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Intravenous to Oral Conversion of

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Article in Annals of Pharmacotherapy · September 2010

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Critical Care

Intravenous to Oral Conversion of Antihypertensives:

A Toolkit for Guideline Development

Joseph F Dasta, Bradley A Boucher, Gretchen M Brophy, Henry Cohen, Erkan Hassan, Robert MacLaren,

Karina Muzykovsky, Steven J Martin, Steven E Pass, and Amy L Seybert

ue to the high cost of an intensive

D care unit (ICU) stay, ranging from
$3000 to $4000 per day, opportunities are
OBJECTIVE: To provide a toolkit of information for hospitals to use in developing
intravenous to oral conversion protocols for antihypertensives.
being sought to increase the quality of care DATA SOURCES: Articles describing intravenous to oral conversion protocols for
while decreasing length of stay (LOS).1 any therapeutic category were identified in an English-language MEDLINE
Strategies include protocols for sepsis, se- search (1990–April 2010) using a wide variety of MeSH terms. References from
selected articles were reviewed for additional material.
dation, deep venous thrombosis prophy-
STUDY SELECTION AND DATA EXTRACTION: Experimental and observational
laxis, and switching patients from intra-
English-language studies and review articles that focused on oral transition of
venous to oral medications, such as antibi-
intravenous drugs were selected.
otics.2,3 The rationale for oral conversion
DATA SYNTHESIS: Most of the literature on conversion from intravenous to oral
protocols consists of the oral dosage form formulations involves antimicrobials. There is considerable evidence docu-
being less expensive than its intravenous menting reduced costs and improved patient flow through the health-care system
counterpart, an increased risk of adverse following implementing these protocols with drugs like antimicrobials, histamine-2
drug reactions associated with intravenous receptor antagonists, and proton pump inhibitors. Although antihypertensives have
administration, and as importantly, the po- not been studied, principles and implementation strategies used for other drug
classes can be applied to antihypertensives. Guidance is provided on framing the
tential to transfer the patient sooner from
problem, issues surrounding oral absorption principles, information pertaining to oral
the ICU. Despite considerable research conversion in specific disease states, and implementation and documentation
documenting the positive clinical and eco- strategies. Detailed tables of oral and intravenous antihypertensives are provided.
nomic impact of oral transition protocols CONCLUSIONS: We recommend that hospitals consider developing protocols on
for drugs such as antibiotics, histamine-2 conversion of intravenous to oral antihypertensives in an attempt to reduce
receptor antagonists, antiarrhythmics, non- unnecessarily prolonged intravenous therapy. Information contained in this article
steroidal antiinflammatory compounds, can be used as a toolkit to select information specific to the characteristics of
individual health-care systems.
and proton pump inhibitors, there are no
KEY WORDS: acute hypertension, hypertensive crisis, oral conversion program,
studies describing the design, implementa-
oral transition program.
tion, or evaluation of intravenous to oral
Ann Pharmacother 2010;44:1430-47.
conversion protocols involving antihyper-
tensives. 4 Published Online, 11 Aug 2010, theannals.com, DOI 10.1345/aph.1P086
Hypertensive crisis is an important
medical problem. A recent registry of
1500 patients with severe acute hypertension revealed a sig- venous antihypertensive drugs.6 Despite widespread usage of
nificant all-cause in-hospital mortality rate of nearly 7%, with intravenous antihypertensives, national guidelines on their
59% of patients developing acute/worsening end-organ dys- use are limited to the seventh report of the Joint National
5 Committee on Prevention, Detection, Evaluation, and Treat-
function during hospitalization. A recent survey revealed
that most hospitals do not have guidelines for use of intra- ment of High Blood Pressure (JNC 7), which devotes only 1
table and a 519-word discussion and documents pertaining to
patients with stroke.7-9 Furthermore, there is minimal infor-
Author information provided at end of text. mation on intravenous to oral conversion.10,11

1430 n The Annals of Pharmacotherapy n 2010 September, Volume 44 theannals.com

 Lack of protocols on oral conversion can lead to pro-
longed duration of intravenous antihypertensives, resulting
in excessive costs. As such, we have developed a toolkit of
information to assist hospitals in developing intravenous to
oral protocols. Readers are referred to recent reviews on
the pharmacologic management of acute hypertension as
background material.10-15 We performed an English-lan-
guage MEDLINE search (from 1990 to April 2010) to
identify articles on factors affecting oral absorption, intra-
venous antihypertensives, and oral transition. Appropriate
references from selected articles were also reviewed. Since
few data exist on conversion from intravenous to oral anti-
hypertensive therapy, expert opinion was often used.
Benefits of Oral Conversion Programs
The impetus for hospitals to convert treatment from in-
travenous to highly bioavailable oral dosage forms began
with the advent of oral fluoroquinolones and is predicated
on savings from reduced drug acquisition costs, decreased
LOS, and increased bed turnaround with improved patient
flow to discharge.16 A recent survey of hospitals with intra-
venous to oral conversion programs indicated that of the
87 hospitals that reported cost savings, 47% reported annu-
al cost savings of at least $50,000.17 Drug acquisition cost
was the most common parameter used (80% of institu-
tions) to calculate cost savings.
The conversion from intravenous to oral antibiotics may
result in savings beyond reduced acquisition cost of phar-
maceuticals. Intravenous to oral conversion of antibiotics
for patients with community-acquired pneumonia has been
suggested to shorten hospital LOS, as clinicians and pa-
tients consider oral therapy to be a prerequisite for dis-
charge.18 This principle likely applies to antihypertensives,
but oral conversion may be a marker for discharge from
the ICU, rather than from the hospital.
There are additional benefits beyond financial advan-
tages to an oral conversion program for antihyperten-
sives. Intermittently administered intravenous antihyper-
tensive agents typically have a short duration of action
and can produce rapid changes in blood pressure shortly
after administration and just prior to readministration. 14
Oral dosage forms commonly provide a longer duration
of effect and produce a more sustained effect on blood
pressure than parenteral dosage forms. However, the du-
ration of hypotension may also be prolonged with oral
drugs.
Elimination of intravenous administration allows re-
moval of intravenous catheters and reduced risk of nosoco-
mial catheter infections and bacteremia.4 Infusion-related
adverse drug reactions, including hypotension, are com-
mon with intravenous antihypertensives. Oral administra-
tion of antihypertensive therapy may reduce those risks.
Oral therapy is less labor intensive for nurses and increases
theannals.com The Annals of Pharmacotherapy
comfort and mobility for the patient. Intravenous antihy-
pertensives require an infusion pump, which introduces
potential programming errors and increases cost.
Intravenous to oral conversion programs with other
agents have been successful in many institutions. They cre-
ate a mutually beneficial environment for the patient and
hospital.17 The concept of intravenous to oral conversion is
generally well accepted by medical staff, and implementa-
tion of a program for antihypertensive agents is likely to be
successful, based on previous success shown with other
drugs.
Barriers to Protocol Implementation
Designing and implementing a protocol requires an un-
derstanding of the complexities and local politics of the or-
ganization, particularly the ICU. Clinicians may not readily
appreciate the applicability of oral transition protocols to
antihypertensives. This is due, in part, to lack of data, in-
cluding absence of national guidelines. An additional barri-
er is that few oral counterparts of intravenous antihyperten-
sives exist. Furthermore, patients often receive several in-
travenous antihypertensives, making oral transition even
more challenging.5 Finally, the financial benefit of convert-
ing from an intravenous to oral antihypertensive is not as
readily apparent as with drugs like antibiotics.
General Principles of Oral Transition
RISK OF HYPERTENSION AND TREATMENT GOALS
The goals of therapy for acute hypertension in the ICU
include maintaining adequate myocardial oxygen supply,
reducing blood pressure to an acceptable range, and mini-
mizing complications of antihypertensives. Selection of the
appropriate agent requires an understanding of the primary
cause of the elevated blood pressure.1 The therapeutic goal
of hypertensive crisis according to JNC 7 is to reduce
mean arterial blood pressure (MAP) by no more than 25%
(within minutes to 1 hour) and then, if stable, to
160/100 –110 mm Hg within the next 2– 6 hours.8 This is
typically accomplished with the use of an intravenous anti-
hypertensive agent (Table 1),19-32 followed by a transition to
an oral agent (Table 2).19-21,33,34
TRANSITION TIMING CONSIDERATIONS
There are some clear indications for the appropriate tim-
ing of oral transition therapy, but there are often unclear
circumstances that make the timing of the transition more
complex. Transition to oral therapy may be delayed despite
attainment of the target blood pressure depending on the
underlying acute illness, the patient’s ability to tolerate oral
medications, or availability of enteral access. As such,
these variables should be assessed at least daily.
n 2010 September, Volume 44 n 1431
 Table 1. Pharmacologic Summary of Intravenous Antihypertensives

1432
Drug Pharmacokinetics Metabolism/Elimination Dosing Precautions Adverse Reactions Clinical Notes

n
β-Blockers
JF Dasta et al.

Labetalol O: 2–5 min M: Hepatic Initial bolus dose: 20 mg over 2 min Use caution in impaired Dizziness, fatigue, nausea, Discontinue infusion once
P: 5 min E: 55–60% in urine as glucuro- Initial infusion dosage: 2 mg/min hepatic function increased serum target BP goals achieved;
D: 2–18 h nide metabolite or titrated to a total dose of 300 mg transaminases switch to bolus dose or
unchanged; also bile, feces oral dosing
Metoprolol O: 2–5 min M: Hepatic Initial bolus dose: 1.25–5 mg every 6 h CI in sinus bradycardia, Bradycardia, first- degree Used primarily for heart rate
P: 20 min E: Urine as inactive metabo- over 1 min second- or third-degree heart block, dizziness, control
D: 5–8 h lites; <5–10% unchanged Maximum dose: 15 mg every 3 h heart block; use with fatigue, rash, dyspnea
caution in CHF
Esmolol O: 2–10 min M: Ester hydrolysis Initial bolus dosage: 500 µg/kg over 1 min CI in advanced aortic Bradycardia, thrombophlebitis, Used primarily for heart rate
P: 30 min E: Urine as inactive metabo- Initial infusion dosage: 50 µg/kg/min stenosis; use with diaphoresis, nausea, control
D: 10–20 min lites; <2% unchanged Increase by 50 µg/kg/min every 4 min to caution in impaired headache
a maximum of 300 µg/kg/min renal function

The Annals of Pharmacotherapy

Calcium-channel blockers

n
Nicardipine O: 10 min M: Hepatic Initial infusion dosage: 5 mg/h Use with caution in CHF, Headache, tachycardia,
P: 30–60 min E: As inactive metabolite; 49– Increase by 2.5 mg/h every 5–15 min to impaired hepatic or renal nausea, vomiting
D: ≤8 h 60% urine, 43% feces a maximum of 15 mg/h function; CI in advanced
aortic stenosis
Clevidipine O: 2–4 min M: Ester hydrolysis Initial infusion dosage: 1–2 mg/h Soy/egg allergies, CI in Headache, nausea, vomiting 20% Lipid formulation
P: 30 min E: As inactive metabolite; 63– Double every 90 sec; then every 5–10 severe aortic stenosis
D: 5–15 min 74% urine, 7–22% feces min as closer to goal to a maximum of
32 mg/h
ACE inhibitors
Enalaprilat O: 15 min M: Prodrug; hepatic Initial dose: 1.25 mg every 6 h Severe aortic stenosis, may Headache, nausea, fatigue, Not considered first-line therapy
P: 1–5 h E: Urine, >90% unchanged Maximum dose: 5 mg every 6 h cause hyperkalemia; use dizziness, fever, rash, due to unpredictable effects;
D: 6 h Administer slow bolus over 5 min with caution in impaired constipation, cough, reduce initial dose to 0.625
renal function angioedema mg if CrCl <30 mL/min

2010 September, Volume 44

Vasodilators
Hydralazine O: 5–20 min M: Hepatic Initial dose: 10–20 mg q4–6 h Use with caution in CAD Headache, anorexia, nausea, Not considered first-line
P: 10–80 min E: Urine as inactive metabo- Maximum dose: 40 mg every 6 h and mitral valvular vomiting, diarrhea, palpita- therapy due to unpredict-
D: 1–4 h lites; 14% unchanged Administer slow bolus at 5 mg/min rheumatic heart disease tions, tachycardia, angina able effects
Nitroglycerin O: 1–2 min M: Hepatic Initial dosage: 5–10 µg/min CI in pericardial tamponade, Headache, lightheaded- Requires frequent dosing
P: 1–2 min E: Urine as active metabolites Increase by 5 µg/min every 5 min to restrictive cardiomyopathy, ness, syncope, angina, increases due to
D: 3–5 min 20 µg/min, then by 10 µg/min every constrictive pericarditis rebound hypertension development of
5 min to a maximum of 200 µg/min nitrate tolerance
Nitroprusside O: 1–2 min M: Hemoglobin, hepatic Initial dosage: 0.3 µg/kg/min Use with caution in CHF Nausea, vomiting, dizziness, Monitor cyanide concentrations
P: 1–2 min E: Renal (thiocyanate) Increase by 0.5 µg/kg/min and renal insufficiency; headache, methemoglobi- in hepatic impairment;
D: 1–10 min Maximum dosage: 10 µg/kg/min may cause increase in ICP nemia, cyanide toxicity, thiocyanate concentrations in
thiocyanate toxicity renal impairment
Dopamine agonist
Fenoldopam O: 10 min M: Hepatic No bolus dose May increase intraocular Headache, flushing, dizziness, May induce natriuresis and
P: 20 min E: As inactive metabolites; Initial dosage: 0.1–0.3 µg/kg/min pressure; may cause tachycardia/bradycardia diuresis
D: 60 min urine 90%, feces 10% Maximum dosage: 1.6 µg/kg/min hypokalemia
Increase by 0.05–1 µg/kg/min every 15 min

ACE = angiotensin-converting enzyme; CAD = coronary artery disease; CHF = congestive heart failure; CI = contraindicated; CrCl = creatinine clearance; D = duration of effect; E = excretion; ICP = intracranial

theannals.com
pressure; M = metabolism; O = onset of action; P = peak effect.

THE ART OF TRANSITION
Experts agree that the success of oral transition is depen-
dent on the pharmacokinetics and pharmacodynamics of
the selected medications. As the patient’s hemodynamic
status stabilizes, one approach to conversion is to begin
with a downward titration of the intravenous infusion or in-
termittent dosing regimen to the minimal effective dosage
to maintain the patient’s blood pressure at a desired level
without excessive variability. Once accomplished, an ini-
tial dose of an oral agent is given. For intermittent intra-
venous dosing regimens, the oral dose is generally admin-
stered at the end of the dosing interval and the intravenous
regimen is discontinued. In the case of intravenous infu-
sions, the infusion is discontinued 1–2 hours after the oral
drug is administered; however, this may differ, depending
on the absorption characteristics of the oral agent and off-
set of the intravenous drug (Tables 1 and 2). For drugs with
a fast offset of action, like clevidipine and sodium nitro-
prusside, the oral drug should be started 1–2 hours before
the intravenous agent is discontinued. Another option, es-
pecially in cases of severe blood pressure elevations, is to
start low dosages of an oral agent concurrently with the in-
travenous infusion. The dosage of the oral agent can be
titrated upward daily toward optimal or maximal dosages
as the infusion is slowly reduced and discontinued. Based
on experience and the absorption characteristics of oral
dosage forms, this approach results in minimal fluctuations
in blood pressure. The patient should be closely monitored
during this transition phase for either hypotensive or hyper-
tensive episodes.
INITIAL AGENT SELECTION
When transitioning from intravenous to oral antihyper-
tensives, it is important to select an appropriate oral agent
for the patient. There are several ways to accomplish this,
and each has benefits that depend on specific patient fac-
tors. One approach is to resume all or part of the patient’s
preadmission drug regimen, unless there is a clinical indi-
cation to alter the medication based on a newly discovered
comorbidity. If the patient required multiple antihyperten-
sives before admission, restarting 1 or 2 of those drugs in
the acute setting may help avoid prolonged use of intra-
venous antihypertensives in patients with difficult-to-con-
trol hypertension (eg, chronic kidney disease). Patients
with preoperative essential hypertension should have their
preadmission antihypertensive medications, especially β-
blockers, continued until their surgical procedure is com-
pleted and restarted postoperatively when their condition is
stable to avoid antihypertensive withdrawal syndrome.3 A
second approach is to choose an agent of the same class (or
the same agent) as the intravenous antihypertensive used.
A third approach is to discontinue the patient’s preadmis-
theannals.com The Annals of Pharmacotherapy
Intravenous to Oral Conversion of Antihypertensives
sion drug regimen and select a regimen that is specific for
the patient’s current status. Numerous oral drugs are used
following intravenous therapy. One recent study of 17 pa-
tients receiving nicardipine examined oral therapy follow-
ing nicardipine discontinuation.35 A wide variety of oral
drug classes were selected, with 5 out of 17 patients receiv-
ing >1 oral antihypertensive. The shortest mean nicardi-
pine infusion duration (23 ± 19 hours) occurred when oral
calcium-channel blockers were used, while the longest du-
ration (72 ± 63 hours) was seen when oral β-blockers were
prescribed.
The appropriate drug class should be chosen for oral
transition in patients with a compelling indication for a par-
ticular class.3 If there is not a compelling indication, then
the selection of an oral agent centers on other factors, such
as ease of administration, likelihood of adherence, adverse
effect profile, available dosage forms, and cost. Ease of ad-
ministration is an important factor to consider. Oral agents
dosed once or twice daily may offer advantages in adher-
ence to regimens over agents requiring more frequent dos-
ing. Another consideration is that several agents are also
available in alternative dosage forms, such as extended-re-
lease or transdermal formulations that may provide admin-
istration advantages. A similar problem may be encoun-
tered for patients with health insurance, as certain agents
may not be on formulary. It is therefore important to take
into consideration the hospital formulary and the formula-
ry of the patient’s pharmacy benefit management compa-
ny.
Gastrointestinal Absorption Criteria
Drug absorption from the gastrointestinal tract may be
altered in critically ill patients. Variables affecting absorp-
tion may be classified as abnormalities of the gastrointesti-
nal tract (pH, blood flow, surface area, motility), the patient’s
ability to tolerate oral/enteral administration, and/or physico-
chemical characteristics of the environment (tube size and
location, dosage form).36-41 The effects of acute hyperten-
sion on gastrointestinal motility and drug absorption are
unknown. Hemodynamic parameters should be stable be-
fore transitioning to the oral or enteral route.
All immediate-release antihypertensive medications are
absorbed along the intestinal tract with predominance in
the small intestine.42 Critically ill patients frequently re-
ceive gastric acid suppressant therapy to prevent stress-re-
lated gastrointestinal hemorrhage. Unfortunately, data are
not available addressing the impact of intraluminal pH
variations on the absorption of antihypertensive medica-
tions. Regional perfusion abnormalities and intestinal atro-
phy may reduce bioavailability after oral or enteral admin-
istration.36,37 Verapamil is the only antihypertensive agent
with documented diminished extent of absorption in criti-
cally ill patients, but few agents have been studied. Other
n 2010 September, Volume 44 n 1433
 Table 2. Pharmacodynamics and Pharmacokinetics of Oral Antihypertensive Agents

1434
Onset of Oral Fraction Oral to
Action Peak Duration of Absorbed Intravenous Dosage

n
Drug (h) Effect (h) Action (h) (%) Metabolism Excretion Equivalent Form May Crush Interact with Food
JF Dasta et al.

Centrally acting adrenergic agents (α

α2-agonists)
Clonidine 0.5–1 2–4 8 75–95 Hepatic 40–60% Urine Intravenous Tablet, Yes Unknown
(unchanged) formulation not injectable,
20% Feces indicated for HTN transdermal
Guanabenz 1 2–7 Manufacturer: 75 Extensively metabo- 70–80% Urine Intravenous Tablet Unknown Unknown
6–8 h, substantial Absolute F in lized, site unknown; (parent drug formulation not
decrease in humans extensive first- and metabolites) available
hypotensive effect unknown pass metabolism 10–30% Feces
Baseline BP: at
12 h
Hypotensive
effect >12 h

The Annals of Pharmacotherapy

Guanfacine 2 1–4 Manufacturer: 80 50–70% Hepatic (via 40–75% Urine Intravenous Tablet Unknown Unknown

n
6–8 h, may oxidative metabolism) via tubular formulation not
persist for >12 h; to inactive metabolite: excretion available
however, hypo- 3-hydroxy-derivative, (unchanged),
tensive effect which is conjugated 30–40%
diminishes sub- glucuronide,
stantially at 12 h. 8% sulfate
Methyldopa 3–6 3–6 12–24 50 Extensively metabo- 70% Urine 1:1 Tablet, Use liquid; liquid Unknown
lized in GI tract and (parent drug injectable, may be
liver to sulfate and metabolites) liquid compounded as
conjugates Feces well
(unchanged)
ACE inhibitors

2010 September, Volume 44

Benazepril ≤1 2–4 24 37% Hepatic, hydrolyzed Urine Intravenous Tablet Liquid compounded Rate of absorption
to active Minor: biliary formulation not with glycerol slower with food
benazeprilat available
Captopril 1 (fasting) 1–2 2–6 (increases 60–75% 50% Hepatic Urine Intravenous Tablet Liquid compounded Extent of absorption
with increasing formulation not with glycerol decreased 30–40%
doses) available with food
Enalapril 1 0.5–1.5 12–24 55–75% Prodrug, hepatic 60–80% Urine If no diuretic: Tablet, Liquid compounded Unknown
(enalapril), (enalapril), Feces initiate at 5 mg injectable with glycerol and
3.0–4.5 3–12% orally daily and sodium citrate
(enalaprilat) (enalaprilat) titrate as needed;
If on diuretic and
responding to
0.625 mg
intravenously
q6h: initiate at
2.5 mg orally
daily and titrate
as needed

theannals.com
 Fosinopril 1 3 24 36% Prodrug, intestinal Hepatic and Intravenous Tablet Unknown Rate of absorption
wall and hepatic renal formulation not slower with food
esterases available
Lisinopril 1 7 24 25% Not metabolized Urine Intravenous Tablet Liquid compounded Unknown
(16% NYHA (unchanged) formulation not with glycerol and

theannals.com
class II–IV available sodium citrate
heart failure)
Moexipril 1 3–6 24 13% Hepatic Feces and urine Intravenous Tablet Unknown Extent of absorption
formulation not decreased 40% with
available food
Perindopril 1.5 Chronic 80–90% Perindopril: Hepatically hydrolyzed Urine Intravenous Tablet Unknown Extent of absorption
therapy: Inhibition of 75% to perindoprilat; formulation not decreased
perindopril: ACE at 10–12 Perindoprilat: prevalent first-pass available 35% with food
1h 24% Inhibition 25% metabolism
perindoprilat: of ACE at 24
3–7 h
Quinapril 1 2–4 24 60% Hepatic, hydrolyzed Urine Intravenous Tablet Liquid may be Extent of absorption
to quinaprilat formulation not compounded reduced with food
available
Ramipril 1–2 Ramipril: 1 80% Inhibition Ramipril: 28% Hepatic, hydrolyzed Urine, feces Intravenous Tablet, Liquid compounded Rate of absorption
Ramiprilat: of ACE at 24 Ramiprilat: to ramiprilat formulation not capsule with water or slower with food
2–4 44% available apple juice
Trandolapril 80% Trandolapril: 1 24+ Inhibition of Trandolapril: Hepatic, hydrolyzed Feces > urine Intravenous Tablet Unknown Rate of absorption
inhibition Trandolaprilat: ACE declines by 10% to trandolaprilat; formulation not slower with food
of ACE 4–10 10% Trandolaprilat: prevalent first- available
at 4 70% pass metabolism
Angiotensin II receptor blockers
Candesartan 2–4 6–8 24+ 15 Candesartan cilexetil: 33–59% Urine Intravenous Tablet Unknown Unknown
hydrolysis (unchanged) formulation not
Candesartan: 36–76% Feces available
O-deethylation (via bile)
Eprosartan 1–2 1–2 (fasting) Unknown 13 Not by CYP; no 90% Biliary Intravenous Tablet Unknown Rate slower, but

The Annals of Pharmacotherapy

pharmacologically (unchanged) formulation not extent of absorption
active metabolites 7% Renal available increased 25–55%

n
detected with food
Irbesartan 2 1.5–2 24 60–80 Hepatic (CYP2C9), 20% Urine Intravenous Tablet Unknown None
glucuronide conjuga- 80% Feces (via formulation not
tion and oxidation to bile) available
inactive metabolites
Losartan 6 1 (parent 24 33 CYP2C9: pharmaco- 35% Urine (4% Intravenous Tablet Liquid may be Extent of absorption
compound) logically active meta- unchanged, 6% formulation not compounded increased 10% with
3–4 (metabo- bolite active meta- available food
lites) CYP3A4: inactive bolite)
metabolites 60% Feces
Prevalent first-pass (via bile)
metabolism

2010 September, Volume 44

n
ACE = angiotensin-converting enzyme; BP = blood pressure; F = fraction absorbed; GI = gastrointestinal; HTN = hypertension; NYHA = New York Heart Association.
(continued on page 1436)

1435
Intravenous to Oral Conversion of Antihypertensives
 Table 2. Pharmacodynamics and Pharmacokinetics of Oral Antihypertensive Agents (continued)

1436
Onset of Oral Fraction Oral to
Action Peak Duration of Absorbed Intravenous Dosage

n
Drug (h) Effect (h) Action (h) (%) Metabolism Excretion Equivalent Form May Crush Interact with Food
JF Dasta et al.

Angiotensin II receptor blockers

Olmesartan Unknown 1–2 24 26 Olmesartan medoxomil 35–50% Urine Intravenous Tablet Unknown None
hydrolyzed to olme- 50–65% Feces formulation not
sartan; no further (via bile) available
metabolism or CYP
metabolism
Telmisartan <3 0.5–1 24+ 40 mg: 42 Hepatic, via conjuga- >97% Unchanged Intravenous Tablet Unknown None
160 mg: 58 tion to inactive in feces (via bile), formulation not
metabolite <1% in urine available

Valsartan 2 2–4 24 10–35 Hepatic 83% Feces Intravenous Tablet Liquid compounded Extent of absorption
(unchanged) formulation not with glycerol decreased 40 %

The Annals of Pharmacotherapy

13% Urine available with food

n
β-Blockers
Atenolol 1 2–4 24+ 50–60 Limited hepatic 40–50% Urine Intravenous Tablet Liquid Extent of absorption
(unchanged); formulation not compounded with decreased 20% with
remainder in available glycerol ± food
feces as polyethylene
unabsorbed glycol
drug
Betaxolol <3 1.5–6 12–24 89 Hepatic Urine (15% Intravenous Tablet Unknown None
unchanged, formulation not
remainder available
metabolites)

2010 September, Volume 44

Carvedilol 0.5 1.5–7 24 25–35 Substantial, Feces (metabo- Intravenous Tablet, Liquid may be Rate of absorption
stereoselective lites), <2% formulation not extended- compounded slower with food
first-pass unchanged in available release
metabolism urine capsule
Labetalol 0.3–2 1–4 200 mg: 8–12 Absolute 25 Hepatic and GI 30% Feces 200 mg orally Tablet, Liquid compounded Extent of absorption
300 mg: 12–24 tract mucosa; Urine (55–60% followed by 200– injection with glycerol increased with food
prevalent first- as metabolite, 400 mg orally 6– or syrup
pass metabolism <5% 12 h later based
unchanged) on BP response
Can be titrated by
100 mg twice
daily for 1 day
while hospitalized
or every 3 days
as outpatient
Metoprolol 0.17 1.5 3–6 Absolute 50 Hepatic; prevalent Urine 2.5:1 Tablet, Liquid compounded Extent of absorption
first-pass (metabolites) injection with glycerol increased with food
metabolism
Nadolol 3–4 2–4 24+ 30–40 Not metabolized Unchanged in Intravenous Tablet Unknown Unknown
feces (76.9%) formulation not
and urine available
(24.6%)

theannals.com
 Propranolol 0.5 1–1.5 IR: 6–12 Absolute Hepatic; prevalent Urine Intravenous Tablet, Use liquid Extent of absorption
16–60 first-pass metabolism 1–4% Feces formulation not solution, increased 50% with
(unchanged and available; not capsule, food
metabolites) commonly used injection
for HTN

theannals.com
Timolol 0.25–0.75 1–2 4 90 Hepatic 80%; prevalent Urine (unchanged Intravenous Tablet Unknown Unknown
first-pass metabolism and metabolites) formulation not
available
Dihydropyridine calcium-channel blockers
Amlodipine NA 6 –12 24+ 64–90 Hepatic, to Urine (metabo- Intravenous Tablet Liquid compounded Unknown
inactive lites 60%, formulation not with methylcellulose
metabolites unchanged 10%) available
Felodipine 2–5 2.5–5 24 Absolute Hepatic, by Inactive metabo- Intravenous ER tablet No: ER formulation High-fat/high-carbo-
20 CYP3A4 lites in urine formulation not should not be hydrate increases
(70%) and available crushed peak concentration
feces (10%) by 60%
Grapefruit juice in-
creases F by ~2-fold
Isradipine Unknown 1.5 >12 (capsules) 15–24 Hepatic, completely 60–65% Urine Intravenous ER Extemporaneously Decreases time to
metabolized by 25–30% Feces formulation not tablet, compounded peak plasma con-
CYP3A4 to inactive available capsule liquid centration by 1 h
metabolites;
prevalent first-pass
metabolism
Nicardipine 0.5–2 0.5–2 8 35 Hepatic 49–60% Urine Oral Equiv- Capsule, Unknown Extent of absorption
35–43% Feces dosage alent injectable decreased 20–30%
intra- with food
venous
infusion
rate
20 mg q8h 0.5 mg/h
30 mg q8h 1.2 mg/h
40 mg q8h 2.2 mg/h

The Annals of Pharmacotherapy

Nisoldipine Unknown 6–12 24+ 5 Hepatic 60–80% Urine Intravenous ER No: ER formulation High-fat meal
formulation not tablet should not be increases peak

n
available crushed plasma concentra-
tions by ~300%, but
decreases extent of
absorption by 25%
Nondihydropyridine calcium-channel blockers
Diltiazem 0.25–1 IR: 2–3 ≤8 Absolute 40 Hepatic Urine and bile Oral = [(intrave- Tablet, Liquid compounded Unknown
as metabolites, nous rate × 3) capsule, with sorbitol
2–4% unchanged + 3] × 10 (start injectable
in urine 3 h post bolus)
Verapamil IR: 1–2 IR: 1–2 IR: 6–8 IR: 20–35 Hepatic Urine (70% as Intravenous Tablet, Liquid compounded Extent of absorption
metabolite, 3–4% formulation capsule, with glycerol decreased with food
as unchanged not commonly injectable

2010 September, Volume 44

drug) used for HTN

n
16% Feces

BP = blood pressure; ER = extended release; F = fraction absorbed; GI = gastrointestinal; HTN = hypertension; IR = immediate release.

1437
Intravenous to Oral Conversion of Antihypertensives

(continued on page 1438)

 Table 2. Pharmacodynamics and Pharmacokinetics of Oral Antihypertensive Agents (continued)

1438
Onset of Oral Fraction Oral to
Action Peak Duration of Absorbed Intravenous Dosage

n
Drug (h) Effect (h) Action (h) (%) Metabolism Excretion Equivalent Form May Crush Interact with Food
JF Dasta et al.

Direct arterial vasodilators

Hydralazine 0.3–0.5 2 2–4 66 By GI mucosa during Urine (metabo- 20–25 mg Intra- Capsule, Liquid compounded Extent of absorption
absorption lites) venous tablet, in mannitol or increased with food
Hepatic: acetylation 10% Feces hydralazine injectable sorbitol ± propylene
(genetic), hydroxy- = 75–100 mg glycol or parabens
lation, glucuronida- oral hydralazine
tion
Minoxidil 0.5 2–8 48–120 90 Glucuronidation 90% Urine by Intravenous Tablet Unknown Rate of absorption
glomerular formulation slower with food
filtration not available
Loop diuretics

The Annals of Pharmacotherapy

Bumetanide 0.5–1 1–2 4–6 85–95 Partial hepatic 80% Urine 1:1 Tablet, Unknown Unknown
oxidation (50% unchanged) injectable

n
10–20% Feces
(mostly
metabolites)
Ethacrynic 0.5 2 <12 100 Hepatic Feces, urine 1:1 Tablet, Liquid may be Unknown
acid (30–60% injectable compounded
unchanged) with parabens
Furosemide 0.5–1 1–2 6–8 64, Tablet Hepatic 50% Urine; 1–1.5: 1 Tablet, IR liquid dosage Rate of absorption
60, Solution remainder injectable, form available slower with food
degraded in liver, oral solution
excreted
unchanged in
feces

2010 September, Volume 44

Torsemide <1 1–2 6–8 80 Hepatic, 80% Urine, 20% Intravenous Tablet Unknown Rate of absorption
unchanged formulation not slower with food
available
Thiazide diuretics
Chlorothia- 2 3–6 6–12 Poor Not metabolized Urine 1:1 Tablet, Use liquid Extent of
zide suspension, absorption doubled
injectable with food

Chlorthali- 2.5 1.5–6 <72 65 Hepatic Urine (30–60% Intravenous Tablet Unknown None
done unchanged), formulation
feces not available
Hydrochloro- ≤2 3–6 6–12 65–75 Not metabolized Urine Intravenous Tablet, Use liquid Extent of absorption
thiazide (unchanged) formulation capsule, decreased with food
not available liquid
Indapamide 1–2 2–2.5 8–12 (up to 36) 100 Hepatic (glucuronide 70% Urine Intravenous Tablet Unknown Absorption not
and sulfate (metabolites) formulation affected by food
conjugates) 16–23% Feces not available
(bile)
7% Unchanged

theannals.com
 Intravenous to Oral Conversion of Antihypertensives

agents, such as furosemide, may have delayed or reduced

ER tablets should be
taken with morning
absorption in patients with heart failure, presumably due to

Rate of absorption

Rate of absorption
slower with food

slower with food

hindered intestinal circulation and intestinal edema.42
Motility disorders may delay absorption, but bioavailabili-
ty may be increased due to longer intestinal exposure.36,37
meal

Agents with extensive first-pass metabolism (Table 2)8,42

may demonstrate reduced systemic exposure with motility
ER tablets should

dysfunction, assuming that hepatic function is not compro-

not be crushed

mised.38,39
Patient-related characteristics will determine whether
the patient is ready to tolerate oral/enteral administration of
No

No

antihypertensives.43 The physicochemical environment will

determine whether a specific antihypertensive medication
should be administered via the oral or enteral route. Oral
Capsule

Capsule

administration requires the patient to swallow and tolerate

Tablet

ingestion of liquids or solids. Studies often define readiness

for oral/enteral administration as the absence of nausea,
formulation not

formulation not

formulation not

vomiting, or gastrointestinal disturbances (eg, cramping,

Intravenous

Intravenous

Intravenous

distension, bloating) for at least 4 hours following inges-

available

available

available

tion.44-47 This definition may be applied to the ICU patient

who is able to swallow, when the oral route of administra-
tion is being considered for drug delivery.
urine (20%, 10%
4.8% unchanged

biliary excretion)
Metabolites: 63%
feces, 9% urine;

60% Feces, 40%

Medications may be administered through enteral tubes,

feces and urine
90% Feces (via

respectively)
6–10% Urine

unchanged,

depending on patient-related variables and the physico-

chemical environment. Medications may be considered for
enteral administration when the tube size is ≥8 French (Fr)
gauge and either (1) enteral nutrition being delivered at a
2D6, 2C9; O-demeth-
ylation, hydroxylation)

rate sufficient to supply at least half the daily caloric re-

Hepatic (CYP3A4,

quirement and gastrointestinal abnormalities (eg, vomiting,

and conjugation)
(demethylation

cramping, distension, bloating) are absent and gastric

ER = extended release; F = fraction absorbed; GI = gastrointestinal; IR = immediate release.

residual volumes do not exceed 150 –250 mL if gastric

Hepatic

Hepatic

feeding is used or (2) other medications are being delivered

through the tube with evidence of adequate absorption.38-40,48
Medications should not be delivered via this route when
Absolute oral

tubes are being used for frequent or continuous suction-

(43–82)

ing.39,40 If drug administration via this route is necessary,

F 60

then the tube should be flushed with 15–30 mL of water

65

90

before and after administration and clamped for at least 30

minutes after drug delivery before resuming suctioning.39,40
Solutions, suspensions, elixirs, or other liquid formulations
of medications should be chosen whenever possible (Table
18–36

2).8,43 Extended-release formulations should never be deliv-

8–10

24

ered through a tube, since any modification to the formula-

tion may cause the immediate release and subsequent sys-
temic exposure of the entire dose.38-41 Similarly, enteric-coat-
ed or microencapsulated formulations should not be
α-Adrenergic blocking agents
2–6

2–3

crushed, as they may clog tubes. The intravenous formula-

tion of an antihypertensive agent should not be administered
enterally as absorption may be erratic. Immediate-release
2–3

tablets may be crushed and capsules opened and diluted pri-

2

or to administration; however, the tube should be flushed

Doxazosin

Terazosin

with at least 30 mL of water before and after medication de-

Prazosin

livery.38,41 Medications should never be mixed with tube

feedings. The absorption profiles of some antihypertensives

theannals.com The Annals of Pharmacotherapy n 2010 September, Volume 44 n 1439

JF Dasta et al.
change when the drugs are administered with food (Table
2),8,42 since systemic absorption may be altered. Clinicians
may temporarily stop the administration of enteral nutrition
around the enteral delivery of these agents (eg, 30 minutes
before and 2 hours after).38-41
The tube size and anatomic site of delivery must also be
considered.38-41 Larger tubes (≥14 Fr) are less likely to be-
come occluded than are small-bore tubes (4–12 Fr) when
medications are administered.38,39 In general, medications
should not be delivered through tubes <8 Fr gauge due to the
risk of clogging.40 The stomach is able to tolerate more con-
centrated and hyperosmolar formulations than the small
bowel.38,39 This is particularly important for extemporaneous-
ly compounded liquid formulations of antihypertensives that
may contain diluents and preservatives (Table 2).38-42 There-
fore, hypertonic solutions may require additional dilution if
they are administered into the small bowel.40 Diluents such as
sorbitol or glycerol may cause cramping or diarrhea. Small
bowel feeding tubes may end in the duodenum or jejunum.
Hence, jejunal administration of medications may limit the
extent of first-pass hepatic metabolism, resulting in increased
absorption, but the small lumen may limit their use for ad-
ministering medications.38,39
Disease State–Specific Issues
CARDIOVASCULAR DISEASE
Nearly 75% of patients with cardiovascular disease have
hypertension, validating that hypertension is a major risk
factor for the development of coronary artery disease.49
Generally, transition to oral therapy in patients with cardio-
vascular disease can begin once the systolic blood pressure
is approximately <120 mm Hg for 24 hours and the patient
can tolerate oral therapy, with appropriate monitoring. A
key factor in transitioning these patients is to consider their
intravascular volume status. If the patient is volume deplet-
ed, restoration of volume will be necessary to maintain ad-
equate organ perfusion and for maximum benefit of anti-
hypertensive therapy.13
In patients with heart failure who are receiving aggres-
sive dosing of diuretics, transition of antihypertensives
should be undertaken with extra caution to avoid hypoten-
sion. This is particularly relevant for angiotensin-convert-
ing enzyme (ACE) inhibitors that can cause first-dose hy-
potension in patients with intravascular depletion. Caution
is also needed while initiating afterload-reducing agents
with other antihypertensives. Additionally, if the patient
was receiving intravenous or intramuscular hydralazine,
the antihypertensive effect is variable and can last up to 12
hours.50 In patients with myocardial infarction or acute
coronary syndrome, it is important to evaluate risk factors
and ejection fraction when considering transitioning to
ACE inhibitors and it is paramount to continue β-blockers
unless contraindicated.
1440 n The Annals of Pharmacotherapy n 2010 September, Volume 44
Finally, in patients who undergo cardiothoracic surgery
or those with aortic aneurysm, it is best to avoid using hy-
dralazine and nifedipine. If treatment is being transitioned
to an oral agent that is associated with reflex tachycardia,
such as hydralazine or minoxidil, β-blockers must also be
administered. Maintaining intravascular volume status dur-
ing the oral transition in these patients is also important.
SURGERY/TRAUMA
Acute postoperative hypertension (APH) develops in
3–34% of patients undergoing surgical procedures, includ-
ing trauma patients.51 The overall frequency depends on
the patient population, type of surgery, and the hyperten-
sion definition used. Elevations in blood pressure most
commonly occur within 30 – 60 minutes postoperatively
but can last for hours or days despite treatment.51 The ex-
ception is patients with preexisting essential hypertension
who may require antihypertensive therapy throughout their
hospitalization and following discharge.
Management strategies for APH should first be focused
on reversible or treatable causes postoperatively.52 Most
notable are pain and anxiety that may elevate blood pres-
sure, requiring the use of analgesics and sedatives. Fluid
overload can also lead to APH. Hypervolemia-associated
APH may require the use of loop diuretics, and hence care-
ful attention to input and output values.
Patients with preoperative essential hypertension should
have their preadmission antihypertensive medications, es-
pecially β-blockers, continued until their surgical proce-
dures are completed and restarted postoperatively when
they are stable to avoid antihypertensive withdrawal syn-
drome.52 Often, alternative parenteral antihypertensives
may be needed until the patient is able to tolerate oral med-
ications. Thereafter, his/her preadmission antihypertensive
therapy can be restarted. Other surgery and trauma patients
with APH unresponsive to nonspecific therapy noted
above (eg, analgesia, sedation, diuretics) or without any
treatable cause should be considered candidates for short-
term administration of intravenous antihypertensives.
Transition to oral therapy will be based on whether or
not ongoing blood pressure control is needed. Patients
without a history of essential hypertension prior to admis-
sion may have their intravenous antihypertensives discon-
tinued after 24 hours following blood pressure normaliza-
tion without transition to oral therapy. This will ensure the
absence of diurnal variations relative to blood pressure sta-
bility. Patients with a history of essential hypertension or
with evidence of ongoing APH may be considered for
transitioning to oral antihypertensives after approximately
24 hours of reaching their target blood pressure. Daily as-
sessment of these latter variables should occur throughout
hospitalization as the patient is evaluated for conversion
from intravenous to oral antihypertensives.
theannals.com

MEDICAL ICU
The most common presentation upon admission to the
medical ICU for elevated blood pressure is hypertensive
urgency or emergency. Selection of the appropriate agent
for use in these patients requires knowing the primary
cause for the elevated blood pressure, as treatment will be
driven by management of the underlying disease state(s)
and avoidance of target end-organ damage.12,13 Due to the
wide variability of patients admitted to medical ICUs, no
single methodology can be used.
STROKE
During the acute phase of stroke, cerebral autoregula-
tion is impaired in the ischemic tissue, which could lead to
inadequate cerebral perfusion and further injury. Poor out-
comes in patients with stroke have been associated with
very high or very low blood pressures causing cerebral
edema and hemorrhage or further ischemia.53 Therefore,
the key to pressure regulation in the stroke population is to
avoid changing blood pressure “too far, too fast” and rou-
tine monitoring of the patient’s neurologic status. Mean
arterial pressure changes of less than 15–20% in the first
24 hours of injury, or more quickly (approximately 2
hours) in the presence of end-organ damage, are suggest-
ed.8
Acute blood pressure goals differ between patients with
ischemic and hemorrhagic stroke, but treatment recommen-
dations are similar.7,8 Intravenous antihypertensives may be
needed for rapid control of hypertension in the acute stroke
period; however, starting or converting to oral therapy can be
considered in the first 24 hours after injury. Studies have
shown that the use of oral antihypertensive agents (eg, la-
betalol, lisinopril, and candesartan) in the acute stroke setting
are safe and may improve outcomes.54-56 Two large prospec-
tive, randomized trials evaluating whether or not to continue
antihypertensives following acute ischemic and hemorrhagic
stroke patients are ongoing.57,58
In the clinical setting, several items should be considered
prior to administering oral medications to patients with
Table 3. Advantages and Disadvantages of Oral Antihypertensive Transition Programs
Advantages
Decreased health-care costs
Increased patient flow through the system
Decreased length of stay
Longer duration of action with oral agents
Fewer infusion-related adverse events
Expedited removal of intravenous catheters
Easier administration for nursing
Increased patient comfort and mobility
theannals.com The Annals of Pharmacotherapy
Intravenous to Oral Conversion of Antihypertensives
stroke. A swallowing study should be conducted prior to
the first dose of any oral medication to determine the ap-
propriate route (oral vs enteral) of delivery. Drug onset and
offset of action (Tables 1 and 2) should also be considered,
especially in patients with stroke and elevated intracranial
pressure, as their blood pressure may fluctuate to maintain
cerebral perfusion pressure. Agents shown to prevent pri-
mary and/or secondary ischemic stroke include ACE in-
hibitors and angiotensin receptor blockers, calcium-chan-
nel blockers, and thiazide diuretics; any of these may be
appropriate therapeutic options for these hypertensive pa-
tients.59-63
Implementing and Maintaining an Oral
Conversion Program
Implementation of an intravenous to oral conversion
program for antihypertensives requires a strategic planning
process to ensure that the objectives of the program are ev-
ident and clear and the outcomes are measurable by the in-
stitution within a reasonable time period. Advantages and
disadvantages of an oral transition program can be dis-
cussed (Table 3).
Early identification of program objectives is important.
Although the conversion from intravenous to oral antihy-
pertensives is not well studied, several common themes
from successful antimicrobial oral conversion programs
can be applied.3 Stakeholders in an intravenous to oral
conversion program include patients, physicians, nurses,
pharmacists, and administrators. Nurses can play an im-
portant role in the success of an antihypertensive intra-
venous to oral conversion program and should be in-
volved in the initial design of the program. Nurses recog-
nize when patients may be ready for oral conversion and
can collaborate with the pharmacist to make that recom-
mendation even before physicians change diet or other
orders to oral. A proposed pathway for this oral conver-
sion program is shown in Figure 1 and a checklist assess-
ing a patient’s readiness for oral conversion is shown in
Table 4.
Disadvantages
Lack of data and guidelines, including national guidelines
Longer duration of action with oral agents (in cases of overshoot)
Few oral counterparts to intravenous antihypertensives
Less drug acquisition cost savings compared to antibiotics
Different adverse effect profile
Lack of information on equivalent dosing of oral antihypertensives
n 2010 September, Volume 44 n 1441
JF Dasta et al.
SELECT TARGETED DRUGS (OR CLASSES) FOR THE
PROGRAM
Many successful programs begin with one targeted drug
or drug class.4 Targeting one antihypertensive, such as
nicardipine or nitroprusside, will simplify the implementa-
tion of the program and promote the likelihood of success
and program expansion. Selection of the initial candidate
agent for the conversion program should also be based on lo-
cal formulary and practice patterns. Although economic in-
centives are always present, the primary determinant of the
initial agent selected should be one that can successfully be
converted from the intravenous to oral formulation and lead
to meeting program objectives. Select the unit where the con-
version program will be targeted. For an antihypertensive
conversion program, starting in the cardiac or surgical ICU
may be beneficial, particularly if that unit is well organized
and has a team-based approach to patient care. Personnel in
the unit must be willing to implement new strategies to im-
prove patient care, and the communication among practition-
ers in the unit must be open and effective. Once the program
is successful in one location, others can be added.
All stakeholders should be involved in the design and
approval of the program. This involves identifying the key
steps in the adequate management of intravenous to oral
antihypertensive conversion, associating each step with a
responsible party and ensuring that communication among
the team members is maintained.
Table 4. Suggested Checklist for Determining Readiness for
Intravenous to Oral Antihypertensive Transitiona
Gastrointestinal criteria
Eating or taking other oral medications WITHOUT
nausea, vomiting, or gastrointestinal disturbances
(eg, cramping, distension, bloating) for at least 4 h
following ingestion OR
Tube feeding is being delivered through tube size ≥8 Fr
gauge AND at a rate sufficient to supply at least half the
daily caloric requirement AND gastrointestinal
abnormalities (eg, vomiting, cramping, distension,
bloating) are absent AND gastric residual volumes do
not exceed 150–250 mL if gastric feeding
Hemodynamic criteriab
CV patients: SBP ≤120 mm Hg for 24 h
Surgical/trauma patients: target BP for 24 h (oral therapy
may not be required if no history of chronic hypertension)
Medical patients: BP ≤160/100 mm Hg for 6 h
Stroke patients: achieved BP goals based on stroke type
(approximate decrease in MAP ≤15–20% of presentation
for 24 h)6,7
BP = blood pressure; CV = cardiovascular; MAP = mean arterial pres-
sure; SBP = systolic blood pressure.
a
These criteria are best developed by a multiprofessional team with a
stake in managing patients with acute hypertension.
b
These are suggested criteria based on expert opinion and are only
meant to be a general guide to therapy.
1442 n The Annals of Pharmacotherapy n 2010 September, Volume 44
UNDERSTAND PRESCRIBERS
Physicians may not initially recognize the value of an
intravenous to oral conversion program and may be un-
willing to participate.64 Loss of autonomy and pressure to
discharge patients have been reported as predominant
physician concerns when confronted with intravenous to
oral conversion programs.64 A survey of physicians identi-
fied reasons that prevented them from prescribing oral
(antimicrobial) therapy for patients for whom this would
be appropriate.65 Common reasons for continuing patients
on parenteral therapy included instability of the patient,
uncertainty about the patient’s gastrointestinal function,
lack of knowledge about which oral alternatives would be
appropriate and the bioavailability of oral agents, belief
that intravenous therapy is required by third-party payers
to keep patients in the hospital (or ICU), and simply not
considering oral conversion.4 Prescribers could also be
queried on perception of cost differences between intra-
venous and oral therapy and the role that oral therapy
plays in discharge readiness, either from ICUs or the hos-
pital.
EVALUATE METRICS
It is important to establish clear and measurable metrics
in order to determine the program’s success. Even with these
metrics in place, other unmeasured confounders can influ-
ence program success. These metrics should consist of at
least 4 sections: financial, quality, operational, and satisfac-
tion. For each metric identified, the team should provide not
only what is to be measured, but also who is responsible for
obtaining the metric, how often it should be measured, and
whether baseline data are needed before starting the project.
¨
There may be significant overlap among these 4 areas.
Financial metrics do not solely include the acquisition cost
of the medications, but also LOS in the ICU and hospital.
¨
To have appropriate meaning, the average daily census of
the ICU and illness severity measurements may be re-
quired. Quality metrics include the ability to successfully
convert patients from intravenous to oral therapy. In ad-
dition to collecting audit data on patient readiness for
oral conversion, as suggested in Table 4, one should also
¨
consider measuring (1) the date and time the hemody-
¨
namic goals were reached, (2) the date and time the oral
¨ conversion program was initiated, (3) the clinical reason,
¨ if any, that the patient could not be converted to an oral
regimen, (4) the oral therapy conversion option used
(Figure 1), and (5) the date and time that the patient
completed intravenous to oral conversion. Operational
metrics assess how well each person completed his/her
role and responsibilities. Staff and patient satisfaction
surveys would indicate how effectively the program is
working. For an antihypertensive conversion program,
theannals.com
 Intravenous to Oral Conversion of Antihypertensives

Figure 1. Intravenous to oral transition pathway. AHM = antihypertensive medication; BP = blood pressure; ICU = intensive care unit.

theannals.com The Annals of Pharmacotherapy n 2010 September, Volume 44 n 1443

JF Dasta et al.
maintenance of goal blood pressure and timely discharge
from the critical care or step-down unit are reasonable
primary objectives. Secondary objectives could include
cost savings, in addition to the outcome measures identi-
fied above. Once identified, baseline outcomes measures
should be determined to allow measurement of progress
from the program.
CREATE AND CONDUCT EDUCATIONAL PROGRAMS
Educational programs should be designed to reach all
clinicians involved in the care of patients with acute hyper-
tension. The primary purpose of the education should be to
have team members understand their roles and responsibil-
ities and to work as a team. Typically, initial and ongoing
educational efforts are needed.
CREATE AN IMPLEMENTATION STRATEGY
Identification of appropriate candidates for intravenous to
oral conversion can be accomplished by various screening
methods. For example, the intravenous label could include
a statement to assess the patient for whether the next bag or
bottle is needed or computerized prompts could identify
patients admitted to ICU for greater than 24 hours. One
study described a computerized algorithm that reviewed
patient orders daily to identify targeted drugs in their con-
version protocol.4 Once identified, the patient’s orders were
automatically examined for scheduled oral medications or
an order for an oral diet. The appropriate patient was iden-
tified for intravenous to oral conversion and an electronic
message was generated for the prescriber to review. Anoth-
er group distributed written materials to house officers,
medical students, and pharmacists.66 A nurse was used to
intervene with physicians in another study.67 The nurse
served as a hospital committee member and presented sug-
gestions for oral antibiotic conversion to physicians. Clini-
cal pharmacists have been used to suggest oral replace-
ments for intravenous antibiotics and found decreased drug
use for patients in whom the medications were converted.68
It has been suggested that decentralized pharmacists
should be targeted to speak with physicians at the appropri-
ate time in the medication use process to suggest oral con-
version.69
COMMUNICATE CLEARLY
Clear articulation of the objectives and outcome mea-
sures will improve the chances for participation by pre-
scribers and other health-care workers success of the pro-
gram. Data collection should occur concurrently, if possi-
ble, and an automated data collection system using
electronic medical records and computerized prescriber or-
der entry is ideal. Early and frequent sharing of outcome
data with stakeholders are essential to maintaining partici-
1444 n The Annals of Pharmacotherapy n 2010 September, Volume 44
pation. Data can be shared in various ways. Protocol
changes may be required when problems arise or new in-
formation becomes available.
Summary
Protocols for successful conversion to oral from intra-
venous therapies for selected drug classes are well estab-
lished and often result in improved patient care and re-
duced costs. Antihypertensives represent an additional im-
portant drug class for implementing oral conversion
programs. However, lack of national guidelines for optimiz-
ing treatment of hypertensive crisis, coupled with the wide
variety of available oral antihypertensives and the lack of a
health-care professional focused on acute hypertension, may
be reasons for the reluctance in hospitals to develop proto-
cols involving antihypertensive drugs. This article provides
hospitals with a variety of resources and practice considera-
tions that can be individualized for their environment. We
suggest that research on the impact of an antihypertensive
conversion protocol be conducted in a similar way that such
studies were performed with antimicrobials. In the interim,
hospitals can consider developing protocols for conversion
to oral antihypertensives as an attempt to reduce unnecessar-
ily prolonged intravenous therapy.
Joseph F Dasta MSc FCCM FCCP, Professor Emeritus, The Ohio
State University, Columbus, OH; Adjunct Professor, The University
of Texas, Hutto, TX
Bradley A Boucher PharmD FCCP FCCM, Professor of Clinical
Pharmacy, University of Tennessee Health Science Center, Mem-
phis, TN
Gretchen M Brophy PharmD BCPS FCCP FCCM, Professor of
Pharmacotherapy & Outcomes Science and Neurosurgery, Virginia
Commonwealth University, Medical College of Virginia Campus,
Richmond, VA
Henry Cohen MS PharmD FCCM BCPP CGP, Professor of Phar-
macy Practice, Arnold & Marie Schwartz College of Pharmacy and
Health Sciences, Long Island University; Chief Pharmacotherapy
Officer, Kingsbrook Jewish Medical Center, Brooklyn, NY
Erkan Hassan PharmD FCCM, Director of Pharmacotherapy,
Philips VISICU, Patient Monitoring Informatics; Adjunct Associate
Professor, University of Maryland School of Pharmacy, Department
of Pharmacy Practice and Science, Baltimore, MD
Robert MacLaren PharmD FCCM FCCP, Associate Professor of
Clinical Pharmacy, University of Colorado, Aurora, CO
Karina Muzykovsky PharmD, Critical Care Pharmacotherapy Spe-
cialty Resident (PGY-2), Kingsbrook Jewish Medical Center
Steven J Martin PharmD BCPS FCCP FCCM, Professor and Chair,
Department of Pharmacy Practice, College of Pharmacy, The Uni-
versity of Toledo, Toledo, OH
Steven E Pass PharmD FCCM BCPS, Associate Professor, Texas
Tech University Health Sciences Center School of Pharmacy, Dallas,
TX
Amy L Seybert PharmD, Associate Professor of Pharmacy and
Therapeutics, University of Pittsburgh School of Pharmacy; Cardio-
vascular Critical Care Clinical Pharmacist, University of Pittsburgh
Medical Center, Pittsburgh, PA
Correspondence: Professor Dasta, jdasta@mail.utexas.edu
Reprints/Online Access: www.theannals.com/cgi/reprint/aph.1P086
Conflict of interest: Professor Dasta is a consultant for and mem-
ber of the speaker’s bureau of The Medicines Company; Drs. Bouch-
er, Brophy, Hassan, MacLaren, Martin, and Pass are consultants to
theannals.com

The Medicines Company. Logistical support from The Medicines
Company is acknowledged.
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3. Athanassa Z, Makris G, Dimopoulos G, Falagas ME. Early switch to oral
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venous to oral medications. Arch Intern Med 2003;163:2585-9.
5. Katz JN, Gore JM, Amin A, et al., on behalf of the STAT Investigators.
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1446 n The Annals of Pharmacotherapy n 2010 September, Volume 44
Conversión a la vía Oral de Medicamentos Antihipertensivos
Utilizados por vía Intravenosa: Colección de Recursos de
Información Para el Desarrollo de una Guía
JF Dasta, BA Boucher, GM Brophy, H Cohen, E Hassan, R MacLaren, K
Muzykovsky, S J Martin, S E Pass, y A L Seybert
Ann Pharmacother 2010;44:1430- 47.
EXTRACTO
OBJETIVO: Proveer una colección de recursos de información para ser
utilizada en los hospitales que estén desarrollando protocolos de
conversión de medicamentos antihipertensivos usados intravenosamente
(IV) a medicamentos por vía oral (PO).
FUENTES DE DATOS: Se realizó una búsqueda de la literatura en el sistema
de información MEDLINE (1990–abril 2010) utilizando diversos
términos MESH. Se revisaron los artículos publicados en el idioma
inglés que describían protocolos para la conversión de medicamentos de
cualquier categoría terapéutica que se utilizaban por vía intravenosa para
cambiar a medicamentos por vía oral. Se evaluaron las referencias de los
artículos seleccionados para obtener información adicional.
SELECCIÓN DE ESTUDIOS Y EXTRACCIÓN DE LA INFORMACIÓN: Se
seleccionaron todos los estudios experimentales y observacionales,
además de los artículos de revisión de la literatura, publicados en inglés
y que se enfocaban en la transición a medicamentos orales cuando se
utilizaban medicamentos por vía intravenosa.
SÍNTESIS DE LOS DATOS: La mayoría de la literatura disponible discute la
conversión de IV a PO de medicamentos antimicrobiales. Existe
considerable evidencia que documenta la reducción en costos y el mejor
movimiento del paciente en el sistema de salud luego de implantados
estos protocolos con medicamentos como antimicrobiales, antagonistas
de los receptores de histamina -2 y los inhibidores de la bomba de
protones. Aunque los medicamentos antihipertensivos no han sido
estudiados, los principios, y estrategias de implantación utilizadas con
estos otros medicamentos se puede aplicar con el uso de
antihipertensivos. En este manuscrito se presenta el problema y los
beneficios de la conversión y se discuten diferentes asuntos relacionados
a cómo y cuándo hacer la conversión, los principios de absorción oral de
los medicamentos, la información pertinente a la conversión oral cuando
el paciente presenta diferentes condiciones de salud como enfermedades
cardiovasculares, trauma y cirugía, las estrategias de implantación de
estos protocolos de conversión y la documentación necesaria. También
se presentan tablas con información sobre los medicamentos
antihipertensivos orales e intravenosos, parámetros farmacocinéticos y
farmacodinámicos, regímenes de dosificación, efectos secundarios, y
precauciones de uso.
CONCLUSIONS: Los autores recomiendan que en los hospitales se
considere utilizar protocolos de conversión a vía oral de medicamentos
que se utilizan por vía intravenosa con el propósito de tratar de reducir
una terapia intravenosa prolongada. La información que se provee en
este manuscrito se puede utilizar como una colección de recursos de
información para seleccionar los datos más específicos para desarrollar
una guía de conversión de IV a PO, de acuerdo a las características
individuales de los sistemas de salud.
Traducido por Mirza Martinez
Conversion des Antihypertenseurs de la voie Intraveineuse à la Voie
Orale: des Outils pour le Développement de Lignes Directrices
JF Dasta, BA Boucher, GM Brophy, H Cohen, E Hassan, R MacLaren, K
Muzykovsky, S J Martin, S E Pass, et A L Seybert
Ann Pharmacother 2010;44:1430- 47.
RÉSUMÉ
OBJECTIFS: Fournir des outils d’information pour les hôpitaux qui
souhaitent développer des protocoles de conversion de la voie
intraveineuse (IV) à la voie orale pour les médicaments
antihypertenseurs.
theannals.com
 Intravenous to Oral Conversion of Antihypertensives

SOURCES DE L’INFORMATION: Les articles décrivant des protocoles de
conversion de la voie intraveineuse à la voie orale, pour toutes catégories
thérapeutiques, publiés en langue anglaise, et indexés dans MEDLINE
(1990–avril 2010) sous divers mots-clés MESH. Les références de
certains articles ont aussi été fouillées pour retrouver d’autre matériel.
SÉLECTION DES ÉTUDES ET DE L’INFORMATION: Les études expérimentales
et observationnelles et les articles de revue portant sur la transition de la
voie intraveineuse à orale et publiés en anglais ont été sélectionnés.
les principes et les stratégies de mise en application utilisés pour les
autres classes de médicaments peuvent leur être appliqués. Des règles
sont préposées pour identifier le problème, les éléments importants
concernant l’absorption orale, les caractéristiques de la conversion à la
voie orale propres à certaines pathologies, et les stratégies d’instauration
et de documentation. Des tableaux détaillés portant sur les
antihypertenseurs oraux et intraveineux sont présentés.
CONCLUSIONS: Les auteurs recommandent aux hôpitaux d’envisager le

SYNTHÈSE DES DONNÉES: La majorité des informations publiées portent
sur les agents antimicrobiens. De nombreuses évidences supportent une
réduction des coûts et une amélioration du cheminement du patient dans
le système de santé suite à l’implantation de protocoles de transition vers
la voie orale pour des médicaments comme les antimicrobiens, les
antagonistes des récepteurs H-2, et les inhibiteurs de la pompe à protons.
Bien que les antihypertenseurs n’aient pas été étudiés spécifiquement,
développement de protocoles visant la conversion à la voie orale
d’antihypertenseurs intraveineux dans une tentative d’abréger des
thérapies intraveineuses autrement non requises. Les informations
présentées dans cet article peuvent servir de base pour choisir les
informations afin de les adapter aux divers systèmes de santé.
Traduit par Marc Parent

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