3. Stages Pathogenesis Symptoms Signs
Proposed
Therapeutic
Strategies
Based on Limited
Data
1
Viral response/early
infection
Constitutional
Respiratory
Gastrointestinal
Mild leukopaenia,
lymphopenia.
Elevated PT, D
dimer, LDH, CRP;
ferritin;
IL6.Procalcitonin
may be normal
Antimicrobial
therapy
Reduce
Immunosuppressan
ts if needed
2
Inflammatory
phase/pulmonary
phase
Shortness of breath
Hypoxia:
PaO2/FiO2 ratio <
300
Increasing
Inflammatory
markers including
cardiac biomarkers
(Troponin, BNP)
Abnormal CT chest
Supportive care.
Restrictive IV fluid
strategy.
Antimicrobials,
Immunotherapy per
ID.
3
Hyperinflammatory
phase/Cytokine
release storm
ARDS
SIRS, Sepsis
Cardiac failure
Multiorgan
dysfunction,
Shock, DIC
Markedly elevated
inflammatory
markers, cardiac
biomarkers
Antimicrobial,
Immunotherapy per
ID.
Supportive care
including
vasoactive drips if
indicated.
Table 1
Stages of COVID-19 infection.
4. 1. SARS-CoV-2 is an enveloped, positive-sense single-stranded
RNA virus.9 SARS-CoV-2 and other similar coronaviruses
use the ACE 2 (ACE2) protein for ligand binding before
entering the cell via receptor-mediated endocytosis.
2. More than 7.5% of myocardial cells have positive ACE2
expression, based on single-cell RNA sequencing, which
could mediate SARS-CoV-2 entry into cardiomyocytes and
cause direct cardiotoxicity.
8. Chest PainKey points•
Chest pain and breathlessness is a frequent symptom inCOVID-
19infection;
Chronic and acute coronary syndrome presentations can be associated
with respiratory symptoms.
The symptom of chest pain or tightness is common in patients with
activeCOVID-19infection. It is usually poorly localized and may be
associated with breathlessness due to the underlying pneumonia.
Electrocardiographic changes suggestive of myocardial ischaemia.
Where biomarkers are altered, Type 2 myocardial infarction (MI) may
be suggested
9. The same ECG diagnostic criteria for cardiac
conditions apply in patients affected by the SARS-
CoV-2 infection and in the general population.
10. Prolonged QTc
• monitoring at least daily QT assessment
•• Monitor electrolytes; Keep K >4.5, Mg >2.2
•• Monitor for QT prolongation if on QT prolonging medications
•• QTc=QT/√RR interval (in sec, Bazett correction). QTc will
approximately be equal to QT if HR 60–70 bpm.
•
Key thresholds:• If QTc ≥470 ms in males and ≥480 ms females
but <500 ms: close surveillance and stop QT prolonging
medications
•• If QTc >500ms or >550 ms with BBB or increase in QTc >60 ms
after drug initiation: place pacer pads, stop QT prolonging
medication and maintain HR >80 bpm with isoproterenol or
dobutamine.
11.
12. Polymorphic VT
Sustained VT
Ventricular fibrillation
Torsades de Pointes (TdP)
•• Amiodarone bolus 150 mg IV Isoproterenol + Lidocaine or
temporary pacing if bradycardia induced torsade de pointes.
•• Monitor electrolytes: Keep K >4.5, Mg>2.2
•• VT: Amiodarone 150 mg bolus then infusion 1 mg/min if
QTc<450 ms (300 mg IV i; Avoid amiodarone if QTc markedly
prolonged.
•• VT: Lidocaine if QTc>550 ms: bolus 75–100 mg then infusion
0.5–2 mg/min, avoid if poor hepatic function or severe heart
failure
•• TdP/polymorphic VT: Maintain heart rate of >80 bpm (may
need beta agonist such as dobutamine, isoproterenol or
epinephrine; transvenous pacing).
•• Magnesium IV 2–4 gm for Torsade de Pointes
••
13. Do not perform routine cardiac imaging in patients with
suspected or confirmed COVID-19.
Perform imaging studies in patients with suspected or
confirmed COVID-19 only if the management is likely to be
impacted by imaging results.
The imaging protocols should be kept as short as possible.
Non-urgent or elective cardiac imaging should not be
performed routinely in patients with suspected or
confirmed COVID-19 infection. Accordingly, non-urgent or
elective exams should be postponed until the COVID-19
infection has ceased
14. Cardiac troponin T/I andBNP/NT-proBNPconcentrations
should be interpreted as quantitative variables;
In patients hospitalized withCOVID-19, mild elevations in
cardiac troponin T/Iand/orBNP/NT-proBNPconcentrations
are in general the result of pre-existing cardiac disease
and/or the acute injury/stress related toCOVID-19;
15. Marked elevations in cardiac troponin T/I concentrations
(e.g. > 5 times theULN) may indicate the presence of shock
as part ofCOVID-19, severe respiratory failure, tachycardia,
systemic hypoxaemia, myocarditis, Takotsubo syndrome
orT1MI triggered byCOVID-19.
In the absence of symptoms or ECGchanges suggestive of
T1MI, echocardiography should be considered in order to
diagnose the underlying cause.
16. Severe COVID-19 disease is associated with features of
disseminated intravascular coagulation (DIC) and
hypercoagulable states which can manifest as venous
thromboembolism (VTE) and/or microthrombosis.
•Critically ill patients with COVID-19 have been reported to
have a VTE incidence rate around 30% which is significantly
higher than non-COVID-19 critically ill populations
17.
18.
19.
20. There is currently no evidence to suggest that
hypertension per se is an independent risk factor for severe
complications or death from COVID-19 infection;
Despite much speculation, evidence from a recently
published series of observational cohort studies suggests
that prior or current treatment with ACEIs or ARBs does
not increase the risk of COVID-19 infection when
compared to the risk in patients taking other
antihypertensive drugs
21.
22.
23.
24. Cardiovascular concerns Treatment considerations
STEMI and NSTEMI Primary PCI vs thrombolytics
Myocardial injury Worse prognosis, monitoring rising trends
Hypercoaulable state Thromboprophylaxis
ACEI or ARB use Continue treatment currently, await further studies
HCQ, CQ and/or azithromycin use QTc monitoring, avoid other QTc prolonging drugs
Immunosupression/Immunomodulation Maybe helpful in selected patients with cytokine
storm
MCS IABP and VA ECMO might be used for support in
cardiogenic shock
Cardiovascular considerations in treatment
Possible mechanisms of cardiovascular injury due to COVID-19. DIC, disseminated intravascular coagulation; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.
