ECG in Weakness and Neurological Symptoms

In this ECG Cases blog we review how the ECG can help in diagnosing a variety of causes of generalized weakness and acute neurological symptoms.

Written by Jesse McLaren; Peer Reviewed and edited by Anton Helman. September 2023

10 patients presented with generalized weakness or acute neurological symptoms. What does the ECG show, and how does this help guide diagnosis and management?

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Case 2: 75 year old with generalized weakness for days and not eating. Old then new ECG:

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Case 3: 25 year old with anorexia nervosa, presenting with generalized weakness

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Case 4: dialysis patient with generalized weakness and paresthesias. Old then new ECG:

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Case 5: 50 year old, recent unstable angina treated with stent and started on dual anti-platelets, presenting with weakness and dizziness. Prior and new ECG:

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Case 6: 90 year old, remote MI, with generalized weakness and falls, normal vitals. Old then new ECG:

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Case 7: 45 year old with headache and BP 220/130. 15 lead ECG recorded

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Case 8: 60 year old, previously healthy, with dizziness, ataxia and slurred speech

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Case 9: 80 year old, chest pain two days prior, now presenting with hemiparesis

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Case 10: 90 year old previously healthy, found aphasic and with hemiparesis

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The ECG in weakness and neurological symptoms

The ECG is a quick an easy test to get for patients with generalized weakness or acute neurological symptoms. Interpreting the ECG can be more challenging, but is vital for the early diagnosis and risk stratification of electrical, metabolic, cardiovascular and neurological emergencies.

ECG in generalized weakness

1. Dysrhythmias, fast and slow

General weakness can be associated with bradyarrhythmias/block (including from secondary causes like hyperkalemia or acute coronary occlusion) and tachyarrrhythmias. Weakness in patients with atrial fibrillation could be from slow ventricular response requiring pacemaker or reduction of AV nodal blockers, or fast ventricular response where the first step is to identify and treat secondary causes.

2. Electrolyte emergencies

Weakness can also reflect electrolyte emergencies. Hypokalemia can produce peaked P waves, ST depression, flat/flipped T waves, and prominent U waves – whereas hyperkalemia can produce absent P waves, bradycardia, conduction abnormalities, ST elevation and peaked T waves. Hypercalcemia shortens the ST segment while hypocalcemia elongates it. Patients with end stage renal disease are at risk for the combination of hyperkalemia/hypocalcemia – with a long ST segment followed by a narrow peaked T wave – both of which are improved with calcium

3. Cardiovascular emergencies and demand ischemia

Like shortness of breath and epigastric pain/vomiting, weakness can be an anginal equivalent – with the ECG revealing acute coronary occlusion.

Whereas diffuse ST depression with reciprocal ST elevation in aVR is a nonspecific sign of subendocardial ischemia – which in the context of weakness could be secondary to demand ischemia states like GI bleed or sepsis, as well as cardiac ischemia including triple vessel disease.

ECG in neurological symptoms

Assessing acute neurological symptoms puts attention on the brain, but we can’t forget about the heart. Headaches can be associated with hypertension and the ECG might reveal longstanding LVH (though headache alone doesn’t qualify as a hypertensive emergency). Seizure-like activity can be caused by syncope from heart block, Brugada syndrome or polymorphic VT with long QT.[1] Or true seizures can have ECG changes reflecting their cause, eg metabolic, toxic, or raised intracranial pressure.

Stroke or TIA might have a cardiac etiology like atrial fibrillation[2], including paroxysmal Afib only present on prehospital ECGs[3]. Stroke and MI can occur simultaneously from aortic dissection, but the more likely cause is LV thrombus from old or subacute anterior MI. As the American Heart Association explains, “the severity and extent of cardiac injury increase the risk of developing an LV thrombus…Larger injury (higher peak troponins), delayed reperfusion attributable to late presentation, and faint or no antegrade coronary flow (TIMI grade 0 or 1) after reperfusion are other risk factors.”[4]

The causal effect can also be reversed, with spontaenous or traumatic neurological emergencies causing cardiac complications like stress-induced cardiomyopathy, with QT prolongation and anteroapical T wave inversion.[5-7]

Back to the cases

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Case 2: 75 year old with weakness for days and not eating – with AF and rapid ventricular response secondary to dehydration

• H: new atrial fibrillation with rapid ventricular response
• E: old RBBB
• A: old left axis from inferior Q
• R: early R waves from RBBB
• T: normal voltages
• S: secondary repolarization abnormalities

Impression: AF with rapid ventricular response secondary to dehydration. Initially treated with fluids, later rate control. Repeat ECG:

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Case 3: 25 year old with anorexia nervosa, presenting with generalized weakness – from hypokalemia

• H: sinus bradycardia
• E: pseudo-long QT from prominent U wave (eg lead II)
• A: normal axis
• R: normal R wave progression
• T: prominent P waves
• S: T waves flat, inverted in V3-4

Impression: weakness with multiple signs of hypokalemia. Potassium was 2.4, and ECG normalized after potassium replacement:

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Case 4: dialysis patient with generalized weakness and paresthesias. Old then new ECG:

• H: borderline sinus tach
• E: long ST segment
• A: right axis deviation
• R: normal R wave progression
• T: normal voltages
• S: diffuse peaked T waves

Impression: dialysis patient with long ST and peaked T waves (and new axis deviation), from hyperkalemia (6.6) and hypocalcemia (1.8mmol/L). ECG normalized after calcium and dialysis.

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Case 5: 50 year old, recent unstable angina treated with stent and started on dual anti-platelets, presenting with generalized weakness and dizziness. Prior and new ECG:

• H: borderline sinus tach
• E: normal conduction
• A: normal axis
• R: normal R wave progression
• T: normal voltages
• S: inferolateral primary ST depression with reciprocal ST elevation in aVR

Impression: nonspecific subendocardial ischemia in post-PCI patient with weak and dizziness. POCUS showed hyperdynamic heart and labs revealed significant drop in hemoglobin. Patient diagnosed with upper GI bleed secondary to anti-platelets, and ECG normalized after fluid resuscitation.

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Case 6: 90 year old, remote MI, with generalized weakness and falls, normal vitals. Old then new ECG:

• H: normal sinus with PVCs
• E: IVCD
• A: left axis from LAFB
• R: old anterior Q wave
• T: normal voltages
• S: anterolateral ST elevation and hyperacute T wave (including concordant ST elevation in the PVC), with inferior reciprocal ST depression

Impression: proximal LAD occlusion. Because of the Q waves and the presentation with weakness, these changes were assumed to be old, and initial troponin of 65ng/L (normal <26 in males and <16 in females) was attributed to demand ischemia. Troponin rose to 160,000 and echo showed new anterolateral regional wall motion abnormality corresponding to LAD occlusion, but patient was treated medically due to age. Discharge ECG had further Q waves across the precordium:

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Case 7: 45 year old with headache and BP 220/130. 15 lead ECG recorded

• H: normal sinus
• E: normal conduction
• A: right axis from right arm/left arm reversal (P wave inverted in I and upright in aVR)
• R: normal R wave progression
• T: LVH
• S: discordant and proportional ST/T wave changes

Impression: LVH with limb lead reversal, falsely labeled as STEMI. Patient had no cardiorespiratory symptoms, so stat cardiology consult. Repeat 12-lead ECG with correct lead placement confirmed LVH with secondary repolarization abnormalities.

Serial troponins were normal and echo revealed concentric LVH without wall motion abnormalities, and patient admitted for BP control due to acute renal failure.

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Case 8: 60 year old, previously healthy, with dizziness, ataxia and slurred speech

• H: atrial fibrillation with normal ventricular response
• E: incomplete RBBB
• A: normal axis
• R: small R waves V2-3 but normal R wave progression
• T: normal voltages
• S: no ST/T changes

Impression: stroke symptoms with new atrial fibrillation. CT revealed cerebellar stroke

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Case 9: 80 year old, chest pain two days prior, now presenting with hemiparesis

• H: normal sinus rhythm
• E: normal conduction
• A: physiological left axis
• R: loss of anterior R waves
• T: normal voltages
• S: anterolateral ST elevation and hyperacute T waves, with reciprocal ST depression III/aVF

Impression: stroke symptoms with chest pain two days prior, and ECG revealing subacute but ongoing LAD occlusion. Code STEMI and code stroke activated: CT head showed acute stroke, and angiogram showed 100% proximal LAD occlusion. Echo showed anterior regional wall motion abnormality, EF 30% and apical thrombus. First troponin was 22,000ng/L and rose to 50,000. Discharge ECG showed ongoing LV aneurysm morphology (QS waves with residual ST elevation), with reduction in hyperacute T waves but failure to develop reperfusion T wave inversion:

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Case 10: 90 year old previously healthy, found aphasic and with hemiparesis

• H: borderline sinus tach
• E: RBBB
• A: left axis from LAFB
• R: early R wave from RBBB, but preceded by anterior Q waves
• T: normal voltages
• S: anterolateral ST elevation, with reciprocal ST depression III/aVF

Impression: RBBB/LAFB/anterolateral ST elevation, a high risk pattern seen in proximal LAD or left main occlusion, in a patient with stroke symptoms. Stat cardiology consultation and stat CT head/chest: CT head showed acute stroke, CT chest ruled out aortic dissection, and then cath lab activated: 100% proximal LAD occlusion, and patient arrested.

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Take home points for ECG in Generalized Weakness and Neurologic Symptoms

1. Generalized weakness: look for ECG signs of dysrhythmias, electrolyte emergencies, acute coronary occlusion, and demand ischemia
2. Acute neurological symptoms: consider predisposing factors like LVH; seizure-like activity from cardiac syncope; TIA/CVA embolic sources like atrial fibrillation or LV thrombus; or cardiac complications like stress-induced cardiomyopathy

References for ECG Cases 45 ECG in Weakness and Neurological Symptoms

1. Wong SH, Adams P, Jackson M. The electrocardiograph (ECG) in a first seizure clinic. Seizure 2008 Dec;17(8):707-710
2. Sposato LA, Ciprinano LE, Saposnik G, et al. Diagnosis of atrial fibrillation after stroke and transient ischaemic attack: a systematic review and meta-analysis. Neurol 2015;14:377-87
3. Bobinger T, Kallmunzer B, Kopp M, et al. Diagnostic value of prehospital ECG in acute stroke patients. Neurology 2017 May 16;88(20):1894-1898
4. Levine GN, McEvoy JW, Fang JC, et al. Management of patients at risk for and with left ventricular thrombus: a scientific statement from the American Heart Association. Circulation 2022;146:e205-e223
5. Perron AD, Brady WJ. Electrocardiographic manifestations of CNS events. Am J of Emerg Med 2000 Oct;18(6):715-720
6. Goldberger ZD, Creutzfeldt CJ, Goldberger AL. Catastrophic neurological syndrome with dramatic ECG changes. J Electrocardiol 2014 Jan-Feb;47(1):80-83
7. Lee JH, Lee DH, Lee BK, et al. Role of electrocardiogram findings in predicting 48-h mortality in patients with traumatic brain injury. BMC Neurology 2022;22