Tag Archives: cardiology

modified valsalva maneuver (quick reference)

12 Jan

for a more in-depth look, check out last May’s ACEP Now article.

brief highlights:

  • 428 patient study
  • modified valsalva maneuver
    • forced strain (e.g. blow into 10 cc syringe)
    • lie patient flat
    • elevate legs to 45 degrees x 15 seconds
  • return to sinus rhythm at 1 minute:
    • 43% with modified valsalva
    • 17% standard valsalva (strain x 15 sec, no position change)
    • NNT = 4


quick visual aid (start at the 1:17 mark if short on time):


There you go.  Add it to the toolbox.

References: ACEP Now article; video


Hypertrophic Cardiomyopathy (HCM)

25 Jun


-only about 50% of patients will have positive family history

-average age of diagnosis is 30-40 years -> not always a teenager or young adult!

-clinical features: syncope, chest pain, palpitations, dyspnea

systolic murmur at apex or LLSB

  • increases with valsalva and standing
  • decreases with trendelenburg and squatting

-ECG abnormalities present >85% of the time

            high left ventricular voltage, left atrial enlargement

            tall R wave in V1 (mimics posterior MI)

            deep, narrow Q-waves in inferior, lateral leads

-definitive diagnosis Doppler ECHO

-treatment: beta blockers, calcium channel blockers; these patients should be urgently referred to cardiology and be counseled to avoid strenuous activity

Source: lifeinthefastlane.com, Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.; picture

Submitted by K Estes.

Rapid Bedside Diagnosis of Massive PE (Looking for R heart strain)

8 Jan


-RV failure can be seen in massive PE but also in RV infarct and other conditions therefore this is NOT specific for a PE.

-Echo findings NOT sensitive for PE. Increased PA pressure not seen until >30 % obstruction (beyond my US skills- looking at tricuspid regurg jets…) and RV failure not seen until >50% ACUTE obstruction.

-BUT this is a good tool to have for the unstable patient in whom you have a high clinical suspicion for a PE.


US findings of increased RV pressure:

  1. Large RV
  2. Underfilled LV
  3. Paradoxical septal wall motion
  4. RV apex dominance
  5. McConnell’s sign


Findings by US view:

  1. Parasternal Long
    1. Large RV



Note: Normal ratio of RV: Aortic outflow: LV should be 1:1:1.


  1. Underfilled LV



  1. Parasternal Short
    1. Large RV
    2. Underfilled LV
    3. Paradoxical septal wall motion (“D” sign)


 The LV should be circular. Increased RV pressure pushes on the LV, causing it to look more like a “D”. Also, will see bowing of the septum toward the LV or flattening of the septum during diastole.


  1. Apical 4 Chamber
    1. RV apex dominance



  1. McConnell’s sign
    • Acute RV failure, 77% sensitive and 94% specific for PE in RV failure
    • Hypokinetic free wall and hyperkinetic apex (looks like a little person is jumping on a trampoline at the apex)
    • Here is an example: McConnell’s Sign


Submitted by Heather Groth.









how good is your precordial thump?

7 Nov


tough finding data on this (if you find more, please send it my way):

one study with 2 cardiologists:

  • cardiologist 1: 6.3–7.1 J
  • cardiologist 2: 8.8–10.4 J
  • ventricular arrhythmia terminated in only 2/155 patients


The Good:

deliver mechanical force to attempt defib (see mechanism below)

you can’t kill dead (little downside, aside from possible trauma, depending on strength)


The Bad:

if its not v-fib, and you induce it with an R-on-T

rarely successful (0/180 successful thumps with fist or 30-40mph lacrosse balls in one study)

The Mechanism (theory):

  • conversion of mechanical energy to electrical current (mechanoelectric coupling)
  • initiated by chest impact with a rapid, transient rise in left ventricular pressure.
  • Increased pressure results in myocardial stretch
  • stretch-activated ionic channels including the K+ATP channels are activated and open, resulting in an inward current and subsequent depolarization.

In commodio cordis, this depolarization induces a premature ventricular beat which, if precisely timed during the upstroke of the T wave in the P-QRS-T electrical cycle, can result in ventricular fibrillation—in essence, the R-on-T phenomenon.

In intentional precordial thump, this depolarization can indeed defibrillate the myocardium and thus interrupting the ventricular dysrhythmia.

References: cardiologist thumps; lacrosse ball thumps + picture;  mechanism

magnesium sulfate: great NNT, ? mechanisms

6 Nov

from October’s EP Monthly article:


IV magnesium sulfate: to prevent hospital admission in severe asthmatics

  • NNT = 3


Mechanisms for…

  • concurrent hypokalemia
    • magnesium repletion is required to prevent renal excretion of potassium by inhibiting ROMK channels in the distal tubules
  • eclampsia
    • unclear but may be due to systemic or cerebral vasodilation
  • tocolytic
    • calcium antagonism
  • dysrhythmias
    • magnesium is required for functioning of the Na/K ATPase enzyme, and hypomagnesemia can lead to prolonged QT and PR.
  • severe asthma exacerbations,
    • bronchodilation, though the mechanism by which it produces this is not well established


References: epmonthly article, theNNT.com; picture

LVAD: do you know enough?

29 Sep

Raging Hypothetical:

You are working overnight in a single coverage emergency department and the next patient walks in with a wire hanging from his chest and no palpable pulses. He needs help because the alarm on his device is going off. You look at the external device and it reads “low volume”. Before you start to treat this patient, a few important things to keep in mind…


Who gets LVADs?

Severe heart failure

EF <25%

VO2max <15

And a few other less common criteria


What in the world is it?

LVAD = Left Ventricular Assist Device 

=An external pump unit outside the body with an intake channel (draining blood from the left ventricle) and output channel (ejecting blood into the aorta)


Why might these patients come into the ED?

Infection of the driveline at skin insertion site

Bleeding (these patients are anticoagulated while using this device)


Pump thrombosis

Machine alarming

Patient is coding or pump not running (this is pretty much the same thing)


What to do?

All situations:

-contact the patient’s VAD coordinator

-listen over the heart to hear if the monitor is working (sounds like a “muffled blender”)

-evaluate mental status, skin color for perfusion, skin driveline site for infection

-evaluate the machine for battery function, lines plugged in, alarms of “low flow” or “low volume”

MAP should be 65 on manual Doppler (automated cuffs less accurate)

EKG to look for RV problems, arrhythmia, STEMI

-consider beside echo to assist with your differential (heart failure, focal wall motion abnormality, PE, etc.)


The patient should have extra batteries or there should be a special power pack option to plug into the wall


VADs love volume! Fluid bolus if poor perfusion, give PRBC if bleeding, but… think twice about correcting elevated INR or reversing coumadin (is this worth clotting off the patient’s device???)


Consider inotropes. Right heart failure à dobutamine; sepsis or reduced afterload à norepinephrine


Signs of pump thrombosis à hot device, working hard with high RPM, dilated RV/LV on bedside echo, low MAP. Consider heparin bolus.


And for the coding patient… avoid CPR. You can rip out the driveline. Yikes! But use your clinical judgment. The patient may need CPR if the pump is not working and the patient has lost their BP (MAP = zero).


Submitted by K Estes.


Sources: EMCrit Blog, EM:RAP podcast; picture

Left Anterior vs. Posterior Fasicular Blocks

16 Jun

Left Anterior Fasicular Block (more common of the two)

  • Left axis deviation (usually between -45 and -90 degrees)
  • Small Q waves with tall R waves in leads I and aVL
  • Small R waves with deep S waves in leads II, III, aVF



Left Posterior Fasicular Block (almost always associated with RBBB)

  • Right axis deviation (> +90 degrees)
  • Small R waves with deep S waves in leads I and aVL
  • Small Q waves with tall R waves in leads II, III and aVF



Clinical Significance

  • By itself with no symptoms, these blocks are not significant. May indicate underlying CAD which led to impairment or that the patient is at risk for progressing to LBBB.
  • LAFB can be seen in about 4% of acute MI cases. It is the most common type of intraventricular conduction defect seen in acute anterior MI, the LAD usually the involved vessel.
  • LPFB plus RBBB in acute MI associated with high mortality rate.  However, CAD is less common in RBBB with LPFB than in RBBB with LAFB or isolated LAFB.


Submitted by Joran Sequeira.


References: Biagani et al. Prognostic Significance of Left Anterior Hemiblock in Patients With Suspected Coronary Artery Disease. Journal of the American College of Cardiology. Volume 46, Issue 5, 6 September 2005, Pages 858–863; Elizari et al. Hemiblocks revisited. Circulation. 2007; 115: 1154-1163