Tmatthews
Contributor
My question on the following report is can you bill 93462 twice and do you think the documentation supports 93655? Are these the codes you would use:
93653
93462
93462,59
93662
93621
93623
93655
male with history of flail mitral leaflet s/p mitral annuloplasty in 1/2015 with concomitant MAZE/left atrial appendage suture ligation, hypertension, nonobstructive CAD, IVC filter, and atrial fibrillation. He was on flecainide in the past however was noted to have prolongation of his QTc interval. He was on amiodarone/eliquis/coumadin in the past well however as self-discontinued his most recent therapies. He was planned for possible discontinuation of his anticoagulation 3-6 months post-MAZE if CT imaging demonstrated occlusion of the appendage and if free of AF recurrence. However, had a prolonged, highly symptomatic recurrence of tachycardia with heart rates in the 160's and associated with hypotension recently for which his metoprolol dose was increased. The tachycardia was not documented. Various options were discussed with patient and he wished to proceed with an ablative strategy for management of his tachycardia. He is now planned for evaluation of his pulmonary veins and possible AF ablation and EPS.
PROCEDURE
TThe patient was brought to the Cardiac Electrophysiology laboratory in a post-absorptive, fasting state. Informed consent was obtained. A peripheral IV was in place. Continuous electrocardiographic, blood pressure, O2 saturation and expired CO2 monitoring was initiated. Self-adhesive cardioversion patches were positioned on the chest. General anesthesia was effectuated by the anesthesia service. The patient was then prepped and draped in the usual sterile fashion. Both groins were infiltrated with a 50/50 mixture of Lidocaine (1%) and bupivicaine (0.5%). Vascular access was obtained and an SL1 sheath, SL0 sheath and an 8F sheath were placed in the right common femoral vein using the modified Seldinger technique. All wires/catheters were advanced without difficulty through the IVC filter under fluoroscopic visualization. Through these sheaths, an 8F phased-array intracardiac ultrasound catheter was advanced to the right atrium where the surrounding structures were visualized and the fossa ovalis was localized. Through the SL sheaths, two 0.032, 145-cm Cook J wires were advanced to the level of the superior vena cava. After the guidewire was withdrawn, a Bayliss transseptal needle was introduced into the sheath. The needle/sheath assembly was withdrawn under fluoroscopic and ICE guidance until the tip of the sheath prolapsed into the fossa ovalis. Appropriate positioning was confirmed with multiple fluoroscopic views and ICE imaging. Transseptal access was obtained following delivery of RF energy with the Bayliss needle. The dilator was advanced over the wire, followed by the sheath. The dilator and wire were removed. A circular duodecapolar Lasso mapping catheter was advanced into the left atrium. Systemic heparinization was initiated and the sheath was flushed continuously with heparinized saline. Anticoagulation status was monitored with frequent ACT measurements. Heparin was given in interrupted doses to maintain an ACT > 300 sec. Using the CARTO3 mapping system, detailed mapping was performed and a 3D electroanatomical, geometric rendering of the left atrium was created. The Lasso catheter was then exchanged for a 3.5 mm, bi-directional, externally-irrigated contact-force sensing ablation catheter and further detailed mapping was completed. This electroanatomic map was then merged with a previously obtained cardiac MRI. Over the second 0.032 145-cm wire, a second transseptal access was obtained. The ICE catheter was then exchanged for a 7F octapolar electrode catheter which was utilized to catheterize the coronary sinus for left atrial activity recording and pacing. Esophageal temperatures were monitored using a temperature probe. The height of the esophageal temperature probe was adjusted throughout the procedure in relation to the position of the ablation catheter. Entrance and exit block across all four pulmonary veins was demonstrated. Isuprel 10 mcg/min infusion was initiated in an attempt to induce atrial fibrillation however during atrial burst pacing from the CS, a wide complex tachycardia with a TCL of 320 msec and positive concordance that was hemodynamically intolerable. The tachycardia was terminated with ventricular overdrive pacing. Isuprel infusion was discontinued and atrial burst pacing was performed once again and induced a tachycardia with similar morphology at a TCL of 427 msec (VA interval 200 msec) that was also hemodynamically intolerable (SBP 50's). VOP reproducibly terminated the tachycardia. Comparison of the two tachycardia morphologies and demonstrated similar QRS morphology to that observed during sinus rhythm. Catheters were then positioned at the His and HRA. Retrograde conduction was concentric and decremental. AV nodal function curves were smooth and continuous antegrade and retrograde. During once induction of the tachycardia, a short VA interval was observed (VA 28 msec). Given the short VA interval, suspicion for AVNRT as the underlying mechanism of the tachycardia was heightened. The SL0 sheath was then exchanged from an 8.5F SR0 sheath and the 3.5 mm-irrigated tip ablation catheter was exchanged for a 4 mm non-irrigated tip bi-directional tip ablation catheter. Several applications of RF energy were delivered anterior and inferior to the CS ostium. Occasional junctional beats were evident. Tachycardia remained inducible and further applications were delivered while monitoring VA conduction. Further ablation at these additional sites rendered the tachycardia no longer inducible on/off/washout of isuprel infusion. At the completion of the study, both transseptal sheaths were withdrawn to the RA. Catheters were placed in the RA and RV for recording and pacing as well as the His position for recording. Following a test dose, protamine 50 mg was administered and once the ACT was found to be < 180 seconds, all catheters and sheaths were removed under fluoroscopic visualization without disruption for the IVC filter and hemostasis obtained by direct manual compression. The patient was extubated, hemodynamically stable, tolerated the procedure well and was transferred in stable condition. There were no immediate complications encountered during the procedure. There was minimal blood loss and no specimen were removed.
CONDUCTION INTERVALS
V-V
813 P-R
153 QRS
164 Q-T
333 A-H
48 H-V
43
FINDINGS
1. The baseline ECG revealed sinus rhythm
2. The intracardiac intervals were normal (HV = 43 msec).
3. Retrograde conduction was concentric and decremental.
4. AV nodal function curves were smooth and continuous antegrade and retrograde.
5. All pulmonary veins were successfully mapped using 3D mapping and ICE imaging and demonstrated persistent entrance/exit conduction block.
6. Isuprel 10 mcg/min infusion was initiated in an attempt to induce atrial fibrillation however during atrial burst pacing from the CS, a wide complex tachycardia with a TCL of 320 msec and positive concordance that was hemodynamically intolerable. The tachycardia was terminated with ventricular overdrive pacing.
7. Isuprel infusion was discontinued and atrial burst pacing was performed once again and induced a tachycardia with similar morphology at a TCL of 427 msec (VA interval 200 msec) that was also hemodynamically intolerable (SBP 50's). VOP reproducibly terminated the tachycardia. Comparison of the two tachycardia morphologies and demonstrated similar QRS morphology to that observed during sinus rhythm. During once induction of the tachycardia, a short VA interval was observed (VA 28 msec). Entrainment of the tachycardia was precluded by reproducible termination of the tachycardia with VOP. 3D activation mapping was precluded by hemodynamic instability of the tachycardia.
8. Given the short VA interval, suspicion for AVNRT as the underlying mechanism of the tachycardia was heightened. The SL0 sheath was then exchanged from an 8.5F SR0 sheath and the 3.5 mm-irrigated tip ablation catheter was exchanged for a 4 mm non-irrigated tip bi-directional tip ablation catheter. Several applications of RF energy were delivered anterior and inferior to the CS ostium. Occasional junctional beats were evident. Tachycardia remained inducible and further applications were delivered while monitoring VA conduction. Further ablation at these additional sites rendered the tachycardia no longer inducible on/off/washout of isuprel infusion.
RADIOLOGY SUMMARY
See attached report
CONCLUSIONS
1. Successful AVNRT ablation via slow pathway ablation.
2. Successful mapping of all pulmonary veins demonstrating entrance/exit conduction block.
3. Monitor on telemetry overnight.
4. Resume anticoagulation with eliquis 5 mg po bid, first dose tonight
5. Resume all other home medications.
6. Follow up in 1 month in EP clinic
93653
93462
93462,59
93662
93621
93623
93655
male with history of flail mitral leaflet s/p mitral annuloplasty in 1/2015 with concomitant MAZE/left atrial appendage suture ligation, hypertension, nonobstructive CAD, IVC filter, and atrial fibrillation. He was on flecainide in the past however was noted to have prolongation of his QTc interval. He was on amiodarone/eliquis/coumadin in the past well however as self-discontinued his most recent therapies. He was planned for possible discontinuation of his anticoagulation 3-6 months post-MAZE if CT imaging demonstrated occlusion of the appendage and if free of AF recurrence. However, had a prolonged, highly symptomatic recurrence of tachycardia with heart rates in the 160's and associated with hypotension recently for which his metoprolol dose was increased. The tachycardia was not documented. Various options were discussed with patient and he wished to proceed with an ablative strategy for management of his tachycardia. He is now planned for evaluation of his pulmonary veins and possible AF ablation and EPS.
PROCEDURE
TThe patient was brought to the Cardiac Electrophysiology laboratory in a post-absorptive, fasting state. Informed consent was obtained. A peripheral IV was in place. Continuous electrocardiographic, blood pressure, O2 saturation and expired CO2 monitoring was initiated. Self-adhesive cardioversion patches were positioned on the chest. General anesthesia was effectuated by the anesthesia service. The patient was then prepped and draped in the usual sterile fashion. Both groins were infiltrated with a 50/50 mixture of Lidocaine (1%) and bupivicaine (0.5%). Vascular access was obtained and an SL1 sheath, SL0 sheath and an 8F sheath were placed in the right common femoral vein using the modified Seldinger technique. All wires/catheters were advanced without difficulty through the IVC filter under fluoroscopic visualization. Through these sheaths, an 8F phased-array intracardiac ultrasound catheter was advanced to the right atrium where the surrounding structures were visualized and the fossa ovalis was localized. Through the SL sheaths, two 0.032, 145-cm Cook J wires were advanced to the level of the superior vena cava. After the guidewire was withdrawn, a Bayliss transseptal needle was introduced into the sheath. The needle/sheath assembly was withdrawn under fluoroscopic and ICE guidance until the tip of the sheath prolapsed into the fossa ovalis. Appropriate positioning was confirmed with multiple fluoroscopic views and ICE imaging. Transseptal access was obtained following delivery of RF energy with the Bayliss needle. The dilator was advanced over the wire, followed by the sheath. The dilator and wire were removed. A circular duodecapolar Lasso mapping catheter was advanced into the left atrium. Systemic heparinization was initiated and the sheath was flushed continuously with heparinized saline. Anticoagulation status was monitored with frequent ACT measurements. Heparin was given in interrupted doses to maintain an ACT > 300 sec. Using the CARTO3 mapping system, detailed mapping was performed and a 3D electroanatomical, geometric rendering of the left atrium was created. The Lasso catheter was then exchanged for a 3.5 mm, bi-directional, externally-irrigated contact-force sensing ablation catheter and further detailed mapping was completed. This electroanatomic map was then merged with a previously obtained cardiac MRI. Over the second 0.032 145-cm wire, a second transseptal access was obtained. The ICE catheter was then exchanged for a 7F octapolar electrode catheter which was utilized to catheterize the coronary sinus for left atrial activity recording and pacing. Esophageal temperatures were monitored using a temperature probe. The height of the esophageal temperature probe was adjusted throughout the procedure in relation to the position of the ablation catheter. Entrance and exit block across all four pulmonary veins was demonstrated. Isuprel 10 mcg/min infusion was initiated in an attempt to induce atrial fibrillation however during atrial burst pacing from the CS, a wide complex tachycardia with a TCL of 320 msec and positive concordance that was hemodynamically intolerable. The tachycardia was terminated with ventricular overdrive pacing. Isuprel infusion was discontinued and atrial burst pacing was performed once again and induced a tachycardia with similar morphology at a TCL of 427 msec (VA interval 200 msec) that was also hemodynamically intolerable (SBP 50's). VOP reproducibly terminated the tachycardia. Comparison of the two tachycardia morphologies and demonstrated similar QRS morphology to that observed during sinus rhythm. Catheters were then positioned at the His and HRA. Retrograde conduction was concentric and decremental. AV nodal function curves were smooth and continuous antegrade and retrograde. During once induction of the tachycardia, a short VA interval was observed (VA 28 msec). Given the short VA interval, suspicion for AVNRT as the underlying mechanism of the tachycardia was heightened. The SL0 sheath was then exchanged from an 8.5F SR0 sheath and the 3.5 mm-irrigated tip ablation catheter was exchanged for a 4 mm non-irrigated tip bi-directional tip ablation catheter. Several applications of RF energy were delivered anterior and inferior to the CS ostium. Occasional junctional beats were evident. Tachycardia remained inducible and further applications were delivered while monitoring VA conduction. Further ablation at these additional sites rendered the tachycardia no longer inducible on/off/washout of isuprel infusion. At the completion of the study, both transseptal sheaths were withdrawn to the RA. Catheters were placed in the RA and RV for recording and pacing as well as the His position for recording. Following a test dose, protamine 50 mg was administered and once the ACT was found to be < 180 seconds, all catheters and sheaths were removed under fluoroscopic visualization without disruption for the IVC filter and hemostasis obtained by direct manual compression. The patient was extubated, hemodynamically stable, tolerated the procedure well and was transferred in stable condition. There were no immediate complications encountered during the procedure. There was minimal blood loss and no specimen were removed.
CONDUCTION INTERVALS
V-V
813 P-R
153 QRS
164 Q-T
333 A-H
48 H-V
43
FINDINGS
1. The baseline ECG revealed sinus rhythm
2. The intracardiac intervals were normal (HV = 43 msec).
3. Retrograde conduction was concentric and decremental.
4. AV nodal function curves were smooth and continuous antegrade and retrograde.
5. All pulmonary veins were successfully mapped using 3D mapping and ICE imaging and demonstrated persistent entrance/exit conduction block.
6. Isuprel 10 mcg/min infusion was initiated in an attempt to induce atrial fibrillation however during atrial burst pacing from the CS, a wide complex tachycardia with a TCL of 320 msec and positive concordance that was hemodynamically intolerable. The tachycardia was terminated with ventricular overdrive pacing.
7. Isuprel infusion was discontinued and atrial burst pacing was performed once again and induced a tachycardia with similar morphology at a TCL of 427 msec (VA interval 200 msec) that was also hemodynamically intolerable (SBP 50's). VOP reproducibly terminated the tachycardia. Comparison of the two tachycardia morphologies and demonstrated similar QRS morphology to that observed during sinus rhythm. During once induction of the tachycardia, a short VA interval was observed (VA 28 msec). Entrainment of the tachycardia was precluded by reproducible termination of the tachycardia with VOP. 3D activation mapping was precluded by hemodynamic instability of the tachycardia.
8. Given the short VA interval, suspicion for AVNRT as the underlying mechanism of the tachycardia was heightened. The SL0 sheath was then exchanged from an 8.5F SR0 sheath and the 3.5 mm-irrigated tip ablation catheter was exchanged for a 4 mm non-irrigated tip bi-directional tip ablation catheter. Several applications of RF energy were delivered anterior and inferior to the CS ostium. Occasional junctional beats were evident. Tachycardia remained inducible and further applications were delivered while monitoring VA conduction. Further ablation at these additional sites rendered the tachycardia no longer inducible on/off/washout of isuprel infusion.
RADIOLOGY SUMMARY
See attached report
CONCLUSIONS
1. Successful AVNRT ablation via slow pathway ablation.
2. Successful mapping of all pulmonary veins demonstrating entrance/exit conduction block.
3. Monitor on telemetry overnight.
4. Resume anticoagulation with eliquis 5 mg po bid, first dose tonight
5. Resume all other home medications.
6. Follow up in 1 month in EP clinic
