“When can you discontinue anticoagulation when someone has converted from atrial fibrillation to sinus rhythm?”

Let’s say you admit a 75 year old man with pneumonia and sepsis. His EKG shows atrial fibrillation, which as far as anyone knows, is new. He is treated with antibiotics, fluids, and started on a heparin drip for the atrial fibrillation.

Two days later, his telemetry shows normal sinus rhythm. The patient feels much better than when he came in. Past medical history is significant for hypertension and hyperlipidemia. A TTE shows no valvular disease. The patient asks you, “Doc, do I have to keep taking a blood thinner? Do I have to take it for the rest of my life?”

In this case, the conversion to NSR was spontaneous. My brief search did not turn up studies looking at anticoagulation dosing/duration in patients who spontaneously convert to NSR, so I’m extrapolating from recommendations for patients who undergo planned cardioversion.

In cases of planned cardioversion, short-term vs. long-term anticoagulation afterwards is based on the CHADS VASC score and patient-specific risk factors for stroke/thromboembolism. This is regardless of how long atrial fibrillation has been present for (the all-important “48 hours” is arbitrary and most helpful for categorizing afib for study purposes).
CHADS VASC=0 : most cardiologists would anticoagulate for 4 weeks
CHADS VASC ≥ 1: most cardiologists would anticoagulate for at least 4 weeks…and might continue long-term anticoagulation if the CHADS VASC is considered “high risk,” and definitely if there is history like valve disease or replacement, or past stroke.

Our patient in the case above is relatively healthy but has a CHADS VASC score of 3. It would be reasonable to keep him anticoagulated and discharge with your favorite anticoagulant. He and his primary care doctor should discuss risks/benefits of anticoagulation, and if the patient agrees, it would be preferable for him to continue anticoagulation long-term.

Remember: when making decisions about anticoagulation, it’s not the kind of atrial fibrillation that matters (it doesn’t matter if it’s unprovoked, provoked, or new onset)–it’s the patient’s underlying risk factors.

When should you consider cardioversion for atrial fibrillation?


  • afib with rapid rate that causes hemodynamic instability or severe heart failure, MI


  • symptomatic, persistent afib (causing CHF exacerbations, for example)
  • symptomatic, new afib due to an underlying cause (e.g., hyperthyroidism, post-op, PE) after that cause is treated
  • before cardioverting, ask about anticoagulation–if afib has been present for >48 hrs, either TEE to rule out atrial thrombus or 3-4 weeks of anticoagulation is recommended. That being said, even when cardioversion is done in the ER with no anticoagulation the risk of clot at 30 days is 0% – 0.7%


  • patients with infrequent, but symptomatic episodes who don’t have a pattern of spontaneously converting back to sinus rhythm
  • as part of a plan for long-term rhythm control, cardioversion is performed before starting patients on oral antiarrhythmics

Cardiology is more likely to say no to patients who are…

  • stable, completely asymptomatic patients 🙂
  • >80 years age, multiple medical comorbidities
  • patients who have not been anticoagulated or are not candidates for anticoagulation
  • left atrial dilation or other structural features that make afib more likely to recur

What is catheter-directed therapy? (EKOS)

Catheter-directed lysis therapy delivers thrombolytics (like tPA) via a catheter. Consider it for extensive DVT or submassive or massive PE when you have concerns about bleeding risks.

EKOS (EndoWave Catheter Infusion System) is a device that is supposed to enhance catheter-directed therapy with the use of ultrasonic waves. Ooh! There are several parts of the EKOS experience to be aware of:

  • Control unit–the pump. Can adjust settings and infusion rates. Beeps at you when there are problems.
  • Catheter/drug delivery device–infuses the thrombolytic at a set rate
  • Ultrasound core–supposedly increases thrombolytic efficacy, decreases fibrin clotting
  • Coolant (usually normal saline or heparin-infused normal saline)–to prevent the ultrasound core from overheating/causing tissue damage

A video is worth a thousand pictures: check out the EKOS inservice video on YouTube.

This review goes into some of the nitty-gritty of managing EKOS. The thrombolytic of your choice is usually set to an infusion rate of 1-5 mg/hour. The catheter usually stays in for 18-24 hours. Consider stopping thrombolysis once a maximum dose has been given (like 18-24 mg), 18-24 hours has passed, or repeat ECHO or CTA shows improvement. Once the clinical goal is achieved, the catheters may be removed without repeat imaging. Trend fibrinogen levels: most conservative protocols would reduce or stop the infusion when fibrinogen <200 mg/dL.

While there are studies proving the efficacy and relative safety of EKOS (such as SEATTLE II), there are no high-quality studies that compare EKOS with other kinds of catheter-directed therapy, or against the oldie goodie systemic tPA. Therefore, EKOS seems promising, but people are reluctant to recommend it over other kinds of therapy.

Tangent: not all contraindications to tPA are created equal; see this review on the absolute and relative contraindications to thrombolytics. In addition, even when there are contraindications to tPA, you might still be able to use it and get lucky, as in this interesting case report.

Are orthostatics useful?

Yes. But only in certain situations. Read on.

Typical case: 80-year old woman with severe ILD and pulmonary hypertension on 6 L nasal cannula coming in with dizziness and presyncope. “I feel fine now,” she says after one day of being in the hospital (her son warns you she is eager to get home to see a new grandchild). She has been on Lasix for several months for leg edema (which on exam is 3+), and despite saying she’s not dizzy anymore, her orthostatic vital signs (VS) are positive by SBP and DBP. Should you stop Lasix? Can you send her home?

Orthostatic symptoms include lightheadedness, dizziness, confusion, weakness, blurry vision, etc. Orthostatic VS are positive if after 1-3 minutes, the heart rate increases >30, systolic BP decreases >20, diastolic BP decreases >10 (the 30-20-10 rule). For patients who have hypertension, using a cutoff of systolic BP decreases >30 is more specific. This paper provides a great physiologic review of orthostatic hypotension (OH). In up to 1/3 of cases, the cause of orthostasis will not be identified.

Studies such as this meta-analysis and this prospective population study have linked OH to increased all-cause mortality as well as stroke, CHF, and MI. Positive orthostatic VS can be linked to serious chronic illnesses, but these studies showed patients with OH had worse outcomes independently of other conditions.

Just some of the diseases associated with OH:

  • Neurodegenerative disease: primary autonomic failure, MSA, Parkinson’s, MS
  • Neuropathies: diabetes, amyloidosis, renal failure, stroke
  • Cardiovascular disease: heart block, pulmonary HTN, heart failure
  • Endocrinopathies: adrenal insufficiency, hypothyroidism
  • Cancer: paraneoplastic syndromes, multiple myeloma

Known factors that can make OH worse:

  • Fever
  • Dehydration, excessive urination
  • Increased venous pooling
  • Immobilization and deconditioning
  • Post-prandial state
  • Certain medications (diuretics, some antipsychotics, etc…)

The above information shows that not all orthostasis will be fixed by fluids. Don’t overload patients if they’re not responding.

More recently, orthostatic VS have been critiqued. Anand Swaminathan’s presentation on the “urban legend” of orthostatics in the ED is very informative. He cites a study showing that in a population of 900 nursing home residents, 50% had orthostatic VS changes. The numbers are similar for young, healthy adults. Positive orthostatics could indicate a new problem…or not. See this: a letter to the editor on the lack of evidence showing positive orthostatic VS in syncope require additional diagnostic testing/admission. For triaging purposes, orthostatic VS are not as useful as orthostatic symptoms (getting so lightheaded they might fall or injure themselves at home).

Orthostatic VS should only be obtained if they will change decision-making or result in new treatment. I propose that orthostatic VS are useful for:

  • in certain presenting complaints, like pre-syncope or syncope, which based on a patient’s background, may lead to cardiac testing (I say this as an internal medicine doctor dealing with patients already admitted to the hospital)
  • determining how aggressively someone’s supine hypertension should be treated
  • determining if someone’s lightheadedness, dizziness, or hypotension should be treated with compression stockings or meds like droxidopa or midodrine
  • evaluating functional status or quality of life in patients with above-mentioned chronic illnesses (very specific situations)

Returning to the case: the patient’s positive orthostatic VS were thought to be due to underlying pulmonary HTN and deconditioning. Lasix was thought to be necessary for pulmonary and peripheral edema. She was sent home. She was re-admitted <48 hrs later with syncope and found to be normotensive lying on her back, but profoundly hypotensive (SBP 50s) with just turning in bed; this failed to improve with IV fluids. TTE showed new RV dilation and a thrombus vs. vegetation on a pacemaker lead. In retrospect, this TTE should have been performed during her first hospitalization. This case is a good example that the significance of positive orthostatics depends on the clinical context, and while you may not need to treat the orthostatics per se, they can be a warning sign of a high-risk patient or a brewing problem.

“Why does potassium have to be repleted to 4?”

There is general agreement–but not an official statement that I could find–that in all comers, K <3.0 should be repleted. In patients with a history of past cardiac surgery, heart disease, and definitely in the post-MI population, K<3.5 should be repleted for a goal of 4.0. When there is acute concern for torsades or other arrhythmia, there is again general agreement but no official consensus that the goal is raised to >4.5.

Remember action potentials? The ins and the outs with K, Na, and Ca with the alphabet soup of channels? (Brief review in the first section of this editorial.) In the short-term, having a low serum K affects repolarization and has a chain effect on the action potential, causing increased automaticity, excitability, and QT prolongation, potentially triggering fatal arrhythmia. In the long-term, hypokalemia is associated with cardiovascular mortality in patients with underlying heart disease, arrhythmias like RBBB, and heart failure.

NB: Kind of supporting this are findings that higher doses of thiazide diuretic are linked to sudden cardiac death. Some argue that the mortality benefit of ACE inhibitors and beta-blockers in heart failure comes in part from an ability to better stabilize potassium levels. (Beta-blockers keep potassium extracellular through beta-2 receptors.)

Many studies linking hypokalemia to arrhythmia were relatively smaller studies (it seems like anything fewer than n=5,000 is not impressive in general cardiology) done in the 1980s, with mixed patient populations of mostly acute MI, hypertension (looking specifically at thiazide diuretics), or heart failure. These studies implied that the higher the potassium (K>4.5) the better:


A more recent population-based cohort study of post-MI patients in JAMA (n>38,000), on the other hand, showed the following:

Because the lowest rate of mortality was found in the group with K 3.5-4.5, a goal of 4.0 is generally set for post-MI patients, which was extrapolated to any patient with heart disease. A similar distribution was found in patients who also had renal disease, and this study based on data from MERLIN-TIMI 36. This is a good reminder that hyperkalemia is linked to increased cardiovascular mortality, too.

What is a pericardial window?

A window is also called a transthoracic pericardiostomy, a surgical procedure done for large and/or recurrent pericardial effusion in which a 4-cm flap of pericardium is removed from the heart so that pericardial fluid can drain into the chest cavity. The pericardial flap can be used for biopsy (if there is concern for infectious or malignant pericardial effusion). When a pericardial window is performed, there may initially be a large-bore drain as well. However, the point of the window is to allow fluid to continuously drain into the chest cavity until the tissue fibroses and scars and the window “closes.” Only 5-10% of patients who get a window will have reaccumulation of the effusion, as demonstrated in this study.

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Source: http://onsopcontent.ons.org/Publications/SIGNewsletters/images/PDFs/acc/Table1.pdf


The least invasive technique for relieving pericardial effusion is pericardiocentesis; the most invasive is pericardiectomy. A pericardial window is somewhere in-between. (There is also something called balloon pericardiotomy which is analogous to balloon valvuloplasty.) Risks include arrhythmia, infection, clot, and very rarely, cardiac perforation.

When pericardiocentesis is performed, there may be a decision to place a pericardial drain (a small-bore catheter) to allow extra fluid to be removed. The drain is usually removed when output decreases to 25-50 cc over 24 hours. Unfortunately, up to 60% of patients who receive pericardiocentesis may have reaccumulation of the effusion.


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“What does it mean to be intravascularly dry but extravascularly overloaded?”

This excellent question comes from Esther!

Digging back into basic physiology, approximately 2/3 of body fluid is INTRAcellular and 1/3 is EXTRAcellular. We are only talking about EXTRAcellular fluid here. Extracellular fluid is divided into the intravascular space and extravascular space. Screen Shot 2018-06-29 at 10.51.45 PM.png

As above, fluid shifts are affected by factors like endothelial permeability (which is affected by direct tissue injury or inflammatory cytokines, etc.), hydrostatic pressure (free water in the plasma that goes into the interstitium), and osmotic pressure (proteins in the interstitium that pull water in).

Clinically, patients who are “intravascular dry and extravascularly overloaded” are patients who don’t have enough volume in their vascular system because all their fluid is getting pushed into other parts of the body, like the abdomen, lungs, extremities, and dependent areas. These patients will often have pitting edema on exam or “wet sounding” lungs with crackles or decreased breath sounds indicating pleural effusions.

Severe heart failure is a good example. The heart cannot pump blood effectively (there is poor “forward flow”) so fluid is retained in the veins, leading to fluid leaking out into the interstitium because of increased hydrostatic pressure. These patients develop “volume overload” which refer to the edema and lung findings above, but because there is not enough fluid in the vascular system, they are also “dry” and can be at risk for hypotension and poor perfusion of organs like the brain and kidneys. If a patient has acute kidney injury from poor perfusion, they may have low urine output, but this is not always present.

We use diuretics (like furosemide or bumetanide) to treat heart failure exacerbations because they cause Na/K/Cl loss in the urine, which leads to water getting pulled from the interstitium back into the vascular system. Treatment success is measured in terms of increased urine output (peeing out extra fluid that had built up in the interstitium) and weight loss.