In our protocols we have two beta blockers to choose from depending on the patient’s problem. The two are Metoprolol and Labetalol and they are actually quite different in their actions and therefore, their use.

Metoprolol is a selective beta 1 blocker which will specifically block the effects of epinephrine and norepinephrine on the heart. For our purposes this will blunt their chronotropic and inotropic effects thereby reducing CO and blood pressure. Additionally Metoprolol also has been shown to reduce the incidence of post MI arrhythmias.

Labetalol on the other hand is a non-specific beta blocker and also has alpha 1 blocking effects. This alpha blocking effect would make it specifically useful for lowering a high DIASTOLIC pressure as that number is driven primarily by peripheral vascular resistance.

Our protocols allow for Metoprolol is cases of ACS/MI and allow for either one in cases of hypertensive crisis and CVA with associated hypertension. We also can use nitroglycerin in the latter two but NTG has more of an effect on the veins (preload) than the arteries (afterload). I imagine that the choice would be based on whether its the systolic or diastolic that is really high.

According to the AHA, Nitrates should not be given both to someone with a systolic of less than 90 OR 30 or more points below their normal baseline!! (Also severe bradycardia <50BPM or Tachycardia >100BPM) This obviously makes sense, as someone with a normal BP of 160 needs close to that 160 to maintain adequate tissue perfusion. A BP of 130 will not cut it for him as he will be in a state of relative hypovolemia.

Also, with regard to O2, according to study published in the 70s high flow o2 may actually be detrimental to a patient experiencing an uncomplicated MI (i.e. no CHF, COPD, etc). This is because o2 is known to have vasocontrictive effects and as such by increasing afterload (increased peripheral vasoconstriction) you are reducing the cardiac output for a patient that really needs whatever he can get. The AHA it seems, advocates high concentration o2 only when the patient has an spo2 of less than 90% – Also see this study published in 2009 – relevant quote below.

Oxygen
Supplemental oxygen is given because of the theoretical benefit of maximizing oxygen delivery in a patient with an ischemic condition. This was first recommended for myocardial infarction over 100 years ago. However, there have been several studies dating back to the 1950s demonstrating concerning harmful effects. Specifically, they have shown that when supplemental oxygen is given to non-hypoxic patients, it produces increased systemic vascular resistance and decreases cardiac output. In hypoxic patients, the data have varied between no effect to improvement. Our current practice is based on the first randomized controlled clinical trial done on the effects of oxygen therapy for MI patients. It showed a reduction in MI-associated enzyme elevation, but these results did not achieve statistical significance (p=0.08). Given the small numbers involved in this study (n=151), it may have been underpowered to detect an actual clinical and/or statistical effect (type II error), but the results are not sufficient enough to support the routine administration of oxygen to all MI patients. In line with this evidence, the ACC/AHA’s STEMI guidelines  only recommend supplemental oxygen for hypoxic patients. It is worth noting that all but one of these studies were done before the advent of the pharmacologic agents, fibrinolytics, or PCI. In conclusion, the evidence is thin, and this highlights the need to re-consider the risks and benefits of oxygen therapy in both hypoxic and non-hypoxic patients, in the context of modern medical management of STEMI.

Comments welcome!

Doing rotations on 27v out of Montefiore and had this patient:

69 yea old female – chest pain x 7 hours started after grandson was taken in by EMS due to a febrile seizure. Pt has history of multiple stents placed a few years ago out of the country, no follow up care since then. Pt takes a statin and a beta blocker for HTN. Pt describes a substernal dull pain 8/10 radiating down left arm. Vitals are HR 84, BP 122/100, RR 24, Spo2 99% on room air, lungs C&E Bilat. ECG is NSR without ectopy. 12 Lead ECG  obtained with our Lifepak 12 reveals ST Elevations in Leads II, III, aVf, V1-V4, poor R wave progression and a curious rsR pattern in V1, width of 89ms. Reciprocal changes noted in Lead I and aVl. After ascertaining that there were no allergies pt was given 162mg of chewable ASA and placed on 3lpm via Nasal cannula.

Prior to administration of NTG a V4r lead was obtained which revealed ST elevations of 1mm. IV placed, 18ga Left A/C and 250cc fluid bolus administered. NTG admin 0.4m SL which offered minimal relief. B/P now 110/p – NTG repeated 0.4mg SL, this time patient offers that her pain is now 5/10. Repeat B/P is 102/64. Normal Saline left running wide open.

At this point we are at the ED, a STEMI alert had been called. 12 Lead in ED confirms the same and cardiologist calls it positively based on the V4r obtained in the field. NTG repeated in the ED causes BP to fall to 84 systolic, squeezing the bag and another 250 cc of NS gets her back up to 94 systolic.

Pt is transported to the cath lab on our stretcher and my preceptor is kind enough to allow me to stay and watch the case. LAD and LCx both freely flowing. RCA – 100% proximal occlusion.

I’ll be getting a v4r on every IWMI before NTG.

(Also see this great article :Recognition and Treatment of Right Ventricular Myocardial Infarction)

And this one too: http://ems12lead.blogspot.com/2009/02/right-ventricular-infarction-part-i.html

Tim Phalen – 10/13/09

STEMI vs. Non STEMI – STEMI is ultimate candidate for reperfusion therapy – non STE-MI – much higher mortality rate.

Is the early part of the ST segment elevated – 1mm elevated at beginning – at J point only (J point elevation)

Pick one good segment – pick one where T-P matches that of T-P before it –pick a steady baseline

Notch in ST segment – not always BBB – Not STEMI

Always use the T-P segment to measure elevation

aVR – Looks from top at chamber of Left ventricle – not used because we can’t localize the injury. Also looking at endocardial tissue – wont have same meaning or significance

Evolution of AMI

• Ischemia – Endocardial Hypoxia – St Depression – T wave inversion
• Injury – Epicardial Hypoxia – causes ST Elevations – being that the epicardial cells have a rich blood supply – must be an occlusion.
• Hyperacute Phase -  T waves – Tall & peaked – first change – may give illusion of a wide based t wave (vs hyperkalemia) – Tall = in limb leads elevations of  >5mm – in chest leads more >10mm – Peaked = don’t want to sit on it
• Acute Phase -
• Pathological Q wave – =>.04 – or greater than 1/3 of R wave. –Age undetermined
• A normal 12 lead does not rule out an AMI

Reciprocal Leads

• II III aVF vs. I aVL, V-Leads
• Inferior wall MI – single most likely reciprocal lead is aVL
  • Some MIs start with reciprocals and then show elevations

More than 50% of ST Elevations are not caused by AMI – called STEMI imposters (first 3 make up 80%)

• LVH – Primary cause is HTN
  • increased QRS amplitude – variety of formulas exist – read the interpretation – machine does the math. (Or – look at v1 – from baseline to most negative deflection – count mm – then look at v5 and v6 and count the tallest. add depth of v1 to highest of v5 or v6 – if over 35 you have LVH (if under age 35 use 53mm)
• BBB – Primary cause is aging process
  • Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
• Ventricular Rhythms including paced
  • Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
• Benign Early Repolarization (BER)
  • ST elevations often in lateral leads and lead II
  • Tall peaked T waves – and tall QRS
  • Fishhook ST segment
  • Young healthy male (20-40 years, +African Americans)
  • does not typically produce reciprocal changes
• Pericarditis (epicardium may be inflamed too)
  • May be in all leads
  • May be in leads not grouped anatomically
  • sharp pain
  • localize with a finger
  • positional – prefer leaning forward
  • radiates to base of neck or shoulder blade
  • might hear friction rub on auscultation
  • does not typically produce reciprocal changes

5 step analysis

• 1. Rate & rhythm
  2. Waveform analysis
     1. st segment
     2. T wave
     3. Q wave
  3. Suspected STEMI
     1. location
  4. Additional considerations
     1. voltage criteria for LVH
     2. QRS width
     3. Reciprocal leads
  5. STEMI Decision
     1. Definitely NOT a STEMI
     2. Definite STEMI
     3. Definite Maybe – EMS needs a plan for definite maybes – Transmit ECGs to ER for consult.

see www.ecgsolutions.com

Right and Posterior Leads

• • Inferior wall MI – most likely RCA – 40% of time will also have a Right Ventricular MI – Add v3r through v6r (at minimum look at v4r)
  • Anywhere else – Most likely LCA -
  • Posterior wall MI – reciprocal changes in v1- v4 (reciprocal q wave would manifest with taller R waves, sometimes)– indicative changes in V7, v8 and v9 (keep going around back – posterior axiallary mid scapular, just left of spine)

BBB Recognition

• forget the notch
• suspect with wide QRS
• normal sinus, a-fib, or any sinus rhythm – suspect BBB
• v1 – back off j point – which direction is tail end of QRS – RBBB – points up – LBBB turns down
• LBBB – new onset – indication for reperfusion – (Sgarbossa criteria)
  • Normally BBBs produce discordant QRS-ST (direction of QRS is in opposition to ST)
  • Both in same direction in any one lead – infarct.
  • If you have LBBB with concordant (both downward) QRS & ST depressions – suspect MI if it occurs in V1 or V2 or V3
  • More than 5mm of elevation from baseline to j point – suspect MI in any one lead
• Serial EKGs – changes are hallmark of AMI

Dr Bonaris – 12 Lead EKG

The three Is

Ischemia

• Lack of oxygenation to myocardium
• ST Depression or T wave inversion
• may or may not result in infarct or Q wave

Injury

• Prolonged ischemia
• ST elevations (injury pattern)
• usually results in an infarct may or may not result in a Q wave

Infarction

• Death of tissue
• May throw pathological Q waves (.04 wide and greater than 1/3 of height of R wave)

T to P is the baseline you compare to for comparing ST segment, do not use the the PRI!

T wave inversions may be normal in some leads, but think cardiac.

What to look for

• ST elevations in two or more anatomically contiguous leads
• T wave – tall and round – Tombstone pattern

12 lead EKG Injury Patterns

Evolution of MI

• Hyperacute T waves – Tall Peaked- Suggestive of MI (Also hyperkalemia)
• Tombstone appearance – ominous sign, severe

Reciprocal changes

A change detected electrocardiographically in a wall of the heart opposite the site of a myocardial infarction. In acute inferior wall infarction, reciprocal changes are considered a sign of more extensive myocardial damage. Not always present.

(Electrical alternans – seen in cardiac tamponade)

Some more from http://medinfo.ufl.edu/~ekg/Infarct%20&%20Ischemia.html

Coronary Anatomy: Relation to the Site of Infarct

• The most common cause of Acute MI is sudden total occlusion of a major coronary artery.
• Sudden total occlusion of the RCA (Right Coronary Artery) causes acute inferior MI and/or posterior or right ventricular MI (ST elevation in lead V4R helps diagnose RV infarction.). Mobitz I is common with inferior MI (the RCA supplies the AV nodal artery).
• Sudden occlusion of the Left Main coronary artery leads to sudden death (from massive infarction).
• Sudden occlusion of the LAD (Left Anterior Descending) artery leads to anterior infarction; bundle branch block/Mobitz II 2° AV block may be seen.
• Sudden occlusion of the Circumflex artery leads to lateral infarction.  In about 10% of patients this artery (rather than the RCA) also supplies the inferior and posterior walls of the left ventricle.
• Note -  Collateral development changes the above patterns.