Stress cardiomyopathy is an acute, reversible dysfunction of the left ventricle that appears when the heart is suddenly overwhelmed by a surge of catecholamines. During the perioperative period, powerful sympathetic triggers such as anxiety, induction, airway manipulation, hypoxia, pain, blood loss, or emergence can replicate the severe emotional or physical stressors known to precipitate this syndrome outside the operating room.
The challenge for anesthesia practice is that stress cardiomyopathy:
Mimics acute myocardial infarction in ECG patterns
Presents suddenly with hypotension, pulmonary edema, or shock
Has normal coronary arteries despite profound dysfunction
Worsens with catecholamine inotropes—drugs commonly used during anesthesia
Improves when sympathetic activity is reduced
Can be triggered by anesthesia itself, including laryngoscopy, insufficient analgesia, hypoxia, or abrupt hemodynamic shifts
Its recognition requires mastery of the molecular pathways controlling myocardial contraction, receptor signaling, and the autonomic responses activated during surgery.
Stress cardiomyopathy is known by multiple names, each highlighting a different dimension of its appearance or mechanism.
Originally described in Japan, the condition was named after the “takotsubo”, a traditional ceramic pot used to trap octopuses. It has:
A narrow neck
A rounded, balloon-shaped bottom
On ventriculography, the left ventricle in systole shows:
A hypercontractile base
A ballooned, akinetic apex
The overall silhouette strongly resembles the octopus pot, which is why this descriptive anatomical term became the primary medical name.
This name emphasizes the role of intense emotional or physical stress in triggering the syndrome through a massive catecholamine surge. Surgical stress activates the same neurohumoral pathways, making the operating room a high-risk environment for susceptible individuals.
This popular term reflects how emotional trauma—such as bereavement, shock, or severe distress—can precipitate acute, profound left ventricular dysfunction. It highlights the strong link between the brain's emotional centers and the heart's autonomic regulation.
This name directly describes the characteristic apical akinesis with ballooning observed on echocardiography or ventriculography, which remains one of the hallmark diagnostic features.
Takotsubo syndrome is not a problem of blocked coronary arteries. It is a problem of cellular signaling, receptor overstimulation, and myocardial metabolic dysfunction triggered by catecholamine excess. The following mechanisms form the scientific foundation needed to understand clinical presentations and anesthetic implications.
Stress activates:
The sympathetic nervous system
The adrenal medulla
This results in sudden, massive elevations in:
Norepinephrine (from sympathetic nerve terminals)
Epinephrine (from adrenal medulla)
Circulating catecholamine levels in Takotsubo syndrome often exceed those seen in myocardial infarction...
