Cardiovascular FAQ

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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 placement 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.

Q: Is this combination of therapeutic treatments ( (i.e., that is, ramipril/Altace: angiotensin-converting enzyme (ACE) inhibitor; propranolol: agents that block beta-adrenergic receptors; a diuretic: furosemide/Lasix; and calcium channel blockers) a standard for all cardiac patients? If so, why is this? If not, are there factors which dictate what is attended to or corrected first and foremost? Christy McDonald, Daniel David, & Denise Caron. November 17, 2003.

A: This turns out to be a very complex question with quite a complex answer. In terms of clinical practice guidelines, combination drug therapy is now more the norm, depending upon the cardiac disease. In BC, it will take some digging to find out what drives which combination therapy decision-making. In the interim, the AHA has published the ACC/AHA/ESC Guidelines for the
Management of Patients With Atrial Fibrillation, and the quick answer is "it depends..." To get more information, try the Professional Atrial Fibrillation heart profiler ( the amazing thing about this heart profiler is that it allows one to modify various factors and look at the evidence-based support for various interventions, including combination drug therapy). In fact, one can get a health care professional view of the evidence to support therapies for a variety of cardiac conditions, including:

a mind-boggling decision support software!

Q: I noticed , while in the hospital, as I administered cardiac drugs, that some beta blockers are selective, while others are non-selective.....Can you explain what would be the indication either way? Is it that selective work just on the heart, while non-selective works on the heart and vasculature? Ebony Lees, November 17, 2003.

A: A selective beta blocker is one that has much higher antagonist activity for a beta-1 receptor than a beta-2 receptor, or the converse. In the heart, we have many more beta-1 receptors than beta-2, which when stimulated, increase force and rate of contraction. Beta-2 receptors are found mainly in smooth muscle of the respiratory tract, the uterus, and the vasculature, where stimulation produces relaxation. Beta-3 receptors are found in fat cells in adipose tissue. Examples of selective beta-1 blockers are: metoprolol, acebutolol, atenolol, and betaxolol. The only selective beta-2 blocker I know about is butoxamine, which is used in research, but has no known clinical indications. Most of the other beta blockers are mixed affinity, i.e. have similar affinities for beta-1 and beta-2 receptors, including propranolol, pindolol and timolol. Indications are usually based upon target tissues and symptoms, so all other things being equal we might want to use selective beta-1 blockers for their cardiac effects, while minimizing or avoiding systemic side effects. However, carvedilol, which is a mixed antagonist (beta-1 = beta-2 > or = alpha-1 > alpha-2) has proven very useful in treatment of heart failure, because of its mixed antagonist features. (see Packer et al, The effect of carvedilol on morbidity and mortality in patients with chronic heart failure: US Carvedilol Heart Failure Study Group. N Engl J Med 1996: 334(21): 1349-55. )

Q: As I am reading about cardiac meds I am realizing that many of them are hard on the kidney. Therefore I am curious as to what cardiac medication would be most appropriate for a pt who has chronic kidney disease and why? Ben Faulkner, November 18th, 2003.

A: It depends on the exact cardiac pathology. With all drugs, we have to be aware of the dose adjustments needed for chronic renal failure and ESRD based upon impaired ability to eliminate and clear drugs. This is particularly true for renal patients with co-morbid cardiac pathology (many of them), so the decision then is usually based on the therapeutic index and degree of impact on the kidneys. But it is a two way street, such that if renal disease is not properly managed, there are significant cardiac implications and vice-versa, so it becomes a balancing act. You could dig deeper into some interesting full text articles here.

Q: Should cardiac meds be held if an idividual is to have hemodialysis shortly after their cardiac med administration. If the meds are to be held what would be the protocol (i.e. the hemo wards?). I am aware that many meds are dialysed out during a dialysis run, but that one of the main risks facing hemo patients is cardiac arrest. James Madden, November 18th, 2003.

A: The basic principle is first to decide if the drug is dialyzable or not. If, like digoxin, it is not then the next issue is whether the fluid loss during dialysis could provoke an increased concentration of the non dialyzable drug and to make allowances for that. For most dialyzable drugs, a catch up post dialysis dose can be calculated based upon clearance data, especially since 90% of current hemodialysis machines are hi-flux (averaging dialysis times of 4 to 4.5 hrs) . Many nephrologists will simply order a post dialysis dose to catch up any loss due to dialyzability, or in situations where intra-dialysis coverage is important, may order SR versions of the drug, e.g. diltiazem. Practices may vary in different hospitals and for home dialysis patients too. Most modern drug guides carry a list of dialyzable drugs, and Amgen publishes a yearly update. In many cardiac diseased ESRD patients, significant dialysis fluid loss can provoke BP bottoming out or spiking, so varying approaches to drug management may occur. At VH this may include more frequent, but smaller volume removal to avoid hypotensive periods or the use of SR nifedipine to prevent post dialysis hypertensive episodes. (they used to use SL nifedipine, but this caused a rebound rise in BP). As with many things, the answer is often "it depends..." so we always need to think about drug factors and patient variables, including past experience with dialysis and cardiac symptoms.

Q: When I was vacationing this summer I had the opportunity to go on a diving excursion in the tropics. When we were preparing for the dive, during our a pre-teaching session each of us were asked if we were currently using any heart medications. One person was on an antiarrhythmic and was told that due to his condition he would be unable to dive. He was told that certain lung and heart conditions (while on medications) could lead to adverse effects due to pressure changes under the water. I have heard that while on cardiovascular drugs, diving can lead to lung fibrosis, syncope and bleeding- are you able attest to this or expand on it further? Jenica Burns, November 19th, 2003.

A: Cold water immersion, and water on the face produce a diving reflex, which includes short and longer term bradycardia, depending upon water temperature and depth, and diver experience and fitness, amongst other factors. (see the Divers Alert Network FAQ and Cardiovascular Fitness and Diving). If you look at diving fatalities, 20-30% are due to cardiovascular causes, often in people with no previously known condition. I suspect that fatalities would be even higher with known conditions PLUS medications, since the person is also under duress from bradycardia, exercise, cold water immersion, hyperbaric states, transient hyperoxia and dry tank gas. Anyone with long QT syndrome is at particular risk from bradycardia and may be at extreme risk if taking cardiac meds with bradycardiac or bradydysrhythmic side effects. Many recreational divers (i.e. while on vacation) take dimenhydrinate to combat boat motion sickness, while getting to the dive spot. This can lead to further bradycardia and decreased mental acuity. It is known that post-dive "silent" gas bubbles can damage pulmonary endothelium and trigger the reactive cascade that leads to fibrosis, similar to ARDS. My guess is that syncope could be a result of exercise, and the hyperbaric state itself combined with bradycardia. Barotrauma or baro-exposure is known to be associated with bleeds of various types (sub-arachnoid, hemoptysis, and varices).

Q: What cardiac meds are indicated after cardiac valve surgery? Are the meds different if the valve is tissue or mechanical? How does valvular surgery effect the electrical conductivity in the heart? Joshua Clarke, Nov 20th, 2003.

A: Mechanical valves require that the recipient maintain lifetime anticoagulation, whereas homograft (cryopreserved human valves and xenograft (treated animal tissues) do not. Graft rejection is a much bigger problem with tissue valves. All patients usually undergo a short course of antibiotic prophylaxis to prevent infection and receive steroids to suppress tissue graft rejection. Although infection rates are much less than graft rejection rates, infection is often more lethal. Pre-surgically patients may receive immunoglobulin with low-dose cyclophosphamide to reduce allosensitivity. Since left ventricular dysfunction is common following cardiac surgery, many patients will receive positive inotropes (like amrinone, dobutamine, epinephrine, or dopamine) to support LV recovery. AF is common after cardiac surgery, and abnormal EKGs are fairly common, in fact some are quite strange (see this post mitral valve tracing). We should not forget pain medications (post-surgical), diuretics (to support pre-load reduction and LV re-modelling), and laxatives and softeners to prevent straining (and hence intra-thoracic pressure fluctuations). For an interesting account of what to expect from a patient perspective, see here.

Q: I was wondering if someone had CHF and was taking digoxin but had a history of a dysrythmia and a had pacemaker implant would the 'prolonged refractory period' effect of the medication still be present? It seemed to me that the effect of the digoxin slowed the SA node, but it might cause some weird(v. medical term) effect. And a more anatomy/physiology completely off the medication topic but still cardiac related question, do ventricular septal defects in infants ever cause damage to the av bundle? Robbie Dunbar, Nov 21st, 2003.

A: In patients with electromechanical pacemakers AND digoxin, the pacemakers overide the negative dromotropy of the digoxin, which is usually given at a lower dose. If pacemakers are in place to correct AV block, then digoxin is still safe. Embryonically, it seems that the bundle of His still manages to work its way around both types of VSD, namely perimembranous or muscular types, although following VSD repair there are often EKG irregularities, even if damage to one or other bundle is avoided through shallow suturing. It appears that the occurrence of early postoperative dysrhythmias after repair of congenital heart disease is significantly associated with procedure-related risk factors such as extracorporeal bypass time and aortic crossclamp time.In contrast, adults with small VSDs that were not corrected in childhood do remarkably well and may not show EKG irregularities.

Q: I've heard that the bioavailability in blood pressure meds can increase when given with food. I'm curious to know why that is? Erika Cervantes, Nov 22nd, 2003.

A: Food enhances the bioavailability of many drugs through food stimulation of the gastric and enteric vasculature, enhancing absorption and transport. Lipophilic drugs may be absorbed better in the presence of fatty foods and conversely with lipophobic drugs. Bioavailability is the fraction of unchanged drug reaching the systemic circulation following adminsitration by any route, so IV admin is generally considered to be equal to unity. So the biggest factors are the extent of absorption, rate of absorption and degree to which first pass elimination occurs. Food can affect all three of these factors.

Q: I've read an article online on the heart and stroke foundation website stating that digoxin may be harmful to women. It says that a clinical trial in 1997 shows that digoxin could increase a women's relative risk of death by 23% when compared to women taking a placebo. But the same threat is not present for men. It states that since the 18th century, the same dose of digoxin has been prescibed to both men and women. However, in the past 20 years, it has been discovered that women metabolized drugs differently, therefore doses have been altered. I was wondering if you have heard anything about this? Kendall Korda, Nov 23rd, 2003.

A: This first appeared in The Digitalis Investigation Group The effect of digoxin on mortality and morbidity in patients with heart failure N Engl J Med 1997 Feb 20; 336:525-533. However, the conclusions were based upon a post hoc (remember the fallacies!) sub group analysis which can be misleading. There was a later article, Sex-Based Differences in the Effect of Digoxin for the Treatment of Heart Failure by Rathore, M.P.H., Yongfei Wang, M.S., and Krumholz, H. M. The New England Journal of Medicine. Oct 31, 2002. Vol. 347, Iss. 18; followed by Digoxin--new perspective on an old drug. Digoxin--new perspective on an old drug. Eichhorn, Eric J., Georghiade, Mihai. The New England Journal of Medicine. Oct 31, 2002. Vol. 347, Iss. 18; pg. 1394 which suggested: the retrospective analysis reveals a 4.2 percent increase in mortality with digoxin therapy in women but no such effect in men. These findings may have been as a result of an imbalance in baseline characteristics between the treatment groups, and the increase in mortality in women may have been due to the use of a digoxin dose that was too high. Therefore, the use of digoxin in women with heart failure should not be abandoned. Rather, a dose that will result in serum concentrations lower than 1.0 ng per milliliter should be used. This year, I saw a letter that pointed out the big differences between the men and the women in the original trial, namely that there were striking differences between men and women in the causes of congestive heart failure. Women more often had cardiomegaly, severe heart failure, diabetes, and idiopathic heart failure; men more often had ischemic heart failure and heart failure due to prior myocardial infarction. My guess is that a proper study has yet to be conducted.

Q: I 've read about beta-blockers and impotence in men. Probably playing a significant role in men complying with this med. Is there anything out there to help men with this unwanted adverse affect. I don't think Viagra is an option is it? Tony Falcos, Nov 23rd, 2003.

A: PDE5 inhibition (Viagra) does not worsen exercise capacity and exercise-induced myocardial ischemia in patients with chronic stable angina whose symptoms and exercise test response are well controlled by beta-blocker therapy. So, safety seems OK. However, there is some fascinating work that suggests that men who know about side effects of beta blockers are much more prone to ED than those who do not, plus it is reversed by placebo, so it may be an anxiety related phenomenon. If this were the case, supportive counselling, psychotherapy and even recerational drugs might be of benefit. Other studies support safety of Viagra with beta blockers. I have anecdotal reports from one of my sexology practitioner friends that similar results can be observed in women on beta blockade who take Viagra. Apart from headache, flushing, dizziness and occasional priapism (uncomfortable for men and women) sildenafil appears OK for many cardiovascular patients. Remember that cardiac symptoms and disease are very anxiety provoking and anxiety dampens libido big time in men and women. This also explains why cardiac patients (men mostly but also women) often act out sexually while in hospital.