Cardiovascular FAQ

Q: Why do EKG techs sometimes use 4 lead and sometimes 12 lead EKGs? Tamara Chan, November 5th, 2002.

A: 4 lead EKGs give a quick and dirty measure of rate and rhythm and will show obvious ST changes, but they are useless for accurate diagnostic purposes. If the leads are correctly placed, the monitor "sees" lateral and anterior aspects of the cardiac waveforms. However, the leads are not always placed systematically, so arbitrary palcement will give difficult to interpret tracings. 12 lead electrodes are systematically and carefully placed and give standardized views of the heart, which can be compared with millions of other EKGs stored in databases. These are used for diagnostic purposes and are very sensitive and specific. Some manufacturers now market 5 lead monitors (Easy-electrode, Eze-electrode) that purport to show (through mathematical derivation) the equivalent 12 lead tracing, but the jury still seems to be out on this approach.

Q: Is the method of treatment for hypertension the same regardless of the age or are elderly people recommended to take antihypertensive even if their BP is stable? Rie Yoneda, November 6th, 2002.

A: Treatment may vary with age and other circumstances. Elderly people do not need to take antihypertensives if they have a stable BP WNL. The JNC VI (USA The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure) report makes the following recommendations for the treatment of hypertension in people over the age of 65:

Q: How does a physician determine which class of anti-hypertensive to use on his or her patient? For example, how will he or she know whether or not to use an angiotensin II receptor antagonist (Avapro) or a nonselective beta-adrenergic blocking agent (Pindolol)? Karen Madayag, November 7th, 2002.

A: The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997;157(21):2413-46 (known as JNC VI) concluded in 1997 that "a diuretic and/or a beta-blocker should be chosen as initial therapy unless there are compelling or specific indications for another drug." There are some critical views (see for example Initial antihypertensive therapy: What are the current drugs of choice?) Since the JNC VI is a lot to wade through, I have extracted its recommendations into an algorithm, which should be helpful.

Q: 1) what's the most commonly prescribed antihypertensive drug and why? Glorissa Contaoe, November 8th, 2002.

A: Outside of North America, it is furosemide (Lasix) because it is safe and inexpensive. In North America, it is probably enalapril (Vasotec) an ACE inhibitor, because it is aggressively marketed and profitable. Probably followed by hydrochlorothiazide (diuretic) which is safe and inexpensive and not very profitable.

Q: 2) at what point would a physician recommend a cardioversion (since I was able to see how one is done in the PACU)? Would a recurrent cardioversion do damage to the heart? How?

A: Cardioversion is used for correcting dysrhythmias that are non responsive to antidysrhythmics, either on an emergency basis, or as a scheduled procedure when antidysrhythmics need a "helping hand." Synchronized cardioversion is indicated for atrial fibrillation, atrial flutter, atrial tachycardia and supraventricular tachycardias. Unsynchronised cardioversion/defibrillation is indicated for ventricular tachycardia - compromising and ventricular fibrillation. Pacing cardioversion is done through an electrode wire placed in the femoral vein. Complications may affect the patient or health care workers. Injury incidence is 1 per 1700 shocks for paramedics in the field and less for in hospital care. The patient may become hypoxic or hypoventilate from sedation. Most burns from shocks are superficial partial-thickness burns, but a few are deep. Cardiac complications include dysrhythmia, hypotension, and pulmonary edema. Repetitve cardioversion is used with v tach and v fib and serial troponin assays indicate minimal myocardial damage. On a personal note, I have a colleague who underwent unsynchronised cardioversion/defibrillation 11 times until his heart responded. He is still alive and his enzyme markers were fine.

Q: I have seen that there is an antidote for digoxin which is digoxin immune FAB but have had difficulty finding this anywhere and where would we have to obtain it on a unit? Is it common? Nancy Vos, November 10, 2002.

A: Digoxin Immune Fab (Fragment antigen binding), also known as Digibind, is a sterile lyophilized powder of antigen binding fragments (Fab) derived from specific antidigoxin antibodies raised in sheep. Production of antibodies specific for digoxin involves conjugation of digoxin as a hapten to human albumin. Sheep are immunized with this material to produce antibodies specific for the antigenic determinants of the digoxin molecule. The antibody is then papain-digested and digoxin-specific Fab fragments of the antibody are isolated and purified by affinity chromatography. Each vial, which will bind approximately 0.5 mg of digoxin (or digitoxin), contains 38 mg of digoxin-specific Fab fragments derived from sheep plus 75 mg of sorbitol as a stabilizer and 28 mg of sodium chloride. The vial contains no preservatives.

Digibind is administered by intravenous injection after reconstitution (gently - no foaming) with sterile water for injection (4 mL per vial). Indications: Treatment of potentially life threatening digoxin intoxication. Includes ventricular arrhythmias (V-tachycardia, V-fibrillation), progressive bradyarrhythmias (severe sinus bradycardia or second or third degree AV block not responsive to atropine), acute ingestions of >10 mg in adults or >4 mg in children, or serum potassium concentrations > 5 mEq/L and/or post distribution serum digoxin concentrations >10 ng/ml. Most large hospital pharmacies carry digibind, although many do not. It has a shelf-life of about 5 years, and has saved many lives!

Q: My question concerns a patient I had in my med-surg rotation. He was admitted with a diagnosis of unstable angina. He also had a history of two previous MI's. He was on nitropatch .4mg daily and sl spray .4mg prn. Also atenolol 50mg, ticlopidine 250mg, amlodipine 5mg and simvastatin 5mg. My question is that he was going for a cardiac catheterization and his pre procedure blood work showed that he had had some kidney damage. He did not have any S+S of this but the blood work showed it was there. Anyway he was asked to particpate in a study of patients who had angina because they were beginning to see kidney damage related to anginal therapy. I am wondering do the drugs cause this and if so how do they or is it something else. Apparently these cases had been found when doing the blood work prior to doing cardiac catheterizations. Anita Hine, November 11th, 2002.

A: The approach to this is to examine the drug profiles and look for renal adverse effects. Of all of the drugs, only ticlopidine (platelet aggregation inhibitor) has shown renal failure (rarely). Then we have to look at the indications for each of the drugs, as this patient shows a history of unstable angina, hypertension and previous MIs. It could be that with a sufficient history of uncontrolled or poorly controlled hypertension (common) we might see incipient renal impairment and damage, via changes in renal function tests like creatinine, creatinine clearance and CPK. It would be useful to run a Clinical Queries Medline search on angina therapy to scan for renal damage. Finally, it might be fun to try a case study on coronary syndrome with unstable angina. Another excellent resource for individual patients themselves (advising), or health care professionals (evidence basd practice) is the heart profilers which matches each patient’s medical information or profile with published clinical research studies, whether the patient has coronary artery disease, heart failure, atrial fibrillation, high blood pressure or cholesterol. It makes me think that the same technology could be used with learning needs of BSN students!

Q: I was always told that if the pulse rate is <60 bpm in an adult, you withhold giving the pt. digoxin. In past clinical practices, different agencies have policies on certain drugs and digoxin is one. Some say withhold if pulse rate is <60 bpm, other agency's policy say withhold if
<50 bpm. So which one is the ideal value to follow and why? Does it really matter if it's <60 or <50, is there much of a difference? Does it depend on the pt's condition or does it mean different agencies, therefore different preferences/policies? Celestine Bote, November 14th, 2002.

A: I always use a pulse rate of < 60 to trigger witholding digoxin and informing the physician, but do so because I am aware that digoxin toxicity may lead to bradydysrhythmias. It is not an issue that we see bradycardia itself, since we know that digoxin is vagomimetic (mimics stimulation of the vagus) and will slow SA and AV nodal transmission and increase the PR interval. The problem arises because without an EKG it is difficult to pick up bradydysrhythmias simply through taking a pulse, so a rate < 60 is simply a potential bradydysrhythmia waiting to be detected. When in doubt be guided by the specific agency policies PLUS nursing judgment, i.e. what other patient specific factors would warrant action at < 60 versus < 50 bpm?

Q: Some of the information I came across said that CHF was a cause of atrial fibrillation, and some information said that atrial fibrillation was a cause of CHF. I'm pretty sure there is a relationship between AF and CHF, but I'm not sure how it comes about. Any ideas? Jennifer Armstrong, November 16th, 2002.

A: AF and CHF tend to occur together in patients in the setting of structural heart disease. Persistent tachycardias lead to tachycardia-induced cardiomyopathy, most often demonstrable in the case of sustained ectopic or reentrant supraventricular tachycardia. However, a persistently high and poorly controlled ventricular rate in the case of AF may induce CHF with a greater morbidity or mortality.
Discussion of the natural history of AF occurring in the setting of CHF is of therapeutic interest. When we want to examine causality, we first look for correlation. The incidence of AF associated with CHF ranges from 10% to 50%, with the highest incidence in those with the most severe symptoms. The prevalence of AF increases from 10% of patients in New York Heart Association (NYHA) class II heart failure to 40% of those with NYHA class IV symptoms. The incidence of AF increases with age as well as with increasing severity of ventricular dysfunction. We have to figure out which has priority, rate or rhythm control. The issue here is whether AF is the result of CHF or the converse. In patients with CHF, atrial transport may contribute up to 30% of total cardiac output. The resulting loss of forward output after the onset of AF may result in rapid and severe decompensation as a consequence of a faster ventricular rate. This may be associated with 2 important consequences, thromboembolism and worsening heart failure, both of which might lead to reduced survival. Whether AF is an independent risk factor for survival in CHF is not certain, but its presence in any setting has been shown to increase mortality 2-fold. So the bottom line is that in some cases CHF can provoke AF and AF will definitely exacerbate CHF. However, it is possible to have one without the other.

Q: Why does a physician prescribe a low molecular weight heparin such as Enoxaparin rather than Heparin? I have had patients on Enoxaparin however an extraordinary number are administered Heparin for anti-coagulant therapy? Christine Smith, November 17th, 2002.

A: Usual indications for LMW heparin are for treatment and prophylaxis of DVT, where the efficacy is similar to regular heparin (Merli (2001) Ann Intern Med 134:191-202) . However, the LMWs show better outcomes for unstable angina and MI (Cohen (1997) N Eng J Med 337:447-52 ). For some patients, the LMWs are preferred because they do not cause thombocytopenia, they have fewer bleeding complications, do not cause paradoxical thrombotic events, and show less hypersensitivity. However, unles specifically contraindicated regular heparin is much less expensive. So the decision is based on a combination of patient factors (reasons for anti-coagulation, religion - regular heparin is derived from pigs, avoidance of bleeding complications and thrombocytopenia) and drug factors (expense, efficacy for treatment, side effect profiles).

Q: We hear so much about different ways to change the course of our illnessess "naturally" and since I'm sure we all have family secrets or have learned or heard about something, I was wondering if you could help me to find some natural ways to lower your blood pressure. The
obvious eat less or no salt come to mind, and increase exercise but what if those are already in action and yet there still is no change? Shannon Lal, November 18th, 2002.

A: Nutritionists and some herbalists would suggest dietary modifications, some supplements and some herbs. For example, avoid saturated fats, excessive salt and alcohol, caffeine, tobacco, and sugar, all of which contribute to the development of hypertension. A vegetarian diet supplemented by fish and low in high-fat dairy products is often helpful. Eat plenty of garlic and onions, which have been shown to lower blood pressure, every day. Consuming foods rich in potassium, such as vegetables and fruits, helps normalize the sodium-potassium balance of the blood and prevents the fluid buildup that contributes to high blood pressure. These foods, along with whole grains and beans, are also rich in fiber, which helps prevent hypertension. I would add to this systematic relxation and actual stress management.

Supplements that may help lower high blood pressure include:

The literature on herbs and hypertension frequently mentions hawthorne, garlic, linden blossom, yarrow, and valerian, so you may wish to do some research on those plants. However, remember that these so called "natural" products all contain potent chemicals which may be involved with the active ingredients. I would use scientifically sound databases like MicroMedex. They have several databases, including AltMedDex® System, AltMedDex® Protocols, and Herbal Medicines.

Q: Grapefruit juice apparently contains enzymes which decreases the efficacy of some antihypertensive drugs. Can you please clarify this and explain it further? Glorissa Contaoe, November 18th, 2002.

A: This is an easy one! The final common degradative pathway for many drugs includes the cytochrome oxidases, particularly P450. See the animation here. If P450 is inhibited, dangerous levels of active drug metabolites may build up. Grapefruit juice contains several P450 inhibitors (such as flavonoids) and could cause this. There was a Health Canada warning about this, issued in the summer. The concentration of flavonoids and other cytochrome oxidase inhibitors in juice is higher than in segments, where some is bound to fibrous material. If you cannot bear to give up grapefruit juice, avoid it 2 hours before and 5 hours after taking any medications known to be metabolized by the P450 and P3A4 and P1A2 cytochromes.

Q: I was wondering why hydrochlorothiazide is more effective in individuals of African descent. Jivan Chhokar, November 20th, 2002.

A: This is a tricky one in that it looks more at patient factors than at drug factors. There is considerable evidence that there is a link between ethnicity and cardiovascular disease. If we look at the work by The International Society on Hypertension in Blacks, we see that some of the factors point to increased risk in African Americans, such as high sodium and high fat diets, leading to disproportionate representation in the incidence of hypertension. It is much easier to get data for African Americans than for African Africans, however similar studies in South Africa show similar results. The most recent conference of ISHIB 2002 shows that there may be some hard wired (genetic) factors as well as dietary practices. For example, some evidence points to increased Endothelin-1 Gene Polymorphism (ET-1/C198) sensitivity in Black youths compared with White - this leads to oversensitive vasoactive stress responsivity. Similarly, Brain Natriuretic Peptide (BNP) seems less effective in African Americans in reducing stress mediated vasopressor responses. It is also known that hydrochlorothiazide was 60 to 78 percent more effective in reducing blood pressure for the group with two copies of the T-variant of the GNB3 gene compared to those with two copies of the C-variant of the gene. This suggests that there may be a greater distribution of GNB3 TT variant in Afriacn decent than in non African. Interestingly, it is not simply African descent that leads to increased hypertensive rates, since Somali immigrants to USA show less incidence of hypertension, presumably due to cultural food preferences remaining dominant over North American high sodium, high fat preferences. Anyway, the bottom line seems to be high sodium loading, which would explain the increased effectiveness of sodium wasting diuretics like hydochlorothiazide. If you are interested in the mechanism of action of hydrochlorothiazide, is is almost identical to furosemide.

Q: I was just wondering if leg exercises after surgery are efficacious enough to stop DVT's from occuring--ie does a patient have to have pharacological treatment to stop them from occuring if they are in the high risk category? I am just interested because it would make sense for RN's to assess Hx of pt's for these problems if nonpharmacological measures aren't adequate enough? Nicky Aaronson, March 9th, 2003.

A: For folks who do not have a biologic loading for DVT and for whom other risk factors are not present, leg exercises post surgery may be sufficient. However, it is easy enough to screen all pregnant women as part of their prenatal care, and all patients admitted for surgery, for a family history of clotting and other risk factors like:

Interestingly calf pain while flexing the foot upwards— known as Homans' sign—was once considered the classic sign of DVT, but is now known to be unreliable and produces many false positives.

If one or more of the risk factors are present, it would be reasonable to treat prophylactically with low molecular weight heparins, or use venous compression stockings to assist in venous return.

You may be interested in searching for DVT risk factors on a new and powerful search engine Teoma, which is an offshoot of Google.