After reading through findings in the Chinese clinical report recommended by the American Cardiology Association, and listening to the webinar from March 18 2020, here is a summary of what was presented. Please feel free to question, comment and correct these points by commenting below, as I am simply trying to create a quick summary based on the presentation for those who are not able to watch the two hour-long webinar. Feel free to use this as a starting point and modify as additional reliable studies are released. For those wanting to monitor their vitals at home, please refer to diagnostic questionnaires provided by your healthcare providers, or use this table as a start and consult your clinician to add or modify parameters.

Recommended workflow for the pandemic:

• Non-symptomatic patients: Asked stay home, avoid unnecessary hospitalization. (Honest rational notes to stay informed and monitor vitals in case a clinic visit becomes necessary).
• Symptomatic patients: Patients with fever or respiratory issues asked to visit fever clinics that were set up at the entrance of hospitals to determine whether a patient was a high risk case based on temperature determination at the clinic’s entrance.
• Patient consultation: Do routine blood work, take CT scan of the chest, and assess travel history for contact tracing.
• Suspected COVID-19 cases: Isolate patients in separate area or clinic equipped with catheterization lab.
• Confirmed COVID-19 cases: Isolation of patients in situ (in the original location).

Suspected case parameters: While conducting both nucleic acid and antibody testing with patient samples (blood, stool, urine), doctors used the following parameters to label patients as suspected COVID-19 cases:

(a) contact tracing of patients with a travel history or residential history in Wuhan or communities where COVID-19 has been found in a 14-day period,

(b) clinical symptoms such as fever or respiratory problems, and

(c) blood panel results to check for normal/decreased White Blood Cell and Lymphocyte counts.

Confirmed case parameters: If patient has the etiology evidence above, then additional information from antibody and nucleic acid testing were used to confirm suspected COVID-19 cases. Antibody testing is seen to prevent false negatives from nucleic acid testing, but patients with steroids in their system may create a false positive result with antibody testing. Several questions remain unanswered as to the nature of the nucleic acid testing, such as whether the testing parameters and evaluation criteria for the viral tests have been or can be standardized.

Recommendations on what to monitor in severe COVID-19 cases:

(a) White Blood Cell and Lymphocyte counts, abnormal coagulation via increased D-dimer formation

(b) Biochemical indicators (liver, myocardial enzymes and renal function),

(c) inflammation markers (serum ferritin, interleukin-6, cytokine production), and

(d) chest imaging.

Treatment options for severe or critical COVID-19 cases:

(a) Respiratory and circulatory support.

(b) Renal replacement therapy

(c) convalescent plasma and blood purification treatment

(d) immunotherapy

Antiviral interventions: No evidence-based medicine data as of March 18 2020, trials ongoing (Remdesvir).

Discharge criteria: Body temperature normal for more than three days, improvement of respiratory and pulmonary systems, and no viral nucleic acids found in patient respiratory specimens for two consecutive days, and 24 hours between each test. Doctors saw that some patients who initially tested negative in nucleic acid and antibody tests then tested positive when returning to the clinic. Permanent damage to heart may occur over in patients.

Biggest point of confusion in video at the 1 hour 3 minute point: Why does the self-management quadrant at the top left state that we need to “Induce COVID-19 infection,”???? Did the presenter mean *reduce* COVID-19 infection? If you have any feedback, please comment below.

Here are other notes taken during the video, feel free to add or edit by commenting below:

1. Both oral and written reports prepared in seven editions by medical doctors working in Wuhan, China over a two month period.
2. Sars-CoV-2 is 80% genetically identical to SARS, and seems to be most susceptible to alcohol and surfactant based cleaning.
3. Droplets from, and close contact with, infected people are biggest form of transmission, N95 masks are best for healthcare workers to prevent their infection and death.
4. 80% of cases were mild with no pneumonia, rest needed respiratory/ventilator help for 13 days.
5. Infections can last up to 37 days, survivors still had cough after hospital discharge
6. Viral particles released by infected cells are causing severe inflammatory response in lung, heart, liver and kidney tissues. Hypoxia-induced myocardial injury, and cardiac microvascular damage seen.
7. COVID-19 may cause sepsis, cardiac and kidney injury as additional complications of viral sepsis
8. Viremia (viral RNA in blood) seen.
9. CT scan of lungs show rapid organ deterioration in critical cases (24 hours to two weeks), possibly monitor decrease in pericardial adipose tissue as this has been seen with severe COVID-19 cases.
10. Decreased lymphocytes, unsure whether this is a direct or immune-modulated response
11. IgM/IgG kinetics- IgM higher and IgG lower, but level flips after two weeks
12. TNF-alpha and Interleukin-2 are amongst the inflammatory responses from infection, T cells severly decreased, cytokine storm in patient.
13. Over-expression of ACE-2 receptors in vascular endothelial cells, as expected since this is also seen with previous SARS infections.
14. Abnormal coagulation due to increased d-dimer formation, so need to carefully monitor antiplatelet drugs and statins.
15. Lopinavir and Ritonavir may lower heart rate, incease blood lipid levels, and may also increase liver injury for those taking statins.
16. Chloroquine may cause sudden cardiac death.
17. Corticosteroids usage is still debated due to contraindications.
18. Anti-RAS medications inhibit angio-II activity and reduce lung inflammation, but inhibition of angio-II may increase ACE2 mediated SARS-CoV-2 viral infection.
19. Spike proteins in SARS-CoV-2 virus mediate ACE2 based infections, as also seen with previous SARS cases. Previous SARS cases display chronic cardiovascular organ damage.