SIlverollbars

• Aspirin
• Plavix.

• -Hi lev of lipids in blood (major factor for CV disease)
• -most familiar (plaque buildup
• Statins (at end of word) (aka HMG-CoA reductase inhibitors
• Other
• exetimbe (Zetia)
• B vitamin (niacin)

• Atorvastatin *(Lipitor)
• 1st drug of choice in reducing lipids
• Dec LDL by up to 40%, raises HDL lev, mostly at night, mostly safe, monitor liver functions
• Serious adverse effects
• myopathy-injre muscle tissue. Rabdomyolysis (rel CK and K and in severe cases can cause renal impairment)
• Hepatox-don't give to active/chronic liver disease
• Link to Parkinsons
• Preggo-stop meds
• Reduces

• Baseline lipid and LFT
• drugs- inc digoxin, don't take w grapefruit juice, effects warfarin (won't be on exam)

• Atorvastatin *(Lipitor)
• MI, cardiac event, stenosis, leg circ problems, all about plaque buildup (plaque can build up pretty much anywhere, stroke (plaque can build up in carotids)

• Blocks absorption and reabsorption of cholesterol in intestines
• LDL levels are reduced and slt ic HDL
• GI- mayt affect liver, abd pain, diarrhea, resp-cough upper respiratory infections

• Best for reducing LDL inc HDL
• Very safe, but Unppleas SEs ^ noncompliance
• Skin-itching intense flush of face, neck, ears
• GI NVD, liv dam
• endo-hyperglycemia

Used to be gold stand. Cardiac cells die, cell enz and prots are rel into circ. Important diagnostic tol. Higher lev can tell ext of dam. Do serial check. CK, CKMB start to rise w/ in 2-3 h of beginning MI. eak lev 24 h return to norm 24-38.

• (T not gold stand, found in skeletal muscle, so not as big a deal)
• 3-5 h after MI, may stay up to 21 days, affected by skeletal muscle, renal dis
• Troponin I is #1 gold standard
• the specific cardiac marker, not aff by skel muscle or renal. 3 h after MI, peaks at 14-18h, returns to norm 5-7days

• B-type natriurtic peptide
• higher the #, the more severe the heart failure.

• Sodium channel blockers (class I)
• Beta blockers (Class II)
• K+ blockers (Class III)
• Ca++ channel blockers (Class IV)
• Other

• abnorm.s of elec cond in heart. may be harmless or deadly. Need ECG to know for sure. Atrial dysrhythmias-15% have strokes
• AFib affects 2 mill people in USA
• May need cardioversion (may have arrhythmia that can be converted into normal sinus rhythm. Energy given, not as much as defib). or defib (someone in vfib is dead-no heartbeat)

blocking ion channels (Na+, Ca++, K+). Keep or slow stuff from going in and out of cells. Ex: Ca++ channel blockers are supposed to slow the HR down (Ca ion responsible for myocardial contraction)

• -right after depolarization. Need smoke break. cell cannot initiate another action potential. R on T.
• -everything is resetting

• Both slow impulse conduction across myocardium
• Make sure you check elytes

not rec but still used

• rapid control of ventric dysrhythmia (IV), Na+ channel blocker, slow rhythm. Fast vtach into normal rhythm.
• Lidotoxicity- if on more than a day or 2 check levels
• confusion, hypotension, worsened arrhythmia, bradycardia (heart block) cuz slowing HR down.
• Resp-resp arrest, rare. status asthmaticus
• neuro- conf seiz, ltheadedness, drowsiness

assess prior, cardiac monitor, vitals and Elytes, tox (seiz, conf), widening of QRS

• blood pressure, HR
• help protect heart from second MI (dec contractility of muscle, dec HR). most common now ACE inhibitors are almost #1
• Slows HR thru AV. Reduce automaticity (waiting to beat, excitability) in SA node.

Antidysrhythmics, HTN, MI (everyone who's had one), stage fright

• heart
• lungs

• People w asthma
• diabetes (B2 can stop glyconeogenesis)

bradycardia, heart block, heart failure (makes sense because contracting softer)

• K+ channel blockers
• Amiodarone (cordarone)

• Now since 05, first antiarrhythmic used in CODE
• Tx resistant ventric tach
• Tx of atrial tach (atrial fib)
• Half life long, for a month
• Resp- sev pulm tox, pneumonia like sx Can cause lungs to
• stiffen (fibrosis)
• Hepatic dysfunction (LFTs once a year)
• Neuro- photosensitivity, dizziness
• Inc effects of digoxin
• Enhances actions of anticoags
• Caution w herbal supps
• Review CV, pulm, liver fnctn before, reg
• IV- continuous EKG monitoring
• Clotting factors made in liver
• Monitor for pulm tox-fatal
• Monitor elytes

• Monitor BP, HR
• Fairly common CV disorders
• Slows conduction velocity, slows impulse through AV node
• Prolongs resting stage
• Only a few “approved” to treat dysrhythmias
• HTN, AFib (cause slows AV node down)

• Also treats vasopspastic angina
• Helps coronary arteries relax
• HTN
• A Fib or flutter
• CV-AV block, brady, arrhyth, HF,
• hypotension
• CNS- hache, insomnia,
• photosensensitivity
• Verapamil (Calan) old. Grapefruit may inc levels
• Grapefruit juice w any drug?
• No

• Common.
• Before dijoxin, apical pulse for 1 minute.
• Slows impulses through heart
• Works on SA, also by AV. Double whammy.
• Possible toxicity.
• Increases contractility in myocardial cells contract
• Excessive levels cause serious dysrhythmias
• SOB, brady, dizziness, diaphoresis, chest pain, syncope
• Antidote: binds
• to dij, decreases level
• Increases contractility, so good to a point, but can cause
• HF
• (heart work increases, gets bigger, stiffer, floppier)
• worry about K+ linked w hypo K, can make pt have
• hyperkalemia
• CV arrhythmias, HF, hypotension
• GI- anorexia, rise in K+

• Anicoags
• Antilpt
• Tissue plasminogen
• Nitrates
• Bnete-ad blockers/Ca++ channel blockers
• Salicylates
• Antidystrhythmics
• Stool softener
• Diuretics
• Elyte replacement

resp arr, slows GI, GU, NVD. PPl allergic to preservatives, not morphine

• IV
• short acting-PRN
• when long acting:
• if long term stable angina, long acting one. Patch, sign, date. If hypotensive, take nitro patch off, wipe chest

• Severe hypotension sildenafil (Viagra), tadalafil (Cialis)
• subling spray, sublingual tabs, paste
• make sure to sign and date

• CV- hypotension, tachy, flushing, palp
• CNS-h ache, throbbing, dizziness
• EENT- sublingual burning

• 911 if angina unrelieved X3 doses
• avoid alcohol
• store in cool dark place
• tell about SEs
• replace after 6 mos in book, 30 days
• cotton absorbs drug

• red workload of heart
• SLow HR
• reduce contractility
• dec O2 demands, anti hypertensive, reduce myocardial necrosis post MI
• Selected B blockers treat angina

dilates coronary arteries, relax them

decrease BP slow HR

• can't pump enough blood to sustain body's needs
• circ cong
• pulm, systemic cong, combo of any.

• yes. Backs up to pulm artery, pulm artery BP goes up.
• Rt ususally 2ary to something else

• SOB
• depression (dx moderate heart failure), pain, angina

100-110

• Digoxin increases contraction
• apical pulse for one minute
• antidote binds to dij, but slow

• Ace Inhibitors, 1st BP med we use for HTN. Use for HF by trying to offset HTN
• catching up to Dig
• Managing HTN, less risk of dev into heart failure.

gets aldosterone

• SEs
• hyperkalemia, angioedema (facial region)

• hydrochlorothiazide (hydrodiuril)
• the most prescribed diuretic or HTN and or HF. If doesn't work on own add a pril. Most common combo with Lisinopril
• Reduces BP 10-20 mmHg
• acts on different part of kidneys to increase urine production
• CV-hypotension

• Spironolactone (aldoactone)
• a diuretic used that spares K+
• Inhibiting aldosterone in distal tubule
• Metab Hyperkalemia
• (super rare, angioedema). Not used as much cuz not as powerful- Lasix most powerful

• HF
• pt drown in own sec
• code without immediate and aggressive interventions