Respiratory failure

DefinitionSevere dysfunction of pulmonary ventilation and/or oxygenation caused by various diseases, characterized by hypoxia and/or retention of carbon dioxide, manifested as multiple systemic syndromes with a series of pathophysiologic changes

The standard for definition: PaO26.67kPa(50mmHg), under the circumstances as at sea-level atmospheric pressure, at rest indoor, excluding the interference of other diseases such as intracardiac shunt

ClassificationHistory & Course

Acute: no primary pulmonary D, accordant to the standard of RF in several Hrs or daysChronic: long history of chronic pulmonary D, e.g. COPD, interstitial D, etcPathophysiology

Hypoventilation, airway obstructionOxygenation (gas exchange disorder), ARDSCombination of the above: COPDSite of Primary Diseases

PeripheralCentral

Arterial gas analysis

Type : hypoxia, PaO2

Etiology

Pump RF: insufficiency of respiratory drive (center), or limited respiratory movement (paralysis of peripheral nerve, fatigue of muscles, thoracic deformity, etc)Lung RF: caused by airway obstruction, pulmonary parenchymal or interstitial D or pulmonary vascular D.

EtiologyIn terms of pathogenesis: hypoventilation, oxygenation, or the combination

Ventilation dysfunctionObstructiveChronic bronchitis, COPD, late stage of asthma, sleep apnea, bronchial foreign body, oppression of inflammatory granuloma, tumor or enlarged LNLimited

LimitedDiseases of Chest wall: such as thoracic deformity, trauma, Rheumatic Arthritis(central type), severe pleural adhesion and hypertrophyDiaphragmatic movement limited by abdominal surgery, exuberant ascites, huge mass, etcLimited lung expansion: pleural effusion, pneumothorax, atelectasis, lung consolidation, etcCNS diseases: cerebral injury, tumor, stroke, encephalitis, etcNeuromuscular D, such as poliomyelitis, myasthenia gravitas, progressive myatrophy, etcRespiratory center inhibited by drugs such as morphine, barbitals, & other sedatives, pesticides

Oxygenation dysfunction

Pulmonary edema caused by cardiac or other DChronic pulmonary interstitial D such as primary interstitial fibrosis, sarcoidosis, silicosis, radio pneumonia, oxygen intoxication, etcOcclusive pulmonary vascular D: pulmonary embolism and infarction, thrombosisARDS (acute respiratory distress syndrome)

PathogenesisAlveolar insufficient ventilationVentilation/perfusion mismatchingDiffusion dysfunctionIncreased intrapulmonary shuntRespiratory muscular fatigue

1. Alveolar insufficient ventilationNormal ventilation depends on:Airway, thoracic and pulmonary compliance Obstruction or compliance insufficient ventilation hypoxia and retention of CO2.

PaCO 2 equation, which show the relationship between PaCO 2 and alveolar ventilationPaCO2 = 0.863 (VCO2/VA)VCO2: Minute production of CO2 -- relatively invariableVA: Minute alveolar ventilationNegative relationship between VA & PaCO2VAVEVD. VE: minute ventilation; VD: physiologic dead (ineffective) volumeVE and VD VA hypoxia and retention of CO2

2. Ventilation/perfusion mismatchingEffective gas exchange realized by matched alveolar ventilation & blood perfusion

N: ventilation 4L/Min; perfusion: 5L/Min; V/Q0.8V/Q>0.8: N ventilation, but perfusion, termed as dead-volume effect, occurrs in shock or pulmonary embolismV/Q

3. Intrapulmonary shunt increaseN: shunt

4. Diffusion dysfunctionGas exchange realized via respiratory membranealveolar-capillary membraneComposed of 6 layers: surfactant, alveolar epithelium, alveolar basic membrane, interstitia, capillary basic membrane and capillary endotheliumAverage thickness: 0.7m

Diffusion effect is determined byEquation: D = d A P1--P2/TD: diffusion amountMembrane area (A) Thickness (T) Diffusion coefficient: (d) Differential pressure between alveoli and capillary (P1P2)

In COPD, alveolar injury Area reducedIn pulmonary edema & interstitial fibrosis thickness increasedDiffusion coefficiency of CO2 is 20 times of O2, so diffusion dysfunction is for O2 only in most cases

5. Respiratory muscular fatigueImportant part of respiratory pumpReasons

Insufficient drive of Respiratory centerNeuromuscular DRespiratory burden increasedEnergy support insufficiency

PathophysiologyKey or basic changes: hypoxia, retention of CO2, and acidosisSystemic changes including

Central nervous system Respiratory systemCirculatory systemDigestive systemAnd others

1. Influence on CNSDetermined by the severity, velocity and duration Hypoxia: cerebral cortex most sensitive, O2 consumption: 3ml100gMin. abrupt halt for 20Secspasm and coma; if hypoxia occurs slowly attention and orientation delirium comaRetention of CO2: headache and excitement somnolence coma (CO2 anesthesia)Both hypoxia & retention of CO2: brain vascular dilation, permeability, intracranial pressure cerebral edema

2. Influences on respiratory systemHypoxia (PaO250% O2 inhalation may induce R. inhibition, so 16% is recommended.CO2 strong respiratory stimulant. 5% CO2 inhalation ventilation 3-4 times, but >12% R. inhibitionPaCO210.7kPa, no stimulation on R. center. At this time, hypoxia is the only trigger for ventilation, thats why high-dose O2 therapy may reduce ventilation aggravate retention of CO2 pulmonary encephalopathy

3. Influence on circulatory systemHypoxia: slight sympathetic nerve (+) tachycardia, myocardial retraction, output, Bp. Severe hypoxia arrhythmia, bradycardia, myocardial retraction (-), output. output pulmonary vascular retraction pulmonary A hypertension RV hypertrophy cor pulmonaleRetention of CO2: slight sympathetic nerve (+); severe retention bradycardia, output and Bp, skin vessel dilation dermatorrhea (excessive sweat), facial flush

4. Influence on hematologySecondary erythrocytosisIncrease the burden of heartHypoxia and toxin capillary injury DIC

5. On digestive and urinary systemHypoxia dyspepsia, abdominal distention, nausea, vomiting, stress ulcer, gastrointestinal bleedingLobular necrosis, enzymes and bilirubinRetraction of renal artery, renal perfusion reduced, GFR ; imbalance of acid-base and electrolyte

6. On acid-base & electrolyteRetention of CO2 PaCO2, respiratory acidosispH may be in normal range, because it determined by the ratio of PaCO2/HCO3-. pH calculated by Henderson-Hanalbach equation:pH = 6.1 + (-HCO3)/PaCO2pH is normal: termed as compensatory respiratory acidosis, or else, decompensatory respiratory acidosis

If acidosis in tissue fluid, Ktransferred outward, while Na and H inward cellular acidosis, extracellular hyperpotassemiaPaCO2 hypochloremia & hypochloremia alkalosisTherapy on type RF, administration of glucose, uretics and glucocorticoids loss of K hypopotassemia and hypochloremia alkalosisAlkalosis left shift of oxygenation curve O2 release aggravate hypoxia, inhibit respiration

Clinical manifestationtypeTypical: dyspnea, esp. exertional.Tachypnea, cyanosis, waving nose, assistant R. movement In early stage, attention & orientation disorders delirium, tachycardia, Bp spasm, coma, bradypnea, BpManifestation in other system

Type RFSimilar with typeBesides, headache, somnolence, sleep rhythm disorder, warm skin, facial flush, bulla conjunctiva edemaPulmonary encephalopathy

Diagnosis & Differentiation DiagnosisCombination of history, signs and results of arterial gas analysisIf accompanied with neuropsychic presentations, be distinguished from

StrokeSevere imbalance of acid-base and electrolyteInfectious intoxicated encephalopathy

TreatmentAIMCorrect hypoxia and retention of CO2Etiological therapy: different with various DEmphasis on treatment of aggravation stage in chronic RF

Main principlesAirway opening & ventilation improvementOxygen therapyAntibiotics and infection controlRegulation of acid-base & electrolyte disorderNutrition & supportive measurementsothers

1.Airway opening & ventilation improvementPhlegm excretionBronchodilatorsHeparinSteroidsRespiratory stimulantsAirway intubation or incisionMechanical ventilation

Phlegm excretion

Phlegm dilation: infusion >20002500ml, but monitoring CVP (central vein pressure); inhalation of nebulized 2~4% carbonate natrium monitoring cardiac functionactive cough (position alternation) is encouragedexpectorants

Bronchodilators

2 selective inhalation agents is recommendedAnticholinergicsTheophyllines: monitor blood drug concentration

Heparin

Non-specific anti-inflammatory. Anti-allergic action Viscosity of blood and airway excretions. Dosage: 50100 m g/day, duration: 1 week. Examination for platelet counting, clotting and bleeding time, and prothrombin time before administration

SteroidsAirway spasm, inflammation and excretionMethylpredisolone inhalation is recommended (5 times of pharmacologic effect, lower inhibition on HPA axis). 2~4mg/kg

Respiratory stimulantsIndication: significant retention of CO2 respiration inhibitedDrugs: CoramineMechanism: directly stimulates R. center, and stimulates chemical receptors in carotid and aortic body. Administration: 0.3757~10+ 500ml ivgtt, or together with lobelineContraindication: R. muscular fatigue or airway obstruction is not relieved

Airway intubation or incision

Indication: not relieved by bronchodilators and phlegm excretionsMethods: intubation & incisionIntubation: commonly used, via nasal cavity, 2~5cms above carina of trachea

Airway intubation or incisionIncision: intubation is not effective, or long period of mechanical ventilation is required. Advantages: significant reduction of dead volume and consumption of respiratory movement, convenient for phlegm clearance and diet. Disadvantages: more nosocomial infections, difficult for nursing

Mechanical ventilationIndication: ineffective by all above treatments, or oxygenation disorders AIM: improve ventilation & gas exchange, reduce consumption of R. movement Methods: non-invasive or invasive.

Indications for non-invasive mechanical ventilation

Moderate to severe dyspnea, accompanied with assistant muscle involvement and paradoxical thoracic-abdominal respirationModerate to severe acidosis (pH 7.30~7.35) and hypercapnea (PCO2 45~60mmHg) R>25tpmAt least met 2 items

Exclusive standard (any 1 of items)

Respiratory inhibition or apnea Unstable circulatory system (hypotension, arrhythmia, or myocardial infarction)Somnolence, abnormal consciousness, not cooperatedAbnormal swallowing reflex, severe upper digestive bleedingLarge amount of viscous airway excretionRecent facial or gastroesophageal surgery Nasopharyngeal abnormality, cephalofacial injurySevere fatnessSevere gastrointestinal distention

Indications for invasive M. ventilation

NIPPV failed or existence of contraindicationssevere dyspnea, accompanied with assistant muscle involvement & paradoxical thoracic-abdominal respirationR>35tpm Life threatened hypoxia, PO2< 45~60 or PO2/FIO2

Mode selectionDetermined by 2 factors

Autonomic respiratory capability or R. driveAim for mechanical ventilation

CMVControlled Mode of VentilationFor acute attack of COPD patientsProvide sufficient tidal volume, reduce respiratory consumption, relieve R. muscular fatigueIf autonomic R reversed and infection controlled, SIMV PSV, in order to practice the capacity of autonomic respiration preparation for stop M. ventilationSIMV: simultaneous intermittent mode of ventilationPSV: pressure support ventilation

Indexes setup FiO2 (oxygenation flow fraction): >50%--alert for intoxicationVT (tidal volume)

6~10ml/kg, generallyRegulated in real time by the results of arterial gas and dynamic changes of respirationAim: avoiding too much high airway pressure (high pressure cause injury)For patients with reduced effective ventilation volume (ARDS), 68ml/kg is recommended

Breath rate

1216tp, for patients with COPD and asthmaMore rapid frequency in D of limited ventilation such as ARDS, assisted with lower VT, which benefit for overcoming elastic resistance and cardiovascular side effectsI/E (ratio of inspiration to expiration)

1:2, generally.Smaller I/E (1, even 2:1 ventilation, used in ARDS, helpful for gas distribution & oxygenation

Time of Positive end-inspiratory pressure

Period between end of inspiration and start of expirationIn general, < 20 respiratory cycleLonger: benefit gas distribution, reduce dead-volume ventilation, but increased average airway pressure and harmful to hemodynnamicsPEEP: Positive end-expiratory pressureFor patients with COPD, endogenous PEEP exist, because of airway resistance and thoracic-pulmonary elastic retraction. Proper PEEP (2-5cmH2O) improve alveolar ventilation and oxygenationWhile in ARDS, PEEP is key to improve oxygenation

Complications in M. ventilationAtmospheric pressure injury

Such as interstitial, mediastinal, subcutaneous emphysema, or pneumothoraxPrevention: limit & avoid abrupt increase of airway pressureHypotension

Occurred when insufficient effective blood volume, excessive VT, or too high PEEP Prevention: monitoring cardiovascular function (CVP by Swan-Ganz catheter), compensate blood volume

Nosocomial infection

Occurrence rate: 967, death rate: 3376Reasons: poor resistance, administration of wide-spectrum antibiotics, intubation & incision, phlegm aspiration, etcPulmonary infection is most commonPrevention

Avoid cross-infectionUse antibiotics reasonablyStop M. ventilation as soon as possible

Other complications

Insufficient or excessive ventilationGastrointestinal bleedingDysfunction of liver & kidney Oxygen intoxicationDependence on M. ventilation, etc.

Indications for weaning

Primary D is controlledReversion of autonomic respiration to some degreeMonitoring of autonomic respiration by a -type tube or CPAP mode, the indexes are for reference only. CPAP: continuous positive airway pressureCurrently, mainly relied on integral analysis and experience

Procedure for weaning

CMVSIMV+PSVPSV weaning from M. ventilationPatients with COPD need long period of M. ventilation and have difficulty in weaning (which caused VAP, ventilation-weaning associated pneumonia)Recent evidence suggest: non-invasive M. ventilation used before weaning is very helpful to shorten period of assistant ventilation, to reduce the occurrence of VAP and other nosocomial infections

2. Oxygen therapyImportant for RF, the mode is determined by different types of RF

Non-controlled: FiO2 no need to be strictly controlled, but regulated by clinical status; More in patients without ventilation disorderControlled: FiO2 is controlled strictly. Aim: PaO2

Methods

Unilateral nasal catheter Bilateral nasal catheter Air diluted VenturiCalculation for oxygen concentration: FiO2214oxygen flow (L/min)

3. Infection controlInfection is the commonest trigger for RFIn RF, airway excretion, mucosal edema, bronchial spasm, lower resistance susceptible to infection, hard to be controlledEmphasis on reasonable administration of antibiotics

Based on result of repeated culture and sensitivity testExperience: G coccus or G bacillus

4. Correction of disturbance of acid-base & electrolyteR. acidosis

Key measurement: Improve alveolar ventilation, PaCO2Generally, alkaline drugs not required, which only used when PH

Metabolic acidosis: lactic acid, improve ventilation, correct hypoxiaMetabolic alkalosis

Caused by hypopotassemia or hypochloremialeft shift of oxygenation curve, aggravate hypoxiaMore dangerous, more difficult for weaningPrevention: chloridion & potassium compensation

Disturbance of electrolyteHypopotassemia, hypochloremia, and hyponatremia is commonSevere hyponatremia is corrected by infusion of 10% chloride natrium (diluted in 3%). Attention: rapid infusion may aggravate heart failure

5. Nutrition & supportive therapyMalnutrition is common, because

High consumption exist in both ARDS & COPD- acute attackInsufficient ingestion, malabsorptionOxygen consumption in mechanical ventilationMalnutrition lower immunity, and reduce both of central and peripheral driveImprove nutritional status is vital Basic everyday energy support (BEE) calculated by Harris-Benedict equation BEE (M)=66.47+13.75W+5H-6.8A(kcal)BEE (F)=655+9.68W+1.7H-4.68A(kcal)W: weight (kg), H: height (cm), A: age (year)For patients with COPD, the value is rectified by multiply a coefficiency (1.16 for M, 1.19 for F)

Ratio of nutrientsCarbohydrate

PasswayEnteric catheter-- safer: better for maintenance of functional integrity of GI tract, benefit for the growth of normal bacteria, which inhibit the shift of bacteria & the production of toxin.Parenteric: including ivdrop, only used when EN is dangerous, e.g. comatous patients (aspiration). EN should be used as soon as possible

6. Treatment on other complicationsImprove cardiac functionPrevent against shock, DIC and arrhythmia, DICPay much attention to DM and hypertensionSevere airway structure, but without M. ventilation, be alert for use of sedatives & diuretics

Appendices antibioticsCephalosporin4th generation

Wider spectrum, more effective on Gcoccus, especially for penicillin-resistant S. pneumoniaeStronger activity on G- bacilliMore stable to - lactamase

CephalosporinG coccusG- bacilli1st generationCephazolin ()Sensitive2nd generationCefuroxime ()SensitiveSensitive 3rd generationCeftriaxone ()WeakStrong4th generationCefepime )StrongStrong

CarbopenemRepresentatives: tienam composed of Imipenem and cilastatin sodiumMost effective in the worldQuite stable to - lactamase because of trans structure formed by hydroxyl lateral chain and -lactate loopCilastatin inhibit enzymes (degrade imipenem) in kidney

Tienam

Wide spectrumaerobic or anaerobic G coccus and G- bacilli, including those with super -lactamase (ESBL), and resistant against 3rd-generation cephalosporinImipenem combine with PBP-2 and PBP-2Ib induce rapid resolution, production of endotoxin

QuinolonesRepresentative: levoflaxacin ()Advantages

No need for cutaneous sensitivity testOral administrationWide-spectrumLess side-effect on liver & kidneyEffective on intracellular pathogens such as legionella and mycobacterium, mycoplasma, Chlamydia, etc.Disadvantages

Weaker effective on G+ coccusToxic to long bones and article, not recommended to be used in youth (< age of 16)

MacrolidesRepresentative: erythromycin, roxithromycin, clarithromycin, azithromycinvery effective on G coccusEffective on atypical infections

AminoglycosidesRepresentations: kanamycin, amikacin, netimicin, etimicin ()G- bacilliToxin injury to Ear, auditory Nerve, kidneyEtimicin more effective than gentamicinNetimicin, etimicin less side-effect

Anti fungus drugsRepresentatives: Amphotericin B, ketoconazole, fluconazole Candida, cryptococcus, aspergillusAnti anaerobic bacteriaPenicillin, metronidazole, tinidazole, chloromycetin, clindamycin. Erythromycin is only against anaerobic coccus, metronidazole against all anaerobic bacteria