In my fellowship, we had a handbook for every rotation outlining all of our responsibilities. But the things I’m talking about here were never in it. They’re the unwritten rules that can make you a really great co-fellow (or co-resident).

Reflecting on my training now, I don’t remember every guideline, or every lecture, or even most of the clinical scenarios that I handled. But I do remember the co-fellow who brought me coffee on call, who took extra consults when I was really busy, or who dealt with a messy situation so that I didn’t have to when I started my shift.

I remember the co-fellows I loved working with.

I’m sure there are plenty more, but these are the ones that stood out to me. And to be clear, I didn’t always get these right myself. Some I learned to do, and others I really wish I had done more often!

Here are 10 small things you can do to make life a little easier for your co-fellows or co-residents during training:

1. Give the sign-out you would actually want to receive.

   There are people who recite the entire chart and others who give you three words about the patient. There’s a happy (and relevant) medium. I want to know what happened, what I’m waiting for, what could go wrong, and what I am likely to get called about overnight. In person, message, or email: it all works. Just give the relevant headlines, please.

2. If there is a weird, messy, or very particular situation (or person), give your co-fellow or co-resident a heads up.

   Guys, this isn’t about gossip. It’s literally an act of service. If there is an attending who is super particular about something, takes hours to round, or just has certain preferences, please give the next person a heads up. The same goes for anything you know is about to become someone else’s problem. Tell them before it does.

3. Don’t leave your own task unfinished just because your shift is over.

   I’m super protective of the idea that when your shift is over, you should wrap up and go home because… self-care. However, if you’re already standing there and can consent the patient, make the phone call, or finish closing the loop in the next five minutes, don’t deliberately leave it for the next person just because your shift technically just ended. Your co-fellow or co-resident will be eternally grateful.

4. Don’t be too quick to say “that’s not my patient.”

   I’ve seen this one a lot. Maybe you weren’t assigned that particular patient on the wards, in the ICU, or on the consult list, but if you’re part of that team, they’re still your team’s patient. Boundaries are important, and no one should constantly be expected to pick up someone else’s work. But residency and fellowship work because, when we can, we help each other.

5. If you switch a call day or ask for coverage, remember the favor.

   If you’re the person who agrees to cover or switch a day for a co-fellow, that’s great. But if you’re the person who remembers the favor and asks when you can return it, that’s even better. Reciprocity matters. Don’t be the person who always needs coverage but disappears when someone else does.

6. Share the good stuff.

   During training, you come across so many cool cases. For me, it was uncommon ECGs, interesting echos, or cool angiogram findings. Every specialty has its version of these. Don’t keep them to yourself; sharing is caring! If you come across a great case, article, or boards resource, send it to your co-fellows or co-residents. Trust me, learning together is better.

7. Don’t throw your co-fellow or co-resident under the bus in front of an attending.

   This is a biggie. If something needs to be addressed, do it privately. Fellowship is not the Hunger Games. You don’t need to make someone else look bad to make yourself look good.

8. Protect your co-fellow or co-resident when they’re absolutely getting slammed.

   Black cloud or not, we all have bad days. If you see your co-fellow or co-resident struggling, offer to take the consult, or help with one of their patients. They will definitely remember the people who helped when they needed it.

9. Don’t make someone else’s mistake a story.

   Even the best people make mistakes. I was always told that if you haven’t made a mistake doing something, you probably haven’t done enough of it yet. Of course, if an error needs to be addressed for patient safety or discussed for educational purposes, that’s different. But please be kind and don’t turn someone else’s mistake into a story that gets passed around. They probably already feel terrible about it. There’s no need to make it worse.

10. Be the person who makes a bad call day 10% less terrible.

    This can be anything. Bring them a coffee. Give them some encouragement. Let them vent. Order food. Answer a page while they’re stuck doing a procedure. Tiny things like these become surprisingly memorable during training.

That’s it! No one is perfect, but we can all try to make training a little easier for the people around us. If you think of any more unwritten rules, feel free to leave them in the comments. And if you’re currently in training, I hope some of this resonates with you, and I hope you’re almost done 😂.

Sending a big hug to all of you.

-Iv 🪽🤍

I literally had no idea what to do with that information when I first started out. All I knew was that at some point, if the PVCs were too frequent, we would consult cardiology.

This is the reason I decided to make this post.

When it comes to PVCs, do they matter? When should you worry about them? When should you treat them?

I hope my Mini Guide helps answer these questions and more. For the purposes of this guide, I’ll focus on the general framework I use as a cardiologist and avoid getting into the EP-heavy details.

I’ll start off by saying that PVCs, or premature ventricular contractions, are pretty common. And not all PVCs are inherently abnormal. They are known to occur more frequently with older age, higher blood pressure, a sedentary lifestyle, smoking, and underlying heart disease.

PVCs can occur in isolation, in couplets or triplets, and in patterns such as bigeminy (every other beat) or trigeminy (every third beat).

However, PVCs aren’t always benign. Several studies have shown that a high PVC burden is associated with heart failure, LV dysfunction, and increased mortality. That being said, we don’t have enough evidence to suggest that suppressing PVCs in everyone prevents these outcomes. The major exception is PVC-induced cardiomyopathy (CM). This is what you should watch out for, because eliminating (or significantly reducing) the PVC burden can lead to improvement of LV function.

Okay, let’s get to it. These are the 3 main questions that I ask myself when I encounter a patient with frequent PVCs:

1. Are the PVCs a marker of structural heart disease or are they coming from a normal heart?

2. How much is too much PVC burden? What is the % burden and is it high enough to put the patient at risk of PVC-induced CM?

3. Do the PVCs need to be suppressed? Are they causing symptoms or contributing to LV dysfunction?

THE INITIAL EVALUATION

• Take a good history.

  • Ask about palpitations, skipped beats, fatigue, dizziness, presyncope, syncope, exercise intolerance, etc.

  • Ask about family history (especially premature sudden cardiac death), as well as drug or stimulant use.

  • It’s important to know that symptoms are super variable. Someone with a high burden of PVCs may be completely asymptomatic, whereas someone with relatively few PVCs can be very symptomatic.

• We NEED to see the PVC! Obtain a 12-lead ECG.

  • We want to know: Where is the PVC coming from, and how many different morphologies are there? The morphology can help determine the likely site of origin (RVOT/LVOT, fascicular, papillary muscle, etc.) and whether the PVCs are unifocal or multifocal.

  • These characteristics are important for many reasons, but most especially for guiding therapy.

• An echo is indicated to rule out structural heart disease.

  • If a patient has rare PVCs that were incidentally noted and they are asymptomatic, you don’t necessarily need an echo. However, if someone has frequent PVCs or the PVC morphology is concerning, an echo is warranted to rule out a reduced EF or other pathology that is contributing to presence of PVCs or its symptoms.

• Ambulatory ECG monitoring is key.

  • If I have a patient with frequent PVCs, in addition to getting an ECG and echo, I order a an ambulatory monitor to quantify the PVC burden.

  • Since PVC burden can vary from day to day, data shows that at least 6 days or more are needed to properly assess the maximal burden. This is why in my practice I prefer a 30-day event monitor over a 12-48 hr Holter monitor.

  **A note on CMR: A CMR can be considered even with a normal echo, particularly when the PVCs are multifocal or have an atypical morphology, or when there are other concerning features such as a family history of sudden cardiac death, NSVT, or suspicion for underlying myocardial disease (like myocarditis, cardiac sarcoidosis, ARVC…).

  **A note on exercise testing: This is most useful when the symptoms are exercise-related, and can help rule out ischemia. PVCs that improve with exercise could be reassuring. But more importantly, if they worsen, or if high grade PVCs persist into recovery, this is associated with a higher risk of future cardiovascular death.

HOW MUCH IS TOO MUCH?

PVC burden is essential in the evaluation of PVCs. It is the percentage of total heartbeats on ambulatory monitoring that are PVCs. This is reported by the event monitor.

There’s not an absolute cut off that separates safe from dangerous, and different thresholds have been proposed. In general the way I think about it is:

Low burden: <5%; Gray zone: 5-10%; High burden >10-15%; Higher risk for PVC-induced CM >15%.

Important to know: a high PVC burden alone does not automatically mean the PVCs need to be suppressed. In an asymptomatic patient with preserved LV function, a high burden warrants surveillance for development of LV dysfunction, while treatment is individualized (based on symptoms, burden, and patient preference).

And if you see a high burden of PVCs and a low EF, you need to ask: Are the PVCs causing the CM? Is the CM causing the PVCs? Or is it a little bit of both?

CLINICAL SCENARIOS

Before moving into therapies, here are some useful scenarios to think about when encountering a patient with PVCs in clinical practice:

Asymptomatic + low PVC burden + normal echo: Reassurance. No treatment is needed at this time.

Symptomatic + normal echo: If symptoms are attributed to the PVCs, symptom-directed therapy is reasonable.

High PVC burden + normal echo: These patients should be followed for surveillance of LV function. The treatment will depend on symptoms, PVC burden, and patient preference.

High PVC burden + reduced LVEF: Further evaluation of the LV dysfunction is warranted. PVC-induced CM should be considered, particularly when other common causes of cardiomyopathy have been excluded. In this setting, PVC-suppressive therapy is recommended.

THERAPIES

Beta blockers (BB) or nondihydropyridine calcium channel blockers (CCB; verapamil or diltiazem) are first-line medications for symptomatic PVCs. These can be uptitrated as tolerated.

If a patient cannot tolerate BBs or CCBs, or their symptoms are refractory to these medications, we consider catheter ablation or antiarrhythmic drugs. At this point, EP should be involved in their care.

Catheter ablation is the most effective at eliminating PVCs (but we must weigh the procedural risks). When do we favor ablation?

• Symptomatic idiopathic PVCs, particularly those arising from the RVOT or fascicular system, where ablation can be considered first-line therapy.

• PVC-induced CM, particularly when the PVCs are predominantly monomorphic.

• Highly symptomatic PVCs despite medical therapy or when medications are not tolerated or desired.

• Patients with CRT device when frequent PVCs interfere with adequate BiV pacing.

For patients who are not good candidates for ablation or who prefer medical therapy, commonly used antiarrhythmics include flecainide*, propafenone*, sotalol, or amiodarone**, depending on the patient's clinical profile and underlying heart disease.

*avoid in pts with structural heart disease or CAD.

**reserved for select cases due to its potential long-term toxicities.

TAKE HOME POINTS:

• PVCs are common and often benign, especially when arising from a structurally normal heart. However, a high PVC burden can contribute to LV dysfunction and PVC-induced CM.

• The basic evaluation includes a 12-lead ECG to assess PVC morphology, an echo to rule out LV dysfunction and structural heart disease, and ambulatory monitoring to quantify PVC burden.

• There is no absolute PVC burden that separates benign from harmful, but >10% is worth paying attention to and >15% is a high burden with the risk of PVC-induced cardiomyopathy increasing as the burden rises.

• Asymptomatic patients with a low PVC burden and a normal echo generally do not require treatment. However, for symptomatic PVCs, BBs or nondihydropyridine CCBs are first-line medications.

• Catheter ablation is the most effective therapy for eliminating PVCs and should be considered in appropriate patients with highly symptomatic or refractory PVCs, those who prefer ablation, or when PVCs are causing LV dysfunction.

• Ultimately, PVC suppression is primarily indicated when PVCs are causing symptoms or contributing to LV dysfunction, while patients with a high burden but preserved LV function require appropriate surveillance and individualized treatment.

Ok lots of info in this one. I had frequent PVCs just writing it! But I hope some of it makes sense and helps you manage your patients. As always, thank you for reading and subscribing :)

-Iv 🪽🤍

The truth of the matter is that it takes time to get comfortable reading ECGs. Throughout my training, I was always told that the more ECGs I looked at, the easier it would get. I still found them difficult. But it was true. At some point, things started to click. The concepts got easier, and the more common patterns became recognizable. In the end, two things that will help the most: learning the physiology of the ECG (sorry) and looking at hundreds of ECGs and rhythm strips (sorry #2).

Similar to my Mini Guide series, I would rather highlight 10 high-yield ECGs that are important to recognize. There are some emergent ECGs on here, but not all of them are. I wanted to include a few that are unique, can fool you, or are simply worth knowing. Some concepts are straightforward; others are more complex. I like variety.

Of note, these ECGs are in no particular order!

1. Atrial Fibrillation (AF) with Pre-Excitation

   

   AF with pre-excitation occurs in Wolff-Parkinson-White (WPW) syndrome. It’s essential to recognize because this is the one situation where you should avoid AV nodal blockers for AF. In pre-excited AF, the atria are firing chaotically at very high rates. Electrical conduction from the atria to the ventricles (A to V) can occur through either the AV node (which is protective because it slows conduction) or the accessory pathway. If you block the AV node, rapid atrial impulses can preferentially conduct through the accessory pathway instead, resulting in extremely fast ventricular rates and potentially degenerating into VFib.
   

   ECG CLUES: This is a chaotic ECG. Look for an irregularly irregular rhythm indicative of AF, a very rapid ventricular rate (often into the 200s), and QRS complexes that vary in width and morphology. Some beats may be very wide from greater conduction through the accessory pathway, while others may appear narrower due to greater conduction through the AV node.
   

2. Ventricular Tachycardia (VT)

   

   VT is an essential arrhythmia to recognize because it is emergent. In this case, the ventricle is running the show. It is wide-complex tachycardia originating from the ventricles. As a general rule, wide complex tachycardia is VT until proven otherwise, especially in a patient with a history of MI or structural heart disease.
   

   ECG CLUES: For monomorphic VT, seen in the ECG above, the QRS will be wide (>120 ms) and regular. Findings that support VT (rather than SVT, as we will see on the next ECG), include AV dissociation (sometimes you will catch a P wave), capture beats (narrow complex beats that make it from the sinus node), fusion beats (product of fused narrow and wide complex beats), extreme axis deviation (+AVR), and concordance (all prec ordial leads either + or -).

3. Supraventricular Tachycardia (SVT) with Aberrancy

   

   This is the mimicker of VT. Most people can recognize SVT right away (a narrow-complex tachycardia without clearly discernible P waves), but when ventricular conduction is aberrant, the QRS can widen and appear similar to VT. Distinguishing the two is important because SVT with aberrancy may respond to adenosine, whereas VT requires a different management approach.
   

   ECG CLUES: Features favoring SVT with aberrancy include absence of AV dissociation, capture beats, and fusion beats. The QRS morphology may resemble a typical RBBB or LBBB pattern. Other clues favoring SVT with aberrancy include an initial negative deflection in aVR and absence of positive or negative concordance across the precordial leads.

4. Complete Heart Block (CHB)

   

   Many of you have seen this ECG at least once if you’re in medicine or critical care. It’s a cannot-miss kind of ECG. CHB is third-degree AV block, which occurs when there is complete absence of conduction from A to V. There are some reversible causes, like ischemia or AV nodal blocker medications, but more often than not, it means that your patient will need a pacemaker.

   
   ECG CLUES: In CHB, you will see P waves that are not associated with (or conducting to) the QRS complexes; this is AV dissociation. The QRS complexes originate from an escape focus below the level of the block. A junctional escape rhythm is typically narrow, while a ventricular escape rhythm is typically wide. The P-P and R-R intervals are each regular and independent of one another, with the atrial rate faster than the ventricular rate.
   

5. Left Bundle Branch Block (LBBB), Right Bundle Branch Block (RBBB), and Alternating Bundle Branch Block
   
   These first two ECGs show a LBBB pattern, followed by a RBBB pattern. We’re often taught to look for things like “bunny ears,” but I wanted to include the actual criteria for each. I’ve been called about a patient with sinus tachycardia and a LBBB because it was mistaken for VT.

   

   LBBB criteria: Wide QRS (≥120 ms, or 3 small boxes if complete); broad, often notched or slurred R waves in the lateral leads (I, aVL, V5, V6) with absence of normal Q waves; and predominantly negative QRS complexes in V1–V3 (typically a deep, broad S wave). Additionally, the ST segment and T wave are generally directed opposite to the QRS deflection.

   

   RBBB criteria: Wide QRS (≥120 ms, or 3 small boxes if complete); V1-V2/V3 have an M-shaped R wave (or rSR’/rsR’) with an appropriate T wave inversion and ST depression; and lateral leads have a slurred S wave.

   ---

   

   The ECG above is very high-yield. It’s not common, but it’s important to recognize. This is alternating bundle branch block. It’s easiest to see in the V1 rhythm strip. Beats 1 and 3 are normal sinus beats, while beat 2 has a RBBB morphology and beat 4 has a LBBB morphology. Throughout the rhythm strip, you can see the QRS morphology alternate between RBBB and LBBB.

   
   Why does this matter? Alternating bundle branch block indicates advanced disease of the His-Purkinje conduction system and a high risk of progression to CHB. For this reason, it is an indication for permanent pacemaker implantation.
   

6. Atrial Flutter (AFL) with 2:1 AV Block

   

   AFL with 2:1 AV conduction is a difficult ECG because it can look very similar to sinus tachycardia or even SVT. If you look closely, you may see subtle notches embedded within the ST segment or T wave, without clear sinus P waves preceding each QRS. These subtle deflections may actually be flutter waves. See the sample beat from V1 below. I have circled the two flutter waves associated with each QRS. It is extremely subtle. Looking closely at V1 can be particularly helpful, since the inferior leads will not always show the classic sawtooth pattern.

   

   
   
   ECG CLUES: Suspect 2:1 AFL when you see a very regular narrow-complex tachycardia around 150 bpm without convincing P waves. The atrial rate is typically around 300 bpm, with every other flutter wave conducting to the ventricles. Look carefully within the ST segment and T wave for the “hidden” flutter wave, particularly in V1.
   

7. Brugada Type 1 Pattern

   

   If you don’t recognize a Brugada ECG, it’s possible the cath lab gets wrongly activated for a “STEMI.” I saw this happen a couple of times during my training. There are several Brugada ECG patterns, but Type 1 is the most important because it is diagnostic. Important to know that the Brugada pattern ≠ Brugada syndrome. Patients with this ECG and a history of cardiac arrest or cardiogenic syncope, have Brugada syndrome and benefit from an ICD.
   
   ECG CLUES: Look for the characteristic “coved-type” ST elevation in the right precordial leads (V1–V2), with ≥2 mm of ST elevation followed by T-wave inversion. Sometimes the pattern becomes more apparent when V1 and V2 are placed higher (2nd or 3rd intercostal spaces).
   

8. Posterior ST Elevation Myocardial Infarction (STEMI)

   

   A posterior STEMI on a standard 12-lead ECG looks different from most STEMIs because you are essentially seeing the reciprocal changes of the infarct. It’s important to have a high suspicion for posterior MI in a patient presenting with chest pain and these ECG changes. We don’t obtain posterior leads as often as we should, but this pattern should tip you off and prompt you to get them.
   
   ECG CLUES: Look for horizontal ST depression in V1–V3, often with tall R waves and upright T waves. Think of this as the “mirror image” of posterior ST elevation and Q waves. If you see this pattern in the right clinical setting, obtain posterior leads V7–V9 to confirm posterior STEMI.
   

9. Bidirectional VT

   

   You may never see this in practice, but it’s unique and worth knowing about. Bidirectional VT is classically associated with two clinical scenarios: severe digoxin toxicity and catecholaminergic polymorphic VT (CPVT). Unlike torsades, where the QRS morphology appears to twist around the baseline, bidirectional VT has a beat-to-beat alternating QRS axis.
   
   ECG CLUES: Look for wide complex tachycardia in which the QRS axis alternates from beat to beat (+, -, +), producing a characteristic back-and-forth appearance of the QRS complexes.
   

10. Long QT Syndrome (LQTS)

We’ve reached the end! Last but not least, long QT syndrome (LQTS) deserves a mention. We all look out for QT prolongation on our patients’ ECGs, so it’s worth being familiar with LQTS and its most common inherited types. There are three classic types, and the ECG above demonstrates LQT1.

ECG CLUES: Look for a prolonged QTc (QTc ≥480 ms should raise suspicion). LQT1 classically has a broad-based, prolonged T wave. LQT2 has a low-amplitude, notched or bifid T wave, while LQT3 typically has a long isoelectric ST segment followed by a late, narrow/peaked T wave.

Hope this list is helpful for some of you! ECGs are very polarizing, but if you love them, then cardiology and/or EP is not a bad place to be. Either way, learning to recognize different ECG patterns will only make you a better clinician and ultimately help your patients.

See ya next time!

-Iv 🪽🤍

I would also say that as a medicine resident, I called in/placed this cardiology consult a lot. I also rotated through the surgical co-management service as a resident and dealt with these patients frequently. However, it seemed like no matter what risk stratification we provided in medicine, the final recommendations were still needed from cardiology.

Hence, this mini guide.

While cardiology will still be consulted on these patients, I would like to give some insight into how we make these decisions. This guide is largely based on the 2024 AHA/ACC/ACS/ASNC/HRS/SCA/SCCT/SCMR/SVM (wow, so many acronyms!) Guideline for Perioperative Cardiovascular Management for Noncardiac Surgery. I will also briefly reference the 2022 ESC guidelines.

Before I get into it, I do want to make one very important point: Cardiology doesn’t CLEAR anyone for surgery. We ASSESS the patient’s perioperative cardiac risk and estimate their risk of MACE (major adverse cardiovascular events), such as MI, stroke, pulmonary edema, ventricular fibrillation, or primary cardiac arrest.

Every patient has some risk of MACE. Our aim is to mitigate that risk, whether by doing further testing, optimizing their cardiac conditions, or adjusting their medications. Sometimes this is feasible, and other times we can’t do much to improve their cardiac risk. Either way, the patient’s risk is never zero, and thus, they are never truly “cleared” of cardiac risk before surgery.

Okay! So, I am consulted on a patient with a cardiac comorbidity or complaint that is going for non-cardiac surgery, and I’ve been asked to provide perioperative cardiac risk stratification. These are my 5 steps:

STEP 1: Is the surgery emergent*?

*immediate threat to limb/life without surgery, typically <2hr.

If yes, then the answer is: take the patient to surgery. There’s not enough time to make any major changes, the benefit of proceeding with surgery outweighs the risk of delaying it, and I will deal with the cardiac aftermath later.

If no, then I’m dealing with urgent (typically 2-24 hrs.), time-sensitive (can be delayed up to 3 mo.), or elective surgery, and I have time to evaluate:

STEP 2: Do they have unstable cardiac disease?

I ask myself: Does this patient have ACS (acute coronary syndrome), ADHF (acute decompensated heart failure), or an unstable arrhythmia?

If yes, then I manage their cardiac disease first. I will treat their ACS, diurese them as close to euvolemia as possible, or get their arrhythmia under control prior to surgery. Once optimized, they can proceed with surgery.

If no, then:

STEP 3: Calculate their risk of MACE.

This includes the clinical and surgical risk.

First, the type of surgery matters. To keep things simple, high-risk surgeries include vascular, thoracic, and transplant surgery. There is a full list of low, intermediate, and high-risk surgeries, but the risk calculator will take this into account.

Second, we estimate the perioperative clinical risk using a validated risk calculator.

***Of note, if the patient has any of these risk modifiers (severe valvular disease, pulmonary hypertension, congenital heart disease, recent stroke, prior PCI/CABG, or cardiac implanted device), then regardless of the calculated risk, they benefit from a cardiology consult for a heart team approach to decide what diagnostic testing and management are needed prior to surgery.

Risk calculation: I use the National Surgical Quality Improvement Program (NSQIP) Surgical Risk Calculator the most. I’ve also used the Gupta Myocardial Infarction or Cardiac Arrest (MICA) and Revised Cardiac Risk Index (RCRI). However, the RCRI is validated for non-emergent and elective surgeries (mostly orthopedic and female reproductive) and performs poorly for vascular surgery, so I don’t use it much. Using NSQIP (or any other validated tool), I categorize patients as low risk (<1%) or elevated risk (>1%) of MACE.

If the patient is low risk, they can proceed with surgery. So far, this would be a patient going for non-emergent, non-cardiac surgery, with stable cardiac disease, who has a risk of MACE of <1%.

If the patient is at elevated risk, then:

STEP 4: Assess their functional status.

I’ve done this by simply asking questions, but I’ve found the Duke Activity Status Index (DASI) score to be the most reliable. A patient who can do more than 10 METS is excellent (this is someone who swims, plays basketball, or plays tennis), but for surgery, I am looking to see if the patient can do 4 METS or greater. This is someone who takes care of themselves, walks around their house, can climb 2 flights of stairs, etc.

If the patient can do >4 METS, they can proceed with surgery.

If they have poor functional status (or it is unknown), then I ask myself this question: Will further testing impact decision-making or perioperative care? Will it change the patient’s need for surgery or its timing? Will it change the medications in the perioperative period? If not, then there is no need for cardiac testing, and the patient should proceed with surgery.

If yes, then this is when we can obtain biomarkers and/or non-invasive testing.

STEP 5: Non-invasive testing

If a patient has a cardiac condition, is >65 years old, or has a cardiac complaint, it’s reasonable to get a pre-op NT-proBNP. It may be reasonable to also get a pre- and post-op troponin. However, these have no proven impact on postoperative clinical outcomes. The ESC guidelines vary on this point. They recommend obtaining pre-op and post-op day 1 and day 2 troponins for intermediate/high-risk patients undergoing intermediate/high-risk surgery.

In my personal practice, I don’t often obtain biomarkers (only in select cases). And if a troponin is positive after surgery, it’s not necessarily an MI. There have to be signs of ischemia (see my last mini guide); otherwise, it is MINS (myocardial injury after surgery).

Now, by this point, you can see that stress testing/CCTA is reserved only for patients who are going for intermediate- to high-risk surgery AND are at elevated risk or have low/unknown functional capacity, if it will change management. It’s not a strong recommendation (2B in the ACC/AHA guidelines).

If we decide to perform a stress test and it’s positive, we treat it as we would any other positive stress test.

Other tests I get for my patients, depending on the indication:

• EKG: reasonable in patients with cardiac disease/sx

• Echo: only recommended in sx of HF, HF on exam, or concern for LV dysfunction (and reasonable in a patient with known HF with a clinical change)

• Cath: unstable sx, high-risk stress test, concern for severe CAD (same as non-pre-op patients)

Most importantly, who gets revascularized in the pre-op setting? This is what you need to know. If we do cardiac testing and the patient has severe coronary artery disease, who will we actually intervene on?

Only patients who are going for elective surgery AND either have ACS (class 1) or have >50% left main stenosis on angiogram (class 2a). This is the only time we PCI and commit to DAPT prior to surgery.

VALVULAR HEART DISEASE:

There’s a lot to this but I’ll keep it short. The bottom line for patients with moderate to severe valvular disease:

In asymptomatic patients with moderate to severe AS and normal LV function, elective surgery is reasonable with appropriate hemodynamic/operative monitoring*. The same goes for patients with moderate to severe rheumatic MS and a PASP <50 mmHg.

It is also reasonable for patients with moderate to severe MR or AR, particularly if EF is normal and PASP is <50 mmHg.

*What is the appropriate intraoperative and hemodynamic monitoring for these patents? Where we have a cardiac anesthesia team, the ability to do intraop TEE, an arterial line, and the ability to put in a Swan Ganz catheter.

This is how I assess preoperative cardiovascular risk. 5 steps.

Major take home points:

• If the surgery is emergent, take the patient to surgery.

• If a patient has unstable cardiac disease (ACS, ADHF, unstable arrhythmia), we optimize and treat prior to surgery.

• If a patient has stable cardiac disease with low risk of MACE, they can go for surgery.

• If a patient is at elevated risk of MACE, but has good functional status, they can go for surgery.

• If a patient is going for an intermediate to high risk surgery, they have elevated risk, poor functional status, and testing will make a difference in their management, your friendly cardiologist may obtain biomarkers +/- non-invasive testing.

• We do not routinely revascularize prior to surgery to reduce perioperative events; revascularization is only recommended prior to elective surgery in patients with ACS or severe LM disease.

Again, this is a mini guide. There are a lot of other details and more individualized patient clinical scenarios, but this will work for most patients we encounter in practice.

If you enjoyed this or want more info, feel free to comment below. If you want a mini guide to perioperative medication management, including anticoagulation, let me know!

Thank you all for reading!

Iv 🪽🤍

Why is this important? Because we encounter elevated troponins all the time in clinical practice. More importantly, whether due to true myocardial ischemia or not, an elevated troponin is associated with an adverse prognosis.

In my experience, clinicians tend to hyperfocus on an elevated troponin, assuming the patient is having an MI and needs a cath right away. Meanwhile, if the patient is hospitalized for another important reason, that tricky troponin elevation can delay other testing or therapies they may actually need. And sometimes it is an MI. But many times it’s not. And it can be useful to discern the difference.

At the start of my cardiology fellowship, one of my faculty members pointed me to the Fourth Universal Definition of Myocardial Infarction. This is an amazing document from 2018, produced by the ESC/ACC/AHA/WHF Task Force. This is where my mind goes whenever I get consulted for an elevated troponin. Since it helped me so much, I figured I’d take some of the important points and incorporate them into my guide. For the purposes of this guide, I will make it as simple as possible, but of course there is much more detail and complexity to all of this.

Okay... I just got consulted for an elevated troponin. Here’s exactly how I think through it.

1. The Patient

   1. First, I want to estimate their pretest probability (PTP) of actually having coronary artery disease that could warrant invasive testing (i.e., coronary angiography/left heart cath) for an MI.

   2. Older age, a history of CAD, or risk factors like HTN, HLD, DM, or smoking all increase that PTP.

   3. Then I look at the vitals to assess for shock or brady-/tachyarrhythmias.

2. The Presentation

   1. Why is the patient in the ED? Or, if they're admitted, what are they in the hospital for? What has their hospital course been like so far?

   2. Most importantly: Do they have chest pain, pressure, tightness, or heaviness (or an anginal equivalent)? And if they do, what kind? Is it cardiac? Does it come on with exertion or emotional stress, and is it relieved with rest or nitroglycerin?

   3. A lack of chest pain does not rule out ischemia. But, as we'll see later, chest pain plus an elevated troponin sends me down one path, while an elevated troponin without chest pain sends me down another. So this distinction is key.

3. The TROPONIN

   1. When looking at an elevated troponin, the question is: “Is this myocardial infarction or myocardial injury?”

   2. The first thing I do is look for either a rise and/or fall pattern or a stable pattern. If the pattern is stable, meaning there’s little variability between the values and it appears to have plateaued, then this is chronic myocardial injury. These patients almost always have an elevated troponin. A flat, recurrent, mild troponin elevation is not ischemia; it is longstanding myocardial injury. We commonly see this in patients with ESRD/CKD or structural heart disease (HF, etc.). Their chronic troponin elevation alone does not warrant a cardiac cath or an urgent cardiology consult.

   3. If the troponin is rising and/or falling significantly (meaning at least a 20% variation between values), then this represents either acute myocardial ischemia or acute myocardial injury. Now the question is simple: Are there signs of ischemia? How to tell: ischemia manifests through symptoms (chest pain!), EKG changes (new ST changes or T-wave inversions), or echo findings (new wall motion abnormalities).

   4. If the patient has no chest pain, an EKG without signs of ischemia (or one that looks unchanged from their prior EKG), and an echo without any acute findings (no new wall motion abnormalities or drop in EF), then this is acute myocardial injury. Not an MI. Although it does not warrant ACS protocol or a cath, it unfortunately still carries negative prognostic risk. More on this shortly.

   5. If the patient has a significant rise and/or fall in troponin plus any signs of ischemia (as discussed above), then this is what we refer to as an acute MI. This is when I'm initiating ACS protocol and planning the timeline for coronary angiography. More on the two most commonly encountered types of MI later in this article.

I hope my approach is helpful!

These are my last few, but relevant, points on myocardial infarction and acute myocardial injury:

ACUTE MI

There are actually five types of MI, but we most commonly diagnose Type I and Type II MI. These require a cardiac cath to distinguish between the two.

Type I MI is the one we are most familiar with and worry about the most in our patients. It results from rupture or erosion of an atherosclerotic coronary plaque, leading to thrombus formation and ultimately myocardial necrosis. The culprit thrombotic lesion will be seen on the angiogram (hence why it’s one of the criteria for diagnosis).

Type II MI, on the other hand, is not caused by plaque disruption and clot formation. It occurs most commonly in patients with stable or known CAD who then experience an acute stressor that results in insufficient blood flow to the myocardium. In other words, coronary blood flow can no longer meet the increased myocardial oxygen demand created by the stressor (or “demand ischemia,” as many of you call it). There are many potential stressors, including GI bleeding, sepsis, hypoxic respiratory failure, tachyarrhythmias, and more.

Important to know is that even when we call it “demand ischemia,” the patient will need further work up (possibly with a cath down the line), to assess for underlying obstructive CAD.

***Of note, patients do not need to have underlying CAD to develop Type II MI. It can also occur from coronary vasospasm, coronary embolism, severe anemia, and other conditions. See the figure below.

Last, but not least:

ACUTE MYOCARDIAL INJURY

So, what exactly is acute myocardial injury? And why do we care if we don’t necessarily treat it the same way we treat ACS?

It’s important to know that acute myocardial injury precedes myocardial infarction. In fact, myocardial injury caused by ischemia is an MI. However, for simplicity and based on the Universal Definition, myocardial injury is discussed as its own entity.

This is still an evolving diagnosis. We commonly refer to it as “benign troponinemia.” But although we don’t treat it with ACS protocols or routine invasive testing, it is far from benign. And it’s extremely common. Studies estimate that approximately 70% of patients who present to the ED with an elevated hs-Tn ultimately have acute myocardial injury, rather than an MI.

The bottom line is that acute myocardial injury carries a poor prognosis. Based on the current data, patients with acute myocardial injury have a one-year rate of cardiovascular death or MI that is qualitatively comparable to patients with Type I MI, and they have a higher rate of death.

There was a lot of information in this post, but it has all helped me understand what I’m dealing with when I get called for an elevated troponin. Hopefully you found this helpful too. If so, feel free to comment. I’m interested in starting a mini guide series on topics I feel are common/important. Lmk if you would be interested!

-Iv 🪽🤍

I’ve always been a fan of Legally Blonde. That’s why, when I heard there was a series created based on the movies, I was really excited. I may not be a teenager, or even in my 20s anymore, but I couldn’t help but give it a try.

At first, it felt pretty silly of me. Elle is a girl starting high school in Seattle after moving from L.A. Though Lexi Minetree makes for an amazing Elle Woods, and the show really is so grounded in the character, honoring major parts of the movies and the person Elle will one day become, the first couple of episodes were mainly smiles, laughs, and nostalgia.

But at some point, it became more than that. Elle’s character makes me think of little me, Ivie. She also makes me think of women all around the world. Female empowerment. Though I’m not an outspoken feminist, I believe in the inner power and strength that all women have. It is woven into each one of us so delicately.

Elle shows that through and through. She’s fun and fearless. She can’t be defined by only one word. She makes comebacks and overcomes. She smiles at life and puts her best foot forward each time. She cares about herself and her well-being, and of course her appearance, without compromising good deeds, kindness, and compassion for others. She makes you laugh because, yes, she is naïve, but also because she is constantly finding herself.

We’re all finding ourselves. Our lives change throughout the years, and parts of us do too. As we move from one thing to the next, we continue to discover parts of ourselves we didn’t know existed. There is nuance and beauty in this.

I love watching it through Elle because it reminds me how important it is to care about your loved ones, to be there for them, to be vulnerable, curious, and open to learning and adapting. She reminds me how special it is to be kind and giving. She reminds me of the importance of being strong and rooted in who you are.

Anyway, I just wanted to put this out there. Let’s keep believing in ourselves and finding the better versions that are yet to come.

-Iv 🪽🤍

But maybe greed isn’t always what we imagine it to be. It’s not just an excessive desire for more overt wealth or power. It goes much deeper than that. Greed can be that quiet voice that whispers, I need more. It’s not enough.

This is so common in the world that we live in today. Our minds tell us this, in so many aspects of life. For me, this is how it can show up…

I go to the gym, and I didn’t work out hard enough because I haven’t lost enough weight yet. I need to do more next time.

I make a delicious meal at home, but somehow it isn’t enough because it doesn’t have all the beautiful ingredients I see in recipes online. It doesn’t look picture perfect for social media. I can make a better meal tomorrow.

I wear an outfit I recently bought, but it’s not good enough. I could use a new pair of shoes. A new purse. Something else. I want to look better.

I don’t have enough people viewing my stories or liking my posts. I need to get more followers on Instagram. I need better content.

I don’t have enough subscribers on Substack yet. Maybe I need to write something different? Be someone else? I want more.

Even in my career. I’m a cardiologist, but right now I’m on a break before starting my next job. Sometimes I feel like I’m getting rusty because I’m not seeing patients. I need to read more. Learn more. Be better. Prove myself. Get a better job one day.

Right?

It’s. Never. Enough.

I’m sure I’m not the only one who thinks this way. We’re all hungry for more in different areas of our lives. We’re human, after all. We want the incredible vacation, the beautiful wardrobe, the perfect body, the happy family, the recognition, the influence, the public platform.

We want it all.

And maybe that is how greed shows up quietly in our lives. It may not look like greed on the surface, but it hides within us.

There’s nothing wrong with having goals or wanting to grow. Ambition itself isn’t the problem. But there is something profoundly beautiful about being content. About recognizing that what we have today is enough because God has already provided enough.

When we allow our hearts to be truly content, we create space for something greater. We begin to notice God instead of constantly chasing the next thing. We recognize the blessings we’ve overlooked, the quiet moments of beauty around us, the people we love, and the impact we’re already making.

Instead of seeking more possessions, more status, or more validation, we seek God.

We become grateful. We thank Him. We rest. We rest in God’s goodness, and our hearts begin to change. We discover a peace that the world can never offer.

In the end, it’s a paradox. The more status, possessions, and validation we accumulate, the more dissatisfied we often become. Our relentless pursuit of worldly things will never bring lasting fulfillment. It feels great for a moment, until it suddenly feels empty. And it never brings us closer to God.

So let’s not allow greed to overshadow contentment and gratitude. I hope some of you can relate to this. More than anything, I hope you can recognize the countless blessings God has already given you, thank Him for His faithfulness, and trust that His provision is far from over.

P.S. I’m a work in progress on this matter. If you related to this, you’re welcome to spend the next 5 minutes in prayer. I had a great chat with Him this morning and it made a big difference in my day.

-Iv 🪽🤍

I was a bit obsessed with the heart. My maternal grandfather died of a large heart attack in his 40s, on the dance floor while dancing with my grandmother, and in front of my mother when she was 18 years old. My paternal grandfather had multiple heart attacks, a bypass surgery, and two strokes, before he eventually died from a complication of carotid endarterectomy. Cardiovascular disease is prevalent, and my family is no exception.

I think it was around 14 years of age that I decided I had to be a cardiologist. Being a doctor was already a given for me, but it was cardiology that I was truly excited about. I think a lot about My Why. Actually, I had to give a speech about My Why at an American Heart Association event. I feel like it’s a tough question to answer but as the years have gone by, it’s gotten clearer for me.

My grandparents are My Why. My parents. My environment. The people around me. Every time I succeed at getting close to a patient and making a difference. Every time tears well up in my eyes when I learn that my patient has died. The fact that after all this time, I still get surprised that a patient died from their heart disease, or their heart failure, or their malignant arrhythmia.

It’s crazy how often I think I know exactly what I’m doing, reassure myself that I’m doing everything right, and feel pride about how good I am at my job. Then I’m in a situation where that only matters to a certain extent, or doesn’t even matter at all. I am either totally humbled (because truly none of us are perfect, neither is the medicine or the science, and doctors don’t have an exact recipe) or it’s just up to God.

God is also My Why. I don’t believe that I just think of an idea myself. I believe God puts His thoughts in my head. It was His idea that I become a cardiologist. To honor Him and give Him all the glory. When someone sick starts to feel better, when they understand their disease, when they feel cared for, or know they’re not alone, in some way because of me, I know that God smiles. It was His plan.

And just to wrap it up, I am a general cardiologist. I finished training a month ago. I initially wanted to keep going and specialize further in heart failure or in electrophysiology. But TBH, 14 years of school is enough. I’m too tired and ready to start practicing solo! I start my new job in November… wish me luck!

Also, may I continue to always draw hearts in random places everywhere I go… see below.

-Iv 🪽🤍

I have many interests. I’m 33 years old (thirty, flirty, and thriving!) and I’m a general cardiologist based in Texas. Which means I can potentially post cardio educational content…

However, I also like to read, draw, cook, and create. I love collecting beautiful pictures and quotes.

I’m spiritual. I love God and have a relationship with Jesus.

I’m also happily married to the best guy ever. You guys would love him. He’s my soulmate.

Maybe I can share a little bit of everything! I’m used to keeping my thoughts and likes pretty private. It’s my first try at this so go easy on me.

I can’t help but to feel excited!

-Iv 🪽🤍