Rodney Shandukani 14/03/2012
OXYGEN THERAPY Aerobic metabolism accounts for 90% of Oxygen consumption by tissues. generates ATP by oxidative phosphorylation. Oxygen cascade: Oxygen exerts a partial pressure, which is determined by the prevailing environmental pressure. The oxygen cascade describes the process of declining oxygen tension from atmosphere to mitochondria. 160mmHg to about 1mmHg Convection-ventilation: On inspiration the air is humidified ( PIO 2 = FiO 2 x Patm-47mmHg) mixed with exhaled carbon dioxide (CO 2 )> PAO 2 = PIO 2 - PaCO 2 /R at the alveolus the PAO 2 is =100 mmhg
Pulmonary oxygen transfer Is affected by V/Q mismatch and intra pulmonary right to left shunt. 1. V/Q = 1 Ventilation-perfusion is matched- Normal gas exchange 2. V/Q > 1 - Dead space ventilation : PaO 2 & PaCO 2 (when Vd/Vt>50%) 3. V/Q < 1 - Venous admixture : PaO 2 ; PaCO 2 or normal. A-a gradient(pao 2 -PaO 2 ) varies with FIO 2 and age. Intrapulmonary shunt V/Q < 1 -Blood flow is excessive to ventilation (does not exchange gas) The fraction of the cardiac output that represents intrapulmonary shunt is known as the shunt fraction (Qs/Qt) is normally less than 10% Types of Intra pulmonary shunts 1. V/Q =0 - No gas exchange = true shunt 2. V/Q 0-1 - Some gas exchange = Venous admixture
Haemoglobin binding: Bound O 2 = [1.34 x Hb x SaO 2 ] The relationship between (SaO 2 ) and PO 2 forms a sigmoidal shape. The P50 is the PaO 2 at which 50% of the haemoglobin is saturated. Systemic interventions such as alteration in PCO 2 or ph will influence the curve and therefore oxygen dissociation and availability.
Cardiovascular The cardiovascular system is the solitary delivery system of oxygen to the cells CaO 2 = [1.34 x Hb x SaO 2 ] + 0.003 x PO 2 = 20ml/100ml Delivery of O 2, DO 2 (ml/min)= 10 x CO (l/min) x CaO 2 o Normal resting DO 2 is approximately 1000ml/min Oxygen uptake(vo 2 ) = 10 x CO(l/min) x CaO 2 -CvO 2 o O 2 consumption at rest is approximately 250ml/min(25%) Oxygen extraction ratio : the ratio of uptake VO 2 to delivery DO 2 o O 2 ER = VO 2 /DO 2 [ VO 2 = O 2 ER x DO 2 ]
Diffusion from blood to mitochondrion Diffusion of O 2 from oxyhaemoglobin to mitochondrion follows the principle of diffusion: 1.Fick s law of diffusion 2. Position of oxygen haemoglobin dissociation curve.
Pathology of oxygen delivery ( DO 2 ): Oxygen transport operates to maintain constant flow of O 2 into the tissues in the face of varying O 2 delivery. This is made possible by the ability of O 2 extraction to adjust to O 2 delivery. SaO 2 =98%, SvO 2 = 50% SaO 2 =98%, SvO 2 = 73% Critical DO 2, is the point at which VO 2 becomes supply dependent.
Diagnosis and monitoring of DO 2 SaO 2 and PaO 2 Generally oxygen is indicated when PaO 2 falls below 60mmHg and SaO 2 is below 90% Acid-base balance acidosis and base deficit of -2mmol/l may indicate inadequate DO 2. Lactate level may indicate inadequate tissue oxygenation, but not specific Other causes of hyperlactaemia : Hepatic insufficiency( lactate clearance) Thiamine deficiency(inhibit pyruvate entry into mitochondrion) Severe sepsis(cytokine mediated inhibition of pyruvate dehydrogenase) SvO 2 /ScO 2 A falling DO 2 can be compensated for by increase in Oxygen extraction which leads to lower Hb saturation in venous blood. Ideally SvO 2 > 70%.,a low SVO 2 may indicate an increase in uptake or decrease in delivery.
The PaO2/FiO2 Ratio The PaO2/FiO2 ratio is used as an indirect estimate of shunt fraction. it is used to define Acute lung injury and ARDS. It cannot distinguish hypoxaemia due to alveolar hypoventilation from other causes. The ratio is markedly FiO 2 dependent. PaO2/FiO2 Qs/Qt <200 >20% ARDS >200 <20% ALI
Arterial hypoxaemia vs. Tissue hypoxia poor correlation between arterial hypoxaemia and tissue hypoxia hypoxaemia is not a marker of hypoxia. (PaO 2 should not be used as evidence during oxygen inhalation therapy for tissue oxygenation.) Hypoxaemia PaO 2 <60mmHg O2 deficiency in blood ( O2 delivery from atmosphere to blood) Mostly lung level problem Inspired PO 2 ( Altitude) Alveolar hypoperfusion (Sleep apnoea) V/Q mismatch (Asthma, atelectasis) R L Shunt Hypoxia O 2 Deficiency in tissues ( Delivery, Uptake) PaO 2 may be normal or even elevated Types Hypoxic Hypoxia Anaemic Hypoxia Ischaemic/Stagnant Hypoxia Histotoxic Hypoxia
Oxygen therapy Oxygen inhalation is a therapeutic intervention designed to correct tissue hypoxia. Indications Cardiac and respiratory arrest Respiratory failure Type 1 (Hypoxaemia without CO 2 retention) Asthma, pneumonia, pulm. oedema, pulm. embolism Type 2 (Hypoxaemia with CO 2 retention) -COPD, chron. bronchitis, chest injuries, post op. hypoxaemia, neuromuscular diseas Cardiac failure, M.I. Shock Metabolic demands (Burns, multiple injuries, severe infection) Carbon monoxide poisoning.
Methods of Oxygen Inhalation Variable perfomance systems Nasal cannulae Semirigid face mask with or without reservoir bag Tracheostomy mask T piece Fixed perfomance Venturi mask CPAP
COMPLICATIONS OF O 2 therapy Pulmonary toxicity General recommendations CO 2 narcosis Keep FiO 2 < 50% FiO 2 of 60% can be tolerated for +- 48hrs FiO 2 of 100% should not be maintained > 24hrs When high FiO 2 is administered to patients with dependence on hypoxic (chemoreceptor) drive, a respiratory depression occur Neurological O 2 toxicity Idiopathic epilepsy occurs with exposure to O 2 > 3 atmospheres Retrolental fibroplasias In preterm babies
Hyperbaric Oxygen Therapy (HBO) Delivers 100% oxygen at a pressure above atmospheric Increases the amount of oxygen carried in plasma Indications Decompression sickness CO poisoning Burns Gas gangrene Osteomyelitis Necrotizing fasciitis Osteoradionecrosis Crush injuries Ischaemic skin grafts