Respiratory system includes: CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature
WE SHOULD DIFFRENTIAT BETWEENRESPIRATORY INSUFFICIENCY ANDRESPIRATORY FAILURE
Respiratory insufficiencyThe condition in which the lungs can not take in sufficient oxygen or expel sufficient carbon dioxide to meet the needs of the cells of the body..
Respiratory failureRespiratory failure is a syndrome in which the respiratorysystem fails in one or both of its gas exchange functions:oxygenation and carbon dioxide elimination.
In practice : respiratory failure defiend as Pao2 value lessthan 60 mm Hg or PaCO2 value more than50 mm Hg.
classification（1）according to PaCO2■ hypoxemic (Group Ⅰ) respiratory failure PaO2 of less than 60 mm Hg with a normal or low PaCO2. Cause of: Edema, Vascular disease, Chest Wall.■ hypercapnic (Group Ⅱ ) respiratory failure PaO2 low 60 mm Hg and PaCO2 of more than 50 mm Hg. Cause of: Airway obstruction, Neuromuscular disease.
（2）according to pathogenic mechanism ■ ventilatory disorders 1-obstructive ventilatory disorders asthma, emphysema, chronic bronchitis, and bronchiectasis 2-restrictive ventilatory disorders deformity of thorax , fracture of several ribs, tension pneumothorax diffuse interstitial fibrosis ■ gas exchange disorders 1-diffusion disorders 2-ventilation-perfusion mismatching
（3）according to primary site ■ central respiratory failure ■ peripheral respiratory failureairway obstruction between the glottis and the carina ■Obstruction is located in the airway outside the thorax： inspiratory dysnea ■Obstruction is located in the airway inside the thorax： expiratory dysnea expire inspire
■ peripheral respiratory failure Peripheral airway obstruction may be caused by: specific chemical mediators (such as histamine, leukotrienes, prostaglandins ), other substances released during inflammatory and allergic responses（4）according to duration ■ acute respiratory failure minute to hours ■ chronic respiratory failure several dayes or longer
Shunt An extreme V/Q mismatch((Perfusion without ventilation))Shunting is the most common cause for hypoxaemic respiratory failurein ICU patients.The deoxygenated blood bypasses the ventilated alveoli and mixes withoxygenated blood → hypoxemiaPersistent of hypoxemia despite 100% O2 inhalationHypercapnia occur when shunt is excessive > 60%
CausesI- Anatomic shuntBlood passes through parts of respiratory system thatreceives no ventilationII- IntracardiacRight to left shuntFallot’s tetralogyEisenmenger’s syndrome III- IntraPulmonary A/V malformation Pneumonia Pulmonary edema Atelectasis/collapse Pulmonary Hge Pulmonary contusion
Diffusion limitationDistance between alveoli and pulmonary capillary isone- two cells thickWith diffusion abnormalities:there is an increased distance between alveoli and pulmonary capillary.causesA.R.D.SSever emphysemaRecurrent pulmonary emboliPulmonary fibrosis
Alveolar hypoventilationIs a generalized decrease in ventilation of lungsand resultant buildup of CO2CausesRestrictive lung diseaseCNS diseaseChest wall dysfunctionNeuromuscular disease
Hypercapnic Respiratory Failure (Type II) This occurs in patients with chronic CO2 retention who worsen and have rising CO2 and low pH. Mechanism: respiratory muscle fatigue
Common causes Hypoxemic RF • Hypercapnic RF •Chronic bronchitis, emphysema Chronic bronchitis,emphysemaPneumonia, pulmonary edema Severe asthma, drug overdosePulmonary fibrosis Poisonings, Myasthenia gravisAsthma, pneumothorax Polyneuropathy, PoliomyelitisPulmonary embolism, Primary ms disordersPulmonary hypertension 1ry alveolar hypoventilationBronchiectasis, ARDS Obesity hypoventilation synd.Fat embolism, KS, Obesity Pulmonary edema, ARDSCyanotic congenital heart disease Myxedema, head and cervicalGranulomatous lung disease cord injury
Effects of respiratory failure 1- Acid-base disturbances & disorders of electrolyte balance 2- Alteration of the respiratory system peripheral chemoreceptor■ PaO2↓ ＜60mmHg respiratory center(+) respiratory movement↑ ＜30mmHg respiratory center (-) respiratory movement ↓■ PaCO2↑ central chemoreceptor ＜80mmHg respiratory center (+) respiratory movement↑ ＞80mmHg respiratory center (-) respiratory movement ↓
3. Alteration of the cardiovascular system ■ compensatory reaction PaO2<60 mmHg，PaCO2 increase cardiovascular center(+) increase in cardiac output : increase in stroke volume and heart rate redistribution of blood flow ■ injurious changes PaO2< 40 mmHg，PaCO2> 80 mmHg cardiovascular center(-) rate slow, decreased blood pressure cardiac output decrease pulmonary hypertension
4. Alteration of the nervous system(1) Hypoxia: the nervous system is very sensible to oxygen lack. < 40~50 mmHg, serious but reversible deterioration in cerebral function ( orientation, arithmetic tasks, memory) occurs, and restlessness and confusion are common. < 30 mmHg, loss of consciousness results. < 20 mmHg, irreversible damage of neural cells.(2) Hypercapnia: CO2 nacosis.condition of confusion, tremors, convulsions, and possible coma thatmay occur if blood levels of carbon dioxide increase to 80mm Hg or higher
5. Alteration of the renal function6. Alteration of the digestive system
Clinical diagnosisRespiratory compensationTachypnoea RR > 35 Breath /minAccessory musclRetraction intercostal msNasal flaringSympathetic stimulation HR BP Tissue hypoxiasweating Altered mental stateHaemoglobin desaturation HR and BP (late)Low spo2Cyanosis (late)
Causes of error Pulse oximetry Poor peripheral perfusion Dark skin False nails or nail PAINTING Bright ambient light Poorly adherent probe Excessive motion Carboxyhaemoglobin or methaemoglobin
ASSESSMENT OF PATIENT1-Careful history2-Physical Examination3-InvestigationsI- ABG analysis :PaO2PaCO2pHAlveolar-Arterial PO2 Gradient P(A-a)02 = (PiO2 - PaCO2) – PaO2 R
where PiO2 = partial pressure of inspired air, R = 0.8i.e, at sea level, breathing air;PAO2 = 20 - PaCO2/0.8 A-a Gradient = 20 - PaCO2/0.8 -PaO2Normal P(A-a)O2 gradient: 5-10 mm of HgA sensitive indicator of disturbance of gas exchange.Useful in differentiating extrapulmonary and pulmonary causes ofresp. failure.
Management of Respiratory Failure PrinciplesHypoxemia may cause death in RFPrimary objective is to reverse and preventhypoxemiaSecondary objective is to control PaCO2 andrespiratory acidosisTreatment of underlying diseasePatient’s CNS and CVS must be monitoredand treated
Management Correction of hypoxemiaSupplemental O2 therapy essentialTitration based on SaO2, PaO2 levels and PaCO2Goal is to prevent tissue hypoxiaTissue hypoxia occurs (normal Hb & C.O.)- venous PaO2 < 20 mmHg or SaO2 < 40%- arterial PaO2 < 38 mmHg or SaO2 < 70%Increase arterial PaO2 > 60 mmHg(SaO2 > 90%) or venous SaO2 > 60% Correction of hypercapniaControl the underlying causeControlled O2 supply1 -3 lit/min, titrate according O2 saturationO2 supply to keep the O2 saturation >90% but<93 to avoid inducing hypercapnia
Mobilization of secretionsEncourage pt 4 Effective coughing Positioning Semisetting
Hydration and humidification Chest PhysiotherapyChest percussion to loosensecretion Airway suctioning
Drug TherapyRelief of bronchospasmBronchodilatorsReduction of airway inflammationCorticosteroidsReduction of pulmonary congestionIV diureticsTreatment of pulmonary infectionsIV antibiotics Nutritional TherapyMaintain protein and energy storesEnteral or parenteral nutrition Supplements
Noninvasive Ventilatory support (IPPV) BiPAP CPAPMild to moderate RFNIPPV INDICATED InAcute exacerbation of COPD WITHRespiratory acidosis pH 7.25 Or lessCardiogenic pulmonary edemaAsthmaType II R.F secondary to chest wall deformityor neuro muscular diseasesWeaning off mechanical ventilation
Benefits NIPPV ofImproved alveolar ventilationReduced work of breathing Rest of the respiratory musculature Increased intrathoracic pressure decreases preload and afterload
should not be considered for NPPV? ContraindicationsCardiac or respiratory arrestNonrespiratory organ failureHemodynamic instabilitySevere encephalopathySevere UGI bleedFacial or neurosurgery, traumaUpper airway obstructionInability to cooperate or protect airwayHigh risk for aspiration
Mechanical ventilationIndicationsPaO2< 55 mm Hg or PaCO2 > 60 mm Hgdespite 100% oxygen therapy.Deteriorating respiratory status despiteoxygen and Nebulization therapyAnxious, with deteriorating mental status.Respiratory fatigue: for relief of metabolicstress of the work of breathing
Mechanical Ventilation: Strategies1-SIMV, A/C with PEEPPEEP (positive End-Expiratory pressure)Increase intrathoracic pressureKeeps the alveoli openDecrease shuntingImprove gas exchange
2-High frequency ventilation (HFV)Very small tidal volumes are used(<1ml/kg), very rapid rates and lower meanairway pressures are used3-Lung RecruitmentTo open the collapsed alveoliA sustained inflation of the lungs to higherairway pressure and volumes 4-Permissive HypercapniaAllows the PaCO2 to rise into the 60-70 mm ofHg range, as long as the patient is adequatelyoxygenated (SaO2> 92%), and able to toleratethe acidosis.This strategy is used to limit the amount ofbarotrauma and volutrauma to the patient
5-Prone positioningImprove oxygenation in about 2/3 of alltreated patientsNo improvement on survival, time onventilation, or time in ICUMight be useful to treat refractoryhypoxemiaRoutine use is not recommended
Respiratory failure common in old age due to ↓ Ventilatory capacity Alveolar dilation Larger air spaces Loss of surface area Diminished elastic recoil Decreased respiratory muscle strength ↓ Chest wall compliance