(33.1)
It is a measurement for the time needed to exhale air. The unit is seconds. The normal value in healthy patients is 0.2 s, in ventilated patients 0.3 s. After one time constant 63 % of air is exhaled, after three time constants 95 %, and after five time constants more than 99 % of inhaled air is exhaled.
Patients with chronic obstructive lung disease (COPD) have an extended expiration time with a higher time constant. The value is usually about 0.9 s.
Ideally, 5 time constants should be available to exhale (4.5 s for an asthma patient). If the expiration time is less than 3 time constants, air remains in the lungs. This air trapping results in overinflation of the lung and development of an auto-PEEP. The danger of auto-PEEP formation is especially high in COPD patients, if the set expiratory time is not long enough.
33.1.4 What Are Typical Triggers for Bronchospasm?
Typical triggers include:
Allergic reactions
Pulmonary infections
Exertion [2] (the so-called “Tour de France” asthma)
Manipulations done in and around the airways (e.g., insufficient depth of anesthesia)
Chemical stimuli (e.g., aspiration, irritating gases)
Medications, e.g., noncardioselective β-blockers, cholinesterase inhibitors, and NSAIDS
Apart from that, bronchospasm may be seen as a result of psychological stress in susceptible patients.
>> In the meantime, tech Roger helped Mr. Sanford to sit up and administered 2 puffs of albuterol. “I’m gonna be sick,” Mr. Sanford said after he received the sprays.
“Hopefully it’s not a myocardial infarction!” thought Dr. Spiegel. “Do you have any chest pain?” she asked. Mr. Sanford shook his head. “Oh, man,” she thought. “Why does this always happen to the nicest patients?” She auscultated his lungs; breath sounds were normal. “Can I lie down again, doc?” was all she heard.
“Do you think it’s a myocardial infarction?” Dr. Spiegel asked, turning to tech Roger. “We could give nitroglycerin and see if it helps.”
Tech Roger shook his head. “I don’t think so,” he said, as he started the blood pressure. The measurement appeared as the alarms went off, showing the following values:
Blood pressure 70/40 mmHg
Heart rate 90/min
S P O 2 92 %
33.1.5 What Would You Do Now?
The first suspected diagnosis, asthma attack, seems to have been incorrect. Mr. Sanford is now:
Diaphoretic
Short of breath
Hypotensive
The diaphoresis and the dyspnea can be caused by the hypotension. In the presented case, before a search for the cause of hypotension is done, symptomatic therapy needs to be started, with volume administration and vasopressors.
>> Mr. Sanford received phenylephrine and 1,000 ml of a crystalloid solution IV. His blood pressure stabilized at 110/55 mmHg. Mr. Sanford felt much better. “Thanks, Roger. I’ll call the anesthesiologist–in–charge now,” said Dr. Spiegel.
33.1.6 What Is Your Differential Diagnosis?
Difficult, very difficult to determine. We just don’t know enough at this time, but all too often, that’s the way it is in real life.
33.1.6.1 Reflex Hypotension
Reflex hypotension and bradycardia can occur in very upset or nervous patients. Usually the patients are younger.
33.1.6.2 Cardiogenic Shock
Dr. Spiegel might have been right about her cardiac suspicions. An acute coronary syndrome could explain the symptoms. Pain is not necessarily present, especially when the patients are diabetic.
33.1.6.3 Hypovolemia
Hypovolemia may cause hypotension. Whether or not the preoperative fasting state in combination with the diuretics is sufficient to explain the symptoms is debatable.
33.1.6.4 Pulmonary Emboli
Thrombosis and pulmonary emboli are the most feared complications of every surgeon. Occurrence before an operation is not impossible, but unlikely in patients without additional risk factors.
33.1.6.5 Hypoglycemia
Hypoglycemia must be considered as the cause of the symptoms in diabetic patients.
33.1.6.6 Anaphylactic Shock
33.1.6.7 Septic Shock
Once you know the definition of sepsis, you can explain almost all symptoms as being due to sepsis (see Sect. 25.2.2).
33.1.6.8 Neurogenic Shock
An intracerebral mass can cause neurogenic shock. The possibility of this being the cause of the symptoms in the presented case is unlikely. Mr. Sanford is simply doing too well neurologically.
>> Anesthesiologist–in–charge Dr. Eldridge walked into the preop holding area and listened to the recount of the situation. In the meantime, Roger had done a 12-lead ECG and a glucose. Both were normal/unchanged from the previous readings. Axillary temperature was 35.9 °C, and glucose was 105 mg/dl (reference 70–99 mg/dl).
Dr. Eldridge examined Mr. Sanford, without making a new discovery. Then he reviewed the patient’s medical record on the computer. “Have you seen the labs?” he asked Dr. Spiegel. “Everything is normal except the increased creatinine,” she responded.
“Not exactly,” said anesthesiologist–in–charge Dr. Eldridge. “The C–reactive protein (CRP) yesterday was 232 mg/dl. Maybe Mr. Sanford has an infection. My best differential diagnosis is an allergic reaction. Acute myocardial infarction and pulmonary emboli must be ruled out, even though I think they are unlikely. Put in an arterial line under local anesthesia so we can carefully monitor the blood pressure. I’ll call the neurosurgeon and discuss postponing the surgery until we find out what is going on here.”
33.1.7 Which Parameters Would You Determine?
33.1.7.1 To Rule Out Acute Myocardial Infarction
Lab values: troponin, creatine kinase (CK), CK-MB (heart specific portion of the CK), glutamate oxaloacetate transaminase (GOT), lactate dehydrogenase (LDH)
The lab values are initially negative in an acute myocardial infarction; additional measurements are required. Troponin is the first parameter to increase.
33.1.7.2 Pulmonary Emboli
Lab values: D-dimers, proBNP
Increased D-dimers could be a clue of a thrombosis, but can also be found in many other diseases like infections and tumors. proBNP is a marker of stress on the right side of the heart.
33.1.7.3 Infection/Sepsis
Lab values: complete blood count with differential, CRP, procalcitonin, blood culture
Procalcitonin is a precursor of the hormone calcitonin, which is formed in the C cells of the parathyroid gland. An increase of procalcitonin can have many causes. The value in the diagnosis of sepsis is debated [6]. High procalcitonin levels (>10 ng/ml) are a clue that sepsis is likely; low levels cannot exclude sepsis from the differential.
33.1.7.4 Anaphylaxis
Mast cells play a key role in anaphylactic shock. After activation, they release various mediators, the most important of which are histamine and tryptase (Fig. 33.1). Tryptase is an enzyme with many purposes, which are only partly understood. Known effects are:
Fig. 33.1
Schematic representation of histamine and tryptase degranulation from mast cells. A trigger causes calcium to flow into the cell and activate cAMP, which causes histamine and tryptase to be released from the intravascular vesicles (H histamine, T tryptase)
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