Correlation of invasive and non-invasive blood pressure: A must for management

A 74-year-old male (43 kg, ASA status II)) patient was posted for parotid gland excision. The patient’s medical history was significant for chronic obstructive lung disease. He had fair effort tolerance (New York Heart Association-II). All pre-operative investigations were normal except for moderate obstruction in spirometry and typical hyperinflation features in chest X-ray. His physical examination and airway assessment were unremarkable.

Correlation of invasive and noninvasive blood pressure: A must for management DOI: 10.4103/0019-5049.72658 Sir, Arterial blood pressure (ABP) is a basic haemodynamic index often utilized to guide therapeutic interventions, especially in critically ill patients. Inaccurate ABP measuring creates a potential for misdiagnosis and mismanagement. I would like to share an important and interesting experience with you that would be valuable for the students.
A 74-year-old male (43 kg, ASA status II)) patient was posted for parotid gland excision. The patient's medical history was significant for chronic obstructive lung disease. He had fair effort tolerance (New York Heart Association-II). All pre-operative investigations were normal except for moderate obstruction in spirometry and typical hyperinflation features in chest X-ray. His physical examination and airway assessment were unremarkable.
The patient was induced with i.v. inj fentanyl 2 ug/ kg inj propofol 2 mg/kg and inj atracurium 0.5 mg/ kg after pre-oxygenating with 100% oxygen. His noninvasive systolic blood pressure was between 80 and 90 mmHg. We placed a radial arterial cannula with 100 cm of stiff tubing that was free of air bubbles and used a Flotrac TM sensor for arterial pressure monitoring. Invasive BP was 176/114 mmHg. There was no ringing or resonance and arterial tracing was absolutely normal. Non-invasive BP showed 82/46 mmHg. We cross-checked our BP reading and found it to be correct. Then, we changed the disposable transducer. After changing the disposable transducer, invasive BP correlated with non-invasive BP. The remaining intraoperative period was uneventful and the patient was extubated successfully.
Ideally, the pressure waves recorded through the intravascular catheter should be transmitted undistorted to the transducer and then to the amplifier, display or recording system. [1,2] Unfortunately, the mechanical transmission system oscillates (rings or resonates) after being set in motion by the arterial pressure wave. These oscillations produce small pressure waves that are superimposed on those caused by the pressure pulse itself, thereby introducing artefacts that distort the measured pressure. [1,3] In our case, there was no ringing or resonance as the arterial waveform was not distorted. Most disposable transducers have natural frequencies of several hundred hertz, but the addition of saline-filled tubing and stopcocks that may trap tiny air bubbles results in a monitoring system with a markedly reduced natural frequency. [1,4] We used 100 cm of stiff tubing that was free of air bubbles and a Flotrac TM sensor for arterial pressure monitoring. In our case, the disposable transducer was faulty, probably having a natural frequency in the unacceptable low range [ Figure 1]. [1] Most monitoring systems are underdamped but have a natural frequency high enough such that the effect on the monitored waveform is limited. [2] In conclusion, invasive BP should always be correlated with non-invasive BP, and any discrepancy noted should be rectified to avoid misdiagnosis and mismanagement. Sir, I read with interest the case report by Raiger et al, [1] titled "Non-cardiogenic pulmonary oedema after neostigmine for reversal: A report of two cases." The authors had described two cases of pulmonary oedema after routine surgeries. One patient developed it after tracheal extubation and required a very short period of mechanical ventilation. A laryngeal pack was used in this patient. The other patient developed it before tracheal extubation and required a relatively longer period of mechanical ventilation. This patient was reported to have difficulty in breathing and hence tracheal extubation was delayed.
Post-obstructive pulmonary oedema is caused by significant fluid shifts resulting from changes in intrathoracic pressure. [2] Negative intrathoracic pressure generated, when a patient attempts to inspire against a closed glottis or obstructed airway, leads to increase in venous return and a consequent rise in pulmonary venous pressure. This leads to a hydrostatic gradient with fluid moving from high pressure (pulmonary venous system) to low pressure (pulmonary interstitium and airspaces). [3] The negative intrathoracic pressure, along with the resultant hypoxia, also depresses the cardiac output by increasing myocardial wall stress and systemic vascular resistance, which increases the pulmonary venous pressure further. [4] Laryngospasm has been reported to be the cause in >50% of cases, whilst other causes include tracheal secretions, hiccups, and biting the endotracheal tube.
Drug-induced non-cardiogenic pulmonary oedema may be due to a pulmonary venoconstriction, capillary leak syndrome, intravascular fluid volume overload, and/or reduced serum oncotic pressure. [5] Drugs known to cause the above have been enumerated by Reed and Severe pain and hypertension following intravesical instillation of formalin necessitating epidural analgesia DOI: 10.4103/0019-5049.72660

Sir,
A 75-year-old, American Society of Anesthesiology Grade II male patient, a known case of carcinoma of the urinary bladder, who had previously undergone transurethral resection of the bladder tumour, received intravesical BCG and six cycles of radiotherapy, was referred to our hospital with persistent hematuria for seven months. A diagnosis of post-radiotherapy