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:

Source

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.

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.