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

Pulseless Electrical Activity (PEA)

Treat the cause first! 

  
Causes:  Remember 5 “H’s” and 5 “T’s”

Hypoxia*                                     Tension Pneumothorax              
Hypovolemia*                             Tamponade (Cardiac)
Hypothermia                              Tablets (drug overdose)              
Hyper/hypokalemia                    Thrombosis, coronary (ACS)
Hydrogen ion -acidosis               Thrombosis, pulmonary (embolism)         
*Most common causes     

   
Algorithm “P-E-A”:
Possible causes-always give 500 cc bolus of fluid since hypovolemia is common cause.
Epinephrine 1 mg IV q 3-5 minutes
Atropine 1 mg IV q 3-5 minutes
Consider transcutaneous pacing
Dopamine after rhythm and pulse returns to treat BP

Nursing Information

"For ACLS Algorithms: This if from my Critical Care Syllabus (NU 403-Med.Surg. Nsg II)" Contributed
by Dr. Hatfield
Mgmt of MI patient: MONA Be A Friend, Please!
Morphine
Oxygen
Nitrates
ASA (within 24 hrs of admission and on discharge)
BB (within 24 hrs of admission and on discharge)
ACE-I or ARB for LVSD (EF <40%)
Fibrinolytic within 30 minutes of arrival
PCI within 90-120 minutes of arrival

VT/VF Algorithms:  AAA SCREAM
AAA: Assess the patient first (not the monitor)
Activate Emergency Response
Action- start CPR
SCREAM
Shock at 200 joules(with biphasic defibrillator) or 360 (monophasic)
CPR x 2 min.
Rhythm check: if still in VT?VF give…
EPI or Vasopressin IV or IO ( no more meds down the ET tube)
CPR x 2 min. and shock at 200 joules
Antiarrythmic meds: Amiodarone IV/IO
CPR x 2 min. and shock at 200 joules
Antiarrythmic meds: consider Lidocaine in Amio. not effective
CPR x 2 min. and shock at 200 joules
Antiarrythmic meds: consider Mag Sulfate IV/IO but only if Mg is low or pt in Torsades de Pointes
If pt is acidotic: NaHco3 (draw ABG’s)
If pt converts out of VT/VF: hang a drip based on the med bolus used (Amio or Lidocaine)

Asytole Algorithm:
"maybe we should give some CEA"
CPR
Epi or Vasopressin
Atropine

Bradycardia Algorithm:
"Pacing always ends danger"
Pacer transcutaneous
Atropine
Epi
Dopamine
If the patient is resuscitated, considered differential diagnoses (what caused the code to occur); order CXR, lab work, 12 Lead EKG and speak with the family.

Contiguous and reciprocal lead charts

Prehospital 12 Lead ECG: Contiguous and reciprocal lead charts

See this site for great 12 lead info…(reproduced below)

Here are some charts to help you identify and localize acute STEMI on the 12 lead ECG.
Contiguous leads

What do we mean when we say leads are “contiguous”?

Contiguous leads are “next” to one another anatomically speaking. They view the same general area of the heart (specifically the left ventricle).
For example, these states in the upper-midwest are contiguous, because they are all touching and in the same region of the country.
The “inferior” leads (II, III and aVF) view the inferior wall of the left ventricle. Remember that the inerior leads make up the lower-left corner of the 12 lead ECG.
The “septal” leads (V1 and V2) view the septal wall of the left ventricle. They are sometimes grouped together with the anterior leads.
The “anterior” leads (V3 and V4) view the anterior wall of the left ventricle.
The “lateral” leads (I, aVL, V5 and V6) view the lateral wall of the left ventricle. Leads I and aVL are sometimes referred to as the “high lateral” leads, because their positive electrode is on the left shoulder. Leads V5 and V6 are sometimes referred to as the “low lateral” leads because their positive electrodes are on the lateral left chest.

In addition, any two precordial leads that a next to one another are contiguous. In other words, V4 and V5 are contiguous, even though V4 is an anterior lead and V5 is a lateral lead. This makes sense when you consider that leads V4 and V5 are next to each other on the patient’s chest.
It’s worth mentioning that the standard 12 lead ECG does a relatively poor job examining the lateral wall of the left ventricle, and does not directly examine the posterior wall of the left ventricle. That’s the reason we sometimes miss acute STEMI in the distribution of the circumflex artery.
This image from Rescue One EMS Prehospital Program © 1999 Centric Medical Communications, Inc. illustrates the point nicely. This was from a class sponsored by Centocor (makers of the drug Retavase) that was taught by a Miami-Dade Fire Captain. In case you weren’t aware, Miami-Dade was the largest enroller in ER-TIMI-19 which was a clinical trial involving prehospital administration of thrombolytic therapy.

Think of it this way. There are 3 main epicardial coronary arteries, the right coronary artery (RCA), left anterior descending (LAD) and the circumflex (LCX).
It stands to reason that approximately 33% of documented acute STEMIs should occur in the distribution of each of the 3 main arteries. But that’s not what we find. Most acute STEMIs are documented in the distribution of the right coronary artery or the left anterior descending.
In other words, the standard 12 lead ECG does a relatively poor job examining the lateral and posterior walls of the left ventricle, so there’s a danger of missing STEMI in the distribution of the circumflex artery.
That’s the main reason it’s so important to carefully analyze the right precordial leads (V1-V3) for reciprocal changes that may indicate posterior STEMI. You can also consider using modified leads V7, V8 and V9 to increase the sensitivity.
Right ventricular infarction is another issue that will have to be addressed another time.
Reciprocal leads

What do we mean when we say that a lead is reciprocal? It means that during an acute STEMI, when ST segment elevation is present in leads that face the acute injury, ST segment depression will often be present in leads that face the “ischemic boundary”.
Many theories have been advanced to help explain reciprocal changes. I can’t go into all of them here, but consider this diagram modified from A Mechanism for ST Depression Associated with Contiguous Subendocardial Ischemia by Bruce Hopenfeld. Jeroen Stinstra, and Rob MacLeod. J. Cardiovasc. Electrophys, 15(10), 1200–1206, 2004.

Computer modeling has shown that as the ischemic zone extends from the endocardium to the epicardium, it creates a relatively positive area above the ischemic zone, and a relatively negative area at the ischemic boundaries.
This computer model helps explain why reciprocal changes may appear prior to ST segment elevation. Some authors have suggested that the first sign of acute inferior STEMI is a downsloping ST segment in lead aVL, and I have seen this happen many times.
Regardless of why reciprocal changes occur, clinical experience shows that the most important reciprocal changes can be viewed between the high lateral leads (I and aVL) and the inferior leads (II, III and aVF).
Keep in mind that reciprocal changes can be subtle, and may present as nothing more than a flattening of the ST segment in the reciprocal leads.
*** Update 01/15/09 ***
Check out this case at Dr. Smith’s ECG blog to see just how subtle reciprocal changes can be! And how they can prevent you from discharging a patient home to experience cardiac arrest!
*** End update ***
You will sometimes notice reciprocal changes in the anterior leads (V1, V2, V3 and V4). These usually represent reciprocal changes associated with injury of the posterior wall of the left ventricle. Since we don’t usually view modified chest leads V7, V8 and V9, we most often see these changes associated with acute inferior STEMI, because the posterior descending artery branches off the right coronary artery (RCA), which also supplies the inferior wall of the left ventricle.
With anterior STEMI, the occlusion is often in the left anterior descending artery (LAD) which branches off the left main coronary artery. Depending on the patient’s coronary vasculature, the culprit artery, and the location of the occlusion, the blood supply may also effect the lateral wall of the left ventricle, which can create reciprocal changes in the inferior leads (sometimes very subtle depending on the stage of the infarct).
Reciprocal changes may not always be present, but when they are present, it is very strong supporting evidence that the patient is experiencing actue STEMI.
See also:
12 lead ECG – lead placement diagrams
The problem of ST segment elevation

Andy Rodriguez

First Degree Heart Block

• Not a true block
• Conduction delay at AV node
• All impulses are conducted to ventricles
• PRI will be >0.20 consistently across the strip

Second Degree Heart Block

• Intermittent
• Some get through and some don’t
• pathology can be in AV node or below in Bundle of His
• pathology is often blended with other blocks
• Mobitz Type I (Wenckebach)
• Impulses encounter progressive delays at the AV node until one impulse is blocked completely
• PRI starts getting progressively longer and then dropped QRS
• All conducted QRSs present are tight, <0.12 and preceded by a P wave
• Mobitz Type II
• Can be regular or irregular, depending on conduction ratio
• Usually a Brady rhythm
• More than one P wave for every QRS
• PRI constant on conducted beats can be >0.20
• QRS <0.12
• Conduction Ratios
• 2:1, 3:1, etc. two P waves for every conducted QRS

Third Degree Heart Block (Complete Heart Block)

• All impulses generated by Sinus node are being blocked by AV node
• Separate Sinus and Ventricular Pacemakers –
• Complete disassociation between P waves and QRSs
• Regular
• Rate depends on whether its junctional or ventricular
• P waves, normal and upright, more P waves than QRS
• PRI – no relationship between P waves and QRS , occasional superimposed on QRS
• QRS width depends on whether its junctional or ventricular

Heart blocks are best diagnosed using a 12 Lead EKG Machine. This and other used medical equipment can be found easily online.

Download Excel Version Here

UPDATED 6/15/09

Sinus Blocks, Pauses and Arrest

• In all cases, no P, QRS or T wave present – Impulse is blocked a SA node and Atria are never depolarized.
• Sinus Block – Always a multiple of underlying P-P interval. can be more than one missing complex
• Sinus Pause – Not a multiple of P-P interval. Shorter than three times the P-P
• Sinus Arrest – Same as pause but more than 2 missing complexes (consecutive)

Andy Rodriguez

Ventricular Rhythms

• Impulse is generated in the ventricles. Generally recognized by wide QRS complex, >0.12

Premature Ventricular Contraction (PVC)

• Regular – ectopics will interrupt
• Rate – depending on underlying rhythm
• No P wave before PVC
• Wide QRS >0.12
• 
• 
•  

Compensatory Pause

• Allows for heart pick up its rhythm again after a PVC, resumes normal rhythm as was before PVC
• 2x R-R
•  

Interpolated

• R-R stays the same and PVC is between normal R-R
•  

Types of PVCs

• Unifocal – One focus generating the extra beat, generates PVCs that look exactly the same
• Multifocal – Multiple foci generating extra impulses. generates PVCs that look different

R on T Phenomenon

• PVC hits during or end of T wave, can cause Vfib if hits just right
• 

PVC Couplets

• Two PVCs in a row
• May be unifocal or multifocal

PVCs in a run or Run of PVCs

• More than three PVCs in a row
• Also called a “run of vtach”

PVC Groupings

• 1:1 Ratio – Bigeminy (every other is a PVC)
• 2:1 Ratio – Trigeminy (every third is a PVC)
• 4:1 Ratio – Quadgeminy (every fourth is a PVC)

Ventricular Tachycardia

• Usually Regular – can be slightly irregular
• Rate of 150 – 250 (Less than 150 is slow VT, greater than 250 V flutter)
• No P waves
• PRI – None
• QRS- wide and bizarre >0.12
• 

Ventricular Fibrillation

• Multiple foci firing in an uncoordinated fashion
• Grossly irregular
• Wide QRS – Fibrillating
• No pulse
• Shockable Rhythm
• Most lethal rhythm
• 

Idioventricular Rhythm

• Regular rate at 20-40 BPM (above 40 -120 called an accelerated idioventricular rhythm)
• No P waves
• No PI
• QRS wide and bizarre
•  

Asystole

• Absence of any electrical activity

Andy Rodriguez

Impulse is generated somewhere near the AV node. Impulses can travel up or down causing absent or inverted P wave – sometimes after the QRS. QRS is normal and tight.

Premature Junctional Contraction (PJC)

• Irritable site in AV junction fires prematurely producing a single ectopic beat.
  • Regularity depends on underlying rhythm
  • Rate – same
  • P Wave: Inverted, can fall before, during or after QRS
  • PRI, if measurable, <.12
  • QRS <.12
  • 

Junctional Escape Rhythm

• Higher pacemaker sites fall and AV junction takes over, atria are depolarized via retrograde conduction. Ventricular conduction is normal.
  • Regular
  • Rate: 40-60
  • P Waves, inverted, during or after QRS
  • PRI – only if there is a P wave and before and will be <.12
  • QRS <.12
  • 

Accelerated Junctional Rhythm

• Irritable focus in the AV junction fires repeatedly at a rate faster than the SA node. Retrograde conduction to atria and conduction to ventricles is normal
• Regular
• Rate: 60-100
• P Wave: inverted, before or after QRS
• PRI – only if there is a P wave and before and will be <.12
• QRS <.12
•  

Junctional Tachycardia

• Irritable focus in the AV junction fires repeatedly at a rate faster than the SA node. Retrograde conduction to atria and conduction to ventricles is normal
• Regular
• Rate: 100-180
• P Wave: inverted, before or after QRS
• PRI – only if there is a P wave and before and will be <.12
• QRS <.12
• 

Supraventricular Tachycardia (SVT)

• Rapid, Regular, SV rhythm that is so fast that you cant see P waves. Normal QRS
• Rate >150
• 

Paroxysmal Supraventricular Tachycardia (PSVT)

• A short burst of SVT that occurs in a rhythm strip
•