A 2 am Tamponade: Critical call to action

ArchanaViswanathan1, Abdul Salaam2, Venkatesh3, Ramanathan4

1DNB Emergency Medicine resident, Kauvery Hospital, Trichy

2Consultant Emergency Medicine, Kauvery Hospital, Trichy

3Consultant Critical care, Kauvery Hospital, Trichy

4HOD Emergency Medicine, Kauvery Hospital, Trichy

Abstract

A 52-years – aged male, with chronic kidney disease (CKD) on hemodialysis, admitted for pulmonary edema secondary to volume overload, and with severe metabolic acidosis and hyperkalemia, from Day 1 of admission. Despite initial treatment, he continued to experience vague left-sided chest pain. On Day 8 of admission, the patient developed acute chest pain, breathing difficulty and hypotension, prompting transfer to critical care. Bedside echocardiography revealed a significant pericardial effusion consistent with cardiac tamponade. Urgent pericardiocentesis was performed, leading to immediate hemodynamic stabilization. This case emphasizes the necessity for vigilance and timely intervention in patients with complex comorbidities presenting with chest pain.

Introduction

A pericardial effusion refers to when the pericardial fluid exceeds 15-50 mL. Pericardial tamponade refers to hemodynamic instability and clinical symptoms owing directly to that effusion. This occurs when the pressure exerted on one or more cardiac chambers by the pericardial effusion (i.e. the intrapericardial pressure) exceeds the pressures within the cardiac chambers (i.e. the intracardiac pressure), leading to obstruction of normal chamber filling.

Case Presentation

A 52 years male, known to have CKD on medical management / HTN / T2DM,

His diagnoses on admission were

  • Acute pulmonary edema- cardiogenic, volume overload status
  • Acute on CKD
  • Severe metabolic acidosis(since resolved)
  • Hyperkalemia (since corrected)
  • Anemia

Lab reports on admission

ABG – metabolic acidosis pH 7.16, HCO3 4.3 mmol/L, pCO2 12 mmHg, pO2 119 mmHg

Potassium – 6.0 mmol/L

Urea – 393 mg/dl

Creatinine – 31.8 mg/dl

Troponin – 0.2 ng/ml

NT Pro BNP >30,000 pg/ml

Management

The patient was admitted to the nephrology department and underwent immediate hemodialysis, which resolved most symptoms, but the chest pain persisted. He completed 5 cycles of HD, last HD done on day 7 of admission.

His ECG on day 1 of admission revealed Sinus rhythm with heart rate of 80, inverted T waves in inferior leads II, III and aVF. Cardiac enzyme – Troponin I was found to be 0.7 ng/ml. After cardiology evaluation for NSTEMI, he was started on antiplatelets on day 1 of admission. He still had vague chest pain on and off during his stay in the hospital. Cardiology evaluation attributed his pain to pleuritic origins, and anti-inflammatory medications were initiated.

On 8th day of admission, around 2 am, he was transferred to critical care in view of left sided chest pain for past 2 hours along with breathing difficulty  and hypotension.

Previous ECHO findings were global hypokinesia of LV anterior wall> inferior wall, EF 42%, Mild LV dysfunction, grade 2 diastolic dysfunction, mild MR, trivial TR and concentric LVH. No intra cavitary masses/thrombus/pericardial effusion.

During the initial evaluation following his transfer to critical care:

Patient was shifted with oxygen support, was conscious, oriented to time, place, person and tachypneic.

  • Airway- patent, vocalizing.
  • Breathing- Spontaneously breathing, RR- 30/min,SpO2- 98%, with 6 litres of oxygen via facemask.
  • Circulation- BP 70/40mmHg , HR- 108/min, peripheral pulses were felt.
  • Disability- GCS- E4V5M6, pupils- bilaterally equal ,and reacting to light
  • Exposure- Temp- normal. CBG- 98mg/dl
  • Raised JVP noted.

Systemic examination

  • CVS- heart sounds not clearly audible.
  • RS- Vesicular breath sounds heard in both lung fields, no added sounds.
  • PA- soft, non tender.
  • CNS- alert, obeying commands,E4V5M6

Patient was noted to have Beck’s triad, consisting of hypotension, jugular venous distension and muffled heart sounds.

ECG: Taken on day 8 before shifting to critical care

Impression

  • Sinus rhythm with HR of 92 bpm.
  • T wave inverted in lead III and flattened in aVF.

ABG findings

  • pH 7.30 , PCO2 21mmHg , PO2 132mmHg , HCO3 12mmol/L , SO2 99%
  • Potassium – 7.6mmol/L
  • Hb – 6.4 g%
  • Lactate – 8.0mmol/L

Given the acute presentation, a bedside POCUS was performed, which revealed a large pericardial effusion causing cardiac tamponade. This finding explained the patient’s hemodynamic instability.

POCUS

Heart –             Massive pericardial effusion noted.

  • Inadequate contractility of left ventricle.
  • Right ventricle free wall diastolic collapse and right atrium collapse was present.

IVC – 2.19 cm, distended

Lungs – Right basal minimal effusion with collapse noted.

PLAX – PSAX: 4 chamber view

Therapeutic Intervention

Immediate echo guided pericardiocentesis by sub xiphoid approach was conducted, draining around 600ml of haemorrhagic pericardial fluid. This intervention resulted in a rapid improvement in the patient’s blood pressure and overall clinical condition. He underwent haemodialysis and received a Packed Cell (PRBC) transfusion shortly after stabilization.

Post procedure–

Patient was conscious, oriented

BP- 190/100mmHg, with Inj. Noradrealine support which was tapered gradually and stopped in few hours.

HR-98/min

SpO2-98% with 6L oxygen

RR-30/min

POCUS

Heart – Reduction in pericardial effusion noted.

  • Adequate contractility of chambers seen.
  • RA/ RV contracting well.

Lungs – Bilateral lung sliding present.

IVC – 2cm

PLAX 4 chamber view

Chest X ray showing enlarged globular heart

Pericardial fluid analysis demonstrated predominantly elevated LDH without any evidence of malignancy or tuberculosis.

Repeat echocardiogram demonstrated normal left ventricular ejection fraction of 60% and moderate pericardial effusion still present without any evidence of tamponade.

Outcome and Follow-Up

Following pericardiocentesis, the patient’s haemodynamics stabilized, and his chest pain resolved. He was closely monitored in the critical care unit for any recurrence of symptoms or complications. Further evaluation did not reveal any ongoing sources of infection. However, he had recurrent effusion two days later, around 100ml of haemorrhagic pericardial fluid was drained out. He was eventually transferred back to the general ward in stable condition and later discharged with appropriate follow-up plans.

Discussion

Cardiac tamponade is a medical emergency caused by the accumulation of fluid in the pericardial space, resulting in reduced ventricular filling and subsequent hemodynamic compromise.

Etiology

  1. Pericarditis (Inflammation from infection, immunologic, uremic, post MI)
  2. Trauma causing bleeding in pericardial space/ rupture of ventricles after MI/ ruptured Aorta.
  3. Non-infectious conditions such as:
  • Increase in pulmonary hydrostatic pressure e.g. congestive heart failure.
  • Increase in capillary permeability e.g. hypothyroidism
  • Decrease in plasma oncotic pressure e.g. cirrhosis.
  1. Decrease drainage of pericardial fluid due to obstruction of thoracic duct as a result of malignancy or damage during surgery.

Effusion may be serous, serofibrinous, suppurative, chylous, or hemorrhagic depending on the etiology. Viral effusions are usually serous or serofibrinous; malignant effusions are usually hemorrhagic.

Hemodynamics of cardiac compression

Compensatory changes

  • Increased catecholamines / sympathetic activity:
  • Increases contractility à increases EFà increases CO
  • Increases HR. Tachycardia helps to maintain adequate cardiac output in the face of low stroke volume.
  • Augments venous toneà increases preload àincreases stroke volume.
  • Increases Peripheral arterial resistanceà supports BP

Harm

  • Increase in myocardial oxygen consumption.
  • Increased afterload à increases myocardial work.
  • Arrhythmias

Clinical features

  • Sharp pain in the chest.
  • Shortness of breath.
  • Dizziness/Syncope
  • Palpitations
  • Altered mental status-confused or agitated.
  • Swelling in your abdomen or legs.
  • In advanced stages of tamponade clinical features include hypotension, tachycardia, distended jugular veins and a pulsus paradoxus of > 10mmhg. With progressive increase in intrapericardial pressure, there is further elevation of venous pressure and a drop in cardiac output, which, if untreated, leads to cardiogenic shock.
  • Pulsus Paradoxus- Pulsus paradoxus is a larger-than-normal >10mmHg drop in systolic blood pressure on inhalation.
  • The Kussmaul sign – a paradoxical elevated in JVP and pressure during inspiration is sometimes seen in cardiac tamponade.
  • Compression of lung leading to an area of consolidation (detected as percussion dullness and bronchial breathing) in the left infrascapular region is known as – Ewalt’s sign.

ECG findings in cardiac tamponade

  • Electricalalternans
  • Low voltage complexes

Echo findings in cardiac tamponade

  • Evidence of pericardial effusion
  • RA, RV diastolic collapse
  • Swinging of heart within the effusion

Differential diagnosis

  • Pleural effusion
  • Pneumothorax
  • Pulmonary embolism
  • Constrictive pericarditis
  • Heart failure
  • Shock

Management

Removal of pericardial fluid is the definitive therapy for tamponade and can be done using the following three methods:

  • Emergency subxiphoid percutaneous drainage
  • Pericardiocentesis (with or without echocardiographic guidance)
  • Percutaneous balloon pericardiotomy

Conclusion

This case underscores the complexity of diagnosing chest pain in patients with multiple comorbidities. While the patient’s initial chest pain was attributed to pleuritic pain, the development of cardiac tamponade highlights the necessity for continuous re-evaluation. Cardiac tamponade, although rare, should be considered in patients with sudden hemodynamic collapse, especially in those with risk factors such as recent myocardial infarction and chronic kidney disease.

CPC-EM Capsule

  1. What do we already know about this clinical entity?

Cardiac tamponade is a life-threatening illness that requires emergent recognition and treatment.

  1. What makes this presentation of disease reportable?

This is a case report of a patient who developed severe, life-threatening cardiac tamponade in under 24 hours that necessitated immediate intervention.

  1. What is the major learning point?

Cardiac tamponade can develop rapidly, and recent negative imaging does not rule it out. Point-of-care ultrasound can help rapidly identify this disease process.

  1. How might this improve emergency medicine practice?

Emergency physicians must always consider cardiac tamponade in hypotensive, tachycardic patients.


Dr. Archana viswanathan
DNB Emergency Medicine

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