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Cardiovascular Alterations and Management 239
increased concentrations are present in the loop, attract-
Practice tip ing more water and increasing urine volume. Intrave-
nous administration of frusemide is often used to
Heart failure is a disease of the elderly. Many elderly patients manage preload in acute exacerbations. In fluid-
have arthritis. However, elderly patients with heart failure must overloaded patients, the aim is to achieve increased urine
avoid taking NSAID medications especially when taking ACEIs output and a weight reduction of 0.5–1 kg daily, until
as NSAIDs counter the action of ACE inhibitors. In such cases clinical euvolaemia is achieved. Hypokalaemia is a
we usually recommend taking glycosamine for relief from common adverse effect, and patients on long-term
arthritis pain. diuretics need regular monitoring and may require
potassium supplements. Hyponatraemia may also
Beta-adrenergic blocking agents occur at high doses, and needs careful management in
All patients with symptomatic systolic left ventricular dys- heart failure patients. Ototoxicity, presenting as tinnitus,
vertigo and deafness, can occur at high doses, so IV deliv-
function should be prescribed a beta-adrenergic blocking ery of frusemide should be no faster than 4 mg/min.
agent. Beta-adrenergic blocking agents (carvedilol, meto- ● Thiazide and thiazide-like diuretics: These drugs (chlo-
prolol, bisoprolol) are used in CHF to inhibit the adverse rothiazide, hydrochlorothiazide, chlorthalidone) act
effects of chronic activation of the sympathetic nervous on the ascending loop of the nephron and decrease
system and improve ventricular function (see Chapter 10). sodium reabsorption. As a result, the fluid in the col-
In heart failure beta-2 receptors predominate with beta-1 lecting ducts is more concentrated and attracts more
receptors being downregulated. In heart failure beta- water. Thiazides also cause peripheral arteriole vasodi-
adrenergic blocking agents reduce this neurohormonal lation, which may be beneficial in hypertensive patients.
activity. The addition of a beta-adrenergic blocker has Adverse effects are similar to loop diuretics due to
been demonstrated to reduce symptoms, reduce hospi- potassium and sodium loss, and supplementation may
talisations and prolong survival in patients. 80,81 Similar to be necessary. When ACE inhibitors are prescribed con-
ACE inhibitors the dose of beta-adrenergic blocking agents currently, there is less potassium loss (details below).
needs to be gradually increased. Once the patient is euro- Hyperglycaemia can occur, so diabetics need monitor-
volaemic they should be commenced on low dose and ing. Impotence may also occur, as well as sensitivity
gradually increased to maximal dose over several months. due to the presence of sulphonamide in the drug
In patients with COPD, selective beta-1 blockers are pre- structure.
scribed. Patients will require close monitoring for signs ● Aldosterone antagonists: These are potassium-sparing
of deterioration of their COPD. Other adverse events are: diuretics and include spironolactone. Aldosterone
55
symptomatic hypotension, bradycardia and worsening acts on the distal convoluted tubule of the nephron to
heart failure. Also during the up-titration of beta-adrenergic cause sodium retention and thus water retention,
blocking agents many patients complain of feeling vague although potassium is lost. Antagonists stop this
in the morning; this usually disappears after 2–3 weeks. action, so potassium is not lost and not as much
Angiotensin receptor blocking agents sodium retained, thus there is minor diuresis. Spirono-
lactone is particularly useful in chronic heart failure
The primary use of angiotensin receptor blocking agents because there is excessive aldosterone production,
(ARBs) is in patients who are intolerant of ACE inhibitors causing oedema. There is the potential that spironolac-
such as ACEI cough. They have a similar action as ACE tone, by blocking aldosterone systemically, may prevent
inhibitors, however, ARBs block the angiotensin II recep- the negative effects of aldosterone on the heart, such
tor that responds to angiotensin II stimulation. ACE as fibrosis, hypertrophy and arrhythmogenesis. Adverse
inhibitors on the other hand act on the enzyme that effects include hyperkalaemia, which may occur more
78
produces angiotensin II. They have similar benefits as readily in CHF patients because of renal failure, and
ACE inhibitors, improving survival, LVEF and heart failure because of its potentially lethal effects requires regular
symptoms and a reduction in hospitalisations. 82,83 Similar monitoring. Other effects include hyponatraemia and
to ACE inhibitors, ARBs are commenced on a low dose feminisation effects such as gynaecomastia. Spirono-
and gradually up-titrated to optimal dose over two lactone is recommended for use in patients with severe
months. Adverse effects are: deterioration in renal func- symptomatic (NYHA class III–IV) systolic heart failure
tion, hyperkalaemia and symptomatic hypotension. 61 in addition other pharmacotherapy such as ACE inhib-
Diuretics itors. Aldosterone antagonists have additional survival
84,85
Diuretics are one of the mainstays of management of benefits and reduce hospital readmission.
heart failure, primarily to decrease the sodium and water Inotropic agents
retention response to the low cardiac output state. A com- This category of drugs increases cardiac contractility. The
bination of diuretics may be used if oedema persists on group includes cardiac glycosides (digoxin) and dopa-
one diuretic. Most often diuretics will be used in combi- mine agonists (dopamine, dobutamine), sympath o-
nation with ACE inhibitors. mimetics (adrenaline, noradrenaline), and calcium
● Loop diuretics: These drugs (frusemide, ethacrynic acid sensitising agents (levosimendan). Inotropes are used as
and bumetanide) act on the ascending limb of the loop IV infusions in severe heart failure, acute exacerbations of
of Henle of the nephron. They prevent the reabsorption chronic heart failure and for palliative care or bridging to
of chloride and sodium ions from the loop, so that transplant in very severe chronic heart failure. These drugs

