ResusEdu

THAM is not routine, but it is worth understanding. Compared with sodium bicarbonate, it avoids CO₂ generation and avoids adding more sodium to the patient. It also has the potential to buffer intracellular acidosis. In the right scenario, those differences matter, especially when ventilation or sodium balance is already a problem.

This is where blanket algorithm thinking can miss the nuance. Buffering agents are not routine in resuscitation, but the OR is one of the few places where severe metabolic derangements can be recognized in real time with ABGs, trends, and immediate clinical context. That does not mean give them reflexively. It means there are situations where the physiology may support their use.

Lidocaine still makes a lot of sense in perioperative resuscitation. It tends to preserve blood pressure and contractility better than many other antiarrhythmics, which matters when the patient is already unstable. In a setting where hemodynamics can fall apart fast, that lower hypotension burden is a real advantage.

Endotracheal medication delivery used to be taught as a backup route during arrest, but that is no longer the recommendation. Absorption is unpredictable, circulating drug levels are often inadequate, and it has been associated with lower ROSC and survival compared with IV or IO administration. Old habits die hard, but this one deserves to.

In the OR, epinephrine is not always approached the same way it is in a generic ACLS scenario. Many anesthesia clinicians use 10 to 100 mcg boluses first, especially in bradycardia or PEA, because the patient is continuously monitored and reversible causes can often be identified and treated quickly. The perioperative environment gives you more physiologic information, which means resuscitation can be more targeted from the start.

Return of spontaneous circulation does not mean the patient is hemodynamically stable.
Hypotension occurs in nearly half of patients following ROSC. Several mechanisms may contribute, including myocardial stunning, relative adrenal insufficiency, and systemic inflammatory responses triggered by ischemia-reperfusion injury.
Early recognition and aggressive hemodynamic support are critical to maintain perfusion and prevent secondary organ injury in the post-arrest period.

Temporary transvenous pacing (TTVP) involves advancing a pacing lead through the subclavian, internal jugular, or femoral vein into the right ventricle. The lead connects to an external pacing generator that delivers controlled electrical impulses to stimulate myocardial depolarization.
Because the electrode sits directly against the endocardium, transvenous pacing requires significantly less current to achieve capture compared with transcutaneous pacing (TCP).

Transcutaneous pacing must overcome skin, soft tissue, and thoracic impedance, which is why higher energy levels are typically required.

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Calcium plays a critical role in both myocardial contraction and vascular smooth muscle tone.
When ionized calcium levels fall, vascular responsiveness to catecholamines decreases and systemic vasodilation can occur. This may present clinically as vasoplegia and refractory hypotension despite escalating vasopressor support.
In critically ill patients, particularly during massive transfusion or prolonged resuscitation, checking and correcting ionized calcium can be an important step in restoring hemodynamic stability.

Anesthesia professionals work in environments where critical events can unfold rapidly and without warning.
Complications, adverse outcomes, and unexpected clinical crises can leave a lasting emotional impact on the providers involved.
This phenomenon is often described as the “second victim,” where healthcare professionals experience psychological distress following a patient-related event.
Recognizing these experiences and creating systems that support clinicians after critical events is essential for maintaining both provider well-being and patient safety.