#LVH WITH IVCD HOW TO#

With aging population and rampant acute and chronic renal disorders it is becoming a daily affair to get calls from medical units for ECG changes.

Contrary to our belief even Inferior leads can show q waves due to inferior septal hypertrophy.

Left ventricular hypertrophy mimics old MI as poor R wave progression in V1 to V3.

LVH with incomplete LBBB – A very common association that can further elevate ST segment in v1 to v3.

LVH can mimic a STEMI due to secondary ST/T changes.

It is confined to septum ,the second clue is a little delayed post QRS thickening of IVS (Septal beaking sign will vouch for benign LBBB with fair degree of success ) One clue is, the motion defects can not extend into anterior wall. Unfortunately, LBBB can induce wall motion defect in septum that may awkwardly simulate an ischemic wall motion. (So a marginal elevation is not going to help!) LBBB due to STEMI will purge a large quantum of cardiac enzymes from the infarcted zone. (They are helpful only if 3 hours have elapsed, can we afford to wait ? ). You can always ask for Troponin T / CPK MB. Role of enzymes and Echocardiogram in LBBB and suspected STEMI. (Almost impossible to differentiate it from rate dependent LBBB with aberrancy ) Here, LBBB is not due to necrosis of the bundle but due to ischemia. We do not know the true incidence and long-term significance of this entity. Of course, there is one another issue to comprehend ie transient ischemic LBBB. (Logic would suggest necrosis of large parts of IVS is necessary to cause LBBB ) Chronic LBBBs are relatively comfortable. If STEMI is causing the LBBB, it should be a large extensive one and you can not expect the patient to be comfortable.

#LVH WITH IVCD HOW TO#

How to overcome this ? Always rely on clinical features. even old MIs are at risk of acute intervention if they have LBBB and vague chest pain ! Still, Sgarbossa will struggle to differentiate an acute STEMI in Chronic LBBB from an acute LBBB in old AWMI. Of course, we can apply criteria of Sgarbossa to differentiate ! however flimsy it may appear. Probably, this is the reason many of the LBBBs are thrombolysed when they present to ER in an acute fashion. ( Physician presumption is a too delicate thread to hang our concepts ! )Įvery LBBB is new onset unless you have a documented proof otherwise. In fact, ACC/AHA guidelines reinforced this behavior, as it added a key word in their STEMI guidelines “New onset” or “presumably new onset ” LBBB is an indication for PCI/Thrombolysis. Unfortunately, this rule is too reverently followed by physician community. Suspicious ones demand observation in step down units, at least ! ERS being a common ECG pattern in general population, it is not wise to label every chest pain in ERS patient as benign. * STEMI in ERS : The issue becomes too delicate, if a patient with ERS develops a true ACS. There is some evidence ERS may confer a risk of primary VF, if they experience a true STEMI (Michel Haïssaguerre 2008 NEJM ).( False alarm of STEMI is the major risk !)

On EST it is expected to the touch the baseline.ST elevation can be dynamic ( Further confusing the picture ! ).The ST elevation in ERS is often global.Especially in vago-tonic persons with relative baseline bradycardia If the repolarisation starts even by 10 milli- second earlier, it would have early take off from descending limb of R wave and the J point ST segment appear elevated. The K channel porosity is subjected to high degree of genetic variations. Left bundle branch block(LBBB)/ Left ventricular hypertrophy(LVH).

Top 5 conditions that closely mimic and often mistaken for STEMI !

Lvh with ivcd