This post is for the psychiatry resident who asked me about a patient who had a Bazett’s QTc in the 510’s, but a Hodges QTc of 470:
Generally, we are concerned about QTc because torsades=bad.Practically speaking, a QTc >500 is something to be worried about.
A really shocking number of medications prolong the QTc, and just as a reminder, include things like antiarrhythmics, ondansetron, and haloperidol, but also Benadryl, erythromycin, tacrolimus, and TCAs.
What are the different formulas for QTc?
Bazett’s formula: QTC = QT / √ RR
Fredericia’s formula: QTC = QT / RR 1/3
Framingham formula: QTC = QT + 0.154 (1 – RR)
Hodges formula: QTC = QT + 1.75 (heart rate – 60)
Based on my expert Internet search, it is unclear which is the “best.” I also asked a couple of our attending cardiologists and cards enthusiasts, who didn’t have strong opinions.
The current clinical standard is the most widely used Bazett formula, but with this formula, there is a known overcorrection at high heart rates and undercorrection at lower heart rates. The Fridericia and Framingham correction formulae showed the best rate correction and significantly improved prediction of 30‐day and 1‐year mortality. With current clinical standards, Bazett overestimated the number of patients with potential dangerous QTc prolongation, which could lead to unnecessary safety measurements as withholding the patient of first‐choice medication.
That all being said: use the QTc that will give your patient the safest plan. And if you remain skeptical of a prolonged QTc in a clinically stable patient, get repeat EKGs until it’s…less prolonged…and your problem is solved.
One of the tenets of treatment of ACS (unstable angina, NSTEMI, STEMI) is treatment with an anticoagulant like heparin or enoxaparin. The “heparin vs. enoxaparin” issue is a totally different discussion. What this post addresses is a gray area: does every patient with unstable angina need to be started on a heparin drip?
Heparin is a medication that has potential side effects (bleeding, immune reaction) and takes time and resources (maintaining a patient on a drip, PTT draws).
I think that if a patient has had chest pain within the past 24 hours, then it would be prudent to start a heparin drip, as unstable angina can escalate into an NSTEMI on short notice. There are several high-risk features that should prompt a heparin drip (reference):
history of MI
abnormal stress test
a strong history suggestive of UA
What about aspirin? EVERY patient with suspected unstable angina should get 324 mg of aspirin. There is virtually no harm to giving a single dose of aspirin, so you might as well give it.
The intra-aortic balloon pump (IABP) is one of the devices that you may see in your cardiology/cardiac intensive care unit rotations.
The physiology of the IABP is intuitive. In heart failure, factors such as increased afterload and decreased contractility are negatives, right? The IABP inflates during diastole and deflates during systole, which generates a suction-cup like negative force that propels blood forward out of the heart. Physiologically, this is like the “suction cup” effect that geckos, treefrogs, and other animals have.
Because of the increased forward flow, the IABP can increase myocardial oxygenation (the coronary arteries have more time to perfuse, too), increase cardiac output, and reduce LV workload. It also decreases pulmonary artery pressure (which is why you’ll see a PAP listed on the monitor).
Which patients get IABP? People who have been through cardiac shock, are post-MI, or have severe cardiomyopathy, valvular disease like MR, or high-risk patients who are awaiting stenting. The important common factor is that IABP is a bridge to something: whether that is cardiac surgery, interventional cath, or transplant. It is not meant to be used indefinitely.
How do you titrate the power of the IABP? The IABP’s power is measured in “augmented beats”: the ratio of how many times the IABP “works” to number of heartbeats. If the IABP is 1:1 for instance, that means that it is being activated with every heart beat. As you wean down a patient, you may see a ratio of 1:2 or 1:3 (which is basically equivalent to not having an IABP).
How can you improve IABP performance?
make sure timing of balloon inflation is optimized: there is an ECG monitor and “trigger” system that can be used to determine how to time a patient correctly.
make sure the size of the balloon is correct
heart rate >130 reduces efficiency
preserve kidney function
Warning signs and complications to watch for:
limb ischemia caused by thrombosis at the insertion site…IABP may also be associated with a compartment syndrome or gut ischemia for the same reason
aortic dissection or pseudoaneurysm…ahh!!
if augmentation decreases, ask yourself about the possibility of whether this is due to improving cardiac function, or whether there could be new sepsis or balloon rupture
infection (you may be asked to place the patient on vancomycin…to prevent antibiotic abuse you should make sure there is a plan in place for how long the patient will be on antibiotics for, and if it’s treating anything or just for prophylaxis)
acute renal failure (blockage of the renal arteries, catheter migration)
When and how can you wean the IABP? A complicated decision that basically is about: is the patient’s cardiac function improving? Will it remain that way even if you take them off the device? As far as weaning goes, it’s a process of reducing the ratio of augmented to non-augmented beats from 1:1 to 1:2 or 1:3 (which is the same as no support) or decreasing balloon volume. It takes 6-12 hours.
A “heart monitor” is a device that is ordered when a patient has a complaint of palpitations, syncope, or a known history of arrhythmia that tracks a patient’s heart rhythm. There are different kinds of heart monitors reviewed below:
Holter monitors are about the size of a large deck of cards and continuously record rhythm for 24-48 hours. Patients can’t shower with the monitor on, but sponge baths are ok!
Wireless Holter monitors may be used if a regular Holter doesn’t detect a problem, but the patient continues to have symptoms. These monitors can record for days to weeks, until signs or symptoms of an arrhythmia occur.
Event monitors, unlike the Holter, only record rhythm at certain times.Patients are supposed to start recording when they feel like they have symptoms. These monitors can be worn for weeks if needed, and can be taken off while patients are showering. They are relatively small and worn like a Holter, with sensor pads on the chest. The King of Hearts monitor is a type of event monitor that is worn for 30 days.
Continuous loop records (aka presymptom memory loop recorders) are also worn on the body and are continuously recording and erasing data every few minutes. When a patient feels symptoms, they press a button that stops the erasing process and can save the rhythm strips a few minutes before, during, and after an event.
Implantable loop recorders are, as the name suggests, implanted under the skin and are roughly the size of a pack of gum. They have a long battery life and can be used for monitoring for 2-3 years! They are best in cases of symptoms that occur too infrequently to be picked up by a 30-day monitor, or someone who needs extended monitoring.
In medical school, the pulsus was a Step 1 concept that I learned to associate with tamponade. But now that I’ve seen a couple of cases, I think it’s helpful to have a reminder of how to measure a pulsus and create a differential for when you do hear one.
First: what causes a pulsus?
We often measure the pulsus if we’re worried about tamponade physiology but a very important learning point is that there are many things that can cause pulsus! Pulsus paradoxus is created when there is markedly less left ventricular volume, which can be caused either by lower LV and/or RV volume–as in asthma, myocardial infarction, shock, or PE. Even profound hypovolemia can cause pulsus. So really, it’s only “pulsus paradoxus” in the concerning sense if the variation in systolic blood pressure with inspiration is >10 mm Hg lower than it is with expiration.
Next: how to measure a pulsus.
By knowing how to take a blood pressure, you’re already halfway there! It can be confusing if you’ve never identified a pulsus paradoxus before, or if you feel uncertain because there’s no one else listening along to confirm your diagnosis. My tip is to practice on patients who you know do NOT have cardiac tamponade. Get familiar with when a normal patient’s Korotkoff sounds go away and come back. Let the air out of the cuff slowly. You will learn that you don’t even have to look to see when they’re breathing in and out. Then, when you have a patient who you ARE concerned about, you will be able to identify that point/systolic reading at which the Korotkoff sound remains constant and strong despite their breathing in and out, and calculate what their pulsus is.
Example: go to this Australian EMS Spot Diagnosis! link (video #3 is probably most revealing). Observe that the systolic blood pressures on the arterial tracing go from 100 to 50 in time with respiration.
Example: the ubiquitous and well-done Stanford 25 video (skip to 1:10 for the actual blood pressure-taking part).