Oxygen Therapy PDF

Oxygen Therapy Rinaliza P. Bogsulen, RTRP  Case Study A 36 y/o F patient came into ER with c/c of DOB. Upon assessment, you have observed she has RR of 33; PR – 110. Which of the following O2 delivery device is most appropriate at this time? A. 2LPM via nasal cannula B. 10LPM via simple face mask...

Oxygen Therapy Rinaliza P. Bogsulen, RTRP  Case Study A 36 y/o F patient came into ER with c/c of DOB. Upon assessment, you have observed she has RR of 33; PR – 110. Which of the following O2 delivery device is most appropriate at this time? A. 2LPM via nasal cannula B. 10LPM via simple face mask C. 40% via air entrainment mask D. 15 LPM via non rebreathing mask General Goals & Clinical Objectives 1. Correct documented or suspected acute hypoxemia. 2. Decrease the symptoms associated with chronic hypoxemia. 3. Decrease the workload hypoxemia imposes on the cardiopulmonary system. Assessing the need for O2 therapy Laboratory documentation ◦ PaO2, SaO2, SpO2 Specific clinical problem ◦ e.g., post op px, carbon monoxide poisoning, shock, trauma, AMI Clinical findings at the bedside ◦ Tachypnea, tachycardia, confusion, etc. TYPES OF HYPOXIA Hypoxemic Hypoxia Lack of oxygen in the blood ◦ Low PiO2 ◦ Alveolar hypoventilation ◦ Diffusion defects ◦ V/Q mismatch ◦ R to L shunt  Causes of hypoxemia 1. Low PIO2 / FIO2 ◦ Breathing gases with low O2 concentration at sea level ◦ Pressure less than the atmospheric pressure  E.g. high altitude – “mountain sickness”  to illustrate: PO2 of air = (760- 47) x 0.21 = 149.73 ≈ 150 PO2 in the alveoli = 100 What will happen to the atmospheric pressure at higher altitude? What about the PiO2? 735 – 47 mmHg x 0.21 = 144.48 ≈ 144 2. Hypoventilation High PaCO2, decrease VA Causes: ◦ COPD, SIDS, obesity, OSA, CSA, upper airway obstruction ◦ CNS depression ◦ Head trauma, poliomyelitis, muscular dystrophy ◦ Neuromuscular disorders 3. V/Q Mismatch Most common cause of hypoxemia V/Q = 0.8 V/Q = Higher than 0.8 V/Q = 0.8 V/Q = less than 0.8 IncreasedV/Q – Increased ventilation or decreased perfusion ↑ PAO2 & ↓PACO2 Decreased V/Q – decreased ventilation or increased perfusion ↓PAO2 & ↑PACO2 Wasted Ventilation – ventilation is good but O perfusion ◦ Causes:  Pulmonary emboli  Partial /complete obstruction within the pulmonary capillary  Extrinsic pressure on the pulmonary vessels  Destruction of the pulmonary vessels  Decrease CO Shunted blood – good perfusion in the absence of ventilation Causes: ◦ COPD ◦ RLD ◦ hypoventilation 4. Shunt A. Anatomic Shunt Normal physiologic shunt = 3% (bronchial venous drainage, thebesian veins) Causes: congenital heart disease, intrapulmonary fistula, vascular lung tumors B. Capillary Shunt Causes: alveolar collapse or atelectasis, alveolar fluid accumulation, alveolar consolidation C. Shunt-Like Effect True Shunt- refractory to OT 1. alveoli cannot accommodate any form of ventilation  Shunt equation Qs/Qt = Cc02 – CaO2 CcO2 – CvO2 Where: CaO2 – O2 content in arterial blood CvO2 – O2 content of mixed venous blood CcO2 – O2 content pulmonary capillary blood  CaO2 = (Hbx1.34xSa02) + (PaO2 x0.003) CvO2 = (Hbx1.34xSv02 + (PvO2 x0.003) Cc02 = (Hbx1.34) + (PA02 x0.003) Remember: When shunt percentage is too high, oxygenation becomes an extremely difficult task for the cardiopulmonary system to support 5. Diffusion Impairment Equilibration doesn’t occur between PO2 in the pulmonary capillary and alveolar gas It takes about ¾ sec for the process of diffusion During exercise it takes ¼ sec In diseased condition – thickened alveolo- capillary membrane Causes:asbestosis, Wegener’s granulomatosis, alveolar cell CA, IPF, SLE, rheumatoid lung, scleroderma Responsive to OT Anemic Hypoxia Oxygen carrying capacity of the blood is reduced ◦ Deceased Hgb level (12 – 16g/dL) CO poisoning Excessive blood loss Methemoglobin Iron deficiency Stagnant (Circulatory) Hypoxia Normal oxygen content and carrying capacity but capillary diffusion is decreased ◦ Decreased heart rate ◦ Decreased CO ◦ Shock ◦ embolism Histotoxic Hypoxia Impaired oxidative enzyme mechanism ◦ Cyanide poisoning ◦ Alcohol poisoning ◦ accompanied by increased venous PO2 levels and not hypoxemia Clinical Signs of Hypoxia Finding Mild - Moderate Severe Respiratory Tachypnea Tachypnea Dyspnea Dyspnea Paleness Cyanosis Cardiovascular Tachycardia Tachycardia eventual Mild NPN, bradycardia, peripheral arrythmia vasocontriction HPN and eventual hypotensio Neurologic Restlessness Somnolence Disorientation Confusion, Distressed Headache appearance Lassitude Blurred vision Tunnel vision Loss of coordination Impaired judgment Slow reaction time Manic depressive activity Precautions and hazards of supplemental O2 Oxygen toxicity ◦Primarily affects the lungs and central nervous system ◦ Determining factors include PO2 and exposure time. ◦ Prolonged exposure to high FIO2 can cause infiltrates in the lung parenchyma. Physiological Responses to Exposure to 100% inspired Oxygen Exposure Physiological Response Time 0 - 12 Normal Pulmonary Function Tracheobronchitis Substernal Chest Pain 12 - 24 Decreasing Vital Capacity 25 - 30 Decreasing lung compliance Increasing P(A-a) O2 Decreasing PO2 30 - 72 Decreasing Diffusing capacity  Rule of Thumb To avoid oxygen toxicity Limit patient exposure to: 100% FiO2 – 24 hrs 70% FiO2 – 2 days 50% FiO2 or less – 5 days Precautions and hazards of supplemental O2 (cont.) Depression of ventilation ◦ Occurs in COPD patients with chronic hypercapnia Retinopathy of prematurity ◦ Excessive blood O2 levels cause retinal vasoconstriction and necrosis. ◦ More common in preterm infants * Maintain PaO2 3years – adults FDO2: 5 – 8LPM Adv: good for short term delivery, good mobility Disadv: skin irritation, aspiration of vomitus, claustrophobia, variable FiO2 D. Oxyhood – plastic devices that fits over the head and shoulders of an infant Age Group: preterm -