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Respiratory failure Dr .Ghazi F.Haji Senior lecturer of cardiology
Al-Kindy College of Medicine
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Plan of the Talk *Definition *Physiology *Classification *Pathology *Type 1 RF Causes clinical features diagnosis *Type 2 RF causes *Treatment *ARDS (Adult respiratory distress syndrome)
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True or false
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Definition: Is the production of abnormal blood gases due to diseases of Respiratory system or it is control (Respiratory center) ,intercostals ,phrenic nerve and muscles of respiration or thoracic cage when the patient at sea level and at rest
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Physiology There are 3 important factors must be available: 1- Proper ventilation (o2 to lung tissue and co2 to the outside ) 2-Proper perfusion (circulation) 3- Proper exchange of gases(matching between perfusion and ventilation ) Normally upper zone of the lung (well ventilation and less perfusion)while lower zone vice versa
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Classification There are 2 types : both include hypoxia but in : Type 1 RF – PO2 is low +Pco2 is normal or low (Normocapenia or Hypocapenia) while in Type 2- PO2 is low +Pco2 is high 1-- has cyanosis and Tachypnea(i.e active Respiratory 2– has cyanosis with breathing similar to normal (No excessive drive for ventilation i.e depress Respiratory center )
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Pathology Type 1 RF: *The mechanism of this type if ventilation – perfusion mismatching (well ventilated area has poor perfusion or vice versa) *PO2 Decrease + PCO2 normal or decrease (PO2 Dcrease ;that because less o2 is brought from air to blood while co2 is normal; because of hyperventilation – that washes co2 from blood that because co2 is present in plasma as carbonic acid (it is amount not fixed;dissolved ) so it be can washed easily while o2 is sticky and carry it to haemoglobulin of the RBC and only small amount is dissolved in plasma ,so hyperventilation could not bring enough amount of o2,but it could wash co2
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Type 2 RF: the mechanism is Hypoventilation(mean less o2 will come in and less co2 will come out ) PO2 decrease + PCO2 increase (Hypoxia and hypercapenia)
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Causes of Type 1 RF Possible causes : 3groups 1- Restrictive defect in ventilation :eg infilterative lung diseases,pneumonia ,pulmonary fibrosis ,pulmonary eodema .sudden pnemothorax ,and sudden pleural effusion . 2- obstructive defect of ventilation :acute asthmatic attack(asthma can cause type 2 RF) 3-Vacular causes :pulmonary thermoembolism is the common (mismatching between ventilation and perfusion ; that mean the area has agood ventilation but poor blood flow .
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Clinical features of type 1 RF
Depending on the cyanosis (which can correct by o2 shallow breathing
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Diagnosis of type 1 RF Clinical Radiological Arterial blood gases tests
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Causes;of Type 2 RF 3 groups
1- chronic obstructive airway disease (COAD)-Chronic bronchitis ,chronic asthma (not acute asthma) Despite having central cyanosis ,the patient breath is similar to normal 2-center suppression ((anesthesia, (poisoning narcotic – hypnotic(in suicidal attempt)) , trauma ,tumors, CVA ) ) Nerves (intercostal and phrenic)- guilain barre syndrome (infective polyneuropathy(ferver +abnormal behavior like hysteria +polyneuropathy +cyanosis due involvement of intercostal muscles or nerves; treatment tracheostomy or endotracheal tube and ventilator)) Poliomyelitis (affect intercostal muscles and phrenic nerve – lead to hypventilation ) Myopathies -Myasthenia gravis-Kyphoscoilosis -Flial chest (multiple rib fractures 3- late stage of type 1 RF:all causes of type 1RF (IF NOT TREATED )can cause type 2 RF
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Clinical features of type 2RF
The main finding +despite cyanosis ;hypoventilation means a decrease in breathing rate or normal breathing rate but not properly effective or hypercapenia : SOB+ tiredness at rest or in excretion +tachycardia (bounding pulse)+hyper dynamic circulation(collapsing pulse ;large volume with central cyanosis +flapping tremor +irritability +convulsion and finally coma dueto co2 chronic obstructive bronchitis or asthma there is edema and puffiness of the face so the patient is blue and bloated which mean cyanosis+edema also sleepy +drowsy
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Diagnosis type 2 RF Clinical Radiology Arterial blood gases
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Treatment of RF 1-Treated the cause 2- general measure :
Treat the infection with suitable antiboitic Treat bronchospasm with bronchodilator sometime with steroid therapy Oxygen therapy ;in type 1RF give any o2 percentage ,the best way mask supply 60% Because respiratory center still active while in type 2 RF (the respiratory center is depress and the stimulus for it is action is hyopxia ,so removal of this stimulus will treat cyanosis but it will cause further depression to the respiratory center )
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No more than 35% in type 2RF especially in COAD
*apatient with breathing rate 20 b/m,with hypoxia and hypercapenia .if give high concentrated o2 percent ,that lead to more depression of respiratory center with decrease of breathing rate to 12 that lead to co2 retention – more hypercapenia – co2 necrosis --- irretability ,convulsion and coma so in type 2 RF should start with controlled o2 therapy depending on severity of disease ;the more severe condition need less o2 percent So start with 24%o2 (which is near to normal concentration of o2 in air ) Once the patient improve ;we can gradually increase the o2 concentration to 28% then 30% then 35% No more than 35% in type 2RF especially in COAD
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Clearance of airway from any obstructing material Physiotherapy (trendelenburg position) Assisted ventilation ;indicated in severe hypoventilation such patients usually have paralysis of the muscles ,sometime patients unconscious so in addition to mechanical ventilator ;we must supply the patient with nutrition ,electrolyte . treated bed sore if present mechanical ventilation by either volume- fixed or pressure- fixed ventilator
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ARDS- adult respiratory distress syndrome
Called shock lung :there is pulmonary edema without increase in the venous pressure (unlike left side heart failure in which pul. Edema with increase in venous pressure due to increase in left atrial pressure which cause increase pulmonary venous pressure – lead to oozing of fluid to the lung tissue causing pulmonary edemea ) In this syndrome ;the pulmonary edemea is due to oozing of fluid through capillaries without increase in venous pressure (but the defect in capillaries itself)
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Causes There are many process that precipitated ARDS: 1- Pulmonary infection 2-Injury : Direct –bullet injery ,blast ,embolus.infection Indirect :haemolytic anemia /fracture 3- fractures 4- head injury 5- surgery if prolong 6- septicemia and septic shock 7-acute pancreatitis 8- burns 9- embolization 10- direct damage to the lung by acids (due to vomiting or regurgitation) 11-drowing 12- hanging 13-inhalation of chemical and toxic material (chlorine –irritant to lung ) 14- cardiopulmonary bypass in cardiac surgery 15- multiple blood transfusion
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How would you suspect ARDS?
Any patient with previous serious surgical and medical problem will develop severe progressive SOB after 1-2 days (ARDS- RF type 1) ARDS is a serious condition that may lead to death (toxic gases that cause this syndrome one of which is o2 ,o2 is irretant if given in high concentration so it is mandated to not given high concentrated o2 for more than 24h That happen in mechanical ventilators when received pure o2 over 24h
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What happens during ARDS
Destruction of lung tissue -- this tissue contains endothilum of the blood vessls and epithelum of the alveoli – that destruction leads to stiffness of the lung + capillaries damage –leads to left side heart failure (oozing of fluid from capillaries causing pulmonary edemia)– lead to respiratory failure type 1
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Clinical features Any patient having severe medical or surgical problems and he developed respiratory failure within 1-2 days – you should diagnose as ARDS Progressive SOB- Central cyanosis – Fine cripitation-hypoxia and hypocapenia –wide,spread shadowing (bilateral) on chest X-ray COMPLICATION : Bacterial super infection Multiple organ failure Mortality in best center is about 50% If patient survive might develop pulmonary fibrosis in future
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Treatment *ICU(intensive cure unit) with mechanical ventilator and treat the cause *O2 therapy (not pure o2 because it irritant to lung tissue ) *Ventlation : there is damage of type 2 pneumocytes that lead to decrease in surfactant (so need always to positive pressure to keep the lung inflated and push the fluid away) there are two unit to keep this positive pressure : IPPV(INTERMITTENT POSITIVE PRESSURE VENTILATOR) PEEP(POSITIVE END EXPIRATORY PRESSURE) Treat the infection (antibiotic) *IV nutrition *Cleaning *Prevent bed sore *Electrolyte balance *Steroid therapy ? As antiinflammatory
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True or false
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Thank you for attention
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