Patients Breathing Room Air Research Articles

Continuous Monitoring of Arterial Oxygen Saturation with Pulse Oximetry during Transfer to the Recovery Room

The incidence of hypoxemia in the immediate postoperative period was determined using a pulse oximeter for continuous monitoring of arterial oxygen saturation (Sao2) in 95 ASA class I or II adult patients breathing room air during their transfer from the operating room to the recovery room. Hypoxemia was defined as 90% Sao2 (arterial oxygen partial pressure (PaO2) ≅ 58 mm Hg). Severe hypoxemia was defined as 85% Sao2 (PaO2 ≅ 50 mm Hg). Hypoxemia occurred in 33 (35%) patients; severe hypoxemia occurred in 11 (12%). Postoperative hypoxemia did not correlate significantly with anesthetic agent, age, duration of anesthesia, or level of consciousness. There was a statistically significant correlation (P < 0.05) between hypoxemia and obesity. All three patients with a history of mild asthma became severely hypoxemic even though none had perioperative evidence of obstructive disease, also a statistically significant (P < 0.003) finding.

Therapeutic application of calcium-channel antagonists for pulmonary hypertension

Calcium-channel antagonists may provide an effective approach to the treatment of pulmonary hypertensive disorders. Biochemical evidence suggests that pulmonary vasoconstriction results from the transmembrane flux of calcium into vascular smooth muscle; accordingly, the pulmonary pressor responses in experimental hypoxic pulmonary hypertension can be attenuated by verapamil and nifedipine. In patients with chronic obstructive lung disease, nifedipine decreases pulmonary artery pressures and pulmonary vascular resistance in proportion to the severity of hypoxemia before treatment. However, little pulmonary vasodilator effect is seen when hypoxemia is corrected by inhalation of oxygen, and systemic arterial oxygen desaturation can occur after nifedipine in patients breathing room air; most importantly, long-term studies in patients with chronic lung disease are lacking. In selected patients with primary pulmonary hypertension and other obliterative diseases of the pulmonary vasculature, nifedipine produces short- and long-term hemodynamic improvement at rest and during exercise, and these benefits are frequently paralleled by amelioration of dyspnea and fatigue. However, in patients in whom right ventricular function has been severely compromised by chronic pressure overload, both verapamil and nifedipine may exert notable depressant effects on right ventricular performance, despite the decrease in right ventricular afterload that would be expected to accompany a decrease in pulmonary vascular resistance. These negative inotropic actions may result in serious deleterious clinical reactions. Although calcium-channel antagonists represent a promising approach to the management of patients with pulmonary hypertension, the long-term efficacy and safety of these drugs in this disorder remain to be established.

Radionuclide angiocardiographic assessment of pulmonary vascular reactivity in patients with left to right shunt and pulmonary hypertension

Radionuclide angiocardiography was used to assess pulmonary vascular reactivity in eight patients (nine studies) with a large, relatively unrestrictive intracardiac defect and pulmonary arterial hypertension. Radionuclide angiocardiograms, using technetium-99m pertechnetate, were performed first with the patient breathing room air and then after 10 minutes of breathing a mixture containing 90 percent or more of oxygen. The pulmonary to systemic flow ratios obtained by gamma variate analysis of the radionuclide time-activity curves were compared with those calculated with the Fick principle at the time of cardiac catheterization. There was a good correlation between the two methods both in room air studies (r = 0.88) and in those obtained with 90 percent or more of oxygen (r = 0.94). All six studies (in five patients) with a reactive pulmonary vasculature (judged by a pulmonary vascular resistance at cardiac catheterization of less than 6 units/m2 with oxygen or after tolazoline) had a radionuclide pulmonary to systemic flow ratio of 3.0 or greater with oxygen. The three patients with a nonreactive pulmonary vasculature had a radionuclide pulmonary to systemic flow ratio of 2.3 or less with oxygen, a value that was unchanged from the room air value. These data suggest that radionuclide angiocardiography may be a useful, relatively noninvasive method of assessing pulmonary vascular reactivity in patients with a large, relatively unrestrictive intracardiac defect.

Disposable condenser humidifiers in intensive care.

Two disposable condenser humidifiers were evaluated in nine ventilated intensive care patients. The Portex "Humid Vent" delivered end-inspired absolute humidities of 22--26.3 g/m3 at end-inspired temperatures of 27--28.3 degrees C. Corresponding humidities and temperatures with the Servo "Humidifier 150" were higher and were constant, at 27.7--29 g/m3 and 29.3--29.7 degrees C respectively. These disposable devices can be used for humidification in intensive care, but only for patients breathing room air, or on a short term basis.

EFFICIENCY OF TWO VARIABLE PERFORMANCE TECHNIQUES OF OXYGEN THERAPY IN RELIEVING POSTOPERATIVE HYPOXAEMIA

The efficiency of two patient-dependent, variable performance techniques of oxygen therapy in relieving hypoxaemia after upper abdominal surgery was compared. A high-flow system delivered a humidified mixture of oxygen 2 litre min-1 and air 13 litre min-1 through a cannula inserted into the anterior nares. The low-flow system delivered 2 litre min-1 of dry oxygen into the nasopharynx through a catheter. Thirteen otherwise healthy patients received either high-flow oxygen therapy for 30 min followed by low-flow oxygen therapy for a further 30 min after operation or the same therapy in reverse order. With the patients breathing room air, arterial hypoxaemia could be demonstrated with Pao2 inversely related to age. The increase of Pao2 during either oxygen treatment was significantly greater with the low flow system.

First Pass Radionuclide Assessment of Right and Left Ventricular Ejection Fraction in Chronic Pulmonary Disease: Effect of Oxygen upon Exercise Response

Right and left ventricular ejection fraction (RVEF; LVEF) were determined in patients with severe chronic pulmonary disease (mean +/- SEM [FEV1 percent predicted 36 +/- 3%; PaO2: 64 +/- 3 mm Hg]), utilizing first pass radionuclide angiocardiography. RVEF and LVEF were measured at rest and again during upright bicycle exercise while patients breathed room air, and again during low flow oxygen (O2) administration. Mean RVEF was abnormal (less than 45%) at rest and did not increase with exercise while subjects breathed room air (44 +/- 2 percent vs 44 +/- 3 percent, P = ns), but improved significantly during exercise while patients breathed O2 (45 +/- 5 percent vs 51 +/- 3 percent, P less than .05). Breathing room air, RV exercise ejection fraction was abnormal (less than 5 percent increase in absolute RVEF) in 15 of 18 patients, but only 5 of 10 patients were abnormal during O2 administration. LVEF at rest was normal in all subjects. These data suggest: 1) RV exercise ejection fraction is abnormal in most patients with chronic pulmonary disease; 2) while low flow O2 does not alter RV performance at rest, it improves RV exercise ejection fraction in some patients.

Ventricular Function in Children During Halothane Anesthesia

The effect of halothane on ventricular function in normal children was studied with the aid of echocardiography, which offers a noninvasive method to obtain these measurements safely. Thirteen healthy children ranging in age from 19 months to 12 years (mean=6 years), undergoing elective non-cardiac surgical procedures, were studied. Secobarbital, 4 mg/kg, and morphine, 0.1 mg/ kg, were administered intramuscularly an hour prior to induction of general anesthesia. Echocardiographic measurements were obtained while the patients breathed room air (control) and following nitrous oxide, 60 per cent, and concentrations of halothane ranging from 0.5 to 2 per cent. Increasing inspired concentrations of halothane significantly altered ventricular function in a dosedependent fashion. At halothane, 2 per cent, systolic blood pressure, pulse rate, and cardiac output decreased to 82, 94, and 72 per cent of control values, respectively. Measurements of ventricular performance, ejection fraction (EF), left ventricular enddiaslolic volume (LVEDV), and mean normalized rate of circumferential fiber shortening (Vuf) showed parallel decreases. Following atropine, 0.02 mg/kg, intravenously, improvement in cardiac output and all rate-dependent variables was observed. Although V,.r improved by 18 per cent, other indices of myocardial performance (EF, LVEDV, PEP/LVET) still showed depression. It is concluded that halothane can significantly decrease ventricular function in children undergoing surgical procedures. The accompanying decrease in cardiac output was completely offset by the administration of atropine.

Ventricular function in children during halothane anesthesia: an echocardiographic evaluation.

The effect of halothane on ventricular function in normal children was studied with the aid of echocardiography, which offers a noninvasive method to obtain these measurements safely. Thirteen healthy children ranging in age from 19 months to 12 years (mean=6 years), undergoing elective non-cardiac surgical procedures, were studied. Secobarbital, 4 mg/kg, and morphine, 0.1 mg/ kg, were administered intramuscularly an hour prior to induction of general anesthesia. Echocardiographic measurements were obtained while the patients breathed room air (control) and following nitrous oxide, 60 per cent, and concentrations of halothane ranging from 0.5 to 2 per cent. Increasing inspired concentrations of halothane significantly altered ventricular function in a dosedependent fashion. At halothane, 2 per cent, systolic blood pressure, pulse rate, and cardiac output decreased to 82, 94, and 72 per cent of control values, respectively. Measurements of ventricular performance, ejection fraction (EF), left ventricular enddiaslolic volume (LVEDV), and mean normalized rate of circumferential fiber shortening (Vuf) showed parallel decreases. Following atropine, 0.02 mg/kg, intravenously, improvement in cardiac output and all rate-dependent variables was observed. Although V,.r improved by 18 per cent, other indices of myocardial performance (EF, LVEDV, PEP/LVET) still showed depression. It is concluded that halothane can significantly decrease ventricular function in children undergoing surgical procedures. The accompanying decrease in cardiac output was completely offset by the administration of atropine.

Arterial blood gases in acute pulmonary edema

Arterial blood gas and pH measurements in 82 patients with acute pulmonary edema of cardiogenic origin entering the emergency department varied widely and were unpredictable using clinical examination. The mean arterial oxygen tension (PaO2) measured in 71 patients breathing room air was 59 mm Hg. Fourteen of the 82 patients were acidemic; 35, alkalemic and 33 had a pH in the normal range. The acidemic group had markedly lower PaO2, all under 60 mm Hg. Oxygen and furosemide were used in all cases and effectively corrected the hypoxia and reduced pulmonary congestion. Other drugs used included aminophylline (14 patients), morphine sulfate (9 patients) and digoxin (3 patients). Five of the nine patients who received morphine were hypercarbic initially but the CO2 retention did not worsen. No patient died during the initial 48 hours. This study reiterates the importance of directing therapy at ventilatory and cardiac abnormalities and points out the value of arterial blood gas monitoring to assess the initial status, monitor the patient's course, and to select drug therapy.

Alcohol dependence: provisional description of a clinical syndrome.

BACKGROUND: Oxygen therapy is effective in the prevention and treatment of oedematous exacerbations of cor pulmonale. As renal blood flow is reduced in cor pulmonale a study was designed to investigate whether one of the beneficial effects of oxygen was to increase renal blood flow. The effect of oxygen therapy on renal haemodynamics measured noninvasively was examined in patients with chronic obstructive airways disease and previous episodes of oedema. METHODS: Renal blood flow waveforms were recorded in a single vessel by colour flow Doppler ultrasound in nine hypoxaemic patients (PaO2) (arterial oxygen tension &lt; 8 kPa while they were breathing air) with chronic obstructive airways disease and previous oedema and eight age matched normoxaemic volunteers (arterial oxygen saturation (SaO2) 97% or more when breathing air) while they were breathing air and oxygen. SaO2 and transcutaneous PaO2 (TcPO2) and PaCO2 (TcPCO2) were monitored. Five renal velocity profile recordings were made from the same segmental vessel with the patient breathing room air for one hour followed by oxygen titrated to achieve an oxygen saturation of 95% or more without a rise in TcPCO2 for 15 minutes. Control subjects breathed 35% oxygen. RESULTS: No significant change in the pulsatility index (a measure of distal vascular resistance) or mean height of the waveform (Tamx, a measure of renal blood flow) occurred in the control subjects while they were breathing air or oxygen. The pulsatility index of the patients with chronic obstructive airways disease was significantly greater than that in the control subjects breathing air (1.44 (SD 0.28) v 1.03 (0.14). Breathing oxygen was associated with an increase in TcPO2 in the patients (from 6.9 (1.9) to 11.5 (0.7) kPa), a fall in pulsatility index (from 1.44 (0.28) to 1.26 (0.14) and an increase in Tamx (from 0.187 (0.055) to 0.234 (0.087) m/s). CONCLUSIONS: The results suggest that renal vascular resistance is increased in patients with chronic obstructive airways disease and hypoxaemia and that short term oxygen therapy reduces renal vascular resistance and increases blood flow. Some of the benefits of oxygen therapy in cor pulmonale may be due to improvements in renal haemodynamics.

ARTERIAL OXYGEN TENSION DURING LAPAROSCOPY WITH NITROUS OXIDE IN THE SPONTANEOUSLY BREATHING PATIENT

Arterial blood was sampled from 10 anaesthetized, spontaneously breathing patients before, during and after pelvic laparoscopy using N2O as the insufflating gas. There was little change in Paco2 during the procedure. With an inspired oxygen concentration of approximately 37%, the mean Pao2 decreased during laparoscopy from 163 mm Hg (±24 mm Hg) to 146 mm Hg (±28 mm Hg). In the postoperative period, with the patients breathing room air, the mean Pao2 was 78 mm Hg (± 10 mm Hg). In 2 other patients, who were heavy smokers, arterial Pao2 decreased to less than 100 mm Hg during laparoscopy and the mean Pao2 in the postoperative period with the patients breathing room air was 49 mm Hg (±0.07 mm Hg). One of these patients had significant airflow obstruction and impaired gas transfer. It is concluded that spontaneous ventilation during pelvic laparoscopy may be unsuitable for patients with lung disease, and that arterial hypoxaemia may occur in patients with apparently normal lung function.

Factitial Pulmonary Edema

To the Editor.— A recent experience at this hospital prompts recognition of an additional cause of noncardiac pulmonary edema. A 42-year-old woman was brought to the emergency room after she was found in the street obtunded, with labored respirations. Her blood pressure was 130/90 mm Hg; pulse rate, 110 beats per minute; temperature, 36.6 C; and respiration, 30/min, with peripheral cyanosis and frothy pink sputum. There was no jugular venous distension, and auscultation of the chest disclosed coarse breath sounds with both rales and rhonchi. Heart sounds were normal and there was no gallop. Other results of the examination were normal except for the patient's obtunded mental state. Arterial blood gas values with the patient breathing room air disclosed pH, 7.52; Po 2 , 44 mm Hg; and Pco 2 , 28 mm Hg. Chest roentgenograms showed bilateral, fluffy perihilar infiltrates. The electrocardiogram was within normal limits except for sinus tachycardia. The

ARTERIAL OXYGEN TENSION DURING LAPAROSCOPY WITH NITROUS OXIDE IN THE SPONTANEOUSLY BREATHING PATIENT

Arterial blood was sampled from 10 anaesthetized, spontaneously breathing patients before, during and after pelvic laparoscopy using N2O as the insufflating gas. There was little change in Paco2 during the procedure. With an inspired oxygen concentration of approximately 37%, the mean Pao2 decreased during laparoscopy from 163 mm Hg (±24 mm Hg) to 146 mm Hg (±28 mm Hg). In the postoperative period, with the patients breathing room air, the mean Pao2 was 78 mm Hg (± 10 mm Hg). In 2 other patients, who were heavy smokers, arterial Pao2 decreased to less than 100 mm Hg during laparoscopy and the mean Pao2 in the postoperative period with the patients breathing room air was 49 mm Hg (±0.07 mm Hg). One of these patients had significant airflow obstruction and impaired gas transfer. It is concluded that spontaneous ventilation during pelvic laparoscopy may be unsuitable for patients with lung disease, and that arterial hypoxaemia may occur in patients with apparently normal lung function.

Positive expiratory pressure plateau breathing in spontaneously breathing patients with myocardial infarction and pulmonary dema

<b>Kerr, F., Ewing, D. J., Irving, J. B., Sudlow, M. F., and Kirby, B. J. (1974).</b><i>Thorax</i>, <b>29</b>, 690-694. <b>Positive expiratory pressure plateau breathing in spontaneously breathing patients with myocardial infarction and pulmonary oedema.</b> The respiratory effects of breathing with a positive expiratory pressure plateau (PEPP) was studied in 24 spontaneously breathing, alert, nonsedated patients with pulmonary oedema following myocardial infarction. When 20 patients breathed room air with PEPP a small rise in arterial oxygen tension (<i>P</i>ao₂) with a fall in alveolar to arterial oxygen gradient (A—ado₂) occurred. Arterial carbon dioxide tension did not change significantly. When PEPP was used in six patients after breathing 100% oxygen for 20 minutes there was no significant change in <i>P</i>ao₂, A—ado₂ or anatomical shunt (Qs/Qt). Expired air collection in a further six of the patients demonstrated that although PEPP produced an increase in tidal volume (Vt), alveolar ventilation (Va) fell slightly as a result of a decrease in respiratory rate, and oxygen consumption (Vo₂) did not change. In 10 normal subjects functional residual capacity (FRC), measured continuously in a whole-body volume displacement plethysmograph, decreased by a small amount when these subjects breathed with PEPP. Positive expiratory pressure plateau breathing in spontaneously breathing conscious patients with pulmonary oedema produced a small improvement in ventilation/perfusion matching not by an increase in FRC but by an increase in Vt. The increase in Vt probably altered the ventilation/perfusion relationships by a redistribution of inspired gas.

Arterial hypoxaemia in acute myocardial infarction.

Summary: Serial measurements of arterial pO2, pCO2 and pH were made in 99 patients admitted to a coronary care unit with acute myocardial ischaemia or infarction. Samples were taken whilst the patients breathed room air and air enriched with oxygen in a concentration of approximately 40% via nasal cannulae. The degree of arterial hypoxaemia on room air correlated well with the degree of left ventricular failure. The increase in arterial oxygen tension produced by oxygen enrichment of the inspired air was greater in those with mild than in those with severe left ventricular dysfunction. The return of the arterial oxygen tension to normal after myocardial infarction may be protracted, suggesting that prolonged oxygen administration is advisable in the more severely ill patients. Levels of arterial pCO2 and pH were not found to be helpful in management.

NOMOGRAMS FOR CALCULATION OF OXYGEN CONSUMPTION AND RESPIRATORY EXCHANGE RATIO

Nomograms have been prepared whereby the respiratory exchange ratio may be derived from the concentrations of carbon dioxide and oxygen in expired gas and oxygen consumption from the volume and oxygen concentration of expired gas; they apply only to patients breathing room air. The nomogram for the respiratory exchange ratio has an error of less than 0·01, which is the limit of visual discrimination on the nomogram. The nomogram for oxygen consumption has an error of standard deviation 7·73 ml/min. This error may be substantially reduced by excluding cases with a respiratory exchange ratio outside the range 0·70-0·93. Under these conditions the maximum error was 10 ml/min, which is acceptable for a wide range of clinical purposes.

Relationship between pulmonary artery end-diastolic pressure and left ventricular filling pressure in patients in shock

Bedside catheterization permitted 56 simultaneous measurements of left ventricular end-diastolic pressure (LVEDP) and pulmonary artery end-diastolic pressure (PAEDP) in 25 patients in shock. Measurements were made over a wide range of heart rates (60-160 beats/min), arterial oxygen tension (Poo2; 33-562 mm Hg), stroke volumes (9-105 ml), and systolic arterial pressures (65-250 mm Hg), and before and during various therapeutic interventions. There was good correlation between PAEDP and LVEDP (r = +0.85) and PAEDP and left ventricular pre-a pressure (r = +0.82). In 16 patients breathing room air, mean arterial Poo2 was 58 ± 15 mm Hg and rose significantly to 282 ± 16 mm Hg after breathing oxygen (P<0.01), but there was no significant change in the correlation between PAEDP and LVEDP before (r = +0.80) or during oxygen breathing (r = +0.80). Similarly, in seven patients treated with inotropic agents there was excellent correlation between PAEDP and LVEDP before (r = +0.96) and during inotropic therapy (r = +...

Relationship between pulmonary artery end-diastolic pressure and left ventricular filling pressure in patients in shock.

Bedside catheterization permitted 56 simultaneous measurements of left ventricular end-diastolic pressure (LVEDP) and pulmonary artery end-diastolic pressure (PAEDP) in 25 patients in shock. Measurements were made over a wide range of heart rates (60-160 beats/min), arterial oxygen tension (P o o2 ; 33-562 mm Hg), stroke volumes (9-105 ml), and systolic arterial pressures (65-250 mm Hg), and before and during various therapeutic interventions. There was good correlation between PAEDP and LVEDP (r = +0.85) and PAEDP and left ventricular pre-a pressure (r = +0.82). In 16 patients breathing room air, mean arterial P o o2 was 58 ± 15 mm Hg and rose significantly to 282 ± 16 mm Hg after breathing oxygen (P&lt;0.01), but there was no significant change in the correlation between PAEDP and LVEDP before (r = +0.80) or during oxygen breathing (r = +0.80). Similarly, in seven patients treated with inotropic agents there was excellent correlation between PAEDP and LVEDP before (r = +0.96) and during inotropic therapy (r = +0.86). A PAEDP in excess of 15 mm Hg nearly always reflected increased LVEDP while a PAEDP less than 10 mm Hg was always associated with normal LVEDP. Thus in our patients with shock PAEDP represented a good estimate of LVEDP during a variety of therapeutic interventions and therefore represents a useful tool in guiding the therapy of patients in shock.

Respiratory Effects of Ethyl Alcohol Intoxication

<h3>To the Editor.—</h3> Death from acute alcohol intoxication is thought by many to be due to respiratory failure. Yet in recent laboratory studies, moderately intoxicating doses of ethyl alcohol (120 mg/100 ml) had no consistent effect on respiratory rate or minute volume and sometimes increased ventilation. We therefore studied ten severely intoxicated adults brought to the Cincinnati General Hospital emergency unit. Very high blood concentrations of ethyl alcohol (BEC) in these patients caused only moderate respiratory depression. The patients were chronic alcoholics without clinical evidence of cardiopulmonary disease. Screening of blood samples by means of gas chromatography excluded the presence of other drugs in addition to ethyl alcohol. Of the ten patients, two were unconscious and eight were conscious but lethargic, with slurred speech and incoordination. Arterial blood for pH and gas analysis was drawn while the patients breathed room air. Venous BEC were determined by gas chromatography. Arterial blood

Nomograms for calculation of oxygen consumption and respiratory exchange ratio.

Nomograms have been prepared whereby the respiratory exchange ratio may be derived from the concentrations of carbon dioxide and oxygen in expired gas and oxygen consumption from the volume and oxygen concentration of expired gas; they apply only to patients breathing room air. The nomogram for the respiratory exchange ratio has an error of less than 0.01, which is the limit of visual discrimination on the nomogram. The nomogram for oxygen consumption has an error of standard deviation 7.73 ml/min. This error may be substantially reduced by excluding cases with a respiratory exchange ratio outside the range 0.70-0.93. Under these conditions the maximum error was 10 ml/min, which is acceptable for a wide range of clinical purposes.