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Insuficiencia respiratoria aguda y oxigenoterapia
- 1. Insuficiencia respiratoria aguda Leal Lam Sara Li 482 Urgencias UNIVERSIDAD AUTÓNOMA DE BAJA CALIFORNIA Escuela de Ciencias de la Salud Unidad Valle de las Palmas
- 2. Fisiología pulmonar • Componentes • Mantienen capacidad ventilatoria (CD) y cumplen demanda ventilatoria (DV) • Relación CD>DV Vías aéreas Alveolos SNC SNP Músculos respiratorios Caja torácica Riego sanguíneo
- 3. Fisiología pulmonar • Funciones generales Ventilación pulmonar Equilibrio ácido- base Filtración
- 4. Fisiología pulmonar • 3 procesos: • Salida de O2 a través del alveolo • Transporte de O2 hacia los tejidos • Eliminación de CO2 hacia el exterior Intercambio gaseoso •Gradiente de presión alveolo-arterial <15 mmHg •Unidades V/Q Ventilación alveolar •CO2 prod.= CO2 eliminado Zona mejor ventilada (espacio muerto) Zona mejor perfundida (shunts)
- 5. Insuficiencia respiratoria aguda Síndrome en el que el sistema respiratorio falla en una o en ambas funciones de intercambio gaseoso: • Oxigenación → Hipoxémica/ tipo I • Eliminación de CO2 → Hipercápnica/ tipo II • Minutos-horas: • pH <7.3
- 6. Epidemiología • Incidencia y prevalencia total desconocida • H=M, cualquier edad, cualquier raza • Pronóstico depende de la etiología y si hay comorbilidades
- 7. Clasificación Tipo I ↓O2 <60 mmHg; PaCO2 N/↑ El tipo más común Asociado a cualquier enfermedad aguda pulmonar: •Acumulación de líquido •Colapso alveolar Neumonía, hemotórax, edema pulmonar cardiogénico y no cardiogénico Tipo II ↑PaCO2 >50 mmHg ± hipoxemia No tan común pH depende de los niveles de HCO3- Sobredosis con opiáceos, enfermedad neuromuscular, anormalidad de tórax, enfermedades graves de vías aéreas
- 8. Etiología
- 9. Fisiopatología Tipo I •2 mecanismos que aumentan gradiente de presión alveolo-arterial ≥15 mmHg •Alteración V/Q → Responden a O2 al 100% •↑V/Q: Casos severos •↓V/Q: •↓ventilación + perfusión normal •Ventilación normal + ↑perfusión •Cortocircuitos → NO responden a O2 al 100% (se agrega hipercapnia si shunt >60%) Tipo II •2 mecanismos que ↑CO2 en sangre: •↓ventilación/minuto (<6 L/min) •Sist. nervioso •Ap. muscular. •↑espacio muerto •↓O2 corregible con oxigenoterapia •Gradiente de presión alveolo-arterial normal
- 10. Fisiopatología Tipo I •2 mecanismos que aumentan gradiente de presión alveolo-arterial ≥15 mmHg •Alteración V/Q → Responden a O2 al 100% •↑V/Q: Casos severos •↓V/Q: •↓ventilación + perfusión normal •Ventilación normal + ↑perfusión •Cortocircuitos → NO responden a O2 al 100% (se agrega hipercapnia si shunt >60%) Tipo II •2 mecanismos que ↑CO2 en sangre: •↓ventilación/minuto (<6 L/min) •Sist. nervioso •Ap. muscular. •↑espacio muerto •↓O2 corregible con oxigenoterapia •Gradiente de presión alveolo-arterial normal
- 11. Cuadro clínico Tipo I •Convulsiones •Taquicardia, arritmias, bradicardia con hipotensión, soplos cardíacos •Disnea ± uso de músculos respiratorios accesorios •Cianosis •Diaforesis •Fiebre Signos •Ansiedad, alteración del estado mental, confusión Síntomas Tipo II •Asterixis •Vasodilatación periférica (palidez), taquicardia, arritmias, pulsos limítrofes •Signos de obstrucción de vía aérea (estridor, sibilancias) •Extremidades calientes Signos •Somnolencia, letargo, inquietud, dificultad para hablar, cefalea, ↓nivel consciencia Síntomas
- 13. Diagnóstico HC + EF Radiografía de tórax Gases arteriales o pulsioximetría Ecocardiografía Pruebas de función pulmonar Cateterización de VD
- 14. Gases arteriales Parámetro Valores normales Valores críticos pH 7.35-7.45 <7.2; >7.6 pO2 80-100 mmHg 35-45 mmHg pCO2 <60 mmHg >50 mmHg PaO2 y la PaCO2 sólo reflejan la función pulmonar o respiración externa, (oxigenación y ventilación de la sangre)
- 15. Radiografía de tórax No SDRA Cardiomegalia Redistribución vascular Engrosamiento peribronquial Derrame pleural Líneas septales Distribución perihiliar en “alas de murciélago” de opacidades SDRA Ninguna de las anteriores
- 16. Neumonía SDRA
- 18. <
- 20. Tratamiento • Tx de elección: Oxigenoterapia • Riesgos: intoxicación por O2 y narcosis de CO2 • Manejado en UCI (idealmente) • Dispositivo depende de si el Px tiene respiración espontánea o no Corregir causa de base Tratar/ prevenir hipoxemia Suplemento de O2 Ventilación mecánica ± intubación endotraqueal
- 21. Ventilación mecánica • Objetivos: • ↑PaO2 y ↓PaCO2 • Ventaja: Da un “descanso” a los músculos de la respiración (para evitar fatiga) • Riesgos: barotrauma, daño directo a parénquima pulmonar, sobredistensión alveolar Tipos No invasivo Puntillas nasales Mascarilla completa Invasivo Intubación endotraqueal Traqueostomía
- 22. Ventilación mecánica • Objetivos: • ↑PaO2 y ↓PaCO2 • Ventaja: Da un “descanso” a los músculos de la respiración (para evitar fatiga) • Riesgos: barotrauma, daño directo a parénquima pulmonar, sobredistensión alveolar Invasivo No invasivo
- 23. Ventilación mecánica • Actualmente son de presión positiva (CPAP), y toman como variable independiente: • Presión Tiempo • Volumen • Mecanismos iniciadores: • Máquina • Paciente • Requiere de una interfase máquina-paciente Modos ventilatorios PSV IMV Modo asistido Volumen- control Presión control PCIRV
- 24. Ventilación mecánica • Actualmente son de presión positiva (CPAP), y toman como variable independiente: • Presión Tiempo • Volumen • Mecanismos iniciadores: • Máquina • Paciente • Requiere de una interfase máquina-paciente • Máscara “total face” • Máscara oronasal • Máscara nasal • Mouthpieces • Almohadillas nasales • Casco Tipos de interfase
- 25. Valores en VM •12-15 o más (en ausencia de auto-PEEP) Frecuencia respiratoria •6 ml/kg (5-8 ml/kg) del peso corporal ideal Volumen corriente •5 a 8 cm H2O PEEP •100% inicialmente; después FiO2 de menos de 60% para evitar la toxicidad del oxígeno •Si requiere FiO2 mayor del 60%, aumentar la PEEP 5 cm H2O cada 30 min •Si el paciente persiste con hipoxemia y una PEEP de 15 cm H2O, tratar como hipoxemia refractaria FiO2
- 26. Indicaciones y contraindicaciones para iniciar VNI
- 27. Algoritmo Valorar cada 1-2 h y en cada cambio de patrón respiratorio en el ventilador
- 28. Algoritmo
- 29. Indicadores de falla de VNI
- 30. Indicaciones para intubar • Fracaso de mantenimiento o de protección de las vías aéreas • Insuficiencia de oxigenación o ventilación • Curso clínico esperado (necesidad prevista para la intubación)
- 31. Tx farmacológico Diuréticos Nitratos Analgésicos opioides Agentes inotrópicos ß2-agonistas Derivados de las xantinas Anticolinérgicos Corticoesteroides
- 32. Bibliografía 1. Kaynar A. Respiratory Failure. Medscape. 2016. 2. C. Dueñas Castell et al. REVISIÓN: Insuficiencia respiratoria aguda. Acta Colomb Cuid Intensivo. 2016;16(S1):1---24.
Notas del editor
- Componentes del sistema respiratorio: -Vías aéreas -Alveolos -SNC -SNP -Músculos respiratorios -Caja torácica -Riego sanguíneo Respiratory failure can arisa from an abnormality in any of the components of the respiratory system. Px who have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure. Ventilatory capacity is the maximal spontaneous ventilation that can be maintained without development of respiratory muscle fatigue. Ventilatory demand is the spontaneous minute ventilation that results in a stable PaCO2. Respiratory failure may result from either a reduction in ventilatory capacity or an increase in ventilatory demand (or both).
- 3 funciones importantes: -Ventilación pulmonar: La ventilación es el proceso por el cual el aire atmosférico rico en oxígeno entra en los pulmones, los cuales expulsan a continuación aire pobre en oxígeno y rico en dióxido de carbono. Consta de 2 fases, la inspiración y la espiración: La inspiración tiene lugar cuando la contracción del diafragma y los músculos intercostales externos aumentan el volumen de la cavidad torácica y hacen que el pulmón se expanda. La presión intraalveolar se hace negativa con respecto a la atmosférica y entra aire al pulmón hasta que desaparece el gradiente de presión. La espiración ocurre cuando el diafragma se relaja y la cúpula diafragmática sube pasivamente por su elasticidad, la presión intrapulmonar se hace positiva con respecto a la atmosférica, el pulmón disminuye su volumen y el aire sale al exterior hasta que desaparece el gradiente de presión y la presión intraalveolar se iguala a la atmosférica. En estado de reposo el volumen de aire que entra en el pulmón durante una inspiración se llama volumen corriente y es 500 cm³, la frecuencia respiratoria es de 12 ciclos por minuto. La capacidad pulmonar total oscila entre 4000 y 6000 cm³, dependiendo de la edad, peso y sexo; siendo más elevada en los hombres que en las mujeres. -Equilibrio ácido-base: Logrado a través de la espiración de CO2 para mantener niveles de gases arteriales y presiones normales. -Filtración (inmunológica): Los pulmones contrarrestan la contaminación aérea a la que están expuestos por acción del sistema mucociliar y fagocitario de los macrófagos alveolares. La producción de moco por las células de las glándulas seromucosas bronquiales y por las células caliciformes del epitelio bronquial contribuye a atrapar partículas extrañas e impedir su paso a los alveolos.
- Las condiciones que se ven afectadas en la IRA son el intercambio de gases y la ventilación alveolar. El intercambio de gases es el proceso por el cual el O2 atraviesa el alveolo y es llevado a los tejidos a través de la sangre (su vehículo es la albúmina) y el CO2 es eliminado al exterior al cruzar la barrera alveolar; la ventilación alveolar mide cuánto CO2 es eliminado de manera eficiente (lo que se produce de CO2, de manera constante, es lo mismo que lo que se elimina: relación 1:1) y así determina si la ventilación alveolar es adecuada a las necesidades metabólicas del cuerpo. Respiratory physiology The act of respiration engages the following three processes: -Transfer of oxygen across the alveolus -Transport of oxygen to the tissues -Removal of carbon dioxide from blood into the alveolus and then into the environment Respiratory failure may occur from malfunctioning of any of these processes. In order to understand the pathophysiologic basis of acute respiratory failure, an understanding of pulmonary gas exchange is essential. Gas exchange Respiration primarily occurs at the alveolar capillary units of the lungs, where exchange of oxygen and carbon dioxide between alveolar gas and blood takes place. After diffusing into the blood, the oxygen molecules reversibly bind to the hemoglobin. Each molecule of hemoglobin contains 4 sites for combination with molecular oxygen; 1 g of hemoglobin combines with a maximum of 1.36 mL of oxygen. The quantity of oxygen combined with hemoglobin depends on the level of blood PaO2. This relationship, expressed as the oxygen hemoglobin dissociation curve, is not linear but has a sigmoid-shaped curve with a steep slope between a PaO2 of 10 and 50 mm Hg and a flat portion above a PaO2 of 70 mm Hg. The carbon dioxide is transported in 3 main forms: (1) in simple solution, (2) as bicarbonate, and (3) combined with protein of hemoglobin as a carbamino compound. During ideal gas exchange, blood flow and ventilation would perfectly match each other, resulting in no alveolar-arterial oxygen tension (PO2) gradient. However, even in normal lungs, not all alveoli are ventilated and perfused perfectly. For a given perfusion, some alveoli are underventilated, while others are overventilated. Similarly, for known alveolar ventilation, some units are underperfused, while others are overperfused. The optimally ventilated alveoli that are not perfused well have a large ventilation-to-perfusion ratio (V/Q) and are called high-V/Q units (which act like dead space). Alveoli that are optimally perfused but not adequately ventilated are called low-V/Q units (which act like a shunt). Alveolar ventilation At steady state, the rate of carbon dioxide production by the tissues is constant and equals the rate of carbon dioxide elimination by the lung. This relation is expressed by the following equation: VA = K × VCO2/ PaCO2 where K is a constant (0.863), VA is alveolar ventilation, and VCO2 is carbon dioxide ventilation. This relation determines whether the alveolar ventilation is adequate for metabolic needs of the body. The efficiency of lungs at carrying out of respiration can be further evaluated by measuring the alveolar-arterial PO2 gradient. This difference is calculated by the following equation: PAO2 = FiO2 × (PB – PH2 O) – PACO2/R where PA O2 is alveolar PO2, FiO2 is fractional concentration of oxygen in inspired gas, PB is barometric pressure, PH2O is water vapor pressure at 37°C, PACO2 is alveolar PCO2 (assumed to be equal to PaCO2), and R is respiratory exchange ratio. R depends on oxygen consumption and carbon dioxide production. At rest, the ratio of VCO2 to oxygen ventilation (VO2) is approximately 0.8. Even normal lungs have some degree of V/Q mismatching and a small quantity of right-to-left shunt, with PAO2 slightly higher than PaO2. However, an increase in the alveolar-arterial PO2 gradient above 15-20 mm Hg indicates pulmonary disease as the cause of hypoxemia.
- Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic. Acute hypercapnic respiratory failure develops over minutes to hours; therefore, pH is less than 7.3. Chronic respiratory failure develops over several days or longer, allowing time for renal compensation and an increase in bicarbonate concentration. Therefore, the pH usually is only slightly decreased. Curva de disociación del O2: La curva tiene dos partes: Una horizontal(> 60mmHg de PaO2) y otra casi vertical (< 60mmHg de PaO2). El punto de flexión o “rodilla” de la curva, se denomina ”La orilla del precipicio "y corresponde a los 60 mmHg.de Pa02 Cualquier disminución de la PaO2 por abajo de 60mmHg, provocara bruscos descensos de la Sat.HbO2.
- Tipo I: trastornos de la ventilación-perfusión Tipo II: trastornos estructurales o funcionales Common causes of type I (hypoxemic) respiratory failure include the following: COPD Pneumonia Pulmonary edema Pulmonary fibrosis Asthma Pneumothorax Pulmonary embolism Pulmonary arterial hypertension Pneumoconiosis Granulomatous lung diseases Cyanotic congenital heart disease Bronchiectasis Acute respiratory distress syndrome (ARDS) Fat embolism syndrome Kyphoscoliosis Obesity Common causes of type II (hypercapnic) respiratory failure include the following: COPD Severe asthma Drug overdose Poisonings Myasthenia gravis Polyneuropathy Poliomyelitis Primary muscle disorders Porphyria Cervical cordotomy Head and cervical cord injury Primary alveolar hypoventilation Obesity-hypoventilation syndrome Pulmonary edema ARDS Myxedema Tetanus
- Hypoxemic respiratory failure The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are V/Q mismatch and shunt. These 2 mechanisms lead to widening of the alveolar-arterial PO2 gradient, which normally is less than 15 mm Hg. They can be differentiated by assessing the response to oxygen supplementation or calculating the shunt fraction after inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. -V/Q mismatch V/Q mismatch is the most common cause of hypoxemia. Alveolar units may vary from low-V/Q to high-V/Q in the presence of a disease process. The low-V/Q units contribute to hypoxemia and hypercapnia, whereas the high-V/Q units waste ventilation but do not affect gas exchange unless the abnormality is quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low-V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the PaCO2 generally is not affected. -Shunt Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation: QS/QT = (CCO2 – CaO2)/CCO2 – CvO2) where QS/QT is the shunt fraction, CCO2 is capillary oxygen content (calculated from ideal PAO2), CaO2 is arterial oxygen content (derived from PaO2 by using the oxygen dissociation curve), and CvO2 is mixed venous oxygen content (assumed or measured by drawing mixed venous blood from a pulmonary arterial catheter). Anatomic shunt exists in normal lungs because of the bronchial and thebesian circulations, which account for 2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac origin. Hypercapnia generally does not develop unless the shunt is excessive (> 60%). Compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by means of oxygen administration. Hypercapnic respiratory failure At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation according to the following equation (a restatement of the equation given above for alveolar ventilation): PaCO2 = VCO2 × K/VA where K is a constant (0.863). The relation between PaCO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, PaCO2 rises precipitously. A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy. Hypoventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.
- Hypoxemic respiratory failure The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are V/Q mismatch and shunt. These 2 mechanisms lead to widening of the alveolar-arterial PO2 gradient, which normally is less than 15 mm Hg. They can be differentiated by assessing the response to oxygen supplementation or calculating the shunt fraction after inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. -V/Q mismatch V/Q mismatch is the most common cause of hypoxemia. Alveolar units may vary from low-V/Q to high-V/Q in the presence of a disease process. The low-V/Q units contribute to hypoxemia and hypercapnia, whereas the high-V/Q units waste ventilation but do not affect gas exchange unless the abnormality is quite severe. The low V/Q ratio may occur either from a decrease in ventilation secondary to airway or interstitial lung disease or from overperfusion in the presence of normal ventilation. The overperfusion may occur in case of pulmonary embolism, where the blood is diverted to normally ventilated units from regions of lungs that have blood flow obstruction secondary to embolism. Administration of 100% oxygen eliminates all of the low-V/Q units, thus leading to correction of hypoxemia. Hypoxemia increases minute ventilation by chemoreceptor stimulation, but the PaCO2 generally is not affected. -Shunt Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes with oxygenated blood that has flowed through the ventilated alveoli, consequently leading to a reduction in arterial blood content. The shunt is calculated by the following equation: QS/QT = (CCO2 – CaO2)/CCO2 – CvO2) where QS/QT is the shunt fraction, CCO2 is capillary oxygen content (calculated from ideal PAO2), CaO2 is arterial oxygen content (derived from PaO2 by using the oxygen dissociation curve), and CvO2 is mixed venous oxygen content (assumed or measured by drawing mixed venous blood from a pulmonary arterial catheter). Anatomic shunt exists in normal lungs because of the bronchial and thebesian circulations, which account for 2-3% of shunt. A normal right-to-left shunt may occur from atrial septal defect, ventricular septal defect, patent ductus arteriosus, or arteriovenous malformation in the lung. Shunt as a cause of hypoxemia is observed primarily in pneumonia, atelectasis, and severe pulmonary edema of either cardiac or noncardiac origin. Hypercapnia generally does not develop unless the shunt is excessive (> 60%). Compared with V/Q mismatch, hypoxemia produced by shunt is difficult to correct by means of oxygen administration. Hypercapnic respiratory failure At a constant rate of carbon dioxide production, PaCO2 is determined by the level of alveolar ventilation according to the following equation (a restatement of the equation given above for alveolar ventilation): PaCO2 = VCO2 × K/VA where K is a constant (0.863). The relation between PaCO2 and alveolar ventilation is hyperbolic. As ventilation decreases below 4-6 L/min, PaCO2 rises precipitously. A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercapnic respiratory failure, the hypoxemia is easily corrected with oxygen therapy. Hypoventilation is an uncommon cause of respiratory failure and usually occurs from depression of the CNS from drugs or neuromuscular diseases affecting respiratory muscles. Hypoventilation is characterized by hypercapnia and hypoxemia. Hypoventilation can be differentiated from other causes of hypoxemia by the presence of a normal alveolar-arterial PO2 gradient.
- Tipo I:Px con ↑trabajo respiratorio (taquipnea), más “agresividad” (por ansiedad), cianosis Tipo II: Px con ↓trabajo respiratorio/ bradipnea (por ↓fuerza necesaria para respirar, ya sea por fatiga muscular, dolor, menor actividad nerviosa o como consecuencia de presentación clínica prolongada de tipo I que “cansa” al paciente y deja de respirar), cefalea, más “sopor”
- Radiography Chest radiography is essential in the evaluation of respiratory failure because it frequently reveals the cause (see the images below). However, distinguishing between cardiogenic and noncardiogenic pulmonary edema is often difficult. Increased heart size, vascular redistribution, peribronchial cuffing, pleural effusions, septal lines, and perihilar bat-wing distribution of infiltrates suggest hydrostatic edema; the lack of these findings suggests acute respiratory distress syndrome (ARDS). Arterial blood gas Once respiratory failure is suspected on clinical grounds, arterial blood gas analysis should be performed to confirm the diagnosis and to assist in the distinction between acute and chronic forms. This helps assess the severity of respiratory failure and helps guide management. Echocardiography Echocardiography need not be performed routinely in all patients with respiratory failure. However, it is a useful test when a cardiac cause of acute respiratory failure is suspected. The findings of left ventricular dilatation, regional or global wall motion abnormalities, or severe mitral regurgitation support the diagnosis of cardiogenic pulmonary edema. A normal heart size and normal systolic and diastolic function in a patient with pulmonary edema would suggest ARDS. Echocardiography provides an estimate of right ventricular function and pulmonary artery pressure in patients with chronic hypercapnic respiratory failure. Pulmonary Function Tests Patients with acute respiratory failure generally are unable to perform PFTs; however, these tests are useful in the evaluation of chronic respiratory failure. Right-Sided Heart Catheterization Right-sided heart catheterization (also known as pulmonary artery catheterization or Swan-Ganz catheterization) remains a controversial issue in the management of critically ill patients. Invasive monitoring probably is not routinely needed in patients with acute hypoxemic respiratory failure, but when significant uncertainty about cardiac function, adequacy of volume resuscitation, and systemic oxygen delivery remain, right-sided heart catheterization should be considered. Measurement of pulmonary capillary wedge pressure may be helpful in distinguishing cardiogenic from noncardiogenic edema. The pulmonary capillary wedge pressure should be interpreted in the context of serum oncotic pressure and cardiac function.
- PaO2 y la PaCO2 sólo reflejan la función pulmonar o respiración externa, (oxigenación y ventilación de la sangre), NO EXPRESA la respiración celular o interna (consumo de oxígeno, producción de energía y liberación celular de CO2)
- SDRA: Sx de distrés respiratorio agudo perihilar bat-wing distribution of infiltrates suggest hydrostatic edema
- El objetivo de la oxigenoterapia es mantener una adecuada ventilación alveolar al dejar permeables los alveolos, reducir el trabajo respiratorio muscular para evitar la fatiga y asegurar una vía aérea (si se requiere intubar). Many factors affect the decision to begin mechanical ventilation. Because no mode of mechanical ventilation can cure a disease process, the patient should have a correctable underlying problem that can be resolved with the support of mechanical ventilation. This intervention should not be started without thoughtful consideration because intubation and positive-pressure ventilation are not without potentially harmful effects. Mechanical ventilation is indicated when the patient's spontaneous ventilation is inadequate to sustain life. In addition, it is indicated as a measure to control ventilation in critically ill patients and as prophylaxis for impending collapse of other physiologic functions. Physiologic indications include respiratory or mechanical insufficiency and ineffective gas exchange. Assurance of an adequate airway is vital in a patient with acute respiratory distress. The most common indication for endotracheal intubation is respiratory failure. Endotracheal intubation serves as an interface between the patient and the ventilator. Another indication is airway protection in patients with altered mental status. Once the airway is secured, attention is turned toward correcting the underlying hypoxemia, the most life-threatening facet of acute respiratory failure. The goal is to assure adequate oxygen delivery to tissues, generally achieved with an arterial oxygen tension (PaO2) of 60 mm Hg or an arterial oxygen saturation (SaO2) greater than 90%. Supplemental oxygen is administered via nasal prongs or face mask; however, in patients with severe hypoxemia, intubation and mechanical ventilation are often required.
- Positive-pressure ventilation (CPAP) means that airway pressure is applied at the patient's airway through an endotracheal or tracheostomy tube, this in order to achieve a positive pressure at the end of the expiration (PEEP) and diminish respiratory function that consumes oxygen. The positive nature of the pressure causes the gas to flow into the lungs until the ventilator breath is terminated. As the airway pressure drops to zero, elastic recoil of the chest accomplishes passive exhalation by pushing the tidal volume out. Classifications of Positive-Pressure Ventilators Modern ventilators are classified by their method of cycling from the inspiratory phase to the expiratory phase. That is, they are named after that parameter that signals the termination of the positive-pressure inspiration cycle of the machine. The signal to terminate the inspiratory activity of the machine is either a preset volume (for a volume-cycled ventilator), a preset pressure limit (for a pressure-cycled ventilator), or a preset time factor (for a time-cycled ventilator). Volume-cycled ventilation is the most common form of ventilator cycling used in adult medicine because it provides a consistent breath-to-breath tidal volume. Termination of the delivered breath is signaled when a set volume leaves the ventilator.
- Positive-pressure ventilation (CPAP) means that airway pressure is applied at the patient's airway through an endotracheal or tracheostomy tube, this in order to achieve a positive pressure at the end of the expiration (PEEP) and diminish respiratory function that consumes oxygen. The positive nature of the pressure causes the gas to flow into the lungs until the ventilator breath is terminated. As the airway pressure drops to zero, elastic recoil of the chest accomplishes passive exhalation by pushing the tidal volume out. Classifications of Positive-Pressure Ventilators Modern ventilators are classified by their method of cycling from the inspiratory phase to the expiratory phase. That is, they are named after that parameter that signals the termination of the positive-pressure inspiration cycle of the machine. The signal to terminate the inspiratory activity of the machine is either a preset volume (for a volume-cycled ventilator), a preset pressure limit (for a pressure-cycled ventilator), or a preset time factor (for a time-cycled ventilator). Volume-cycled ventilation is the most common form of ventilator cycling used in adult medicine because it provides a consistent breath-to-breath tidal volume. Termination of the delivered breath is signaled when a set volume leaves the ventilator.
- La identificación de pacientes susceptibles de beneficiarse de la VNI puede considerarse un proceso de 2 pasos: -En la primera etapa, se debe determinar la necesidad de ventilacion mecanica para el paciente, identificada por signos de dificultad respiratoria. -En la segunda etapa, el paciente no debe tener contraindicaciones para VNI, tales como la necesidad de una via aerea artificial para la proteccion de la via respiratoria, la incapacidad para adaptarse a una interfaz, la alta gravedad de la enfermedad (por ejemplo, un paro respiratorio), que el paciente no coopere o que no deje colocarse la interfaz y un diagnostico en el que se haya demostrado que la VNI no es efectiva (por ejemplo, SDRA grave). La tasa de fracaso de la VNI reportada es del 5-40%91. Algunos pacientes fallan debido a la progresion de la enfermedad. La experiencia del clinico y la experticia en la aplicacion de la VNI se asocian con una mayor tasa de exito92. Algunos pacientes no obtienen una ventilacion adecuada con VNI y, por lo tanto, requieren intubacion. No siempre es evidente que pacientes se beneficiaran de la VNI, pero los factores de riesgo reconocidos para fracaso de la VNI se muestran en la figura 13 93. Los signos clinicos que solo son equivocos en la presentacion se vuelven más predictivos de fracaso definitivo si persisten despues de 2 h de la VNI. Por lo tanto, es importante para evaluar la respuesta clinica despues de 1-2 h de la iniciacion de la VNI para establecer si es exitosa o no.
- Las razones por las que a menudo se usa la intubación se conocen muy bien; como por ejemplo: 1) proteger la via respiratoria; 2) necesidad de ventilación continua y, por lo tanto, sedación y a veces bloqueo neuromuscular; 3) inestabilidad hemodinámica grave y 4) uso de altas fracciones de oxígeno inspirado.