Hypoxia In Anesthesia Essay Research Paper HypoxiaHypoxiaIntraanesthesia

Hypoxia In Anesthesia Essay, Research Paper


Intra-anesthesia hypoxia may be due to a problem with the anesthesia delivery system or a problem within the patient. The following are possible causes of hypoxia.

1) Decreased O2 supply.

A low supply of oxygen may be due to an inadequate FiO2 mixture. If the proportioning system fails to allow a proper ratio of N2O to O2 (3:1) then a hypoxic mixture will be delivered. A bobbin in the flowmeter that is stuck can fool the anesthetist into believing that more O2 is being delivered than in actuality. A depleted O2 supply will also cause hypoxia, as a decreased volume of O2 will be administered to the patient. If the pipeline valves or cylinder valves are closed then no O2 reaches the breathing circuit. The hospital should have an O2 backup supply on facility grounds for emergencies. It is important to note that cylinders are full and that hoses for pipelines are hooked up correctly and function prior to anesthetizing a patient. Pipeline pressures should read a minimum of 50 psig and O2 cylinders a minimum of 600 psig to assure adequate supply. Leaks can occur inside the machine, the CO2 absorber, at hose connections, in the bellows (especially hanging bellows), in the ventilator, flowmeter, and proportioner.(4) Broken valves allow leakage within the circuit. Tests for high and low pressure leaks should be performed prior to use of the machine. Do not use hoses that are damaged or frayed and have a potential for leakage. Incompetent unidirectional valves may cause rebreathing of gases and a hypoxic mixture.(3) Leaks can be detected by low expired volume, increase in ETCO2, or inadequate bellow expansion after expiration. Ventilator alarms for low airway pressures indicate a leak in the ventilator. Applying soapy water on connectors will result in bubbling if a leak is present.(1) Obstruction of flow into the circuit will prevent O2 from reaching the patient. This can occur as a result of sticking flow control valves, kinking of tubes, or foreign bodies in the system. Be sure to inspect all tubes and valves prior to use. When a cylinder or pipeline is hooked up incorrectly the DISS and PISS systems have been violated. Make sure that O2 connections are green, air is yellow, and N2O blue. Check to be sure that each cylinder has only 1 gasket at the connection. Closed circuits (Maplesons) give rise to the risk of rebreathing when inadequate gas flow is supplied. Be sure to identify the amount of FGF needed for each Mapleson system in order to prevent hypoxic rebreathing. A scavenger that is hooked up to high suction will pull FGF in and bypass the patient if the negative pressure relief valve is dysfunctional and cannot entrain air. A negative pressure alarm will alert the anesthetist to this problem. The collapsing reservoir bag will be the first indication that negative pressure is in the system. Any catheter that is inadvertently passed into the trachea with suction will steal O2 supply from the lungs.(1) Be sure to check NG placement after insertion by listening to air being injected into the stomach via the NG. An improperly placed ETT results in right mainstem bronchus or esophageal intubation. Verify ETT placement by chest movement, ETCO2 response, and bilateral breath sounds ausculated post intubation. It is a good standard of practice to preoxygenate the patient with O2 prior to intubation to store O2 in the FRC for physiologic backup. Reposition the ETT as indicated if improper placement is suspected. Inadequate O2 supply can be prevented by performing a machine checkout of the anesthesia equipment each day. Problems occurring intraoperatively should be detected by troubleshooting the equipment for disconnects or leaks. Temporary increase of FiO2 can be of assistance until the problem is found. O2 analyzers on the inspiratory limb should ensure adequate O2 delivery to the patient. The analyzer should alert the anesthetist when O2 delivery is less than 21% but may be as high as 100%.

2) Hypoventilation.

Anesthetic drugs and diseases that depress medullary function can cause deep sedation with low respiratory volume exchanges. Inadequate MV or apnea occurs frequently with use of anesthesia drugs.(4) MV for each patient should be calculated according to IBW prior to putting the patient to sleep to ensure adequate ventilation and perfusion. Extended intubation time sometimes requires intermittent ventilation and O2 via the ambu bag to prevent hypoxia between attempts. Patients who have been oversedated can be reversed with anti-narcotic drugs such as Narcan. Be sure to set proper TV and RR to meet each patients required MV. Watch the bellows to see that the volume being delivered is the volume you have set. If the ventilator is not delivering the set MV, ambu the patient until the problem with the machine has been fixed. Watch the patients chest rise and fall appropriately. Note any pathologic changes in patients history that may affect MV status. Airway resistance prevents delivery of O2 to the lungs. First be sure that the ETT is correctly placed. Monitor for laryngospasm for bronchospasm by ausculation. If present, administer positive airway pressure by ambu or PEEP.(4) Assess for pneumothorax or CHF. Notify the surgeon for possibility of CXR/chest tube if indicated. Administer diuretics as needed for pulmonary edema in CHF. Increasing amounts of secretions in the lungs and airway also increase resistance. Suction as needed to clear the airway. A lightly anesthetized patient may breathe against the ventilator. Administer more anesthetic if indicated. Check the inspiratory valve for condensation and stickiness. Is the ceramic valve moving to allow inward flow? Clean and dry the valve or replace a broken ceramic valve as needed.(3) Be sure that the APL valve is not fully open during ventilator mode. Any delivery of gases to the patient including O2 will escape the open valve. The knob should be partially closed and adjusted to control ventilatory pressure.(3)

3) Rebreathing.

If expired gases are inadvertently rebreathed then hypoxia can occur as well as hypercapnia. Incorrect placement of the PEEP valve on the inspiratory limb will not only result in failure of end expiratory pressure, but inspiration may be obstructed or diminished by the valve. Be sure that the PEEP valve is only placed on the inspiratory limb for proper inspiratory air flow.(3)

4) AV shunting

Pathologic changes in patients respiratory systems can contribute to the prevention of O2 delivery at the alveolar membrane. Some of these causes are sepsis, liver failure, AV malformation, pulmonary emboli, and right to left shunting. Increasing the amount of FiO2 delivery does not generally help the problem. The anesthetist must treat the underlying pathology in order to improve oxygenation.(4)

5) V/Q mismatch.

When ventilation and perfusion ratios are not in balance, O2 can not be delivered to the tissues at an adequate rate. Some causes of V/Q mismatch are atelectasis, positioning (especially lateral decubitus), bronchial intubation, bronchospasm, pneumonia, plugs, ARDS, airway obstruction, and decreased FRC. One lung ventilation can cause a mismatch if the DLT is malpositioned. Most V/Q mismatches will improve with increase in mean airway pressure or PEEP. Treatment of underlying problems is also very important.(4)

6) Decrease O2 carrying.

Anemias including carboxyhemoglobinemia and methemoglobinemia prevent O2 delivery to the tissues. Low Hgb impedes carrying of O2 while Met and COHgb carry O2 but do not release it to the tissues. CO poisoning increases the amount of carboxyhemoglobin in the blood therefore any rebreathing potentiates the problem. Some anemias can be detected by pulse oximetry. Severe anemias from blood loss should be treated by blood replacement.(4)

7) Decrease O2 delivery.

A patient with severe vasoconstriction as is shock cannot get adequate perfusion of vital organs. If perfusion is decreased then the O2 is not being delivered to the organ. An algorithm for severe vasoconstriction in shock should be followed.(4)

8) Left shift of oxyhemoglobin curve.

When the oxyhemoglobin curve shifts to the left there is a decreased affinity of O2 for the Hgb and less O2 being carried to the tissues. Some causes of the shift are hypothermia, alkalosis, and hypocarbia. Prevention by adequate warming intraoperatively, adequate MV’s and control of blood pH can deter the shift. Shivering from hypothermia will increase O2 consumption which can be monitored by comparing O2 analyzer and ETO2 readings.(4)

9) Diffusion hypoxia.

When N2O is suddenly discontinued there is a rapid diffusion of N back into the alveoli displacing O2. Pre-treatment with 100% O2 during emergence can help curve the detrimental effects of duffusion hypoxia. A decrease in SaO2 should be minimal and short-lived to prevent hypoxic events.(3)

10) Surgical considerations.

Always check the surgical field for events contributing to hypoxia. Severe blood loss, retractors, and positioning can cause rapid and negative effects on O2 delivery. Keep the surgical team informed of patients O2 status as needed.(3)

The O2 analyzer and pulse oximeter are the main monitors to assess O2 delivery to the patient. The pulse oximeter reflects arrival of O2 in the patients tissue and the O2 analyzer ensures delivery of O2 from the machine to the patient. Both monitors have audiovisual alarms for low oxygen levels that need immediate attention by the anesthetist.


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