Cardiovascular system Rx Flashcards
What is the mechanism of action of Diuretics?
Ion transport inhibitors, impacting reabsorption of electrolytes => water follows electrolytes to maintain osmotic pressure gradient
NOT WATER TRANSPORT INHIBITORS
Where do Thiazide diuretics work?
luminal (inner) surface of proximal convoluted tubule= Na+, Cl-, and K+ excretion
requires adequate renal perfusion to work
What are adverse effects of diuretics?
Dry mouth/mucous membranes
Electrolyte imbalances
Can potentiate drugs that cause ototoxicity and nephrotoxicity
What is a unique adverse effect of thiazide diuretics?
Potentiate uric acid retention => gout
What lab evaluations are important for diuretics?
serum electrolytes- especially K+
renal function- BUN/creatinine
Thiazides- additionally Na+ and uric acid if hx of gout
What is the mechanism of action of Beta Adrenergic Antagonists?
1) “Beta Blockers” prevent sympathetic stimulation of the heart =>block action of epinephrine
2) prevent renin release from glomerulus => decrease outflow and water retention in kidney
* Cardio-selective or noncardio-selective
Cardioselective beta blockers
-selective for B1 receptors =>cardiac effect only; may lose selectivity in high doses Atenolol (Tenormin) Acebutolol (Sectral) Esmolol (Brevibloc) Metoprolol (Lopressor) Penbutolol (Levatol)
Non-cardioselective beta blockers
-Also block B2 receptors of smooth muscle => inhibits smooth muscle relaxation=>vasocontriction, bronchospasm Lebetolol (Trandate) Nadolol (Corgard) Propranolol (Inderal) Pindolol (Visken)
What are the Third Generation Beta Blockers?
- combination agents that produce vasodilation and beta blockade
- Nebivolol (Bystolic) and Carvedilol (Coreg)
What are the common adverse effects of Beta Blockers?
Bradycardia, hypotension
B2 receptor inhibition => bronchospasm, inability to present sympathetic response, weakness/fatigue, erectile dysfunction
What is the mechanism of action of Alpha adrenergic antagonists (alpha blockers)?
block alpha receptors => relaxation of arterial and venous smooth muscle => decrease peripheral vascular resistance and lower BP
Name Alpha adrenergic antagonists
“-zosin”
Prazosin (Minipress)
Terazosin
Doxazosin
What are common adverse effects of Alpha adrenergic antagonists?
Orthostatic hypotension HA drowsiness N/V impotence *NSAIDs block antiHTN effect
What is the mechanism of action of ACE inhibitors?
Angiotensin Converting Enzyme Inhibitors
- block conversion of Angiotensin I to Angiotensin II in RAAS=> decreases aldosterone release, ADH release, and vasoconstriction => less Na + water retention and vasodilation
Name ACE inhibitors
“-pril”
Captopril, Lisinopril, Ramipril, Benazepril, Fosinopril, Quinapril, Enalapril, Perindopril
What are common adverse effects of ACE inhibitors?
HA/dizziness; tachycardia
neutropenia/agranulcytosis
*angioedema
*cough; maculopapular rash
What lab evaluations are considered for ACE inhibitors?
-WBC with diff @ baseline
-baseline urine protein
-renal function studies
Lab interference- may produce false ANA titers; transient BUN/creat. elevations; increase K, prolactin and LFTs; may decrease fasting blood glucose
What is the mechanism of action of ARBs?
Angiotensin II Receptor Blockers => block vasoconstrictive effect of angiotensin II at receptor site => decrease periph vascular resistance
Name ARBs
"-sartan" Losartan potassium valsartan irbsartan candesartan telmisartan eprosartan
What are common adverse effects for ARBs?
rare- hyperkalemia
no cough issues and fewer renal issues
contraindications- caution if on diuretics or with renal impairments
drug interactions- issues with K+ in drugs
Aliskiren (Tekturna)
- Renin Inhibitor
- Direct renin inhibitor- decreases conversion of angiotensinogen to angiotensin I and plasma renin activity not increased
- Indicated for HTN
- Adverse effects similar to ACE inhibitors- angioedema, cough, diarrhea
Entresto
- Entresto (valsartan/sacubitril)- combination agent of ACE I with Neprilysin Inhibitor
- Indicated for CHF
- Adverse effects: hypotension, hyperkalemia, cough
- do not administer with ACE I or with pregnancy/planning pregnancy
How do HCN channel blockers work?
ivabradine (Corlanor)
Inhibits funny current in SA node => lowers HR by slowing depolarization in SA node
What is the mechanism of action of Calcium Channel Blockers?
Blocks Ca entry into cell => inhibits constriction => vasodilation => lower BP
Name Calcium Channel Blockers
“-dipines”
Amlodipines, isradipine, nicardipine, nifedipine, nisoldipine, clevidipine, verapamil
What are the adverse effects of calcium channel blockers?
r/t vasodilation
- HA, dizziness, hypotension constipation
- peripheral edema
- AV block
What are other vasodilators?
-directly relax arterial smooth muscle Sodium Nitroprusside (Nipride) Hydralazine (Apresoline) Minoxidil (Rogaine) Diazoxide (Hyperstat)
What is the mechanism of action of Clonidine?
centrally acting antiadrenergic derivitive
activates alpha2 receptors in CNS to sympathetic nervous centers => decrease plasma norepi => inhibits renin release from kidney
What adverse effects are related to Clonidine?
CNS depression
Caution with recent MI, SA node dysfuntion, CKD, depression
What lab evaluations are important for Clonidine?
May decrease urinary aldosteron, catecholamines, and VMA (mask pheochromacytoma)
What are the first line drugs for hypertension?
1) Thiazide diuretics
2) ACE inhibitors or ARBs
3) CCBs
What are the first line drugs for hypertension in the Black population?
Thiazides and DHP CCBs
What is the drug class of choice for CKD patients with Hypertension?
ACE I or ARBs
In general, when are patients treated for HTN?
BP >130/80- pts with comorbid disease or high risk
BP>140/90- general population
How is hypertension treatment managed?
If goal is not readed after 1 month, increase dose or add 2nd agent => continue to assess and modify until goal reached => add third agent if necessary
What is the goal of treatment for coronary artery disease (CAD)?
increase oxygenation or decrease workload to equalize supply and demand => decrease preload or afterload and dilate coronary arteries
What are the drugs of choice for CAD?
Beta blockers- decrease workload by decreasing contractility and HR
What drugs are often used to manage CAD?
Beta blockers- decrease workload by decreasing contractility and HR
CCBs- decrease contractility and inhibit vascular constriction
Nitrates- vasodilate coronary arteries, decreases preload
Ranolazine (Ranexa)- decreases episodes of angina
What are Nitrates?
cause direct vasodilation of coronary arteries to increase oxygenation to heart; venodilate and can dilate arteries in high doses
isosorbide dinitrate- used for acute anginal attack
isosorbid mononitrate- long acting
How is CAD treatment managed?
1) beta blocker
2) CCB
3) long acting nitrites
4) angiography/angioplasty
What is Ranolazine (Ranexa)
“Metabolic modulator”
for chronic angina unresponsive to other drugs
CYP450 substrate and prolongs QT
Decreases episodes of angina and increases exercise tolerance (small benefit)
What is are the management strategies for congestive heart failure?
1) correct underlying problem- CO insufficient to meet metabolic demands
2) decrease workload of heart (preload/afterload)
3) increase contractility of heart
What drugs are used to manage CHF?
Loop diuretics- for acute, symptomatic HF to immediately decrease preload
*ACE I/ARB- decrease afterload by inhibiting vasoconstriction
*Beta Blocker- Carvediolol, Metroprolol, Bisoprolol
Entresto- Neprilysin inhibitor/ACE I
Aldosterone Antagonist- for severe disease (spironolactone); watch K closely
HCN channel blockers- if on max beta blocker, stable but symptomatic, HR >70
Hydralazine/Nitrates- esp in African Americans
Cardiac Glycosides- slows HR, but increases contraction
Dobutamine and Dopamine- increase HR and BP
Vasodilators- decrease preload
Phosphodiesterase Inhibitors- increase contractility
What is the mechanism of action of cardiac glycosides?
Digoxin
inhibit Na-K pump => increase release of Ca => increase force of contraction
increases sensitivity of AV node to vagal stimulation =>slows conduction of impulse
What are adverse effects of cardiac glycosides?
Dig. toxicity (very narrow therapeutic range)
Fatigue, muscle weekness, nausea, AV block
Contraindications- hypokalemia, acute MI
What labs are important for cardiac glycosides?
Digoxin levels, K (watch for hypokalemia)
How do Dopamine and Dobutamine work?
Dopa- catecholemine that is precursor to norepi; acts like epi in high doses; stimulates B1 receptors of heart and A1 receptors of arteries => increase contractility and vasoconstriction
Dobut- B1 agonist and dopamine receptor agonist
increase HR and BP
What are adverse effects of dopamine and dobutamine?
angina, palpitations, HA
Contraindicated for HTN and pheochromacytoma
Beta blockers and Alpha blockers- block effects
What are Phosphodiesterase Inhibitors?
Amrinone, Milrinone, Cilostazol
inhibits breaking of cAMP =>increases smooth muscle contraction => increases heart contractility
Adverse effects- hypotension, dysrhythmias
Contraindications- severe valve disease, hypokalemia, dehydration
How is CHF treatment managed?
symptomatic CHF- loop diuretic
chronic CHF: ACE I/Neprilysin Inhib. and beta blocker; HCN channel blocker, Aldosterone antagonist, cardiac glycoside
Severe, inpatient CHF- loop diuretic, morphine, inotropes, vasodilators
What are adverse effects and contraindications of Nitrites?
Adverse effects- H/A, dizziness, flushing; postural hypotension, palpitations
Contraindications- increased ICP, glaucoma, hypotension, hyperthyroidism
What medication can interfere with effectiveness of antihypertensives?
Ibuprofen
Nebivolol (Bystolic)
- Third generation beta blocker
- extremely cardioselective
- increases nitric oxide release
- only approved for HTN
Carvedilol (Coreg)
- not cardioselective
- indicated for *CHF, HTN, LV dysfunction after MI
What contraindications are there for beta blockers?
symptomatic SB
>1st degree heart block
RAD
What drug interactions are there for beta blockers?
antacids- decrease absorption
anticholinergics- increase absorption
What are contraindications are there for ACE Inhibitors?
B/L renal artery stenosis *pregnancy *renal impairment on immunosuppressants collagen vascular disease severe salt/volume depletion
What are Neprilysin Inhibitors?
Metabolizes to LBQ657 => inhibits neprilysin => increases circulating amounts of vasoactive peptides => promotes natriuresis, diuresis, vasodilation, attenuates cardiac fibrosis
*Used in Entresto- combination with ACE I
Ivabradine (Corlanor)
- HCN Channel Blocker
- Indications:
- reduce hospitalizations for stable symptomatic CHF with LVEF <35%
- beta blockers on max doses
- resting HR >70
- Contraindicated for decompensated CHF, SBP <90, A. Fib
DHP vs non-DHP calcium channel blockers
Non-dihydropyridines (nonDHP)- primary site of action @ cardiac monocyte; best choices for CAD; Diltiazem, verapamil
DHP- primary site of action @ arterial smooth muscle; best choice for HTN; “-dipines”
Contraindications and drug interactions for CCBs
Contraindications: *>1st degree heart block severe CHF sick sinus syndrome SBP <90 *aortic stenosis Drug interactions- beta blockers increase CHF risk; CCBs potentiate other antihypertensives
