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PEDIATRIC EMERGENCYSilvia TriratnaDivisi Pediatri Gawat DaruratBagian Ilmu Kesehatan Anak FK UNSRI PalembangRESPIRATORY EMERGENCYCIRCULATORY EMERGENCYNEUROGY EMERGENCYENDOCRINE EMERGENCYTRAUMAPOISONING/ INTOXICATION.......A fundamental concept in pediatric emergency care is that children are not simply scaled-down adults and cannot be treated as such. Pediatric considerationA childs physiologic response to a critical illness or injury is different from an adults..Children are also developing mentally and behaviorally. Infants and young children cannot tell you what the problem is or where it hurts.

PEMERIKSAAN SULIT DILAKUKANKOMINIKASI SULITCENDRUNG KETAKUTANPENILAIAN KEGAWATAN SULIT DILAKUKANCHILD IS NOT SMALL ADULT

The key differences to consider in children are:1. Weight2. Anatomical size and shape3. Physiological cardiovascular, respiratory, immune function4. Psychological intellectual ability and emotional response

Infant is nasal breatherNose is responsible for 50% of total airway resistance at all agesInfant: blockage of nose = respiratory distress or failureSoSometimes, oral and nasalsuctioning is all that is needed!!

TongueLarge in proportion to rest of oral cavityLoss of tone with sleep, sedation, CNS dysfunctionFrequent cause of upper airway obstructionPositioning with or without oral airway can be enough.

Pediatric Cardiopulmonary ArrestAlmost all pediatric codes are of respiratory originInternal Data. B.C. Childrens Hospital, Vancouver. 1989.

10%10%80%100%75%SurvivalrateHenti NapasHenti Kardiopulmonal75 90 %7 11 %

9KEHILANGANCAIRANPERDARAHANGELUKA BAKARMALDISTRIBUSICAIRANSYOK SEPTIKPENY.JANTUNGANAFILAKSISDISTRESPERNAPASANASPIRASIASMABPDEPRESIPERNAPASANKEJANGTIK KERACUNANGAGAL SIRKULASIGAGAL NAPASGAGAL KARDIOPULMONALHENTI JANTUNGPenyebab Kegawatan Kardiopulmonal10Pediatric-CPRRESPIRATORY EMERGENCYThe Need for Oxygen

0 1 minute: cardiac irritability0 4 minutes: brain damage not likely4 6 minutes: brain damage possible6 10 minutes: brain damage very likely> 10 minutes: irreversible brain damageRespiratory EmergenciesIn children, illness and injury frequently result in respiratory compromise, a leading cause of pediatric morbidity and mortality; Management of the airway and breathing should be your first concern in all pediatric patientsRespiratory EmergenciesRespiratory distress is one of the most common chief complaints for which children seek medical care.nearly 10 % of pediatric emergency department visits and 20 % of hospitalizations Respiratory distress in children, particularly neonates and infants, must be promptly recognized and aggressively treated because they may decompensate quickly. 15Respiratory arrest is the most common cause of cardiac arrest in children and outcomes are poor for patients who develop cardiopulmonary arrest as the result of respiratory deterioration 16Peningkatan penggunaan SubstratOksigen/Glukosa PulsesMottledDinginPucat CRT Respon (voice, pain)GelisahIrritableKejangKomaSSPKulitKardiovaskulerOrgan AbdomenGinjalThird spacing fluidsIleusDysmotilityBowel sloughAnuriaOliguriaUrine output Gagal jantungResistensi kapilerTakikardiBradikardiAsystolePediatric-CPRManifestasi klinis1718Pediatric considerationsThe frequency of acute respiratory failure is higher in infants and young children than in adults, for several reasons. 19Factors that contribute to rapid respiratory compromise in children smaller airways, increased metabolic demands, decreased respiratory reserves, inadequate compensatory mechanisms as compared to adults. 20Extrathoracic airway differencesThe area extending from the nose through the nasopharynx, oropharynx, and larynx to the subglottic region of the trachea constitutes the extrathoracic airway.

This area differs in pediatric versus adult patients21Extrathoracic airway differencesNeonates and infants are obligate nasal breathers until the age of 2-6 months because of the proximity of the epiglottis to the nasopharynx.

Nasal congestion can lead to clinically significant distress in this age group.

22Extrathoracic airway differencesThe airway is small; this is one of the primary differences in infants and children younger than 8 years compared with older patients.Infants and young children have a large tongue that fills a small oropharynx.Infants and young children have a cephalic larynx. The larynx is opposite vertebrae C3-4 in children versus C6-7 in adults.

23Extrathoracic airway differencesThe epiglottis is larger and more horizontal to the pharyngeal wall in children than in adults.

The cephalic larynx and large epiglottis can make laryngoscopy challenging.24Extrathoracic airway differencesInfants and young children have a narrow subglottic area. In children, the subglottic area is cone shaped, with the narrowest area at the cricoid ring.A small amount of subglottic edema can lead to clinically significant narrowing, increased airway resistance, and increased work of breathing. 25Extrathoracic airway differencesAdolescents and adults have a cylindrical airway that is narrowest at the glottic opening.

26Extrathoracic airway differencesIn slightly older children, adenoidal and tonsillar lymphoid tissue is prominent and can contribute to airway obstruction.Uncorrected congenital anatomic abnormalities (eg, cleft palate, Pierre Robin sequence) or acquired abnormalities (eg, subglottic stenosis, laryngomalacia/tracheomalacia) may cause inspiratory obstruction27Intrathoracic airway differences

The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, the lung lymphatics, and the pulmonary circulation. 28Intrathoracic airway differences

The intrathoracic airways and lung include the conducting airways and alveoli, the interstitia, the pleura, the lung lymphatics, and the pulmonary circulation. 29Intrathoracic airway differences

Infants and young children have fewer alveoli than do adults. The number dramatically increases during childhood, from approximately 20 million at birth to 300 million by 8 years of age.The alveolus is small. Alveolar size increases from 150-180 to 250-300 m during childhood.Therefore, infants and young children have a relatively small area for gas exchange30Collateral ventilation is not fully developed; therefore, atelectasis is more common in children than in adults.

Smaller intrathoracic airways are more easily obstructed than larger onesInfants and young children have relatively little cartilaginous support of the airwaysIntrathoracic airway differences

31The respiratory pump includes the nervous system with central control (ie, cerebrum, brainstem, spinal cord, peripheral nerves), respiratory muscles, and chest wall. Respiratory pump differences

32The respiratory center is immature in infants and young children leads to irregular respirations and an increased risk of apnea.The ribs are horizontally oriented. During inspiration, a decreased volume is displaced, the capacity to increase tidal volume is limited compared with that in older individuals.Respiratory pump differences

33The small surface area for the interaction between the diaphragm and thorax limits displacing volume in the vertical direction.The musculature is not fully developed. The slow-twitch fatigue-resistant muscle fibers in the infant are underdeveloped.Respiratory pump differences

34The soft compliant chest wall provides little opposition to the deflating tendency of the lungs.

This leads to a lower functional residual capacity in pediatric patients than in adults, a volume that approaches the pediatric alveolus critical closing volume.

Respiratory pump differences

3536Causes of acute respiratory compromise in childrenRespiratory tractCardiovascularNervous systemGastointestinalMetabolic and endocrine diseasesHematologyPoisoningINFECTION, etc37Causes of acute respiratory compromise in childrenRespiratory tract

38Decrease muscle toneInfectionAsthmaAnaphylaxisForeign body (upper airway, lower airway, esophagus)Airway anomalies (eg, laryngomalacia, laryngospasm, tracheoesophageal fistula, tracheal stenosis, tracheal ring)Biologic or chemical weapons (eg, anthrax, nerve agents, ricin)Chest wall abnormalities (eg, flail chest, open pneumothorax)Thoracic cavity conditions (eg, pneumothorax, hemothorax, pleural effusion, empyema, mediastinal mass)Pulmonary contusionPulmonary embolismSmoke inhalationSubmersion injury (near-drowning)Causes of acute respiratory compromise in childrenRespiratory tract

39INFECTIONUvulitis, EpiglottitisRetropharyngeal abscess, Peritonsillar abscessCroupBacterial tracheitis;Bronchiolitis, PneumoniaCauses of acute respiratory compromise in childrenCardiovascular

40Congenital heart diseaseAcute decompensated heart failureMyocarditisPericarditisShockCardiac tamponadeSmoke inhalationSubmersion injury (near-drowning)Causes of acute respiratory compromise in childrenNervous system

41Depressed ventilation (eg, ingestion, CNS trauma, seizures, or CNS infection)Hypotonia (variety of etiologies causing poor airway or respiratory tone and ineffective respiratory effort)Pulmonary aspiration due to loss of airway protective reflexesCauses of acute respiratory compromise in childrenGastrointestinal system

42Splinting from abdominal pain (intraabdominal trauma)Abdominal distention (eg, small bowel obstruction, bowel perforation)Gastroesophageal reflux with pulmonary aspirationCauses of acute respiratory compromise in childrenMetabolic and endocrine diseases

43Metabolic acidosis (eg, diabetic ketoacidosis, severe dehydration, sepsis, toxic ingestions)HyperthyroidismHypothyroidismHyperammonemiaHematologicDecreased O2 carrying capacity (eg, acute severe anemia from hemolysis, methemoglobinemia, carbon monoxide poisoning)Acute chest syndrome (patients with sickle cell disease)Causes of upper and lower airway problems in children44Upper AiwayLower AirwayBothTraumaCroupBacterial TracheitisAbscessEpiglotitisNeck ImjuryAsthmaBronchiolitisPneumoniaBruising of the LungCollapse LungSubmersion InjuryForeign BodySmoke InhalationAllergic ReactionRespiratory problems have 3 levels of severityRespiratory distress,Respiratory failure, and Respiratory arrest. 45Respiratory EmergenciesRespiratory distress is a state where a child is able to maintain adequate oxygenation of the blood, but only by increasing his or her work of breathing.

Respiratory failure occurs when a child cannot compensate for inadequate oxygenation and the circulatory and respiratory systems begin to collapse.

Respiratory EmergenciesRespiratory arrestare unresponsive and limp, with cyanosis around the lips. Respiratory rate and work of breathing may be very slow or absent, or you may note agonal respirationinfrequent, gasping breaths with no chest risea pattern that is seen in dyingRespiratory arrestChildren are unresponsive and limp, with cyanosis around the lips.Respiratory rate and work of breathing may be very slow or absent, or you may note agonal respirationinfrequent, gasping breaths with no chest rise48Respiratory arrest is the most common cause of cardiac arrest in children and outcomes are poor for patients who develop cardiopulmonary arrest as the result of respiratory deterioration 49Clinical evaluation of Respiratory EmergencyHow do you initially assess a patient in respiratory distress?50should be rapid and quickly determine if patient needs emergent interventions and rule out life threatening conditionsPENAMPILANUPAYA NAFASSIRKULASI KULIT51T = TonusI = Interactiveness C = ConsolabilityL = Look/GazeS = Speech/CrySuara nafas abnormalPosisi abnormalRetraksiNapas cuping hidungMottledPucat Sianosis

SEGITIGA PENILAIAN PEDIATRIK (PEDIATRIC ASSESSMENT TRIANGLE = PAT)After completing the Triangle, begin a more complete

pediatric primary survey.AIRWAYBREATHINGCIRCULATIONDISABILITYTachypnea: World Health OrganizationAgeBreaths per minuteLess than 2 months>60 breaths/min2 to 12 months>50 breaths/min1 to 5 years>40 breaths/minMore than 5 years>20 breaths/minReproduced with permission from: World Health Organization. The management of acute respiratory infections in children. In: Practical guidelines for outpatient care. World Health Organization, Geneva, 1995. Copyright 1995 World Health Organization.Diagnostic studies for evaluation of acute respiratory distressBedside testing: Pulse oximetry

INDICATION:All patients with respiratory distress

54Diagnostic studies for evaluation of acute respiratory distressBedside testing: Pulse oximetry

Normal values despite hypoxia seen in patients with severe anemia, carboxyhemoglobin, or sickle cell disease

Falsely low values obtained in patients with pulse oximeter not correlating with pulse, poor peripheral perfusion, venous congestion, methemoglobinemia, certain nail polish colors, and in patients receiving vital dyes (eg, methylene blue) during surgical procedures

55Diagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsBedside testingEnd-tidal CO2 (ETCO2) measurementConfirmation of succesful endotracheal intubationNoninvasive monitoring of ventilation in intubated patientsNoninvasive monitoring for sedation in childrenMeasurable in non-intubated and intubated, patientsDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsBedside testingElectrocardiogramClinical suspicion of cardiac disease (eg, cardiac murmur, gallop, differential pulses or blood pressure between upper and lower extremities)Typically combined with chest radiograph to assess heart size and pulmonary vasculature in order to determine need for echocardiographyDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsLaboratory testingArterial blood gasDetermine PaO2 for calculation of physiologic measures of oxygenation (eg, A-a gradient, PaO2/FiO2 ratio)Correlate pCO2 with end-tidal CO2 measurmentsMeasure pH and correlate with venous pHEnd-tidal CO2, pulse oximetry, and venous blood gases may be used as less invasive methods for ongoing monitoring of oxygenation, ventilation, and acid-base status if they correlate with arterial blood gas measurementsDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsLaboratory testingElectrolytes, blood urea nitrogen, creatininePatients with metabolic acidosisAssesses for the presence of an anion gap and renal dysfunctionGlucoseAltered mental statusAmmoniaAltered mental status and other findings suggestive of urea cycle defectsDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsLaboratory testingCarboxyhemoglobinSmoke inhalationAltered mental status, headache, vomiting and possible exposure to carbon monoxide (eg, blocked furnace flue)Pulse oximetry is falsely elevated in the presence of carboxyhemoglobinMethemoglobinCyanosis in the presence of a normal PaO2 on arterial blood gasExposure to agents known to cause methemoglobinemia (eg, nitrites, benzocaine, aniline dyes)Oxygen saturation by cooximetry identifies the presence of an abnormal hemoglobin if specific measure of methemoglobin is not availableDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsLaboratory testingD-dimerClinical findings suggestive of pulmonary embolus (eg, low oxygenation, pleuritic chest pain, wedge-shaped infiltrate on chest radiograph, and predisposing condition [eg, sickle cell disease, thrombotic condition])Pulmonary embolus is a rare cause of respiratory distress in childrenImaging options in patients with moderate to high clinical probability and elevated D-dimer include ventilation/perfusion scan, ultrasound of extremity veins and deep veins, CT pulmonary angiography, and pulmonary angiographyDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsImagingLateral neck radiographClinical findings suggestive of epiglottitism retropharyngeal abscess or ingested foreign bodyCroup can usually be diagnosed clinically without a radiographChest radiographAll children with significant respiratory distress and those with focal lung findingsDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsImagingForced expiratory or bilateral decubitus chest radiographSuspected foreign body aspirationHyperaeration noted on the side with the bronchial foreign bodyUnilateral decubitus chest radiographAssess whether lung opacity is due to parenchymal disease or effusionLoculated effusions and very large effusions may not show evidence of layeringDiagnostic studies for evaluation of acute respiratory distressTestIndicationsCommentsImagingAbdominal radiographs (supine and upright, or cross-table lateral)Significant abdominal tenderness and/or distension with concern for intestinal obstruction or perforationOther testing (eg, ultrasound, upper gastrointestinal contrast study, abdominal CT) may also be indicated depending upon clinical findings and likely etiologiesComputed tomography (CT) of the headClinical findings suggestive of increased intracranial pressure or intracranial mass lesionSteeple sign65

The AP view demonstrates tapering of the upper trachea, known as the "steeple sign" of croup. Note that the finding can be simulated by differing phases of respiration even in normal children. Courtesy of the Department of Diagnostic Imaging, Texas Children's Hospital.Croup lateral neck radiograph66

Lateral neck radiograph showing subglottic narrowing and distended hypopharynx consistent with acute laryngotracheitis. Courtesy of Joe Black, Diagnostic Imaging, Texas Children's Hospital.

Bacterial tracheitis67

Lateral neck radiograph showing intraluminal membranes and tracheal wall irregularity consistent with bacterial tracheitis. Courtesy of R. Paul Guillerman, MD, Department of Radiology, Baylor College of Medicine.

Retropharyngeal abscess68

Lateral neck radiograph demonstrating widening of the retropharyngeal space and reversal of the normal cervical spine curvature. The retropharyngeal space is considered widened if it is greater than 7 mm at C2 or 14 mm at C6. The epiglottis and subglottic area in this radiograph are normal. Courtesy of Joe Black, Department of Diagnostic Imaging, Texas Children's Hospital.

GENERAL ASSESSMENT OF PEDIATRIC RESPIRATORY EMERGENCIES69

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AIRWAY ASSESSMENT AND MANAGEMENT71

Airway and Breathing ManagementPositioning is the first step in airway management. Infants : should be placed in the "sniffing position" by a head tilt-Chin lift or jaw-thrust maneuver that brings the angle of the chin up 90 degrees from the bed72Airway ObstructionCroupA viral infection of the airway below the level of the vocal cords EpiglottitisInfection of the soft tissue in the area above the vocal cordsForeign body airway obstructions73Croupis a common viral infection that usually affects children 2 to 4 years old. affects the larynx and trachea, although this illness may also extend to the bronchi.85% of children to have mild croup, less than 1% with severe croup. 74CroupTypical signs include a low-grade fever of 38C to 39C,a seal-bark cough, and stridor, particularly if the child is agitated. onset is gradual.Breathing problems worsen at night, and may appear severe and extremely upsetting to caregivers.75Severity level of croupMild severity - Occasional barking cough, no audible stridor at rest, and either no or mild suprasternal and/or intercostal retractionsModerate severity - Frequent barking cough, easily audible stridor at rest, and suprasternal and sternal wall retractions at rest, with no or minimal agitationSevere severity - Frequent barking cough, prominent inspiratory (and occasionally expiratory) stridor, marked sternal wall retractions, significant agitation and distressImpending respiratory failure - Barking cough (often not prominent), audible stridor at rest, sternal wall retractions may not be marked, lethargy or decreased consciousness, and often dusky appearance without supplemental oxygen support76Severe Croup ManagementABCNebulized Racemic Epinephrine (2.25%)observe for at least 3 hours post last treatment because of concerns for a rebound phenomenon of bronchospasm,Dose: 0.05 ml/kg (maximum 0.5 ml in children)Child under 6 months: 0.25 mlChild: 0.5 mlAdolescent: 0.75 ml

L Epinephrine 1:1000 Dose: 0.5 ml/kg (maximum 5 ml)77Severe Croup ManagementCORTICOSTEROIDSdecreasing edema in the laryngeal mucosa, usually effective within six hours of treatment.decreases the need for additional medical care, hospital stays, and intubation rates and duration. 78Epiglottitis

A bacterial infection that usually affects children 4 to 6 years oldusually presents with a higher fever ranging from 39C to 40C. Difficulty swallowing may cause the child to drool. Stridor will be present even if the child is resting. Children with epiglottitis often assume a tripod position to maximize breathing comfort.As with most upper airway problems, onset is rapid..79Bacterial tracheitis

This bacterial infection causes the trachea to swell, resulting in partial airway obstruction. High fever, low-pitched stridor (a snoring sound)a productive cough are usually present80

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Questions ?83

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Congenital anomalies associated with stridorMalformationCharacteristicsNoseNasal deformitiesChoanal atresia or agenesis, septum deformities, turbinate hypertrophy, vestibular atresia or stenosis.PharynxCraniofacial anomaliesAnomalies causing facial retrusion are associated with upper airway obstruction, including Crouzon's, Pierre Robin, and Apert's Syndrome.TongueMacroglossia and glossoptosisLarynxLaryngomalaciaMost common cause of chronic stridor in infants. Almost all patients present by 6 weeks of age. Symptoms are more pronounced after upper respiratory infections.Laryngeal webs75 percent located in the glottic area. Complete webs cause respiratory distress at birth, partial webs produce stridor, weak cry and different degrees of respiratory distress.Laryngeal cystsLocated in supraglottic area may cause respiratory distress and stridor.Subglottic hemangiomaPresents as progressive loud stridor with increased respiratory distress. Associated with hemangiomas in other parts of the body.Subglottic stenosisMay be congenital but more often acquired secondary to intubation. Usually located 2- 3 mm below the glottis.TracheaTracheal stenosisUsually present with stridor or both stridor and wheezing. If stenosis is significant, respiratory distress occurs.Vascular rings or slings74 percent of vascular rings are symptomatic.TracheomalaciaAssociated with other congenital anomalies. May be secondary to a vascular ring or cysts. Worsens with upper respiratory infections, crying, coughing or feeding. May cause severe spells with cyanosis.Definitions86Acute respiratory failure

inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or failure of CO2 homeostasisDefinitionshypoxaemic respiratory failure:PaO2 50 mm Hg when breathing room air

hypercapnic respiratory failure:PaCO2 50 mm Hg.Basic respiratory physiology88O2CO2The major function of the lung is to get oxygen into the body and carbon dioxide out90Oxygen inDepends onPAO2Diffusing capacityPerfusionVentilation-perfusion matching

Carbon dioxideWater vapourOxygenNitrogen

Oxygen inDepends onPAO2FIO2PACO2Alveolar pressureVentilationDiffusing capacityPerfusionVentilation-perfusion matchingCarbon dioxide outLargely dependent on alveolar ventilation

Anatomical deadspace constant but physiological deadspace depends on ventilation-perfusion matching

Carbon dioxide outRespiratory rateTidal volumeVentilation-perfusion matching

Pathophysiology

Hypoxemia, defined as a decreased level of oxygen in the bloodhypoxia, defined as a decreased level of oxygen in the tissues.

.97These 2 conditions may be closely related and may or may not coexist, but they are not synonymousCauses of HypoxemiaMismatch between alveolar ventilation (V) and pulmonary perfusion (Q)Intrapulmonary shuntHypoventilationAbnormal diffusion of gases at the alveolar-capillary interfaceReduction in inspired oxygen concentrationIncreased venous desaturation with cardiac dysfunction plus one or more of the above 5 factors98The 3 most important abnormalities in gas exchange that lead to respiratory failure are V/Q mismatch,intrapulmonary shunt, and hypoventilation99FIO2Ventilation without perfusion(deadspace ventilation)Diffusion abnormalityPerfusion without ventilation (shunting)HypoventilationNormal75%75%100%75%87.5%Perfusion without ventilation (Shunting)Intra-cardiacAny cause of right to left shunteg Fallots, EisenmengerIntra-pulmonaryPneumoniaPulmonary oedemaAtelectasisCollapsePulmonary haemorrhage or contusionPerfusion without ventilation (shunting)Intra-pulmonarySmall airways occluded ( e.g asthma, chronic bronchitis)

Alveoli are filled with fluid ( e.g pulm edema, pneumonia)

Alveolar collapse ( e.g atelectasis)

V/Q mismatch:Dead space ventilation Alveoli that are normally ventilated but poorly perfused

Anatomic dead space Gas in the large conducting airways that does not come in contact with the capillaries e.g pharynx

V/Q mismatch:Dead space ventilation

Physiologic dead space Alveolar gas that does not equilibrate fully with capillary blood Dead space vantilationDSV increase:Alveolar-capillary interface destroyed e.g emphysemaBlood flow is reduced e.g CHF, PEOverdistended alveoli e.g positive- pressure ventilationDiffusion abnormality:Less common

Abnormality of the alveolar membrane or a reduction in the number of capillaries resulting in a reduction in alveolar surface area

Causes include:Acute Respiratory Distress SyndromeFibrotic lung disease

Hypoventilationcan be caused bydisease at any of the anatomical sites involved in ventilation. Brainstem injury or disease may result in impaired functioning of the respiratory centre, impaired functioning of the respiratory centre which suppressed by depressant drugs108BrainstemSpinal cordNerve rootAirwayNerveNeuromuscular junctionRespiratory muscleLungPleuraChest wallSites at which disease may cause ventilatory disturbance110The nerve roots may be damaged by trauma or tumour nerve injuries and neuropathies such as Guillain Barre or critical illness neuropathy may affect motor neurons supplying respiratory musclesNeuromuscular blockers or disease of the neuromuscular junction (eg myasthenia gravis) may impair transmission of nerve impulses to respiratory musclesOr the problem may be in the muscle itself. Respiratory muscle fatigue, disuse atrophy and malnutrition are important causes of respiratory muscle failure in the ICUAlternatively the problem may be a problem of increased resistance to airflow. For example due to obstruction of the upper airway or bronchospasmOr the problem may be decreased compliance of the lung itself, the pleura or the chest wall.

Respiratory FailureSymptomsCNS:HeadacheVisual DisturbancesAnxietyConfusionMemory LossWeaknessDecreased Functional PerformanceRespiratory FailureSymptomsPulmonary:CoughChest painsSputum productionStridorDyspnea

Respiratory FailureSymptomsCardiac:OrthopneaPeripheral edemaChest pain

Other:Fever, Abdominal pain, Anemia, BleedingClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaHaemoglobin desaturation

Clinical signs of respiratory failure can be divided into signs of respiratory compensationClinicalRespiratory compensationTachypnoeaAccessory musclesRecesssionNasal flaringSympathetic stimulationTissue hypoxiaHaemoglobin desaturation

Such as tachypnoea, use of accessory muscles, recession and nasal flaringClinicalRespiratory compensationSympathetic stimulationHRBPsweatingTissue hypoxiaHaemoglobin desaturation

ClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaAltered mental stateHR and BP (late)Haemoglobin desaturation

Signs of tissue hypoxia such as altered mental status and at a very late stage bradycardia and hypotensionClinicalAltered mental statePaO2 +PaCO2 acidosis dilatation of cerebral resistance vesseles ICP

DisorientationHeadachecomaasterixispersonality changesClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaHaemoglobin desaturationcyanosis

And signs of haemoglobin desaturationRespiratory FailureLaboratory TestingArterial blood gasPaO2PaCO2PHChest imagingChest x-rayCT sacnUltrasoundRespiratory FailureLaboratory TestingOther testsHemoglobinElectrolytes, blood urea nitrogen, creatinineCreatinine phosphokinase, aldolaseEKG, echocardiogramElectromyography (EMG)

PaO2 (kPa)Hb saturation (%)890Pulse oximetryThe pulse oximeter is an extremely useful monitor which estimates arterial saturationthe relationship between saturation and PaO2 is described by the oxyhaemoglobin dissociation curvea saturation ~90% is a critical threshold because below this level a small fall in PaO2 produces a sharp fall in SpO2 .Conversely a rise in arterial PO2 has little effect on saturation and therefore little effect on oxygen delivery to tissuesSources of errorPoor peripheral perfusionDark skinFalse nails or nail varnishLipaemiaBright ambient lightPoorly adherent probeExcessive motionCarboxyhaemoglobin or methaemoglobin

126 Each minute is critical to achieving both survival and a favorable neurologic outcome.

Chart214.7451.2679

Sheet1Oxygen14.74Carbon dioxide5Water vapour1.26Nitrogen79

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