Broken Heart Syndrome: Cardiovascular Manifestations of Traumatic Brain Injury

1. Broken Heart Syndrome:
Cardiovascular Manifestations of
Traumatic Brain Injury
Dr Amit Agrawal, MCh
Department of Neurosurgery
Narayana Medical College and Hospital
Chintareddypalem, Nellore (AP), India

2.  Conflict of interest: None

3.  Up to 89% patients with severe TBI can show significant organ
dysfunction*
 It is shown to be independently associated with worse
outcomes*
 Cardiovascular
 Respiratory
 Immunological
 Haematological
 Endocrinological systems
Introduction
*Zygun DA, Kortbeek JB, Fick GH, et al. Nonneurologic organ dysfunction in severe
traumatic brain injury. Crit Care Med 2005; 33:654660.

4.  An increasing appreciation of the role of neurocardiac
interactions in TBI
 Associated with increased morbidity and mortality
 Although most patients succumbed to serious brain injury
 15.7% of patients developed global systolic dysfunction and
regional wall motion abnormalities***
 Increased sympathetic or reduced vagal activity may result in
ventricular tachyarrhythmias and sudden cardiac death**
Neurogenic cardiovascular
abnormalities
van der Bilt IAC, Hasan D, Vandertop WP et al. Impact of cardiac complications on outcome after aneurysmal
subarachnoid hemorrhage: a meta-analysis. Neurology 2009; 72: 635-42
Zygun D. Non-neurological organ dysfunction in neurocritical care: impact on outcome and etiological
considerations. Curr Opin Crit Care 2005; 11: 139-43
***Huttemann et al. Left ventricular dysfunction in lethal severe brain injury: impact of transesophageal
echocardiography on patient management. Intensive Care Medicine 2002; 28: 1084-8.
**Henden et al. Can Baroreflex Sensitivity and Heart Rate Variability Predict Late Neurological Outcome in Patients
with Traumatic Brain Injury? J. Neurosurg. Anesthesiol. 2014, 26, 50-59.

5.  Hypotension
 Hypertension
 ECG changes
 Cardiac arrhythmias
 Release of biomarkers of cardiac injury
 Left ventricular (LV) dysfunction
Cardiovascular complications
Gregory T, Smith M. Cardiovascular complications of brain injury. Continuing Education
in Anaesthesia Critical Care & Pain 2012;12:67-71.

6.  Less well understood
 Potentially a protective mechanism intend to maintain cerebral
perfusion in the presence of raised intracranial pressure (ICP)
 However can have several adverse effects
Pathology
Clifton GL, Ziegler MG. Circulating catecholamines and sympathetic activity after head
injury. Neurosurgery 1981; 8: 10-4.
Clifton GL, Robertson CS, Kyper K, Taylor AA, Dhekne RD, Grossman RG. Cardiovascular
response to severe head injury. Journal of Neurosurgery 1983; 59: 447-54.
Tamsin Gregory. Cardiovascular complications of brain injury

7. Direct stimulation of specific trigger zones
Including A1, A5
Nuclei of solitary tract
Area postrema within the medulla and hypothalamus
Raised intracranial pressure
Catecholamine
excess
Autonomic
dysfunction
Systemic
inflammatory
response
The
catecholamine
surge may
cause direct
injury to the
myocardium
Intense systemic
vasoconstriction
Hyperdynamic
circulation
Tachycardia
Hypertension
Increases cardiac
afterload
Myocardial
workload
Increase
myocardial
oxygen demand
Sedy J, Kunes J, Zicha J. Pathogenetic mechanisms of neurogenic pulmonary edema. J Neurotrauma 2015; 32:1135-1145.
Elenkov IJ, Wilder RL, Chrousos GP, Vizi ES. The sympathetic nerve - an integrative interface between two supersystems: the brain and the
immune system. Pharmacol Rev 2000; 52:595-638.
Clifton GL, McCormick WF, Grossman RG. Neuropathology of early and late deaths after head injury. Neurosurgery 1981; 8: 309-14.
Nguyen H, Zaroff JG. Neurogenic stunned myocardium. Curr Neurol Neurosci Rep 2009; 9: 486-91
The degree of catecholamine release directly related to the
severity of the brain injury

8.  Conventional teaching suggests that isolated head injury does
not result in hypotension in adults
 Neurogenic hypotension: 13% of patients with isolated head
injury
 Associated with a higher mortality than haemorrhagic
hypotension
Hypotension
Mahoney EJ, Biffl WL, Harrington DT, Cioffi WG. Isolated brain injury as a cause of
hypotension in the blunt trauma patient. Journal of Trauma 2003; 55: 1065-9.

9.  Often associated with diffuse axonal injury
 Disruption of brainstem centers for hemodynamic control
 As the catecholamine surge subsides
 The initial hyperdynamic response is often followed by significant
hypotension because of unopposed peripheral vasodilatation and
ventricular dysfunction
 Injury to diencephalic region-Reduction of systematic vascular
resistance
 The development of adrenal insufficiency
Neurogenic Hypotension
Chesnut et al. Neurogenic hypotension in patients with severe head injuries. Journal of Trauma 1998; 44: 958-63.
Deleu et al. “Neurogenic stunned myocardium following hemorrhagic cerebral contusion,” Saudi Medical Journal, vol. 28, no. 2, pp.
283-285, 2007.
Kocsis et al. Effects of pre-existing brain ischaemia on sympathetic nerve response to intracranial hypertension. Journal of Applied
Physiology 1991; 70: 2181-7.

10. 
Cushing’s phenomenon revisited
(N=16047, Valid Records=10200)
Bhandarkar et al. On-admission blood pressure and pulse rate in trauma patients and
their correlation with mortality: Cushing's phenomenon revisited. Int J Crit Illn Inj Sci
2017;7:14-7.

11. Cushing’s phenomenon revisited
(N=16047, Valid Records=12/10200)
Bhandarkar et al. On-admission blood pressure and pulse rate in trauma patients and
their correlation with mortality: Cushing's phenomenon revisited. Int J Crit Illn Inj Sci
2017;7:14-7.

12. Cushing’s phenomenon revisited
(N=16047, Valid Records=12/10200)
Bhandarkar et al. On-admission blood pressure and pulse rate in trauma patients and
their correlation with mortality: Cushing's phenomenon revisited. Int J Crit Illn Inj Sci
2017;7:14-7.

13.  In TBI, up to 73% of patients will demonstrate ECG changes*
 Sinus tachycardia
 Ischaemic mimics
 Repolarization abnormalities (i.e. ST segment changes,
pathological T waves, QTc prolongation and U waves )**
 Prolonged QTc syndrome may predispose to ventricular
arrhythmias***
 ECG changes correlate with the severity of TBI and poorer
outcomes****
ECG
*Fan X, Du FH, Tian JP. The electrocardiographic changes in acute brain injury patients. Chin Med J (Engl) 2012; 125:3430-3433.
**Fan X, Du FH, Tian JP. The electrocardiographic changes in acute brain injury patients. Chin Med J (Engl) 2012; 125:3430-3433.
**Krishnamoorthy V, Prathep S, Sharma D, et al. Association between electrocardiographic findings and cardiac dysfunction in adult
isolated traumatic brain injury. Indian J Crit Care Med 2014; 18:570-574.
***Collier BR, Miller SL, Kramer GS, Balon JA, Gonzalez LS. Traumatic subarachnoid hemorrhage and QTc prolongation. Journal of
Neurosurgical Anesthesiology 2004; 16: 196200.
****Krishnamoorthy V, Prathep S, Sharma D, et al. Association between electrocardiographic findings and cardiac dysfunction in
adult isolated traumatic brain injury. Indian J Crit Care Med 2014; 18:570-574.

14.  Echographic findings are often transient but are associated with
significant mortality*
 Regional wall motion abnormality (RWMA)**
Echographic findings
*Prathep S, Sharma D, Hallman M, et al. Preliminary report on cardiac dysfunction after
isolated traumatic brain injury. Crit Care Med 2014; 42:142-147.
*Clifton GL, McCormick WF, Grossman RG. Neuropathology of early and late deaths after
head injury. Neurosurgery 1981; 8:309-314.
**Krishnamoorthy V, Prathep S, Sharma D, Gibbons E, Vavilala MS. Association between
electrocardiographic findings and cardiac dysfunction in adult isolated traumatic brain
injury. Indian J Crit Care Med 2014;18:570-4

15.  Most of the data from SAH
 Elevation of cardiac troponin I (cTnl)
 Usually peaks within 24-36 h
 Possibility to explore the role biomarkers of cardiac origin in TBI
Biomarkers of cardiac injury
Bruder N, Rabinstein A. Cardiovascular and pulmonary complications of aneurysmal
subarachnoid hemorrhage. Neurocrit Care 2011; 15: 257-69

16.  Differentiating between neurogenic and coronary events*
 No history of cardiac problems,
 Temporal relationship between brain injury and cardiovascular
abnormalities
 ECG changes in isolation,
 Modest elevations in cTnI,
 New onset LV dysfunction
 Cardiac wall motion abnormalities that do not correspond with coronary
vascular territories,
 Inconsistency between echocardiographic and ECG findings
 Inconsistency between cTnI and LV ejection fraction
Management
*Tamsin Gregory. Cardiovascular complications of brain injury
**Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al., Neurocritical Care Society. Critical care management of
patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care
Society’s Multidisciplinary Consensus Conference. Neurocrit Care 2011; 15:211240.
***Nguyen H, Zaroff JG. Neurogenic stunned myocardium. Curr Neurol Neurosci Rep 2009; 9: 486-91

17.  Treatment of the underlying brain injury*
 Hemodynamic optimization (Avoid hypovolemia)**
 The abnormalities are usually reversible
 Coronary angiography is the definitive diagnostic test to
exclude coronary artery disease but is seldom indicated in this
high-risk group of patients***
 In any case, the presence of significant coronary artery disease
does not exclude co-incidental neurogenic stunned
myocardium
Management
*Tamsin Gregory. Cardiovascular complications of brain injury
**Diringer MN, Bleck TP, Claude Hemphill J 3rd, et al., Neurocritical Care Society. Critical care management of
patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care
Society’s Multidisciplinary Consensus Conference. Neurocrit Care 2011; 15:211240.
***Nguyen H, Zaroff JG. Neurogenic stunned myocardium. Curr Neurol Neurosci Rep 2009; 9: 486-91

18.  Cardiac injury is common in patients with severe head trauma
 It is associated with increased mortality.
 Abnormal echocardiographic findings
 Neurogenic hypotension needs to explored further
 What is unclear is whether neurogenic cardiac injury is
independently associated with poor outcome or whether it is
an epiphenomenon reflecting the severity of the underlying
brain injury
Conclusion

19.  Entire team of WACEM 2018
 Dr Sagar Galwankar
 Research Team, Narayana Medical College and Hospital, Nellore
Acknowledgement