I. Severe hypotension in the operating room
1, cause analysis (1) patient factors: ① hypovolemia; ② venous obstruction resulting in poor reflux; ③ tension pneumothorax and other causes of increased intrathoracic pressure; ④ allergic reaction; ⑤ embolus dislodgement (gas/air/thrombus/bone cement/fat/amniotic fluid); ⑥ cardiac pump failure/rapid arrhythmia; ⑦ systemic septic sepsis, etc.
(2) Technical causes: ① monitoring errors; ② too deep anesthesia; ③ high regional block (including accidental diffusion from the periocular or oblique angle muscle gap to the center); ④ medical medication errors, including local anesthetic poisoning, porphyria due to barbiturates, etc.
2. Emergency management measures include 100% oxygen inhalation; check surgical blood loss; check ventilation; reduce shallow inhalation anesthesia; elevate legs (if feasible); intravenous rehydration; vasoconstrictor or positive inotropic drugs. Further examination: electrocardiogram, chest X-ray, arterial blood gas, cardiac enzyme profile, etc. to clarify the diagnosis.
2. Risk factors
(1) Preoperative untreated hypertension or “white coat hypertension” (increased instability);
(2) Inadequate preoperative fluid volume (dehydration, diarrhea, vomiting, blood loss);
(3) Mediastinal/liver/renal surgery (blood loss, vena cava compression);
(4) Preoperative cardiac disease or arrhythmia;
(5) Multiple injuries;
(6) septic sepsis;
(7) benign tumor syndrome (bradykinin);
III. Differential diagnosis
(1) Erroneous monitoring: touch the distal pulse while re-testing non-invasive blood pressure; check the monitor deflation value when the pulse recovers. Sensor height must be checked when monitoring invasive blood pressure.
(2) Tension pneumothorax: When intermittent positive pressure ventilation (IPPV) is removed from one side of the reactive hyperemic lung field and is accompanied by loss of breath sounds after removal of the tracheal tube, the possibility of tension pneumothorax should be highly suspected (especially after insertion of the central catheter). The manifestation is jugular vein filling. A catheter must be placed immediately through the second intercostal space in the midclavicular line for thoracic decompression.
(3) Dehydration: The patient is conscious of thirst, dry tongue extension, dark urine, elevated values of complete blood count, urea nitrogen, inosine and electrolyte ions.
(4) Hypovolemia: The patient has a heart rate >100 beats/min, respiratory rate >20 breaths/min, capillary reflux >2s, cold extremities, venous atrophy, and weak pulse, or central venous pressure (CVP) and pulse strength vary with respiration.
(5) Heart failure: patient’s heart rate >100 beats/min, respiratory rate >20 breaths/min, central venous filling, capillary reflux >2s, syncopal cold extremities, pulmonary edema, and SaO2 decreases with increasing fluid load.
(6) Air or gas embolism: Patients with preoperative low CVP and open venous vascular bed should be alert for air or gas embolism. The manifestations of air or gas embolism are varied and include a sudden drop in ETCO2, a drop in SaO2, an inaccessible pulse, electro-mechanical separation of the heart, and a concomitant decrease in CVP.
(7) Fat embolism and bone cement reaction: should be considered in multiple fractures or intraosseous surgery of long bones.
(8) Drug reactions: prohistamine-releasing drugs, etc., or dilution solution errors.
(9) High central nerve block: may manifest as Horner`s syndrome (pupil narrowing, eyelid drooping, loss of smell, no sweating).
(10) Allergic reactions: cardiovascular reactions 88%, erythema 45%, bronchospasm 36%, angioedema 24%, drug rash 13%, rubella 8.5%.
4. Primary measures
1. ABC…check the surgeon’s operation on the operating table (for vena cava compression or bleeding); clamp or directly compress the vessel to prevent further blood loss. Increasing the concentration of inhaled oxygen to ensure organ perfusion and oxygenation is far more important than simply maintaining BP. BP = SVR x CO, so increasing cardiac output can increase perfusion pressure.
2. 1) “Optimal preload” (if a manometry device has been placed, the starting CVP can be measured first. the trend of CVP is more meaningful than its actual value): elevating the legs can increase central venous blood return, while increasing afterload. Use a pressurized infuser to rapidly replenish crystalloid or colloid fluids at 10 ml/kg. Assess the patient’s response to rapid rehydration (BP/HR/CVP) and repeat the procedure if appropriate.
3. (2) Increase myocardial contractility: ephedrine 3-6mg iv (direct and non-direct dual action); epinephrine 10ug
iv (β1,2 and α receptor agonist effect); can consider slow sedation of calcium (maximum amount of 10% calcium chloride 10ml).
4. (3) Constriction of systemic blood vessels (NB: alpha agonists can reduce cardiac output while increasing tissue perfusion pressure): methoxamine 1-2mgiv; meprobamate 1-2mgiv; phenylephrine 0.25-0.5mgiv; epinephrine 10ugiv.
5. Secondary measures
(1) Correct acidosis and improve myocardial responsiveness to drugs. According to the results of blood gas analysis, correct respiratory acidosis first. If there is severe metabolic acidosis (arterial blood pH 100 times/min, respiration >20 times/min, capillary reflux >2s, cold extremities, weak pulse, or CVP and arterial pulses change significantly with respiration.
(7) Heart failure: heart rate > 100 beats/min, respiration > 20 beats/min, jugular venous filling, capillary reflux > 2s, cold extremities, pulmonary edema, SaO2 decreases with increasing fluid intake.
(8) Air or gas tethering: The possibility of air or gas tethering should be considered when the patient has low preoperative CVP and an open venous vascular bed. The presentation varies, including a sudden drop in ETCO2, a drop in SaO2, an inaccessible pulse, electro-mechanical separation of the heart, and a subsequent rise in CVP.
(9) Fat tethering or bone cement reaction: in multiple fractures, or in long bone intramedullary procedures.
(10) Malignant hyperthermia: When accompanied by elevated ETCO2, increased respiration, increased heart rate and ectopic heart rhythm, high alert for malignant hyperthermia is warranted.
(11) Allergic reactions: 88% cardiovascular reactions, 45% erythema, 36% bronchospasm, 24% vasogenic edema, 13% drug rash, 8.5% rubella.
5. Primary measures
8. ABC: Expose the chest, all breathing circuits and all parts connected to the airway. Hand-controlled breathing with 100% pure oxygen, starting with 3-4 large tidal volumes to help collapsed alveoli reopen (continuous hand-controlled ventilation also allows sensing changes in airway status). If conditions do not improve.
(1) Determine FiO2: If the inhalation oxygen concentration from the anesthesia machine is suspected to be incorrect, separate bottles of oxygen can be used (room air can also be inhaled with hand-controlled breathing as a final step, when the inhalation oxygen concentration is 21%).
(2) Wrong position of the endotracheal tube? Auscultate the upper abdomen and bilateral axillae, monitor the carbon dioxide concentration, and repeatedly determine the thoracic rise and fall.
(3) Ventilation failure: simplify the breathing circuit until the problem is resolved. For example, instead of ventilator, use balloon hand-controlled breathing; instead of circulatory circuit, use Bain circuit; use self-expanding balloon; instead of endotracheal tube, use face mask breathing, etc.
(4) Finding air leaks or obstructions: This is not as important as ensuring the patient’s oxygen supply in the beginning. The patient’s safety should be ensured first, followed by a systematic examination to find the air leak or obstruction. The fastest way to find the problem may be to perform a dissection. For example, splitting the circuit at the tracheal tube connection into two parts and then determining whether the problem is on the patient’s side or on the side of the anesthesia machine?
(5) Severe right-to-left shunt: When SVR is reduced, blood flow returns through a congenital defect on the heart, producing a bypass pulmonary circulation, at which point severe hypoxia occurs. The resulting hypoxemia can in turn cause hypoxic pulmonary vasoconstriction and increased pulmonary vascular resistance (PVR), aggravating the shunting of blood flow through the cardiac defect, thus further worsening the condition. There are dual measures for this: ① Elevate SVR: elevate legs, use epinephrine, and intravenous rehydration. This is particularly emphasized in septic sepsis. (2) Decrease PVR: discontinue PEEP, prevent excessive intrathoracic pressure, and increase FiO2.
(6) Bronchospasm: Use a resin elastic probe to auscultate the tracheal tube and rule out tube obstruction. Treatment can be done by increasing the concentration of inhaled anesthetics and intravenous albuterol (250ug) (see Asthma persistence, P848).
6. Other
9. u Patients with chronic bronchitis have a bronchial circulation shunt of up to 10% of cardiac output.
10. In 20-30% of patients, the foramen ovale is not closed, but is usually in a closed state due to higher left ventricular pressure than the right ventricle. However, IPPV, PEEP, breath-holding, CCF, open-heart surgery, and pulmonary tethering can reverse the pressure gradient between the two ventricles, resulting in shunting.
IV. Severe laryngospasm
1. Causal analysis: Acute vocal fold closure caused by vocal fold closure, showing high pitched inspiratory sounds, disappearance of inspiratory sounds, and visible obvious tracheal traction (tracheal tug).
2, emergency management measures: avoid painful stimulation; 100% oxygen inhalation; continuous positive airway pressure (CPAP); jaw support; removal of airway irritants; deepen anesthesia. Follow-up measures: muscle relaxants can be used when the situation is difficult. However, it is still necessary to consider: ① bronchospasm; ② laryngeal injury/airway edema (especially if a pediatric tracheal tube is used without air leakage); ③ reoccurrence of laryngeal nerve injury; ④ tracheal softening; ⑤ inhalation of foreign body; ⑥ epiglottitis or pseudomembranous laryngitis.
3. Risk factors
(1) Barbiturate-induced or shallow anesthesia, especially in anxious patients;
(2) High intensity of surgical stimulation: dilation, neck dilatation, abscess incision and drainage;
(3) extubation of a contaminated airway;
(4) Thyroid surgery;
(5) Hypocalcemia (increased neuromuscular excitability);
(6) Multiple crown (inhalation of foreign body).
IV. Primary measures
(1) Remove laryngospasm inducing irritants;
(2) Check the airway to ensure that it is free of obstruction and potential irritants;
(3) Close the circuit expiratory valve, inhale high concentration of oxygen, and if necessary, clasp the mask with both hands to ensure the entire circuit tightness and maintain CPAP. the degree of CPAP can be adjusted by intermittently loosening the mask and relaxing the circuit tightness.
(4) If laryngospasm occurs during induction, it can be relieved by deepening anesthesia: additional propofol (disadvantage: potential risk of respiratory depression), or increasing the concentration of inhaled anesthetics (disadvantage: changes in airway excitability, which can be reduced by sevoflurane and reversed by isoflurane). N2O should not be used, as it can reduce oxygen reserve.
(5) If laryngospasm fails to improve, remove any ventilation tract that may irritate the pharynx.
(6) Succinylcholine 0.25-0.5 mg/kg may relieve laryngospasm. If intravenous administration is not possible, 2-4mg/kg intramuscular or sublingual route may be considered.
V. Secondary measures
(1) Close monitoring to prevent pulmonary edema.
(2) Since gas may enter the stomach during CPAP and cause gastric distension, a transoral gastric tube may be placed for decompression and the patient should be kept in the lateral position.
6. Other
(1)Combination of opioids, intravenous lidocaine (lignocaine) or local spraying of lidocaine (lignocaine) before peeking into the throat during induction (1mm.
(8) It is believed that signs and symptoms of air tethering can occur after intravenous gas injection of 0.5 ml/kg/min.
5. Primary measures
11. ABC: exclude disconnection of breathing circuit; inhale 100% pure oxygen; check ECG and pulse.
(1) Prevent continued entry of gas/air into the circulation. Ask surgeon to compress the main perfusion vessel, flush the wound with flushing solution or cover the wound with wet dressing, stop enlarging the wound operation, etc.
(2) Decompress the distended system or cavernous organs, e.g., the abdominal cavity in laparoscopic surgery.
(3) Lower the surgical site to below the level of the heart.
(4) Shut down N2O (as it expands the volume of gas in the vessel).
(5) Rapidly rehydrate intravenously or co-administer antihypertensive agents to elevate venous pressure.
(6) If electro-mechanical separation of the heart occurs, perform external cardiac compressions and begin further life support steps for cardiac arrests that are not ventricular fibrillation or ventricular tachycardia in nature.
(7) Aspirate the CVP catheter. The classic textbook approach is to place the patient in a left-sided, head-down position so that the foam is located in the right atrium or right ventricular apex until the gas dissolves in the blood or is withdrawn via a central venous catheter extending into the right atrium. In practice, it is quite difficult to extract the gas without prior placement of a CVP catheter.
(8) It has been suggested that moderate CPAP during gas tethering can rapidly elevate intrathoracic pressure and CVP. although hand-controlled breathing has the potential to precede allegations of the extent and progression of tethering, it must be noted that 10% of patients have an unclosed foramen ovale. Persistent elevation of right atrial pressure will lead to right-to-left shunts and unexpected air tethering of the cerebral circulation.
6. Secondary measures
(1) Have the surgeon smear bone wax on the exposed bone ends.
(2) Correct the previous hypovolemia.
(3) Avoid the use of N2O for the rest of the anesthesia and maintain high FiO2.
(4) Monitor 12-lead ECG for myocardial ischemia. Intracoronary air suggests the possibility of air tethering.
(5) Consider the use of hyperbaric oxygen therapy when available: elevated ambient pressure (3-6 bar) may reduce gas embolic volume.
7. Other
Carbon dioxide is the safest gas to use as a pneumoperitoneum for laparoscopic surgery, is non-flammable and more soluble than other gases. Even if gas tethering occurs, the embolus will dissolve quickly. The prerequisite for gas tethering is to limit the extent of tethering and slow down the process of gas frothing in the heart, thus reducing the impact on the systemic cardiovascular system.
VI. Misaspiration
1. Analysis of causes
(1) Pathological state: chemical pneumonia; foreign body obstruction and pulmonary atelectasis.
(2) manifestations: shortness of breath, tachycardia, reduced pulmonary compliance, and decreased SaO2.
2.
Emergency treatment measures: minimize further misaspiration; ensure airway patency; suction. Follow-up measures: inhale 100% oxygen; consider CPAP; gastrointestinal decompression. Further examination: chest X-ray; bronchoscopy. Still need to consider: ① pulmonary edema; ② embolism; ③ ARDS.
3. Risk factors
(1) full stomach; (2) known reflux; (3) elevated intragastric pressure (intestinal obstruction, pregnancy, laparoscopic surgery);
13. recent trauma; (4) perioperative opioid use; (5) diabetes mellitus; (6) typical post-anesthesia airway.
4. Diagnosis
(1) Clinical: croup and twang sounds can be heard on auscultation, and the endotracheal aspirate is acidic (aspirate is negative cannot exclude the possibility of misaspiration)
(2) Chest radiograph: diffuse exudative changes, especially in the right lower lobe (but not often seen in the acute phase)
5. Primary measures
(1) Avoid the use of general anesthesia in high-risk patients. Fast induction (rapid sequence technique) can be used when appropriate.
(2) Give 100% oxygen inhalation to minimize continued contamination of the airway by inadvertent inhalation.
(3) If the patient is awake or semi-conscious, aspirate the oral and nasopharyngeal cavities and place the patient in a modified position.
(4) If the patient is unconscious but still breathing spontaneously, apply pressure to the cricoid cartilage. If the patient is vomiting on his own (beware of esophageal rupture), avoid pressing on the cricoid cartilage and place the patient in a left-sided, head-down position. After endotracheal suctioning, the patient can be intubated and mechanically ventilated.
(5) If the patient loses consciousness and stops breathing, intubate immediately and start mechanical ventilation.
(6) Follow the treatment of airway foreign body: when positive pressure ventilation is performed, the positive pressure is as small as possible until the tracheal tube is inserted, the airway has been aspirated, and all misaspirated material has been removed.
6. Secondary measures
(1) Lower the thick nasogastric tube before extubation and evacuate the gastric contents.
(2) Monitor respiratory function and take chest radiographs. Look for evidence of pulmonary edema, alveolar collapse or pulmonary fusion.
(3) CPAP (10 cmH2O) and chest physiotherapy can help improve pulmonary atelectasis when SpO2 is maintained at 90-95%.
(4) SpO2 25-30mmHg when on 100% oxygen).
(3)Chest radiograph: lung base shadowing, upper lobe entrapment, batwing-like or antler-like changes, hilar shadowing, bronchial cuff sign, Kerley B line, pleural exudate, septal line or interlobular fluid line.
(4) ECG: evidence of right heart strain; evidence of infarction.
5. Primary measures
(1) ABC…management is dependent on the patient’s current status.
(2) Awake spontaneously breathing patients: sit up, reduce pulmonary vascular load, increase functional residual air volume; inhale 100% oxygen through mask with storage balloon; tachyphylaxis 50mg IV; diacetylmorphine 5mg IV; consider CPAP 5-10mmHg with hypertension with vasodilators (e.g., nitro glycerin 0.5-1.5mg sublingual, or 10mg transdermal dressing, caution must be exercised when intravenous nitro-glycerin is not available for invasive blood pressure monitoring).
(3) Anesthetized intubated patients: head high 15. position, IPPV combined with PEEP (5-10cmH2O) to reduce pulmonary atelectasis and increase functional residual air volume; intermittent suctioning of overflowing fluid in the trachea; pharmacotherapy as above.
6. Secondary measures
(1) Reasonable fluid therapy based on monitoring serial CVP to maintain plasma colloid osmotic pressure. If there is doubt about CVP, PCWP can be monitored by pulmonary artery catheter.
(2) If filling pressures remain high or circulation remains unstable, consider beta agonists to enhance myocardial contractility (e.g., dobutamine) or intravenous bloodletting (500 ml).