Cardio Pharm Flashcards
(30 cards)
ACE Inhibitors
-Examples
-Mechanism
-Use
-Other
-Drugs that end in “-pril”
-Lisinopril, Enalapril, Ramipril, Captopril
-Mech = Inhibiting the conversion of angiotensin 1 to 2 (also blocks aldo)
Also inhibits bradykinin degradation by kininase 2
Leading to vasodilation
-1st line agent for primary HTN
-Pt w/ DM + microalbuminuria
-CHF, non-stage 4 CKD
-CAD/CVD risk factors
-Other:
-afterload or preload reducer, or arterial dilator
-SE = compromised GFR, blocked aldo leading to hyperkalemia, angioedema, dry cough
CI in pregnancy!
Angiotensin Receptor Blockers (ARBs)
-Examples
-Mechanism
-Use
-Other
-Drugs “-artans”
-Losartan, Irbesartan, Valsartan, Candesartan
-Mech:
-Selectively antagonizing the action of ANG2 at AT1 receptors on blood vessels & heart = indirectly increases vasorelaxant AT2 receptor activity = dilating
-1st line in primary HTN
-Pt w/ DM + microalbuminuria
-CHF, non-stage 4 CKD
-CAD/CVD risk factors
-Other:
-afterload/ preload reducer or arterial dilators
-SEs = compromised GFR, blocked aldo leading to hyperkalemia, hypotension, renal fail, URIs
-CI = pregnancy!
Can you use ACEi & ARBs together?
No, need to pick one or the other
What is the recommended HTN regimen in African American patients?
-ACEi/ARBs should not be used alone
-ACEi/ARB + site 3 diuretic + CCB
Dihydropyridine Calcium Channel Blockers (CCBs)
-Examples
-Mech
-Use
-Other
-Ending in “-dipines”
-Amlodipine (PO), Nifedipine (PO), Nicardipine (IV), Clevidipine
-Mech:
-Afterload reducer
-Block voltage-gated CCs in the vascular smooth muscle of blood vessels = peripheral arterial vasodilation = more blood into capillary bed
-1st line in HTN, esp. African American pts
-Pts w/ uncomplicated/ no comorbidities primary HTN
-Can be used as anti-anginal agent, esp. if pt is maxed on CAD meds & still require additional BP control)
-Can be used in pregnancy (Nifedipine)
-SEs = peripheral edema (increased hydrostatic pressure), gingival hyperplasia, constipation, hyperglycemia
-CIs = Severe aortic stenosis, cardiogenic shock, unstable angina or recent MI, hypotension
Hydralazine
-Use
-Mech
-Other
-Inpatient IV control of out of range BP & slow HR
-Added to ISDN, used as 1st line for HF in African American pts
-Mech:
-Direct vasodilator = inducing release of NO = smooth muscle relaxation (working on arteries)
-Afterload reducer
-Can have reflex tachycardia
-High-dose = drug-induced lupus (anti-histone antibodies + joint/skin symptoms w/out visceral involvement)
-CIs = LES, severe renal disease, severe CAD
Aldosterone Antagonists (potassium-sparing diuretics)
-Examples
-Use
-Mech
-Other
-Spironolactone, Eplerenone
-Preload reducers
-Specifically block the effects of aldosterone only
-Aldosterone is normally responsible for the insertion of channels that passively reabsorb sodium from the collecting duct. Potassium is forced into the urine to keep things electroneutral
-Working at site 4/ collecting duct
-inhibition of sodium reabsorption
-Potassium excretion (K-sparing)
-Adjuncts in volume overload = 4th line in the management of CHF
-1st line + loop diuretic to treat ascites
or
-K-sparing + thiazide/loop diuretic to prevent hypokalemia
-May provoke hyperkalemia (less K is entering the urine to be excreted)
-induces H/K-ATPases to counteract the increase in serum K
-K enters cells in exchange for H = amplified acidosis
-Hyponatremia = arrhythmias
-GI disturbances
-Spironolactone = gynecomastia & ED in men, amenorrhea in women
Thiazide Diuretics
-Examples
-Mech
-Use
-Other
-Hydrochlorothiazide, Chlorthalidone, Metolazone, Indapamide
-Preload reducers
-Block sodium reabsorption in the distal convoluted tubule (site 3) of the nephron = increases distal sodium delivery to the collecting duct
The collecting duct tries, but fails, to handle the excess sodium burden (overall, more sodium in the urine, water follows sodium, and you have decreased preload) = diuresis
-Increased excretion of sodium, chloride, potassium = hyperpolarization of smooth muscle cells = vasodilation
-For edema associated with CHF
-Mild to moderate HTN
-Alone = stage 1 (130-139)
-Combo with ACEi/ARB = stage 2 (>140)
-Prevention of calcium oxalate kidney stones
-SEs:
-Hypokalemia & metabolic alkalosis
-Hyponatremia, hypomagnesemia, hypercalcemia
-Precipitation of gout flares (prevents urate secretion)
-Rare, pancreatitis
-CIs = hypokalemia, anuria, not recommended in pregnancy
Loop Diuretics
-Examples
-Use
-Mech
-Other
-Ending in “-semide”
-Furosemide/Lasix, Torsemide
-Preload reducing/ elimination
-Acting at site 2/ thick ascending limb of the Loop of Henle, inhibition of the sodium-potassium-chloride co-transporter (NKCC2) = inhibition of Na, K, Cl reabsorption = rapid diuresis & reduction of intravascular volume
-Short acting in duration (not effective BP management)
-Potent = they take off too much volume too quickly
-Hypervolemic states (CHF + volume overload or ascites)
-Not used to treat HTN, but do have BP effect
-Used to maintain urine output in chronically failing kidneys
-SEs:
-Hypokalemia, hypomagnesemia (can result in arrhythmia)
-Other electrolyte levels lowered
-Metabolic alkalosis
-Excess volume removal = prerenal azotemia (AKI due to volume depletion)
-Ototoxicity (accumulation of furosemide)
-CIs = anuria (little fluid in the body already), not recommended in pregnancy
Nitrates
-Examples
-Use
-Mech
-Other
-Nitroglycerin = sublingual rapid acting
-Nitroprusside = IV
-Isosorbide dinitrate (ISDN) or Isosorbide mononitrate (ISMN) = daily PO
-Nitrates work on veins the way hydralazine works on arteries (NO induces venodilation)
-Blood pools in capacitance veins = preload is reduced (not long-term)
-ISDN + hydralazine = heart failure
-ISMN = anti-anginal treatment (see above)
-HTN emergency via parenteral route
-SEs:
-Headache
-Nitroprusside:
-Turns into cyanide after prolonged use (try to use something else)
-CIs = cannot be used with PDE5is (Viagra or cialis) due to dangerous drop in BP
Beta-Blockers (BP perspective)
-Nonselective blockers (B1/B2):
-Propranolol
-Nadolol
-Timolol
-Beta1 Selective blockers:
-Metoprolol (PO, IV)
-Esmolol
-Atenolol
-Bisoprolol
-Nebivolol
-Beta1-alpha1 blockers:
-Carvedilol
-Labetalol (IV)
-Use/Mech
-Non-selective:
-Block both beta1 (heart) & beta2 (lungs/skeletal muscle) adrenergic receptors
-Beta1 Selective:
-Rate control agents
-Anti-arrhythmic treatment
-BP Perspective:
-Propranolol/ nadolol = indicated for preventing esophageal varices from bleeding, reducing panic attacks/nervousness
-Timolol = eye drop for glaucoma, not ideal for cardio due to SEs
-Metoprolol = tachy arrhythmias (ex: Afib or comorbid Afib), CAD, HFrEF + BP reduction not needed
-Nebivolol = induces NO production via activation of Beta3 receptors
-Beta1-alpha1 blockers = chosen when Beta blockade is required for another diagnosis (CAD, HFrEF), & rate control is not a concern or additional BP reduction is desired
-Labetalol = end-stage renal disease patients, inpatient
Beta-Blockers Continued
Side effects & CIs
-Nonselective = induction of asthma due to blocking Beta 2 (bronchospasm)
-Generally = AV block, bradycardia, hypotension, dizziness, nausea, constipation, insomnia, etc.
-BB Overdose = bradycardia, blunt hypoglycemic response (treat with glucagon)
-CIs = severe bradycardia, sick sinus syndrome, 2nd/3rd degree AV blocks, cardiogenic shock, decompensated HF, etc.
What part of the RAAS Path does beta blockers impact?
-They are blocking SNS stimulation
-The start of the pathway at Renin (kidney) is blocked = downstream effects blocked
-No change in bradykinin
Alpha 1 Antagonists
-Examples
-Use
-Mech
-Other
-Ending in “-zosin”
-Selective blockers
-Terazosin
-Doxazosin
-Prazosin
-Non-selective blockers
-Phentolamine
-Phenoxybenzamine
-Selective alpha1 blockers in arterioles & venules
-Inhibition of NE-mediated vasoconstriction = vasodilator
-Non-selective = vasodilators
-Used to dilate the ureters & urethra in the management of BPH
-Adjunts for medical expulsion therapy in kidney stones
-PTSD
-Raynaud phenomenon
-Non-selective = pheochromocytoma (secondary HTN)
-SEs = Orthostatic hypotension, priapism
Minoxidil (Rogaine)
-Direct vasodilator
-Causes the opening of potassium channels in smooth muscle cells, leading to hyperpolarization, reduced calcium influx, and subsequent relaxation
-Consider drug as a super-potent arterial vasodilator, a mega-upgrade to hydralazine/ used to replace hydralazine when it fails to control BP at max doses
-Typically used by nephrologists & cardiologists in pts on 3+ antihypertensive meds
-Use:
-Resistant HTN (4th or 5th drug)
-Replaces hydralazine when max dose it not effective
-SEs = sodium & water retention (peripheral edema), pericarditis that can progress to tamponade, hypertrichosis (facial hair)
-CIs = pheochromocytoma, severe renal disease, uncontrolled HTN
-If BP is this unstable, cardio should be managing anyway
Centrally Acting Sympathoplegics
-Examples
-Use
-Mech
-Other
-Clonidine, alpha-methyldopa
-Clonidine:
-Consider as a bad drug with minimal use
-It stimulates alpha 2 receptors/ inhibition of E/NE from adrenergic nerve terminals
UWorld - decreasing presynaptic release of NE
-alpha-Methyldopa:
-alpha2 receptor agonist/ inhibition of E/NE from adrenergic nerve terminals
-Overall, decreases sympathetic outflow & decrease in BP
-Alpha-methyldopa used in pregnancy
-Other:
-Clonidine has to be taken 3x daily (risk of rebound HTN if missed dose due to release of stored NE)
-SEs clonidine = sedation, dizziness
-SEs alpha-M = drug-induced lupus, myocarditis, hemolytic anemia
Pt has MI involving the right atrium & develops sinus bradycardia & hypotension. Management?
-IV atropine
-Anticholinergic to increase HR
Treatment for hypertensive emergency (HTN + signs of end-organ damage)?
-(Uworld) Fenoldopam = peripheral dopamine-1 receptor agonist = vasodilation of most arterial beds & a decrease in systemic BP
-Especially helpful in pts with HTN & renal insufficiency
Temporary options for bradyarrhythmia
-Atropine = PNS blocker/ anti-cholinergic
-Epinephrine (or Dopamine, Dobutamine) = Stimulating Beta 1 (heart) + vasoconstriction
-Correct etiology or pacemaker placement
What can we consider of Class 1 & 3 anti-arrhythmics?
-Classes 1 (Sodium blocker) & 3 (Potassium blocker)
-Myocyte anti-arrhythmics = working at the myocyte action potential
-For rhythm control (helping to return back to sinus)
Describe the MOA of Sodium Channel Blockers
Give examples of the classes
-MOA = inhibition/ reduction of depolarization (phase 0) or reducing the likelihood of AP discharge
-Class 1a = can also block K channels:
-Quinidine, Procainamide, Disopyramide
-SEs = Cinchonism (tinnitus, ocular dysfunction, CNS excitation), Arrhythmia, Hypotension, Lupus-like syndrome
-Class 1b:
-Lidocaine, Mexiletine
-Lido can be used for post MI Vtach or Vfib
-Used if amiodarone or electricity does not work/not available
-SEs = Lido has toxic metabolites (may have metal taste in mouth), Arrhythmia, CNS effects
-Class 1c:
-Flecainide, Propafenone
-Used for refractory Vtach, WPW, Afib without structural or valvular changes
-SEs = Arrhythmia, Visual disturbances
-Note: try to not have pts on these drugs unless they were started by cardio
Describe function of potassium channel blockers (class 3)
-Myocyte rhythm control
-Prolonging the AP duration & refractory period/ repolarization phase
-Amiodarone (most efficient)
-Sotalol (non-selective BB)
-Ibutilide, Dofetilide
-Uses = SVT, Vtach/Vfib, Afib/Aflutter, may be used as rate control in HFrEF in exacerbation with Afib with RVR
-SEs:
-Amiodarone = trigger other arrhythmia, interstitial lung disease!!, long-term can see corneal opacities, thyroid issues, lung infiltration
-Interactions = Warfarin (risk of stroke), Digoxin (hyperkalemia), procainamide, Phenytoin, etc.
-Use with caution in addition to TCAs
What can we consider of Class 2 & 4 anti-arrhythmics?
-Class 2 (Cardioselective Beta-Blocker) & 4 (non-DHP Calcium blocker)
-Working at the pacemaker action potential
-For Rate control (helping to slow down ventricular rate)
Describe the function of Beta-blockers
-MOA = blocking Beta 1 receptors of the SNS
-Reducing myocardial O2 consumption/ demand by keeping the rate slow & steady
-Decreased conduction velocity through the AV node
-Decreased contractility in non-PM cells
-Esmolol = selective B1
-Propranolol = non-selective B1/B2
-Labetalol = non-selective B1/B2 & selective a1
-Metoprolol, Carvedilol (see list above)
-Use in Afib/aflutter, Heart failure with reduced EF (HFrEF) because it reduces neurohormonal remodel/ increased survival, post-MI or angina
-SEs = Arrhythmia, hypotension, insomnia, nightmares (propranolol)
-Do not initiate or increase during HF exacerbation
-CIs = COPD, asthma
