The document discusses COVID-19 and its impact on the cardiovascular system. It covers the epidemiology of COVID-19 and how it can lead to myocardial infarction through several pathways. The pathophysiology involves three phases - early infection, pulmonary, and hyperinflammation - that can result in direct myocardial injury, cytokine storm, or stress-induced cardiomyopathy. Those at highest risk are the elderly, those with pre-existing cardiovascular conditions, and those with other comorbidities. Assessment of cardiac issues in COVID-19 patients involves evaluating symptoms like chest pain and dyspnea, as well as diagnostic tests. Management depends on the specific cardiovascular presentation, such as protocols for STEMI patients or those with cardiogenic shock.

1. COVID and Myocardial Infarction
JASMIN ANAND

2. “Nothing in life is to be feared; it is only to be
understood. Now is the time to understand
more, so that we may fear less.” —
Marie
Curie

3. • Introduction
• Epidemiology
• Structure of COVID
• Pathophysiology
• What happens in the CVS
• MI –Etiology
• Assessment
• Management
• Recovery
• Rehabilitation

4. • COVID is a pandemic since March11, 2019 as declared by WHO
• Human to human transmission is intense by way of droplet infection
• Incubation period is 4-5 days although it may continue for 14 days
• Affected patients have fever, dry cough, dyspnea, headache
and pneumonia, similar to SARS epidemic in 2003
• Case-fatality ratio is highly variable depending on how the
cases are defined, the testing practices, the health system
access and other unknown factors.
• The interaction between COVID-19 and the cardiovascular
system has been a subject of special attention right from the
beginning
INTRODUCTION

5. EPIDEMIOLOGY
• GENDER – Male > Female cause Unknown
> mortality
• AGE - 2-3% in patients < than 19 years of age have a risk of hospitalization
2-45 % in ages 20-45 yrs.
11% to 31% in ages 75 to 84 yrs.
31% in patients > than 85yrs.
Case fatality rates of 0.1% to 0.2% in patients less than
44 yrs. and 10.4% to 27.3% in patient 85 years or older.
( Recently there have been reports of a rare multi‐system inflammatory syndrome
associated with COVID‐19 disease resembling Kawasaki disease in children.)

6. EPIDEMIOLOGY : SOCIOECONOMIC FACTORS
•Nursing Homes and Assisted living facilities
• Inmates and correctional staff in prisons
• Homeless shelters
Low Socio‐economic factors have been shown to
worsen outcome with COVID‐19 disease.

7. Epidemiology - Co‐morbidities
Mortality Rates
•Cardiovascular disease -10.5 %
•Diabetes Mellitus 7.3%
•Hypertension 6%

8. CURRENT STATUS IN THE COUNTRY

10. CORONA VIRUS STRUCTURE
•Coronaviruses are enveloped viruses, minute in size
(65–125 nm in diameter) and contain a single-stranded
RNA as a nucleic material, size ranging from 26 to
32kbs in length
•Enters human cells: by binding to the membrane-
bound aminopeptidase angiotensin-converting
enzyme 2 (ACE2)

11. • COVID-19 results in respiratory illness, but some patients can
have cardiac injury.
• Patients with underlying cardiac disease have worse outcomes
with COVID-19.
• ACHD ( Adult Congenital Heart Disease) patients may be at
increased risk of worse outcomes with COVID-19.
• No treatment exists currently, the focus is on supportive care
and prevention.
International journal of cardiology. The cardiovascular burden of coronavirus disease 2019 (COVID-19) with a
focus on congenital heart disease
COVID & CARDIOVASCULAR SYSTEM

12. PATHOPHYSIOLOGY OF COVID‐19 AND CARDIAC
INVOLVEMENT
Three intermingling phases
1.Early infection phase
2.Pulmonary phase
3.Hyperinflammation phase
The three stages are characterised by a different type
of biological interaction with the virus.

13. PATHOPHYSIOLOGY OF COVID‐19 AND CARDIAC
INVOLVEMENT
1.Early infection phase- virus spread and proliferation in lung
tissues with initial innate immunity including recruitment of
monocytes and macrophages, characterized by mild
constitutional symptoms.
Some early phase symptomatic patients suffer from mild
respiratory symptoms and may require supportive care like
supplemental oxygen followed by an adaptive immunity stage
with falling titers of the virus and resolution of symptoms

14. PATHOPHYSIOLOGY OF COVID‐19 AND CARDIAC INVOLVEMENT
Three intermingling phases
2.Pulmonary phase -The second stage includes several mechanisms leading
to pulmonary tissue injury, vasodilation, endothelial permeability and
leukocyte recruitment that cause further pulmonary damage, hypoxemia,
and cardiovascular stress.
Ten percent may experience further exacerbation of immune response
(hyperinflammation stage) become critically‐ill, and may suffer from ARDS,
acute cardiac injury, multi‐organ failure, secondary bacterial infections,
sepsis and require intensive care

15. PATHOPHYSIOLOGY OF COVID‐19 AND CARDIAC
INVOLVEMENT
Three intermingling phases
3.Hyperinflammation phase .The third, hyperinflammatory phase, occurs
when a hyperactivated immune system may cause injury to the heart,
kidneys, and other organs.
In this phase, a “cytokine storm”occurs where the body attacks its own
tissues
Ten percent of patients in the second stage may experience further
exacerbation of immune response (hyperinflammation stage) become
critically‐ill, and they may suffer from acute respiratory distress syndrome
(ARDS), acute cardiac injury, multi‐organ failure, secondary bacterial
infections, sepsis and require intensive care

18. Stage III and cardiac Involvement ?
• Systemic Inflammation
• Hypoxemia or Lung failure
• Direct Myocardial injury
• Cytokine Storm
• Disseminated Intravascular Coagulation ( DIC )
• Stress Induced Cardiomyopathy

19. WHO IS AT RISK FOR CARDIOVASCULAR COMPLICATIONS ?
Potential Risks
• Old age
• Immunosuppressive Disease
• Hypertension
• CVD
• Obesity
• Renal Abnormalities
• Multiorgan failure
• Chronic Resp.Disease
• DM
• Coagulation Aberration
• Tumor or Cancer
Cardiovascular Complications
• Cytokine storm
• Systemic Inflammation
• Myocardial Infarction
• Heart Failure
• Myocarditis
• Arrhythmia
• Myocardial Injury
• Cardiac Arrest
• Thrombotic Events
• Cardiotoxicity

20. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS
OF COVID‐19

21. Differential diagnosis when in Chest Pain
• Type 1: MI caused by acute atherothrombotic CAD and usually
precipitated by atherosclerotic plaque disruption (rupture or
erosion).
• Type 2: MI consequent to a mismatch between oxygen supply and
demand.
With COVID-19 infection, the majority of MIs are type 2 and related
to the primary infection, hemodynamic, and respiratory
derangement.
If a Type 1 infarction is thought to be the primary etiology of the MI,
standard therapies can be considered.

22. Diagnosis - In-Patient
ASSESSMENT
1.Chest Pain
• Chest pain or tightness ,poorly localized and associated with
breathlessness may be due to the underlying pneumonia.
• Profound hypoxaemia together with tachycardia may result in chest
pain
• When biomarkers are altered, Type 2 myocardial infarction (MI) may
be suggested.
• Patients with ACS do, however, experience the more typical
symptoms related to ischaemia.
The presence of a COVID-19 infection can make the differential
diagnosis more difficult, as shortness of breath and respiratory
symptoms may be present and may precede or precipitate cardiac

23. S Severity
O Onset
C Characteristic
R Radiation
A Associated factors
T Time
E Exacerbating factors
S Severity ( use 1-10 scale )
DIAGNOSIS & ASSESSMENT AT CHEST PAIN TRIAGE

24. Diagnostic Tests as In-Patient

26. Diagnosis - In-Patient
ASSESSMENT
2. Dyspnoea, Cough, Respiratory distress
• COVID-19 patients may present with cough, dyspnoea,
and ARDS
• Dyspnoea 18.7% present with dyspnoea. With
increasing disease severity, the proportion of dyspnoea
significantly increases (31–55% in hospitalized patients
and up to 92% of patients admitted to ICUs).
• Cough is present in 59.4–81.1% of patients
with COVID-19, irrespective of disease
severity. Unproductive (dry) cough is more frequent,
whereas sputum production is present in 23.0–33.7%..

27. Diagnosis - In-Patient
ASSESSMENT
3.Acute Respiratory Distress Syndrome
• ARDS is characterized by bilateral opacifications on chest imaging
(e.g. bilateral ground glass opacifications on CT) and hypoxaemia
that cannot be explained by other causes.
• The median time from disease onset to ARDS is 8–12.5 days.
• The risk of ARDS increases with older age (≥ 65 years old),
presence of comorbidities (hypertension, diabetes), neutrophilia,
lymphocytopenia, elevated laboratory markers of organ
dysfunction (e.g. lactate dehydrogenase [LDH]), inflammation (C
reactive protein) and D-dimer. Mortality of patients treated
for ARDS in COVID-19 is high (e.g. 52–53%).

28. Clinical pathway for suspected or confirmed COVID-19 ST-elevation
myocardial infarction patients

29. Diagnosis - In-Patient ASSESSMENT
4.Cardiogenic Shock (CS)
• In COVID-19 patients with impaired end-organ perfusion is at risk
of cardiogenic shock (e.g. large acute myocardial infarction ),
consider also sepsis as possible or mixed aetiology;
• Myocarditis should be considered as precipitating cause of CS.
• An early, accurate, and rapid diagnosis of CS in patients with
confirmed or suspected COVID-19 is essential. The exact
incidence of CS in these patients is unknown.
However, the median duration between onset of symptoms and
admission to ICU in critically ill COVID-19 patients has been 9–10
days, suggesting a gradual onset

30. Diagnosis - ASSESSMENT
Simple, actionable classification scheme for CS diagnosis .
• In critically ill COVID-19 patients at risk for CS (such as those with
large AMI, acute decompensated HF; ) and sepsis, a mixed aetiology
of CS and septic shock should be considered in addition to the sole
cardiogenic component.
• Parameters for a differential diagnosis between CS and septic shock
is to check for presence of vasodilatation and decreasing central
venous oxygen saturation values

31. Diagnosis - In-Patient
ASSESSMENT
•In patients with unclear reasons for haemodynamic
deterioration,a pulmonary artery catheter may provide
useful information.
• key diagnostic testing in patients with suspected CS, include
electrocardiogram (ECG), bedside echocardiography, and
urgent/emergent coronary angiography (with dedicated
and/or protected equipment)

32. Suspected cardiogenic shock in COVID
patients

33. MANAGEMENT for NSTE ACS

34. Acute Cardiac Injury and Myocarditis in COVID-19
• Can occur several days after initiation of fever (indicates viral
infilteration )
• ACE 2 in the heart and coronary vessels
• Resp.failure & hypoxia may cause damage to myocardium &
immune mechanism with myocardial Inflammation
• Mechanisms of SARS-CoV-2-induced myocardial injury may be
related to ACE2 in the heart and coronary vessels.
• Respiratory failure and hypoxia in COVID-19 may cause damage
to the myocardium and immune mechanisms of myocardial
inflammation
• Cardiac injury leads to activation of the innate immune response
with release of proinflammatory cytokines.

35. Pathophysiology - Mechanism of Disease in Relation with the
Cardiovascular System –KEY POINTS
• SARS-CoV-2 binds to the host receptor angiotensin-converting
enzyme 2 (ACE2) to mediate entry into cells
• ACE2, which is expressed in the lungs, heart and vessels, is a key
member of the renin angiotensin system (RAS) important in the
pathophysiology of CVD;
• CVD associated with COVID-19, likely involves dysregulation of
the RAS/ACE2 system due to SARS-CoV-2 infection & due to
comorbidities, such as hypertension

36. Pathophysiology - Mechanism of Disease in Relation with
the Cardiovascular System –KEY POINTS
• CVD may be a primary phenomenon in COVID-19, but may be
secondary to acute lung injury, which leads to increased cardiac
workload, potentially problematic in patients with pre
existing HF
• Cytokine release storm, originating from imbalance of T cell
activation with dysregulated release of interleukin (IL)-6, IL-17
and other cytokines, may contribute to CVD in COVID-19. IL-6
targeting is being tested therapeutically;
• Immune system activation along with immunometabolism
alterations may result in plaque instability, contributing to
development of acute coronary events.

37. Relationships Between Hypertension, Angiotensin-
Converting Enzyme 2 and COVID-19
• HT and ARDS ( age was not studied )
• No clear evidence that using angiotensin-converting enzyme
inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) lead
to up-regulation of ACE2 in human tissues.
• The available data from blood samples suggest that there is no
association between circulating levels of ACE2 and use
of RAAS antagonists.
• .This is in line with prior guidance from major CV Societies, that
stated that patients on ACEIs or ARBs should not stop their
treatment.51,61

38. Immune System Dysregulation and
Cardiovascular Disease in COVID-19
• Inflammatory mechanisms and activation of immune responses
underlie a large range of CVDs including atherosclerosis, HF and
hypertension.
• This dysregulation may have different degrees in COVID-19. Firstly
another receptor through which SARS-CoV-2 may enter cells is
cluster of differentiation 209 (CD209).
• In severe cases of COVID-19, systemic increases of numerous
cytokines including IL-6 IL-2, IL-7.
• Altered vascular permeability can result in non-cardiogenic
pulmonary oedema and promotes ARDS as well as multi-organ
dysfunction.
• T cell dysfunction & development of CVD.

39. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS OF
COVID‐19
• Myocarditis
• Arrhythmias
• Acute coronary syndrome
• Heart failure

40. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS OF
COVID‐19
2.Arrhythmias
I. Symptomatic/asymptomatic tachycardia.
II. Bradycardia
III. Others
( Arrythmia may occur in the setting of myocarditis, myocardial
ischemia and in critically ill patients with hypoxia and shock.)
Potential causes include electrolyte disturbance (mainly hypokalemia),
adverse effects of therapies (eg, chloroquine/hydroxychloroquine and
azithromycin) that prolong QT interval with potential development of
polymorphic ventricular tachycardia (VT) and fever which may unmask
cases of cardiac channelopathies such as Brugada syndrome and long
QT syndrome.

41. COVID‐19 complicated by acute myocardial infarction with extensive thrombus burden
and cardiogenic shock
Catheterization and Cardiovascular Interventions, First published: 19 May 2020, DOI: (10.1002/ccd.28992)

42. COVID‐19 complicated by acute myocardial infarction with extensive thrombus burden and
cardiogenic shock

43. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS OF
COVID‐19
1.Myocarditis
7% of the COVID‐19‐related deaths are linked to myocarditis.
The spectrum of symptoms may vary from mild symptoms such
as mild chest pain, dyspnea and fatigue to more severe
symptoms with left and right ventricular failure, cardiogenic
shock, arrythmia, and sudden cardiac death with fulminant
myocarditis.
- likely due to a combination of direct cell injury and
T‐lymphocytes‐mediated cytotoxicity - cytokine storm syndrome
- may mimic an acute coronary syndrome with ST segment
elevation and elevated enzymes due to acute cardiac injury and
hence, providers should be aware of this presentation.

44. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS OF
COVID‐19
3. Acute coronary syndrome (STEMI, NSTEMI,unstable
angina )
• There are no clear statistics for STEMI from intracoronary plaque
rupture or obstruction.
• Acute coronary events may be triggered by plaque rupture and
coronary thrombosis due to inflammation/increased shear stress
in high risk patients
Attributed to patients reluctance, delays in evaluating patients
with STEMI after hospital arrival due to precautions such as
detailed travel and contact history, symptomatology, and chest
X‐ray, delayed patient transfer to cath. Lab.& precautions in cath
lab )

45. 4 PECULIAR CARDIAC‐RELATED MANIFESTATIONS OF
COVID‐19
4.Heart failure
There is a lack of data on the incidence of left ventricular systolic dysfunction,
acute left ventricular failure, and cardiogenic shock.
One study demonstrated heart failure in 52% of deceased patients and 12%
of discharged patients. Many critically ill patients may develop reversible
sepsis‐related cardiomyopathy with left ventricular dilatation, impaired
systolic function and recovery within 7 to 10 days.COVID‐19 infection can
cause decompensation of underlying heart failure and may lead to mixed
shock syndrome (combination of septic shock and cardiogenic shock).
Invasive hemodynamic monitoring, if feasible, may be helpful to manage the
cardiac component of shock in such cases.

46. OUTCOMES - CVS
• Long‐term cardiovascular outcome
• It is too early to predict long term cardiovascular outcome for
patients who have recovered from COVID 19 infection, However, the
potential outcome may be similar to that seen in the severe acute
respiratory syndrome (SARS) caused by the SARS‐CoV virus. The
outcome studies of patients who recovered from SARS and were
followed for 12 years showed that 40% had cardiovascular
abnormalities, 60% with altered glucose metabolism and 68% with
abnormal lipid metabolism.2

47. THERAPEUTIC OPTIONS IN COVID TREATMENT:
CARDIAC IMPLICATIONS

48. • Recommended thrombolysis as first choice
• PCI later

50. NURSING CARE
• Triage & Assessment ( “happy hypoxic” patient or “silent hypoxemia”40%-
60%)
• Diagnostic tests
• Precautions & Isolation –Use of PPE (a nasal swab is considered an
“aerosolizing procedure”)
• Vigilance on fast decline of the disease ( Skin findings (rashes and “COVID
toes”) & neurologic findings (altered mental status, dizziness, headache, and
loss of taste/smell)
• Care of the critically ill ( high flow nasal cannula is preferred ),negative
pressure rooms, Proning, avoiding aggressive fluid administration, PEEP
,avoid frequent auscultation)
• Unit setup for COVID care

51. NURSING CARE
• Drug Therapy –watching for complications ( QT prolongation,
hypoglycemia, irreversible eye damage, seizures, liver damage
,several vit.& its effects eg.Vit C (IV ), propofol infusion syndrome
• Need for dialysis & ECMO
• Self care & care of health care personnel
• Supportive care
• Rehabilitation & follow up

52. Managing circulatory failure
• Fluid resuscitation : increasing the circulating volume of the blood by giving
the patients fluids (direct in to veins via a catheter) which can boost the
volume of blood going through the system.
• Drug treatments : can act on different mechanisms in the body to increase
blood pressure e.g. increase the output of the heart, cause veins to
constrict to increase blood pressure, etc.
• Treat underlying cause : not possible in this case but in bacterial
pneumonia – antibiotics.
Aim is to assist the patient to sustain an adequate volume of circulating
blood at an adequate pressure until an immune response is mounted which
will improve the situation and the body can take over and manage this on its
own.

53. NURSING CARE
• Quarantine & Contact policies update (14 days )

54. Consideration for Continuity of Non-COVID-19
Rehabilitation Services
Essential rehabilitation needs continue for:
• Patients with new acute injuries, such as burns,
amputations or spinal cord injuries who may develop
serious preventable complications.
• Patients recovering from surgery.
• Patients with conditions who are at risk of suboptimal
recovery, such as those recovering from stroke,
myocardial infarction or perinatal complications.
• Patient requiring long-term rehabilitation in hospitals,
residential centres or community settings who may
experience a loss of function or develop complications.
• Patients who are unable to be discharged to a setting
and be safe, or who may return to a setting that is a
very long distance from the service and likely preclude
them from future access.

55. Rehabilitation for Severe COVID-19
Severe COVID-19 patients
• The illness may be complicated by respiratory failure
and other forms of multi organ failure, resulting in
ICU admission with likely invasive mechanical
ventilation.
• Rehabilitation needs are typically related to the
consequences of ventilatory support, and prolonged
immobilization

56. Rehabilitation along the continuum of care
in COVID-19
Acute
Objectives
- Optimize oxygenation
- Manage secretions
- Prevent complications
Input:
Specialist Respiratory
physiotherapist /therapist
and/or rehabilitation staff
experienced with ICU/HDU
setting
Setting: ICU/HDU
Post-acute
Objectives
- Identify and manage
impairments for affected
functioning domains
- Facilitate safe discharge and
onward referral
Input: Multidisciplinary
Setting: Rehabilitation
ward/unit, stepdown facility,
home
Long-term
Objectives
- Optimize functioning/
minimize impact of
impairments on independence
and quality of life
Input: Multidisciplinary
Setting: Home, outpatient
facility, clinic

57. Rehabilitation for severe COVID-19
• Impairments most likely to encounter:
• Physical deconditioning and muscle weakness, fatigue
• Impaired lung function
• Delirium and other cognitive impairments
• Impaired swallow and communication
• Mental health disorders and psychosocial support needs.
• Multi-disciplinary team approach is key
• Still many unknowns related to the pathophysiology of COVID-19
and the long-term complications, many organs can be affected

58. Common country experiences
• Rehabilitation services significantly reduced and often without full consideration of the
consequences. Decisions made locally regarding continuation of rehabilitation services, limited
national direction. Inadequate consideration of all four factors regarding service continuation :
I. Risks associated with cessation or reduction of services for different patient groups
II. Feasibility and appropriateness of alternative modes of service delivery e.g. telehealth, home outreach
III. Access to PPE and robustness of IPC measures in different settings
IV. Capacity of the rehabilitation workforce, e.g. available for redistribution
• COVID-19 related rehabilitation needs increased in tertiary settings and major urban areas, but
less ‘new’ need in rural areas. Generally, reduced demand in line with reductions in elective
surgery, transportation, lockdowns etc
• Where face to face rehabilitation has not been an option a re-purposing workforce towards
alternatives like tele-health, advice/help lines and developing self management plans has
occurred, as has re-purposing for triage and other urgent needs

59. Common country experiences
• PPE for rehabilitation personnel is essential but concerns repeatedly raised about limited access.
Unmet rehabilitation needs & lack of resources reported to ministries of health, advocacy by
professionals essential, value of involving rehabilitation workforce in service decisions highlighted
• Telehealth (primarily phone calls) being utilised for service delivery for patients - important way
forward
• Online videos for patient rehabilitation and pre-developed pamphlets used for COVID-19 clients
• Supply chains for assistive products interrupted
• Greater task-sharing, upskilling and transdisciplinary teamwork occurring – but must be within
scope of practice.
• Rehabilitation professionals undertaking online training
• Inadequate social support services for people with disabilities repeatedly highlighted as a concern

60. Rehabilitation sector reflections
 No perfect response
 Context vary, teams vary - need to adopt, adapt and evaluate approaches
 Opportunity to highlight the value of rehabilitation
 Opportunity to strengthen teams and efficiencies
 Opportunity to harness telehealth for the long term
 Importance of social sector support services for people with disabilities, and
continuation of health and social sector collaboration
 Opportunity to learn and link with international groups/ resources / training

61. LIFE STYLE IN PREVENTION &
CURE
N utrition
E xercise
W ater
S unshine
T emperence
A ir
R est
T rust in God

62. Thankyou
WISH YOU A HAPPY HEALTHY LIFE