April 6, 2026

This month, we discuss the importance of EKGs and why they remain one of the most essential tools we use in the prehospital setting—and why continued practice and review are so important for all of us.

EKGs are simple, non-invasive, but incredibly powerful. They save lives by helping us identify critical and life-threatening conditions early, thereby helping us reduce morbidity and mortality. Having knowledge of important EKG findings can help guide key decisions, such as transport destination and early activation of resources, including the cath lab. It can even help us prevent cardiac arrests if we can identify concerning rhythms early on, before our patients decompensate. It’s no surprise that this topic is consistently requested for continuing education — mastery requires constant review, and the stakes are high.

To better understand what we’re seeing, it’s important to revisit some fundamentals of cardiac anatomy and physiology. The heart functions through a coordinated electrical conduction system that drives rhythmic contraction and ensures effective perfusion of both the coronary arteries and the body as a whole. At rest, myocardial cells maintain a polarized state through ion exchange — pumping sodium out and potassium in. When stimulated, sodium rushes back into the cell, causing depolarization and triggering calcium release, which leads to muscle contraction. Afterward, the cell resets through repolarization, entering a refractory period that allows the heart chambers to refill. This is a well-coordinated dance that requires the right balance of electrolytes, healthy, well-perfused tissue, and impeccable timing. 

This electrical activity is what we capture on the EKG. As a positive wave of depolarization moves through the heart toward a lead, it produces a positive deflection on the tracing. Each component of the waveform corresponds to a specific event: the P wave represents atrial contraction, the PR interval reflects conduction time from atria to ventricles, the QRS complex indicates ventricular depolarization, and the T wave shows ventricular repolarization. The ST segment is particularly important, as elevation or depression may indicate myocardial ischemia, and abnormalities in the QT interval can predispose patients to dangerous arrhythmias. Remembering what each portion of the EKG tracing looks like and how long it takes is crucial to being able to identify defective areas and help arrive at a diagnosis.

Electrical activity is not the only important information that can be discerned by looking at a tracing. Knowing coronary perfusion territories can help identify the area of infarct by examining the affected leads. Coronary arteries deliver oxygenated blood to the myocardium, and different vessels supply specific regions of the heart. The left coronary artery primarily supplies the left atrium and most of the left ventricle, with its major branches — the left anterior descending artery (LAD) supplying the anterior wall, septum, and apex, and the left circumflex (LCX) supplying the lateral and posterior walls. The right coronary artery (RCA) supplies the right atrium and ventricle, much of the conduction system (including the SA and AV nodes in most individuals), and portions of the posterior heart. Additional branches, such as the posterior descending artery and right marginal artery, further supply the ventricles. Understanding these territories helps us correlate EKG changes with the affected area of the heart.

Since the heart is a three-dimensional structure, we rely on multiple leads to give us different perspectives. The 12-lead EKG allows us to view specific regions: inferior (II, III, aVF), lateral (I, aVL, V5, V6), septal (V1, V2), and anterior (V3, V4). Contiguous leads provide insight into localized areas of the heart, helping us pinpoint where pathology may be occurring. Proper lead placement and interpretation are key, and sometimes initial findings will prompt us to obtain additional or serial EKGs — especially when clinical suspicion remains high or when early changes are subtle. Remember, we are not just putting stickers on a patient; we are choosing the most appropriate vantage point to get the clearest picture of what is going on. 

It’s also important to remember that STEMIs and obvious ischemic changes are not the only time-sensitive findings. Subtle abnormalities, evolving patterns, and early warning signs can be just as critical and must be recognized promptly.

Ultimately, a well-functioning heart is central to a healthy patient, and the EKG is one of our best tools for assessing that function in real time. As we will see, however, cardiac pathology is not the only thing we can discern from a timely performed EKG. The more comfortable and confident we are in interpreting these tracings, the better equipped we are to make rapid, informed decisions that truly impact outcomes.

Thank you all for your continued dedication to learning and excellence in patient care,

Cristina M. Carpintero-Ramirez, MD

April 13, 2026

Good morning! 

Last week we discussed the basics of how an EKG works; today, we’ll discuss how to interpret this data and translate what we read into life-saving actions for our patients.  

First off, the tried-and-true method for EKG reading is as follows:  

1. Rate: Count R-R intervals. 300 ÷ large boxes between peaks. Normal: 60-100 bpm. 

2. Rhythm: Are R-R intervals regular? Use calipers or mark paper. Regular vs. irregular? 

3. P waves: Present? Upright in lead II? One before every QRS? Normal: <0.12 sec wide. 

4. PR interval: From start of P to start of QRS. Normal: 0.12-0.20 sec (3-5 small boxes).

5. QRS complex: Is it narrow or wide? Any weird morphology? Normal: <0.12 sec (3 small boxes). 

6. ST segment: Elevated, depressed, or at baseline (isoelectric)? Elevation may = STEMI — act fast! 

7. T waves: Upright in most leads? Peaked, flat, or inverted? Flat/inverted can = ischemia 

8. QTc interval: Corrected QT — risk for dangerous arrhythmia. Normal: <0.44 sec in men, <0.46 in women.

While the above is one way of dealing with a critical patient, it may be helpful to interpret the EKG in a faster, more action-driven approach as follows: 

1. Do you see a STEMI?

2. Is the patient unstable vs stable?

3. Is the pattern wide or narrow?

4. Is it regular vs irregular?

5. Is it fast vs slow?

Now that we have discussed how to approach reading EKGs, let’s discuss critical rhythms that can kill your patient now and what we can do in real time to treat these patients: 

• Critical rhythms in pulseless patients: 

• Asystole: appears like a flatline

• PEA: looks like a wave, but the patient is without a pulse 

• Actions/approach to these patients: (non-shockable rhythms) 

• IV (IO), O2, Monitor, make sure to perform good compressions to ensure proper perfusion to critical organs.  

• Administer epinephrine per ACLS guidelines  

• Consider clinical context (ESRD, etc.) for next steps, including the need for calcium and sodium bicarbonate administration.  

• Evaluate patient to note any reversible causes that may have prompted the arrest: Hs and Ts  

• V-fib: chaotic, no organized QRS → immediate defib, 

• V-tach: wide, fast, regular rhythm without pulse → immediate defib and meds (shockable rhythms) 

• ACTIONS will again include: 

• V (IO), O2, Monitor, Good compressions, epinephrine, and consider clinical context (ESRD, etc.) for next steps, including need for calcium and sodium bicarbonate administration.

• But these you will defibrillate and consider amiodarone  

• Patients with pulse: Unstable tachycardias: wide, fast complex:

• V-tach with pulse 

• ACTIONS: 

• Synchronized cardioversion for monomorphic 

• AMIODARONE: 150 mg IV / IO 

• IF PREGNANT – USE LIDOCAINE 

• Polymorphic VT or VF with long QTc is Torsades de Pointes: is rarely ischemic, and should NOT generally receive amiodarone or other QTc-prolonging medications. Torsades de Pointes is French for “twisting of the points,” describing its appearance. It can be STABLE or UNSTABLE but always appears IRREGULAR. It is caused by an “early afterdepolarization,” which occurs during a vulnerable time in repolarization (on the T-wave, also called “R-on-T phenomenon”). It is important to treat early because it can degenerate into V-fib.  

• ACTION: Mg Sulfate 2g IV over 20 mins max of 4G if stable 

• Defibrillate if pulseless or unstable 

• Unstable narrow tachycardias:

• SVT: REGULAR and narrow complex tachydysrhythmia arising from above the level of the Bundle of His, usually 140s-280s HR, P waves rarely visible.

• ACTIONS: Attempt vagal maneuvers first (avoid carotid massage) 

• Administer adenosine 6mg, 12mg 

• Call Medical Command for RED BOX: Metoprolol

• AFib with RVR: appears IRREGULARLY IRREGULAR with no P waves, Variable R-R intervals. It is a problem with pacemaker cells firing inadequately, and can lead to hemodynamic compromise at high rates. 

• ACTIONS: If unstable (hypotensive, chest pain, acute heart failure) →  

• synchronized cardioversion 

• If stable: IV access transport  

• If not responding RED BOX: Metoprolol 

• Remember to avoid adenosine in rapid AFib and WPW, as it works by blocking the AV nodal pathway and can lead to unobstructed depolarization through accessory pathway. This increases the risk of life-threatening arrhythmia.

• Slow, narrow, and unstable:

• Severe sinus bradycardia: Usually sinus rhythms with heart rates less than 50 bpm. Can lead to hypotension, AMS, CP, or signs of acute heart failure. When you see this, always consider drug overdose and note the patient's medication list.  

• ACTIONS: Atropine 1mg up to 3mg (avoid in high degree blocks) 

• External pacing if highly unstable 

• Look for second degree (Mobitz II) as it has a high risk of developing complete heart block 

• Complete heart block: high risk. P waves do not correlate to QRS complexes. Slow escape rhythm (34-40 bpm). Look for regular P-P interval and regular R-R interval without a relationship between them 

• ACTIONS:  

• Need to pace if symptomatic (hypotensive, AMS, CP).  

• Apply pacing pads, notify receiving facility 

• Avoid atropine in 2nd and 3rd degree blocks as it may worsen ischemia  

• Transcutaneous pacing how-to: 

• Apply pads 

• Push pacer button 

• Choose rate (start at 60) 

• Push the CURRENT button and increase the milliamps until you reach electrical and mechanical (pulse) 

• Monitor closely 

Next week, we will discuss STEMIs and how to identify and treat them.

Have a great week everyone!  

Cristina M. Carpintero-Ramirez, MD

April 20, 2026

Good morning team, 

As we continue to refine our cardiac care in the field, I want to reinforce key concepts in recognizing and managing ST-Elevation Myocardial Infarction (STEMI), including important mimics and high-risk equivalents. 

STEMI on EKG represents acute myocardial ischemia most often caused by complete occlusion of a coronary artery, typically due to atherosclerotic plaque rupture with subsequent thrombosis. Identifying these patients early is critical, as they benefit from rapid reperfusion therapy. 

Our system goal aligns with national standards: 

• Door-to-balloon time < 90 minutes 

• If PCI cannot be achieved within 120 minutes, fibrinolytic therapy should be considered within 30 minutes of hospital arrival (when no contraindications exist) 

STEMI ECG Criteria 

• ST elevation ≥ 1 mm in two contiguous leads 

• Exception: 

• V2–V3: look for ≥ 2 mm in men, ≥ 1.5 mm in women 

• Reciprocal ST depressions (in opposing leads) increase suspicion for true STEMI 

Reciprocal Changes – When seen in conjunction with STE in opposing leads, it is very highly suggestive of true MI. I like the “PAILS” mnemonic to remember where the reciprocal changes should appear, as follows: 

• Posterior ↔ Anterior 

• Anterior ↔ Inferior 

• Inferior ↔ Lateral 

• Lateral ↔ Inferior 

• Septal ↔ Posterior 

These patterns help confirm ischemia and localize the infarct territory. Remember that, as outlined below, coronary perfusion territories can be identified by specific leads. 

• LAD (Anterior/Septal): V1–V4 

• RCA (Inferior): II, III, aVF 

• LCx (Lateral): I, aVL, V5–V6 

Critical EMS actions that should be taken when the clinical picture and EKG are highly suggestive of acute MI: 

• Acquire a 12-lead ECG within 10 minutes of patient contact 

• Give aspirin 324 mg (if no allergy) 

• Administer nitroglycerin 0.4 mg SL if: 

• SBP > 90 mmHg 

• No evidence of right ventricular infarction 

• No recent phosphodiesterase inhibitor use (e.g., sildenafil within 24–48 hours) 

• Consider: 

• Antiplatelet therapy (e.g., ticagrelor/Brilinta®) per protocol 

• Heparin per protocol (after assessing bleeding risk, anticoagulant use, and concerning symptoms such as tearing chest pain) 

• Activate the nearest PCI-capable center early 

• Perform serial ECGs when suspicion remains high despite an initial non-diagnostic tracing. Remember, a normal EKG does not necessarily mean a safe patient. 

Remember to avoid or be cautious of nitroglycerin administration in: 

• Suspected right ventricular infarction 

• Hypotension 

• Strong suspicion of preload dependence 

Keep in mind that seeing ST elevation or anomalies on an EKG doesn’t always mean the patient is suffering an acute MI. 

Be cautious of conditions that can resemble STEMI (known as STEMI mimics): 

• Early Repolarization: Younger patients, STE in V2–V4 with J-point notching.

• Pericarditis: Diffuse STE, PR depression, not confined to a vascular territory. 

• LVH with Strain: ST changes with high-voltage QRS complexes.

• LBBB: Requires use of Sgarbossa criteria; defer interpretation to ED/cardiology when uncertain.

When in doubt, call Med Command to discuss further. Be cautious and call it if there is a high index of suspicion.  

Finally, there are findings on an EKG that do not adhere to the standard STEMI criteria but have been found to identify patients who may still benefit from early PCI. These are collectively known as STEMI Equivalents and should be treated as such in the right clinical setting. They likely represent coronary occlusion without classic ST elevation: 

• De Winter Pattern: Upsloping ST depression with tall symmetric T waves in precordial leads (anterior occlusion).

• Wellens Syndrome: Biphasic or deeply inverted T waves in V2–V3, often pain-free but indicates critical proximal LAD stenosis.

• Posterior MI: ST depression in V1–V3 (reciprocal changes); consider posterior leads.

• Right Ventricular MI: Often with inferior MI; look for STE in V1 and confirm with right-sided ECG. 

• These patients are preload dependent.

• aVR Elevation with Diffuse ST Depression: Suggests left main or multi-vessel disease.

• Hyperacute T Waves: Early sign of occlusion; broad, tall, disproportionate to QRS.

• Early Inferior MI Clue: T-wave inversion in aVL with hyperacute inferior T waves.

Important take-home points: 

• A normal initial ECG does not rule out STEMI → Repeat if suspicion remains high.

• Time is myocardium: early activation of PCI is one of the most impactful actions you take. 

• Always consider right-sided ECGs in inferior MI before giving nitroglycerin. 

• Reciprocal changes strengthen your diagnosis — don’t ignore them. 

• STEMI equivalents may be just as dangerous as classic STEMI.

• Always treat the patient, not just the ECG — clinical presentation matters. 

• When in doubt, err on the side of early notification and transport to PCI.

Thank you for your continued commitment to delivering high-quality cardiac care in the field, 

Cristina M. Carpintero-Ramirez, MD

April 27, 2026

Team, 

As we wrap up our critical EKG findings series, this final installment focuses on additional high-risk patterns that require rapid recognition and decisive prehospital management. These conditions may be subtle at first glance but carry significant morbidity and mortality if missed. 

1. Hyperkalemia 

A dialysis patient with weakness should always be considered hyperkalemic until proven otherwise. Severe hyperkalemia can lead to cardiac arrest, ventricular brady dysrhythmias, and tachydysrhythmias. 

EKG changes can be progressive, so it is important to identify them early to avoid decompensation into a critical rhythm. Changes may correspond to the level of potassium as follows: 

• Peaked T waves (K+ 5.5–6.5) 

• Loss of P waves, PR prolongation (K+ 6.5–7.5) 

• Widened QRS (K+ 7.5–8.0) 

• Sine wave pattern (>8.0, pre-arrest state → VF/asystole) 

As always, remember that the clinical picture matters a great deal. Look for changes that may indicate hyperkalemia in patients with a history of dialysis, renal failure, burns, trauma, certain medications (ACE inhibitors, potassium-sparing diuretics). Remember to ask for recent labs, if available.  

Management of these patients should be based on EKG changes and include: 

• Continuous cardiac monitoring! 

• Albuterol (shifts potassium intracellularly) 

• Calcium gluconate/chloride for cardiac membrane stabilization 

• Sine wave: calcium + bicarbonate 

• Early hospital notification, as these patients may require emergent dialysis. 

• Serial EKGs 

2. Sodium Channel Blocker Toxicity 

Most commonly from TCA overdose, but also seen with procainamide and antimalarials. Highly cardiotoxic. 

Presentation may be varied and include altered mental status, hypotension, tachycardia, seizures, wide complex dysrhythmias, and anticholinergic signs (dry mouth, mydriasis).  

EKG findings: 

• Wide QRS (>100 ms, especially in lead II) 

• Sinus tachycardia 

• Terminal R wave >3 mm in aVR or R/S ratio >0.7 

• QT prolongation 

• Management: 

• Sodium bicarbonate 

• Serial EKG monitoring 

3. Long QT Syndrome 

Represents delayed ventricular repolarization and increases the risk for Torsades de Pointes. 

EKG changes will include:  

• QTc >500 ms = high risk 

• QT interval should be <½ the R-R interval 

Causes: 

• Medications (antipsychotics, antibiotics, methadone) 

• Electrolyte abnormalities (low K+, Mg++, Ca++) (remember the dance!) 

• Congenital conditions 

Management: 

• Magnesium sulfate 2g IV over 10 minutes if Torsades develop 

• Defibrillation, if the patient becomes pulseless 

4. Brugada Syndrome 

A sodium channelopathy associated with sudden cardiac death!  

Considered in: 

• Syncope or near-syncope, especially in young males 

• Family history of sudden cardiac death 

• Patient may be feeling better, but it is very important that you do not let these patients sign out without discussing with Medical Command.  

Triggers for these patients may include fever, medications, alcohol, and electrolyte disturbances. 

EKG Finding:

• Type 1 pattern: coved ST elevation in V1–V2! 

Management: 

• Early notification 

• Avoid medications that worsen the condition (AV nodal blockers, nitrates, etc.) 

5. Pulmonary Embolism (PE) 

Classic S1Q3T3 pattern is present in only ~20% of cases; however, the most common finding is sinus tachycardia.

EKG Findings: 

• Sinus tachycardia (most common) 

• Right heart strain pattern 

• S1Q3T3 (deep S in I, Q in III, inverted T in III) 

Clinical Presentation: 

• Sudden dyspnea, pleuritic chest pain 

• Risk factors: recent surgery, cancer, immobilization, DVT history 

Management: 

• Oxygen, IV access 

• Early notification, especially if unstable 

6. Pericarditis 

Inflammation of the pericardium. 

Presentation: 

• Chest pain (worse when lying flat), SOB, fever 

• Possible pericardial friction rub 

EKG Findings: 

• Diffuse ST elevation with PR depression 

Management: 

• Oxygen 

• NSAIDs 

• Antibiotics, if an infectious cause is suspected 

7. Wolff-Parkinson-White (WPW) 

Accessory pathway leading to abnormal conduction and tachyarrhythmias. 

Risks: 

• Atrial fibrillation with rapid conduction → ventricular fibrillation 

Critical Reminder: 

• In WPW with atrial fibrillation (irregular wide complex tachycardia): DO NOT give adenosine, diltiazem, or amiodarone. Avoid all AV nodal blockers 

Management: 

• If unstable: immediate cardioversion.

8. Cerebral T Waves 

Associated with increased intracranial pressure. 

EKG Findings: 

• Widespread, deep T wave inversions 

• Prolonged QT (~600 ms) 

Cause: 

• Sympathetic surge from CNS injury  

The EKG is one of the most lifesaving tools in our arsenal. It is noninvasive, quick, easy, and has the power to identify life-threatening etiology! As we have seen this month, STEMIs are important -- but not everything that can kill has ST elevation. Knowing all critical EKG findings and their corresponding actions is a crucial part of patient care. 

Always remember: when in doubt—call it! Early recognition and aggressive management in the prehospital setting save lives. Many of these EKG findings represent evolving, time-sensitive conditions where your interpretation directly impacts patient outcomes. Treat the patient, not just the monitor, but never ignore what the monitor is telling you. Hyperkalemia changes are progressive — act early. Communicate clearly with the receiving facility, provide early notification for critical findings, and ensure thorough documentation, including timing of EKGs, interventions, patient response, and confirmation of EKG transmission. 

Your role in early identification and intervention is often the difference between deterioration and survival. Stay vigilant, trust your training, and continue to advocate for your patients from first contact through handoff.

Now go out there and make a difference! 

Cristina M. Carpintero-Ramirez, MD