Drug therapy for congestive heart failure poses several risks during dental treatment

Cynthia R. Biron, RDH

More than 250,000 new cases of congestive heart failure (CHF) are diagnosed each year, and these patients join the millions who have already experienced it. We must be aware of the risk factors of treating these patients who are taking several drugs concomitantly.

The disease`s symptoms vary in severity, depending on the region and extent of disease of the myocardium. Simply speaking, the myocardium has impaired pump performance, and oxygenated blood is not adequately perfusing (saturating) all of the bodily organs and tissues. The same failing pump is inadequate in returning deoxygenated blood back through the lungs for reoxygenation.

In early stages of CHF, there is frequently both left and right heart failure in a chronic state. The telltale signs are exhibited in combination as pedal edema (granny ankles), extended jugular veins, dyspnea (cardiac asthma), elevated heart and respiratory rates, and a blood pressure that usually has a narrow pulse pressure. The pulse pressure is the difference between the systolic and the diastolic pressures. Sometimes only the diastolic is elevated, and the normal difference of 50 is not seen in CHF. Instead, the difference is 20 or 30.

The most common causes of CHF include coronary artery disease, long-term hypertension, and valvular damage leading to or after myocardial infarction. A host of other causes include, but are not limited to, those categorized as infective, metabolic, toxic, and infiltrative.

Left heart failure usually occurs first. The left ventricle is unable to provide the adequate contractile force (inotropic) necessary for pumping the blood out through the aorta to the body. The first signs of this include fatigue and difficulty breathing on exertion.

An increased respiratory rate, coughing, and expectoration can prompt the patient to see their physician. The latter manifestation is frequently referred to as "cardiac asthma." The congestion in the lungs is due to left ventricular failure.

Right ventricular failure occurs most frequently after left ventricular failure. When the right ventricle is failing, the venous blood is not pumped into the lungs completely, and there is a backup of blood into the venous system as evidenced by pedal edema, distended jugular veins, and cyanosis of nailbeds and lips.

The heart attempts to compensate for inadequate pumping and reduction in cardiac output. As a result, ventricular dilation, hypertrophy, and increased sympathetic activity occurs. The ventricular dilation causes an increase in the preload volume which, in turn, causes increased stroke work during contractions. Ventricular hypertrophy is an increase in heart muscle mass for pumping against increased resistance.

The enlarged heart is not completely perfused with oxygenated blood, and it is unable to provide adequate contractility. The sympathetic activity is a response to decreased blood pressure and cardiac output. The sympathetic response involves increasing the peripheral vascular resistance to elevate the blood pressure. This general understanding of the CHF myocardial dysfunction can lead us into the understanding of specific drug therapy for improving each aspect of heart function for overall management of the patients with this disease.

The therapeutic objectives for drug management of CHF include:

- Restoring inotropic and chronotropic ventricular function.

- Reducing both preload and afterload.

- Relieving symptoms of atrial hypertension.

- Improving cardiac output.

- Maintaining adequate blood pressure for organ perfusion.

Primary Drug Therapies

Inotropic Therapy Agents. The cardiac glycosides (digitalis glycosides), digoxin and deslanoside/digoxin, increase the force and velocity of myocardial systolic contraction, the refractory period of the AV node, and the total peripheral resistance. Digoxin has a narrow margin of safety, and toxicity is easily brought on by changes in dosage, patient metabolism, or interaction with other drugs.

Drugs used in dentistry that increase levels of digoxin are: aminoglycosides, benzodiazepines, erythromycin, ibuprofen, and tetracycline.

Side effects of anorexia, nausea, and vomiting in a mild form can be a usual adverse effect of the digitalis drugs. But persistent, more dramatic representations of these symptoms are indications of toxicity.

Sympathomimetics interact with cardiac glycosides. Therefore, vasoconstrictors used in dentistry should be avoided in patients taking digoxin as the combination could cause cardiac arrhythmias.

All other inotropic agents are used in emergency or hospital management of acute pulmonary edema. These inotropic agents include amrinone, milrinone, dopamine, dobutamine, and aminophylline.

Diuretics. These are used in the management of CHF to enhance renal excretion of sodium and water, decrease preload, reduce blood volume, and lower ventricular filling pressures to prevent systemic and pulmonary congestion. The three types of diuretics used in the management of CHF include the thiazides, loop diuretics, and potassium sparing diuretics.

The thiazides increase urinary excretion of sodium and chloride. They also increase potassium and bicarbonate excretion. Sodium depletion in initial therapy results in reduced cardiac output and extracellular volume. In long-term therapy, cardiac output normalizes while peripheral vascular resistance decreases, causing a lowering in blood pressure.

The thiazides can cause hypokalemia (potassium depletion), and this upset in the balance of electrolytes can cause cardiac arrhythmias and/or contribute to digitalis toxicity. For this reason, potassium-sparing diuretics are more often used in CHF patients in combination with thiazides.

Some very commonly prescribed thiazide drugs include: chlorothiazide (Diuril) and hydrochlorothiazide (Hydrodiuril), but there are several thiazide drugs in this group.

Loop diuretics are very potent diuretics that can cause profound electrolyte depletion if not carefully prescribed. The most common examples, furosemide (Lasix) and ethracrynic acid (Edecrin), inhibit reabsorption in proximal and distal tubules, as well as the loop of Henle.

The loop of Henle is the site of action that is affected by these diuretics. The drugs get the name "loop diuretics" from this unique mechanism that contributes to such profound efficacy. This drug is reserved for rapid onset of diuresis in CHF patients when edema must be reversed rapidly or when other diuretics are ineffective. The drug is used in the management of other types of edema associated with renal function, malignancy, or idiopathic edema.

The potassium-sparing diuretics interfere with sodium reabsorption at the distal tubule. They decrease potassium secretion by inhibiting aldosterone and the formation of the protein which is the carrier of sodium. Frequently, the potassium-sparing diuretic is used with the thiazide diuretic to potentiate thiazide activity while preventing potassium depletion.

The potassium-sparing diuretics include: spironolactone (Aldactone), amiloride (Midamor) and triamterene (Dyrenium).

All of the diuretics are capable of causing the adverse effect of orthostatic hypotension. This is a concern in dentistry. Patients who are placed in a supine position may not adjust to postural changes that require abrupt movement to a sitting or standing position without a drop in blood pressure.

Without warning or symptoms, the patient may faint. This can be prevented by raising the back of the dental chair slowly and allowing the patient to sit upright for a few minutes before allowing him/her to stand.

Vasodilators. In the treatment of CHF, vasodilators reduce preload, afterload (which is responsible for decreasing left ventricular end-diastolic pressure), and systemic vascular resistance. The nitrates such as nitroglycerine (Nitrostat) and isosorbide (Isordil) are one category of vasodilators. Another example is hydralazine (Apresoline), which exerts a peripheral vasodilating effect on vascular smooth muscle, lowering blood pressure and increasing the heart rate, stroke volume, and cardiac output.

Minoxidil (Loniten) is a potent vasodilator that is used for high blood pressure. The side effect of a rapid heart rate can be avoided by concomitant use of beta-blocking agents such as clonidine or sympatholytics such as methyldopa.

Another side effect has caused minoxidil to become better known among consumers - hypertrichosis (extensive hair growth). Some 80 percent of the patients taking minoxidil experienced elongation, thickening, and enhanced pigmentation of hair within six weeks of taking the drug. The hair grows in specific areas and not always in areas desired. The drug should be reserved for those patients with cardiac conditions that suggest its need.

Some patients find physicians who will prescribe the drug for male-pattern baldness. This can pose a risk and prescribing it for hair growth is not an approved use. The topical minoxidil (Rogaine) is approved for hair growth use.

Prazosin (Minipress) is one of the Alpha-1-adrenergic blockers used in refractory CHF. The drug decreases cardiac afterload and preload, improving cardiac output as well as relieving pulmonary congestion. It is also used alone in cases of hypertension.

Angiotensin-converting enzyme inhibitors (ACE inhibitors) are added to conventional CHF therapy to improve symptoms of heart failure and manage hypertension. Some ACE inhibitors are captopril (Capoten), enalapril (Vasotec), and lisinopril (Prinivil, Zestril). Vasoconstrictors should be avoided in patients taking ACE inhibitors.

Other drugs for CHF treatment

Other drugs may alleviate CHF symptoms and very often drugs are taken concomitantly to complement one another. Concomitant drug use in CHF allows safer drug therapy. When one drug cancels adverse effects of another drug, only the desired effects are elicited.

Of all the cardiac patients, CHF patients usually take the greatest number of drugs. Several of the drugs cause orthostatic hypotension, xerostomia, and nausea. All of the drugs should be looked up in a pharmacological reference book to ascertain that drugs used in dentistry will not interact adversely with those taken by the CHF patient.

New drugs are approved by the FDA weekly, and it is impossible to be familiar with every one of them. Patients are frequently given the new drugs in samples before they are listed in most reference books. A call to the pharmacist or the patient`s physician can clear up any concerns about dental treatment.

Most CHF patients have coronary artery disease and may also be on antiplatelet or anticoagulant therapy. This always requires consultation with the physician since there may be a risk of hemorrhage with dental prophylaxis or surgery.

The medical emergency that is associated with CHF is acute pulmonary edema (APE). Although the onset of the emergency is sudden, careful questioning of the patient will reveal that the condition is worsening during recent weeks. The questioning should take place at the beginning of the appointment. Dental treatment can then be postponed until the patient returns to his physician for medical treatment.

Acute pulmonary edema

Waiting until the patient is in distress to ask questions does not prevent emergencies. Usually the patient will say that they have had increased difficulty in breathing at night, are sleeping upright (orthopnea), and feeling more congested (experiencing wheezing and coughing more) than in the past.

Additional stressful situations of an emotional or physical nature can be the catalyst for the severe ventricular failure that results in blood and fluid accumulations in the lungs. Coughing followed by respiratory distress that resembles an asthmatic attack are the initial signs of the emergency. The patient becomes panic stricken from the sense of suffocation and the lack of oxygen. Cyanosis, sweating, pallor, and a pink frothy sputum are characteristic signs of APE.

If a patient experiences severe chest pain prior to APE, it is most likely because an extensive myocardial infarction caused such severe damage to the left ventricle that it fails to pump, causing the APE. Cardiac arrest could occur. An emergency plan is of paramount importance in these types of emergencies.

Calling out a secret number can rally the office team while the receptionist summons EMS immediately. It is most important to administer high concentrations of oxygen to the patient to improve blood-oxygen perfusion. A non-rebreather face mask may be connected to a low flow regulator to deliver a 90 percent concentration of oxygen to the patient.

A 10 milligram capsule of nifedipine may be opened and poured under the patient?s tongue, or a nitroglycerine tablet may be placed sublingually if the systolic blood pressure is at least 100. Nifedipine is milder and takes 10 minutes to provide vasodilation while nitroglycerine is stronger and faster acting at 2 minutes. Vasodilation reduces ventricular filling pressure and alleviates pulmonary congestion.

Calming the patient and providing basic life support while awaiting the arrival of EMS are the other additional measures the dental team can take in managing this emergency. These patients are difficult to manage due to the anxiety from the sense of suffocation they are experiencing. Oxygen! Oxygen! Oxygen! Give it freely.

The CHF patient has a cardiac disease that is often misunderstood or mistaken for bronchitis, emphysema, or any of the pulmonary diseases. Being familiar with the manifestations, drug therapy treatments, and signs of progression of the disease enables us to employ proper risk management during dental treatment. Understanding the breathing difficulties these patients endure makes us more tolerant of their demands for semi-supine positioning, short appointments, and special treatment.

References available upon request from the author.

Cynthia R. Biron, RDH, is chair of the dental hygiene program at the Tallahassee Community College. She is also a certified emergency medical technician.

Precautionary Measures For Treating CHF Patients

1. Monitor vital signs at every appointment. Cardiovascular changes may have occurred and the patient may need to be referred to their physician.

2. Look up any new drugs the patient is taking.

3. Evaluate patient anxiety and possible trauma from procedure.

4. Employ stress reduction protocols (shorter appointments, alternate treatment plan, etc.).

5. Position patient for easier breathing (semi-supine).

6. Avoid orthostatic hypotension by allowing patient to sit upright for two minutes before standing.

7. Administer supplemental oxygen by nasal cannula or hood (3 - 5 ml flow rate) during treatment.

8. Avoid vasoconstrictors, especially EPI retraction cord.

9. Be mindful of sensitive gag reflex, avoid rubber dams, and be cautious with impressions, radiographs, etc.

Emergency Management of Acute Pulmonary Edema

- While calling out secret number for EMS, position patient upright

- Calm patient while you administer oxygen (90%).

- Take vital signs.

- Administer sublingual vasodilator.

- Provide basic life support.

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