Ready for the next steps of the case challenge? Prof. Dr. Sundeep Mishra reveals more details of the case from the previous week and evaluates your responses from the first part.

Study the next stage case and answer the questions in the boxes below. Get your responses evaluated from the expert. Our expert will share comments as the case progresses. Stay tuned!

Click to read other articles from Dr. Sundeep Mishra.

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Case summary

An elderly lady, known case of COAD and hypertension, presented with symptoms of severe chest tightness, breathlessness and sweating. She had a history of being unwell and ↓mobility in the near past.

Patient could have a cardiac or respiratory system affliction. The D/D are as follows;

Cardiac:

• Acute coronary syndrome/acute myocardial infarction
• Acute myocarditis/acute decompensated heart failure
• Pericarditis ± effusion

Respiratory

• Severe pneumonia/acute respiratory failure
• Pulmonary thromboembolism
• COAD exacerbation/status asthamaticus
• Pneumothorax

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Vital parameters & general examination

Hypotension, tachycardia, tachypnoea, cold clammy skin, possible decreased urine output and mild desaturation suggests shock which seems cardiac in origin (because no evidence of sepsis or blood loss).

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ECG

• Sinus tachycardia
• ? ST elevation in III and aVF
• T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF)
• No evidence of right axis deviation, RVH, right atrial overload

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X-ray chest PA view

• No cardiomegaly- rules out pericardial effusion ± tamponade
• No evidence of pneumothorax
• No pleural effusion
• ? areas of patchy consolidation
• No B/L hyper-inflation of lung fields but?right lung fields translucent.

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Laboratory evaluation

• ↑Hb (18.2)- probably reflective of chronic hypoxemia – point in favour of significant COAD
• Leucocytosis- TLC 11,370 suggestive of inflammation; point in favour of pneumonitis or myocarditis ± of COVID origin
• Renal function tests are within normal limits
• Slight increase in bilirubin levels

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ABG

Normal pH, mild hypoxemia (PO2 <79), mild hypercarbia (PCO2 >30) and ↑HCO3 (>28 mEq/L) suggestive of mild compensatory respiratory acidosis.

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Discussion of questions and answers from part 1

Question 1: What is the possible diagnosis?

There was a fairly broadspread likely-hood (voted by respondents) which shows that the case was fairly interesting. The choices in decreasing order of frequency were;

• Acute coronary syndrome/acute myocardial infarction with shock
• Pneumonitis with respiratory failure possibly due to COVID infection
• Congestive heart failure probably as a result of myocarditis, possibly due to COVID infection
• COAD with exacerbation
• Acute pulmonary thrombo-embolism

Some even considered the possibility of acute pericarditis, pneumothorax, LVH, and dehydration due to hyperglycaemia. Let us consider these possibilities one-by-one in line of the evidence we have.

Acute coronary syndrome/acute myocardial infarction with shock – Nearly half the respondents (42%)

1. Clinical findings: Symptoms are highly suggestive of acute myocardial infarction; a strong possibility.
2. Vital parameters and general examination: Suggests shock; likely cardiac origin, consistent with diagnosis.
3. ECG: Sinus tachycardia with possible ST elevation in III and aVF, T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF)– seems consistent with diagnosis of ACS.
4. X-ray chest PA view: No cardiomegaly, no evidence of pneumothorax, no pleural effusion,? areas of patchy consolidation – doesn’t rule out ACS.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, slight increase in bilirubin levels. Acute myocardial infarction ST-elevation (STEMI) is frequently associated with leukocytosis and relative increased in neutrophil count. It is believed that the peripheral leukocyte count have important prognostic implication in AMI.
6. ABG: It is suggestive of mild respiratory acidosis. It could be a consequence of early pulmonary oedema due to left ventricular failure subsequent to large myocardial infarct.

Discussion: ACS/AMI remains a likely diagnosis in this patient subject to subsequent confirmation.

Pneumonitis with early respiratory failure possibly due to COVID infection – 205 of respondents felt this was the correct diagnosis

1. Clinical findings:
   1. Points in favour- H/O lack of social isolation, prodrome could represent viral infection, severe breathlessness
   2. Points against- Sudden onset of disease (possible if pneumonia was less symptomatic but suddenly ARDS set in), symptom of chest tightness, no cough
2. Vital parameters and general examination: It is suggestive of shock; likely cardiac origin. It is inconsistent with the diagnosis because shock seems cardiac not septic (cold clammy skin). Cardiac origin shock is a rather late event in pneumonitis and develops only in full-fledged respiratory failure.
3. ECG: Sinus tachycardia, ? ST elevation in III and aVF, T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF). ECG is not fitting into diagnosis of pneumonia/respiratory failure.
4. X-ray chest PA view: No cardiomegaly, no pleural effusion, and possible areas of patchy consolidation. Generally, one would expect a more gross derangement in pulmonary parenchyma, but atypical pneumonias can happen.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, slight increase in bilirubin levels; leucocytosis is consistent with lung infection.
6. ABG: It is suggestive of mild respiratory acidosis. This finding actually does not fit into the diagnosis because with this kind of clinical picture, particularly shock, we would have expected a far worse respiratory acidosis.

Discussion: Considering all the points and the main diagnosis of pneumonitis, respiratory failure seems very unlikely, but possibility of some chest infection in conjunction with another main diagnosis cannot be ruled out.

Congestive heart failure probably as a result of myocarditis ± COVID infection – 12% of respondents felt this was the main diagnosis

1. Clinical features:
   1. Points in favour- H/O lack of social isolation, prodrome could represent viral infection, doubtful H/O of ↓ urination could suggest developing heart failure
   2. Points against- Rather sudden onset (onset is generally sub-acute, but acute onset possible if rhythm disturbance), no fever (but presence of fever is not mandatory in viral infections); no H/O of COVID disease in contacts
2. Vital parameters & general examination: It is suggestive of shock; likely cardiac origin. Decompensated heart failure can explain occurence of shock. However, it generally takes a longer time for shock to set in; this is rather abrupt.
3. ECG: Sinus tachycardia, non-specific ST-T changes may fit into diagnosis of myocarditis.
4. X-ray chest PA view: No cardiomegaly, no pleural effusion,? areas of patchy consolidation– neither proves, nor disproves diagnosis of myocarditis/ADHF.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, slight increase in bilirubin levels. Leucocytosis is likely with myocarditiis.
6. ABG: It is suggestive of mild respiratory acidosis. It could be a consequence of early pulmonary oedema due to myocarditis → acute decompensated heart failure.

Discussion: Diagnosis of myocarditis/ADHF is possible, but unlikely because of rather sudden onset of the whole disease with no prodrome of viral infection.

COAD with exacerbation – 12% of respondents felt this was the correct diagnosis

1. Clinical findings:
   1. Points in favour- Past H/O COAD exacerbation, acute breathlessness which may be accompanied by chest tightness, symptom of trouble eating and sleeping
   2. Points against- No precipitating factor, no coughing
2. Vital parameters and general examination: It is suggestive of shock; likely cardiac origin. Inconsistent with diagnosis of COAD exacerbation because shock will be a rather late event and develops only in full-fledged respiratory failure.
3. ECG: Sinus tachycardia, no evidence of right axis deviation, RVH, right atrial overload, possible ST elevation in III and aVF, T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF). ECG is not fitting into diagnosis of COAD exacerbation
4. X-ray chest PA view: No cardiomegaly, no pleural effusion, possible areas of patchy consolidation, no B/L hyper-inflation of lung fields. Not fitting into COAD exacerbation. COAD may show on an X-ray with hyperinflated lung fields (lungs appear larger than normal), diaphragm may look lower and flatter than usual, and the heart may look longer than normal. However, these findings appear late on the X-ray. In this case, on the other hand, with severe long lasting disease leading into shock, one would expect at least some changes on X-ray. Thus, X-ray picture is inconsistent with the diagnosis.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, and slight increase in bilirubin levels. This finding is more in favour than against diagnosis of COAD with exacerbation. ↑Hb doses suggest chronic hypoxemia due to long standing COAD and leucocytosis may be due to lung infection which might have precipitated COAD exacerbation.
6. ABG: It is suggestive of mild respiratory acidosis. This finding actually does not fit into the diagnosis, because with this kind of clinical picture, particularly shock, we would have expected a far worse respiratory acidosis.

Discussion: While COAD is undeniable, ↑Hb but the clinical course, ECG, X-ray and ABG does not suggest that it is the prime diagnosis.

Acute pulmonary thrombo-embolism (PTE) – 10% of respondents felt this was the main diagnosis

1. Clinical picture:
   1. Points in favour- Presenting symptoms possible with PTE, elderly status (risk factor for PTE). H/O of immobilisation (risk factor for PTE). PTE is possible but this is generally a diagnosis of exclusion
   2. Points against- No H/O cough, no H/O haemoptysis
2. Vital parameters and general examination: It is suggestive of shock; likely cardiac or distributive origin; consistent with diagnosis.
3. ECG: Sinus tachycardia with possible ST elevation in III and aVF, T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF). Would have expected some right axis deviation, right ventricular hypertrophy and right atrial overload in chronic PTE but this finding can happen with acute PTE.
4. X-ray chest PA view: No cardiomegaly, no pleural effusion, and possible areas of patchy consolidation; no B/L hyper-inflation of lung fields but possible hyper-inflation in right lower field; consistent with diagnosis of PTE.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, slight increase in bilirubin levels. Lab values neither confirm nor rule out diagnosis of PTE.
6. ABG: It is suggestive of mild respiratory acidosis; could be a consequence of pulmonary infarcts. It may be consistent with diagnosis of PTE.

Discussion: Most of the features fit into diagnosis of PTE. However, PTE is generally a diagnosis of exclusion and appropriate investigations are necessary to rule in or rule out the diagnosis.

Pericarditis ± pericardial effusion – 2% of respondents kept this as the main diagnosis

1. Clinical features:
   1. Points in favour: Symptom of chest pain 
   2. Points against: Symptom of sudden, acute pain with breathlessness so much so that it can cause sweating very unlikely
2. Vital parameters and general examination: It is suggestive of shock; likely cardiac or distributive origin. Pericarditis is very unlikely unless massive effusion and tamponade develops (which is very rare with this disease)  and moreover, it is likely to be terminal.
3. ECG: Sinus tachycardia with possible ST elevation in III and aVF, T-wave inversions in the anterior (V1-4) and inferior leads (II, III, aVF). Some points in favor of diagnosis but ECG alone can neither rule in / rule out the diagnosis.
4. X-ray chest PA view: No cardiomegaly (rules out large pericardial effusion), no pleural effusion, ? areas of patchy consolidation- doesn’t fit into diagnosis of pericarditis with pericardial effusion.
5. Laboratory evaluation: ↑Hb (18.2), leucocytosis, normal renal function tests, slight increase in bilirubin levels. Leucocytosis can happen in pericarditis but overall, lab values neither confirm nor rule out diagnosis of pericarditis.
6. ABG: It is suggestive of mild respiratory acidosis- not consistent with diagnosis of pericarditis.

Discussion: Overall does not fit into the diagnosis of pericarditis.

Pneumothorax – 1 respondent felt it could be a case of pneumothorax

However, X-ray chest clearly rules out a significant pneumothorax which may cause shock and this kind of ABG.

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Question 2: What investigations do you need?

Nearly half the respondents advised diagnostic test for COVID (rt-PCR) including HRCT chest (28%), 2 out of 5 (40%) advised an echocardiogram, 30% advised some cardiac markers, 1 in 4 (25%) advised some inflammatory marker, 12% advised coronary angiogram, and another 12% advised CT pulmonary angiogram. 10% advised D-dimer test. Whereas, 5% advised full pulmonary function tests. Other tests that were advised were; TMT, Blood culture, cystatin and even peri-cardiocentesis.

What we did-

1. A nasopharyngeal swab was obtained for rtPCR for COVID
2. hsTroponin T revealed a value of 24 ≥14 pg/mL . CPK & CPK-MB levels were sent
3. D-dimer revealed a value of 0.3 ɥg / ml
4. Simplified Geneva Score to determine the probability of PTE

Variables	Score
Age >65	1
Previous DVT or PE	1
Surgery or fracture within 1 month	1
Active malignancy	1
Unilateral lower limb pain	1
Haemoptysis	1
Pain on deep vein palpation of lower limb and unilateral oedema	1
Heart rate 75 to 94 bpm	1
Heart rate greater than 94 bpm	2

Based on this, the score was 3.

5. Based on overall picture, acute myocardial infarction was suspected. The patient was loaded with dual anti-platelet therapy using ticagrelor.
6. Since oxygen saturation was 92% with tachypnoea and accompanied with shock, we decided to deliver oxygen by NIV to keep oxygen saturation >95%.
7. Broad spectrum antibiotics were instituted.

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While waiting for report of COVID, the patient suddenly collapsed, became unconscious with an idioventricular rhythm of 40/min with no pulse or blood pressure recorded. Cardiac arrest with pulseless electrical activity followed. Following the aseptic precautions mandated in a COVID patient and with full protective personal equipment for the healthcare workers, the patient was intubated and standard cardiopulmonary resuscitation (CPR) was initiated. There was a return of spontaneous circulation but blood pressure was in the range of 80-90 systolic; the total CPR duration was >1 hour.

Bedside echocardiography revealed diffuse hypokinesis, with left and right sided ventricular dilatation with LV ejection fraction of 25%. The patient was immediately rushed to the cath lab with two teams at work simultaneously; coronary angiogram being performed from right groin and intra-aortic balloon pump support instituted from the left groin. However, the coronary angiogram showed no obstructive lesions in the coronary artery.

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This is a special, real-life case challenge series. Send in your responses latest by December 14 (Monday).

Stay tuned for the next part which will cover the third stage of the case and the expert's discussion of the answers to the questions posted above.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author, Dr. Sundeep Mishra is a Professor of Cardiology.