Ios Exam 2

Front 1

Alternative Agents for HTN
Key Point

Back 1

Alternative antihypertensive agents have not been proved to reduce the risk of CV events
compared with first-line antihypertensive agents. They should be used primarily in
combination with first-line agents to provide additional BP lowering.

Front 2

Characteristics of Alternative HTN Agents

Back 2

• Most have a high risk of side effects
• Reserved for difficult to control patients as last-line agents
• Use only in combination with other agents
• Are very inexpensive, except aliskiren
• Most are dosed several times daily
• Do not have outcomes data showing ↓ hypertension-associated complications

Front 3

Alpha 1 Blockers

Back 3

Doxazosin(cardura)
Prazosin(Minipress)
Terazosin(Hytrin)

1st dose should be given at bedtime; counsel patients to rise from a sitting/laying position slowly to minimize risk of orthostatic hypotension; have additional benefits in men with BPH

*stopped early in ALLHAT trial b/c not as effective long term as ACE, thiazide, CCB

Front 4

Direct Renin Inhibitor

Back 4

Aliskiren(Tekturna)

May cause hyperkalemia in patients w/ CKD and diabetes or those receiving K-sparing diuretic, aldosterone antagonist, ACE inhibitor, or ARB; may cause acute kidney failure in pts. w/ sever bilateral renal artery stenosis or severe stenosis in artery to solitary kidney; do NOT use in pregnancy

Front 5

Central Alpha 2 agonist

Back 5

clonidine(catapres/TTS)
methyldopa(aldomet)

Abrupt discontinuation may cause rebound HTN; most effective if used w/ diuretic to diminish fluid retention, clonidine patch is replaced once/wk and not rec. in elderly

Front 6

Peripheral adrenergic antagonist

Back 6

reserpine(generic only)

very useful agent used in many major clinical trials; should be used w/ diuretic to diminish fluid retention

Front 7

Direct Arterial Vasodilators

Back 7

Minoxidil(Loniten)
Hydralazine(apresoline)

Should be used w/ diuretic and beta blocker to diminish fluid retention and reflex tachycardia

Front 8

Resistant HTN Key Point

Back 8

Patients have resistant hypertension when they fail to attain goal BP values while
adherent with an appropriate three drug regimen. This three drug regimen must include
full doses and include a diuretic.

Front 9

What Defines Patients with Resistant HTN?

Back 9

Patient requiring 4 or more antihypertensive agents to treat hypertension,
even if they are at their goal BP
- Patients not at their goal BP on 3 or more antihypertensive agents, at full
doses, one of which is a diuretic

Front 10

Patient Characteristics associated with resistant HTN

Back 10

o Older age
o High baseline blood pressure
o Obesity
o Excessive dietary salt ingestion
o Chronic kidney disease(a lot of renin secretion)
o Diabetes
o Left ventricular hypertrophy(LV thickens, overburdened, early marker of HTN damage)
o Black race(increased risk to not responding to HTN drugs)
o Female sex
o Residence in southeastern United States(lifestyle)

Front 11

Causes of Resistant HTN

Back 11

1. Improper BP measurement
- excess sodium intake
- vol. retention from CKD
- inadequate diuretic therapy

2. Drug-induced/other causes
- nonadherence
- inadequate doses
- agents from table 15-1, secondary causes of HTN (ex. NSAIDS)

3. Associated conditions
- obesity, excess alcohol intake, sleep apnea

4. Secondary HTN

***Evolving data indicate that may patients have some degree of underlying
hyperaldosteronism, emphasizing the role of adding an aldosterone
antagonist (e.g., spironolactone) in resistant hypertension

Front 12

Pharmacotherapy for Resistant HTN

Back 12

1. Assure Diuretic therapy
2. appropriate use of combo therapy
3. know when to use alternative agents

Front 13

Thiazides as drug therapy for Resistant HTN

Back 13

Thiazides have a large role as part of the regimen

Front 14

Aldosterone Antagonist Diuretic Drug Therapy for resistant HTN

Back 14

- An aldosterone antagonist as an add-on agent is highly effective

Front 15

Loop Diuretic Therapy for resistant HTN

Back 15

- Consider using a loop diuretic in patients with resistant hypertension that
have very compromised kidney function (CrCl < 30 ml/min)

Front 16

When to use alternative agents for resistant HTN

Back 16

- Never in place of recommended antihypertensive therapy in patients with
a compelling indication
- After the first line options (ACE inhibitor, ARB, CCB, thiazide) and even
after beta-blockers have been tried (or are contraindicated or not able to
be used for whatever reason)

Front 17

Why Teach Pharmacists About Nutrition?

Front 18

Obesity is the Greatest Risk Factor for:

Front 19

CVD Prevalence

Front 20

Medical Complications of Obesity

Back 20

1. Pulmonary disease
abnormal function
obstructive sleep apnea
hypoventilation syndrome
2. Nonalcoholic fatty liver
disease
steatosis
steatohepatitis
cirrhosis
3. Coronary heart disease
Diabetes
Dyslipidemia
Hypertension
4. Gynecologic abnormalities
abnormal menses
infertility
polycystic ovarian syndrome
5. Osteoarthritis
6. Skin
7. Gall bladder disease
8. Cancer
breast, uterus, cervix
colon, esophagus, pancreas
kidney, prostate
9. Phlebitis
venous stasis
10. Gout
11. Idiopathic intracranial hypertension
12. Stroke
13. Cataracts
14. Severe pancreatitis

Front 21

Why Does Increased Fat Mass Increase
Chronic Disease Risk?

Front 22

“Fat” Fat Cells and Hypertension

Front 23

Diet-Related Lifestyle Modifications That
Effectively Lower BP

Back 23

Moderation of Alcohol Intake : <2 drinks/d for men; <1 for
women

Increased Potassium Intake: 120 mmol/d (4.7g/d) level
provided in DASH Diet

DASH-TYPE Dietary Patterns: Consume diet rich in fruits &
veg (8-10 servings/day), LF
dairy (2-3 servings/d),
reduced sat fat and
cholesterol

Reduce Salt Intake: <1.5 grams/day sodium

Weight Loss: BMI <25 kg/m2

Front 24

Lifestyle Modification

Back 24

Weight reduction: 5–20 mmHg/10 kg weight loss

Adopt DASH eating plan: 8–14 mmHg

Dietary sodium reduction: 2–8 mmHg

Physical activity: 4–9 mmHg

Moderation of alcohol consumption: 2–4 mmHg

Front 25

Weight Loss

Front 26

Dietary Approaches to Stop
Hypertension (DASH)
Trial

Front 27

DASH + Sodium Restriction
Trial

Front 28

Free-Living Study on DASH Diet,
BP and Wt Loss

Front 29

Increased Potassium Intake
(through DASH-Like Diet)

Front 30

Moderate Alcohol Intake

Front 31

How vegetarian Diets effect BP

Back 31

– Have been associated with lower BP
– Some of the lowest BPs in industrialized countries are from strict
vegetarians.

Front 32

how fish oil effects BP

Back 32

Several small clinical trials have shown that high doses of omega-3
fatty acids can lower BP

Front 33

how fiber effects BP

Back 33

Supplemental fiber of 14g/d showed BP reductions of 1.6 & 2.0 mm
HG

Front 34

How Ca and Mg effect BP

Back 34

– Research has shown modest reduction in BP
with dietary calcium intake.
– Best data with women with preeclampsia
– Magnesium data inconsistent

Front 35

How carbohydrates effect BP

Back 35

– Amount and type of CHO may affect BP

Front 36

Points of Concern to think of during HTN URGENCY cases

Back 36

1. Current medications
a. Appropriateness
b. Dosing
c. Cost
2. Patient presentation
3. Plan of action, including follow-up and monitoring

Front 37

HTN Crisis Defn:

Back 37

• Critically elevated blood pressure (BP). Has been defined by different parameters
over time and most authors identify diastolic blood pressure (DBP) as the primary
factor in diagnosis
o DBP > 110-120 mmHg AND/OR
o Systolic blood pressure (SBP) > 179 mmHg
• Occurs in < 1% of all hypertensive patients
• Major risk factor for hypertensive crisis is a history of stage 2 hypertension
***These are fairly loose definitions and require evaluation of the full clinical picture***

Front 38

4 Main Causes of HTN Crisis:
List

Back 38

1. Idiopathic
2. Medication non-adherence
3. undiagnosed HTN
4. Drug Induced

Front 39

Main Causes of HTN Crisis:
Idiopathic

Back 39

Idiopathic – the rise in blood pressure could have no underlying reason behind it.
Just as HTN can occur in various types of patients, so can hypertensive crisis.

Front 40

Main Causes of HTN Crisis:
Medication Non-adherence

Back 40

Medication non-adherence – the MOST COMMON reason for hypertensive crisis.
Typically occurs in patients with diagnosed stage 2 hypertension. Can also occur
when patients abruptly stop certain agents (beta blockers, centrally acting
agents)

Front 41

Main Causes of HTN Crisis:
Undiagnosed HTN

Back 41

Undiagnosed hypertension – about 73 million people in the U.S. are estimated to
have hypertension, about 25% them are unaware, 63% are uncontrolled

Front 42

Main Causes of HTN Crisis:
Drug Induced

Back 42

Drug induced – typically stimulant type illicit drugs (cocaine, methamphetamines,
phencyclidine hydrochloride (PCP), lysergic acid diethylamide (LSD))

Front 43

Other Causes of HTN Crisis
(Besides Top 4 causes)

Back 43

- Neuro: stroke, head injury
- Endocrine: hyperthyroidism, pheochromocytoma
- Obstetric: eclampsia, preeclampsia
- Cardiovascular: MI, aortic dissection, volume overload
- Renal: acute glomerulonephritis, epogen use

Front 44

Two Types of HTN Crisis:

Back 44

1. HTN Urgency
2. HTN Emergency

Front 45

HTN Urgency
characteristics

Back 45

*** W/out immediate/ progressive end-organ damage
- Recommend lowering blood pressure within the next 24 hours
- Managed by oral agents via a few options
- Rapid (but safe) onset medications
- Adjusting current medications
- Adding on another long acting therapy

Front 46

HTN Emergency
characteristics

Back 46

*** w/ current/progressive end organ damage
- Requires immediate BP reduction, but not to normal values
- Initially treated with an appropriate parenteral drug
Ex (FYI): hypertensive encephalopathy, intracranial hemorrhage, unstable
angina, acute myocardial infarction, acute LV failure with pulmonary
edema, dissecting aortic aneurysm, stroke, progressive renal failure, or
eclampsia (in pregnancy)

Front 47

What should you ALWAYS assess for in HTN Urgency?

Back 47

ALWAYS asses for end organ damage
Heart, brain, kidneys, and eyes (Think about the risks of long-term hypertension)
What questions to ask?

Front 48

Signs of end organ damage in..
brain, eyes, heart and kidney

what do these signs mean?

Back 48

Brain: HA, mental status change

eyes: vision change, blurred vision

heart: chest pain, N/V

Kidney: increase freq. urinatino

These signs constitute EMERGENCY and pt. needs IMMEDIATE medical attn.

Front 49

HTN urgency goal:

Back 49

GOAL: decrease BP gradually over 24 hours
o Avoiding excessive/abrupt reductions in BP is advised because this can
precipitate renal, cerebral, and coronary ischemia
o Adaptive autoregulatory mechanisms of essential organs

Front 50

How do you interpret the "Cerebral Blood Flow vs. MAP" curve on pg. 3 in the notes?

Back 50

Cerebral BF remains constant over a large range of MAP(~50-150mmHg)
Patients w/ chronic HTN have a shift in the curve to the right(~125-200mmHg)
If decrease BP too quickly/try to "normalize" BP values in pts. with chronic HTN, precipitous drop in cerebral perfusion occurs(renal, cerebral, coronary ischemia)

It is IMPORTANT to understand autoregulation in this concept b/c it is integral in making rec. for managing HTN urgency

Front 51

Before you start making suggestions for treatment of HTN urgency, what must be assessed prior to your recommendation?

Back 51

Adherence

Front 52

In the clinic setting, which labs would you recommend to rule-out end-organ
damage? (this may rely heavily on the patients past medical history)

Back 52

Think about organ systems effected acutely by incrased BP
Labs:
Kidney: BMP, urinalysis
heart: EKG, chest X-Ray
Endocrine: TSH

Front 53

Two different ways to manage HTN Urgency:
List

Back 53

1. Adjust Chronic/maintenance meds
Preferred Approach

2. Initiate short-term fast-acting anti_HTN medication to patient's current regimen. Pref. add agent that coincides w/ guidlines for long term control of BP

Front 54

Managing HTN Urgency:
Adjusting chronic/maintenance medications (preferred approach)

Back 54

Adjusting chronic/maintenance medications (preferred approach)
• Adjust dose of current medication(s). This will provide a gradual reduction in BP,
which is much safer than a rapid decrease in BP.
• Add on an additional antihypertensive medication to the patient’s current
regimen. Preferably adding an agent that coincides with guidelines for long term
control of blood pressure.

Front 55

Managing HTN Urgency:
Initiate a short-term fast-acting antihypertensive agent that will help acutely
manage the patient.

Back 55

Initiate a short-term fast-acting antihypertensive agent that will help acutely
manage the patient.
• If short acting is chosen, monitor BP every 15-30 minutes
• Loop diuretics should be used with caution:
o Patients may be volume depleted secondary to BP-induced natriuresis
o Unless there is clear evidence of volume overload, avoid diuretics
• AVOID immediate-release nifedipine:
o Very rapid (too rapid) onset of action that can decrease cerebral blood flow
o Not FDA approved for treatment of hypertension (immediate release form)
o Heightened risk for MI and stroke (confirmed by multiple case reports)
o NEVER USE, especially for this indication

Front 56

Short Acting Agents for HTN Urgency
List

Back 56

labetalol
metoprolol tartrate
captopril
clonidine

Front 57

Labetolol

Back 57

alpha/beta blocker
short acting agent
SE: bronchoconstriction, heart block, bradycardia
caution: asthma, COPD

Front 58

Metoprolol Tartrate

Back 58

beta blocker
50/200 mg PO bid
SE: bronchoconstriction, heart block, bradycardia
caution: asthma, COPD

Front 59

Captopril

Back 59

ACE-inhibitor
SE: hyperkalemia, may worsen renal function
caution: CKD

Front 60

clonidine

Back 60

alpha 2 agonist
useful in cocaine related HTN
may cause rebound HTN

Front 61

How to choose treatment choice in HTN urgency

Back 61

With regard to these treatment choices, there is NO right or wrong answer; however,
one option may be more appropriate in a given patient. Look at the whole clinical
picture.
o There may be a compelling indication for a particular antihypertensive (ie
ACE inhibitor in patients with diabetes, chronic kidney disease, or congestive
heart failure)
o Monitor patients in 1 to 7 days. Appropriate follow-up is necessary to
ensure continued, optimal hypertension management
o Use JNC 7 guidelines to recommend monitoring strategies

Front 62

When to follow up HTN urgency:

Back 62

1-7 days

Front 63

Why is it important to make sure HTN urgency pts. are controlled acutely and chronically?

Back 63

Hypertensive Urgency is associated with increased risk for future cardiovascular events.

Prospective trial in Journal of Hypertension (Vlcek et al, 2008) collected data
comparing cardiovascular events suffered by hypertensive patients who were
diagnosed with hypertensive urgency (n=384) and those who were not (n=295).
o 88 patients (22%) in hypertensive urgency group vs. 42 patients (14%) in
control group had a cardiovascular event during follow-up (p = 0.005)
o Both groups had similar rates of blood pressure control ( < 135/85 mmHg)
after presentation (p = 0.12)

Front 64

Etiologies of HTN Emergency:
List

Back 64

1. pheochromocytoma crisis(CCA surge)
2. drug induced
3. eclampsia
4. head injuury
5. severe epitaxis(nosebleed)
6. cardiac
7. CNS

Front 65

Drug induced causes of HTN emergency

Back 65

Drug-Induced
- MAOI-tyramine interactions
- Overdose with PCP, cocaine, or LSD
- Drug interaction-induced hypertension
- Clonidine withdrawal

Front 66

Cardiac causes of HTN emergency

Back 66

Cardiac:
- Acute aortic dissection
- Acute left ventricular failure
- Acute or impending MI
- Coronary bypass surgery

Front 67

CNS causes of HTN emergency

Back 67

CNS
- Intracranial bleed
- Subarachnoid hemorrhage

Front 68

Onset HTN Emergency

Back 68

abrupt to hours,
occurs immediately

Front 69

DBP HTN emergency

Back 69

> or = 140 mmHg
usually b/w (110-140 mmHg)

Front 70

Ocular Findings HTN Emergency

Back 70

Papiloedema,
Blurry vision, loss of sight,
Wool spots,
Retinal hemorrhages

Front 71

cardiac findings HTN emergency

Back 71

S1/S3(swish b/c increased preload)
MI, LVH, angina
Aortic dissection

Front 72

pulmonary findings HTN emergency

Back 72

Acute pulmonary edema
Rales(fluid accumulation)

Front 73

renal findings HTN emergency

Back 73

Acute renal failure (Scr > 3 mg/dl)
(double Scr = ARF)

Front 74

CNS findings HTN emergency

Back 74

Dizziness, encephalopathy,
Confusion, weakness, stroke
Intracranial/subarachnoid hemorrhage,
Seizures

Front 75

GI findings HTN emergency

Back 75

Nausea/ vomiting

Front 76

Prognosis HTN emergency

Back 76

fatal w/in hours

Front 77

Goals of therapy
HTN Emergency
(rules of thumb)

Back 77

1. DBP ~100-110
dont aim for <100
2.calculate MAP
(2*DBP + SBP)/3
reduce MAP by 10-20%
DONT reduce by >50mmHg

Front 78

Why don't we want to NORMALIZE BP in HTN emergency?

Back 78

in HTN, body autoregulates, and shifts curve to the right.
if decrease BP too quickly, body's autoregulattory mechs can't respond.
want to decrease MAP no more than 50 mmHg in HTN pts because too much can lead to no/not enough cerebral perfusion=>stroke

Front 79

Advantages vs. Disadvantages:
Esmolol

Back 79

Advantage:
Easily titrated; continuous infusion, rapid onset,
short duration;
Metabolized by easterases in the blood and not
metabolized hepatically or cleared renally;

disadvantage:
Can’t use really use in those with
COPD or asthma (e.g.,
bronchospastic disease);
shouldn’t use in patients with
heart failure or those with heart
block or bradycardia

Front 80

Advantages vs. Disadvantages:
Clevidipine

Back 80

advantages:
Easily titrated; continuous infusion, rapid onset,
short duration;
Undergoes hydrolysis in the blood and not
metabolized hepatically or cleared renally

disadvantages:
Bottle is only good for 4 hours,
can’t use if I already have
hypertriglycerdeima or soy, soy
bean, egg allergy, every
expensive

Front 81

Advantages vs. Disadvantages:
Nicardipine

Back 81

Advantages:
Easily titrated; continuous infusion, rapid onset,
short duration; while metabolized hepatically no
dosing adjustments needed for hepatic or renal
impairment, beneficial in heart failure patients by
reducing afterload

Disadvantages:
Reflex tachycardia and expensive

Front 82

Advantages vs. Disadvantages:
Fenoldopam

Back 82

Advantages:
Easily titrated; continuous infusion, rapid onset,
short duration; vasodialtes renal arteries so may
improve GFR and urine output but this is
debateable; no dosage adjustments needed for
renal or hepatic dysfunction

disadvantages:
Reflex tachycardia and expensive

Front 83

Advantages vs. Disadvantages:
Nitroglycerin

Back 83

Advantages:
Easily titrated; continuous infusion, rapid onset,
short duration, coronary vasodilator so will help with chest pain, very cheap, works in heart failure
patients as it reduces preload, no dosing
adjustments needed for hepatic or renal
impairment

Disadvantages:
Tolerance will develop, HA,
inorder to reduce BP will need higher doses

Front 84

Advantages vs. Disadvantages:
Nitroprusside

Back 84

Advantages:
Easily titrated; continuous infusion, rapid onset,
short duration, , very cheap, works in heart failure
patients as it reduces preload and afterload

Disadvantages:
Should not use in patients with
chest pain due to coronary steal
phenomena (see below) or those
with hepatic impairment (as the
cyanide will have trouble being
converted to thiocyanate) or renal
impairment (as both cyanide and
thiocyante are cleared renally)

Front 85

What is coronary steal?

Back 85

When nitroprusside is administered it can cause a coronary steal phenomena. After an acute myocardial
infarction, the coronary arteries within the necrotic tissue are subsequently damaged. Rather than taking on the characteristics of
an artery, they act more more veins. Remember that nitroprusside is more of an arterial than a venodilator. So, when we administer
nitroprusside we vasodilate the healthy coronary arteries and NOT the damaged arteries which are actually more like veins. Blood
always follows the path of least resistance so the vasodilated coronary arteries steal away the blood away from the damaged tissue
that truly needs it thus leading for increasing necrosis. To prevent this phenomena from happening, we can administer a
venodilator like nitroglycerin with nitroprusside so that we dilate those damaged coronary arteries.

Front 86

MR is 55 year old black male, who presents to the ER with a 4-day history of increasing SOB. Over the past 2
days, he developed a severe HA unrelieved by NSAIDS, as well as substernal chest pain, anorexia, and
nausea.
PMH: Meds: NKDA
Asthma Albuterol MDI Lisinopril
Angina x 5 years Furosemide ISDN
AMI ( 2months ago) Felodipine
Physical Exam:
Current Wt: 150 lbs Ht: 5'10" BP(standing): 220/145 BP (supine): 220/142
Oxygen sat: 88% HR: 125 RR: 36 Temp: 989
Gen: slightly cachectic, anxious-appearing male
HEENT: arteriolar narrowing and AV nicking without hemorrhages, exudates, papilledema
-JVD, + bilateral carotid bruits
Card: RRR. + S3/S4 galllop , no murmurs
Resp: inspiratory rales and decreased breath sounds
GI: + Bowl signs
GU: Denies dysuria or incontinence
Extremities: warm with no edema
Neuro: Alert and Oriented x 3.
Labs:
Na = 142 mEq/L, Cl = 101 mEq/L, K = 4.9 mEq/L, CO2 = 23 mEq/L, BUN = 30 mg/dl, Scr = 1.5md/dl, Gluc = 100
mg/dl; INR = 1.08, WBC = 8.0, Hgb = 13 g/dl, Hct = 38%.

Case: Address for Signs of End organ damage

Back 86

1. CNS: severe HA unrelieved by NSAIDS, + bilateral carotid bruits. This last sign means that a
“swishing” sound can be heard over the carotid arteries that are feeding the brain. Normally I
would hear this swishing sound. By hearing this sound, this means that I have constriction
ongoing in the carotid arteries. The good thing is that this patient is still alert and oriented x 3,
meaning to time (e.g., they can tell you the time), place (eg., they know where they are) , and
person (e.g., they know their name). In the eye exam, the patient has + papilledema and arteriolar
narrowing of the vessels of the retina.
2. Cardiovascular: +S3 sound (meaning increase preload), EKG indicative of left ventricular hypertrophy, chest Xray
indicative of cardiomegaly (enlarged heart), + chest pain
3. Pulmonary: inspiratory rales and decreased breath sounds, shortness of breath
4. Renal: Increased serum creatinine (we will need to see the baseline to know if he really has acute renal
failure) but he is spilling protein and blood into his urine.
So, does he have organ dysfunction…YES. Remember this patient has multiple signs and symptoms of organ dysfunction. He only
needs ONE to qualify for HTN emergency

Front 87

Furosemide

Back 87

bad at decreasing BP, better as preload reducer
causes volume depletion, hypokalemia

Front 88

Hydralazine

Back 88

SE: drug induced lupus, tachycardia, flushing, HA, vomiting, aggravation of angina
dosed intermittently, not really used in HTN emergency

Front 89

Enalaprilat

Back 89

SE: variable response, first dose response, worsen renal failure

Front 90

labetolol

Back 90

dosed intermittently, not really used in HTN emergency
SE: vomiting, scalp tingling, heart block, orthostatic HTN

Front 91

Furosemide Dosing

Back 91

20-40 mg in 1-2 min
onset: 5-15 mins
DOA: 2-3 hrs

Front 92

Nitroprusside Dosing

Back 92

0.25-10 mcg/kg/min
(max 2 mcg/kg/min, max 7 days)
onset: immediate
DOA: 1-2 mins

Front 93

Nitroglycerin dosing

Back 93

5-100 mcg/min
(double q 10 mins if needed)
onset: 2-5 mins
DOA: 5-10 mins

Front 94

Fenoldopam dosing

Back 94

0.1-0.3 mcg/kg/min
onset: 4-5 mins
DOA: 30 mins

Front 95

Nicardipine Dosing

Back 95

5-15 mg/hr
(easily titrate q 10 mins)
onset: 5-10 mins
DOA:15-30 mins, may exceed 240 mins

Front 96

Clevidipine dosing

Back 96

1-2 mg/hr (32 mg/hr max)
onset: 2-4 mins
DOA: 5-15 mins

Front 97

Hydralazine dosing

Back 97

10-20 mg IV
10-50 mg IM
Dose intermittently
onset: 10-20min IV, 20-30 min IM
DOA: 1-4 hrs IV, 4-6 hrs IM

Front 98

Enalaprilat Dosing

Back 98

0.625-1.25 mg IV q 6 hrs
onset: 15 mins
DOA: 6 hrs

Front 99

Esmolol dosing:

Back 99

200-500 mcg/kg/min for 4 mins, the 50-300 mcg/kg/min IV
Slowly titrate up
onset 1-2 mins
DOA:10-20 mins(cleared by esterase in blood)

Front 100

Labetolol dosing

Back 100

20-80 mg IV bolus q 10 mins
dose intermittenly
onset: 5-10 mins
DOA: 3-6 hrs