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week 9: treatment of HTN, CAD, and CHF

Terms in this set (72)

what is the most preventable risk factor for premature death?
HTN
prevalence of HTN increases with what 2 things?
increases age and low socioeconomic status
JNC 8 guidelines suggest starting HTN treatment for adults 60+ y.o. when BP goes above...?
150/90
JNC 8 guidelines suggest starting HTN treatment for adults under the age of 60 when BP goes above...?
140/90
JNC 8 guidelines suggest starting HTN treatment for adults w/ diabetes or CKD regardless of age when BP goes above...?
140/90
JNC 8 guidelines suggest keep DBP under what value for patients between the age of 30-60?
< 90
what are the 4 initial HTN treatment drug classes of choice? what 2 should be used in black populations? (bolded)
-thiazide diuretic
-CCB
-ACE-1
-ARB
if target BP is not reached in 1 month after starting initial HTN treatment, what 2 things can be done?
inc. dosage or add a 2nd mediation
starting at 115/75, CV risk DOUBLES for each ____/____ increase in BP
20/10

therefore, BP of 135/85 means pt's risk of CV complication is doubled
chronic elevated BP also inc. long term risk factors for...
-MI
-stroke
-CKD and renal failure
-peripheral vascular disease
-cognitive impairment and dementia
-retinopathy
-death
What BP indicates an acute hypertensive crisis? what differentiates hypertensive emergency from hypertensive urgency?
> 180/110
HTN emergency is when a pt has this BP PLUS evidence of end organ damage or impending damage (whereas urgency is just the BP w/o other major issues)
what limits a single drug's effect in many patients?
natural compensatory mechanisms
ex. vasodilators promote tachycardia and salt retention
loop diuretics, such as _________________, act by selectively inhibiting __________ absorption in the _____________________ (resulting in dec. Na+ and H2O absorption). they are most commonly used or CHF than HTN!
loop diuretics, such as furosemide, act by selectively inhibiting NaCl absorption in the ascending loop of henle (resulting in dec. Na+ and H2O absorption). they are most commonly used or CHF than HTN!
what is the most common side effect of diuretics? what are some other side effects?
hypokalemia (induced metabolic acidosis)
-digitalis, arrhythmias, LV dysfunction, MI
thiazide diuretics, such as ______________________, act by inhibiting _________ absorption in the ______________________. compared to loop diuretics, they actually enhance _______________________ as a secondary effect.
thiazide diuretics, such as hydrochlorothiazide (HCTZ), act by inhibiting NaCl absorption in the distal convoluted tubule. compared to loop diuretics, they actually enhance Ca2+ reabsorption as a secondary effect
what 3 conditions are thiazide diuretics used to treat?
-HTN
-CHF
-nephrolithiasis (kidney stones) due to hypercalcemia
spironolactone and eplerenone are _________________________________. Their MOA is to antagonize __________________ in the _________________________
spironolactone and eplerenone are K+ sparing diuretics. Their MOA is to antagonize aldosterone in the collecting tubules
what kind of diuretic would you NOT want to use to treat HTN in a middle age man? why not?
K+ sparing diuretics (such as spironolactone and eplerenone) b/c side effects include ED and BPH
diuretics are effective at lowering BP by _____-_____ mmHg. At first, they cause a transient drop in BP due to _______________ and dec ________________, which cause a reflexive inc. in __________. After 6-8 weeks, this reflex goes away as ____________ normalizes.
diuretics are effective at lowering BP by 10-15 mmHg. At first, they cause a transient drop in BP due to hypovolemia and dec CO, which cause a reflexive inc. in SVR. After 6-8 weeks, this reflex goes away as CO normalizes.
hydrochlorothiazide (HCTZ) and thiazide diuretics in general are more effective at lower BP than __________________ diuretics. Their efficacy peaks with _________ doses
loop diuretics
low doses
calcium channel blockers' primary anti-HTN mechanism is by causing...
vasodilation
what drug class are dihydropyridines? what are two common drugs in this class? where do they mainly act on? what reflexive effect can they cause
-calcium channel blockers
-amlodipine and nicardipine (also clevidipine and nifedipine)
-act as vasodilators (less cardiac depression)
-reflex SNS activation and mild inc. in HR
verapamil has the greatest ____________________ effects of all calcium channel blockers and is therefore more useful at treating _____________________
verapamil has the greatest cardiac depressant effects of all calcium channel blockers and is therefore more useful at treating arrhythmias
what short-acting CCB is used in the OR/ICU for vasodilation
nicardipine (also clevidipine = ultra short acting)
what is a common side effect of CCBs
edema
angiotensin inhibitors work particularly well in HTN patients that have high ________ activity (20%)
renin
patients w/ what 3 comorbidities particularly benefit from angiotensin inhibitors?
-DM due to renal protection from ACE-I
-CHF
-post-MI
ACE-I, such as _____________, work by blocking the production of ______________________
lisinopril (others: captopril, enalapril, fosinopril)
angiotensin II
diuretic induced Na+ loss is uncompensated when combined with a ______________ because they block the body's _______________-mediated response to Na+ loss
diuretic induced Na+ loss is uncompensated when combined with an ACE-I because they block the body's aldosterone-mediated response to Na+ loss
what are 4 major side effects of ACE-I
-angioedema (rare but life threatening)
-cough (ACE-I only)
-HYPERkalemia
-large BP drop w/ initial dose
angiotensin receptor blockers (ARBs), such as ______________, are antagonists at the ________ receptor. they act by causing peripheral _______________ via _________ and ___________ excretion. full effects make take ____________
angiotensin receptor blockers (ARBs), such as losartan, are antagonists at the AT-1 (AngII) receptor. they act by causing peripheral vasodilation via salt and H2O excretion. full effects make take weeks
ß-blockers: Even though lowered HR can actually increase _________________________, they still cause an overall net *decrease in ______________________ consumption via their negative ________________ and __________________ effects + slight dec. in ___________.
*more ____________ time increases blood flow "supply"!
ß-blockers: Even though lowered HR can actually increase systolic contraction time (WORK), they still cause an overall net *decrease in myocardial O2 consumption via their negative chronotropic and inotropic effects + slight dec. in SBP.
*more diastolic time increases blood flow "supply"!
myocardial ischemia is due to a decreased ratio of O2 _______________ vs _____________
supply vs. demand
ß-blockers are a major part of CV care and extremely beneficial for patients with _________ because they help inc. ___________ and dec. ______________
ß-blockers are a major part of CV care and extremely beneficial for patients with CAD because they help inc. O2 supply and dec. O2 demand
ß-1 antagonists, such as _______________, block ß-1 mediated activation of what system?
metoprolol (+ esmolol)
RAS
labetalol is a ß and alpha antagonist in approximately a ___:___ ratio. It is used in the treatment of these 2 things
3:1 (ß:alpha)
HTN emergency and pheochromocytoma
carvedilol antagonizes what 2 receptors (at what ratio?)? what 2 things is it excellent at treating?
-mixed ß and alpha antagonist (10:1 ratio)
-HTN and heart failure
central acting drugs, such as _______________, are rarely used nowadays due to _______________________ except in ____________ HTN
central acting drugs, such as clonidine, are rarely used nowadays due to lots of side effects except in refractory HTN
"Monday morning headaches" is due to what phenomenon linked to what drug
tachyphylaxis from nitroglycerin
nitroglycerin releases ______________ resulting in _________ formation and SM ______________ (MAINLY __________________!). It results in reduced ________________ (which transiently decreases ________ and ________)
nitroglycerin releases nitric oxide (NO) resulting in cGMP formation and SM relaxation (MAINLY VENOUS dilation!). It results in reduced pre-load (which transiently decreases CO and BP)
hydralazine is a direct ___________________ that results in powerful __________________ stimulation due to _______________ reflex
hydralazine is a direct vasodilator that results in powerful sympathetic stimulation due to baroreceptor reflex (reflex tachycardia)
sodium nitroprusside is ______________ and mainly acts on ________________. what is the major side effect associate with it?
-ARTERIAL vasodilator
-cyanide toxicity
what drug acts on D1 receptor to cause arteriole vasodilation and natriuresis and is used to treat HTN emergencies?
fenoldapam
in general arteriolar vasodilators decrease what (1) and increase what (4)?
-dec. peripheral resistance
-inc. HR, CO< plasma volume, and plasma renin activity
66 y.o. male presents to pre-op clinic prior to Lap nephrectomy.
PMH: HTN, DM, CAD s/p DES (drug-eluting stent) 2 y.o., dyslipidemia.
vitals: HR: 82, BP: 151/93
your most effective recommendation to his PCP for BP management that has mortality benefits would be?

A. furosemide
B. amlodipine
C. hydralazine
D. metoprolol
D. metoprolol

explanation: ß-blockers are particularly beneficial for pts with CAD b/c in increases supply to demand ratio and time in diastole
68 y.o. M for TKA.
PMH: HTN, dyslipidemia, DM, CKD (Cr. 1.6)
Vitals: HR 78, BP 148/94
Meds: HCTZ 25 mg QD, metoprolol 12.5 mg BID, atorvastatin, insulin
what agent would you add that provides renal protection?

A. lisinopril
B. Diltiazem
C. Furosemide
D. Atenolol
A. lisinopril
there are higher rates of CHF in what 3 ethnicities
-African American
-hispanic
-Native American
what are the two classification of CHF?
-systolic failure: HF w/ REDUCED EF (HFrEF)
-diastolic failure: HF w/ PRESERVED EF (HFpEF)
CHF leads to ________________ activation, _______________ inefficiency, and _______________ congestion
CHF leads to neuroendocrine activation, circulatory inefficiency, and vascular congestion
2 common symptoms of CHF
-SOB (shortness of breath)
-peripheral edema
describe the "spiral" of CHF
dec. CO --> inc. NE, AngII, ET (Endothelin) --> inc. afterload --> dec. EF --> dec. CO
CHF treatment is to treat all underlying/contributing conditions such as what 5 common things?
-ischemic heart disease
-dyslipidemia
-HTN
-DM
-arrhythmias
what 2 drug classes can be used to treat CHF?
-ß-blockers (metoprolol)
-angiotensin inhibitors (try ACE-I before ARBs)
phosphodiesterase (PDE) inhibitors prevent inactivation of ____________ and downstream 2nd messengers. What subtype acts directly on cAMP? give an example. What subtype acts on cGMP? give an example
-cAMP: PDE3 (milrinone)
-cGMP: PDE5 (sildenafil)
milrinone increases ________________ in the heart (via inc. ______ channel activation) and causes _________________ in peripheral arterial system. these effects together causes [increased/decreased] cardiac output and decreased _________
milrinone increases contractility in the heart (via inc. Ca2+ channel activation) and causes vasodilation in peripheral arterial system. these effects together causes increased cardiac output and decreased SVR/PVR
what drug is often used in cardiac surgery and heart failure
milrinone
what drug class is used as an end stage/palliative treatment or for acute decompensation to improve CO and symptoms of CHF?
beta agonist
(inc. in mortality seen so only given in extreme circumstances)
Digitalis/Digitoxin
-from cardiac ___________ family
-inhibits _________________
-increases free ___________
-positive _______________ effects
-enhanced [SNS/PNS] effect on HR
-from cardiac glycoside family
-inhibits Na/K-ATPase
-increases free Ca2+
-positive inotropic effects
-enhanced PNS effect on HR
electrolyte disturbance caused by digitalis toxicity is acute ____________________ and chronic ___________________
electrolyte disturbance caused by digitalis toxicity is acute hyperkalemia and chronic hypokalemia
what 2 things can be done to treat digitoxin toxicity?
-supportive care (correct electrolyte imbalances)
-Digibind: digitoxin antibody
how do you treat acute CHF exacerbation based on preload, afterload, and contractility? what drugs can be given to help each of these 3 things?
-preload: normal fluid overloaded so give loop diuretics to help restore CO
-afterload: control HTN (HoTN is good!) and dec. SVR; give low dose ACE-I
-contractility: inc. contractility using milrinone (or beta agonist)
48 y.o. M presents w/ non-ischemic CM (EF 15%) for femur fracture repair. Prior to OR, EBL was 3 L and pt received 3 untie PRBCs and 2 L NS. His breathing is labored, looks distressed, and required NRB O2.
PE: bilateral crackles in lungs, S1S2 + extra heart sound heard
Pt goes to the OR and after induction, his BP is 70/45, HR 86, and SpO2 is 94% on 100% FiO2
Which agent may improve his clinical condition?

A. vasopressin
B. Phenylephrine
C. Dobutamine
D. Norepi
E. Atropine
C. Dobutamine

explanation: improves contractility of heart
48 y.o. M presents w/ non-ischemic CM (EF 15%) for femur fracture repair. Prior to OR, EBL was 3 L and pt received 3 untie PRBCs and 2 L NS. His breathing is labored, looks distressed, and required NRB O2.
PE: bilateral crackles in lungs, S1S2 + extra heart sound heard
Pt goes to the OR and after induction, his BP is 70/45, HR 86, and SpO2 is 94% on 100% FiO2.
you give dubutamine for his BP but his stats are only at 96%.
what drug will best treat his underlying acute exacerbation?

A. digitoxin
B. captopril
C. spironolactone
D. furosemide
E. metoprolol
D. furosemide

expianation: he's hypervolemic--> hiis lungs are drowning in fluid so give diuretic
what 3 things contribute to increased O2 demand in the heart?
-HR
-contractility
-wall stress (tension and thickness)
what 2 thing contribute to decreased oxygen availability/supply?
-coronary blood flow (+ O2 extraction and coronary microcirculation)
-O2 carrying capacity (arterial pO2 Hbg conc.)
how to treat angina (due to ischemic heart disease)?
-nitrovasodilators
-ß-blockers
-CCBs
-coronary plague stabilization
-lifestyle modifications
nitroglycerin is an example of a ______________ because it is metabolized to _________________ in the body, which is what causes its intended effects (which are?)
nitroglycerin is an example of a PRODRUG because it is metabolized to nitric oxide in the body, which is what causes its intended effects which are inc. cGMP levels --> SM vasodilation
*dec. O2 demand/ work by the heart! (dec. pre-load and diastolic pressure)
when autonomic dysfunction is present (old age or DM), dec. BP caused by nitrovadodilators may exacerbate _____________
angina
what is the major benefit to nitrovasodilators?
decreased myocardial workload
what concern is there for patients taking nitro oral meds such as nitroglycerin and isosorbide mononitrate (IsMo) daily? how is this problem solved?
frequent or high doses can head to rapid tolerance and dec. efficacy
-pts undergo a nitrate-free period every night in order to preserve efficacy
nitrovasodilators can cause severe HoTN if combined with what commonly used home medication?
viagra-- PDE5 inhibitor
why do ß-blockers have a low compliance rate as time goes on (1 vs 3 vs 5 years)?
lots of annoying side effects:
-fatigue and weakness
-SOB
-sleep disturbances
-dec. sexual drive
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