Cardiac Flashcards by Kasey May

Thiazide Diuretics

Drugs- hydrochlorothiazide (microzide), chlorthalidone, indapamide, metolazone (zaroxolyn)
MOA- lower BP by increasing sodium and water excretion, decreased CO and renal blood flow
Used as initial therapy
Useful in combo
ADE- hypokalemia, hyperuricemia, hyperglycemia, hyponatremia, hypomagnesemia, hypovolemia

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Loop diuretics

Drugs- furosemide, torsemide, bumetanide, etharynic acid
MOA- blocks sodium and chloride reabsorption in the kidneys, decreases renal vascular resistance
ADE- hypokalemia, hypocalcemia, ototoxicity
Used alone or in combo for HTN, CHF, peripheral edema

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Potassium sparing diuretics

Drugs- amiloride (midamor), triamterene (dyrenium) inhibit sodium transport in late distal and collecting ducts
Spironolatone (aldactone) and eplerenone (inspra) are aldosterone receptor antagonist
MOA- all reduce potassium, aldosterone antagonist have benefit for improving cardiac remodeling and SHF
Used in combo with loop or thiazides to reduce potassium loss
Also used in PCOS
ADE- hyperkalemia, gynecomastia

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Beta blocker

See neuro slides
Acebutolol, atenolol (tenormin), betaxolol, bisoprolol, carvediolol (coreg), esmolol (brevibloc), labetolol (trandate), metorprolol (lopressor, toprol), nadolol (corgard), nebivolol (bystolic), pindolol, propranolol (inderal, innopran)

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ACEI

Drugs- benazepril (lotensin), captopril, enalapril (vasotec), fosinopril, lisinopril (prinivil, zestril), moexipril, quinapril (accupril), perindopril, ramipril (altace), trandolapril
MOA- inhibit ACE which converts angiotensin 1 to angiotensin 2, decreases secretion of aldosterone, decrease cardiac preload and after load
Uses- HTN, MI, CHF, CKD, increased risk for CAS
ADE- dry cough, angioedema, increased potassium
Monitor renal function
Tetrogenic

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ARBs

Drugs- azilsartan (edarbi), candesartan (atacand), irbesartan (avapro), losartan (cozaar), olmesartan (benicar), telmisartan (micardis), valsartan (diovan)
MOA- blocks Angiotensin 1 receptors and decrease angiotensin 2 production
Can be used as first line for HTN especially in DM, CKD, CHF
ADE- similar to ACEI, but cough and angioedema less likely
Do not give with ACEI or in pregnancy

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Renin inhibitor

Drug- aliskiren (tekturna)
MOA- selective renin inhibitor, inhibits renin and acts earlier in the renin angiotensin aldosterone system
Uses- HTN
do not used with ACEI or ARB
ADE- diarrhea, cough and angioedema but less likely
Tetrogenic
CYP3A4 metabolite

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CCB

Drugs- amlodpine (norvasc), clevidipine (cleviprex), diltiazem (cardizem, cartia, tiazac), felodipine, isradipine, nicardipine (cardene), nifedipine (adalat, procardia), nisoldipine (sular), verapamil (calan, verelan)
1st line for BP in AA
Subclasses
-diphenylalkylamines- verapamil-slows cardiac conduction and decreased HR for angina, SVT, migraines, clusters
-benzothiazepines- diltiazem-similar to verapamil but less ADE
-dihydropyridines- nifedipine, amlodipine, felodipine, isradipine, nicardipine, nisoldipine, grater affinity for calcium channels, HTN, minimal effect on conduction and HR
MOA- block calcium in the heart and smooth muscles
Uses- HTN in asthma, DM, PVD, angina, afib
ADE- heart blocks, constipation, diltiazem and verapemil should be avoided in CHF or blocks, dizziness, HA, fatigue, peripheral edema

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Methyldopa

MOA- alpha agonist
ADE- sedation, drowsiness
Uses- HTN in pregnancy

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Vasodilators

Drugs- hydralazine, minoxidil
Reserved for resistant HTN
MOA- produce relaxation of vascular smooth muscles, increase myocardial contraction and can increase HR and oxygen consumption
Can cause angina, MI or CHF
Can increase sodium and water concentrations
Hydralazine- HTN and pregnancy Induced HTN, ADE- HA, tachycardia, nausea, sweating, arrhythmias, angina, lupus like syndrome
Minoxidil can cause body hair growth so can be used for male pattern baldness

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HTN crisis

DOC- CCB like nicardipine and clevidipine, nitroglycerin, adrengeruc receptor antagonist like phentolamine, esmolol, labetalol, hydralazine

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Carbonic anhydrase inhibitors

Drug- acetazolamide (diamox)
MOA- inhibits carbonic anhydrase in proximal tubules, bicarbonate is released more
Uses- glaucoma, altitude sickness
ADE/ metabolic acidosis, potassium depletion, renal stone forming, drowsiness, paresthesia
Avoid in cirrhosis

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Osmotic diuretics

Drugs- mannitol (osmitrol)
MOA- filtered substances undergo little or no reabsorption so results in higher osmolarity in tubular fluid, Limits additional water reabsorption
Not useful for conditions in which sodium retention occurs
Use- maintain urine flow following acute toxic ingestion of substances that can cause ARF, and increased ICP
ADE- dehydration, extracellular water expansion

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Sacubitril/valsartan (Entresto)

MOA- combines ARB with neprilysn inhibition and results in increased concentration of vasoactive peptides leading to natriuesis, vasodilation and inhibition of fibrosis
Decrease preload and after load
Uses- use in place of ARB/ACEI in SHF
ADE- similar to ACEI/ARB,
Do not give in hx of angioedem

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Ivabradine (corlanor)

Class- hyperpolarization activtated cyclic nucleotide gates channel blocker
MOA- acts slowly on If current in SA node to reduce heart rate without reducing contractility, AV conduction, ventricular repolarization, or blood pressure
Uses- SHF
ADE- bradycardia
Not to be used in pregnancy or BF, with heart blocks or potent 3A4 inhibitors

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Vericiguat (verquvo)

Class- soluble guanylate cyclase stimulator
MOA- directly simulates sodium guanylate and signals activation of cGMP to improve left ventricular compliance, vasodilation, reduce inflammation, and prevent hypertrophy and fibrosis
Uses- SHF recently hospitalized and in GDMT
ADE- minimal but due to vasodilators effects, hypotension, anemia, syncope
Contraindicated in pregnancy or BF
Avoid in use with other nitrates or phosphodiesterase inhubutirs

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Milirinone

MOA- phosphodiesterase inhibitor that increases cAMP
Results in increase cardiac contractility
Usually given IV for SHF
Dobuatmine and milirinone can be used for intermediate term treatment for OP palliative care
Can also be used for right sided HF and pulmonary HTN

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Class 1a anti arrhythmics

MOA- acts by blocking voltage sensitive sodium channels, slows phase 0 depolarization in cardiac myocytes and slows down QRS and QT
Drugs- quinidine, procainamide, disopyramide (norpace)
Uses- quinidine for variety, procainamide for atrial and ventricular, disopyramide for afib or flutter or ventricular
ADE- worsen HF, blurred vision, tinnitus, HA, disorientation, psychosis, hypotension if IV, disopyramide anticholinergic SE
D-D- CYP2D6 for quinidine and disopyramide
Do not use in atherosclerosis or HFrEF

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Class 1B antiarrthymics

Drugs- lidocaine (xylocaine), mexiletine
MOA- sodium channel blocker shortens phase 3 repolarization in cardiac myocytes
ADE- worsening ventricular arrhythmia, syncope, dizziness, tremor, ataxia, paresthesia, confusion, seizures, liver failure, n/v, dyspepsia, dysphasia
Uses- alternative for VT VF, used in combo with amiodarone in VT storm
Mexiletine has narrow therapeutic range
D-D- CYP2D6

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Class 1C anti arrhythmics

Drugs- flecainide (tambocor) and propafenone (rythmol)
MOA- sodium channel blockers phase 0 depolarization,
ADE- bradycardia, long QT, worsening arrthymias, acute HF, dizziness, hypotension, constipation, HA, tremor, visual disturbances, bronchospasm, liver failure, agranulocytosis, anemia, edema
Uses- af and a flutter, refractory ventricular arrhythmias

Avoid in structural heart disease

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Class 2 anti arrhythmics

Beta blockers
Atenolol, esmolol, metoprolol
MOA- inhibit phase 4 depolarization in SA and AV node
Uses- tachy arrhythmia

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Class 3 anti arrhythmics

Drugs- amiodarone (cordarone, pacerone), dofertilide (tikosyn), dronedarone (multaq), ibutilide (corvert), sotalol (betapace, sorine)
MOA- potassium channel blocker, prolongs phase 3
-Amiodarone- refractory SVT or ventricular arrhythmias, afib and flutter, ADE- pulmonary fibrosis, neuropathy, hepatotoxicity, corneal deposits, optic neuritis, blue gray skin discoloration, thyroid issues
-dronedarone- similar to amio, better ADE than amio, but liver failure still issue, do not given in symptomatic CHF, or permanent AF due to increase risk of death
-sotalol- also non selective blocker activity, afib, a flutter, refractory paroxysmal SVT, and ventricular arrhythmia, can be used in LVH or CAD, similar ADE to BB, initiate in hospital for QT monitoring
-dofetilide- first line for AF or HF or CAD, must be IP due to risk of proarrhymias
-ibutilide- DOC for chemical conversion of a flutter, IP due to risk of arrhythmias

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Class 4 anti arrhythmics

Drugs- diltiazem (cardizem), verapamil (calan, verelan)
MOA- calcium channel blockers, inhibit action potential in SA and AV nodes
ADE- bradycardia, heart block, active HF, peripheral edema; hypotension, dizziness, constipation, gynecomastia, sexual dysfunction, gingival hyperplasia
Uses- atrial arrhythmia, re entrant SVT, reduce ventricular rates in AF or flutter

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Other anti Arrhythmia

Digoxin (also for CHF)
Adenosine- decreases automaticity in AV node, IV for converting SVT, flushing, CP, and hypotension, very short DOA
Magnesium sulfate- torsades
Ranolazine- similar to amiodarone, antianginal properties, refractory atrial and ventricular arrhythmias in combination with others

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Anti angina drugs

-Beta blockers- nadolol (corgard), propranolol* (inderal, innopran), sotalol (betapace, sorine), atenolol (tenormin), bisoprolol, metoprolol, nebivolol, as they decrease oxygen demand in myocardium, decrease CO, and BP, first line except vasospastic which can make it worse
-CCB- amlodipine (norvasc), felodipine (plendil), nifedipine (adalat, procardia), diltiazem (cardizem), verapamil (calan, verelan), ateriorvasodulators, decrease vascular resistance, decrease after load

Non selective versus selective BB

Non selective
Nadolol, propranolol, sotalol
Selective
Atenolol, bisoprolol, metoprolol, nebivolol

Nitrates

Drugs- nitroglycerin, isosorbide mono nitrate and isosorbide dinitrite
Can also be used in CHF
MOA- relax smooth muscle by nitric oxide causing dilation
ADE-HA, postural hypotension, facial flushing; tachycardia
DO NOT USE WITH PDE 5 INHIBITORS SEVERE HYPOTENSION
Tolerance

Ranolazine (Ranexa)

MOA- inhibits sodium current improving oxygen supply and demand
Improves diastolic function
Has anti arrhythmic properties
ADE- long QT

HMG CoA reductase inhibitors aka statins

Drugs- atorvastatin (Lipitor), fluvastatin (lescol), lovastatin (altoprev), pitavastatin (livalo), pravastatin (pravachol), rosuvastatin (crestor), simvastatin (zocor)
MOA- competitive inhibitors of HGM CoA reductase the rate limiting step in cholesterol synthesis, decrease LDL, for ASCVD risk factors
ADE- elevated liver enzymes, myalgia, myopathy, rhabdomyolysis,

Cholesterol absorption inhibitors

Drugs- ezetimibe (zetia)
MOA- selectively inhibits absorption of dietary and biliary cholesterol in small intestine
Lowers LDLin combo with statin
Do not give in hepatic insufficiency
ADE- uncommon

Bile acid sequestrants

Drugs- colesevelam (welchol), colestipol (colestid), cholestyramine (questran, prevalite)
MOA- binds cholesterol to bile and is excreted via feces
Statin preferred but for those who cannot tolerate others
Can also be used in diabetes (colesevelam)
ADE- GI disturbances like constipation, nausea, flatulence, interfere with vitamin absorption
D-D- digoxin, warfarin, thyroid

PCSK9 inhibitors

Drug- alirocumab (praluent), evolocumab (repatha)
MOA- inhibits protein converts substilisin kexin type 9 in the liver and leads to degradation of LDL receptors
Maximize statin therapy or those intolerant to statins or with familiar hypercholesterolemia
SQ injection
Well tolerated some injection site reactions, allergic reactions, diarrhea, myalgia, URI, nasopharyngitis

Adenosine triphosphate citrate lyase inhibitor

Drugs- bempedoic acid (nexletol)
MOA- lowers LDL by inhibiting cholesterol synthesis in the liver with ATC further upstream of HGM CoA reductase
Uses with max statin therapy and familial hypercholesteremia
Well tolerated- can cause hyperuricemia, back pain, muscle spasm, tendon rupture

Microsomal triglyceride transfer protein inhibitor

Drug-lomitapide (juxtapid)
For familial hypercholesterolemia
MOA- inhibits microsomal triglyceride transfer and lows VLDL
Uses as adjunct
ADE- liver toxicity, chest pain, fatigue, GI distress, infection, respiratory issues
D-D- CYP3A4

Fibrates

Drugs- fenofibrate (triglide, tricor) and genfibrozil (lopid)
MOA- bind to peroxisome proliferator response elements which decrease triglyceride levels throwing increased expression of lipoprotein lipase
Used in hypertriglyceridemia
ADE- GI issues, gallstones, myositits, muscle weakness
Do not give with simvastatin or in severe liver disease, or renal dysfunction or pre existing gall bladder disease, biliary cirrhosis
D-D- warfarin

Niacin

Reduced triglycerides you 20-50%, and reduces LDL and increases HDL
Use in combo with statin
MOA- strongly inhibits lipolysis in adipose and reduces production of free fatty acid
Used in familial hyperlipidemia or intolerant to other agents like statins
ADE- flushing, ASA 30 minutes prior can help, nausea, abdominal pain, predisposition to gout, hepatotoxicity

Omega 3 fatty acid

Drugs- lovaza, vascepa
MOA- exogenous fatty acid that is used for TG lowering 4 grams can decrease serum concentrations of TG, lower some LDL and raise HDL
OTC, naturally eating fish products or rx
Can reduce risk of CV evens as secondary prevention with statin
ADE- GI, bleeding with anti platelet or anticoagulant

ferrous sulfate, ferrous glycine, ferrous fumarate, ferrous aspartate, carbonyl iron

PO iron-ferrous sulfate DOC
MOA- elemental iron supplement
ADE- GI disturbances, staining of teeth, n/v/c, toxicity- diarrhea, shock, acidosis, gastric necrosis, liver failure, pulmonary edema, vasomotor collapse
D-D PPI, antacids, tetracycline, asorbic acid

Folic acid

For Anemia due to demand like pregnancy, or poor absorption, alcoholism, dihydrofolate reductase inhibitors, antibiotics or methotrexate, inhibit DNA synthesis like anti seizures

Cyanocobalmin and hydroxocobalmin (vitamin b12)

For Anemia, celiac, enteritis, Bariatric surgery, alcoholism, PPI, metformin, megaloblastic Anemia, measurable B12
IM hydroxocobalmin is preferred as fast acting
ADE- hypokalemia

Erythropoietin (epogen, procrit) and darbepoetin (aranesp)

For anemia
EPO regulates blood cell proliferation
Can be due to ESRD, HIV, bone marrow disorder, prematurity and malignancy
IV in dialysis patients or SQ for others
ADE- high concentrations can cause CV events, BBW increased risk of death
Pearls- co administer with high potency iron, dialysis need IV, use with caution not for acute treatment

Neutropenia drugs

Drugs- filgrastim (neupogen) tbo-filgrastim (granix), and pegfilgrastim (neulasta), sagramostim (leukine)
MOA- stimulate granulocyte production in bone marrow to increase neutrophil count and reduce severe neutropenia following chemotherapy and bone marrow transplant
ADE- bone pain, sickle cell crisis, growth factor for tumor, splenic rupture, ARDS

Drugs for sickle cell

-hydroxurea (droxia, hydrea) oral ribonucleotide reductase inhibitor that reduces frequency of sickle crisis, increased fetal hemoglobin, diluting abnormal HbS is delayed and reduces crisis. Can take 3-6 months. ADE- bone marrow suppression, cutaneous vasculitis
-cruzanlizumab (adakveo) Monoclonal antibody blocks interaction between endothelial cells, RBC, platelets, and leukocytes, ADE- infusion related, nausea, arthralgia, back pain, phrexia
-voxelotor (oxbryta) inhibits polymerization HbS by binding to alpha chain of HbS,decreased concentration which is thought to lead to sickling
Well tolerated- HA, diarrhea, GI issues

HTN

Greater than 130/80 on two separate occasions
If SBP greater than 20 above goal or DBP 20 above goal need to start two anti hypertensive
So those with a BP 160/90 need two drugs from the get go

ASA

MOA-inhibits thromboxane A2 synthesis on COX 1 irreversibly, anti aggregation effects
Uses- prevent TIA, reduce recurrent MI, decrease mortality on primary and secondary prevention of MI, complete inactivation of platelets occurs
ADE- high doses can increase toxicity, increase bleeding time

P2Y12 receptor antagonist

Drugs- ticlopidine (ticlid), clopidogrel (plavix), prasugrel (effient), ticagrelor (brillinta), cangrelor (kengreal)
MOA- PY212 ADP receptor inhibition block platelet aggregation, block protein needed for platelets to bind to fibrinogen
cangrelor is not oral
Plavix-prevent CV event in those with recent MI, stroke; prevent thrombosis of ACS, prevent thrombosis post PCI
Ticlid- uses similar to plavix but ADE worse reversed if intolerant to others
Prasugrel- decrease CV even in ACS
Brillinta- prevent VTE in unstable angina, acute MI and PCI
Cangrelor -add in during PCI to prevent VTE
Requires loading dose
D-D- CYP450 PPI
ADE- heme reactions, TTP,
BBW FOR BLEEDING

Glycoprotein 2b/3b inhibitors

Drugs- abciximab (reopro), eptifibatide (integrelin), tirofabib (aggrastat)
MOA- GP 2b/3b plays a role in platelet aggregation, blocks binding of fibrinogen
Uses- IV with heparin and ASA as add on in PCI, unstable angina when non responsive to others
ADE- bleeding

Dipyridamole (persantine)

MOA- coronary vasodilator increases cAMP and inhibits phosphodiesterase resulting in less thromboxane , decrease platelet adhesion to surfaces
Given with ASA as well
Do not give in unstable angina
ADE- HA, dizziness, orthostatic BP

Cilostazol

Oral anti platelet with vasodilators effects
MOA- inhibits phosphodiesterase which prevents breakdown of cAMP and prevents platelet aggregation and vasodilation
Uses- can reduce symptoms of intermittent claudication
D-D- CYP450, 3A4, 2C18 and many others
ADE- HA, diarrhea, abnormal stools, dyspepsia, abdominal pain, thrombocytopenia, leukopenia, INCREASED MORTALITY IN CHF pts

Heparin and low molecular weight heparin

Heparin, LMWH enoxaparin (lovenox), dalteparin (fragmin)
IV/SQ
MOA- binds to antithrombin 3 with inactivation of coagulation factors, inhibits factor Xanax
Uses- prevent VTE, acute DVT/PE, prevent post op VTE, DOC for pregnancy women
Heparin bolus
ADE- bleeding, HIT, osteoporosis
OD- use protamine sulfate

Argatroban (acova)

MOA- direct thrombin inhibitor
uses- prevent or tx of VTE in HIT, Post PCI at risk for HIT
ADE- bleeding

Bivalurudin (angiomax), desirudin (lprivask)

MOA- direct thrombin inhibitor
Angiomax is alternative for heparin in those having PCI at risk for HIT or unstable angina
Lprivask is used to prevent DVT in hip replacement
ADE- bleeding

Fondaparinux (arixtra)

MOA- inhibits factor Xa
Uses- DVT, PE, prevent DVT in ortho and abdominal surgery
SQ
Less monitoring required compared to heparin
contraindicated in severe renal disease
ADE- bleeding no antidote, HIT but less likely

Coumadin (warfarin)

MOA- vitamin K antagonist, factor 2, 7, 9, 10 require vitamin K as a cofactor
INR is standard used to monitor, very narrow index
Many D-D and good interactions- Tylenol, quinolones, other antibiotics, vitamin K foods
Uses- DVT, PE, stroke prevention in afib and prosthetic heart valves, protein C, antiphospholipid, protein S deficiency
ADE- bleeding, skin lesion and necrosis, purple toe syndrome, tetrogenic

Direct acting Agents

Drugs- dabigatran (pradaxa),
MOA- thrombin inhibitors, both clot and bound thrombin and free thrombin are inhibited by Pradaxa
Uses- prevent stroke and embolism in non valvular AF, DVT, PE in those who have already gotten parenteral anticoagulants and prevent reduce recurrent DVT/PE
Contraindicated in mechanical heart valves, not recommended in bio prosthetic valves
ADE- bleeding, Use in caution with renal disease and greater than 75, GI side effects
Antidote- idarucizumab (praxbind)

Direct oral factor Xanax inhibitors

Drugs- apixaban (Eliquis), betrixaban (bevyxxa), edoxaban (savaysa), rivaroxaban (Xarelto)
MOA- oral inhibitors of factor Xa, inhibiting factor Xa decreased production of thrombin from prothrombin
Uses- stroke in non valvular AF, DVT, PE, bextrixban for hospitalized pt at risk for DVT/PE
ADE- bleeding, renal disease can prolong effects
No antidote

Thrombolytic agents

MOA- directly or indirectly to covert plasminogen to plasma which cleaves fibrin thus lysing thrombi, increased local thrombi can occur as clot dissolves leading to enhanced platelet aggregation and thrombosis given ASA or heparin to prevent
Uses- DVT, PE, used less due to serious bleeding, in MI via intra coronary delivery, dissolve clots in stroke
Given IV
ADE- hemorrhage as it cannot differentiate between fibrin of an unwanted clot and fibrin of beneficial clot
Do not give in pregnancy, healing wounds, CVA, brain tumor, ICP, metastatic CA
-alteplase (TPA)-for MI, massive PE, acute ischemic stroke: can cause angioedema, increased risk when combined with ACEI
-tenecteplase- recombinant TPA. Used for acute MI

Drugs for bleeding

Drugs- amino caproic acid (amicar), tranexamic acid (cyclotron/lysteda)
MOA- decreases plasmin formation and fibrinolysis
ADE- intravascular thrombosis

Protamine sulfate

Antagonizes heparin
ADE- hyper sensitivity, dyspnea, flushing bradycardia, hypotension

Vitamin K

Phytonadione (mephyton/aquamephyton)
Can stop bleeding from warfarin by increase vitamin K
Oral, SQ, IV,

Idarucizumab (praxbind)

Monoclonal antibody fragment used to reserve bleeding from dabigatran
Binds to dabigatran and neutralizes it
Used in emergency
IV
ADE- thrombosis

Iron dextran, ferric glycine complex, iron sucrose IV

Dextran- used for intolerant or ineffective oral iron
ADE- anaphylaxis, hypotension, HA, fever: uriticaria, arthralgia, persistent pain with injection
Glyconate complex- IDA, and CKD in HD, always used with erythropoietin, ADE- transient flushing, hypotension, lightheadness, malaise, fatigue, weakness, severe pain in chest, back, flanks or groins
Iron sucrose-uses for IDA, CKD ADE- hypotension, cramps, heart failure, sepsis, taste perversion

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