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Causes of PEA
Jun 24th, 2009 by RH-111
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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

Miscellaneous Mnemonics for ACLS
Jun 24th, 2009 by RH-111
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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.

STEMI Imposters
Jun 15th, 2009 by RH-111
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Updated in this post – See here http://www.rhmedicclass.com/index.php/12-lead-ekg-in-acs/

(From Tim Phalen’s lecture)

  • 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
Orotracheal Intubation – Medical Procedures – Medstudents
Jun 15th, 2009 by RH-111
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Orotracheal Intubation – Medical Procedures – Medstudents

The height of the table where the patient is lied, should be adjusted so that the patient’s face is at the level of the xiphoid cartilage of the standing person who is performing the procedure. Elevating the patient’s head about 10 cm with pads under the occiput and extension of the head at the atlanto-occipital joint (sniffing position) serve to align the oral, pharyngeal, and laryngeal axis, so that the passage from the lips to the glottic opening is almost a straight line. This position permits better visualization of the glottis and vocal cords and allows easier passage of the endotracheal tube. For children under 1 month of age, the head should be in a neutral position. See Figure 1.

Figure 1:Letter A shows the wrong and letter B shows the correct position of patient’s head.

Prehospital 12 Lead ECG: Contiguous and reciprocal lead charts
Jun 15th, 2009 by RH-111
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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

Intro to 12 Lead EKGs
Jun 7th, 2009 by RH-111
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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

Lead Location Coronary Reciprocal Leads Notes
II, III, aVF Inferior (IWMI) RCA (LCA) I, aVL Always suspect RVI (40-50% of patients), use V3R, V4R (no nitro, first fluids small doses of MS – RVI patients are preload impaired – nitro or MS can precipitate sudden and catastrophic hypovolemia in these patients. )
V1, V2 Septal (SWMI) LCA -  
V3, V4 Anterior (AWMI) LCA II, III, aVF Widow maker, L Ventricle failure, CHF, Cardiogenic Shock
I, aVL, V5, V6 Lateral (LWMI) LCA V1, V2  
V7, V8, V9 (Back) Posterior RCA or LCX V1 throughV4 usually extends from of IW or LWMI

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.
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