Page 597 - Cardiac Nursing

1:4
0
3 P
1:4
009
6/2
0
009
g
Pa
g
g
M
3 P
Pa
M
6/2
5-5
94.
xd
5-5
q
q
94.
q
3
3
0/0
0/0
3
xd
55
55
0-c
ara
t
24_
ara
LWB K34 0-c 24_ p p pp555-594.qxd 30/06/2009 01:43 PM Page 573 Aptara
LWB
K34
LWBK340-c24_
t
73
73
e 5
e 5
A
p
p
p
A
C HAPTER 24 / Heart Failure and Cardiogenic Shock 573
Arterial Dilators. As a direct arteriolar vasodilator with direct
Table 24-11 ■ MANAGING SIDE EFFECTS DURING inotropic effects, hydralazine can improve LV function by reducing
TITRATION OF -BLOCKERS afterload and myocardial oxygen consumption, augmenting stroke
volume, and improving cardiac output. It is used in combination
Vasodilator Effects (Dizziness or Light Headedness)
Give drug with food as described in the previous section.
Give drug 2 hours before vasodilator agents or stagger doses of vasodilator
medications or other medications affecting blood pressure Calcium-Channel Blockers. The net benefits of calcium-
Reduce diuretic or vasodilator therapy temporarily channel blocker use rest in their ability to decrease afterload and
Reduce -blocker dose if symptoms persist after diuretic and vasodilator to exert anti-ischemic effects. Calcium-channel blockers are a di-
decreased two times verse group of agents with complex actions. They do not seem to
Significant Bradycardia ( 60–65 bpm with Symptoms) have a place in systolic dysfunction and may be harmful, although
(
(
Reduce -blocker dose risks may not accompany the use of the longer-acting agents (e.g.,
Clarify digoxin dosage
Temporarily stop digoxin or reduce digoxin dose amlodipine) in patients with concomitant hypertension or angina.
Monitor digoxin levels Calcium-channel blockers may be of benefit in diastolic dysfunc-
Clarify concomitant drug use tion because of improvement of diastolic relaxation, control of
Amiodarone blood pressure, and prevention of myocardial ischemia, and they
Calcium-channel blockers (verapamil or diltiazem)
may reverse LVH.
Worsening Heart Failure (Dyspnea, Weight gain, Edema)
Increase diuretic dose (if qd increase to bid; if bid, consider increasing the dose) Natriuretic Peptides. Natriuretic peptides such as nesiritide
Intensify salt restriction are intravenously delivered compounds that promote diuresis and
Reduce -blocker dose (if symptoms persist after diuretic increased)
have vasodilator properties that suppress neurohormonal activation
and indirectly improve myocardial performance. 95,96 Nesiritide in
the acute setting has been shown to rapidly reduce symptoms of
congestion, but the effects on morbidity and mortality remain un-
slowing of the sinus pacemaker and atrioventricular conduction clear. There are recent data linking nesiritide use to worsening re-
97
(negative chronotropy and dromotrophy), and neurohormonal nal function and increased mortality and thus it should be used
modulating effects including a sympathoinhibitory effect. 91 Little cautiously. 54,98
controversy exists as to the benefit of digoxin in patients with symp-
tomatic systolic dysfunction and concomitant atrial fibrillation, but Antiarrhythmics. HF is the most arrhythmogenic disorder in
the debate still continues over its current role in patients in normal cardiovascular disease. Management of arrhythmias in this group
sinus rhythm. Digoxin should be considered as a fourth-line med- of patients is difficult and remains far from satisfactory. Many
ication in patients who have LV systolic dysfunction while receiving patients with HF experience frequent and complex ventricular
standard therapy. 1,92 In the majority of patients with HF and nor- tachyarrhythmias, and the imminent risk of sudden death appears
mal sinus rhythm, the starting dosage of digoxin should be 0.125 or to be present for all patients with HF. Experimental and clinical
0.25 mg once daily (no loading dose) based on ideal body weight, evidence indicates that circulatory neurohormonal and electrolyte
age, and renal function. In patients with HF and rapid ventricular deficits (potassium and magnesium) interact to provoke malig-
response, higher doses are not recommended. If amiodarone is nant ventricular ectopic rhythms. In general, antiarrhythmic ther-
added, the dose of digoxin should be reduced. Studies support a apy in patients with HF is reserved for symptomatic arrhythmias
1
lower-serum digoxin concentration target in the range of 0.5 to 0.8 or for control of ventricular responses to atrial fibrillation. Class 1
ng/dL, because higher concentrations were associated with increased antiarrhythmics demonstrated an increase in mortality in patients
99
mortality. 93,94 with ventricular arrhythmias in HF. -Blockers can prevent up
to 40% to 50% of SCD, which adds to their benefit in managing
Vasodilator Therapy. The venous and arterial beds are often patients with HF. Amiodarone has undergone the most extensive
86
inappropriately constricted. Venoconstriction tends to displace evaluation for efficacy and safety in LV dysfunction, but has had
blood in the thorax causing pulmonary congestion, whereas arteri- equivocal effect on SCD. Survival of patients with life-threatening
olar constriction increases the impedance to LV emptying. Arteri- arrhythmias is improved with ICD placement as compared with
olar dilatation results in a reduction of afterload and may augment antiarrhythmic therapy. 100,101 Amiodarone is the preferred drug in
cardiac output, whereas venodilatation tends to produce a reduc- patients with HF with supraventricular tachycardia not controlled
tion in preload, lowers ventricular filling pressure, and reduces by -blocker or digoxin, or for those patients who are not candi-
symptoms of pulmonary congestion. Vasodilators may be sepa- dates for ICD placement. 1,102
rated into three categories: venous dilators (preload reducers), arte-
rial dilators (afterload reducers), and mixed venous and arterial Other Important Considerations
dilators (preload and afterload reducers).
Diabetes Mellitus. An association between Type II DM and
Venous Dilators. Nitroglycerin and the closely related isosor- HF has been clearly seen now for over a decade, the question re-
bide dinitrate are primarily reducers of preload because they dilate mains does insulin resistance (IR) cause a cardiomyopathic process
the systemic veins and reduce venous return, ultimately to reduce that leads to HF and/or does HF lead to IR? Diabetes affects 20 mil-
LV filling pressure. Nitrates are indicated for the treatment of lion Americans; it is highly associated with factors known to cause
1
angina in patients with HF. A combination of hydralazine with HF, such as hypertension and CAD. In addition, diabetes has long
isosorbide dinitrate combines the effect of improved preload and been known to be an independent risk factor for the development
afterload (see next section on hydralazine) and may be adminis- of HF. 10 Therefore, anomalies in glucose metabolism may syner-
tered to patients on standard therapy who cannot be administered gistically act to increase the prevalence of HF. There are several ge-
an ACE inhibitor because of renal insufficiency or true intolerance. netic disorders (Alström syndrome and Bardet–Biedl syndrome)