Don’t break my heart…

Over the past couple weeks, I have been haunted by the unexplained symptoms experienced by someone very close to me. After consulting the primary care provider, an EKG revealed the presence of a heart arrhythmia, which was ultimately diagnosed as atrial fibrillation (Afib). Although not as serious as ventricular fibrillation (Vfib), Afib can cause the atria of the heart to sort of twitch in a way that can lead to unorganized electrical activity an can render the heart ineffective as a pump. Because of this, arrhythmias such as Afib can result in poor blood circulation and organ perfusion, and if severe enough, can lead to detrimental outcomes such as ischemic stroke, blood clots, and heart failure. There are several different classifications of Afib, which is based on the duration of the arrhythmia, and can be essential for determining a plan of care. The first is paroxysmal Afib, which is associated with episodes that last less than 7 days, and will return to normal function on its own. Persistent Afib episodes are often longer than 7 days, and do not terminate without treatment of antiarrhythmic agents and/or a cardioversion procedure (essentially delivering electric shocks to the heart from a device). Arrhythmias that have persisted longer than 1 year with failed treatment attempts is classified as permanent Afib (Edmunds & Mayhew, 2009).

Initially, my grandmother sought treatment for a sensation of hearing loss, and the primary care doc started her on a treatment for an inner ear infection with antibiotics, an antihistamine, and an intranasal steroid to relief symptoms of congestion associated with sinus inflammation. She was also prescribed a beta-blocker (metoprolol), in addition to the two antihypertensive ACE Inhibitors she was already taking (Diovan and fosinopril).

The ACE inhibitor drugs are particularly beneficial in treating hypertension, because they can reduce peripheral blood pressure without having a significant effect on heart rate or cardiac output. However, the mechanism of action of these agents works on the way the kidney reabsorbs water by altering the sodium-potassium exchange, resulting in less fluid absorption (Edmunds & Mayhew, 2009). In some instances, this can not only pose a risk for dehydration, but it can lead to renal insufficiency and result in elevated levels of potassium (hyperkalemia) that can cause irregular heartbeats and muscle weakness. Recall that digoxin toxicity is often related to levels of potassium. Interestingly enough, Edmunds and Mayhew (2009) recommend that anyone taking a combination of ACE inhibitors and dig should have their blood levels monitored, and dig levels should not exceed 1.0 ng/mL, especially in women, and the elderly, since their body mass composition can predispose them for drug toxicity. Furthermore, due to the metabolic pathways of ACE inhibitors, it is not uncommon to see drug interactions resulting in increased levels of digoxin.

So, we have our hypertension treatment plan consisting of two ACE inhibitors and now a beta blocker.

However, the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure no longer recommends beta blockers as a first line therapeutic for hypertension, especially in the elderly, due to the high risk of development or exacerbation of diabetes mellitus. This is caused by the adverse metabolic effects that can cause an elevation of blood glucose levels, as well as increased insulin resistance. Furthermore, antihistamines can increase the efficacy of beta blockers, leading to serious adverse effects.Interestingly enough, antihistamine agents such as loratidine are not recommended in patients with hypertension and diabetes, and special formulations are indicated for these patients (of which my grandmother was not on). The mechanism of action of beta blockers is to act on the receptors in the heart (and often the lungs) to help relax and dilate blood vessels and airways, which results in decreased heart rate, lowered blood pressure that reduces the force exerted by cardiac contractions (Edmunds & Mayhew, 2009). As expected, common side effects would be related to the reduced cardiac output, such as bradycardia (slow heart rate), dizziness, fatigue, weakness, nausea, vomiting, depression, hyperglycemia, renal failure, and stroke. In some patients, compensation for hypotension may result in rapid, unorganized heart rates (sound familiar?) and slowing the electric conduction system in the heart.

After being referred to the cardiologist, she was started on Multag (a similar drug to amiodarone, which is an antiarrhythmic) that acts by reducing the irregular impulses from the electric conduction system in the heart. This drug is often initially prescribed with a beta blocker to prevent a rapid atrioventriacular spasm in response to the drug (which would likely explain the increase in Metoprolol from 50mg to 100mg). However, providers should always express caution when managing patients that are taking multiple cardiac drugs to prevent additive effects or interaction that can cause drug toxicities, and cardiac depression. Many other drug effects, including beta blockers, digoxin, and ACE inhibitors, are increased with use of Multag. It is also known that this agent can also worsen arrhythmias, and may contribute to severe sinoatrial node dysfunction and heart block (Edmunds & Mayhew, 2009). In monitoring for toxicity, drug levels and EKGs should be frequently reevaluated, and patients should be educated to seek consult if there are any new or uncomfortable symptoms.

After one week of treatment, my grandmother returned to the cardiologist for EKG results, and her medications were changed once again. She was told to discontinue the metoprolol, switched instead to nadolol (also a beta blocker), and have her anticoagulant increased (which would normally be expected since arrhythmias carry the potential to create blood clots, however I’m curious about the awareness of the increased potential of the anticoagulant from the cardiac drug interactions). Additionally, she was advised to start taking Digoxin. She began feeling increased nausea and light head-ness around this time.






Digoxin is a potent drug that works by decreasing the heart rate and blood pressure to produce stronger contractions and make the heart work more effectively as a pump. Because of the potency of this drug, there is a narrow therapeutic range for blood levels, increasing the risk of toxicity. Therefore it is crucial that anyone that is prescribed these drugs be monitored closely and made aware of the potential for bradycardia, hypotension, stroke and cardiac arrest, all of which are associated with severe digoxin toxicity. When prescribing digoxin, it is essential to take a thorough patient history to determine current medications, and any previous liver or kidney problems, as this can lead to decreased clearance of the drug, causing it to accumulate and become toxic. Additionally, assessing potassium levels is a critical component of therapy, as digoxin can result in hyperkalemia, which can further worsen arrhythmias, and even result in cardiac arrest. ANY patient taking digoxin should be aware of the signs of digoxin toxicity: fatigue, weakness, syncope, dizziness, visual changes i.e. the presence of a yellow halo around objects), sensation of a pounding or racing heartbeat, poor appetite, nausea, vomiting, diarrhea (Edmunds & Mayhew, 2009). Furthermore, other medications can have a significant impact on the effects of digoxin, that can lead to increased absorption, reduced renal clearance, and most importantly, an additive effect that is seen with many of the beta blockers and calcium channel blockers (recall that these drugs are often used in combination to treat arrhythmias).

After two days of treatment, my grandmother was still experiencing dizziness and feeling light headed, and eventually fainted while in the shower. The cardiologist decreased the dose of the beta blocker, and advised her to continue taking the other medication. For the next week, her nausea and vomiting got worse, as well as severe weakness and loss of appetite. After 8 days of taking the new regimen of drugs (on top of all the initial anti-hypertensives, the cardiologist finally recommended she discontinue the digoxin (after a week of my advice to consult a pharmacist/stop the digoxin/get a second opinion). Interestingly enough, although the digoxin was discontinued at this time, what the doctor failed to take into consideration was the long life of the drug in the body before it gets excreted (6-8 days!). The following day, the symptoms were unbearable, and following ambulance transport to the ICU, she was diagnosed as having digoxin toxicity. Shortly after being stabilized, EKG revealed problems with the sinoatrial node (SA node) which is the primary pathway of the heart’s elecrical conduction system. The (new) cardiologist recommended that she undergo a cardioversion procedure.

This is similar to the way a defibrillator machine works during CPR. The patient gets sedated, and electrodes that are placed on the chest deliver volts of electricity to the heart in a sort of “atrial kick” to try to jump start it into beating regularly. Following the procedure, my grandmother’s heart rate was extremely low, and the cardioversion electrodes (still in place for monitoring for complications) were required as a temporary pace maker for her.

As a plan of treatment, the focus is to try to safely restore a regular rate and rhythm. Treatment may consist of a variety of medications such as beta blockers, calcium channel blockers, antiarrythmics, and anticoagulants. In most of these agents, the mechanism of action is to slow down the emission of sporadic electrical impulses by prolonging the conduction period in attempt to make the heart contract more efficiently. This often leads to a decrease in the heart rate, and in many cases, these agents are used as antihypertensives due to their effectiveness at lowering blood pressure. In some situations, several agents are combined to produce a more effective response, but it is critical to monitor patients when taking these drugs. Once again, health care providers should be emphasizing the importance of follow-up and evaluation to determine the interactions of the drugs, and strongly educate their patients on early signs of toxicity.

In the personal experience previously mentioned, it seems there not only was a lack of patient education, but poor attention to details, patient history, drug interactions, and evaluation skills. Further, when finding that heart drugs were provided by both the primary care doc and the cardiologist, there also appears to be a absence in the collaboration amongst healthcare providers that is crucial to delivering optimal patient care amongst the different disciplines. Due to the inability to identify early signs as toxicity, there was a prolonged duration of preventable suffering that, with proper patient education and monitoring, could have been eliminated at onset. Regardless of possible association with inconsistent care, complications have resulted in bigger problems and stress on loved ones. Although nothing is accomplished through blame, I truly believe that early anticipation of problems can result in prevention of further complications through individualizing patient care and improving communication, assessment, and education. Prayers to my dear Grandmother, one of the most loving and genuine people I know. Lucky Lil should not need luck when it comes to her health; those doc’s better know I’m watching their every move.