Congestive Heart Failure And Hypertension In The Frail Elderly
emphasis on diagnosis and treatment in geriatric home care. (Part I)
Gresham Bayne, MD

BACKGROUND:

The frail elderly patient population is characterized not only by age demographics, but by the inadequacy of the office-based medical model to meet their needs when they can no longer reach the physician's office on a regular basis. In addition, we are often called to see the new patient with presenting symptoms of heart failure precipitated by one of many proximate causes.

Congestive Heart Failure (CHF) is the leading cause for hospitalization after the age of 65. There were 875,000 admissions in 1994 for CHF with 80% of the patients over 65 years of age. CHF is the most costly DRG in the United States with annual costs exceeding $10 billion. The incidence and prevalence of CHF are rising in the population with prevalence doubling each decade after age 45. The one year survival for Class III and IV CHF elder patients is about 60%. The best predictor for survival is the cardiothoracic ratio on standard chest Xray.

There is a close and perhaps causative relationship between hypertension and CHF in the elderly due to the complex neurohormonal reflexes involved (see below). As people age the cardiovascular system normally increases in impedance, has lowered beta-adrenergic responsiveness, alters the myocardial energy metabolism, with the heart showing impaired diastolic relaxation and compliance. The net effect is a marked reduction in the cardiovascular reserve.

PRECIPITATING EVENTS:

Precipitating events must be evaluated first, before the patient's CHF can be addressed. The most common of these is the failure to take their medications due to financial, social, or cognitive problems. We may often choose to use this opportunity to switch patients to the more acceptable geriatric approach to congestive heart failure than has often been the case in the past. Briefly state, the philosophy of treatment has changed dramatically over the past two years from a diuretic-based ramp-up to the primary use of ACE inhibitors. The modern approach will be discussed later.

Other precipitating factors for CHF that are common to our population include anemia, hyperthyroidism, infection, new onset arrhythmias such as atrial fibrillation, change in diet, silent myocardial infarction, worsening valvular disease, inappropriate use of the sodium-retaining NSAIDS, and environmental changes such as increased ambient humidity or temperature, and stress. Obviously, these historical and clinical factors must be evaluated in perspective.

When assessing a new patient in the home, the absence of a readily available medical record and EKG/Xray documentation mandates the use of appropriate technology when patients present with symptoms suggestive of failure. Even in non-acute settings, the ability to have medical records may be due to mobility of the physician, cross referral patterns, or difficulty in accessing other databases from referring physicians. In fact, many of the patients will be well-served by an entirely new approach to their clinical symptoms, especially those on multiple medications. Obviously, precipitating causes should be addressed before redirecting the primary interest in care to the failure itself.

PHYSIOLOGY REVIEW:

The function of the heart is to pump arterialized blood forward under sufficient pressure to meet the peripheral tissue metabolic needs. Given adequate oxygenation and a normal hemoglobin, the cardiac output, defined as the pulse times the stroke volume, should pump enough blood to prevent angina (ischemia to the heart), cold knee caps (ischemia to the skin), oliguria or azotemia (ischemia to the kidney) and confusion (ischemia to the brain). Thus, a quick lab check with a portable analyzer and pulse oximetry is required to rule out azotemia, hypoxemia, and a metabolic acidosis demonstrated by the base deficit. Even a venous sample with a normal base excess is adequate to prove the absence of a low perfusion state.

NOTE that the above definition of inadequate cardiac output (CO) did NOT mention the blood pressure at all! In fact, the only time hypotension is an emergency is when the diastolic pressure is below 60 mmHg, and the patient is experiencing angina or failure symptoms. Since 85% of coronary arterial blood flow occurs during diastole, the aortic root pressure is critical in determining myocardial perfusion. In the emergency room, some patients in shock with angina find that dopamine is the best analgesic!

To evaluate the failing heart, one needs to think in terms of myocardial efficiency, NOT blood pressure. Efficiency of the heart is measured in terms of Oxygen Demand by the heart as balanced against the Stroke Work Index. We will first address the Oxygen Demand, which is determined by five factors, of which only three are clinically relevant: the pulse, the mean arterial pressure and the wall tension index. Myocardial oxygen demand is linearly increased by a pulse over 100, dramatically increased by mean arterial pressure (often estimated by a value one-third the distance between the diastolic and systolic pressures), and increased at the same cardiac output with increases in the wall tension index. The wall tension index is impossible to measure on a housecall, but can be inferred from an assessment of left ventricular end-diastolic volume (cardiomegaly).

For example, the patient with a pulse of 110, a blood pressure of 140/100 and cardiomegaly on CXR is demanding much more oxygen for their heart than a patient of normal heart size and vital signs. When the presenting symptoms include angina, the approach to CHF is first to treat the increased demand by using nitrates or calcium channel blockade to lower the MAP, slow the pulse, and vasodilate the coronary arteries. Once stabilized, the failure may be addressed.

Stroke Work Index (SWI) is a complicated measurement that requires the use of a pulmonary arterial catheter, but can be thought of in clinical terms quite simply. Remember, the heart does not have to create higher than normal pressures to increase its cardiac output (CO) if the peripheral vascular resistance (PVR) is reduced. The SWI is calculated basically by multiplying the cardiac output times the PVR. The human heart is a very efficient flow generator, but a very inefficient pressure generator. Thus, oxygen demand to increase cardiac output is efficiently handled under normal loading conditions, but requirements for hypertension are disastrous. It is important to note due to its inefficiencies and maladaptive neurohumoral reflexes, the failing heart simply increase the blood pressure without generating much increase in the CO. Thus, hypertension is the enemy in both ischemic heart disease and congestive heart failure.

The physiological changes in the elderly which occur in the chronic state of heart failure are numerous and complex. They include:

1. Increased renin levels, which increases the conversion of Angiotension I to Angiotension II, the most potent vasoconstrictor known today
2. Increased renin levels stimulating the kidney to increase aldosterone leading to increased retention of sodium and water
3. Increased adrenergic background tone by the adrenal cortex with elevated circulating norepinephrine levels and inappropriate increases in PVR
4. Decreased levels of adenyl cyclase leading to decreased levels of cyclic AMP which can lead to lower protein kinase, calcium entry levels and calcium re-update by the myofibrils

TREATMENT PRINCIPLES:

To maximize the cardiac output, one must think in terms of the three major forces we can effect: Preload, Contractility, and Afterload.

Preload: The hypovolemic patient may be in shock or hypotensive simply because of fluid depletion. This is easily discerned by the history, physical and portable lab testing. The hypervolemic patient is often much harder to evaluate, since chronic rales, interstial lung disease, emphysematous changes, obesity may all affect our confidence level.

Therefore, some simple in-home testing may be useful. The CXR showing cardiomegaly is strong support for a chronic hypervolemic state and elevated left ventricular filling pressures. The presence of LVH or left ventricular strain pattern in the EKG (R waves in V5 and V6 add up to more that 25mv) is often associated with volume overload. A final test, done only in the hypertensive patient, is the so-called "Chatterjee" test when one monitors the pulse before and after a single dose of sublingual nitroglycerine. Since NTG predictably lowers the pulmonary capillary wedge pressure (PCWP) (left ventricular filling pressure), the hypervolemic patient will NOT have a tachycardic change in pulse with NTG. The normal or hypovolemic patient will increase their pulse by 10% or more. Thus, the absence of tachycardia to NTG is de facto evidence of increase PCWP and needs treatment.

The use of nitrates alone to control preload and subsequent CHF symptoms is complicated by the tolerance that all patients develop for the longer acting versions. The use of nitrates in the elderly is most often useful on the acute housecall when the patient has suddenly decompensated and has hypertension in addition to the symptoms of CHF. One must be cautious in the home when using nitrates to be able to place the patient in recumbency before administration, as the "nitrate syncope" syndrome is much more likely in our patients.

Another preload reduction strategy is diuresis. The use of diuretics has been the mainstay of treatment for both hypertension and failure for some forty years, despite the fact that diuretics have yet to be shown in controlled prospective clinical trials to increase survival rates. Currently, some 35-40% of all seniors over the age of 65 are taking a diuretic in some form. However, cumulative studies now clearly show a number of adverse effects from the use of diuretics:

1. 60% of all toxic drug reactions are due to diuretics in the elderly
2. diuretics are the most common drug reaction requiring hospitalization
3. both types cause increased serum cholesterol, although subsequent cardiac disease is unproven
4. both can cause increased uric acid levels with subsequent tophaceous gout
5. both can cause glucose intolerance in Type 2 prone patients, and the instigation of Type 2 diabetes is NOT reversible by stopping the diuretic (bumex less than lasix)
6. both an cause deafness, even in chronic oral dosing regimes (bumex less than lasix)
7. both can cause decreased calcium absorption and worsen osteoporosis (loop worse than thiazides)
8. both can cause behavioral risks with incontinence in the female, urinary retention in the male
9. both can lead to hyperkalemia in the elderly as well as hypokalemia
10. both can cause severe hyponatremia in the elderly

Contractility: The state of inotropy of the heart in CHF patients is compromised by many of the maladaptive neurohormonal changes discussed above as well as the loss of cardiac tissue from current ischemic heart disease and past infarcts. Unfortunately, the use of phosphodiesterase inhibitors in the elderly to increase inotropy has been clinically unsuccessful. Use of adrenergic agents such as dopamine and dolbutamine requires monitoring and infusion therapy along with the hassles of an intravenous. More and more, however, Stage IV failure patients are doing well on home dobutrex drips, and we can anticipate seeing more of this especially when patients place longevity over quality of life.

The essential difference between the two adrenergic agents in common use today is important. Whereas, dopamine causes a more potent increase in inotropy and blood pressure, it has little or no effect on PCWP, increases ventricular irritability, and requires much more care. Dobutamine, on the other hand, not only has less toxicity at the same cardiac output, but lowers the PCWP dramatically, thereby restoring the normal cardiac anatomy and reducing myocardial oxygen demand.

To reduce the oxygen demand of the heart, the eighties and early nineties saw a increase in the use of beta blockers even in failure patients. Unfortunately, the use of beta blockers to control hypertension in the elderly involves much more toxicity, and has shown to increase mortality due to side effects, including the increase in cholesterol for all age groups. The current new enthusiasm for beta blockade in the elderly needs to be analyzed more closely with ambulatory cardiac output monitoring to improve patient selection.

The use of digoxin remains controversial in patients without the need for rate control in atrial fibrillation. Although digoxin is the oldest and most proven inotropic agent, and the only inotroph that also decreases the wall tension index (cardiomegaly), its toxicity and need for periodic serum measurements makes it risky for some patients.

A NEJM study in 1997 on Class II or III CHF patients showed no change in mortality with digoxin therapy in addition to ACE inhibition (see below), but a significant improvement in functional status and decrease in hospital days. Most patients with an ejection fraction of over 45% will do well on digoxin alone for control of symptoms of CHF.

Suffice to say, patients with cardiomegaly and/or a S3 gallop should have a trial on digoxin alone before using multiple drug combinations. Finally, no one argues about the use of digoxin to control rapid ventricular response in the patient with atrial fibrillation and CHF.

Afterload: If the SWI can be reduced by reducing the MAP, one might be able to both increase the forward flow of blood (CO) as well as decrease the myocardial oxygen demand. This would be the best of both worlds! Indeed, the newer studies show that peripheral vasodilatation has less morbidity and better survival rates with better functional status than conventional beta blocker/diuretic combinations. The geriatric literature offers many studies confirming the observation that the ACE inhibitors alone can control hypertension and should be used for patients with risk of CHF (such as LVH or cardiomegaly on CXR) even when they are asymptomatic.

By using ACE inhibition at lower doses beginning at night, one can often avoid orthostatic hypotension and preserve the peripheral vasomotor reflexes so important to prevent side effects. Many patients can be converted from 2-4 older medications (digoxin, lasix, KCL, tenormin) to a single dose of benzapril 10 mg hs. Titrating the benzapril up to 80 mg daily may control the blood pressure while relieving the symptoms of failure as well. The therapeutic effects must be evaluated by the patient's subjective reports of exercise tolerance or orthopnea, as well as objective weights. If CHF is to be controlled on ACE inhibitors alone, the patient will lose weight on it.

In addition, the Cooperative North Scandinavian Enalapril Survival Study showed that ACE inhibition improves symptoms and exercise tolerance, while affording significant survival benefits among patient with severe CHF. These agents not only decrease afterload, but preload as well, and deter activation of the neuroendocrine system leading to reduced risk of hypertensive episodes, stress reduction, less fluid retention, and perhaps less arrhythmogenicity.

A newer class of drugs similar to ACE inhibitors is on the horizon with studies in England. The angiotensin-receptor blocker Losartan (ELITE) was shown in a 1997 Lancet article to provide better survival than captopril and have no patients afflicted with the chronic cough syndrome.

Before reverting back to diuretics, which some patients simply must have, adding a calcium channel blocker may be useful to improve inotropy by increasing coronary blood flow and further decreasing the peripheral vascular resistance. In addition, the newer calcium-channel blockers such as amlodipine have been show to increase end-diastolic ventricular relaxation, promoting ventricular filling and increasing stroke volume at the same filling pressures. Once the hypertension is under control, the SWI is decreased enough to allow no further therapy requirements for heart failure. Should such therapy be required, a diuretic should be cautiously introduced since their effect is additive to both ACE inhibition and calcium channel blockade.

What has been lacking in both the critical care and outpatient arenas is an ability to measure the systemic vascular resistance. Thus, we are still basing our clinical decisions on non-physiological parameters: i.e., mean arterial pressure. Although MAP may be a useful guideline, many patients with borderline or low cardiac outputs have normotension while their SVR is markedly elevated. We cannot know this without measurement of the cardiac output, which heretofore has been invasive and expensive with the pulmonary arterial catheter. The advent of non-invasive, inexpensive cardiac impedance studies in the outpatient and home settings has opened up a dramatic opportunity to not only titrate therapies toward maximum lowering of the SVR to improve cardiac output, but also to titrate therapies both acutely and chronically toward optimal cardiac efficiency, since impedance can track the pre-ejection period and minimize isovolumetric contraction time.

ATRIAL FIBRILLATION:

No discussion of CHF or hypertension in the elderly can be completed without mention of the importance of anticoagulation for patients with atrial fibrillation (AF). Although coumadin has severe toxicity problems, INR measurements should be coordinated with home health to prevent significant events. Studies have not been done to show the use of coumadin in addition to vitamin E and/or baby ASA daily, but they clearly have shown that coumadin is preferable to vitamin E or aspirin alone.

In one study of 651 patients with AF published in Stroke (1997) by the School of Medicine at SUNY, a significant bias against using warfarin in patients over 45 years old existed. This bias was still present when risk factors such as diabetes, heart disease, history of prior CVA, or GI bleeding were accounted for. Fully 42% of the AF patients were discharged from the hospitals with no specific anticoagulation therapy. Of the patients with no contraindication to anticoagulation, 40% went untreated, although patients between the ages of 45 and 54 were twice as likely to be treated as those between 75 and 84.

The clinical benefit of anticoagulation in younger patients is now a mainstream concept. A meta-analysis of five prospective clinical trials of stroke prophylaxis in nonvalvular AF published in 1994 demonstrated that anticoagulation reduced stroke rates by 68% and overall mortality by 33%. The overall stroke rate was 4.5% for controls and 1.4% yearly for the warfarin-treated group. In these studies, aspirin reduced stroke rate by 3.6% but had no effect on mortality rates.

The Framingham and other studies have clearly shown that stroke risk in patients with AF increases with advancing age. Predictors of increased risk besides age include, prior stroke, history of hypertension, mitral valvular disease, diabetes, history of MI, CHF. In data pooled from numerous trials, the risk of intracranial hemorrhage older than 80 was 0.3%, about the same as the over 65 year old age group.

Given that warfarin anticoagulation reduces deaths and strokes significantly, that CHF increases the risk factors for stroke and heart attack, and that recent data suggests there is no greater complication rate in older patients with anticoagulation, it seems prudent to offer anticoagulation to patients with AF and discuss the relevant issues of quality of life, safety of medication compliance, supportive care in the home, etc.