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heart stretch, left ventricular end diastolic pressure (at the end of relaxation) |
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the resistance the heart has to pump against |
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the forceful contraction of the heart, greatly influenced by preload |
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what happens under circumstances of low blood volume |
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the kidney detects it, renin is secreted from the adrenal medulla that triggers a cascade of physiological effects , angiotensin released, vasoconstriction -> periphery -> inc systemic vascular resistance and improve BP. In HTN this system can be activated, so one way to treat it is to interrupt this system |
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angiotensin-converting enzyme inhibiting class blocks the conversion of angiotensin I to angiotensin II, its active potent vasoconstricting peptide. The main purpose of these medications is to decrease the afterload that the heart has to pump against, which overall will lower blood pressure |
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ACE inhibitor agents and notes |
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Definition
Captopril (cat pril )(short-acting, rare leukopenia, contains sulfhydryl, taste disturbances), Quinapril (quinn pril), Lisinopri (list pril)l (5x more potent than captopril, most commonly prescribed), Ramipril (ram it pril), Benazapril (benz pril), Enlarpril (enlarge pril) (analaprilat is IV formulation), Fosinopril (fossil pril) (only ACEI hepaticaxlly cleared) lcqrbef (liquor beef), pril's |
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angiotensin receptor blockers, block angiotensin II's effect on the actual angiotensin I receptor. Overall, this decreases the ability for angiotensin II to cause vasoconstriction. So it's an indirect vasodilator, decreases afterload and lowers BP |
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ARB agents and most common |
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Definition
Losartan (lost spartan) (most common), Valsarta (val sorta), Irbesartan (herb spartan), Telmisartan (tell me spartan), Candesartan (clandestine spartan), Olmesartan (oh mess spartan) LIVCOT, a(n)'s |
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not available IV, not dosed more than once a day |
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adverse effects of ACEI and ARBs |
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Definition
hypotension w first dose (bc they have overactive RAS systems- very high levels of circulating renin and angiotensin II), monitor for 1st 30 min, hyperkalemia (interfere w downstream aldosterone reabsorption), elevations in creatinine (prevent angiotensin II's affect) but renal protective over time ACEI- can cause dry cough (breaks down bradykinin which can irritate the throat)- switch to ARB -most severe side effect of these medications is angioedema bc of effect on bradykinin (laryngeal vasodilator), tongue can swell- discontinue (10 fold higher risk of this in African Americans), counsel pts to call 911 or present to ER |
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direct renin inhibitor agent, MOA, adverse effects |
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Definition
aliskiren (Alaskan), It's mechanism is to directly block the release of renin from the adrenal medulla and delaying the ability for renin to be released from the adrenal medulla prevents downstream formation of ACE conversion to angiotensin II. Again, overall, this decreases afterload, just like the ACEs and ARBs, which works to lower systemic vascular resistance, and therefore lower blood pressure Adverse effects- diarrhea, hyperkalemia |
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contraindicated in pregnancy |
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2 classes of calcium channel blockers and agents w notes |
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Definition
nondihydropyrodines (relieve angina and atrial fibrillation)- Diltiazem (dialed em) (Immediate release slow disperse over 3 hrs, should not be crushed), Verapamil (very pam ill) (available in immediate, sustained, extended release, and IV formulations) (attracted to more neg charge)
dihydropyroidines- Amlodipine (a lord pine) (takes 3 days to reduce blood pressure), Nifedipine (n-confetti pine), Nicardipine (nicu pine) (available both oral/IV formulations, preferred in pregnancy), Clevidipine (clever pine) (only available IV, ultra short acting) |
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calcium channel blocker MOA |
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Definition
Antagonize L-type voltage gated calcium channels, decreases afterload and contractility, prevent vasocontriction peripherally
DHP: Vasodilates vascular smooth muscle Non-DHP: Depresses cardiac conduction at atrioventricular (AV) and sinoatrial node (SA) node |
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calcium channel blocker adverse effects |
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Definition
non-DHP: bradycardia, heart block DHP: pedal edema |
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predominately expressed in the peripheral arterial circulation, arteries and veins. Agonism of the alpha 1 receptor causes peripheral vasoconstriction in these areas, which will increase systemic vascular resistance |
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commonly expressed in the gastrointestinal tract, it's also expressed centrally as well, so agonism of either of those two things will typically promote a down-regulation of adrenergic activity, so it decreases the tone of the other adrenergic receptor types. You can think of it as an anti-adrenergic receptor |
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is most commonly prescribed in the cardiac myocardium, so agonism of beta 1 will increase contractility and improve cardiac output |
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expressed on skeletal muscle, as well as in the peripheral vascular system, as well as in the bronchial smooth muscle. So agonism of beta 2 will typically cause vasodilation. In the lungs, this will cause bronchodilation, or in the peripheral vasculature, it will cause vasodilation. So it can have the opposite effects of alpha 1 |
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alpha 2 stimulation in the brain stem |
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Definition
by methyldopa or clonidine (or guanfacine), as I mentioned, down-regulates the effect of other adrenergic receptors. So it delays conduction across the ganglion |
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alpha 2 stimulation in the periphery |
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Definition
adrenergic antagonists blunt the downstream effects of this central activation in the postsynaptic terminals |
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alpha 1 blockers agents, MOA, SE |
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Definition
doxazosin, prazosin, used to be used to treat HTN. block endogenous epinephrine and norepinephrine on alpha 1 receptors in the vascular smooth muscle (prevent peripheral vasoconstriction/indirectly vasodialte), decrease afterload. SE: postural hypertension and dizziness |
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alpha 2 agonists MOA, agents, indication |
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Definition
bind alpha 2 peripherally or centrally and cause down regulation of adrenergic receptor activity. most common = clonodine (also methyldopa and guanfacine). not that effective for HTN |
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beta blockers MOA, utility, contraindicated in, SEs |
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Definition
down-regulate cardiac output or lower contractility, block cardiac conduction activity across AV node and slow HR, doesn't affect SVR so not that good at lowering BP, commonly used for heart attack treatment, contraindicated in anyone who has developed an allergy to another beta blocker or anyone who develops severe heart failure as cardiogenic shock or pts w resting HR <50pbm, pts w second or third degree heart block unless they have a pacemaker. SE: bradycardia, AV nodal block, hypotension, dizziness and in asthmatic pts bronchospasm (can also block beta 2), also fatigue that can go away and depression that can last |
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Nonselective -ISA Beta Blocker Agents |
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Definition
Nadolol, Propanolol, Sotalol, Timolol |
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Nonselective +ISA Beta Blocker Agents |
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Selective -ISA Beta Blocker Agents |
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Atenolol, Betaxolol Bisoprolol, Esmolol, Metoprolol, Nebivolol |
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Selective +ISA Beta Blocker Agents |
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B-adrenergic blockers w a-blocking activity |
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Labetalol, Carvedilol (slight) (alpha blocking prevents vasoconstriction) (beta blockers slow HR) |
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most commonly prescribed medicine for cardiac concerns such as atrial fibrillation or heart failure |
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metoprolol (cardio-selective beta blocker with no intrinsics and pathomimetic activity) |
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Intrinsic Sympathomimetic Activity |
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Definition
a beta blocker has ISA if it acts as a partial agonist at the beta 1 receptor (a minimally effective agonist, so ineffective that it blocks adrenaline from doing its job and activating beta 1- ceiling effect- prevents bradycardia)-- so acebuterol may be a good agent for someone w a resting HR of 50-60 bc it would prevent brandycardia. most nonselective beta blockers are rarely used for HTN or cardiac conditions, ex timolol eye drop medication is used for glaucoma and intraocular HTN, nadolol and propanolol are used for performance anxiety |
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Direct acting vasolilators- arterial vasodialating agents, MOA, Adverse effects, SE |
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Definition
hydralazine and minoxidil (Rogaine), MOA- perform direct vasodialatory actions on arterial smooth muscle. sensitive for dilating arteries- decreases SVR/afterload- unfortunate physiological consequence of this is rebound tachycardia (do not prevent physiologic response to inc HR to balance out anti-HTN effects), Rogaine SE of unwanted hair growth- used today to alleviate male pattern baldness |
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HTN combination medication, agent, indication, SE |
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isosorbide dinitrate w hydalazine (fixed dose combination) (BiDil), treats heart failure w reduced ejection fraction in African-American patients, SE: hypotension, strong feelings of headache and weakness, rebound chest pain |
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sodium reabsorption along the nephron |
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Definition
65% in pct, 25% at loop of henle, small amnt at DCT, negligable at collecting duct |
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Diuretics that work at PCT |
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Definition
Acetazolamide, or a carbonic anhydrase inhibitor, osmotic diruetics |
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diruetics that works at loop of henle |
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Definition
loop diuretics, furosemide |
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diuretics that work at dct |
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Definition
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diuretics that work at the collecting duct |
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Definition
potassium-sparing diuretics, or aldosterone antagonists |
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carbonic anhydrase inhibitors, ex, MOA, uses |
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Definition
acetazolamide, inhibit formation of carbonic anhydrase- major buffering enzyme in PCT that controls our formation of bicarb which buffers pH and H+ conc. by preventing bicarb formation, have pH sensitive volume reduction in PCT-> inc's Na reabsorpiton at loop of henle so overall not that good at reducing fluid reabsorption and lowering BP, instead mostly have intraocular uses- glycoma or intraocular HTN- acetazolamide or Diamox. prevents metabolic alkalosis (SE from over diuresis w loop diuretics), can alkalinize urine (hereditary cystinuria |
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thiazides or thiazide-like diuretics, MOA, main effect, agents, SEs |
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Definition
act on DCT and prevent Na reabsorption, mainly effect vasodilation (takes several months), dec SVR, most common is hydrochlorothiazide, or HCTZ (Also chlorthalidone and metolazone). inhibits sodium and chloride cotransporter. hyponatremia is common SE also sodium and potassium wasting, hyperglycemia |
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loop diuretics, use, agents, MOA, SE, delivery, aka |
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Definition
exert a lot of Na excretion into the lumen and remove the most fluid but not particularly effective for HTN, but useful for pts w acute ehart failure or hypercalcemia, furosemide/Lasix (most common), bumetanide (most potent), torsemide, ethacrynic acid. inhibit Na, K, Cl transporter on the apical end of the thick ascending loop of Henle. SE: hypkalemia, hyponatremia, dec mg, dec calcium, cramping esp of leg and calves, hypotension. give w normal saline or sodium chloride, aka high ceiling diuretics (deep dose response curve, may have to inc dose 10x to see an effect- high ceiling for efficacy, safety and toxicity). most of the diuretic response occurs within the first 1-2 hrs, IV is faster for acute congestive failure |
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loop diuretic to give for pt w sulfa allergy |
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K-spacing diuretic agents, use, MOA |
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Definition
spironolactone (most common), eplerenone (hear failure), triamterene, amilodride, only used to treat resistant HTN, act predominantly in the ENaC pathway or the sodium potassium current. They exchanged sodium excretion for retaining potassium, only Na is excreted across the cotransporter and K stays in lumen.block aldosterone-mediated sodium/potassium antiporter. SE: hyperkalemmia esp w ACEI/ARB, gynecomastia (discontiniue) |
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Vasopressin agonists usage, agents |
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Definition
acute heart failure when volume resistance happens on therapy with various other diuretics , Tolvaptan is by far the most commonly prescribed (also conivaptan). MOA: blockvasopressins endogenous effect on the V2 receptor in the collecting duct. They are really only used to ever treat hyponatremia, as they cause aquaresis, or simply, water excretion in the urine. SE: serious, hepatotoxicity and hypernatremia, an excessive thirst (discontinue), monitor BMP 2x day |
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osmotic diruetics, agent, use, MOA, SE |
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Definition
mannitol, used for intraocular pressure, intracranial pressure. draws water into the lumen of the nephron, which is then used to lower volume response because electrolytes will follow that water and you'll diurese electrolytes as well as water to the urine. SE: hypervolemia, and may crystallize at room temperature (keep in fridge), also directly nepherotoxic, can cause some very irritating side effects in the skin, which can appear red, angry, and painful |
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common in pts who are HTN, due to anti-diuretic hormones' resistance that's endogenous in patients. The symptoms include polyuria, hypernatremia, and hypovolemia. Often, hypercalcemia is one of the precipitating factors in diabetes insipidus. So use of loop diuretics is not advised.. treat w low salt and low protein diets, thiazide and K-sparing diuretics are preferred , NSAIDS are useful, may need exogenous anti-diuretic, DDVAP (analog of anti-diuretic, it reverses the resistance to anti-diuretic hormone because it is chemically modified to agonize the receptor with a much higher affinity) it also is used for prevention of bleeding, in patients with uremia or nocturia to prevent overnight urination. SE: hyponatremia, water intoxication, as well as headache, allergies |
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