This question always creeps in any coronary care unit.
Posts Tagged ‘nstemi’
Posted in Cardiac biomarkers, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Infrequently asked questions in cardiology (iFAQs), NSTEMI, tagged cpk mb in nstemi, definition of nstemi, nstemi, troponin positive unstable angina, unstable angina on October 22, 2013| Leave a Comment »
Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged anemia and ST depression, differential daignosis for left main disease, dispropotiante st depresion due to anemai, nstemi, secondary unstable angina on October 31, 2012| Leave a Comment »
This is a true story . . . happened many years ago under my direct vision.
A 48 year old women came with significant breathlessness and catchy sub -sternal chest pain .
“I was exerting too much in recent days doctor” , she said .
Her ECG showed a tachycardia and dramatic ST depression in most leads .
The ER in charge promptly texted the cardiologist .
The moment he saw the ECG ,he had no hesitation , to order for an emergency angioplasty ( How can he plan a angioplasty , without even knowing the coroanry anatomy . some one murmured . May be . . what he probably meant was emergency angiogram the other explained ) Further , he was telling his fellows . . . that this is going top be tough case and a possible left main PCI .
An emergency angiogram was done . On table it was a huge surprise for every one , it was a a classical text book look alike normal coronary arteries !
The moment normal CAG was visualized the consultant concealed his momentary surprise and went on to say it is classical case of syndrome X with severe micro- vascular disease causing ECG changes !
As the patient did not give any opportunity to poke her coronaries she was wheeled out of wheeled out of cath lab.
Meanwhile , first year fellow came rushing with the blood reports and biochemistry .
Is everything alright ? Yeh sir , except her Hb % . . . it is 5.6 Grams !
The bewildered consultant * realized the high coronary drama , that is been enacted over the past 2 hours ! and learnt (and taught) a most important lesson to their fellows !
Hi guys , this is neither a NSTEMI nor a microvascular syndrome X . . . this is simply anemia related extreme ECG changes ! We have erred in our reasoning and our pre cath clinical scrutiny has gone awry !
He went on to say , don’t worry many times medicine is learnt in hard ways . After all nothing adverse has happened here .
The women was subsequently investigated and handed over to gynecologist for a probable hysterectomy .
Please be reminded , anemia can produce variety of ECG changes. In extreme anemia global ST depression is common especially if tachycardia is associated .
The lesson here is , whenever gross ST depression is witnessed with vague chest pain check the hemoglobin first . This is an unusual story of a women , with simple anemia (due to chronic mennorhagia ) landed in cath table in an acute fashion . Luckily she did not have any incidental coronary lesions that prevented her becoming a greater cath lab victim !
* The bewildered consultant is none other than the author of this blog.
Posted in Cardiology - Clinical, cardiology -ECG, cardiology- coronary care, Cardiology-Coronary artery disese, critical care ccu, tagged ecg mimickers of stemi, lvh mimicking stemi, lvh with st depression, lvh with st elevation, non infarct st elevation, non q mi, nstemi on January 23, 2012| 1 Comment »
This is the ECG of a 45 year old man with H/O hypertension and chest pain .The general practitioner who first saw him alerted this patient about a possible heart attack asked to meet a cardiologist immediately. The cardiologist who saw this ECG tended to confirm the diagnosis and advised admission in a coronary care unit .
The patient defied both and somehow landed in my echo lab . Looking at the ECG I also expected it to be a STEMI evolving into a Non Q MI .
I was surprised to find only LVH with absolutely no wall motion defect . There was no evidence of ASH, HOCM or apical cardiomyoapthy as one of my fellows initially suspected . His EF was 70 %. Cardiac enzymes were sent by then. When I spent few minutes with him , listening the history , it was very clear what he had was non cardiac pain . In the anxiety , no one got it right about the character of pain ,which was localised , lasted for few seconds and least suggesed angina.
The moral of the story is listen to the patient however dramatic the ECG may look !
What is special in this ECG ?
It is common for LVH with ST depression to be mistaken for ACS/NSTEMI
Here , there were other observations that added more complexity .
- Presence of ST/T changes in inferior leads(ST elevation in lead 3)
- Bi-phasic T wave in v1 to v3
- ST elevation in precardial leads
In LVH it is usual to note ST depresion , how do you explain ST elevation in LVH ?
ST elevation in LVH may occur in leads v1 to v3 . It is very rare for LVH to inscribe ST elevation in v4 v5 v6 . Why certain leads elevate the ST segment while others depress in LVH is not clear. It may represent incomplete LBBB pattern where the ST segment deviates opposite to the dominant QRS complex. Septal hypertrophy often elevate while free wall hypertrophy depress the ST segment . Since V5,V6 leads are free wall oriented , these leads record classical ST depression .
Importance of Bi-Phasic T waves
Please remember Bi phasic T waves are notorious for it’s unpredictability. An innocuous looking bi-phasic T waves (especially with dynamic behavior ) is a harbinger of proximal LAD or even left main disease.
Finally , what will be ECG changes if a patient with classical LVH who develops a real STEMI ?
- LV strain pattern normalises ?
- Further ST depression occurs ?
- No great changes . ECG Looks near normal ?
Answer : ?
Posted in Uncategorized, tagged ambulance crew as cardiologists, nstemi, pci vs pre hospital thrombolysis, prague danami, timi 3 flow vs timi 2 flow, timi flow in highways on March 27, 2011| Leave a Comment »
Acute STEMI is the numero uno of all medical emergencies. Hundreds of life are lost every few hours in our planet.Significant chunk of them do not even reach the hospital alive . While the emergency crew has many vital responsibilities , the cardiologist job starts only after the patient reaches the hospital . Hence the ambulance crew need to act much more sharper. Please remember even the skills of the driver will have a direct impact on the myocyte survival.
The symptom to first medical ( or second hospital ) contact could be as vital as a primary PCI procedure itself . A 3 minute traffic jam can kill 3 thousand myocytes ! One could imagine the importance of decision making process here.
Distance from the point of contact to PCI lab , the anticipated delay , intensity of traffic matters .
Is it not funny , to realise when we have a reperfusing agent on hand , within the ambulance and the vehicle stuck in the traffic jam waiting to reach a reperfusion room situated 50 km down the high way !
( One may wonder why can’t we thrombolyse every one routinely in the ambulance and do the PCI later in . . . But surprisingly this concept simply does not work !)
When we realise , even in a well developed country like Netherlands , time to shift to cath lab is a big issue (Read the following article ) we will never ever know , how much of myocardium is consumed by traffic jams in a country like India , where the traffic scenarios can be more chaotic than a VF !
Events that unfold following a STEMI are crucial
It begins with chest pain recognition.
Call for first help Spouse/Family doctor /Neighbor
Call for 911/108 . Ambulance arrival time and boarding
Administration of Aspirin + clopidogrel*
Meanwhile spontaneous thrombolysis will begin in most of them !
A promptly administered Aspirin and clopidogrel a shot of heparin and a lytic agent within 30 minutes is distinctly possible and may be more effective at a fraction of cost.
Even though current studies still . . .do not favor primary PCI over thrombolyiss in the first hour , most of the cardiologist do show some favoritism towards pPCI for some unknown reasons.
So by default , many of the ill fated STEMI patients enter an unrealistic hemodynamic race in the deadly highways and urban lanes our country !
For every minute that goes by , the patient not only loses his muscle but also the golden opportunity to get salvaged by the thrombolytic agents .
Since , a delay beyond one hour eliminates the indication of thrombolysis (if a cath lab is available in the vicinity ) many times traffic delays convert a potential hyperacute thrombolysis into a say . . . 3-6 hour old PCI .(Should we feel happy about it ?)
Here , we need to know TIMI 2 flow achieved easily by thrombolytic agents is quiet effective in preventing myocyte death.
Fast track shift to PCI
Helicopter drop over cath lab -( Distant dream ? or better to be in dreams ) It has been noticed even a helicopter was squarely beaten by the thrombolysis in terms of early and timely reperfusion.
Fast -Slow track PCI ? (Like fast slow AVNRT !)
Unexpected delays on road , in many countries financial issues /Insurance sanction etc contribute to the time delay significantly . What starts as a fast track protocol peters out into slow race (Late primary PCI ) and may even end in a grinding halt.(No primary PCI )
Worse still . . . some of these patients are made unsuitable for thrombolysis as well !
Management of STEMI is gradually becoming a team effort. The emergency crew , the command , the destination hospital all need to be alert and proactive. When the initial anticipated delay is getting prolonged , get the ground staff in cath lab ready for an emergency landing .
A word of advice for the ambulance crew .Involve them more in the decision making as they are in a better position to calculate the possible delay. If delays are anticipated propose a thrombolytic order and get clearance from the command and administer the lytic agent as early as possible.
It is highly likely , restoration of TIMI 2 flow right in the middle of national highways is much . . . better than a TIMI 3 flow that is going to come later . . .in a distant cath lab .
Finally use the common sense liberally before you act . . . unfortunately it has become the most elusive sense for man kind !
Here is a study that gives a fresh insight into this enigmatic issue of pre-hospital thrombolysis vs primary PCI
NSTEMI is a common clinical problems in CCU.
When we say NSTEMI it can mean any of the following
- NSTEMI with ST depression
- NSTEMI with T wave Inversion
- NSTEMI with Biphasic T wave
- NSTEMI with normal ECG
- The irony called STEMI evolving as NSTEMI**
By default most of us think , if it is NSTEMI . . . there must be ST depression. This thinking is not logical but traditional. Still, ST depression may be the common presentation. NSTEMI with ST depression has much worse outcome than other forms.
The following ECG is from a 45 year old man with a vague mid sternal chest pain for 48 hours.
His echo showed wall motion defect in LCX territory .A diagnosis of NSTEMI was made.The predominant finding was biphasic T waves .
**One may wonder why can’t we call this ECG as a Classical STEMI ?
There is a 2mm ST elevation , with a infarct as well ? But , the point here is there is no business for T waves to get bi-phasic or inverted in the early hours of a classical STEMI .
This exactly has happened here. Hence we can not call the above event as STEMI . Instead it is , STEMI evolving into NSTEMI . So a combination of features of STEMI/NSTEMI occur together. The best description for above entity is STEMI in transition to Non Q MI
Read the related article in my site Is the terminology of Non Q MI still relevant or obsolete ?
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology journals, cardiology- coronary care, Cardiology-Coronary artery disese, Cardiology-Land mark studies, tagged bari 2 study, cass study, coronary intervention, courage study, high risk unstbale angina, how to do priamry pci, how to manage nstemi, ictus, mass 3 study bari 2d, medical management of cad, nstemi, oasis study, pci, ptca, stemi on December 18, 2010| Leave a Comment »
Cleveland clinic is a leading centre for cardiac care .Major technological breakthrough occurs from this institute than any other place. Thousands of articles come out every year. Some articles , get global attention and make a huge impact. These are usually related to a new hi- tech modality like CRT devices or percutaneous aortic valve deployment etc ,etc.
Some articles , which are very important may not get the due attention . Journal editorial boards often have a scorecard called impact factor .That is , how a journal is impacting the practice habits of medical professionals . Ideally we need to have to grade individual articles with impact factor .Many articles may not have any significant impact however good the impact factor of the journal.
Here is an article, which excellently depicts the principles of management of ACS. It was published in 2003 JACC, by Steven Nissen from Cleveland, Ohio .It deserves more attention . Every cardiologist , involved in ACS management should read this, especially the interventionist.