Tail Sprains and Is All Physiology Research Funded by Cats?

I recently attended the Society of Hospital Medicine’s annual conference and a few people reminded me that I write this newsletter, so I’m back!

When I got back from SHM I picked up my dogs, one from an old neighbor who likes to watch him and the other from boarding at his daycare on account of he may be the incarnate form of some sort of demon or evil spirit. Just kidding, he is v sweet, just sort of a lot. Anyway, the next day I noticed that Satan wasn’t wagging his tail, like, at all, which is very atypical. That dog can’t stop wiggling and his tail wags with such abandon he has a history of ‘happy tail injury’. Basically, he can’t stop wagging it and when he’s in a confined space (kennel at animal control when he got picked up as a stray, kennel at the place I used to board him) he’ll just repeatedly traumatize the tip of his tail until he’s spraying blood all over the walls a la Jackson Pollock. The tip of his tail is now sort of zombified and I take him to this new place where they let the dogs sleep out in the open. I called the daycare to ask if anything happened while he was there and they reviewed the film, he was wagging up until I picked him up. I talked with a vet friend about it (doctors aren’t the only ones coerced into giving free advice) and she thought maybe he had Swimmer’s Tail, otherwise known as acute caudal myopathy. He sprained his tail from wagging it too hard. Lil homie loves me so much he hurt himself with joy when I picked him up. It has gotten better over the last few days and now he’s wagging with abandon once more. In the spirit of being reunited with my guys, here’s a breakdown of a breakdown featuring one of the most famous physiological phenomena in medicine, one derived from the sacrifices of some very good boys.

Berlin DA, Bakker J. Starling curves and central venous pressure. Crit Care. 2015;19(1):55. doi:10.1186/s13054-015-0776-1

The Starling curve comes from a paper published in 1914 by Starling and another dude named Patterson who apparently gets no cred. In the experiments generating the curve, Starling, a British physiologist, turned some soft muzzled martyrs into a simplified closed circuit system by ligating the distal aorta, the branches of the aorta off the arch, and the inferior vena cava, generating one path into the the right atrium (superior vena cava) and a single path for flow out of the left ventricle. Blood proceeded into the aortic arch but was diverted via a cannula into a raised reservoir - it would drain from this reservoir into a cannula feeding the superior vena cava to go back into the right atrium and Starling controlled the amount/rate of flow going back into the RA with a clamp. If he opened the clamp a bit, the RA saw more flow. If he closed it, the RA saw less.

Starling’s closed circuit system.

So, closed system. All that comes out of the left side goes back into the right. He noticed, though, that if he continued to increase flow into the RA from the reservoir it would accommodate it up to a point and then right atrial pressure would begin to rise. He hypothesized that increased venous return (preload) beyond that point caused the heart to fatigue and actually decreased output. He performed the experiment 9 times on 9 sweet, beautiful, loyal, handsome doggos and graphed the results altogether.

Over the ensuing century his findings were assimilated into Big Physiology and built on by the likes of Sarnoff and Berglund, who sound like personal injury attorneys. They sacrificed more perfect angels sent from on high (I’m still talking dogs) and cannulated both atria plus the aorta. They placed a device to detect and measure flow in the aorta to keep track of ventricular work and cardiac output. They demonstrated that increasing atrial filling increased cardiac output to a physiologic limit before it plateaued or decreased. They further demonstrated that increasing the pressure around the heart (we see this clinically in patients on positive pressure (bipap/cpap/vent), with pericardial effusions with or without tamponade, with large pleural effusions, pneumothoraces, etc) would actually decrease cardiac output as right atrial pressure rose. They weren’t done torturing these 4-legged saints of discovery - they increased ventricular afterload and induced myocardial ischemia (they gave them high blood pressure and lil doggy heart attacks!), which also increases right atrial pressure with a concomitant fall in cardiac output. At this point I’m mailing in tear-soaked letters to the editor on the daily saying, “WE BELIEVE YOU! MORE VENOUS RETURN DOESN’T NECESSARILY LEAD TO BETTER CARDIAC PERFORMANCE! USE CATS!”

In the 60’s my dawg Braunwold, who sounds like a Norse folk hero, demonstrated some of this phys in humans. They didn’t have ultrasonographic or magnetic resonant means of demonstrating cardiac output and my guy wasn’t about to send an IRB proposal (did IRB exist in the 60s?) with the same stuff his predecessors pulled, so he sewed some markers into ventricles and used cineradiography (like CT/fluoroscopy I guess?) to examine beat to beat variation in patients with A Fib (variable ventricular filling due to erratically timed atrial contraction). He also demonstrated variable output with valsalva maneuvers (to increase intrathoracic pressure and therefore RAP) and during different parts of the respiratory cycle. His work showed that it was ventricular filling and end diastolic volume independent of right atrial pressure that increases output.

Guyton, who sounds like a trapeze artist, helped complete the picture by including the contribution of the systemic venous circulation. He hypothesized that venous return depended on a pressure gradient between mean systemic filling pressure and right atrial pressure. Systemic pressure has to exceed atrial pressure in order for blood to continue flowing forward and back to the heart, therefore increasing vascular tone (with pressors) or systemic filling pressures (with IV fluids) can improve cardiac performance (to a point) by increasing venous return leading to more end diastolic stretch/filling. This produced the graph below, which is the one I remember from med school physiology with Dr. Peterson, who might be older than the Starling curve.

The red line is cardiac performance and may rotate to the right in a bum ticker. The blue line is venous return under normal circumstances, the dotted line demonstrates manipulating venous return to get more output from the heart. Things like inotropes/chronotropes manipulate the red line, fluids/diuretics/dialysis/stab wounds/vasoconstrictors/positive pressure ventilation/tamponade/etc manipulate the blue line.

Where does that leave us? CVP (which I use interchangeably with right atrial pressure) by itself cannot predict a given patient’s response to volume (IV fluids). To put it another way, since I haven’t even mentioned POCUS yet, your assessment of IVC and the jugular vein is not enough to warrant fluids or dissuade you from giving them. Without another compelling reason for increased CVP (like PPV, MI, CKD/ESRD, pulmonary or severe systemic hypertension, etc) your patient may be overloaded and require diuresis or ultrafiltration. But, keep in mind that those with high CVP might actually need more fluids (saddle embolus, right heart MI, or tamponade) in order to adequately manipulate end diastolic volume and promote cardiac output. If the CVP is low, you’re probably safe to give fluids, but that doesn’t mean you pump em until the IVC and jugular are juicy. It’s a tool in your kit, and just like you ought to question a mechanic using a tire iron to pry open the hood of your car, you ought to question a provider making decisions about fluids based on an IVC or JVP alone.