The patient is a 75 year old male who complained of exertional dyspnea for 6 months. CT coronary calcium score was noted to be high. He was advised coronary angiogram and possible PCI hence admission. Past medical history revealed hypertension for >40 years, prediabetes, and hyperuricemia. Medications include Amlodipine 5 mg once daily, Rosuvastatin 10 mg once daily, Aspirin 80 mg once daily, and Allopurinol 200 mg once daily. PE showed BP 122/71, HR 67, regular rhythm, and good heart sounds.

ECG revealed HR 67 bpm, sinus rhythm, 1st degree AV block, and early repolarization. 2D echocardiogram revealed no wall motion abnormality and normal systolic function with ejection fraction of 62.8%. CT coronary calcium scoring revealed scores of LM 139.5, LAD 590.3, LCX 803.2, RCA 1092.3, and Total of 2625.3.
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The LAD was a good-sized, Type III vessel with an 80% heavily calcified tandem stenosis at the mid segment. The diagonals are fair-sized vessels with luminal irregularities. The LCX is a good-sized non-dominant vessel with a 20-30% distal stenosis. The OM branches are fair-sized vessels with luminal irregularities. The RCA is a good-sized dominant vessel with luminal irregularities. The PDA and PLA are fair-sized vessels with luminal irregularities. 
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PCI was done with a 6F EBU 3.5 guide catheter and a Sion Blue (Asahi Intecc, Japan) wire distalized into the LAD. NC Emerge 2.0 mm balloon (Boston Scientific, USA) was used to dilate the proximal to mid LAD at 12-20 ATM. IVUS was done showing an MLA of 3.46 mm2. A Synergy 3.0 mm x 20 mm stent (Boston Scientific, USA) and an overlapped Synergy 4.0 mm x 20 mm stent (Boston Scientific, USA) were deployed at the proximal to mid LAD. Subsequent fluoroscopy revealed multiple large Type III perforations at the stented segments. Immediate balloon tamponade was performed using the Synergy 4.0 mm x 20 mm stent balloon inflated at 14 ATM for 2 minutes, which revealed resolution of the perforations. Simultaneously, a pericardiocentesis was performed and a 6F pigtail catheter was inserted into the pericardial space for drainage. Fluoroscopy and intrathoracic echocardiogram revealed persistence of massive pericardial effusion. The patient was noted to have rapid hypotension as low as 60/30 mmHg and loss of consciousness, hence he was intubated and placed on norepinephrine. The right femoral vein was accessed using a 6F introducer sheath and this was connected to the pericardial pigtail catheter using a closed tubing and syringe system. Approximately 300 ml of blood was aspirated from the pericardium and directly autotransfused into the femoral vein to relieve cardiac tamponade and prevent further cardiogenic and hypovolemic shock. Reversal of heparin anticoagulation was done with protamine.
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After about an hour, the patient became hemodynamically stable, with a BP of 118-124/68-72 mmHg, on down-titrating norepinephrine, HR of 72-81 bpm, and sinus rhythm on cardiac monitor. Repeat transthoracic echocardiogram revealed trace pericardial effusion with no echocardiographic signs of tamponade, with no wall motion abnormality and LVEF of 65%. He was transferred to the ICU and eventually discharged stable.
Immediate pericardiocentesis and direct autotransfusion of aspirated blood from the pericardium to the femoral artery served as a practical, efficient, and effective method of relieving cardiac tamponade and cardiogenic shock in a patient with iatrogenic Type III coronary perforation.