Anesthetic Outcome and Cardiopulmonary Resuscitation
Michele Barletta, Jane Quandt, Rachel Reed in Equine Anesthesia and Pain Management, 2023
Cardiac arrest in the anesthetized horse is responsible for approximately 30% of mortalities. Factors that may predispose to arrest are an excessively deep anesthetic plane leading to cardiovascular collapse and hypotension. Signs of impending arrest include: Loss of palpebral and corneal reflexes, pupillary dilation.Loss of anal pinch reflex.Hypoventilation, < 4 breaths/min to apnea.Tachypnea > 20 breaths/min.Dyspnea or abnormal breathing pattern and agonal gasps.Cyanosis, injected or gray to white mucous membranes, prolonged CRT of > 2.5 seconds.Weak or irregular peripheral pulses, hypotension, MAP < 70 mmHg.Rapid > 60 beats/min or slow < 25 beats/min heart rate, muffled or absent heart sounds.Abnormal ECG, asystole.
Miscellaneous
Bobby Krishnachetty, Abdul Syed, Harriet Scott in Applied Anatomy for the FRCA, 2020
The most probable reasons are noted below. Classic reason is a high spinal block – sensory block higher than T4 due to the blocking of the sympathetic cardio accelerator fibres to the heart (T1–T4). This can cause severe bradycardia which if not treated can lead to asystole.Reflex bradycardia due to the use of vasopressors (phenylephrine) to maintain the feto-placental circulationReflex cardiovascular depression due to decrease in venous return, known as Bezold–Jarisch reflex or neurocardiogenic syncopeSevere reflex bradycardia has been supported in case studies during the time of placental expulsion and tractionManipulation of the abdominal viscera, peritoneum or traction of the visceral ligaments, uterine exteriorisation and inversionPatient with pre-existing cardiac disease such as sick-sinus syndrome can also have bradycardia
In Vivo and In Vitro Cardiac Preparations Used in Antiarrhythmic Assays
John H. McNeill in Measurement of Cardiovascular Function, 2019
Mice. Test drug is administered and behavior observed for 20 min before the mice are placed in a container containing chloroform (2-1 beaker containing cotton wool soaked with 50 ml of chloroform or 20 ml of chloroform soaked cotton wool in a 300-ml beaker).2,31 Mice are removed after their last shallow breath and pin electrodes are used immediately to record an EKG. The heart is then rapidly exposed and observed for rate and rhythm. Ventricular fibrillation is differentiated from sinus rhythm as fine tremulous movements of the heart and is confirmed by the EKG record.31 Fibrillation should last at least 5 seconds. In controls, fibrillation occurs in a large percentage of mice, and animals are considered protected if ventricular fibrillation does not occur. Protected hearts beat in sinus rhythm. Asystole is often a toxic manifestation of the drug.
Tests for the identification of reflex syncope mechanism
Published in Expert Review of Medical Devices, 2023
Michele Brignole, Giulia Rivasi, Artur Fedorowski, Marcus Ståhlberg, Antonella Groppelli, Andrea Ungar
It has been demonstrated that hypotensive phase during tilt-induced reflex syncope begins approximately 8–9 minutes before the loss of consciousness, while the CI phase begins 1-min prior to syncope [13]. In the real-life scenario, the introductory hypotensive phase may not be fully sensed by the patient who is thus not aware of the imminent syncope. As CI component acts very fast, for most of the affected individuals the sensing of cardioinhibition and imminent syncope may not be sufficient to take countermeasures. In an interesting study of Saal et al., approximately one-third of patients who demonstrated asystole during TT, lost their consciousness prior to the onset of asystole due to profound hypotension [14]. This finding might question the role of pacemaker therapy in such setting [15]. In the context of CI reflex, it is important to mention the role of age. As demonstrated by several independent studies, while vagal cardiac overactivity and sinus depression dominate in younger patients, vasodepression is more prevalent in older age, beginning with the age of 50 years [16,17].
When is a wearable defibrillator indicated?
Published in Expert Review of Medical Devices, 2021
Alexandre Bodin, Arnaud Bisson, Laurent Fauchier
Registries and retrospective studies with numerous patients in different countries showed the safety and effectiveness of the WCD, with a good tolerance to the device with high daily use duration (Table 1) [6,8,10–16]. Appropriate therapy for VT or VF events was between 1.3 and 4% across the different main studies described in Table 1 when inappropriate therapy was observed in 0.5 to 1.2% of patients. The survival rate within the 24 hours after an appropriate therapy was between 84 and 93%. Interestingly, asystole is reported in some studies in 0.03 to 0.6% of patients. Long-term follow-up in the PROLONG-II study showed that mean estimated survival after the WCD was similar between patients with and without WCD shocks. This emphasizes the transitory risk of SCD and the usefulness of WCD.
Intracerebral haemorrhage following spine surgery: a word of caution on the use of suction drains
Published in British Journal of Neurosurgery, 2021
Wei Zhang, Colum Patrick Nolan, Dinesh Shree Kumar, Reuben Chee Cheong Soh, Jacob Yoong-Leong Oh
An 80-year-old man with no significant past medical history and no chronic medication was admitted for severe neck pain after he fell backwards and hit the back of his head in a bus. On examination, his neurology was intact. Computed Tomography (CT) scan of his brain showed no intracranial haemorrhage. CT and Magnetic Resonance Imaging (MRI) of his cervical spine showed an undisplaced type 2 odontoid fracture and C4–C6 stenosis for which he underwent C1–C6 instrumentation, decompression and stabilisation of C4–C6. Surgery lasted six hours without any significant intraoperative events. No dura leak was detected intraoperatively. The estimated blood loss was 1 litre. A closed suction drain (Redivac™) was placed subfascially at the end of surgery. Immediately after skin closure, the patient developed a transient episode of asystole. This resolved spontaneously after few seconds, by which time there was already 850mls of hemoserous fluid in the drain bottle. The drain was clamped and the patient was sent to the surgical intensive care unit (SICU). Ten minutes after arrival at SICU, the patient developed a grand tonic clinic (GTC) seizure CT brain, CT cervical spine with CT angiography were performed urgently, which showed multiple oval shaped acute intracranial haemorrhagic foci scattered in the cerebral hemisphere with associated mass effect and tonsillar herniation (Figure 1). On the same night, the patient’s brainstem functions ceased and he was pronounced brain dead.
Related Knowledge Centers
- Arrhythmia
- Cardiac Arrest
- Defibrillation
- Cardiopulmonary Bypass
- General Anaesthesia
- Ventricular Fibrillation
- Heart
- Ventricular Tachycardia
- Intensive Care Unit
- Antihypotensive Agent