Page 261 - ACCCN's Critical Care Nursing

238 P R I N C I P L E S A N D P R A C T I C E O F C R I T I C A L C A R E

TABLE 10.6 Common medications for the treatment of heart failure 55,64,107,108

Drug/example Action Major adverse effects
First line pharmacotherapy
ACE inhibitor Decrease systemic vascular resistance by stopping angiotensin conversion Symptomatic hypotension
Captopril I to II; decreased sodium and water retention. Hyperkalaemia
Enalapril Unproductive cough
Renal failure
Rash
Loop diuretics Increase urine volume by decreasing reabsorption of chloride and sodium. Hypokalaemia
Frusemide Ototoxicity
Rash
Thiazide diuretics Increase urine volume by decreasing reabsorption of sodium. Hypokalaemia
Chlorothiazide Hyperglycaemia
Hydrochlorothiazide Sensitivity: rash
Beta-adrenergic blockers Reduce systemic vascular resistance and heart rate by blocking Hypotension
Bisoprolol adrenoreceptors in arteries and heart. Bronchoconstriction
Carvedilol
Metoprolol CR/XL
Potassium-sparing Increase urine volume by aldosterone blocking and sodium retention. Hyperkalaemia
diuretics Rash
Spironolactone Gynaecomastia
ARB Block the angiotensin II receptor that responds to angiotensin II Symptomatic hypotension
Candesartan stimulation; decreased sodium and water retention. Alternative to ACEI. Hyperkalaemia
Irbesartan Renal failure
Second line pharmacotherapy
Cardiac glycosides Increase myocardial contractility and decrease heart rate by inhibiting Tachycardia
Digitalis sodium pump in myocytes. AV block
Nausea and vomiting
Disorientation
Visual disturbances

(Beta-adrenergic blocking agents and antiarrhythmic the workload of the heart without affecting heart rate or
drugs are reviewed on page 266). The main actions and cardiac output.
adverse effects of these drugs in heart failure are sum- Common adverse effects of ACE inhibitors primarily
marised in Table 10.6. result from hypotension, including dizziness and head-
ache. Other side effects include hyperkalaemia, deteriora-
Angiotensin-converting enzyme inhibitors tion of renal function, and an unproductive cough, which
ACE inhibitors are the cornerstone of CHF treatment, as may respond to asthma prophylactic medications. Initial
they have been demonstrated to prolong survival, improve doses of ACE inhibitors should be low, as severe – though
patient symptoms and exercise tolerance, prevent transient – symptomatic hypotension can occur, worsen-
hospitalisation and improve ejection fraction in CHF ing of renal function and hyperkalaemia. The dose of ACE
patients. 76,77 All patients with symptomatic systolic LV inhibitors needs to be gradually increased to maximum
dysfunction should be prescribed ACE inhibitors. 55,61 dose over 2–3 months to optimise the survival and func-
Drugs in this group (captopril, enalapril, lisinopril) act tional capacity benefits. This group of drugs is contrain-
on the renin–angiotensin system by specifically prevent- dicated in patients with bilateral renal artery stenosis due
78
ing the conversion of angiotensin I into angiotensin II. to the danger of developing renal failure. One important
As a result, systemic vascular resistance (afterload) is adverse effect of ACEIs is that it cannot be taken in con-
decreased. This is particularly important in preventing the junction with NSAIDs as NSAIDs reduce the action of
progression of CHF, because blockade of the renin– ACE inhibitors. 79
angiotensin system prevents further development of sys-
tolic dysfunction. In addition, because angiotensin II also Practice tip
stimulates the release of aldosterone, sodium and water
retention are decreased (preload). This may also be ben- A dry, non-productive cough is often associated with the intro-
eficial when ACE inhibitors are prescribed with diuretics, duction of ACE inhibitor medication, but is often mistaken for
as potassium loss is limited. Further, ACE inhibitors a symptom of other conditions, so patients may not report the
inhibit the breakdown of bradykinin (a vasodilator), symptom as new. The cough usually begins within 1–2 days of
which also contributes to decreasing vascular resistance. commencing therapy and uptitration of dose.
The total reduction of systemic vascular resistance reduces