COVID-19: Epidemiology and pathophysiology: Difference between revisions
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*[[Cytokine release syndrome|Cytokine Storm]] | *[[Cytokine release syndrome|Cytokine Storm]] | ||
{{COVID-19 Lung Phenotypes}} | {{COVID-19 Lung Phenotypes}} | ||
Revision as of 12:42, 16 January 2021
Virology
- Coronaviruses are common human pathogens
- Cause the common cold
- In epidemics, cause up to one-third of community-acquired upper respiratory tract infections in adults; and may cause diarrhea in infants and children
- SARS-CoV-2 is a novel coronavirus (a new strain not previously identified in humans)
- Likely primary source = bats
- It is a betacoronavirus in the same subgenus as the severe acute respiratory syndrome (SARS) virus. Middle East respiratory syndrome (MERS) virus is another, more distantly related, betacoronavirus. Like the SARS coronavirus, SARS-CoV-2 uses angiotensin-converting enzyme 2 [ACE2] for cell entry
Pathophysiology
- ARDS - Possibly due to direct alveolar damage by the virus AND inflammatory reaction. [1]
- Cytokine Storm
COVID Lung Phenotypes and Their Management
Hypoxemic patients can be divided into two general phenotypes[2]
COVID L Lung Phenotype
- Characterized by Low elastance (i.e., high compliance), Low ventilation to perfusion ratio, Low lung weight and Low recruitability
- Often referred to as the “happy hypoxemic”
- Normal lung volumes and low lung recruitability.
- Hypoxemia may be due to loss of regulation of perfusion and loss of hypoxic vasoconstriction.
- These patients can be damaged iatrogenically if you respond to their pulse ox with standard vent modes
- Do poorly with low tidal volume (TV) and high PEEPs
- Best managed with high FiO2 which allows you to limit the PEEP
- Recommended initial vent settings:
- 8 ml/kg TV, 100% FiO2
- Increase the PEEP only if the patient is desaturating on a high FiO2.
- Can turn into COVID H patients on the vent.
COVID H Lung Phenotype
- Characterized by High elastance, High right-to-left shunt, High lung weight and High recruitability.
- Increased permeability of the lung leads to edema, atelectasis, decreased gas volume, and decreased TV for a given inspiratory pressure.
- High degree of lung recruitability.
- 20 – 30% of patients fit ARDS criteria:
- Hypoxemia
- Bilateral infiltrates
- Decreased the respiratory system compliance
- Increased lung weight and potential for recruitment
- The ARDS ladder applies only to this subset of COVID patients.
Epidemiology
- Disease Severity
- 80% have mild symptoms
- 15% have severe disease requiring hospitalisation
- 5% require mechanical ventilation
- Risk Factors
- Older age
- Underlying conditions (lung disease, Renal Failure, Malignancy, heart disease, diabetes)
- Reproduction Number (R0) SARS-CoV-2:
- R0 = 2.2 - 4.2
- Where R0 = expected number of secondary cases produced by a single typical infection in a susceptible population (basic reproductive rate)
- R0 for seasonal flu ~ 1.3
- R0 for pandemic flu ~ 1.5-1.8
- Incubation Period:
- Incubation = 5 days (median); range of 2-14 days
- Serial interval duration = 7.5 days
- Serial interval refers to the time from illness onset in successive cases in a transmission chain
- Surface survival time of SARS-CoV-2:
- stainless steel: persists for 3 hours (or longer)
- underscores the importance of environmental cleaning / disinfection
- cleaning gets rid of the proteins that would interfere with a disinfectants effectiveness
- How long to shut a patient room down after a COVID patient is in there?
- It’s not about the risk of contracting the infection but about the ability to clean room safely without respiratory protection precautions by the cleaner
- 30-40 minutes usually sufficient (for most modern facilities) as long as no aerosol-generating procedure performed (longer, time not clearly stated at this time)
- Most modern rooms designed to have 12 air exchanges per hour
- Ventilation symptoms vary. So, older / fewer exchanges per hour => more time.
- Note: studied in a simulated lab environment. Lab virions not covered in protein and mucus and other things that would mimic real life and that could prolong survival
See Also
References
- ↑ Xu Z, Shi L, Wang Y et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. The Lancet Respiratory Medicine. 2020;8(4):420-422. doi:10.1016/s2213-2600(20)30076-x
- ↑ Gattinoni L et al. Covid-19 pneumonia: different respiratory treatment for different phenotypes. Intensive Care Medicine. 2020. https://www.esicm.org/wp-content/uploads/2020/04/684_author-proof.pdf