Cardiac Dysfunctions in Neurocritical Care

A variety of brain disorders affect cardiac function, causing increased mortality as well as short- and long-term complications


  • Studies have indicated that patients with Traumatic or Atraumatic, brain injury are more prone to develop cardiac dysfunction within their hospital stay
  • Cardiac Dysfunctions if developed are linked to increased mortality as well as short term and long term complications.
  • Stroke related cardiac dysfunctions can happen, even in the absence of an overt heart disease
  • The severity of brain injury correlates with the severity of cardiac dysfunction.
  • In this chapter, we will review the basis as well as prevention of these dysfunctions
  • The point to note here is that data on this topic is still scarce and the recommendations are still not as strong
It has been seen that some of the brain injuries as well as the heart dysfunctions due to it have some correlation, which has these commonly labeled as “Stroke Heart Syndrome


Intrinsic Cardiac Autonomic Control

  • Sensory receptors in the heart are distributed throughout myocardial, pericardial, and epicardial tissue and at the junction of atria and great veins.
  • Transmission through vagal afferent from above mentioned receptors to nucleus of solitary tract in the medulla
  • Intrinsic nervous system of heart also plays role in autonomic control apart from CNS involvement called the cardiac ganglionic plexus (CGP).
  • CGP is dominantly cholinergic; main neuromodulators involved are norepinephrine, epinephrine, acetylcholine, nitric oxide (NO), vasoactive intestinal peptide (VIP), neuropeptide Y, and intermedin.

Extrinsic Nerve Supply to Heart

  • Parasympathetic nerve supply to heart has its preganglionic neurons located dominantly in nucleus ambiguus and lesser extent in dorsal medial nucleus of vagus nerve
  • Sympathetic nerve supply to the heart arises from cardiac plexus, a bundle of nerves at arch of aorta.
  • These nerves in plexus are post ganglionic projections arise from paravertebral sympathetic ganglions.
  • Paravertebral sympathetic ganglions which receive inputs from higher centers exit CNS via upper 5 T-spine segments as preganglionic fibers.
  • Insular cortex damage is associated with arrythmia, disruption in diurnal blood pressure variation, myocardial injury, and breathing disorders during sleep.
It has been shown that anterior circulation strokes, are more related to cardiac dysfunctions than any other strokes, which is linked to the factor that anterior insular cortex deals with majority of autonomic functions in the body.
  • Cardiovascular autonomic dysfunction is mainly related to increased sympathetic activity via the right hemisphere of the insular cortex
  • Impaired autonomic cardiac control may occur following injury to brain regions such as the prefrontal cortex. For example, using a combination of electroencephalographic dynamics and instantaneous HR estimates to study emotional processing and cardiovascular autonomic responses in brain areas such as the prefrontal cortex and amygdala infract
  • Interomediolateral column at T1-T5 is modulated by rostral ventrolateral medulla and paraventricular nucleus of hypothalamus.
  • The involvement of brainstem in cardiac dysfunction has already been discussed in this chapter
A significant correlation was established between the clinical manifestations of brainstem compression and sinus arrhythmias, multifocal premature ventricular contractions, couplets, and ventricular tachycardias. An explanation for this correlation may be found in the localization of the autonomous cardiovascular centers in the hypothalamus and brainstem. Transtentorial herniation frequently leads to a bilateral lesion of these structures. However, the cardiac arrhythmias are only a partial phenomenon within a complex cardiovascular reaction.
Stober, T., Sen, S., Anstätt, T., & Bette, L. (1988). Correlation of cardiac arrhythmias with brainstem compression in patients with intracerebral hemorrhage. Stroke19(6), 688-692.


There are several hypothesis under research, the ones with the most support are discussed below
  • Sympathetic Over dominance
  • Activation of Hypothalamic-Pituitary-Adrenal axis
  • Mental Stress induced myocardial ischemia
  • Unknown Factors Causing endothelial instability.
  • Sympathetic Over dominance
    • Sympathetic over dominance can cause excess catecholamine concentration at the nerve terminals
      • Etiology is focal damage or dysfunction of CNS structures controlling autonomic outflow
        • Increased cAMP activation and ER Dysfunction → Calcium influx → Altered actin myosin interaction → altered myocardial contraction (consistent contraction) → Disturbance of rate and rhythm + Myocardial necrosis
        • Increased K+ Outflow through delayed rectifiers > Shortening APD and increasing heterogeneity → Disturbance of rate and rhythm + Myocardial necrosis
        • Sustained increase in SVR > decreased endothelial vasodilator agents → Myocardial ischemia
        • Further explanation
          • Heart rate = Action Potential Duration + Diastolic Interval(DI).
          • Increased sympathetic dominance will shorten both APD as well as DI.
          • Shortening of DI has a separate effect on APD, as through negative Feedback, in order to control Heart Rate, it will prolong APD in next cycle. This phenomenon of APD dependency on DI is known as Restitution of APD.
          • This alternative short and long APD, is known as AP Alternans, and increases the susceptibility to arrhythmias.
          • AP duration can be prolonged to the extent that a new stimulus may arise while myocardial cells are still in refractory period of AP → malignant arrythmia (this process corresponds to QT prolongation
  • Activation of HPA + Other factors:
    • Activation of HPA → Cortisol + Inflammatory mediators → Increased myocardial centrality + Increased oxidative stress + Increased vascular contractility → Myocardial necrosis + Coronary demand ischemia.
    • Several Factors lead to sympathetic over dominance and increased activation of HPA
      • Structural damage
      • Excessive stimulation
      • Mental stress
      • 💡
        Trigeminocardiac Reflex is a common cause of hemodynamic disturbance during supratentorial surgery. It manifests as bradycardia and hypotension during stimulation of any of the branches of the trigeminal nerve. It can also be associated with asystole, gastric hypermotility, and apnea.
        Source: Ijaz, M. K. Brainstem Reflexes During Neurosurgery: An Overview.

Table 1: Effects of Neurotransmitters on the Heart

Effects of Neurotransmitters on the Heart (1)
Increased inotropy, increased heterogeneity during repolarization, increased slope of APD restitution, and reduced VFT; Increased HR cardiac output, and perfusion to vital organs. / Increased propensity to ventricular arrythmias and myocardial necrosis
Reduced inotropy, reduced heterogeneity and increased VFT. Reduced HR and inotropy. / Reduced propensity to ventricular arrhythmias.
Accentuation of vagal mediated flattening of APD restitution slope and increase in VFT. / Protection from ventricular arrhythmias
Coronary and peripheral dilataion, LV afterload reduction, enhance myocardial isometric force. / Improves coronary flow during reperfusion and free radical scavenger.
Reduce Ach release from parasympathetic nerve terminals and reduce vagal bradycardic response. / Increased propensity to sympathetic-mediated arrhythmias.
Reduce sympathetic activity, increases VFT and oxidative stress. / Protection from sympathetic mediated ventricular arrhythmias and heart failure in patient with acute MI.

Etiology & Classification

  • Cardiac Dysfunctions can be classified as follows

Table 2: Classification of Cardiac Dysfunctions

Classification of Cardiac Dysfunctions
Clinical Spectrum
· Loss of variability in HR · Prolonged QTc · T wave changes · Severe arrhythmias e.g. atrial fibrillation, SVTs · Sudden cardiac death · Elevated cardiac enzymes
·        Acute stroke ·        Seizures ·        TBI
· Neurogenic stunned myocardium · Exacerbation of heart failure · Myocardial injury · Stress induced cardiomyopathy
·        Psychological stress ·        Critical illness ·        Natural disaster ·        Neurological disorders ·        Catecholamine infusion ·        Spinal cord disorder ·        Acute SAH is major cause for stress induced cardiomyopathy

Table 3: Prognostic Importance of Cardiac Dysfunction

Prognostic Importance
EKG changes including: o QTc prolongation o Cerebral T wave (Inverted T wave after stroke) o ST segment changes
Arrhythmias e.g. atrial fibrillation
Regional wall abnormalities
Takotsubo syndrome

Clinical Syndromes

Impaired Electrical Activity of Heart

  • QTc prolongation in most common; high mortality seen in patients with QTc seen in lead V6
  • Abnormal T-waves or "Cerebral T-waves": T-wave inversion ≥5 mm in depth in 4 contiguous precordial leads

Cardiac Arrest and Sudden Death

  • Most commonly seen in acute aneurysmal SAH patients
  • In ischemic type, more commonly seen in subacute or delayed phase of stroke.
  • SUDEP (Sudden Unexpected Death in Epilepsy) seen with seizures has 1.2 per 1000 patients per year.

Stress Cardiomyopathies

  • Stress cardiomyopathy first described in 1980 as myofibrillar necrotic lesions of heart found at autopsy of physical assault patients but no other internal organ injury
  • Acute chest pain presentation temporally related to emotional stress
  • Ventriculography showed apical and diaphragmatic akinesia along with hyperkinesia of basal segment resulting in apical ballooning
  • Peculiar shape of myocardium (see below) was similar to 'Takotsubu' or Octopus trapping pot.

Figure 1: Takotsubo Cardiomyopathy

notion image
Transthoracic echocardiogram showing LV (left ventricle) dilatation appearing as a pot typical for Takatsubo cardiomyopathy. Kerrigan, D., & Dwyer, K. (2021). Cardiology, Ultrasound. Cardiology

Neurogenic Stunned Myocardium(NSM)

  • Defined as acute left ventricular dysfunction triggered by acute neurologic condition.
  • Can present with left ventricular ejection fraction reduction significantly or normal left ventricular EF with regional wall motion abnormality; can been seen commonly after acute subarachnoid hemorrhage
  • Other risk factors for NSM in acute SAH include female sex, ST elevation anterior leads, high troponin, cocaine or meth use history, or posterior circulation aneurysms.

Risk Factors:

Following are the risk factors that increase the chance of cardiac dysfunctions:
  • Preexisting heart disease
  • Increased burden of cardiac risk factors i.e. smoking, obesity, hypertension, sedentary life style, high cholesterol etc.
  • Factors that increase electrical instability
    • Obstructive sleep apnea
    • Diabetes
    • Electrolyte imbalance
    • Drugs that prolong QTc

Prevention and Therapeutic Options

Several modalities have been considered to prevent cardiac dysfunctions, but none of them are strongly supported by the literature. Following is the list of few
  • Balance electrolyte disturbances
  • Avoid QTc prolonging drugs
  • Factors increasing coronary demand such as hypertension, tachyarrhythmia should be aggressively managed
  • Beta blockers and renin angiotensin pathway inhibitors might work in some cases
  • Centrally acting sympathetic blockers such as clonidine has shown to prevent cardiac dysfunctions
  • Vagal nerve stimulation
  • Inotropes such as dobutamine is preferred than vasopressors in management of cardiac dysfunctions after Stroke.
  • Several other novel treatments are being studied.
Adenosine use can induce temporary asystole and hypotension to decompress the aneurysmal dome, except when the aneurysm is calcified or fibrotic, allowing the surgeon to dissect the aneurysmal plane. It has been used in neurosurgical procedures most notably, aneurysmal clipping.

Further Reading

  • Raad, B., & Sila, C. (2011). Cardiac manifestations of neurologic disorders. CONTINUUM: Lifelong Learning in Neurology17(1), 13-26.
  • Ibrahim, M. S., Samuel, B., Mohamed, W., & Suchdev, K. (2019). Cardiac dysfunction in neurocritical care: an autonomic perspective. Neurocritical care30(3), 508-521.


  • Krishnamoorthy, V., Mackensen, G. B., Gibbons, E. F., & Vavilala, M. S. (2016). Cardiac dysfunction after neurologic injury: what do we know and where are we going?. Chest149(5), 1325-1331.
  • Tahsili-Fahadan, P., & Geocadin, R. G. (2017). Heart–brain axis: effects of neurologic injury on cardiovascular function. Circulation research120(3), 559-572.
  • van der Bilt, I., Hasan, D., van den Brink, R., Cramer, M. J., van der Jagt, M., van Kooten, F., ... & Rinkel, G. (2014). Cardiac dysfunction after aneurysmal subarachnoid hemorrhage: relationship with outcome. Neurology82(4), 351-358.
  • Krishnamoorthy, V., Sharma, D., Prathep, S., & Vavilala, M. S. (2013). Myocardial dysfunction in acute traumatic brain injury relieved by surgical decompression. Case reports in anesthesiology2013
  • S. Oppenheimer and D. Cechetto, “The insular cortex and the regulation of cardiac function,” Comprehensive Physiology, vol. 6, no. 2, pp. 1081–133, 2016.
  • G. Orlandi, S. Fanucchi, G. Strata, L. Pataleo, L. Landucci Pellegrini et al., “Transient autonomic nervous system dysfunction during hyperacute stroke,” Acta Neurologica Scandinavica, vol. 102, no. 5, pp. 317–321, 2000.
  • G. Valenza, A. Greco, C. Gentili, A. Lanata, L. Sebastiani, D. Menicucci et al., “Combining electroencephalographic activity and instantaneous heart rate for assessing brain-heart dynamics during visual emotional elicitation in healthy subjects,” Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences, vol. 374, no. 2067, 2016.