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Cardiovascular Pharmacology (hypertension (Diuretics (loops (edema)…
Cardiovascular Pharmacology
hyperlipidemia
treatments
statins
decrease risk of major cardiovascular events by up the 50%
all patients with ASCVD or diabetes should be on statins
MOA: inhibit HMG-CoA reductase in the liver which is an enzyme that is critical for LDL production
examples: atorvastatin, rosuvastatin, simvastatin, pravastatin, lovastatin
side effects: myopathy
fibrates
can be used to treat hypertriglyceridemia in combination with statins, but they increase muscle pains
fenofibrate and gemfibrozil: bind to receptors in the liver and adipose tissue to increase breakdown of triglycerides, may cause gallstones, myopathy
other LDL drugs
ezetimibe: inhibits cholesterol absorption from small intestines, added to statins may cause diarrhea
bile acid sequestrants: bind bile acids which are then excreted resulting in a decrease cholesterol, may cause constipation
Niacin: various mechanisms that lower LDL raise HDL and lower triglycerides, not sed anymore due to side effects and drug interactions, may cause flushing, increased glucose, increasd uric acid increased liver enzymes
high cholesterol in the blood leads to plaque deposits in the arterial wall that eventually occlude the vessel
if these deposits rupture they can cause thrombosis and infartions
cholesterol
LDL leads to deposits of plaque
HDL transports LDL to the liver to be broken down
triglycerides store extra calories in fat cells
hypertension
Diuretics
thiazides (first line)
hydrochlorothiazides
chlorthalidone
effects: inhibit sodium reabsorption in the kidneys causing retention of water in the nephron resulting in diuresis
loops (edema)
furosimide
torsemide
bumetanide
effects: inhibits sodium and chloride reabsorption in the LoH resulting in diuresis
potassium sparing (second line)
spironolactone
triamterene
effects: prevents potassium secretion in the distal tubule leaving more sodium in the tubule resulting in diuresis
side effects: hypotension, dehydration, hyponatremia, hypokalemia, hyperkalemia
ACE-Inhibitors
MOA: inhibits angiotensin-converting enzyme from converting angiotensin I to angiotensin II
side effects: hypotension, hyperkalemia, dry cough, angioedema
examples: lisinopril, quinapril,ramipril,enalapril,benazepril
ARBs
MOA: block angiotensin II receptors on vascular and other tissues
side effects: hypotension, hyperkalemia
examples losartan
Calcium channel blockers
examples: amlodipine, nifedipine, felodipine, nicardipine
Dihydropyridines MOA: primarily block calcium entry into vasular smooth muscle, limiting contraction, resulting in vasodilation
Non-dihydropyridines MOA: primarily block calcium entry into the myocardial cells, limiting contraction and result in decreased HR and contraction force, may cause bradycardia
side effects: hypotension, peripheral edema, heartburn, constipation, gingival hyperplasia
Beta-Blockers
non selective
carvedilol, labetalol, propranolol, sotalol
cardio selective
metoprolol, atenolol,, nebivolol, bisoprolol
MOA: block fight or flight response, block sympathetic receptors in the heart, causing decreased heart rate and ultimately decreased cardiac output
side effects: hypotension, bradycardia, lethargy/fatigue, depression, bronchoconstriction
other agents
alpha-blockers ((terazosin): block alpha-1 receptors in vascular smooth muscle leading to decreased vascular resistance, may cause hypotension
alpha agonist (clonidine): activate alpha-2 receptors in the CNS decreasing sympathetic output to the heart and vasculature resulting in decreased blood pressure, hypotension, and sedation
vasodilators (hydralazine): directly vasodilates the puerperal vasculature through inhibition of smooth muscle contraction, may cause hypotension, hydralazine-induced lupus erythematosus
angina pectoris
pain and discomfort caused by inadequate oxygenation of the heart muscle, radiates down the left arm and jaw
use drugs that maintain or restore oxygen supply the heart
beta blockers: decrease HR resulting in decreased myocardial oxygen demand
calcium channel blockers: dilate coronary arteries and peripheral vasculature, decreasing exertion of the heart
organic nitrates: converted to nitric oxide which inhibits smooth muscle contraction in the vasculature
nitroglycerine: sublingual fast acting or long lasting tablets, may cause headache, flushing, dizziness/hypotension
coronary artery disease
antiplatelets
chronic heart failure
develops when the heart is unable to pump blood adequately to oxygenate the tissues in the body, congestive refers to accumulation of fluid in the peripheral tissues, decreased exercise tolerance, difficulty breathing, and swelling
types of HF
HFrEF: systolic dysfunction, myocardial damage
digoxin: improve myocardial contraction force, increases intracellular calcium in the myocardium resulting in increased contractility, may cause toxicity and arrhythmias
Diuretic (loops): decrease fluid volume and reduce fluid accumulation, may cause excessive fatigue and weakness
beta-blockers: prevents sympathetic overload of the heart and limits remodeling
ACE-1/ARBs: decrease peripheral vascular resistance and cardiac hypertrophy/remodeling
aldosterone antagonists: block excess aldosterone resulting in mild diuresis and preventing cardiac changes
vasodilators: dilate peripheral vasculature
HFpEF: diastolic dysfunction, thickening of heart walls
treat for hypertension and edema
arrhythmias
antiarrhythmics
class 2 beta blockers
class 1 sodium channel blockers
subclass A
subclass b
subclass c: flecainide, propafenone
class 3 repolarization, prolongation
amiodarone, dofetilide
class 4 calcium channel blockers
diltiazem, verapamil
all antiarrhythmics cause arrhythmias more with class 1 and 3
anticoagulants
normal cardiac conduction is coordinated and predictable, any factor that disrupts this conduction process can result in arrhythmias
factors
metabolic and electrolyte imbalances
cardiac toxicity
cardiac disease
genetic factors
atrial or ventricular arrhythmias
atrial is the most common and could result in clots and cause stroke
DVT/PE
abnormal or undesired formation of blood clots, forms in the veins of the legs occluding the vessels and may travel to the lungs
treatment
antiplatelets drugs (aspirin, clopidogrel): use to prevent heart attack and atherogenic ischemic strokes by affecting platelets
MOA: decreased platelet activity
aspirin: low doses provide antiplatelet effects, secondary prevention, risk of hemorrhage need to be weighed
ADP (adenosine diphosphate) receptor blockers: secondary prevention, used if patient is allergic to aspirin, usually added to aspirin therapy and increases the risk of bleeding
anticoagulants (warfarin, heparin, enoxaparin): used to treat/prevent DVT/PE and prevent cardiogenic ischemic strokes by affecting clotting factors
injectables:
heparin: inactivate clotting factors in the clotting cascade, usually given inpatient via IV
enoxaparin: inactivate clotting factor Xa in the clotting cascade, subcutaneous administration, easier to dose and monitor
orals
warfarin: interferes with vitamin K metabolism in the liver inhibiting the activity of vitamin K- dependent clotting factors, most common anticoagulant, tkes 5-7 days for therapeutic effect, used to prevent recurrent DVT/PE
factors affecting efficacy
adherence
missed or extra doses
vitamin k foods
green leafy veggies, brocoli, mayonaise?
sickness
high fever or diarrhea
drug interactions
antibiotics, acetaminophen >2g per day
Novel oral anticoagulants (NOACs): directly inhibit specific factors in the clotting cascade (Xa or thrombin depending on the drug) given in fixed doses, generally safer with fewer bleeding events, very expensive
antithrombotics ("clot busters"): used on acute MI or ischemic stroke to break down clots by breaking down fibrin, the main component of clots
side effects: bleeding, blood in urine or stool, bleeding gums, unexplained nosebleeds,extensive bruising, unusually heavy menstrual flow, vomiting blood