HTN Flashcards
+New Scheme
Categories of BP in Adults
- Normal:
- Elevated:
- Stage 1 HTN:
- Stage 2 HTN:
Inidividuals with SBP and DBP in 2 categoires should be designated to the ____ BP category
Based on average of > __ careful readings obtained on > __ occasions
- < 120 and <80
- 120-129 and <80
- 130-139 or 80-89
- > 140 or > 90
higher
2, 2
Hypertension
- BP is based on a mathematical equation:
- BP = ____ x _____
- Increased BP can result from either ____ in __ or ___
- Controlled by (2) systems
- Equation
- BP = CO x SVR (cardiac output, systemic vascular resistance)
- Increase, CO, SVR
- Sympathetic nervous system
- Renin-angiotensin-aldosterone system (RAAS)
- CO = SV/HR*
- Renal homeostasis is V important- thats why HTN is so hard to tx in those with CKD*
Regulation of BP
BP = CO x SVR
Sympathetic nervous system:
- Works on CO by?
- Works on SVR by?
Sympathetic nervous system is your “fight or flight” response -> increases BP when needed
- Activation of B1 receptors on the heart
- Activation of a1 receptors on the vasculature
Regulation of BP
BP = CO x SVR
RAAS system
- Angiotension -> Renin -> Antiotensin I -> ACE -> Angiotensin II ->
- Adrenal Cortex -> Aldosterone -> ________________
- Blood Vessels -> _____________
- Sodium and Water Retention
- Vasoconstriction
- Ang II is a very potent vasoconstrictor*
- So unless your in septic shock we don’t want lots of Ang II-> it’ll really boost your BP*
- Aldosterone is very CARDIOTOXIC -> so we try to target in HF*
Determinants of BP
- Afterload = amount of pressure heart has to exert to get blood out*
- End diastolic volume, end systolic volume*
- EF normal = 50%, Normal SV for an adult is about 70cc*
Regulation of BP
- Causes of increased CO
- Increased fluid _____ (____ sodium and water)
- Excess stimulation of _____
- Sympathetic nervous system ______
- Causes of increased SVR
- Excess stimulation of _____
- Sympathetic nervous system ______
- CO
- volume (excess)
- RAAS
- overactivity
- SVR
- RAAS
- overactivity
+Medications Used to Treat Hypertension
(8)
- Diuretics
- B Blockers
- Angiotensin converting enzyme inhibitors (ACEI)
- Angiotensin receptor blockers (ARB)
- Calcium Channel Blockers (CCB)
- a1 receptor antagonists
- a2 receptor agonists
- Vasodilators
Diuretics Patho
- Diuretics MOA are differented by?*
- Proximal tubule is were most of NA is reabsorbed HOWEVER?*
- Where they work in the kidneys*
- Is actually the WEAKEST! Bc other parts later in the kidney adapt/compensate , therefore diuretics that target reabsorption later in the kidneys are more effective*
Diuretics
- Initial BP decrease:
- Decrease blood _____ -> decreases ___
- Compensatory increase in ____
- Sustained BP decrease
- Decrease SVR -> decrease in _____ content of smooth ____ cells
- Inital
- volume, CO
- SVR
- Sustained
- sodium content, muscle
Diuretics that are the most potent are not really used for BP, theyre reserved for ppl with HF -> ex) Loop diuretics not used for HTN
+Diuretics
- SVR decreases overtime*
- CO decreases bc decreases preload*
+Diuretic Medications
(4)
- Classificaton of diuretics are based on the MOA in the _____
- nephron
- Carbonic Anhydrase Inhibitors
- Loop Diuretics
- Thiazide Diuretics
- Potassium Sparing Diuretic
Carbonic Anhydrase Inhibitors
MOA
- Inhibit_______ _______ in the _____ tubule
- Increase ________ fo HCO3 (bicarbonate)
- _____ produce potent diuresis of sodium and water
- carbonic anhydrase, proximal
- excretion
- Does NOT
- So they work where there is most reasorption of Na and Water -> but NOT POTENT for diuresis and HTN bc of all the distal tubules*
- Is used for altitude sickness, breathing on vents, gets rid of excessive bicarb ot help ICU pts breathe, HCO3- alkalinizies urine for icu pts*
- Causes accumulation of carbonic acid by preventing its breakdown*
+Carbonic Anhydrase Inhibitors
(1)
Acetazolamide (Diamox)
+Carbonic Anyhdrase Inhibitors
Therapeutic Uses (4)
Not effective for?
- Glaucoma
- Urinary alkalinization
- Metabolic alkalosis
- Acute mountain sickness
Not an effective class to use for diuresis and management of hypertension
Carbonic Anhydrase Inhibitors
AE (5)
- Metabolic Acidosis
- Renal stones
- Drowsiness
- Parasthesias
- Hypersensitivity reactions
+Loop Diuretcs
MOA
- Inhibits sodium reabsorption in the:
- Promotes up to ___ sodium and water excretion
- Increases urinary excretion of:
- ascending limb of LOOP OF HENLE
- 25%
- other electrolytes
- Water follows salt*
- Main problem is other electrolyte losses*
+Loop Diuretics
(4)
Furosemide (Lasix)
Bumetanide (Bumex)
Torsemide (Demadex)
Ethacrynic acid (Edecrin)
- Ethacrynic = an oldie, only one that doesn’t have a sulfamoity so only really used if allergic to others -> not used bc V expensive esp the IV version*
- LASIX -> aka “Lasts six hours”*
+Loop Diuretics
Routes
PO and IV
+Loop Diuretics Dosing
- _____ is most potent*
- ________ of furosemide is not the best - we use it commonly bc its the first one, nonexpensive, however ppl get tolerant through “diuretic ______”, which is now when we ould ______ to bumetanide or torsemide*
- Bumetanide*
- Bioavailability, “resistance” , switch*
Loop Diuretics
- Oral Bioavaliability
- Furosemide__-__%
- Bumetanide __-__%
- Torsemide __-__%
- Excreted by the ______
- _____ duration in renal dysfunction
- Bioavailability
- 10-70%
- 80-100%
- 80-100%
- Kidneys
- Prolonged
+Loop Diuretics
- Therapeutic Uses
- States of volume ______: ____ effective for fluid _____
- _____ extensively used in the ________ tx of high BP
- Serum electrolyte ______ -> therefore sometimes also used when pts are ____ or ______
- Uses
- overload: very, elimination
- Less, maintenance
- imbalances ,hyperkalemic or hypercalcemic
+Loop Diuretics
AE (8)
- Hypotension
- Hyponatremia
- Hypochloremia
- Hypokalemia*
- Hypomagnesemia
- Hypocalcemia
- Ototoxicity (from high IV doses)
- Azotemia = renal injury (BUN/CR > 20 -> better thing about stopping lasix, pt is dry)
Loop Diuretics
- Loop diuretics have a “______” effect
- ____ doses do ___ further _____ diuresis
- Differ from pt to pt: ____ ____ thresholds identified clinically
- Tolerance
- _____ of distal ____/collecting ___
- ______ sodium reabsorption in ____ segments
- “ceiling”
- Higher, not, increase
- Patient specific
- Tolerance
- Hypertrophy, tubules, ducts
- Increased, distal
- The dose that makes them pee is uaully their max dose*
- Maladaptive process -> gotta start giving more frequently/increasing doses when resistance starts*
+Thiazide Diuretics
MOA
- Inhibits sodium reabsorption in the:
- Promotes up to ___ sodium and water excretion
- Increases urinary excretion of:
- distal tubule
- 5%
- other electrolytes
Less potent than LOOP which is V potent
+Thiazide Diuretics
(5)
- Hydrochlorothiazide (Microzide)
- Chlorothiazide (Diuril)
- Metolazone (Zaroxolyn)
- Chlorthalidone (Thalitone)
- Indapamide (Lozol)
+Thiazide Diuretics Routes
- Hydrochlorothiazide:
- Chlorothiazide:
- Metalazone:
- Chlorthalidone:
- Indapamide:
- PO
- PO, IV
- PO
- PO
- PO
+Thiazide Diuretics
- Therapeutic Uses
- Treatment of:
- Allow for __-__ weeks for max effect on BP
- The effectiveness of diuretics is diminished when ____ falls below ___ mL/min
- Less extensively used in tx of:
- Treatment of:
- Therapeutic Uses
- HTN
- 2-4 wks
- CrCL, <30
- Acute edema
- HTN
- Commonly used ot treat BP but doesn’t work well in advanced/chronic CKD*
- Thiazides are first line agents for BP, but don’t work as well for Edema like Loop Diuretics do*
+Thiazide Diuretics
AE (8)
- Hypotension
- Hyponatremia
- Hypokalemia
- Hypomagnesemia
- Hypercalcemia
- Increased uric acid
- Increased plasma glucose levels
- Azotemia
- Notice its HYPERCALCEMIA -> diff between loop and thiazide*
- Beneift: may help with bone loss in older adults bc of hypercalcemia*
- Con: increases uric acid -> gout “The GOUCH, OUCH it hurts”*
- Slight bump in glucose levels, not significant, still given in DM pts*
Loops and Thiazides
- Loop diuretics block Na+ reabsorption in the ______ of _____
- Results in ____physiologic Na+ concentrations in _____ nephron segments
- _____/hyper-____ of ____ nephron segments
- _____ NA+ reabsorption
- Reduced _____ of loop diuretics
- Use of thiazides in combo with loop diuretics:
- Sample combination regimen:
- loop of Henle
- supra, distal
- Hypertrophy/hyper-function, distal
- Increased
- natriuresis
- blocks Na+ reabsorption in distal nephron segments
- Metolazone 5-10mg PO follwed by Furosemide 80mg IVP
The whole idea is they work in concert together (synergistic effect) - only really done in the hospital though
+Potassium-Sparing Diuretics
MOA
- Acts at _____ _____\_to inhibit sodium reabsoprtion
- Promotes up to ____ sodium and water excretion
- Blocks effects of ______ in kidney
- collecting duct (faaarrr away in very last part of nephron)
- 2%
- aldosterone
+Potassium Sparing Diuretics
(2)
- Triamterene (Dyrenium)
- Spironolactone (Aldactone) (also an aldosterone antagonist)
+Potassium Sparing Diuretics
- Therapeutic Uses
- Protect against _____ with other diuretics
- ____ ____ (aldosterone antagonist)
- _____ hypertension
- Therapeutic Uses
- hypokalemia
- Heart Failure
- Resistant
- Triameterene almost soley used to protect against hypokalemia*
- Spironolactone is a * for HF*
- These drugs not really used for HTN but for SE of other diuretics*
+Potassium Sparing Diuretics
Routes
PO
+Potassium Sparing Diuretics
AE (5)
- Hypotension
- N/V, constipation, diarrhea
- Hypercalcemia
- Hyerkalemia
- Gynecomastia (spironolactone)- (again the gynecomastia more pertinent in HF -10% of male pts get it when taking it for HF)
+B Blockers
MOA
- Blocks B1 receptors in _____ muscle
- ____ HR ( negative _____ effects)
- ____ CO (negative _____ effects
- _____ release of ____ from the kidenys
- Some agents ____ activity of the _____ nervous system
- Some agents directly _____:
- cardiac
- Decrease (chronotropic)
- Decrease (inotropic) - decreasing contractility -> decreases CO
- Inhibit, renin
- inhibit, sympathetic
- decrease peripheral vascular resistance
+B Blockers
MOA
The main thing we care about with B-Blockers is they drop CO, and act pretty quickly after admin
+B Blockers
(6)
- Atenolol (Tenormin) most commonly used - convenient bc once per day
- Carvedilol (Coreg)
- Esmolol (Brevibloc)
- Labetalol (Trandate)
- Metoprolol (Lopressor, Toprol XL)
- Propanolol (Inderal) - oldest and historical gold standard
B Blockers
- Other therapeutic uses
- _____ pectoris
- M_____ i_____
- _____ failure
- Ventricular ______
- ______ prophlyaxis
- _______ thyroidism
- G_______
- Are B Blockers used for HTN ?
- Therapeutic uses
- Angina
- MI
- Heart
- arrhythmia
- Migraine
- Hyperthyroidism
- Glaucoma (eyedrops)
- NOT popular for HTN, 2nd or 3rd line agent, however first line for lots of ther stuff
B Blockers Selectivity
- Pharmacological differences
-
B selectivity
- __B1-adrenergic receptors are located in the ____
- B2-adrenergic receptors are located in the ____
- NOTE: selectivity is?
-
a1 blockade
- __Decrease ______ stimulation causing _______
-
B selectivity
- Differences
- B selectivity
- Heart
- Lungs
- NOT ABSOLUTE
- a1 blockade
- sympathetic, vasodilation
- B selectivity
So obvs with pulmonary disease you want B1 selective
B Blockers
- Pharmacological Differences
- Intrisic ______ activity (ISA)
- Causes activation of _____ receptors producing effects similar to stimulation of the _ _ _
- ______ solubility
- ______ agents have larger volumes of distribution
- ______ agents depend more on renal function for elimination
- Intrisic ______ activity (ISA)
- Pharmacological Differences
- sympathomimetic
- adrenergic, SNS
- Lipid
- Lipophilic
- Hydrophilic
- sympathomimetic
- Not really gonna talk about this bc we tried making a BB agonist/antagonist essentially to derease SE of BB “have my cake and eat it too” but didn’t pan out*
- Lipid solubility -> matters bc contributes to SE*
+B Blockers Chart
Most important things: Beta selectivity bc of SE (don’t really care about ISA)
+B Blockers
AE
- ____tension
- ___________* related to ____ selectivity!!
- _____cardia
- F_____, exercise _____
- D____, C_____, A____, Ps____
Cautions
- What happens with abrupt discontinuation?
- Contraindication with what type of pts?
- Hypotension
- Bronchospasm
- Bradycardia
- Fatigue, exercise intolerance
- Depression, confusion, agitation, psychosis
- Rebound hypertension
- Poorly controlled diabetic pts (masks S/S of hypoglycemia)
Bc they work on sympathetic nervous system -> fatigue, exercise intolerance -> happens quick! “They’re on a walk then boom, i get tired all of sudden -> another reason why we don’t use for HTN bc these patients obv should exercise”
Angiotensin Converting Enzyme Inhibitors (ACEI)
MOA
- _____ RAAS by preventing conversion of ______ to ______ -> decreased ______ -> decreased ___
- Inhibits ______ of ______ and _____ synthesis of _____ prostaglandins
- Inhibits, angiotensin I, angiotensin II, systemic vascular resistance, BP
- degradation, bradykinin, increase, vasodilating
+Angiotensin-Converting Enzyme Inhibitors (ACEI)
MOA
Some SE of ACEI related to inability of bradykinin to break down -> lvls will go up
ACEI
(4)
Routes
How long do they take to work?
Captopril (Capoten) PO
Enalapril (Vasotec) PO
Lisinopril (Prinivil) PO
Ramipril (Altace) PO
Several weeks to see full effect - reevaluate in 2-4 wk of starting or changing dose
All end in pril, like other BP meds gotta give them a few weeks to work
ACEI
- Other therapeutic uses
- _____ failure
- ____ ________ dysfunction
- D____ n_____
- A____ _____ _____
- Chronic ____ ______
- ________* given when pt has HTN and CKD
- Other therapeutic uses
- Heart failure
- LV dysfunction
- Diabetic nephropathy
- Acute MI
- CKD
- NEPHROPROTECTIVE*
+ACEI
AE (5)
- Hypotension
- Hyperkalemia
- Acute renal failure
- Cough
- Angioedema
- Hyperkalemia a major problem with ACEI -> so alway check*
- Higher levels of bradykinin cause Cough, Angioedema -> robitussin doesn’t help it, just gotta swtich to another drug*
- Long term ACEI are nephroprotective but they acutely reduce GFR -> bc kidney relies on Ang II for renal blood flow -> but again long term they are a slam dunk for renal protectors (ARBS are close cousins)*
+ACEI
Significant Drug Interactions (2)
Potassium supplements
or
Potassium sparing diuretics
+ACEI
Contraindications (3)
Pregnancy (bc any drug that works on ang is teratogenic: ACE enzyme is necessary for fetal development)
Aortic Stenosis
Renal Artery Stenosis
Angiotensin Receptor Blocking Agents (ARB)
MOA
- Used in patients that can’t tolerate?
- Should probably not use if?
Selectively blocks the vasoconstrictive effects of angiotensin II by blocking binding of angiotensin II to its receptor
- ACEI due to cough
- not be use if angioedema on ACEI
+ARB
MOA
ARBS just works a bit more ____ than ACE -> net effect/differentiating effect is that it doesn’t effect _______ so only diff is the ___
downstream, bradykinin, SE
ARBS
(2)
Routes
Losartan (Cozaar) PO
Valsartan (Diovan) PO
+ARBS
AE (4)
- Hypotension
- Hyperkalemia
- Acute renal failure
- Angioedema (very rare)
NO COUGH!! Bc doesn’t influence bradykinin
+ARB
Significant Drug Interactions (2)
Potassium supplements
or
Potassium sparing diuretics
+ARB
Contraindications
Pregnancy, Aortic Stenosis, Renal Artery Stenosis
(same as ACEI)
+ACEI/ARB
MOA Chart
Pure ______ don’t really effect (2) -> which is the main way they decrease BP
Vasodilators, CO or Blood volume
Calcium Channel Blockers
MOA
- Blocking calcium entry into smooth ______
- Results in _______
- Can also effect cardiac _______
- muscle
- vasodilation
- conduction
Relaxes smooth muscle -> pure vasodilators
+Calcium Channel Blockers
Dihydrophyridines (3)
Non-dihydropyridines (2)
Routes
- Amlodipine (Norvasc) PO
- Nicardipine (Cardene) PO, IV
- Nifedipine (Adalat, Procardia XL) PO
- Verapamil (Calan) PO, IV
- Diltiazem (Cardizem) PO, IV
+Dihydropyridines (DHP)
MOA Chart
+Non-Dihydropyridines (NON-DHP)
MOA Chart
NON-DHP has additive effect of being negative chronotrope -> decreases HR bc works on AV node
+CCB
MOA Chart
Non-DHP and DHP
Effects on BP
Effects on HR
- Amlodipine is the classic: potent, cheap!*
- The non-dhp are v potent at lowering HR not rly BP -> thats why mostly used for arrhythmias (dilt for Afib)*
CCB
- Other therapeutic uses
- _____ pectoris
- _____ _____ disease
- _____ prophylaxis (non-DHP)
- _____* (non-DHP)
- Other therapeutic uses
- Angina
- PVD
- Migraine
- Arrhythmia
+CCB
DHP AE (3)
NON-DHP AE (3)
- DHP AE
- Hypotension
- HA and flushing
- Peripheral edema
- non-DHP AE
- Bradycardia
- Hypotension
- Constipation (verapamil)
+a1 Receptor Antagonists
MOA
Decrease sympathetic stimulation causing vasodilation and thus reducing blood pressure
+a1 Receptor Antagonists
Agents
Blood pressure, non-selective (3) + Routes
Prostate, selective for 1A subtype (2) + Routes
- Doxazosin (Cardura) PO
- Prazosin (Minipress) PO
- Terazosin (Hytrin) PO
- Alfuzosin (Uroxatral) PO
- Tamsulosin (Flomax) PO
a1 Receptor Antagonists
Indication
Used as last line agent in the treatment of hypertension
Another PURE VASODILATOR - salvage therapy for intoleracne to other meds or really uncontrolled HTN
a1 Receptor Antagonists
AE (2)
- First dose phenomenon -> decreased BP
- Chronic administration -> water and sodium accumulation
+a2 Receptor Agonists
MOA
Decrease sympathetic stimulation to cause vasodilation and thus reduce BP
+a2 Receptor Agonists
(2)
Routes
Clonidine (Catapres) PO, IV, Transdermal patch
Methyldopa (Aldomet) PO
a2 Receptor Agonists
Indication
Used as a last-line agent in the treatment of HTN
also helps with anxiety (clonidine)
a2 Receptor Agonists
AE (2)
Sedation and HA
Abrupt discontinuation may result in rebound HTN
Last line agents bc they have rly bad AE
+Direct Vasodilators
MOA
Causes artery relaxation (vasodilation) resulting in decreased BP
+Direct Vasodilators
(2)
Routes
Hydralazine (Apresoline) PO, IV
Minoxidil (Loniten) PO
Direct Vasodilators
AE (2)
Requires ___ admin -> results in:
Hydralazine -> Tachycardia and fluid retention
Minoxidil -> hirsutism
TID: poor adherence
Direct Vasodilators
Indication
Reserved for pts with severe hypertension
+New 2017 ACC/AHA Guidelines
clinical ASCVD rt ASCVD calculator
+Treatment Choices Part 1
1) For initation of antihypertensive drug therapy first line agents include
Thiazide diuretics
CCBs
ACE inhibitors or ARBS
+Treatment Choices Part 2
- In black adults with HTN but without HF or CKD, including those with DM, initial antihypertensive treatment should include:
- ___ or more antihypertensive medications are recommended to achieve a BP target of < than ___/___ in most adults with HTN, especially in ____ adults with HTN
- thiazides or CCB
- Two, < 130/80, black
- Biological reasoning for not using ACE/ARBS in black patients is because they have “lower renin” -> less reponse to ACE/ARB*
- Statistically significant: most ppl need TWO OR MORE meds*
+Treatment Choices Part 3
- In adults with DM and HTN, antihypertensive drug tx should be initiated at a BP of > ___/___ or higher with a tx goal of:
- In adults with DM and HTN, all first line class of antihypertensive agents are (4) are useful and effective
- In adults with DM and HTN, (2) may be considered in presence of ______.
- > 130/80, < 130/80
- Diuretics, ACEI, ARBS, CCBs
- ACEI, ARBS, albuminuria
+Treatment Choices Part 4
- Adults with HTN and CKD should be treated to a BP goal of:
- In adults with HTN and CKD (stage 3 or higher or stage 1 or 2 with albuminuria (> 300 mg/d, or > 300mg/g albumin:creatinine ratio or the equivalent in the first morning void), tx with ______ is reasonable to slow disease progression.
- In adults with HTN adn CKD (stage 3 or higher or stage 1 or 2 with albuminuria (> 300 mg/d, or > 300mg/g albumin:creatinine ratio or the equivalent in the first morning void) treatment with an ____ may be reasonable if _______ is not tolerated.
- < 130/80
- ACE inhibitor
- ARB
ACE or ARB still preferred agent for CKD*
Select a Drug Treatment Strategy
- _____ first medication before adding a ____
- ___ second agent _____ reaching _____ dose of first medication
- Start with ___ medication classes ______ or as a fixed-dose _____ (ie not typically on an ACEI and ARB)
- Maximize, second
- Add, before, maximum
- 2, separately, combination
+Hypertensive Crisis
-
Hypertensive Urgency
- __SBP > ____ and/or DBP > _____ without:
-
Hypertensive Emergency
- __Presence of an ____ significantly _____ BP (often defined as SBP > ____ and /or DBP > ____) with:
- Hypertensive Urgency
- 180, 110, without evidence of target organ damage
- Hypertensive Emergency
- abrupt, elevated, 200, 120, with concurrent target organ dysfunction (brain, heart, kidneys, eyes)
Organ dysfunction: Chest pain/other symptoms
Hypertensive Crisis Goals
- Urgency
- lower _____ to goal or near goal within ___ hrs: oral ___ can be used
- Emergency
- lower ____ by ___% or ____ pressure to __-__ mmHg within __-__minutes
- Exceptions for (3) conditions
- Urgency
- MAP, 24hrs, meds
- Emergency
- MAP, 25%, diastolic, 100-110 mmHg, 30-60 min
- Acute aortic dissection, Acute ischemic stroke, Intracerebral hemorrhage
- Urgency = Oral meds*
- Emergency = IV meds*
Common IV Drugs Used in Hypertensive Emergency
(3)
- Sodium Nitroprusside (Nipride)
- Nitroglycerin
- Nicardipine (Cardene)
+Sodium Nitroprusside
MOA
- Converts to ___ ____ (NO) -> activates ____ _____ (GC) -> converts ____ ____ ____ (GTP) into ____ ____ ____ (cGMP)
- _____ preload (________) and afterload (______ ______ ) to a similar degree
- ____ cardiac output and ____ heart rate
- nitric oxide -> guanylate cyclase -> guanosine triphosphate -> cyclic guaninine monophosphate
- Decreases, venodilation, arterial dilation
- Reduces CO, Increases HR
- V potent vasodilator -> drops preload AND afterload*
- Its nice bc it has a short half-life usually given as a gtt so if you go to far, just turn it off*
+Sodium Nitroprusside
How is it administered?
What is its half life?
- Continuous infusion (gtt)
- < 10 minutes
+Sodium Nitroprusside
AE (2)
- Conversion to NO generates cyanide** -> liver converts to **thiocyanate -> eliminated through kidneys (Cyanide poisoning when given in v low doses over long periods of time)
- Tachycardia
+Sodium Nitroprusside
Risk of Toxicity
- Doses > ___ mcg/kg/min
- _____ administration
- ____ or ____ insufficiency
- > 2mcg/kg/min
- Prolonged
- Renal, Hepatic
Sodium Nitroprusside
NOT the drug of choice for (3)
(not really on exam?)
- Acute Coronary Syndromes
- Aortic Dissection
- Increased ICP
+Nitroglycerin
MOA
- Combines with _____ groups in vascular ____ that mimics ___ stimulation of _____ ____ and production of ____
- Preferentially relaxes _____ smooth _____
- sulfhydryl, endothelium, nitric oxide’s, guanylate cyclase, cGMP
- venous, muscles
+Nitroglycerin
Indications
Not as potent as nitroprusside for lowering BP
Use more for acute heart failure or ACS
+Nitroglycerin
Admin
Half life
Administered as continuous infusion
HF: 2-3 minutes
+Nitroglycerin
Disadvantages
- _________*
- Prevention includes maintaining a “nitrate ___” interval
- Do not (2)
- Tachyphylaxis (tolerance, even within 24 hours)
- “nitrate free” interval
- DO NOT apply patches for a continuous 24hr period
- DO NOT use oral tablets or sustained release products around the clock
Know that IV and sublingual forms act quickly, and PO/tablets are long acting which is primarily what we want depending on what we use it for
+Nitroglycerin
AE (3)
Hypotension
Headache (nitro HA are real* very common)
Reflex Tachycardia
+Nitroglycerin
Significant Drug Interactions
Phosphodiesterase-5 inhibitors (ie. sildenafil (VIAGRA))
(ED meds)
Nicardipine
- What is it?
- Used for what? or when ___ is no available (ie. post op)
- Normal dose __-__ mg/hr continuous
- Unique ___-phasic elimination, watch for _____
- Intravenous CCB
- Hypertensive emergency, PO
- 5-15 mg/hr
- Tri-phasic, accumulation
- is an IV CCB -> given alot in CCU*
- Be mindful that it can accumulate -> tanks BP*
