Left Atrial Pressure

Left atrial pressure, LAP, is becoming rapidly and important measurement to accurately treat patients in acute decompensated heart failure with congestion but also to rule out a component of pulmonary vascular congestion due to HfpEF.  Due to the dramatic decrease decline in use of pulmonary artery catheters, this is really the next best measurement we have for left ventricular filling/correlate to left ventricular end-diastolic pressure.

However in patients with moderate to severe ARDS that require proning due to severe hypoxemia, I still feel these patient's benefit from a pulmonary artery catheter.  Prior studies that  reviewed  the use of PA catheters was in all-comers in the MICU,  in a very inhomogeneous patient population, an Achilles heel in randomized control trials that limit any credibility regarding external validity.

Notable exception here is that a pulmonary artery catheter still remains a standard of care in post cardiac surgery patients, as well as stage IV class D for treatment decisions for in particular inotropic therapy with milrinone, heart failure patient and cardiogenic shock

I have posted earlier this year on diastolic function and a quick easy approach to assess intracardiac filling pressures.  This is a more complete article with the 2016 guidelines from ASE with attached PowerPoint presentation.

 Realize that most echocardiographic reports are quite inaccurate in determining the degree of diastolic dysfunction and are even more inaccurate in the determination of left atrial pressure. Tissue Doppler imaging from the lateral mitral annulus and medial mitral annulus has become a surrogate quick measure ( E/e' ratio)  for cardiologist and Intensivist ( by bedside US) to determine left atrial pressure. Nothing is farther from the truth : these numbers need to be correlated with additional markers and pressure measurements obtained by echocardiography to give an accurate value. This requires a comprehensive and somewhat time consuming procedure, particularly if done at the bedside.  In most patients on mechanical ventilation, it may not be possible to follow the guidelines to obtain all the measurements that go into the final determination of left atrial pressure/LAP

LBBB and Sgarbossa Criteria in acute MI

What is the diagnosis? What criteria are used to further analyze this EKG ?

Dr Rael Sundy from Tel-Aviv had the immediate answer: this tracing represent an acute anterior wall MI .

Ideally, diagnostic tests for life-threatening conditions (i.e. AMI) need to be highly sensitive.  The reason the original Sgarbossa criteria are limited in clinical practice is the low sensitivity (20%).  This is why a new LBBB alone is no longer a criteria for emergent cath lab activation. Recently, Steven Smith, MD from Dr. Smith’s ECG Blog published a new criterion to replace the third component of the original Sgarbossa Criteria using the ST/S ratio instead of discordant ST-elevation ≥ 5mm. 

 What are the new modified Sgarbossa Criteria?

Scandinavian Clinical practice guidelines for therapeutic hypothermia and post-resuscitation care after cardiac arrest

A little bit of an older article on TTM, but nevertheless a nice overview

The Art of Medicine

My prior TED Talk Blog entry reminded me of a patient I saw in my clinic, many years ago  as a Cardiologist when I was still practicing in a Multi-Specialty Group as well as another "beautiful" TED Talk by Dr Abraham Verhgese ( I published on another Blog I ran during those years) .....

" I recently saw a young woman referred to me for shortness of breath. She had been seen by several physicians and had a recent ER visit for this problem. A week prior she reported some atypical chest pain and a CT scan of the chest was done. She was diagnosed with a "small pneumonia" and given antibiotics. She was told everything else was fine. Her shortness of breath failed to improve, however. She was then referred by her primary care physician to me, because surely there was something wrong with her heart.

 As I walked into the exam room, I noticed she was very pale looking and very anxious appearing. As part of her history she told me that several years ago, she underwent gastric bypass surgery. I asked her if she had blood work done, because my immediate suspicion was that she was anemic. She told me she had it done as recently at the time of her ER visit . My nurse started looking for the labs accessing another database ( even in the community I work, several "Electronic Medical Records" don't "talk" to each other) and not surprisingly, the young woman was profoundly anemic with a hemoglobin of 7.4 ( normal greater then 12), explaining her shortness of breath.

 I don't know what's the saddest part of this story: the fact we don't "look" and "examine" our patients anymore, or being enamored by a CAT scan and completely forgetting to look at a basic blood count or being seen by several physicians, not one of them picking up on the fact that she is a set up for iron deficiency and other micro-nutritional abnormalities because of her gastric bypass surgery and then being referred to a Cardiologist. This is far from being an  isolated case in our current outpatient model of HealthCare. The irony of course is that seeing 30-40 patient a day in clinic is bound to increase the cost rather than curtail it and surely with poorer overall outcomes."

I Know All (in Medicine)

Another excellent TED Talk ....and so so true!

Smartphone electrocardiograms reveal painful left bundle branch block syndrome and illustrate associated electrophysiological phenomena

EP Europace Painfull LBBB syndrome 

A 69-year-old lady presented with exertional chest discomfort. A 12-lead ECG indicated anteroseptal T wave inversion (TWI) (Panel A, left), suspicious for Wellens’ syndrome. However, cardiac catheterization (Panel A, right) and echocardiography were normal. Her symptoms persisted and she purchased a smartphone electrocardiogram (EGM) device (AliveCor KardiaMobile™, USA). Recordings revealed that her pain coincided with the sudden onset and resolution of left bundle branch block (LBBB) (Panel B, top EGM). ‘Painful LBBB Syndrome’ is an increasingly recognized entity and is easily missed following a reassuring ischaemic evaluation. These single lead recordings also illustrate associated electrophysiological phenomena. The LBBB is rate related (Panel B, top EGM), suggesting a phase 3 block. Resolution occurs at a lower rate than onset, due to ‘linking phenomenon’ whereby concealed retrograde invasion of the bundle occurs from the contralateral side. Premature ventricular contractions allowed time for the LBBB to recover (Panel B, middle), consistent with aforementioned explanations for ‘functional’ block. The TWI was also demonstrated on the KardiaMobile™ by recording an anterior precordial lead (Panel B, bottom). Known as ‘cardiac memory’, TWI transiently occurs after a period of abnormal ventricular activation.

In summary, smartphone-based EGM’s continue to improve our diagnostic capability and can illustrate complex electrophysiological phenomena

Painful left bundle branch block syndrome: Clinical and electrocardiographic features and further directions for evaluation and treatment- Heart Rhythm Society 

Narrow QRS tachycardia ("SVT") in the ICU

Supraventricular tachycardias should be described as long RP or short RP tachycardia.

SVT is a general term and has no reference to the underlying pathophysiology or mechanism causing narrow QRS tachycardia. Short RP tachycardias, are most commonly seen in clinical practice,  long RP tachycardias to a lesser extent  (the latter more frequently in  the ICU setting)
. 
One should always look at the initiation of the tachycardia, i.e. is there warm up or ramp-up phase.  How does the tachycardia terminate:  is there a P before conversion to sinus tachycardia after administration of adenosine, or does the tachycardia terminate without a P-wave?  What is the axis of the P-wave during narrow QRS tachycardia, i.e. is axis inferior or superior?

Adenosine should always be administered both as a diagnostic and possible therapeutic agent in the setting of sudden onset hemodynamically stable narrow QRS tachycardia ( and regular monomorphic VT- see below) . Adenosine terminates close to 100% of short RP ( narrow QRS) tachycardias (slow-fast AVNRT as most common rhythm).

Long RP (narrowQRS)  tachycardia's are seen less common but deserve some further attention (higher incidence in the ICU setting) :

1.  Fast-slow AV nodal  reentry tachycardia
2.  AV reentry tachycardia with retrograde conduction over accessory pathway
3.  Ectopic atrial tachycardia/focal atrial tachycardia
4.  Sinus tachycardia

Adenosine will terminate AV nodal reentry tachycardia, but very uncommonly there is an adenosine sensitive accessory pathway.  It will not terminate sinus tachycardia but can cause slowing of the rate.
However, some ectopic atrial tachycardias can be terminated by adenosine.(60-80%)

Of note, adenosine can also be administered for hemodynamically stable regular monomorphic wide complex QRS tachycardia, as it will break AV reentry tachycardia with antegrade conduction over accessory pathway as well as some forms of ventricular tachycardia

The new ACLS guidelines now has adenosine given up to 2 times instead of 3 times.  The first dose of adenosine should be 6 mg administered rapidly over 1-3 seconds followed by a 20 cc normal saline bolus ( use 3 -way stopcock).  If the patient's rhythm does not convert within 1 to 2 minutes,  a second 12 mg dose may be given similar fashion.

A lower initial dose of 3 mg should be used in patients taking dipyridamole or carbamazepine as these 2 medications potentiate the effect of adenosine.

Also, prolonged asystole has been seen with the use of normal doses of adenosine in heart transplant patients and central line use.  Therefore, the lower, 3 mg dose should be considered for patient's with a central venous line or history of heart transplant

Sometimes termination is followed by an immediate return of the tachycardia,  even in AVNRT. In these patients, intravenous verapamil 5-10 mg slow push can be used.  Diltiazem, 20 mg IV as a loading dose followed by 10 mg/min continuous infusion, can be used but is less effective than verapamil.  Intravenous beta blockers i.e. metoprolol, esmolol, can be used as an alternative to verapamil or diltiazem in patients who do not not convert with or are intolerant to adenosine.

This case report in the New England Journal of Medicine is an interesting presentation of focal atrial tachycardia secondary to  hyperthyroidism ( Graves' disease). 
It also highlights that performing contrast studies will cause temporary suppression of  thyroid production due to administration of a high iodine load and " masque" hyperthyroidism for certain period of time.