Direct response question. The question tells the story of a patient with acute pancreatitis who is developing acute respiratory failure. The statement lists the criteria for ARDS (acute respiratory distress syndrome): PaO2/fiO2 < 200 + bilateral pulmonary infiltrates + PCP<18. So the diagnosis is respiratory distress and therefore the correct answer is option 5.

Direct response question. The question tells the story of a patient with acute pancreatitis who is developing acute respiratory failure. The statement lists the criteria for ARDS (acute respiratory distress syndrome): PaO2/fiO2 < 200 + bilateral pulmonary infiltrates + PCP<18. So the diagnosis is respiratory distress and therefore [HIDDEN].

A patient admitted for acute pancreatitis starts with tachypnea, tachycardia, sweating and progressive cyanosis. PaO2 is 55 mm Hg (PaO2/FiO2 ratio<200). CXR shows bilateral alveolar pulmonary infiltrates. Pulmonary capillary wedge pressure is normal. Oxygen therapy does not improve the situation. What is the most probable diagnosis:

ANESTHESIOLOGY, CRITICAL CARE AND EMERGENCIES

[Acute respiratory distress caused by distal neoplastic pulmonary emboli].

In contrast to pulmonary parenchyma metastases or lymphangitic carcinomatosis, neoplastic emboli of small pulmonary arteries and capillaries frequently go unrecognized and are only discovered at autopsy. Five patients (48 +/- 12 years old) were admitted to 3 intensive care units for severe acute respiratory failure and died between the first and the tenth day following hospitalization. Each patient had a history of rapidly progressive dyspnea, and physical examination showed clinical evidence of right ventricular failure. The lungs were clear on chest X-rays and the ECG revealed sinus tachycardia with a right QRS axis. The mean partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2) were, respectively, 50.8 +/- 9.1 mm Hg and 22.2 +/- 2.4 mm Hg. A swan-Ganz catheter, inserted into 4 patients, revealed pulmonary arterial hypertension (55, 43, 37, 28) with capillary wedge pressure within the normal limits and cardiac output normal or low (3.0, 3.8, 4.4, 5.0 l/min). Pulmonary angiograms from each patient showed decreased distal lung perfusion without any proximal defects suggestive of pulmonary embolism. The inferior vena cava always appeared clear. Malignant cells were found upon autopsy (4 cases) in the lumina of the pulmonary arterioles and the primary site of the cancer was determined in 3 patients (2 hepatomas and 1 pancreatic carcinoma). The last patient had a known breast cancer with bone marrow metastases and clinical, hemodynamic and angiographic evidence of neoplastic emboli. The clinical course of neoplastic emboli can suggest acute pulmonary embolism, but the diagnosis can only be advanced after pulmonary angiography, especially if the patient is to have a cancer.(ABSTRACT TRUNCATED AT 250 WORDS)

[Extracorporeal membrane oxygenation for severe acute respiratory and heart failure in a child with severe pneumonia].

To report clinical application of Extracorporeal membrane oxygenation for severe acute respiratory and heart failure in a child with severe pneumonia. A seven-year old male patient with severe pneumonia complicated with heart and lung function failure was admitted to PICU in 28th of December, 2008.Veno-artery access was set up via euthyphoria cannulation in operative incision. Blood was drained from the right atrium through a cannula introduced via femoral veins, and returned via femoral artery. The inter-surface of the ECMO equipment system was completely coated with heparin-coating technique. Anticoagulation was maintained with heparin to keep the activated clotting time (ACT) between 150 and 200 seconds and heparin usage dose was 10 U/(kg.h), mean blood flow was 1/2-2/3 of 80-120 ml/(kg.min) during ECMO assistant period. During ECMO, ventilator settings were gradually reduced to allow lung rest, i.e. peak inspiratory pressure less than 25 cm H2O (1 cm H2O=0.098 kPa), end expiratory pressure 8-10 cm H2O, rate 10-15 breaths per minute and FiO2 30%-40%. In management of ECMO, the incipient blood flow was set at 0.8 L/min, the radio of oxygen and blood flow was 1:1, FiO2 60%. After ten minutes of ECMO working, the blood oxygen saturation of radial artery increased from 40 mm Hg (1 mm Hg=0.133 kPa) to 177 mm Hg, Lac decreased from 3.5 mmol/L to 2.8 mmol/L. Four hours later, blood gas analysis of radial artery showed PaO2 202 mm Hg, PCO2 44 mm Hg, Lac 1.5 mmol/L, blood flow was set at 0.6 L/min, FiO2 60%, PaO2 kept above 150 mm Hg. 96 hours after ECMO supporting, the blood flow was set at 0.4 L/min [20 ml/(kg.min)], the results of blood gas analysis of radial artery was PaO2 190 mm Hg, PaCO2 36 mm Hg, SaO2 100%, Lac 0.9 mmol/L, then the child weaned off successfully from ECMO. Two days later, the child was successfully extubated. After two weeks treatment, the patient was discharged. The main complication associated with extracorporeal membrane oxygenation were bleeding. ECMO is an effective mechanical assistant therapy method for severe pulmonary and cardiac failure in a child.

Acute Respiratory Distress Syndrome diagnosis after coronary artery bypass: comparison between diagnostic criteria and clinical picture.

Acute Respiratory Distress Syndrome (ARDS) is a potential complication of cardiac surgery, given that patients undergoing CABG frequently have hypoxemia and pulmonary dysfunction during initial hours after surgery. Thus, ARDS criteria in these patients are more likely to be positive while these criteria may not match the patient`s clinical picture. We aimed to investigate frequency of rapid onset hypoxemia in Pressure of Arterial Oxygen to Fractional Inspired Oxygen Concentration (PaO2/FiO2) less than 200 and diffuse pulmonary infiltrates as two diagnostic criteria forwards and compared these criteria with the clinical picture of the patients after Coronary Artery Bypass Graft (CABG) in this study. The study was prospective case series which carried out in about six months. All patients admitted to intensive care unit of Tehran Heart Center, who had undergone CABG on cardiopulmonary pump (CPB) recruited in the study. After considering inclusion criteria, age, sex, duration of intubation, arterial blood gas and chest radiography, on 24 hours and 48 hours after admission to the ICU were recorded. Then, patients with rapid onset of hypoxemia (PaO2/FiO2≤200mmHg) and diffuse pulmonary infiltrates and without sign or symptoms of obvious heart failure (probable positive ARDS cases) criteria were recorded and comparison between these probable positive cases with clinician`s clinical diagnosis (blinded to the study) was performed. In this study, a total of 300 patients after on-pump coronary artery bypass surgery were included. Postoperatively, 2 (0.66 %) in the 24 hours and 4 (1.33%) patients in 48 hours after surgery were positive for the two ARDS criteria according to the checklists, but; nobody had saved persistently ARDS criteria persistently during 48 hours after surgery. At the same time, clinician did not report any case of ARDS among 300 patients. In this study patients with ARDS criteria had no significant differences in age (P.value=0.937) and sex (P.value=0.533). Duration of intubation in patients with ARDS (14.26 ± 4.25 hours) in the first 48 hours was higher but not statistically different from the group without ARDS (11.60 ± 5.45 hours) (P.value=0.236). ARDS diagnosis based on rapid onset of hypoxemia (PaO2/FiO2≤200 mmHg) and diffuse pulmonary infiltrates and without signs or symptoms of obvious heart failure criteria in patients undergoing CABG could lead to overdiagnosis or misdiagnosis in less than 24 hours follow up. We recommend following patients for more than 24 hours and revise the current ARDS criteria for CABG patients.

Acute Respiratory Failure in Renal Transplant Recipients: A Single Center Experience.

We evaluated the frequency and cause of acute respiratory failure in renal transplant recipients. Our single-center retrospective observational study included consecutive renal transplant recipients who were admitted to an intensive care unit for acute respiratory failure between 2011 and 2017. Acute respiratory failure was defined as oxygen saturation < 92% or partial pressure of oxygen in arterial blood < 60 mm Hg on room air and/or requirement of noninvasive or invasive mechanical ventilation. Of 187 renal transplant recipients, 35 (18.71%) required intensive care unit admission; 11 of these patients (31.4%) were admitted to the intensive care unit with acute respiratory failure. Six of these patients (54.5%) had pneumonia and had shown infiltrates on chest radiography, which were shown in a minimum of 3 zones of the lung (2 with Klebsiella pneumonia, 1 with Acinetobacter species, 1 with Proteus mirabilis, 2 with no microorganisms). The other reasons for acute respiratory failure were cardiogenic pulmonary edema (2 patients), acute respiratory distress syndrome (2 patients, due to acute pancreatitis and acute cerebrovascular thromboembolism), and exacerbation of chronic obstructive pulmonary disease (1 patient). Six patients (54.5%) needed invasive mechanical ventilation because of pneumonia (3 patients), cardiogenic pulmonary edema (2 patients), and cerebrovascular thromboembolism (1 patient). Hemodialysis was administered in 5 patients (45%). Six of 11 patients died due to pneumonia (3 p atients), cardiogenic pulmonary edema (2 patients), and cerebrovascular thromboembolism (1 patient). Among the 5 survivors, 3 (60%) had recovered previous graft function. Acute respiratory failure is associated with high mortality and morbidity in renal transplant recipients. Main causes of acute respiratory failure were bacterial pneumonia and cardiogenic pulmonary edema in our study population. Extended chemoprophylaxis for bacterial and fungal infection and early intensive care unit admission of patients with acute respiratory failure may improve outcomes.

Early Identification of Acute Respiratory Distress Syndrome in the Absence of Positive Pressure Ventilation: Implications for Revision of the Berlin Criteria for Acute Respiratory Distress Syndrome.

To assess whether patients breathing spontaneously under standard oxygen could be recognized early as acute respiratory distress syndrome patients according to the current Berlin definition. A post hoc analysis from two prospective studies. Twenty-three French ICUs. All patients admitted for acute hypoxemic respiratory failure and treated with noninvasive ventilation were analyzed. Patients with cardiogenic pulmonary edema, acute exacerbation of chronic obstructive pulmonary disease, or hypercapnia were excluded. None. The PaO2/FIO2 ratio was estimated at admission under standard oxygen and then under noninvasive ventilation 1 hour after initiation and within the first 24 hours. Among the 219 patients treated with noninvasive ventilation for acute hypoxemic respiratory failure, 180 (82%) had bilateral infiltrates including 161 patients with PaO2/FIO2 less than or equal to 300 mm Hg under standard oxygen. Among them, 127 were treated with positive end-expiratory pressure of at least 5 cm H2O, and 120 (94%) fulfilled criteria for acute respiratory distress syndrome within the first 24 hours. The mortality rate of patients with bilateral infiltrates and PaO2/FIO2 less than or equal to 300 mm Hg under standard oxygen was 29%, a rate very close to that of intubated patients with acute respiratory distress syndrome in the Berlin definition. Almost all patients with pulmonary bilateral infiltrates and a PaO2/FIO2 less than or equal to 300 mm Hg under standard oxygen fulfilled the acute respiratory distress syndrome criteria under noninvasive ventilation within the first 24 hours. Their mortality rate was similar to that reported in the Berlin definition of acute respiratory distress syndrome. Therefore, spontaneous breathing patients with the acute respiratory distress syndrome criteria could be identified early without positive pressure ventilation.

Diffuse alveolar damage

Berlin Criteria: as stated on UpToDate (2020) Timing: onset of respiratory symptoms within one week of a injury/insult. Chest Imaging: either chest x-ray or CT scan, must show bilateral opacities that cannot be fully explained by other conditions such as effusion, lung/lobar collapse, or lung nodules. Origin of Edema: respiratory failure that cannot be fully explained by cardiac failure or fluid overload, this needs objective assessment such as an echocardiogram. Impaired Oxygenation: this can be determined by looking at the ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) that can be obtained based on an arterial blood gas test. Note: all PaO2/FiO2 ratios used in the determination of the severity of ARDS require that the patient be on a ventilator at a setting that includes 5 cm H2O or more of positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP).

Acute respiratory distress syndrome

Causes may include sepsis, pancreatitis, trauma, pneumonia, and aspiration. The underlying mechanism involves diffuse injury to cells which form the barrier of the microscopic air sacs of the lungs, surfactant dysfunction, activation of the immune system, and dysfunction of the body's regulation of blood clotting. In effect, ARDS impairs the lungs' ability to exchange oxygen and carbon dioxide. Adult diagnosis is based on a PaO2/FiO2 ratio (ratio of partial pressure arterial oxygen and fraction of inspired oxygen) of less than 300 mm Hg despite a positive end-expiratory pressure (PEEP) of more than 5 cm H2O. Cardiogenic pulmonary edema, as the cause, must be excluded.

Increased mortality of older patients with acute respiratory distress syndrome.

To examine the relationship between age and mortality in ARDS patients and evaluate the importance of factors that increase the mortality of older ARDS patients. Prospective inception cohort study. Community-based referral hospital. Two hundred fifty-six ARDS patients identified from May 1987 to December 1990. ARDS was defined by the following: (1) PaO2/PAO2 < or = 0.2; (2) pulmonary capillary wedge pressure < or = 15 mm Hg; (3) total static thoracic compliance < or = 50 mL/cm H2O; (4) bilateral infiltrates on chest radiograph; and (5) an appropriate clinical setting for ARDS. Comparison of organ failure, incidence of sepsis, patient demographics, arterial oxygenation, and level of support in those 55 years and younger and those older than 55 years of age. Withdrawal of support in patients who died. Seventy-two of 112 patients older than 55 years (64%) died vs 65 of 144 patients 55 years and younger (45%) (p = 0.002). Examination of patient groups using age identified older than 55 years as a "cutpoint" above which mortality was greater (p = 0.002). Older nonsurvivors did not differ from nonsurvivors 55 years or younger with respect to gender, smoking history, ARDS risk factors, ARDS identifying characteristics, APACHE II (acute physiology and chronic health evaluation), number of organ failures, or the incidence of sepsis. In the 48 h prior to death, nonsurvivors 55 years and younger had more organ failure (3.4 +/- 0.2 vs 2.8 +/- 0.2; p = 0.03), higher fraction of inspired oxygen (0.82 +/- 0.03 vs 0.68 +/- 0.03; p = 0.008), and higher positive end-expiratory pressure levels (13 +/- 1 vs 8 +/- 1; p = 0.001) than older nonsurvivors. Despite more severe expression of disease, only 32 (50%) nonsurvivors 55 years and younger had support withdrawn. Significantly more nonsurvivors older than 55 years (73%) had support withdrawn (p = 0.009). Even in the absence of chronic disease states, withdrawal was more likely for patients older than 55 years (21/51) than in those 55 years and younger (3/32; p < 0.001). Mortality is significantly higher for patients with ARDS older than 55 years. Decisions to withdraw support are made more often in ARDS patients older than 55 years. These data suggest that age bias may influence decisions to withdraw support.

First_Aid_Step2

Phase 1 (acute injury): Normal physical exam; possible respiratory alkalosis. Phase 2 (6–48 hours): Hyperventilation, hypocapnia, widening A-a oxygen gradient. Phase 3: Acute respiratory failure, tachypnea, dyspnea, ↓ lung compliance, scattered rales, diffuse chest infltrates on CXR (see Figure 2.15-5). F IGU R E 2.1 5-5. AP CXR showing a diffuse alveolar filling pattern 2° to ARDS. (Reproduced, with permission, from Kasper DL et al. Harrison’s Principles of Internal Medicine, 16th ed. New York: McGraw-Hill, 2005: 1497.) ■ Phase 4: Severe hypoxemia unresponsive to therapy; ↑ intrapulmonary shunting; metabolic and respiratory acidosis. The criteria for ARDS diagnosis (according to the American-European Consensus Conference defnition) are as follows: Acute onset of respiratory distress. PaO2/FiO2 ratio ≤ 200 mmHg. Bilateral pulmonary infltrates on CXR. No evidence of cardiac origin (capillary wedge pressure < 18 mmHg or no clinical evidence of elevated left atrial pressure).

Acute respiratory distress syndrome: frequency, clinical course, and costs of care.

To define the occurrence rate of acute respiratory distress syndrome (ARDS) using established criteria in a well-defined general patient population, to study the clinical course of ARDS when patients were ventilated using a "lung-protective" strategy, and to define the total costs of care. A 3-yr (1993 through 1995) retrospective descriptive analysis of all patients with ARDS treated in Kuopio University Hospital. Intensive care unit in the university hospital. Fifty-nine patients fulfilled the definition of ARDS: Pao2/Fio2 <200 mm Hg (33.3 kPa) during mechanical ventilation and bilateral infiltrates on chest radiograph. None. With a patient data management system, the day-by-day data of hemodynamics, ventilation, respiratory mechanics, gas exchange, and organ failures were collected during the period that Pao2/Fio2 ratio was <200 mm Hg (33.3 kPa). The frequency of ARDS was 4.9 cases/100,000 inhabitants/yr. Pneumonia and sepsis were the most common causes of ARDS. Mean age was 43+/-2 yrs. At the time of lowest Pao2/Fio2, the nonsurvivors had lower arterial and venous oxygen saturations and higher arterial lactate than survivors, whereas there were no differences between the groups in other parameters. Multiple organ dysfunction preceded the worst oxygenation in both the survivors and nonsurvivors. The intensive care mortality was 37%; hospital mortality and mortality after a minimum 8 months of follow-up was 42%. The most frequent cause of death was multiple organ failure. The effective costs of intensive care per survivor were US $73,000. The outcome of ARDS is unpredictable at the time of onset and also at the time of the worst oxygenation. Keeping the inspiratory pressures low (30-35 cm H2O [2.94 to 3.43 kPa]) reduces the frequency of pneumothorax, and might lower the mortality. Most patients are young, and therefore the costs per saved year of life are low.

InternalMed_Harrison

MAJOR COMPLICATIONS Cardiopulmonary Complications Ventilation-perfusion mismatching produces a fall in arterial Po2 early in the course. Increasing alveolar epithelial injury and capillary permeability result in increased pulmonary water content, which decreases pulmonary compliance and interferes with oxygen exchange. In the absence of pneumonia or heart failure, progressive diffuse pulmonary infiltrates and arterial hypoxemia occurring within 1 week of a known insult indicate the development of mild acute respiratory distress syndrome (ARDS) (200 mmHg < Pao2/Fio2 ≤ 300 mmHg), moderate ARDS (100 mmHg < Pao2/Fio2 ≤ 200 mmHg), or severe ARDS (Pao2/Fio2 ≤100 mmHg). Acute lung injury or ARDS develops in ~50% of patients with severe sepsis or septic shock. Respiratory muscle fatigue can exacerbate hypoxemia and hypercapnia. An elevated pulmonary capillary wedge pressure (>18 mmHg) suggests fluid volume overload or cardiac failure rather than ARDS. Pneumonia caused by viruses or by

Respiratory failure

This type of respiratory failure is caused by conditions that affect oxygenation, such as: Low ambient oxygen (e.g. at high altitude) Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism) Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe. Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia or ARDS) Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt) Type 2 Hypoxemia (PaO2 <8kPa or normal) with hypercapnia (PaCO2 >6.0kPa). The basic defect in type 2 respiratory failure is characterized by: {| class="wikitable" |PaO2 || decreased (< )or normal |- | PaCO2 || increased (> ) |- | PA-aO2 || normal |- |pH || <7.35 |}

InternalMed_Harrison

This type of respiratory failure occurs with alveolar flooding and subsequent intrapulmonary shunt physiology. Alveolar flooding may be a consequence of pulmonary edema, pneumonia, or alveolar hemorrhage. Pulmonary edema can be further categorized as occurring due to elevated pulmonary microvascular pressures, as seen in heart failure and intravascular volume overload or ARDS (“low-pressure pulmonary edema,” Chap. 322). This syndrome is defined by acute onset (≤1 week) of bilateral opacities on chest imaging that are not fully explained by cardiac failure or fluid overload and of shunt physiology requiring positive end-expiratory pressure (PEEP). Type I respiratory failure occurs in clinical settings such as sepsis, gastric aspiration, pneumonia, near-drowning, multiple blood transfusions, and pancreatitis. The mortality rate among patients with ARDS was traditionally very high (50–70%), although changes in patient care have led to mortality rates closer to 30% (see below).

Fraction of inspired oxygen

Equations Abbreviated alveolar air equation PAO2, PEO2, and PIO2 are the partial pressures of oxygen in alveolar, expired, and inspired gas, respectively, and VD/Vt is the ratio of physiologic dead space over tidal volume. Medicine In medicine, the FIO2 is the assumed percentage of oxygen concentration participating in gas exchange in the alveoli. Uses The FIO2 is used in the APACHE II (Acute Physiology and Chronic Health Evaluation II) severity of disease classification system for intensive care unit patients. For FIO2 values equal to or greater than 0.5, the alveolar–arterial gradient value should be used in the APACHE II score calculation. Otherwise, the PaO2 will suffice. The ratio between partial pressure of oxygen in arterial blood (PaO2) and FIO2 is used as an indicator of hypoxemia per the American-European Consensus Conference on lung injury. A high FIO2 has been shown to alter the ratio of PaO2/FIO2.

Maternal near miss

Cardiovascular dysfunction a) Shock b) Cardiac Arrest c) Severe hypoperfusion (lactate >5 mmol/L or >45 mg/dL) d) Severe acidosis (pH<7.1) e) Use of continuous vasoactive drugs f) Cardio-pulmonary resuscitation Respiratory dysfunction g) Acute cyanosis h) Gasping i) Severe tachypnea (respiratory rate>40 breaths per minute) j) Severe bradypnea (respiratory rate<6 breaths per minute) k) Severe hypoxemia (O2 saturation <90% for ≥60min or PAO2/FiO2<200) l) Intubation and ventilation not related to anaesthesia Renal dysfunction m) Oliguria non responsive to fluids or diuretics n) Severe acute azotemia (creatinine >300 μmol/ml or >3.5 mg/dL) o) Dialysis for acute renal failure Coagulation dysfunction p) Failure to form clots q) Severe acute thrombocytopenia (<50,000 platelets/ml) r) Massive transfusion of blood or red cells (≥ 5 units) Hepatic dysfunction s) Jaundice in the presence of pre-eclampsia

Pulmonary wedge pressure

Noninvasive estimation techniques have been proposed. Clinical significance Because of the large compliance of pulmonary circulation, it provides an indirect measure of the left atrial pressure. For example, it is considered the gold standard for determining the cause of acute pulmonary edema; this is likely to be present at a PWP of >20mmHg. It has also been used to diagnose severity of left ventricular failure and mitral stenosis, given that elevated pulmonary capillary wedge pressure strongly suggests failure of left ventricular output. Traditionally, it was believed that pulmonary edema with normal PWP suggested a diagnosis of acute respiratory distress syndrome (ARDS) or non cardiogenic pulmonary edema (as in opiate poisoning). However, since capillary hydrostatic pressure exceeds wedge pressure once the balloon is deflated (to promote a gradient for forward flow), a normal wedge pressure cannot conclusively differentiate between hydrostatic pulmonary edema and ARDS.

First_Aid_Step2

Removal of the extrinsic cause or treatment of underlying infection if identifed. Corticosteroid treatment may be used if no cause is identif ed. Causes include ventilation-perfusion (V/Q) mismatch, right-to-left shunt, hypoventilation, low inspired O2 content (important at altitudes), and diffusion impairment. Findings depend on the etiology. ↓HbO2 saturation, cyanosis, tachypnea, shortness of breath, pleuritic chest pain, and altered mental status may be seen. Pulse oximetry: Demonstrates ↓ HbO2 saturation. CXR: To rule out ARDS, atelectasis, or an infltrative process (e.g., pneumonia) and to look for signs of pulmonary embolism. ABGs: To evaluate PaO2 and to calculate the alveolar-arterial (A-a) oxygen gradient ([(Patm − 47) × FiO2 − (PaCO2/0.8)] − PaO2). An ↑ A-a gradient suggests a V/Q mismatch or a diffusion impairment. Figure 2.15-4 summarizes the approach toward hypoxemic patients. Is PaCO2 increased? Hypoventilation Yes Yes No No Is PAO2 − PaO2 increased?

Studies on pulmonary function in patients during respiratory treatment. Diagnostic and prognostic evaluations.

Twenty-nine patients, divided into three groups: 1) chronic obstructive pulmonary disease; 2) acute or chronic pulmonary disease with left heart failure; 3) respiratory insufficiency after peritonitis, pancreatitis, and/or sepsis, were studied during respirator treatment with regard to gas exchange, breathing mechanics and central circulation. The dead space ventilation was somewhat greater in group 1 than in the other groups. The alveolar-arterial oxygen tension difference was least in group 1, greater in group 2 and extremely high in group 3. Neither dynamic compliance of the thorax nor inspiratory resistance showed any significant differences between the groups. The cardiac output had the highest values in group 3. The venous admixture was generally small in group 1 and extremely large in group 3. The pulmonary artery pressures were highest in group 2. Three variables proved to be valuable when assessing the prognosis of a patient: a large venous admixture; a large alveolar-arterial oxygen tension difference, and a high pulmonary artery pressure indicated a less favourable prognosis.

THE TREATMENT OF ANOXEMIA IN PNEUMONIA IN AN OXYGEN CHAMBER.

1. The use of an oxygen chamber in the treatment of pneumonia patients makes it possible to administer this gas for long periods of time under exactly known conditions. The medical and nursing care of the patient is greatly facilitated. 2. Prolonged inhalation of oxygen varying from 40 to 60 per cent appears to be without harm. 3. Oxygen administered to intensely anoxemic patients almost immediately clears up this anoxemia. Cyanosis disappears with the anoxemia. 4. The removal of patients from the high oxygen while they are still sick and while examination shows that there are still extensive edema and infiltration of the lung results in a return of the intense anoxemia. 5. It is sometimes impossible to clear up the anoxemia, even when as high as 60 per cent of oxygen is given, especially when there are considerable edema and infiltration of the lungs. 6. Five cases in which the prognosis was grave recovered. Three cases, one of tuberculosis, one with a Pneumococcus Type III infection, and a third with a pneumonia superimposed on a chronic pulmonary condition, died. 7. In all cases there appeared to be an improvement in the patient's condition. In one case, particularly, with an intense degree of anoxemia, the patient became moribund and pulseless. Following the administration of 60 per cent of oxygen there was a lowering of the heart rate from 160 to 120, the return of the pulse to the radial artery, the color became bright pink, and there was a remarkable change in the clinical condition. 8. The anoxemia of pneumonia is due, in large measure, to an impairment of the respiratory surface of the lungs. The greater the lung involvement the greater the anoxemia. Especially is this so when the pneumonic process extends throughout the lungs so that there are many patches of bronchopneumonia, with accompanying bronchitis and edema, as evidenced by the presence of râles throughout the lungs. 9. Rapid and shallow breathing of the degree observed in pneumonia is, as far as present evidence shows, of less importance in the production of anoxemia.

Extracorporeal membrane oxygenation

Guidelines that describe the indications and practice of ECMO are published by the Extracorporeal Life Support Organization (ELSO). Criteria for the initiation of ECMO vary by institution, but generally include acute severe cardiac or pulmonary failure that is potentially reversible and unresponsive to conventional management. Examples of clinical situations that may prompt the initiation of ECMO include the following: Hypoxemic respiratory failure with a ratio of arterial oxygen tension to fraction of inspired oxygen (PaO2/FiO2) of <100 mmHg despite optimization of the ventilator settings, including the fraction of inspired oxygen (FiO2), positive end-expiratory pressure (PEEP), and inspiratory to expiratory (I:E) ratio Hypercapnic respiratory failure with an arterial pH <7.20 Refractory cardiogenic shock Cardiac arrest Failure to wean from cardiopulmonary bypass after cardiac surgery As a bridge to either heart transplantation or placement of a ventricular assist device

Inhaled nitric oxide in acute respiratory distress syndrome.

Inhaled nitric oxide has been shown to improve oxygenation in select patients with acute respiratory distress syndrome (ARDS). The purpose of this study was to evaluate the clinical response to four concentrations of inhaled nitric oxide (NO) in 20 patients with ARDS. All patients with ARDS were eligible for the study. ARDS was defined as (1) the presence of a predisposing factor; (2) a PaO2/FiO2 ratio < 200; (3) bilateral infiltrates on chest radiograph; and (4) absence of evidence of congestive heart failure and pulmonary artery wedge pressure < 18 mm Hg. Patients received each of four doses (1, 15, 30, and 60 ppm) in random order, each for a 3-hour period. Cardiovascular variables were continuously monitored, and arterial and mixed venous blood gas measurements were obtained at 30 minutes and 3 hours. Thirteen of the 20 patients demonstrated a significant increase in their PaO2/FiO2 (> 20% increase) when treated with inhaled NO. The administration of inhaled NO was associated with an increase in oxygenation at doses of 1, 15, and 30 ppm, but not 60 ppm. Increasing NO dose to more than 1 ppm did not significantly improve response. Mean pulmonary artery pressure decreased with increasing NO concentration, but this did not reach statistical significance. Nine of the 13 responding patients and 2 of the 7 nonresponding patients survived. Inhaled NO was successful in increasing PaO2/FiO2 by > 20% in 65% of the surgical patients in this trial. Response to NO could not be predicted by initial PaO2/FiO2 or pulmonary artery pressures. A trial of inhaled NO at a dose of < 10 ppm may be helpful in ARDS patients requiring increasing FiO2 and positive end-expiratory pressure.

High peak PaO2 values associated with adverse outcome in patients treated with noninvasive ventilation for acute cardiogenic pulmonary edema and pneumonia.

Noninvasive ventilation (NIV) has a sigificant impact on mortality in acute respiratory failure (ARF). Predictive parameters for mortality are of high interest. We retrospectively analyzed 3759 blood gas analysis and clinical parameters of 475 patients presenting with ARF based on acute cardiogenic pulmonary edema and/or pneumonia. The influence of peak arterial oxygen partial pressure levels (PaO2) with respect to its predictive value for in-hopital and long-term mortality was investigated. Overall intra-hospital mortality was 24%. Peak PaO2 levels in kPa were significantly higher in non-survivors (20.01±10.11) compared to survivors (15.65±6.79, P<0.001). A univariate Cox proportional-hazards analysis for long-term mortality revealed associations with maximum PaO2 levels (overall cohort: HR= 1.02; 95% CI: 1.007-1.03; P=0.003; CPE: HR= 1.02; 95% CI: 0.99-1.04, P=0.05, pneumonia: HR= 1.02; 95% CI: 1-1.4, P=0.02). A PaO2 cut-off value of 13 kiloPascal (kPa) was calculated by means of Youden Index and remained true even after correction for APACHE 2 Score (HR= 1.50; 95% CI: 1.00-2.25; P=0.05) and for PaCO2 (HR= 1.63; 95% CI: 1.14-2.33; P=0.01). Peak PaO2 levels were associated with worse in-hopital and long-term mortality in patients treated with NIV due to ARF. These findings may indicate that application of high oxygen may be detrimental in such patients.

[Prognosis of chronic obstructive pulmonary disease after acute respiratory failure].

We followed the course of 53 patients (male 38, female 15 and average age 66 +/- 10) with chronic obstructive pulmonary disease hospitalized in our intensive care unit due to acute episode of respiratory failure. Etiologies of acute respiratory failure, patient's clinical data and arterial blood gases analysis were recorded. Most of the results showed no significant difference between the initial survival and the non-survival group. Low hematocrit. hypoalbulinemia and severe hypoxemia were found in the dead group but relative hypercapnea in the survival group was noted. Infection was the most common cause of acute respiratory failure and following by congestive heart failure, pneumothorax and asphyxia. Intubation and mechanical ventilator were needed in all patients except 3 cases to whom only conservative treatment was given. Hospital mortality was 50.9 percent (27/53) and most of the cases (22/53) died in the intensive care unit. Twenty six cases (49.1%) were discharged from the hospital and follow-up was continued for at least two years. Fifteen patients died during two year follow-up and except for one suicide case all died of repeated respiratory failure. The two year survival was only 20.8 percent (11/53). The prognosis of patients with chronic obstructive pulmonary disease following an episode of acute respiratory failure is poor.

[Acute respiratory failure in a medical intensive care unit. Incidence and prognosis].

Acute respiratory failure had occurred in 89 of 1594 patients in a medical intensive care unit (5.6%), 26.8% of all patients (332) on long-term mechanical ventilation. Compared with the other chronically ventilated patients those with acute respiratory failure averaged a lower age, the proportion of women was higher and the duration of ventilation longer. The death rate was significantly higher (78.7% compared with 58.3%). The important prognostic factors included the underlying disease, additional abnormal organ function, severity of pulmonary gas exchange abnormality, and advanced age. If there was septicaemia, peritonitis, liver cirrhosis with bleeding oesophageal varices or polytrauma with acute renal failure the death rate was over 80%; after hypovolaemic shock, pancreatitis or postoperative pulmonary failure it was less than 65%. Patients who had abnormal function of at most one other organ in addition and an inspiratory arterial pO2 difference below 250 mm Hg, measured 12 hours after onset of mechanical ventilation, had a relatively favourable prognosis with a death rate of 33%, while in the other groups of patients it was 86-100%.

First_Aid_Step2

PaO2/FiO2 ratio ≤ 200 mmHg. Bilateral pulmonary infltrates on CXR. No evidence of cardiac origin (capillary wedge pressure < 18 mmHg or no clinical evidence of elevated left atrial pressure). There is no standard treatment. Treat the underlying disease and maintain adequate perfusion to prevent end organ damage. Minimize injury induced by mechanical ventilation by ventilating with low tidal volumes. Use PEEP to recruit collapsed alveoli and titrate PEEP and FiO2 to achieve adequate oxygenation. Goal oxygenation is PaO2 > 60 mmHg or SaO2 > 90% on FiO2 ≤ 0.6. Slowly wean patients from ventilation, and follow with extubation trials (see Table 2.15-6). Pulmonary hypertension is defned as a mean pulmonary arterial pressure of > 25 mmHg (normal = 15 mmHg). It is classifed as either 1° (if the etiology

Factors affecting perioperative pulmonary function in acute respiratory failure.

To determine the magnitude, duration, and associated factors of perioperative changes in pulmonary function, we retrospectively reviewed the medical records of 145 patients who required preoperative mechanical ventilation for acute respiratory failure before undergoing 200 surgical procedures. Patients were grouped into five pulmonary diagnostic categories: (1) adult respiratory distress syndrome (ARDS) (n = 49); (2) pneumonia (n = 20); (3) atelectasis (n = 65); (4) congestive heart failure (n = 11); and (5) acute ventilatory failure (n = 55). Sixty patients underwent intra-abdominal surgery, 135 patients required surgery on the periphery, and five patients had a thoracotomy. For all patients, PaO2/FIO2 declined significantly from 321 mm Hg (mean) preoperatively to 258 mm Hg intraoperatively, and shunt fraction (Qs/QT) increased from 0.16 to 0.23 without a significant change in PaCO2. The magnitude of the increase in Qs/QT did not differ among pulmonary diagnostic groups. Preoperatively, patients undergoing laparotomy had lower PaO2/FIO2 (278 vs 340) and higher Qs/QT (0.19 vs 0.14) than patients requiring surgery on the periphery. Intraoperatively, Qs/QT increased more during abdominal procedures than during peripheral procedures. Intraoperative hypoxemia (PaO2/FIO2 less than 80 mm Hg) occurred during 13 procedures. Hypoxemic patients had a mean increase in Qs/QT of 0.20 (0.25 preoperatively to 0.45 intraoperatively), and a significant increase in PaCO2 from 38 mm Hg to 45 mm Hg intraoperatively). In general, these patients had ARDS (n = 10), sepsis (n = 10), a laparotomy (n = 9), and intraoperative mechanical ventilation via the Ohio Anesthesia ventilator (n = 8), a commonly used operating room ventilator. Their preoperative peak airway pressure (54 cm H2O) and minute ventilation (20 L/min) requirements exceeded the capabilities of the Ohio Anesthesia ventilator and likely contributed to impaired gas exchange intraoperatively. Within the first several hours postoperatively, PaO2/FIO2 recovered to preoperative levels in all patients, even in those who had severe intraoperative hypoxemia develop and who underwent laparotomy. We conclude that most patients with acute respiratory failure receiving preoperative mechanical ventilation experienced mild-to-moderate deterioration in intraoperative pulmonary oxygen exchange that rapidly returned to preoperative levels after surgery. We recommend that necessary surgery not be postponed by concern that pulmonary function will be worsened by surgery and anesthesia.

Effects of high-volume hemofiltration on alveolar-arterial oxygen exchange in patients with refractory septic shock.

High-volume hemofiltration (HVHF) is technically possible in severe acute pancreatitis (SAP) patients complicated with multiple organ dysfunction syndrome (MODS). Continuous HVHF is expected to become a beneficial adjunct therapy for SAP complicated with MODS. In this study, we aimed to explore the effects of fluid resuscitation and HVHF on alveolar-arterial oxygen exchange, the Acute Physiology and Chronic Health Evaluation II (APACHE II) score in patients with refractory septic shock. A total of 89 refractory septic shock patients, who were admitted to ICU, the Provincial Hospital affiliated to Shandong University from August 2006 to December 2009, were enrolled in this retrospective study. The patients were randomly divided into two groups: fluid resuscitation (group A, n=41), and fluid resuscitation plus high-volume hemofiltration (group B, n=48). The levels of O2 content of central venous blood (CcvO2), arterial oxygen content (CaO2), alveolar-arterial oxygen pressure difference P(A-a)DO2, ratio of arterial oxygen pressure/alveolar oxygen pressure (PaO2/PaO2), respiratory index (RI) and oxygenation index (OI) were determined. The oxygen exchange levels of the two groups were examined based on the arterial blood gas analysis at different times (0, 24, 72 hours and 7 days of treatment) in the two groups. The APACHE II score was calculated before and after 7-day treatment in the two groups. The levels of CcvO2, CaO2 on day 7 in group A were significantly lower than those in group B (CcvO2: 0.60±0.24 vs. 0.72±0.28, P<0.05; CaO2: 0.84±0.43 vs. 0.94±0.46, P<0.05). The level of oxygen extraction rate (O2ER) in group A on the 7th day was significantly higher than that in group B (28.7±2.4 vs. 21.7±3.4, P<0.01). The levels of P(A-a)DO2 and RI in group B on the 7th day were significantly lower than those in group A. The levels of PaO2/PaO2 and OI in group B on 7th day were significantly higher than those in group A (P<0.05 or P<0.01). The APACHE II score in the two groups reduced gradually after 7-day treatment, and the APACHE II score on the 7th day in group B was significantly lower than that in group A (8.2±3.8 vs. 17.2±6.8, P<0.01). HVHF combined with fluid resuscitation can improve alveolar-arterial-oxygen exchange, decrease the APACHE II score in patients with refractory septic shock, and thus it increases the survival rate of patients.

The Influence of Hypercapnia and Atmospheric Pressure on the Pao2/Fio2 Ratio-Pathophysiologic Considerations, a Case Series, and Introduction of a Clinical Tool.

The ratio between Pao2 and Fio2 is used as a marker for impaired oxygenation and acute respiratory distress syndrome classification. However, any discrepancy between Fio2 and o2 fraction in the alveolus affects the Pao2/Fio2 ratio. Correcting the Pao2/Fio2 ratios using the alveolar gas equation may result in an improved reflection of the pulmonary situation. This study investigates the difference between standard and corrected Pao2/Fio2 in magnitude, its correlation with the mortality of acute respiratory distress syndrome classification, and trends over time. A register and a retrospective study combined with the development of a mathematical model to determine the difference between standard and corrected Pao2/Fio2 ratio for various levels of Paco2 and atmospheric pressure. ICU in a secondary hospital in The Netherlands. Patients admitted to the ICU for pneumonia or acute respiratory distress syndrome. Register cohort: January 1, 2010, till March 1, 2020 (n = 1008). Retrospective cohort: March 1, 2020, till June 1, 2020 (n = 34). The register was used to determine the 7-day ICU mortality per acute respiratory distress syndrome classification based on the standard and corrected Pao2/Fio2 ratio. The retrospective dataset correlated the Paco2 with Pao2/Fio2 ratio over time in patients with assumed stable oxygenation. The model demonstrated an increased difference between the standard and corrected Pao2/Fio2 ratios by a lower Fio2 and atmospheric pressure and higher Pao2 and Paco2. Reclassification of severe acute respiratory distress syndrome resulted in an increase in mortality from 28.1% for standard Pao2/Fio2 to 30.6% for corrected Pao2/Fio2 ratios. Acute Physiology and Chronic Health Evaluation scores correlated better with 7-day ICU-mortality when corrected Pao2/Fio2 ratio was used for classification. For patients with Fio2 less than 50% (n = 55), change in Paco2 correlated with change in Pao2/Fio2 ratio (r = -0.388; p = 0.003). A corrected Pao2/Fio2 ratio was calculated. Correcting the Pao2/Fio2 ratio for the alveolar gas equation predominantly affects patients with high ratios between Pao2 and Fio2 and Paco2 and at low atmospheric pressure. Using the corrected Pao2/Fio2 ratio for acute respiratory distress syndrome classification results in improved correlation with the 7-day ICU mortality and increases generalization among acute respiratory distress syndrome studies. The authors provide a free, web-based tool.

Atypical Bacterial Pneumonia -- Treatment / Management -- Criteria for Admission

Respiration rate more than 30 bpm Oxygen saturation less than 90% on room air Hypotension Severe lung disease, COPD, emphysema, Heart failure, diabetes Altered mental status Delirium

Acute respiratory distress following liposuction.

An active duty male presented to the emergency room with dyspnea for 2 days after undergoing liposuction surgery. Upon presentation, the patient was afebrile, tachycardic, tachypneic, and hypoxemic. The initial chest radiograph demonstrated bilateral patchy opacities and the PaO2/FiO2 ratio was <200. The patient was admitted to the medical intensive care unit for supportive care. He was treated empirically for pneumonia. Blood and sputum cultures were negative. A computed tomography angiogram of the chest was negative for pulmonary embolism but did reveal a bilateral, perihilar air space process. The patient's oxygen requirement improved and the abnormal chest radiographic findings resolved over the next 48 hours. Given his clinical presentation, negative workup, and rapid recovery, the patient was given a presumptive diagnosis of pulmonary fat embolism. Fat embolism occurs when adipocytes and small blood vessels are damaged during the liposuction procedure. Patients may present with low-grade fever, tachycardia, tachypnea, hypoxemia, and hypocapnia. The differential diagnosis includes venous thromboembolism, aspiration pneumonitis, and pneumonia. The mainstay of treatment for pulmonary fat embolism is supportive care. The risk of mortality is 5 to 15%.

Characteristics of community-acquired pneumonia in patients with chronic obstructive pulmonary disease.

Community-acquired pneumonia is a frequent event in the course of chronic obstructive pulmonary disease (COPD). The aim of the present study was to provide information on clinical and microbiological characteristics and outcome of community-acquired pneumonia in these patients, in a comparative study with the non-COPD population. Prospective study of cases. A university hospital in Lleida, Spain. During a 6 year-period, we prospectively studied the clinical and radiological manifestations, microbiological data and outcome of all patients with community-acquired pneumonia. A comparative analysis of characteristics of pneumonia between 132 patients with a definitive diagnosis of COPD and 575 patients who did not have this underlying disease was performed. COPD was associated with an older and predominantly male population. These patients frequently had concomitant comorbidities such as diabetes mellitus or chronic heart failure. Clinical presentation was more severe, manifested by septic shock, tachypnea, lower values of pH, pO(2) and oxygen saturation, and greater values of pCO(2). Purulent expectoration was also more frequent in this subset of patients. Admission was usually required for patients with COPD, and length of hospitalization was significantly increased; however, difference in the mortality rate was not observed. Although the spectrum of responsible microorganisms was very similar, the incidence of Pseudomonas aeruginosa and other Gram-negative bacilli was increased in COPD, particularly among patients with advanced situation and/or oral corticosteroid treatment. Community-acquired pneumonia in patients with COPD was associated with epidemiological and clinical particularities mainly related to the underlying disease but showed only minor differences in outcome parameters. Gram-negative bacilli and P. aeruginosa are potential pathogens that need to be considered.

Determinants of myocardial performance after blunt chest trauma.

This study investigates whether factors that determine myocardial performance (preload, afterload, heart rate, and contractility) are altered after isolated unilateral pulmonary contusion. Catheters were placed in the carotid arteries, left ventricles, and pulmonary arteries of anesthetized, ventilated (FiO2=0.5) pigs (31.2+/-0.6 kg; n=26). A unilateral, blunt injury to the right chest was delivered with a captive bolt gun (n=17) followed by tube thoracostomy. To control for anesthesia and instrumentation at FiO2 of 0.5, one group received tube thoracostomy only (sham injury; n=6). To control for effects of hypoxia without chest injury, an additional sham-injury group (n=3) was ventilated with FiO2 of 0.12. To generate cardiac function (i.e., Starling) curves, lactated Ringer's solution was administered in three bolus infusions at serial time points; the slope of stroke index versus ventricular filling pressure defines cardiac contractility. By 4 hours after pulmonary contusion, pulmonary vascular resistance, airway resistance, and dead space ventilation were increased, whereas PaO2 (72+/-6 mm Hg at FiO2=0.5) and dynamic compliance were decreased (all p < 0.05). Despite profound lung injury, arterial blood pressure, heart rate, cardiac filling pressures, and output remained within the normal range, which is inconsistent with direct myocardial contusion. The slope of pulmonary capillary wedge pressure versus left ventricular end-diastolic pressure (LVEDP) regression was reduced by more than 50% from baseline (p < 0.05), but there was no significant change in the slope of the central venous pressure versus LVEDP regression. By 4 hours after contusion, the slope of the stroke index versus LVEDP curve was reduced by more than 80% from baseline (p < 0.05). By the same time after sham injury with FiO2 of 0.12 (PaO2 < 50 mm Hg), the regression had decayed a similar amount, but there was no change in the slope after sham injury with FiO2 of 0.5 (PaO2 > 200 mm Hg). After right-side pulmonary contusion, the most often used estimate of cardiac preload (pulmonary capillary wedge pressure) does not accurately estimate LVEDP, probably because of changes in the pulmonary circulation or mechanics. Central venous pressure is a better estimate of filling pressure, at least in these conditions, probably because it is not directly influenced by the pulmonary dysfunction. Also, ventricular performance can be impaired by depressed myocardial contractility and increased right ventricular afterload even with normal left ventricular afterload and preload. It is thus conceivable that occult myocardial dysfunction after pulmonary contusion could have a role in the progression to cardiorespiratory failure even without direct cardiac contusion.