Chapter 38 — Neurocritical Care and Stress Cardiomyopathy

📚 Guideline basis

InterTAK diagnostic criteria and the ESC Heart Failure Association position statement on Takotsubo syndrome (Ghadri JR, et al., Eur Heart J 2018); Neurocritical Care Society guidance on subarachnoid haemorrhage; ASE 2019 comprehensive TTE examination; ASE/consensus documents on echocardiography in the potential organ donor.

Pathophysiology & Mechanisms

Acute brain injury produces cardiac injury through a catecholamine surge originating in the hypothalamus and mediated by direct sympathetic innervation of the myocardium rather than by circulating catecholamines alone. The evidence for local rather than systemic mediation is the distribution: the apical myocardium has the highest density of β-adrenergic receptors, and the resulting injury is regional in a pattern that does not follow coronary territories.

Three mechanisms operate:

Catecholamine-mediated myocyte injury — contraction band necrosis, calcium overload, and a switch in apical β₂-receptor signalling from Gs to Gi coupling, which is negatively inotropic and is the leading explanation for apical stunning with basal hypercontractility.
Microvascular dysfunction and transient vasospasm — reduced coronary flow reserve without epicardial obstruction.
Increased afterload from the sympathetic surge, compounding wall stress at the moment contractility is falling.

The injury is reversible. This is the single most important therapeutic fact: recovery over days to weeks is the rule, and the management goal is to support the patient through a self-limiting process without causing iatrogenic harm.

Neurogenic stunned myocardium after subarachnoid haemorrhage

Feature	Detail
Timing	Within hours to the first few days after ictus
Pattern	Frequently basal or global hypokinesis, distinct from classical apical Takotsubo; any pattern is possible
Associated findings	Troponin elevation, ECG changes (deep T-wave inversion, marked QT prolongation, ST changes) mimicking acute coronary syndrome
Severity correlation	Associated with higher Hunt-Hess and Fisher grades
Recovery	Days to weeks; usually complete
Complications	Pulmonary oedema (cardiogenic and neurogenic), arrhythmia, hypotension compromising cerebral perfusion pressure

The pattern of wall motion abnormality in SAH characteristically crosses coronary territories and is accompanied by a troponin rise that is disproportionately small relative to the extent of dysfunction — the opposite of the relationship seen in infarction. Both features argue against an ischaemic aetiology.

Takotsubo syndrome

InterTAK diagnostic criteria (summarised)

Transient regional wall motion abnormality of the left or right ventricle, frequently preceded by an emotional, physical or neurological trigger; the abnormality typically extends beyond a single epicardial coronary distribution; the presence of coronary artery disease does not exclude the diagnosis; new ECG abnormalities and modest troponin elevation with a significantly elevated BNP are typical; and pheochromocytoma and myocarditis should be considered in the differential.

Morphological variants

Variant	Pattern	Frequency
Apical (classical)	Apical and mid akinesis with basal hypercontractility — "apical ballooning"	Most common
Midventricular	Mid-segment akinesis with preserved apex and base	Second
Basal (inverted / reverse)	Basal akinesis with preserved apex; more common in younger patients and in neurological triggers	Less common
Focal	A single localised segment	Least common

RV involvement is present in a substantial minority and confers a worse prognosis.

Dynamic LVOT obstruction — the complication that inverts management

Hypercontractile basal segments with an akinetic apex produce a small, high-velocity outflow tract and can generate systolic anterior motion of the mitral valve with dynamic LVOT obstruction, reported in roughly 10–25% of Takotsubo cases.

The clinical consequence is decisive. The hypotensive Takotsubo patient with dynamic obstruction becomes more hypotensive with every increment of inotrope. Findings: a late-peaking, dagger-shaped LVOT continuous-wave envelope, SAM on 2D, and a posteriorly directed mitral regurgitant jet.

Management inverts: stop inotropes, volume load, use a pure vasoconstrictor (phenylephrine, or noradrenaline for its α effect), consider beta-blockade, and slow the heart rate to lengthen diastolic filling (Chapter 28).

Every hypotensive patient with apical ballooning requires continuous-wave Doppler through the LVOT before any inotrope is started.

Distinguishing Takotsubo from anterior STEMI

Feature	Takotsubo	Anterior STEMI
Wall motion	Extends beyond the LAD territory; circumferential at the mid/apical level	Confined to the LAD territory
Apical cap	Involved	Involved
Basal segments	Hypercontractile	Normal or hypokinetic
Troponin relative to dysfunction	Disproportionately low	Proportionate
BNP	Markedly elevated	Variable
Recovery	Days to weeks, complete	Regional dysfunction persists

Echocardiography raises the probability; coronary angiography remains necessary in most acute presentations, because the two cannot be reliably separated at the bedside and the cost of missing an occlusion is high.

Haemodynamic management in the injured brain

The central conflict: cerebral perfusion pressure targets require systemic pressure that a stunned myocardium may not tolerate.

CPP = MAP - ICP

Situation	Approach
Induced hypertension for vasospasm with stunned myocardium	Echocardiography-guided: use a vasopressor to raise MAP, and add an inotrope only if measured stroke volume index is inadequate. Serial LVOT VTI documents whether the ventricle is tolerating the pressure target
Pulmonary oedema limiting oxygenation	Distinguish cardiogenic (high E/e′, low VTI) from neurogenic pulmonary oedema (normal filling pressures) — the treatments diverge
Hypotension threatening CPP with dynamic LVOT obstruction	Volume and vasoconstrictor; not inotrope
Euvolaemia targets in SAH	Fluid management guided by measured responsiveness and tolerance rather than by protocol volumes; hypervolaemia is no longer recommended and is harmful in a stunned ventricle

Serial echocardiography is warranted because the myocardium recovers over days while the neurological target persists — the tolerable haemodynamic strategy changes as the ventricle improves.

Echocardiography in the potential organ donor

Consideration	Detail
Timing	Catecholamine storm at the time of herniation causes acute dysfunction that frequently recovers; an early study may under-represent the organ's quality
Serial assessment	Repeat after haemodynamic optimisation and hormone replacement therapy; hearts initially declined for poor function are frequently transplantable on reassessment
Confounders	High-dose vasopressors, diabetes insipidus with profound volume shifts, hypothermia, and thyroid and cortisol deficiency all depress measured function
What to report	LVEF, regional wall motion, RV function, valve structure, chamber dimensions, wall thickness, and the concurrent vasoactive doses

The message is that a single early echocardiogram should not disqualify a donor heart.

Cardiac sources of embolism in stroke

Source	Modality	Notes
Left atrial appendage thrombus	TEE	Not visualised transthoracically
Patent foramen ovale	TEE with agitated saline and provocation	Right-arm injection; watch the LA for 3–6 beats; a positive-pressure breath abolishes the gradient in ventilated patients, so a release manoeuvre is required
Infective endocarditis	TTE then TEE	Chapter 24
Aortic arch atheroma	TEE	Mobile or ≥ 4 mm plaque carries embolic risk
LV thrombus	TTE with contrast; CMR most sensitive	Anterior infarct, apical aneurysm, cardiomyopathy
Intracardiac tumour (myxoma, fibroelastoma)	TTE/TEE	Uncommon

ICU-Specific Limitations

Confounder	Effect	Response
High-dose vasopressors for CPP targets	Raise afterload and depress measured EF	Record the dose; reassess as it weans
Neurogenic pulmonary oedema	Mimics cardiogenic oedema on lung ultrasound	Use E/e′ and TR velocity to separate them (Chapters 8, 41)
Sedation and neuromuscular blockade	Alter loading	Note the state
Cervical collar / raised ICP	Limits positioning; passive leg raise is contraindicated where ICP is a concern	Use end-expiratory occlusion or a mini fluid challenge
Targeted temperature management	Bradycardia and reduced contractility are expected at low temperature	Do not over-interpret

🛑 Critical pitfall: Starting an inotrope in a hypotensive patient with apical ballooning. Dynamic LVOT obstruction complicates a substantial minority of cases, and inotropes make it worse. Put the CW cursor through the LVOT first.

🛑 Critical pitfall: Diagnosing "myocardial infarction" from regional dysfunction plus troponin in a patient with SAH. The pattern crosses coronary territories and the troponin is disproportionately low. Angiography is often still indicated, but the working diagnosis should be neurogenic stunning.

🛑 Critical pitfall: Declining a donor heart on a single echocardiogram performed during catecholamine storm. Reassess after optimisation.

💡 Clinical pearl: A wall motion abnormality that does not respect coronary anatomy — particularly circumferential mid or apical akinesis with hypercontractile bases — is stress cardiomyopathy until proven otherwise.
💡 Clinical pearl: Use the passive leg raise with caution or not at all where intracranial pressure matters. The end-expiratory occlusion test and the 100 mL mini fluid challenge are the alternatives.
💡 Clinical pearl: Serial studies matter more here than almost anywhere else, because the myocardium recovers on a timescale of days while the neurological haemodynamic target does not change.

References

Ghadri JR, Wittstein IS, Prasad A, et al. International expert consensus document on Takotsubo syndrome (Part I): clinical characteristics, diagnostic criteria, and pathophysiology. Eur Heart J 2018;39:2032–46.
Ghadri JR, Wittstein IS, Prasad A, et al. International expert consensus document on Takotsubo syndrome (Part II): diagnostic workup, outcome, and management. Eur Heart J 2018;39:2047–62.
Kerro A, Woods T, Chang JJ. Neurogenic stunned myocardium in subarachnoid hemorrhage. J Crit Care 2017;38:27–34.
Mitchell C, Rahko PS, Blauwet LA, et al. Guidelines for performing a comprehensive TTE examination in adults. J Am Soc Echocardiogr 2019;32:1–64.
Champion S, et al. Dynamic left ventricular outflow tract obstruction. Can J Cardiol 2020. PMID 33173359.