). Therefore, a transfusion is most likely necessary.
>> Dr. Conner called his attending, Dr. Eldridge, because he wasn’t quite sure whether he should transfuse before inducing anesthesia. “You want to get out of here on time tonight, don’t you? Start the anesthesia and transfuse the blood as soon as you get it,” was the answer he received.
“Let’s use a laryngeal mask airway,” Dr. Conner said to Timothy, after hanging up the phone. Dr. Conner discussed the possible complications of the anesthesia and blood transfusion with Mr. Walter and obtained informed consent. Then he began preoxygenation, which didn’t actually work so well, because Mr. Walter didn’t have a single tooth left. The measured end–tidal CO 2 was 19 mmHg.
25.1.4 What Could Be the Cause of the Low End-Tidal CO2?
The most likely cause of the low end-tidal PCO2 during preoxygenation is a leaky mask. Low end-tidal CO2 is also found with an elevated respiratory minute volume or increased dead space ventilation – often seen in the case of a pulmonary embolism or serious pulmonary hypertension.
25.1.5 What Is Preoxygenation? What Is the Purpose of Preoxygenating Patients?
Preoxygenation refers to ventilation with 100 % O2 before inducing respiratory arrest. In spontaneously breathing patients, preoxygenation is done by placing a mask with 100 % oxygen over the patient’s face, instructing the patient to breathe normally (tidal volume respiration) for 3–4 min or by having the patient take 4–8 very deep breaths from the mask (vital capacity respiration). The preoxygenation should achieve an end-expiratory oxygen concentration greater 90 %.
Oxygen is stored in blood, in tissues – especially muscle – and in the lungs. The oxygen stores in tissue and in blood are already almost completely saturated by normal room air ventilation, so that the lungs are most affected by preoxygenation. During preoxygenation, the lung’s nitrogen will be washed out and replaced with oxygen. Through this denitrogenation, the oxygen level in the lungs increases fourfold as it replaces the nitrogen. Altogether, the preoxygenation triples the oxygen content of the body. Correspondingly, the apnea tolerance is extended, delaying the occurrence of hypoxemia, so that more time is available to secure the airway.
25.1.6 When Should a Dramatic Drop in Oxygen Saturation (SPO2) After Induction of Anesthesia Be Expected?
A dramatic decrease in SPO2 after induction can have several causes:
25.1.6.1 Reduced Oxygen Storage Capacity
The oxygen storage of the lung is actually the functional residual capacity (FRC). A reduced FRC, as is usually the case with children, pregnant, and adipose patients, shortens the period of apnea tolerance.
The oxygen storage capacity of the body is also reduced with a reduction in the hemoglobin concentration. SPO2 does not reflect oxygen content (CaO2).
25.1.6.2 Increased Oxygen Utilization
The normal oxygen utilization (
) at rest is 250–300 ml/min. VO2 increases with increasing metabolism, often drastically; for example, children or patients with fever or hyperthyroidism can have very short apnea tolerance times.
) at rest is 250–300 ml/min. VO2 increases with increasing metabolism, often drastically; for example, children or patients with fever or hyperthyroidism can have very short apnea tolerance times.25.1.6.3 Severe Circulatory Depression
Induction of general anesthesia can cause a dramatic decrease in cardiac output; the peripheral perfusion can be so decreased that the pulse oximeter can no longer measure a valid value. With simultaneous respiration, a drastically reduced expiratory PCO2 is the clue for an invalid SPO2 measurement and an inadequate cardiac output.
>> Dr. Conner fiddled with the mask, but was unable to get a tight seal. Finally he asked Timothy to administer 200 μg fentanyl and 120 mg propofol IV. The laryngeal mask airway was then placed uneventfully. As expected, the blood pressure dropped to 82/40 mmHg following anesthetic induction. The heart rate remained at 120 beats/min. “Give Mr. Walter some phenylephrine and turn up the infusion rate,” Dr. Conner said to Timothy. Because the second half of the amp of phenylephrine didn’t have much effect on the pressure, a vasopressin infusion was started. “Come on, let’s get the surgeons to scrub. I don’t want to be here all night!” said Dr. Conner.
He turned up the desflurane to maintain the anesthesia, and the surgeons began their preparations. Mr. Walter’s systolic pressure stayed around 90 mmHg, even though the vasopressin infusion was running. Timothy hung a new bag of normal saline solution. The pulse stayed at 120/min. The packed red blood cells were delivered shortly after the procedure had begun; the bedside tests checked out, so Timothy began the transfusion.
25.1.7 What Are the Determinants of Systemic Arterial Blood Pressure?
The mean arterial blood pressure is proportional to cardiac output (CO) and systemic vascular resistance (SVR):
(25.1)
A drop in CO can be compensated by an increase in SVR, and vice versa. Therefore, blood pressure alone does not allow for accurate determination of CO or SVR (see Sect. 3.2.1).
25.1.8 What Causes Intraoperative Hypotension?
25.1.8.1 Vasodilation
Vasodilation leads to relative hypovolemia. It is triggered by IV and inhalational anesthetics or neuraxial anesthesia. Furthermore, vasodilatation can be caused by anaphylactic reactions, or the release of dilating agents/mediators such as during opening of the abdomen and moving the intestines, or after opening a tourniquet, or by septic bacteremia.
25.1.8.2 Reduced Venous Return
Venous return can be reduced by many mechanisms, such as patient positioning, pneumoperitoneum, high respiratory pressures, tension pneumothorax, or intraoperative accidental compression of the inferior vena cava.
25.1.8.3 Absolute Volume Deficiency
Apart from blood loss, other causes of dehydration must be considered, such as preoperative fasting, perspiration, diuretics, or preoperative bowel preps.
25.1.8.4 Acute Decrease in Afterload
Opening tourniquet or blood vessel clamps results in a sudden decrease in afterload. A sudden drop in blood pressure may be enhanced by the release of vasoactive mediators from the previously ischemic area.
25.1.8.5 Arrhythmia
Arrhythmias can lead to hypotension through a variety of mechanisms. One example is limited left ventricular filling as a result of atrial fibrillation.
25.1.8.6 Abnormal Contractility
Abnormal contraction is a typical result of myocardial ischemia. Administration of IV fluids and negatively inotropic solutions further reduce the contraction capacity.
25.1.8.7 Pulmonary Embolism
An acute embolism of air/CO2, methyl methacrylate bone cement, or a thrombus can lead to acute right heart failure. See Case 11 (Sect. 11.1.5) for complete pathophysiology.
>> All vital signs were stable. “We can stop the vasopressin infusion as soon as the RBCs are in,” thought Dr. Conner as he charted on the computer. Suddenly the respiratory alarm sounded. Dr. Conner looked up and realized that the expiratory CO 2 was too low. One glance at the CO 2 curve and he knew the cause: Mr. Wilson was trying to breathe. “Alright, go for it!” thought Dr. Conner, “Spontaneous respiration is great with laryngeal mask airways.” So he turned the respirator to “spontaneous.” He didn’t want to give additional opioids because the surgery wouldn’t take much longer.
The total surgery time was 25 min. As the abscess was opened, a large amount of smelly pus oozed out. After the second RBC bag, the vasopressin infusion rate could be cut in half. A hemoglobin check showed 10.4 g/l. “Wow, if I hurry, I’ll make it to my movie tonight!” thought Dr. Conner as he shut off the desflurane vaporizer. Mr. Walter was breathing adequately through the laryngeal mask airway. The end–tidal PCO 2 was 21 mmHg. Just as Dr. Conner was removing the laryngeal mask airway, he noticed the heart rate jump to 140 beats/min. The rhythm was no longer regular, and atrial fibrillation was present. The blood pressure remained unchanged.
25.1.9 What Should You Do Now?
Management of new-onset fibrillation depends on the patient’s hemodynamic status. Atrial fibrillation (a-fib) leads to loss of atrial contraction and ensuing atrial dilation. In combination with hypovolemia, the ventricular filling is especially affected, which can lead to a drop in cardiac output. Unstable patients with symptoms and signs of low cardiac output or cardiac ischemia should undergo urgent cardioversion [3, 8].
If cardiac function is unaltered, i.e., no hemodynamic instability, diagnosis may be confirmed with a 12-lead ECG. Rhythm and rate should be monitored and treated pharmacologically. Suitable medications include β-blockers, digitalis, or amiodarone. Anticoagulation therapy is indicated to prevent thromboembolytic complications. A cardiology consultation is recommended (for more information on this topic, please see Case 21, Sects. 21.1.6 and 21.1.7, as well as Fig. 21.2).
25.1.10 What Causes Atrial Fibrillation?
There are many causes of a-fib (Table 25.1 [10]; and Sect. 21.2.3). Clarification of the cause is important, in order to give the proper therapy for rhythm and rate control. Especially important are the reversible causes, for example, hypothyroidism or electrolyte imbalances.
Primary | Idiopathic | |
Secondary | Cardiac causes | Rheumatic or inflammatory heart disease |
Cardiomyopathy | ||
Hypertensive heart disease | ||
Coronary artery disease | ||
Postcardiotomy syndrome
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