When It Looks Like Heart Failure but Isn't

Melissa Walton-Shirley, MD


June 08, 2016

He was 85 years old and often bragged about how well his heart bypass surgery had served him for 25 years. He had remained angina free from the mid-1990s; then, after an episode of atypical chest tightness, a cath demonstrated all grafts were still patent and his left ventricular function was well preserved. For 2 more years his chest tightness would be accompanied by complaints of increasing shortness of air, an increase in abdominal girth and bloating. "My pants need to go up a size," he lamented, with his ankles now sneaking over the tops of his unlaced shoes. "My legs have never swollen in my life until 3 weeks ago. I keep going to my doctor, who just says I'm old and need to take more Lasix," he said, his voice tinged with disappointment. "I have always appreciated Dr Jones, but I think I need to switch doctors," he added.

The echocardiogram demonstrated a still-amazing left ventricular ejection fraction (LVEF) of 60%, but with moderate mitral and tricuspid regurgitation and an estimated right ventricular (RV) systolic pressure of 100 mm Hg. His RV was normal in size and function, not the big bucked-up continuation of his venous system I expected. His chest X ray of course was read as "heart failure," always the scapegoat when pulmonary edema is present. The brain natriuretic peptide (BNP) was of course 400 pg/mL, another often-less-than-reliable witness to the crime of shortness of air. With all the good things his left heart had going for it, I smelled a rat.

Later that evening, the nurse called with the results—a postvoid residual of greater than 1000 ccs; proof his prostate had been holding his bladder hostage for quite some time. A Foley unleashed a torrent of light yellow urine that cascaded into a bulging plastic reservoir. Within 2 days his smile returned. He had ankles again, and both his appetite and his breathing improved. His cardiac function was now vindicated, but it didn't matter for long. Once the diagnosis of CHF found its way onto his chart, his heart was forever guilty.

Postdischarge, the spry 85-year-old gentleman found his way into my office once again with increasing peripheral edema and mild shortness of air. "Do you still have your catheter?" I asked.

"No. I don't need it anymore," he said, relieved. "Did they teach you 'in and out' bladder catheterization?" I asked. "No," he said puzzled.

Did they put in a suprapubic catheter into your bladder?" I asked pointing to his pelvis. "No," he answered. "Did they take out your prostate?" I asked. "No," he said.

"Since we didn't change anything about the bottleneck obstruction of your bladder, you are back to where we started." I could tell that the logic was sinking in.

Another remarkable case involved a gentleman with impaired LV function—always guilty until proven innocent. His LVEF was 30% and was accompanied by moderate mitral regurgitation (MR). When the Foley found its mark, water poured forth like the great Niagara. My echo tech summoned me to her procedure room. "Look at that," she said, pointing to the screen. "What is that?" I asked sheepishly. "That's his bladder up under his armpits," she said, which wasn't much of an exaggeration. He had been walking around like a camel with his own personal reservoir of urine backing up into the gutters of his lungs. The diagnosis on his referral form was of course, "congestive heart failure." Only after a letter to his family doctor, a letter to his urologist, and two phone calls to each was I able to facilitate a prostate surgery. I understood the reluctance because his EF was moderately impaired, but his coronaries were big fat juicy conduits that I knew would not betray him at the time of surgery. He sailed through it and gets to live his life with ankles again.

I've seen a handful of obstructive-uropathy cases masquerading as heart failure in elderly men in recent years. I shudder to think how many times I've missed it. I suspect that it's not just men who suffer. Some of our female patients with "diastolic dysfunction" and overflow incontinence seem to suffer from backpressure that finds its way into the pulmonary vasculature. The mechanism is both direct and indirect. They can't empty their bladders completely and they won't take Lasix to offload because it worsens their incontinence. Sounds like the basis for a good study for someone with more time and resources than I have these days.

Burgeoning bladders aren't the only culprits that fool us into labeling our patients with primary CHF. Calcium-channel blockers and diabetic meds are often culprits for leg swelling. A 24-hour urine protein collection can reveal nephrotic-range proteinuria that turns any patient into the Pillsbury Dough Boy. Sometimes a surprisingly low creatinine clearance in an underweight female with a fairly normal serum creatinine is revealing. We should always ask about sodium loading and overconsumption of liquids in those with LV dysfunction both systolic and diastolic. Chronic hypoxemia and RV stretch from sleep apnea as well as primary pulmonary disorders can be impactful. I once found a thyroid stimulating hormone (TSH) of over 100 mIU/L that improved the patient's LVEF by 30% when corrected. I can assure you that if I'd never checked that TSH, her problem might never have been found. Occult tachyarrhythmias create transient diastology and should be surveilled and addressed in patients with shortness of air or leg swelling.

Twenty years ago, congestive heart failure was one of the most dreaded consult requests. I had nothing but Lasix to offer. Now, I skip to the bedside with a veritable toolbox of diagnostics and treatments. I always enter the room with an air of skepticism, even in those with known cardiac impairment.

Some of the answers to our most frequent questions are not found inside our habitual checklist of cardiac diagnoses. When it comes to "heart failure," even in face of obvious cardiac impairment, we must always think outside the box. If we don't, our patients could be trapped in a misdiagnosis forever.


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