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.

Screen Shot 2018-07-07 at 12.27.44 PM.png
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.

 

Screen Shot 2018-07-07 at 12.34.55 PM.png

 

 

“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.

What do I do if my patient on an antiarrhythmic goes back into atrial fibrillation?!

I had a patient recently who flipped from normal sinus rhythm into asymptomatic afib with RVR with heart rates into the 150s on post-op day 2. Classic. The twist is that she had been in sinus rhythm for years on flecainide prior to the surgery, and was still taking flecainide post-op. I was stymied: did her being on flecainide change management?  Answer at the end of the post!

The urgent question: do you need to cardiovert? The indications for cardioversion are still the same when a patient is on an antiarrhythmic: (1) unacceptable symptoms like syncope, CHF; (2) hemodynamic instability; (3) first episode of new afib within 48 hours (this did NOT apply to my patient because she had a history of afib). Cardioverting whether mechanically or pharmacologically with something like amiodarone carries the same risk of thromboembolism, so the next question should be…

Is the patient anticoagulated? Patients who flip from sinus into afib are at the highest risk of thromboembolism in the first 48 hours. Sometimes patients’ anticoagulation may be held, like in the perioperative period like for my patient. Try to make sure that if there are no contraindications to anticoagulation, it’s restarted.

Is there an underlying trigger? Lots of things can trigger afib: infection, PE, MI, fluid shifts, hyperthyroidism, postoperative stress, etc…If there is a trigger, treating it will make the afib better. Try to make sure there is nothing else going on that could be fixed.

If you are looking for specific discussions on different antiarrhythmics, check out this comprehensive review.

To return to my patient, the goal was still rate control. We decided that it was fine to continue her flecainide, and more than likely her rates would come down and she would convert back to sinus on her own. The biggest concern for her was that she was off anticoagulation. Two days later, she was still in afib, but her rates were in the 90s and she was back on apixaban.

Side note: many cardiologists advocate an antiarrhythmic “pill in pocket” for patients with infrequent afib. If they develop symptomatic afib, they can take the pill right then and there, which increases their chance of going back to sinus. However, if they are also on beta blockers, they should take the beta blocker first, as a medication like flecainide can have greater toxicity if it binds to receptors before the beta blocker does. Flecainide should always be combined with a beta blocker or other rate control agent, as one adverse effect is organization of the atrial rhythm so that the AV node can conduct 1:1 –> conversion of afib into atrial flutter with RVR (rates as high as 200s) which is obviously not sustainable.

How do I select an agent for afterload reduction in a patient with heart failure?

Afterload reduction has been recommended in the management of systolic heart failure since the 1980s. Afterload= arterial resistance as blood is pumped out of the left ventricle. The thought is that by reducing afterload, cardiac filling pressures are decreased, which is beneficial.

What agents reduce afterload? Anything that is an arterial vasodilator. (Venodilators decrease preload, which are thought to have a similar beneficial effect.)

  • Nitrates (venous>arterial vasodilators)
  • Hydralazine (most selective arterial vasodilator, in my experience this has been used the most)
  • Minoxidil (arterial vasodilator)
  • Lisinopril, captopril (about equal veno- and arterial vasodilators)
  • Diuretics (long-term arterial vasodilator)
  • In the ICU: nitroprusside, phentolamine, dopamine
  • Inotropes like milrinone (patients with advanced heart failure may be put on this palliatively)
  • Technically, the intra-aortic balloon pump (IABP) does, too!

What is the diagnostic accuracy of pulsus paradoxus for cardiac tamponade?

A classic Step 1 associations is: increased pulsus paradoxus=cardiac tamponade. But like everything in medicine, it’s not that simple. An abnormal pulsus paradoxus is not really sensitive or specific for cardiac tamponade. Pulsus paradoxus may also be present in patients with labored breathing, asthma attacks, pulmonary hypertension, constrictive pericarditis, PE, etc. This summary cites one report that “15% pulsus paradoxus in the face of relative hypotension was found in 97% of patients with moderate or severe tamponade and only 6% of patients with absent or mild tamponade.”

This review in Clinical Cardiology describes pulsus paradoxus as the “end of a spectrum” in cardiac tamponade, which frames it as what it is: an exam finding that if present, means that it’s more likely the patient is ALREADY in tamponade and you should act quickly…but just because it’s absent doesn’t mean the patient does NOT have tamponade.  This study reports that NHYA Class III symptoms (comfortable at rest but significant symptoms impairing function) were significantly associated the development of cardiac tamponade, which seems like it would be obvious, but can help in ambiguous cases. In my anecdotal experience, this is true, and relative hypotension, a narrow pulse pressure, and distended neck veins have been more sensitive for predicting tamponade.

NB: when trying to figure out if a pulsus paradoxus is abnormal, 20-30 mm Hg is considered high. But remember to take the pulse pressure into account! If the pulse pressure is narrow (like 110/90), then a pulsus of even 10 mm Hg might be abnormal and warrants immediate ultrasound.

What are the PCSK9 inhibitors?

There are two that are FDA approved: alirocumab (Praluent) and evolocumab (Repatha).

What is the biological basis of PCSK9 inhibitors?

LDL-R (for receptor) is found on the surface of hepatocytes. These receptors pick out LDL-c from the circulation, lowering the LDL level in the bloodstream. That’s a good thing!

PCSK9 is a protein that balances out the effect of LDL-R by binding to LDL-R and getting it degraded, thereby not allowing LDL-c to get reabsorbed. This means LDL levels may go up. (See this illustration and explanation) The PCSK9 inhibitors (mAbs) bind to PCSK9, which allows LDL-R to keep doing it’s job, and keep LDL-c levels low.

Are PCSK9 inhibitors effective? 

Yes. They are especially effective at reducing LDL levels when combined with statins. This review goes into exhaustive detail about trial data. However, no one knows for sure if they, like statins, reduce mortality from cardiovascular disease.

What caveats do I need to know about these drugs? 

  • Injected, not in pill form. This may be a barrier for some patients who either can’t (or won’t) inject themselves
  • These drugs are expensive! A year’s supply of evolocucamb is estimated to cost about $14,500. It’s unclear how much of that may be covered by insurance
  • The most common side effects are nasopharyngitis, congestion, and myalgia, but there are concerns about allergic reactions (it’s a monoclonal antibody) and cognitive impairment (subjective, but was reported in the phase III trials).
  • Patients with severe kidney and liver disease were excluded from studies, so if, for example, you have a patient with cirrhosis who wants to start one of these medications, talk with their hepatologist
  • Long-term studies on these drugs are lacking; there is a Cochrane review that reports that overall, follow up times for PCSK9 inhibitor studies have been short (26 months at the longest) and there have been few reported events.

Is is safe to give tPA/thrombolytics to someone who just underwent cardiac catheterization?

At my institution, we recently discussed a case of a patient with acute stroke in the setting of cardiac catheterization (right femoral access). The decision to push tPA was a tricky one, because he had just been cathed. When is it ok? When is it NOT ok?

Here are relative and absolute contraindications (respectively) for giving tPA:

 

As you can see, arterial puncture at a noncompressible site is a relative contraindication for tPA. So depending on where the puncture site was…the typical site for an arterial stick in a catheterization is between the bifurcation of the SFA and PFA and the branching point of the inferior epigastric artery. Typical site=compressible, “high stick”=noncompressible. If there is a “high stick,” tPA will confer a much higher risk of RP bleed and hemorrhage, and should be avoided.

Screen Shot 2018-02-06 at 11.54.23 AM