One lung anesthesia Dr. S. Parthasarathy MD., DA., DNB, MD (Acu), Dip. Diab. Dip. Software statistics PhD ( physiology), IDRA , FICA
Its quite big topic ! I am just touching ! The foundation is Hypoxic pulmonary vasoconstriction
Hypoxic pulmonary vasoconstriction
When does it ( hypoxia )occur Humans encounter hypoxia throughout their lives. This occurs by destiny in utero, disease, desire, in our quest for himalayas !
What is it and why ? Reduces shunt fraction Optimizes PO2 HPV = homeostatic, vasomotor response of resistance of pulmonary arteries to alveolar hypoxia
What happens ! total pulmonary blood flow α RV cardiac output, within the pulmonary vasculature can be altered dynamically. Hypoxia diverts blood flow to better ventilated, non hypoxic lung segments. This phenomenon of HPV, first noted by Von Euler and Liljestrand in 1946
With this base , we will switch to OLV This is a biphasic reaction with early response starting within seconds, reaching a peak at about 15 min followed by a delayed response in 4 h to cause maximal vasoconstriction… this pulmonary vasoconstriction takes hours to reverse when normoxia returns. With this base , we will switch to OLV
When switching from two-lung to one-lung ventilation (OLV), shunt fraction increases, oxygenation is impaired, and hypoxemia may occur hypoxemia may occur in 5–10% of patients undergoing OLV
Normal lung four zones
Normal lung in lateral position Upright : R:L 55:45 Right dependent – R; L 65: 35 Left dependent R:L = 45:55 Ventilation – dome of the dependent diaphragm becomes more convex – better contraction
Patient Anesthetized, Chest Closed Not much change in perfusion Compression by the weight of the mediastinum and the abdominal contents contribute to the decrease in FRC of the dependent lung the nondependent lung receives most of the ventilation but still is less perfused, whereas the dependent lung receives less ventilation but continues to be more perfused, which leads to an increase in shunt
Patient Anesthetized, Paralyzed, Mechanically Ventilated With mechanical ventilation, the highly curved diaphragm in the dependent hemithorax – advantage gone - it is no longer actively contracting. The weight of the abdominal viscera physically restricts expansion of the dependent lung, leading to further preferential distribution of ventilation to the nondependent, less-perfused lung.
Open the chest ! Ventilation may be more but more so in non dependent lung ! The decrease in airway pressure on opening the pleura, along with the increase in cardiac index, results in increased blood flow to the nondependent lung. Exit of CO2 from non dependent lung
Summary Continue ! The anesthetized, paralyzed patient in the lateral decubitus position with an open chest may have considerable V/Q mismatch. The nondependent lung receives greater ventilation and less perfusion and has a V/Q ratio of more than 1. The dependent lung has more perfusion and less ventilation (ie, a low V/Q ratio) and therefore acts as a physiologic shunt.
Starting OLV Back to HPV !! We have not started OLV
A good preoperative spirometry usually predicts bad intra operative hypoxemia A- a O2 gradient is normal – hypoxemia chance more Side
Three knots of one lung anesthesia Oxygenation ( diffusion ) CO2 removal (Ventilation) Anesthesia
Picture clear ?
Redox theory Redox sensor activated Reactive oxygen species Metabolic acidosis Respiratory acidosis Hyperthermia Redox sensor activated Reactive oxygen species Decrease K channels Stimulate calcium channels HPV increases in PA pressure, cardiac output, left atrial pressure, or central blood volume HPV
Does the PA pressure rise after HPV ? High compliance of the pulmonary circulation prevents clinically significant changes in pulmonary vascular resistance or PA pressure
Hypocapnia and hypothermia decrease HPV response Inhalational agents decrease but actual effect – significance ?? Ketamine , propofol and thoracic epidurals does not affect much
Nitric oxide and inhaled prostacyclins Selective pulmonary vasodilators can improve V/Q mismatch in lung surgeries
One lung ventilation Prone for hypoxemia We are better when faced with infective cause and destroyed lungs than carcinoma OLV for esophagectomy and bronchiectasis – different Lungs are destroyed prior , the patient tolerates OLV better !!
They have compensated and knew to live ? Better They have compensated and knew to live but normal lungs by the side – more prone for hypoxemia
Principles of OLV - oxygenation Delay OLV as possible – allow the non dependent lung to collapse ! Suction , Check DLT position Increase FiO2 to get atleast 90 % saturation Increase respiratory rate , tidal volume but check on pressure to be less than 30 mmHg ( barotrauma) Plan for a PaCO2 < 35 mmHg Increased ventilation may wash out CO2 ! Beware
The ETCO2 may be showing differently Paco2 – may be different See the difference at the start Then at least we can correlate Otherwise only ABG
Special !! Special ventilators employing instantaneous breath-to-breath analysis to adjust ventilatory patterns (adaptive lung ventilation) have been used during one-lung ventilation Is there a development of Auto PEEP ?
There is no agreed standard for the definition of hypoxemia during OLV; however, an arterial oxygen saturation of less than 90% with an Fio2 of 1.0 is commonly accepted as a level at which some intervention by the attending anesthesiologist is required. Key strategies To decrease hypoxemia
Oxygen !! Direct insufflation of oxygen to the non dependent lung kept in the carina or just above
PREVENTION OF ABSORPTION ATELECTASIS 100 % oxygen causes absorption atelectasis Why ? What Goes in > what comes out from the lungs Combine N2 10 % with oxygen Nitrogen ( less soluble than nitrous ) splits open the alveoli in areas of low V/Q ratio.
Cut nitrous ! Then MAC will be high Cut agent to inhibit action on HPV Then are we giving anesthesia or not Think of less agents at least with IVA
VERIFICATION OF LUNG ISOLATION Check double lumen tube position Suction secretions Get the airway pressure down
RECRUITMENT MANEUVER Sigh!! single-lung ventilation, lateral decubitus positioning, inhibition of HPV, and periodic disconnection from the ventilator A sustained pressure of about 35 to 40 cm H2O, which would be above the tidal ventilation range, is applied for a period of 30 to 60 seconds in order to inflate lung units. 40/40 !! Sigh!!
VENTILATION USING LARGE TIDAL VOLUMES Start with 6- 8 ml/kg – increase or decrease with ABG and airway pressures Increased airway pressures with the associated the risks barotrauma and increased PVR can divert blood, that is, perfusion, to the non ventilated nondependent lung… Post op pulmonary edema in high inflation pressures !
Maintain PaCO2 ! Hypocapnia should be avoided because it can directly dilate the pulmonary vessels, interfering with HPV in the nondependent lung. Alternatively, hypercapnia will increase PVR and can increase right heart strain CO2 diffuse easily !
SELECTIVE NONDEPENDENT-LUNG CPAP Expand with higher pressure for two three puffs and then start CPAP 20 % blood flow becomes 24 % with isoflurane – 5 – 10 cm CPAP may oxygenate these areas without surgical interference
With or without reservoir bags !
In most situations, an O2 flow rate of 5 to 10 L/min, which creates CPAP of 5 to 10 cm H2O, is sufficient for improving oxygenation. Mediastinal shift and penduluft ventilation Not failed bronchial seal !! Keep oxygen instead of air !!
DEPENDENT-LUNG PEEP
DEPENDENT-LUNG PEEP Diseased lung may be more useful But healthy lungs ? Use may harm ? COPD – both are disaeased but bullectomy on one side – that case , PEEP may open up !!
continuous high-flow apneic ventilation A very high O2 flow rate delivered at or below the carina may improve gas exchange without any tidal exchange, which is known as “continuous high-flow apneic ventilation.”
Other techniques ! If hypoxemia still persists after differential CPAP/PEEP, the nondependent lung may be intermittently ventilated with positive pressure and 100% O2. Selective non dependent HFV Clamp the pulmonary artery
Titbits Because the right lung is larger than the left lung, it is seen that oxygenation during OLV is better during left thoracotomy (i.e., when the larger right lung is the dependent, ventilated lung). In concentrations ranging from 5 to 40 ppm, nitric oxide did not improve oxygenation or decrease the occurrence of hypoxemia during OLV.
Titbits The combination of NO (20 ppm) to the ventilated lung and an intravenous infusion of Almitrene (a pulmonary vasoconstrictor) can restore PaO2 during OLV to levels close to these during two-lung ventilation Epidural may not benefit Better hemoglobin is better Some patients, particularly those with COPD, showed better oxygenation during OLV with a pressure controlled vs volume controlled ventilation.
Thank you all