EMS is called to the residence of a 58 year old male complaining of chest discomfort.
On arrival the patient is found sitting on the edge of the bed. He is anxious but alert and oriented to person, place, time, and event.
He was awakened from sleep by chest discomfort.
Onset: 30 minutes ago while sleeping
Provoke: Nothing makes the pain feel better or worse
Quality: Severe pressure or "ache"
Radiate: The pain does not radiate
Severity: 10/10
Time: He has had chest pain before but "not this bad"
Past medical history: HTN, dyslipidemia
Medications: Lipitor, Norvasc, ASA
Vital signs are assessed.
RR: 24
Pulse: 136
NIBP: 160/98
SpO2: 94 on RA
Breath sounds: basilar rales
The patient admits to mild dyspnea. He states that he has "gained a little weight" recently and his doctor was getting ready to put him "on a water pill."
Temp: 99.1
BGL: 138
The cardiac monitor is attached.
A 12-lead ECG is captured.
The patient is given 324 mg of aspirin, 0.4 mg NTG SL spray and placed on CPAP.
Another 12-lead ECG is captured.
The patient is loaded for transport and another rhythm strip is captured.
What do think is going on with this patient's heart rhythm?
What do you think is wrong with this patient?
You are 15 minutes away from the local non-PCI hospital and 60 minutes away from a STEMI receiving center.
Where would you transport this patient and why?
Given the HPI and PE I would venture to say this patient is experiencing an MI with significant muscle involvement resulting in CHF. The classic CP presentation and elevated B/P and HR indicate neurohumoral and sympathetic response to decreased cardiac output. The crackles and recent fluid retention (aldostorone) in response to decreased CO affirm my initial diagnosis. This patient also has risk factors for this type of event.
ReplyDeleteAs for the ECG... I agree with the LBB and would call this sinus tach with bigeminy PVC's. The heart is looking very irritable from decreased coronary perfusion and the massive amounts of catecholamines released to increase cardiac output. Granted there is no ST-segment elevation but this patient rings to loudly to not signal an MI.
I would consult medical command on transport decision with recommendation geared towards going to PCI capable center and entertain orders for lidocaine or amiodarone due to the ventricular irritability which is precipitous for lethal arrhythmia and ultimately death.
I think the ECG shows tachycardia with a combination of narrow and wide complexes, however, I don't think the wide complexes are due to PVCs as there is p wave before each wide QRS complex (better seen in V1). So this can be considered a ne...w LBBB which in the setting of angina is usually considered equal to STE for treatment purposes.Nevertheless, this is a tricky case here. The reason that new LBBB is considered equal to STE is that masks STE but here we also have narrow QRS (non LBBB QRS) that do not show any STE so in my conclusion this is a case of UA/NSTEMI and can be transfered to the non-PCI closer center!
ReplyDeleteAlso this LBBB appears to be a tachycardia-related BBB (another clue that is not representing transmural MI). In the first tracing with HR of 140 all beats are in LBBB and when the HR comes down to 125 in the ECGs we start to see more narrow QRS complexes and less of LBBB.
I would lean towards a STEMI center. It looks like concordant T waves with the LBBB as the underlying rhythm. The ectopic beats are definitely narrower than the underlying rhythm, but based on the size of the T waves, I'm going that way versus hidden P waves changing the shape. Also across V1-V2, the STE is close to the 20% of the negative deflection of the QRS. The negative deflection is cut off in V3, but everything else looks suspicious to me.
ReplyDeleteAny follow-up to this case?
ReplyDelete