66 (M1176A) Bedside Monitor – Hewlett Packard.
2. Airlife IMV 3 liter anesthesia bag and H-valve assembly.
3. 2 each: 60 cc luer lock syringes.
4. 3 each: 3-way stopcock.
5. 2 each: ABG syringe.
6. Blood gas analyzer (Radiometer).
7. OSM 3 Hemoximeter (Radiometer).
1. Remove the free arm of the H-valve on the IMV bag and place at distal end of ventilator exhalation tubing.
2. Allow expired air to collect for ten minutes to ensure homogeneous expired gas sample.
3. Place 3-way stopcock on 60 cc syringe and ensure there is no air leak. A fractured or loose stopcock allowing aspiration of room air into sample syringe will alter sample analysis.
4. Obtain arterial and mixed venous blood samples from appropriate ports of arterial line and Swan-Ganz (distal port) or triple-lumen (distal port).
5. Aspirate three 60 cc syringes samples of expired gas at end expiration, during inspiration phase.
6. Analyze gas sample and average the 3 results of PECo2 (results should not vary more than 0.5 mmHg).
7. Analyze blood samples and record Sat., Hgb and O2CT from hemoximeter, and blood gas values from blood gas machine.
8. Obtain the cardiac output value, via thermodilution. If this is not available, calculate it by the Modified Fick Equation (below). Note, the calculated cardiac output, from measured saturation values for A-VO2 difference and assumed O2 consumption based on body fat content, is not to be construed as an accurate measurement of cardiac output. The calculated value is only a reasonable estimate of cardiac output to be used as an input value to calculate the shunt fraction (Qs\Qt).
9. Enter the input values requested on theoxygenation, ventilation and hemodynamics screen of “Merlin” bedside monitor.
10. Place computer printouts in front of patient’s chart for evaluation by pulmonologist or cardiologist. Call values to physician immediately.
Modified Fick Method
Cardiac out = 02 Consumption
Arterial O2 Content
-Venous o2 Content
1. Estimate O2consumption multiplying body surface area (BSA) by 130cc if body fat is greater than 15%, and by 140 cc if body fat is less than 5%.
Example: BSA 1.76 x 130 = 288 cc/min O2 consumption.
2. Obtain hemoglobin and o2 saturation values for arterial and venous blood from OSM3 hemoximeter. Multiply hemoglobin x 1.36 cc to obtain the o2 capacity.
Example: Hgb 13.6 x 1.36 cc = 18.49 Vol.% o2 capacity.
3. Multiply O2 saturation values by the O2 capacity to obtain arterial and venous blood O2 contents. Subtract venous o2 content from arterial o2 content to obtain arterial/venous o2 difference. Example:
18.49 Vol. % O2 capacity
x 0.98 Sat.% arterial blood
18.12 Vol.% arterial O2 content
18.49 Vol. % O2 capacity
x 0.70 Sat.% arterial blood
12.94 Vol.% arterial O2 content
18.12 Vol.% arterial O2 content
-12.94 Sat.% venous blood
5.18 Vol.% A-V O2 difference
4. Divide estimated O2 consumption by A-V O2 difference and multiply result by 100 to obtain estimated cardiac output.
(288 cc/5.18) x 100 = 4,401 cc or a CO of 4.401 L.
Case Study #1, Example #1
This patient was admitted to the MICU from an outlying rural hospital with a diagnosis of CHF and pneumonia. She was intubated and placed on a Bear V ventilator.
The radiologist’s reports indicated a totally opacified left lung and raised suspicion of a mucous plug in the main bronchus leading to total atelectasis of the left lung.
Respiratory physiology studies performed immediately after intubation indicated that a perfusion abnormality existed with an elevated Vd/Vt ratio of 83% (range is 25%-40%), and a moderately elevated Qs\Qt fraction of 20.6% (range is 3%-5%).
Hemodynamic calculations revealed an increased pulmonary vascular resistance (PVR) of 280 (range is 100-250), right ventricular stroke work (RVSW) of 33.71, with an index of 19.26 (range is 7.9 - 9.7). Cardiac output was normal at 5.43 by thermodilution, and 5.27 calculated by Modified Fick Equation.
Pneumonia with mucous plugging leading to total atelectasis of the left lung would have revealed a drastically increased Qs\Qt fraction with only moderate elevation of Vd/Vt ratio; because perfusion would have been adequate and increased ventilation would have returned the C02 to normal, or near normal levels, and high Fi02 levels of 80% to 100% would have been necessary to maintain arterial oxygen saturations at an acceptable level.
On clinical grounds alone, a firm diagnosis of embolism cannot be made; the clinical suspicion of embolism requires confirmation by laboratory studies.
Respiratory physiology studies, which yield hemodynamic data, oxygenation and ventilation information may provide a stronger element for the suspicion of thromboembolism., which may then be confirmed by pulmonary angiography or VQ scan.
Case Study #1, Example #2
Repeat respiratory physiology studies four hours after admission seemed to confirm the suspicion of PTE. There was some improvement in RVSWI, which may have been due to compensatory perfusion shifting in the pulmonary vasculature, or possibly that an original large embolus fragmented into smaller emboli and worked their way distally.
At this time the patient began having blood secretions from the endotracheal tube. This too, would further support the possibility of fragmented emboli.
Case Study #2, Example #1
This patient was admitted to the MICU with worsening respiratory failure. Intubation was performed and the patient was placed on a Bear V ventilator. No central line was available for oxygenation and hemodynamic calculations on day one.
Initial diagnosis was pneumonia and possibly tuberculosis bases on radiographic and bronchoscope evidence. Aggressive airway maintenance and hydration diminished pulmonary secretions dramatically.
On day two, a triple lumen catheter was inserted and respiratory physiology studies performed. A Qs\Qt fraction of 14.9% and a Vd/Vt ratio of 41% revealed this patient met weaning criteria as far as ventilation/perfusion ratios were concerned. However, he was not weaned and remained on the ventilator overnight.
On the third day, the chest X-ray revealed intestinal edema. The patient was diagnosed as developing ARDS secondary to pneumonia or possibly tuberculosis.
Case Study #2, Example #2
On day four, respiratory physiology studies revealed a marked increase in Qs\Qt fraction to 30%. The Vd/Vt ratio was inaccurately calculated due to the patient’s spontaneous breathing at a rae of 36 with a shallow ineffective breathing pattern in the SIMV mode.
Copious, viscid secretions at this point required suctioning as often as every 30 minutes. The patient’s level of consciousness was diminished. Oxygen saturation levels remained at 89% to 90%, despite aggressive airway maintenance and an FiO2 of 35% a PEEP of +5.
Case Study #2, Example #3
On day five, the patient showed signs of marked improvement. The patient was alert and cheerful. Secretions were thinner and the amount was markedly reduced. Suction was required every two hours.
Respiratory physiology studies showed a Qs\Qt fraction of 40%. The Vd/Vt ratio was slightly above weaning criteria at 62% but this too was believed to be inaccurately elevated with spontaneous, ineffective shallow breathing at a rate of 26 in the SIMV mode.
Spontaneous weaning parameters were performed and the patient was successfully weaned to a T-piece with an FiO2 of 35%. The patient’s clinical course remained uneventful.
Case Study #3, Example #1
This patient was 21 hours post-op for abdominal abscess. She had been returned to the SICU on mechanical ventilation following late night emergence surgery. Her level of consciousness and lack of cooperation prevented spontaneous weaning parameters from being performed.
Respiratory physiology studies were performed and projected successful weaning probably. The Qs\Qt fraction was 14% and the Vd/Vt ratio 50% were well within weaning criteria. The patient was successfully weaned to a 40% face mask.
 Guyton, Arthur C., Textbook of Medical Physiology. Philadelphia: W.B. Saunders Company, (1976), p. 574.
 Ibid., p. 575.
 Swearinger, Sommers, and Miller. Manul of Critical Care. (C.V. Mosby), pp. 59-60.
 Harrison, Tinsley. Harrison’s Principles of Internal Medicine. (10th edition), New York: McGraw Hill, (1983), p. 1561.
 Guyton. op. cit., p. 575.
 Ibid. p. 541.
 Ibid. p. 575.
 Burton and Hodgkin. Respiratory Care. Lippincott (1984), p. 818.
 Harrison, op. cit., p. 1504.
 Ibid. p. 1504.
 Guyton. op. Cit., p. 575.
 Harrison. op. cit., p. 1563.
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