Research paper published in “Advance for Respiratory Care Practitioners.“ Vol 4, NO 10, Mar 11, 1991: pp.14-15.
Ventilation/Perfusion Abnormalities
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.1
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;2 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.”3 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.”4
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.5
"Merlin" Model66
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.
Ventilation/Perfusion Abnormalities
Due to the difference in the solubility or dissociation of carbon
dioxide (C02) and oxygen (02) at a ratio of twenty to one,6 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.” 7
For instance, the physiologic hallmark of pulmonary vascular
occlusion (a perfusion problem) is the development of an increase in
dead space, or wasted ventilation. 8 "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. 9
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. 10
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."
11
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.
Weaning Parameters
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
Equipment Used
1. “Merlin” Model 66 (M1176A) Bedside Monitor – Hewlett
Packard.
2. Airlife IMV 3 liter anesthesia bag and H-valve assembly.
3.
4.
5.
6.
7.
2 each: 60 cc luer lock syringes.
3 each: 3-way stopcock.
2 each: ABG syringe.
Blood gas analyzer (Radiometer).
OSM 3 Hemoximeter (Radiometer).
Procedure
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.
Example: (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 ven-tricular
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. 12
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.
References
Guyton, Arthur C., Textbook of Medical Physiology. Philadelphia: W.B.
Saunders Company, (1976), p. 574.
1
2
Ibid., p. 575.
Swearinger, Sommers, and Miller. Manul of Critical Care. (C.V. Mosby),
pp. 59-60.
3
Harrison, Tinsley. Harrison’s Principles of Internal Medicine. (10th edition),
New York: McGraw Hill, (1983), p. 1561.
4
5
Guyton. op. cit., p. 575.
6
Ibid. p. 541.
7
Ibid. p. 575.
8
Burton and Hodgkin. Respiratory Care. Lippincott (1984), p. 818.
9
Harrison, op. cit., p. 1504.
10
Ibid. p. 1504.
11
Guyton. op. Cit., p. 575.
12
Harrison. op. cit., p. 1563.