Understanding Cardiovascular Symptoms During Recovery from Covid-19

Post Covid-19 cardiovascular symptoms are a growing concern noted in as many as one fourth of patients hospitalized with the virus and accounting for up to as much as 40 % of all Covid -19 deaths (Williamson, L. 2020). Symptoms expressed include dizziness up to and including syncope, palpitations, irregular heartbeat, shortness of breath and chest pain. Cause has been linked to post viral inflammation in as many as 60% of these patients (Williamson, L. 2020). Dr. Nisha Parikh from the University of California San Francisco states that often Echo, EKG and other traditional cardiac work up may be normal, yet symptoms persist. She also suspects an inflammatory mechanism of injury and reports that people have died unexpectedly post discharge following normal findings with conventional cardiac evaluations.

The goal of this paper is to describe autonomic measurements for patients presenting to Stern Cardiovascular Foundation who have survived Covid-19 and are presenting for evaluation with symptoms mentioned above. Standard thorough cardiac evaluation is performed and if warranted the patient is then sent to the autonomic lab for measurement of neurovascular integration. Similarities in presentation for post Covid-19 patients includes debilitating fatigue, dizziness, syncope, palpitations, labile blood pressure, gastric complaints and sleep dysregulation. Sleep issues are often described as sudden awakenings with tachycardia, palpitations and difficulty going back to sleep.

Autonomic evaluations for post Covid patients consistently demonstrate low parasympathetic tone. This is measured as low heart rate variability, persistent elevation in diastolic blood pressure with upright position and neurogenic changes in blood pressure with upright position with no compensatory change in heart rate.

These changes in autonomic tone have long been described following Epstein Barre Virus (Freeman, 2003). Post viral autonomic injury is an inflammatory response. Resultant oxidative stress leads to damage to the parasympathetic nervous system, in particular vagal output. The above symptoms and autonomic measurements following Covid-19 are consistent with expected post viral decline in parasympathetic tone. Efficacy in treating this population requires a neurovascular strategy which includes cholinergic support and treatments aimed at reversing inflammatory damage.

Additionally, low heart rate variability, described as part of the Framingham Study and throughout recent cardiac literature, is an independent risk factor for sudden cardiac death (Hillebrand, 2013). Heart rate variability is determined by parasympathetic tone. Could this be a possible explanation for unexpected deaths post discharge? It is hoped that this perspective for treatment will be implemented in addition to current regimens and that symptoms will resolve, outcomes improve and lives saved with this approach.

Debra Turner DNP,FNP-C
Stern Cardiovascular Foundation