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214 Cards in this Set

  • Front
  • Back
What is the treatment schedule for a pt with DM?
1) ACE-I or ARB
2) Ca-Channel Blocker
3) Diuretic
4) β-Blocker

Note: Both ACE-Is & ARBs are additionally beneficial due to renal protection
What is the treatment schedule for a pt with HF?
1) ACE-I or ARB
2) Beta-Blocker
3) Aldosterone blocker
4) Diuretics (Loop) are used for symptoms
What is the treatment algorithm for angina?
- β-Blockers
- Calcium Channel Blockers
What is the treatment algorithm for atrial tachycardia?
- β-Blockers
- Non-dihydropyridine CCBs
- ACE-I
- ARBs
What is the treatment algorithm for atrial fibrillation?
- β-Blockers
- Non-dihydropyridine CCBs
- ACE-I
- ARBs
What is the treatment algorithm for Cyclosporine-induced HTN?
- Calcium Channel Blockers
- Thiazide Diuretics (possibly)
What is the treatment algorithm for dislipidemia?
- α-blockers
What is the treatment algorithm for prostatism (BPH)?
- α-blockers
What is the treatment algorithm for essential tremor?
- Non-selective β-blockers
What is the treatment algorithm for hyperthyroidism?
- β-blockers
What is the treatment algorithm for migraine?
- Non-cardioselective β-blockers
- Non-dihydropyridine CCBs
What is the treatment algorithm for osteoporosis?
- Thiazides
What is the treatment algorithm for perioperative HTN?
- β-blockers
What drug class(es) are contraindicated in patients with a co-morbid condition such as bronchospastic disease?
- β-blockers
What drug class(es) are contraindicated in patients with a co-morbid condition such as depression?
- β-blockers
What drug class(es) are contraindicated in patients with a co-morbid condition such as dyslipidemia?
- β-blockers
- Diuretics
What drug class(es) are contraindicated in patients with a co-morbid condition such as DM (Type I/II)?
- β-blockers
- High-dose diuretics
What drug class(es) are contraindicated in patients with a co-morbid condition such as gout?
- Diuretics
What drug class(es) are contraindicated in patients with a co-morbid condition such as HF?
- β-blockers **Except carvediolol, metoprolol & bisoprolol**
- Calcium Channel Blockers **Except amlodipine & felodipine**
What β-blockers can you use in heart failure?
- Carvediolol
- Metoprolol
- Bisoprolol
What Calcium Channel Blockers can you use in heart failure?
- Amlodipine
- Felodipine
Name the four classes of diuretics.
1) Carbonic Anhydrase Inhibitors
2) Thiazides
3) Loop
4) K+ sparing
Name an example diuretic from the class Carbonic Anhydrase Inhibitors
Acetazolamide
Name an example diuretic from the class thiazides
Hydrochlorothiazide & Chlorthalidone

**Hydrochlorothiazide is one heck of a Scrabble word**
Name an example diuretic from the class loop diuretics
Furosemide & Bumetanide
Name an example diuretic from the class potassium-sparing diuretics
Triamterene & Spironolactone
Which is the most effect class of diuretics when used alone?
Thiazides

- Loops and K-sparing are only weakly effective
What are four advantages of diuretics compared to other classes?
1) Cheap
2) Q Daily dosing
3) Lots of data
4) Possible reduction in hip fractures
What are six disadvantages of diuretics?
1) Electrolyte Disturbances - Monitor SCr and K
2) Diabetes - Effects glucose
3) Gout - Effects urea
4) Hyperlipidemia - Effects cholesterol
5) Thiazides lose efficacy as kidney function decreases
6) Orthostasis, especially in the elderly
What is happens when a pt takes HCTZ and cholestryamine?
Reduced HCTZ absorption
What is happens when a pt takes a diuretic and lithium?
Serum lithium concentration is reduced
What is happens when a pt takes a diuretic and a NSAID?
NSAIDS antagonize the effects of diuretics, reducing diuresis
What is happens when a pt takes a diuretic and digoxin?
Increases the risk of digoxin toxicity
What is happens when a pt takes a diuretic and sulfonylureas?

Sulfonylureas are used in DM management and include drugs like glipizide
There is reduced sulfonylurea efficacy
What is happens when a pt takes a diuretic and cylcophosphamide, fluorouracil or methotrexate?
There is myelosuppresion
What is the three mechanisms of action of β-blockers?
1) Reduces CO via Negative Chronotropic and Inotropic Effects
2) Reduces Renin Release
3) Reduce Pulmonary Vascular Resistance
How do we differentiate among the different β-blockers?
By the following:
1) Cardioselectivity
2) ISA - Intrinsic Sympathomimetic Activity
3) Metabolism
Name an example of Non-Selective, -ISA β-blockers
- Propranolol
- Timolol
- Nadolol
Name an example of Non-Selective, +ISA β-blockers
- Pindolol
- Carteolol
- Penbutolol
Name an example of Selective, -ISA β-blockers
- Atenolol
- Metoprolol
- Bisoprolol
- Betaxolol
Name a Selective, +ISA β-blockers
- Acebutolol
What β-blockers are primary excreted via the liver?

i.e. Consider liver function
- Propranolol
- Metoprolol
- Labetaolol
What β-blockers are primary excreted via the kidney?

i.e. Consider renal function
- Atenolol
- Nadolol
What are six advantages of β-blockers?
1) Modest Cost
2) QD/BID dosing
3) Lower CAD mortality and progression
4) Lower post-MI mortality (Not +ISA drugs)
5) Lowers morbidity and mortality in CHF (metoprolol, bisoprolol, carvediolol)
6) No routine lab monitoring
What β-blockers are good for CHF?
- Metoprolol
- Bisoprolol
- Carvediolol
What is the disadvantage of β-blockers and pts with DM?
Causes glucose intolerance while masking hypoglycemia
What are eight disadvantages of β-blockers?
1) DM issues
2) May increase lipids
3) CI in asthma/COPD
4) Caution in CHF
5) Angina with ISA agents
6) Sexual dysfunction
7) Decreased exercise capacity
8) Withdrawl syndrome (rebound HTN)
What are four common side effects of β-blockers?
1) Bradycardia
2) Tiredness
3) Cold extremities
4) CNS
What β-blockers are CI in patients with angina?
ISA Agents

- Pindolol
- Carteolol
- Penbutolol
- Acebutolol
What is Nebivolol?
Bystolic - Newest β-blocker

- Selective β1 antagonist
- Vasodilation via NO release
- Similar tolerance to carvediolol
- Possible better side effect profile (glucose in DM pt)
Carvediol
Coreg

A β-blocker
Tenormin
Atenolol

A selective β-blocker
Toprol
Metoprolol

A selective β-blocker
Coreg
Carvediolol

A β-blocker
Atenolol
Tenormin

A selective β-blocker
Metoprolol
Toprol XL (Extended release form)

A selective β-blocker
Propranolol
Inderal

A non-selective β-blocker
Inderal
Propranolol

A non-selective β-blocker
What are the main concerns with the usage of β-blockers?
They do not reduce central SBP as well and that some, especially atenolol, do not lower stroke risk as well as other classes
What is the drug interaction between cimetidine and metoprolol, labetaol and propranolol?
It decreases the metabolism of these drugs
What is the drug interaction between amiodarone and β-blockers?
Causes hypotension and bradycardia
What is the drug interaction between ritonavir and β-blockers?
Leads to increased metoprolol concentrations
What is the drug interaction between digoxin and β-blockers?
AV nodal block
What is the drug interaction between 2D6 inhibitors (SSRIs) and β-blockers?
Increased metoprolol concentrations
What is the drug interaction between diltiazem/verapamil and β-blockers?
The following is increased:
1) Bradycardia
2) Hypotension
3) AV Node conduction abnormalities
What is the MOA of ACE inhibitors?
It inhibits the converison of angiotensin I to angiotensin II
What are example drugs of the class ACE-I?
- Ramipril
- Enalapril
- Lisinopril
- Benazepril

~ Basically anything that ends in -pril
What class of drug promotes the regression of left ventricular hypertrophy?
ACE-Is
What are the main benefits of ACE-Is?
1) Regression of left ventricular hypertrophy, improving sys and dia function
2) ↓ CHF mortality
3) ↓ DM nephropathy progression
4) ↓ CKD progression
5) ↓ mortality from CV causes (MI, stroke)
What is the main concerns pertaining to fluid balance with a patient taking an ACE-I?
1) Salt substitutes (contain K)
2) K supplements and K sparing diuretics
What are the advantages of ACE-Is?
1) Highly effective in Caucasians and younger pts - AA ↑ response w/ diuretic
2) Lipid neutral
3) Renal protective
4) ↑ survival in HF
5) ↓ mortality in HTN similar to conventional therapy
What are the disadvantages of ACE-Is?
1) ↑ hypotensive response in renovascular HTN, CHF, hypovolemia, + of diuretic
2) Cough (fairly common)
3) SCr and K monitoring
What conditions are ACE-I CI in?
- Pregnancy
- Bilateral renal artery stenosis (RAS) - leads to acute renal failure
What are the common SE of ACE-Is?
1) Rash
2) Angioedema
3) Hyperkalemia
4) Renal Failure (if RAS present)
What two drug classes have the annoying side effect of cough?
ACE-I and ARBs
Altace
Ramipril

ACE-I
Vasotec
Enalapril

ACE-I
Ramipril
Altace

ACE-I
Enalapril
Vasotec

ACE-I
Zestril
Lisinopril

ACE-I
Prinivil
Lisinopril

ACE-I
Lisinopril
Zestril or Prinivil

ACE-I
Benazepril
Lotensin

ACE-I

~Get it, low-tensin... ok maybe not
Lotensin
Benazepril

ACE-I
What is the MOA of angiotensin II receptor blockers (ARBs)?
It competitively inhibits Angiotensin II at the AT1 receptor
Cozaar
Losartan

ARB
Losartan
Cozaar

ARB
Valsartan
Diovan

ARB
Diovan
Valsartan

ARB
Atacand
Candesarten

ARB
Candesarten
Atacand

ARB
What are three advantages to using an ARB?
1) Similar benefits to ACE-I: ↓ CV mortality, DM nephropathy, etc
2) No lipid or glucose changes
3) Useful in combo with other anti-HTN drugs
What are three disadvantages to using an ARB?
1) Expensive
2) Cancer and CV event concerns
3) Has same ACE-I SE profile, although the cough is not quite as bad
What is the MOA of Calcium Channel Blockers?
Smooth muscle relaxation (vasodilation) via negative inotropic and chronotropic effects
What are the three classes of Ca-Channel Blockers and example drugs?
- Benzothiazepines (Diltiazem)
- Phenyalkylamines (Verapamil)
- Diphydrophyridines (Nifedipine, Felodipine, Amlodipine)
What are examples of non-Diphydrophyridines?
Diltiazem and Verapamil
What are the effects of non-Diphydrophyridines Ca-Channel Blockers?
1) Coronary and systemic vasodilation
2) Decreased myocardial contractility
3) Decreased HR
4) Decreased AV node conduction
What are the effects of Diphydrophyridines Ca-Channel Blockers?
1) Coronary and systemic vasodilation
2) None or decreased myocardial contractility
3) None or increased HR
4) NO EFFECT ON AV NODE
What is the primary risk with short-acting Ca-Channel Blockers?
Possible increased mortality via increased risk in MI via reflex tachycardia

Namely with nifedipine
What are five advantages to using Ca-Channel Blockers?
1) Good response in elderly for systolic HTN
2) Effective in CAD, reduces angina sx
3) QD dosing
4) Additive BP effects w/ ACE-I, BB
5) Lipid/Glucose Neutral
What are three disadvantages to using Ca-Channel Blockers?
1) Increased MI risk with short-acting agents
2) More expensive
3) Caution in heart failure (amlodipine, felodipine only)
What are the side effects of Ca-Channel Blockers?
1) Constipation
2) Bradycardia
3) AV Block
4) CHF
5) Edema (Peripheral)
6) Dizziness
7) HA
8) Tachycardia (esp dihydrophyridines)
9) Gingival hyperplasia (nifedipine)
Which HTN drug causes gingival hyperplasia?
The Ca-Channel Blocker Nifedipine
What are the only Ca-Channel Blockers you can use in pts with heart failure?
Amlodipine and Felodipine
Amlodipine
Norvasc

Calcium Channel Blocker
Norvasc
Amlodipine

Calcium Channel Blocker
Nifedipine
Procardia, Nifediac, Adalat

Calcium Channel Blocker
Procardia
Nifedipine

Calcium Channel Blocker
Adalat
Nifedipine

Calcium Channel Blocker
Nifediac
Nifedipine

Calcium Channel Blocker
Plendil
Felodipine

Calcium Channel Blocker
Felodipine
Plendil

Calcium Channel Blocker
Verapamil
Calan

Calcium Channel Blocker
Calan
Verapamil

Calcium Channel Blocker
Diltiazem
Cardizem or Cartia

Calcium Channel Blocker
Cardizem
Diltiazem

Calcium Channel Blocker
Cartia
Diltiazem

Calcium Channel Blocker
What is the MOA of alpha-1 antagonists?
These drugs inhibit efferent sympathetic activity.

Selective alpha-1 antagonists avoid the reflex tachycardia associated with non-selective alpha antagonists
Doxazosin
Cardura

Alpha-1 Antagonist
Cardura
Doxazosin

Alpha-1 Antagonist
Minipress
Prazosin

Alpha-1 Antagonist
Prazosin
Minipress

Alpha-1 Antagonist
What are advantages to using a Alpha-1 Antagonist?
- Positive impact on lipids
- Improves BPH symptoms
What HTN medication class is also effective in treating BPH?
Alpha-1 Antagonists
What are disadvantages to using a Alpha-1 Antagonist?
- Hypotension with 1st dose (take qHS)
- Not recommended as initial mono-tx
What are side effects associated with using a Alpha-1 Antagonist?
- HA
- Fatigue
- Drowsiness
- Weakness
- Vivid dreams
Why did the ALLHAT study not recommend a Alpha-1 Antagonist for initial HTN therapy?
Due to an increased risk in heart failure
What is the MOA for Central Alpha-2 Agonists?
Stimulate central alpha-2 receptors which inhibit sympathetic outflows

Leads to decreased NE, HR, CO and PVR
Clonidine
Catapres

Central Alpha-2 Agonists
Catapres
Clonidine

Central Alpha-2 Agonists
Methyldopa
Aldomet

Central Alpha-2 Agonists
Aldomet
Methyldopa

Central Alpha-2 Agonists
What are the advantages to using Central Alpha-2 Agonists?
- Cheap
- Neutral on lipids
- Available as a patch
- Methyldopa is safe in pregnancy
What HTN medication is first line for a patient who is pregnant?
Methyldopa
What are the disadvantages to using Central Alpha-2 Agonists?
- Withdrawl symptom; rebound HTN due to increase in NE
What are the side effects of Central Alpha-2 Agonists?
- CNS effects (sedation, lowered alertness, depression)
- Dry mouth
- Bradycardia
- Sodium/fluid retention (methyldopa)
What is the MOA of Renin Inhibitors?
Block renin (hard to believe, I know)

Prevents the conversion of angiotensinogen to angiotensin I
Aliskiren
Tekuturna

Renin Inhibitor
Tekuturna
Aliskiren

Renin Inhibitor
What are the side effects to renin inhibitors?
- GI (diarrhea)
- Cough
- Rash
- Hyperuricemia
- Gout
- Kidney Stones
What are the advantages to using a renin inhibitor?
- Well-tolerated
- No dose reduction in elderly or hepatic/mild-renal impairment
- Safe in combo with ARB/CCB/thiazide
- Little hyperalkemia
- Reduced incidence of: rash, cough, angioedemia when compared to ACE-I/ARB
What are the disadvantages to using a renin inhibitor?
- Expensive
- Avoid combo with ACE-I / ARB in diabetics
- High fat meal reduces absorption
- Half-life (Qdaily dosing)
- Metabolized by 3A4
What is the MOA of direct vasodilators?
- Cause direct arteriolar smooth muscle relaxation
What drug class is known as the afterload reducing agents and what does this mean?
Direct vasodilators

- Decrease systemic pressure in the arterial system
- Impedance to myocardial contractility
Hydralazine
Apresoline

Direct Vasodilator
Apresoline
Hydralazine

Direct Vasodilator
Minoxidil
Direct Vasodilator
What are the advantages to using direct vasodilators?
- Cheap
- Added with isosorbide is useful in CHF
What are the disadvantages to using direct vasodilators?
- Reflex sympathetic activation leads to increased HR & CO, renin release
- Increase in angina in pts with CAD
What are the side effects to direct vasodilators?
- Hypertrichosis with Minoxidil (Remember a hairy Heidman)
- Lupus-like syndrome with Hydralazine
- Dermatitis
- Drug Fever
- Peripheral neuropathy
- Hepatitis
- HA
What is the MOA for Postganglionic Sympathetic Inhibitors?
These deplete NE from postganglionic nerve terminals which inhibit NE in response to sympathetic stimulation

Decrease CO and PVR
What are Postganglionic Sympathetic Inhibitors usually reserved for in HTN management?
Almost always for refractory HTN
Guanethidine
Ismelin

Postganglionic Sympathetic Inhibitors
Guanadrel
Hylorel

Postganglionic Sympathetic Inhibitors
Hylorel
Guanadrel

Postganglionic Sympathetic Inhibitors
Ismelin
Guanethidine

Postganglionic Sympathetic Inhibitors
What are the advantages to using
Postganglionic Sympathetic Inhibitors?
- Cheap
- Highly effective
What are the disadvantages to using
Postganglionic Sympathetic Inhibitors?
- Orthostatic Hypotension
- Syncope
What are the side effects for
Postganglionic Sympathetic Inhibitors?
- Impotence
- Diarrhea
- Weight Gain
What is the MOA for Reserpine?
It depletes NE from sympathetic nerve endings, blocking transport of NE into the storage granules.

This decreases sympathetic tone and depletes catecholamines
What are the advantages to using Reserpine?
- Cheap
- Highly efficacious
What are the disadvantages to using Reserpine?
- ***Depression
- Sedation
- Na/Fluid Retention
- Diarrhea
What was the purpose of the ALLHAT Trial?
Antihypertensive and Lipid Lowering Treatment to Prevent Heart Attack Trial

To test whether or not there are differences between classes of anti-HTN agents
What is the BP goal of the ALLHAT trial?
<140/90 mmHg
What was type of control was indicated as needed for patients by the ALLHAT trial?
Therapy requiring at least 2 agents is most likely required.

For diabetics, the name of agents is likely >2 drugs
What type of HTN is a unique characteristic of the elderly population?
Isolated systolic hypertension
What drug class(es) do you use to treat Isolated Systolic Hypertension?
Beta-blockers

Watch changes to lipids, metabolic effects and renal/liver metabolism
What are considerations to be made in choosing a therapy in the elderly?
1) BP reduced slowly and cautiously
2) Lifestyle modifications
3) Target BP <140/90
4) Non-drug therapy
5) Agents started at lowest dose, then titrated
6) ADR more common
What class of drug would you want to avoid in elderly patients with CHF?
CCBs
What is the HYVET study?
Hypertension in the Very Elderly Trial

Age >80 years old, HTN drugs were effective
What is pre-eclampsia?
An increase in BP (30/15) occurring after the 20th week of pregnancy.

Accompanied by edema, proteinuria or both
What drug classes are contraindicated in pregnant women?
ACE-Is and ARBs
When are diuretics okay to use in pregnant women?
If they were used for chronic HTN prior to the pregnancy and if volume depletion is avoided

Do not use for women with pre-eclampsia
What are the drug therapy considerations in african american populations?
1) Use diuretics first
2) CCBs and alpha/beta blockers effective

Avoid mono-tx with beta-blockers and ACE-I (less effective)
How do you treat resistant HTN?
- Use drugs with complimentary MOAs
- Assess efficacy of each new med
- Discontinue those who do not work
- Retry different combinations
- Consider home BP readings
Define: "Hypertensive Emergency"
Acute, marked elevation

DBP > 120mmHG

Leads to acute and progressing end-organ damage
Define: "Hypertensive Urgency"
Acute elevation in BP

Not immediately life-threatening and preventing no symptoms or progressing TOD
Define: "Malignant Hypertension"
Marked elevated BP that is a life-threatening emergency.

Possesses encephalopathy or nephropathy and papilledema
Define: "Accelerated Hypertension"
Similar to malignant HTN, but with no papilledema or other complications

Less rapidly progressive as well
What are the risk factors for a hypertensive crisis?
- Pheochromocytoma
- Renal Vascular Disease
- Poorly-controlled accelerated essential HTN
- Noncompliance with therapy
Describe some of the signs and symptoms of a hypertensive crisis
CNS - HA, dizziness, N/V, anorexia, confusion, slurred speech, nystagmus

Heart - acute CHF, angina, MI

Eyes - Blurred vision, loss of eyesight, funduscopic findings

Kidneys - hematuria, proteinuria, pyelonephritis, elevated BUN & SCr
What are the different signs between urgency and emergency hypertensive crises?
Emergency crisis has TOD, CNS & Heart signs

Urgency crisis has minimal TOD, HTN associated with CAD, post/pre-op HTN
How are hypertensive emergencies treated?
Immediate BP reduction via IV agents

Reduce mean arterial BP by no more than 25% within minutes to 2 hours with a goal of 160/100 within 2-6 hours
How would you treat a hypertensive urgency?
Use of oral antihypertensives over several hours to days
Under what circumstances would you not use oral hypertensives for a hypertensive urgency?
If:

1) Perioperative HTN
2) Intractable epistaxis
3) Sympathomimetic drug overdose
4) Increaed circulating catecolamines
5) MAOI-tyramine interaction
What oral agent should you avoid in a hypertensive crisis and why?
Nifedipine

The short acting form has been associated with CVA, MI and death due to profound hypotensive response precipitating cerebral and coronary ischemia
Name the parenteral agents discussed in lecture
1) Nitroprusside
2) Nitroglycerin
3) Hydralazine
4) Labetaolol
5) Esmolol
6) Fenoldopam
7) Phentolamine
What is the MOA of nitroprusside?
Direct-acting arterial and venous vasodilator

Does not affect CO and increases myocardial contractility and HR in pts without CHF
What is the agent of choice when a minute to minute control is needed in a hypertensive crisis?
Nitroprusside
What are the disadvantages of nitroprusside?
1) Metabolized to cyanide, then thiocyanate. Must monitor levels if infused for >72 hours
2) Increased risk of renal dysfunction
What are advantages to using nitroprusside?
1) Rapid action
2) Fast on/off
3) Can adjust infusion to meet BP goal
4) No sedation
What are the side effects to nitroprusside?
- Fatigue
- Nausea
- Anorexia
- Disorientation
- Psychotic Behavior
- Muscle Spasms
What is the MOA of nitroglycerin?
... Just kidding

Aterial and Venous vasodilator which decreases preload, afterload and myocardial oxygen demand
What parenteral agent should be avoided in patients with hypertensive encephalopathy?
Nitroglycerin

Increases intracranial pressure
What is a concern with prolonged use of nitroglycerin?
Tachphylaxis after a use of >24-48 hours
What is the MOA of hydralazine
Arterial vasodilator which decreases TPR

Reduces dias > sys
What are the disadvantages to using hydralazine as a parenteral agent?
- Increased intracranial pressure
- Increased pressure wave (avoid in aortic dissection)
- Marked reflex tachycardia
- Increased Oxygen demand
- May precipitate chest pain in pts with CAD
What is the parenteral agent of choice for a hypertensive crisis in pregnant women?
Hydralazine
What is the parenteral agent of choice for a hypertensive crisis in patients with renal insufficiency?
Hydralazine
When is using parenteral labetaolol useful?
In pts with CAD or MI as it reduces myocardial oxygen demand
What is the MOA of Esmolol
Fast-acting cardioselective beta blocker for IV use
What are the advantages to using Esmolol?
- Easily titratable
- Rapid onset and cessation
- Metabolized by RBC's (no hepatic or renal involvement)
What are the side effects of Esmolol?
- Diaphoresis
- Dizziness
- Nausea
What is the MOA of Fenoldopam?
Selective post-synaptic dopaminergic receptor aganoist

Peripheral vasodilator causing diuresis and natriuresis while increasing renal blood flow
What are the side effects to Fenoldopam?
- HA
- N & V
- Flushing
- Increased IOP
What are the benefits to using Fenoldopam?
As a parenteral agent it has an immediate onset of action with a similar efficacy to nitroprusside
What is the MOA of Phentolamine?
Non-selective alpha blocker
What drug is most effective in a hypertensive crisis pertaining to excessive catecholamine?

i.e. pheochromocytoma, cocaine, amphetamine ODs, MAOI crisis
Phentolamine
What is the preferred hypertensive crisis treatment in a patient with acute pulmonary edema?
Nitroprusside or Fenoldopam w/ nitroglycerine and a loop diuretic
What is the preferred hypertensive crisis treatment in a patient with acute MI?
Labetaolol or Esmolol in combination with nitroglycerine
What is the preferred hypertensive crisis treatment in a patient with Hypertensive Encphalopathy?
Labetalol, Nicardipine or Fenoldopam
What is the preferred hypertensive crisis treatment in a patient with acute aortic dissection?
Labetalol OR combo of nitroprusside or fenoldopam with Esmolol
What is the preferred hypertensive crisis treatment in a patient with eclampsia?
Hydralazine
What is the preferred hypertensive crisis treatment in a patient with acute renal failure/microangiopathic anemia?
Fenoldopam or nicardipine