by Amy Neglia, RN, MSN, ACNS-BC, CCRN-CMC, CFRN, C-NPT
Very early in my career, I learned a hard lesson. We had a patient at a small, rural facility that was in respiratory failure and needed an airway. He also had a serum potassium of 6.2. My partner and I knew that Succinylcholine could cause an increase in serum potassium, but we thought we would have time to treat the increase. We also thought, that in part, the increase in potassium was caused by fasciculations. If we gave the defasciculating dose of vecuronium, it would counteract the increase in potassium. To make a long story short, the patient ended up dying – there were a lot of factors involved, but this sure didn’t help. His final serum potassium level was 7.2. It turns out that this rise in potassium happens in seconds, and fasciculations have little to do with the potassium shift.
As Prehospital Critical Care Clinicians, we are given the tools to do an incredible amount of good [or an incredible amount of harm] depending on how we use them. We are inevitably going to make mistakes in the course of our careers. If we get lucky, no one gets hurt, and we walk away with some valuable lessons learned. I sure wish I had known a bit more about some of the things that would end up getting me in trouble. This got me thinking: How many times do we cause harm with these tools of ours and don’t even know it? What other patient presentations are out there, that may be rare, but deadly just the same?
You are picking up a 61-year-old female complaining of chest pain. She has tachypnea and dyspnea and signs of right heart enlargement on her EKG, but no acute ischemia. She is mildly hypoxic, has a borderline blood pressure and a heart rate of 150 – sinus tachycardia. You suspect pulmonary embolism. You are concerned that her blood pressure is low and you would like to blame it on the tachycardia; if you could just slow her heart rate down, maybe her blood pressure would come up! So, what do you do? Pull out the intravenous metoprolol and give whatever dose is in your protocol – maybe 5mg. A few minutes later, her heart rate starts to drop along with her level of consciousness. You check her blood pressure and it’s 55/32. You check it again and it’s unobtainable. Sure enough, your patient is in Pulseless Electrical Activity.
Patients with massive pulmonary emboli (PE’s) have historically carried a high mortality, which has decreased in recent years, possibly due to the increased use of CT Pulmonary Angiograms for diagnosis, as well a more effective, timely therapies (Jiminez, et al., 2015). This mortality is largely due to the hemodynamic consequences of the pulmonary embolism, not hypoxia. As the embolism blocks flow in at least 30% of the pulmonary artery bed, pulmonary arterial pressure increases. This causes a release of vasoconstrictive mediators that further increase pulmonary vascular resistance. This sudden increase in resistance causes Right Ventricular (RV) wall stress, ischemia, and dilatation. The RV muscle isn’t conditioned to work this hard and is unable to generate the needed pressures for forward flow; Meanwhile, oxygen demand has exceeded its supply. RV contraction time becomes prolonged and causes the intraventricular septum to bulge to the left (Konstantinides, et al., 2014). And… your patient becomes hemodynamically unstable.
At this point, it’s easy to see why the patient is tachycardic. Her heart rate has increased to compensate for the poor right and left heart pumping ability, as well as for the myocardial ischemia and possible systemic hypoxia. In other words, her extreme tachycardia is normal for this condition. In fact, it is essential to maintain any sort of cardiac output. When you give her beta blockers, you take away her ability to compensate for the problem that is still present. Not only does the metoprolol decrease her heart rate in a failing RV that is very rate dependent, but it also has negative inotropic properties that worsen RV function (Andersen, et al., 2015).
Moral of the story: Some patients with massive pulmonary embolism may survive well-intentioned attempts at beta-blockade, but some won’t…
Nitroglycerin/Left Ventricular Outflow Obstructions
You are landing at a known LZ to rendezvous with a local volunteer BLS crew to pick up a 72-year-old male with complaints of chest pain. You step into the back of the ambulance and find your patient sitting upright and anxious. His chest pain started while he was trying to chop firewood. He tells you that he is usually not that active, but he was worried they would run out of wood before his son could chop it (an Idaho problem). He has taken some ibuprofen, but no other medications. The pain has subsided from a 10/10 to a 7/10 since he stopped chopping wood. His “darn wife” called 911 and here you are. The 12-lead shows signs of left ventricular hypertrophy and contiguous ST depression in the lateral leads. His HR is 110, his BP is 160/100 and his SPO2 is 93%.
You decide he has Acute Coronary Syndrome and expedite your transport. He is loaded into your helicopter and you take off. You note an increase in blood pressure, that he appears more anxious, and again, complains of 10/10 chest pain (…turns out he is afraid to fly). First thing’s first. Sublingual nitroglycerin under the tongue… check! Your patient closes his eyes and after a couple of minutes, you take another blood pressure. You notice that your patient looks a little gray. His blood pressure is now 58/30…. Shoot. You grab the patient history information you scribbled on your trusty notepad and notice that he has a history of Aortic Stenosis (if your patient has a history of hypertrophic cardiomyopathy, you can have the same outcome).
One of the things that Aortic Stenosis and Hypertrophic Cardiomyopathy (and a host of congenital heart diseases) have in common is that in the severe form, the left ventricle can develop Left Ventricular Outflow Tract Obstruction (LVOTO). Patient’s with Takotsubo’s Cardiomyopathy also have LVOTO, but this condition is indistinguishable from other ischemic chest pain syndromes pre-hospital, so we will save that for another day. Let’s look at a quick run-down of our problem.
Patients with advanced aortic stenosis develop a fixed-outflow obstruction. A gradient develops in order for the left ventricle to push past the increased afterload and get blood out to the rest of the body. For example, if the patient’s body has determined that it needs a blood pressure of 120/80 to obtain the desired perfusion, but it takes a systolic blood pressure of 165 to clear the aortic valve, then the gradient is 45mmHg. (A gradient over 40mmHg is considered severe.) The left ventricle eventually becomes hypertrophic in order to meet the demand of the gradient. When a patient exercises or experience other situations that call for a higher cardiac output, the left ventricle can’t meet the demand, though it tries and syncope can happen. Angina occurs from an imbalance of oxygen supply and demand (Czarny & Resar, 2014).
Hypertrophic Cardiomyopathy is also a problem of LVOTO, but instead of a fixed obstruction, there is a “dynamic” outflow obstruction. Many times, this exists because of asymmetric hypertrophy located at the intraventricular septum near the aortic valve. At rest, there may be no afterload gradient, but with physical activity, the obstruction intensifies and an alteration in preload intensifies the obstruction. Once again, an imbalance between myocardial oxygen supply and demand and wall stress occurs, causing ischemia and chest pain. These patients are at risk for Sudden Cardiac Death, due to ventricular arrhythmias induced by ischemia, or exacerbations of outflow obstruction (Marian & Braunwald, 2017). Both of these conditions are very dependent on preload. So, why is nitroglycerin a problem? Nitroglycerin affects venous capacitance, which results in venous pooling and a decrease in venous return (Tarkin & Kaski, 2016). This reduces ventricular volume, causing an increase in the outflow obstruction and prevents forward flow.
Moral of the story: Once again, some patients may do okay… some of these very preload-dependent patients may rapidly decompensate with the administration of nitrates…it’s like playing roulette.
You are picking up a 75-year-old female from a small emergency department. She has been diagnosed with pneumonia and dehydration. She has a history of atrial fibrillation, hypertension, mild congestive heart failure, and depression.
Her heart rate is in the high 50’s; BP is 100/50 and, her SPO2 is 92%. You wonder why her heart rate is so low. Sure enough, when you look at her medication list you find metoprolol. You also notice that she is on Amiodarone, Fluoxetine, Furosemide, and Atorvastatin. You find that the sending RN has given 8mg of Ondansetron, 750mg of Levofloxacin and the patient had received 3mg of Haloperidol for confusion and combativeness. Your patient’s daughter informs you that the patient usually gets airsick. You load her into your helicopter, and because its bound to be a turbulent ride and its been a few hours since the Zofran, you decide to give her another dose IV. 10 minutes into your flight, you notice Torsade de Pointes on the monitor, and you note that she is pulseless.
After a successful resuscitation (because you are that good), you wonder what happened. You look at the 12-lead EKG that was sent with the patient, and you see that she had a corrected QT interval of 550ms. What did you miss? This patient had a long QT interval. We know that’s “not good,” but how long is too long? A QT interval >440ms is generally considered prolonged. Some sources indicate that >470ms is prolonged for females. This patient had a corrected QT interval of 550ms.
Most of us don’t look at the corrected QT interval on every patient… how could we have suspected that this patient was at risk? Let’s look at her risk factors…
Females are more predisposed to long QTs and the effects of QT-prolonging drugs. Heart failure is a risk factor (downregulation of potassium channels), as well as bradycardia (low rate combined with increased repolarization time). Furthermore, she was on several medications that prolong the QT interval, and those drugs have an additive effect on one another: Amiodarone, Levofloxacin, Haloperidol, and Ondansetron. Would it make any difference if I told you her potassium was 3.0 (after all, she was on furosemide)? Low serum potassium is also associated with a prolonged repolarization time and increased arrhythmogenicity (Cubeddu, 2009). Okay…but one dose of Ondansetron can’t increase the QT interval enough to cause Torsades? Yes, it can. Studies have shown that just 4mg of Ondansetron can significantly increase the QT interval for as long as 90 minutes after administration (Haferman, et al., 2011) and corrected QT intervals >500ms put patients at significant risk for Torsades.
To quote the words of a wise man that I wished I had gotten to know: “Just because we transported the patient and he made it alive, doesn’t mean we did it well.”
While these three situations are ones that we might not necessarily run into every day, the consequences can be unfortunate. A good understanding of the pathophysiology behind these processes as well as a basic understanding of how these medications affect the body can prevent the “uh-oh’s,” debriefings and, foremost, the untimely decompensation of our patients. Staying alert for these and similar potential situations will open your eyes to the things you may not have been seeing and improve your patient care. Have you experienced situations like these? What other medication mishaps do you wish you knew about early in your careers
Jiménez, D., de Miguel-Díez, J., Guijarro, R., Trujillo-Santos, J., Otero, Barba, R., et al. (2015). Trends in the management and outcomes of acute pulmonary embolism. Journal of the American College of Cardiology, 67(2), 162-170.
Konstantinides, S.V., Torbicki, A., Agnelli, G., Danchin, N., Fitzmaurice, D., Galie, N., et al. (2014). 2014 ESC Guidelines on the diagnosis and management of acute pulmonary embolism. European Heart Journal, 35: 3033-3080.
Andersen, S., Andersen, A., de Man, F.S. & Nielsen-Kudsk, J.E. (2015). Sympathetic nervous system activation and B-adrenergic blockade in right heart failure. European Journal of Heart Failure, 17:358-366.
Cubeddu, L.X. (2009). Iatrogenic QT abnormalities and fatal arrhythmias: Mechanisms and clinical significance. Current Cardiology Reviews, 5: 166-176.
Czarny, M.J. & Resar, J.R. (2014). Diagnosis and management of valvular aortic stenosis. Clinical Medicine Insights: Cardiology, 8(S1) 15–24.
Marian, A.J. & Braunwald, E. (2017). Hypertrophic cardiomyopathy genetics, pathogenesis, clinical manifestations, diagnosis, and therapy. Circulation Research, 121:749-770.
Tarkin, J.M. & Kaski, J.C. (2016). Vasodilator therapy: Nitrates and nicorandil. Cardiovascular Drug Therapy, 30(4) 367-378.
Haferman, M.J., Namdar, R., Seibold, G.E., & Page, R.E. (2011). Effect of intravenous ondansetron on QT interval prolongation in patients with cardiovascular disease and additional risk factors for torsades: a prospective, observational study. Drug, Healthcare, and Patient Safety, 3: 53-58.
About the Author:
Amy Neglia is a Critical Care Flight Nurse, a National & Regional Speaker on Critical Care Nursing and has been published in AirRescue, a European Flight Magazine. Amy is an Adult Clinical Nurse Specialist, with a focus on Critical Care and Critical Care Transport. Amy holds certifications in Critical Care, Cardiac Care, Flight Nursing and Neonatal Pediatric Transport. Amy is currently a Flight Nurse with Air St. Luke’s out of Idaho, and works PRN for the Critical Care Units in the St. Luke’s Health System.