Pharmacology for Cardiac, HTN, HLD, HF, Arrhythmias Flashcards
“Statins”-AKA
Are HMG CoA Reductase Inhibitors
Statin -MOA
Inhibit LDL synthesis, increase LDL catabolism and have some non steroidal anti-inflammatory activity
Statin -AE
Hepatic Toxicity- elevated transaminases
Myopathy and Rhabdomyolysis
Neuropathy
Small increased risk of DM with high doses
Statin- Contra
Pregnancy category X
Lactation
Active or Chronic Liver disease
Relative-concomitant use of cycolosporins, gemfibrozil and niacin
Statin- Drug interactions
CYP substrate Atorva-3A4 Prava-None Rosuva-limited 2C9 Simva- 3A4&3A5-don't use Myopathy when used with Cyclosporine, gemfibrozil, niacin, azole antifungals and erythromycin
GrapeFruit?
Is a CYP3A4 inhibitor… inhibits metabolism of Atorva and simva causing increase in circulating blood levels
Statin- other Interactions
May potentiate oral anticoagulants
Statin Myopathy Risk Factors
Small body frame,
end stage renal disease or multi system diseases, perioperative,
multiple meds
Statin Monitoring
Check ALT and CK at baseline, document preexisting muscle symptoms
Check fasting lipid panel at 2 months and then every 6-12 months
Recheck ALT and CK as indicated
Monitor for new onset DM, consider lowering dose if 2 consecutive LDL are lower than 40mg/dL
Lipophilic
Atorvastatin
Hydrophilic
Pravastatin and Rosuvastatin
High intensity Statin
Atorvastatin 80mg daily
Rosuvastatin 40Mg Daily
Moderate Intensity Statin
Atorvastatin 20mg Dail
Rosuvastatin 10 mg daily
Low Intensity Statin
Pravastatin 10 mg daily
High intensity Statins are for
lowering LDL by 50%
Moderate statins lower
LDL 30-50%
Clinical ASCVD
Group 1
High intensity STatin if<75
Moderate Intensity if >75 or not candidate for HIS
LDL>190
Group 2
High intensity Statin , moderate if not a candidate
DM and 40-75 yoa
Group 3
High Intensity Statin with ASCVD>7.5%
Moderate intensity for ASCVD <7.5%
ASCVD>7.5%
Group 4
Moderate to high intensity based on Pt
Nonstatins
Use if Triglycerides >500mg/dL
Pt cannot tolerate recommended statin dose or achieve expected statin response
Fibric Acids
Fenofibrate 145 mg daily
Fibric Acid MOA
increases VLDL clearance and decreases VLDL synthesis
Fibric Acid Therapy
Decreases LDL5-20% increases HDL 10-20%
Get a baseline ALT, ALK Phos, repeat at 6-12 weeks
Yearly ALK and FLP
Fibric Acid-AE and Drug interactions
GI complaints
Possible increased effects of warfarin and sulfonylureas
Fibric Acid Contraindications
Hepatic and or severe renal dysfunction
Pre-existing gall bladder disease
Bile Acid Resins(BAR)
Not really used or helpful
Colestipol 4gm BID
Bile Acid Resins(BAR) MOA
Decreases LDL 15-25%
Increase in LDL catabolism, Decrease in Cholesterol absorption,
May increase TG and VLDL
Bile Acid Resins(BAR) AE
Contraindications
GI symptoms- constipation, flatulence, nausea
CI-Monotherapy in TGs>500
-Familial hyperlipidemia
-Hx of Severe constipation
Bile Acid Resins(BAR) Drug interactions
Problems with compliance
-Binds to many coadministered acidic drugs, decreases absorption of Digoxin, warfarin, thyroxine, thiazides, beta blockers, TCN, PCN, Amiodarone
Decreases bioavailability of statins
Take BAR 1 hour Before or 4 hrs after
Bile Acid Resins(BAR) Monitor
FLP at 6 weeks and yearly
Nicotinic Acid MOA
Niacin 1-2 gm TID
decreases LDL and VLDL synthesis
Lowers LDL 5-25% and Increases HDL 15-35%
Nicotinic Acid AE
Flushing of skin, glucose intolerance and increased UA
Hepatotoxicity
Nicotinic Acid contra
Liver disease(absolute cont) DM type 2 Gout and Hyperuricemia
Nicotinic Acid Monitor
Baseline AL, Alk Phos,
6-12 weeks ALT, all phos, Uric acid, BGL, and FLP
Yearly ALT, alk Pos, FLP
Ezetimibe
Zetia 10mg daily
Blocks Cholesterol absorption
Drops LDL by 15% increase HDL by 3%
Ezetimibe AE and Contra
AE- Fatigue, abd pain, diarrhea, back pain, arthralgia
Cont- Combination with statin in active liver disease or with persistent LFT elevations
PCSK9 inhibitors
Evolocumab- SQ q2-4 weeks
PCSK9 inhibitors MOA
Prevents PCSK9 from degrading Liver LDL receptors
Decreases LDL 60%
PCSK9 inhibitors Downside
$14,000/year
Fish Oil
W/O CHD eat fish 2/week
with CHD 1 gm EPA DHA preferably from fish oil
Fish Oil
Omega 3 fatty acid can lower TG, Prescription is Lovaza($184/month)
Class 1a AAD MOA
Sodium channel blockers
Alters the myocardial cell membrane,
Slows conduction velocity, prolongs refractory phase and decreases automaticity
Class Ia AAD Example
Sodium channel blockers
Procainamide
Class Ia AAD Indication
Sodium channel blockers
Supraventricular and ventricular arrhythmias
Class 1a AAD AE
Sodium channel blockers
Widens QRS, Prolongs QT, bradycardia, hypotension, worsening CHF and torsades des pointes
Class 1a AAD Contra
Sodium channel blockers
Hypersensitivity to procainamide, 2nd and 3rd degree HB
Class 1a AAD Monitoring
Sodium channel blockers
MOnitor serum concentration especially in renal failure Pt
Class Ib AAD
Sodium channel blockers
Blocks the rapid influx of sodium ions-
Lidocaine
Class 1C AAD Example
Sodium channel blockers
Flecainide
Class IC AAD MOA
Sodium channel blockers
Conduction slows
Slows conduction in the purkinje fibers and av nodes
Class IC AAD Indications
Sodium channel blockers
SVT, converting fib to NSR
Class IC AAD AE
Sodium channel blockers
dizziness, headache, syncope, SOB, arrhythmias, worsening HF
Class IC AAD Contraindications
Sodium channel blockers
2nd/3rd degree HB, recent MI, cariogenic shock, HF and ischemic heart disease
Class IC AAD monitoring
Sodium channel blockers
monitor for drug interactions CYP system
Class II AAD Example
Beta Blockers
Metoprolol Succinate
Class II AAD MOA
Beta Blockers
Slows conduction velocity, prolongs refectory phase, decreases automaticity, slows AV node conduction
Class II AAD Indications
Beta Blockers
supra ventricular and ventricular rhythms
Class II AAD AE
Beta Blockers
Bradycardia, worsening HF, bronchospasm, hypotension
Class II AAD Contra
Beta Blockers
2nd/3rd degree HB, decompensated HF,
HR<45bpm
Class II AAD Monitoring
Beta Blockers
do not stop suddenly, reflex tacky and HTN, educate Pt on HR and BP
metoprolol tartrate
immediate release
Metoprolol Succinate
extended release
Class III AAD Examples
Potassium Channel Blockers
Amiodarone
Sotalol
Class III AAD Amiodarone-MOA
Increases the action potential
Class III AAD Amiodarone-
Indications
First line for VF/VT in cardiac arrest, stable Vtach, supra ventricular tachs,
Class III AAD Amiodarone-
AE
IV- Hypotension, bradycardia, blocks, phlebitis,
PO-Corneal deposits, optic neuritis, n/v/c, Anorexia, pulmonary fibrosis, elevated LFTs, blue discoloration
Class III AAD Amiodarone-
Contra
2nd/3rd degree HB
Sick SInus syndrome
Class III AAD Amiodarone-Monitoring
EKG monitoring, cautious with asthma Its, annual CXR, LFTs every 6mo, PFTs and Optho if symptoms
CYP interactions
Class III AAD- Sotalol MOA
Prolongs atrial and ventricular refractory period, also has Beta Blocker properties
Class III AAD- Sotalol Indications
Supraventricular and ventricular rhythms
Class III AAD- Sotalol AE
Bradycardia, Torsades, Worsening HF, blocks, bronchospasm
Class III AAD- Sotalol Contra
2nd/3rd degree HB, bradycardia, HF, asthma, and long QT syndrome
Class III AAD- Sotalol Monitoring/special
Pt must be hospitalized for 3 days for initiation of therapy, avoid other qt prolonging drugs, do not stop suddenly
Class IV AAD- Calcium Channel Blockers
Example
Diltiazem
Class IV AAD- Calcium Channel Blockers MOA
Nondihydropyridine- Slows conduction throughAV node
Class IV AAD- Calcium Channel Blockers Indications
PSVT, Afib/A flutter
Class IV AAD- Calcium Channel Blockers AE
dizzy, headaches, edema, blocks, bradycardia, worsening HF, and hypotension
Class IV AAD- Calcium Channel Blockers contra
WPW, caution in HF
Class IV AAD- Calcium Channel Blockers Special considerations
Negative inotrope, careful in combo with BB, dig or clonidine, CYP interactions
Digoxin MOA
Acts on AV node through parasympathetic simulation that increases vagal tone
Digoxin Indication
Controls ventricular rate in supra ventricular rhythms(Afib) and in HF does not convert afib into NSR
Digoxin- AE
anorexia, n/v/d, headache, vertigo, HB, brady
Digoxin- contra
2nd and 3rd degree HB
Digoxin- Special/monitoring
narrow therapeutic window,
requires loading dose
Adenosine MOA
Acts on the atrioventricular node to slow conduction and inhibit reentry pathways
adenosine Indications
PSVT
Adenosine- AE
headache, chest pain, dyspnea, flushing
Adenosine- Contra
2nd and 3rd degree HB, sick sinus
Adenosine special considerations
extremely short half life
will make you feel bad
Atropine MOA
Blocks effects of acetylcholine on the SA and AV nodes. Increasing conduction velocity
Atropine Indication
Symptomatic bradycardia
Atropine AE
Palpitations, tachycardia, dry mouth, dizziness
Atropine Contra
acute angle glaucoma, tachycardia, obstructive GI/GU
Atropine special
give IV and monitor EKG
Vasoactive/inotropes
Epi, Dopamine and Vasopressin
Alpha 1 Stimulators
Norepi-vasoconstriction
Beta 1 Stim
Epi-increased contractility
Dopamine Stimulators
Dopamine-increased renal blood flow
V1/V2
Vasopressin- peripheral vasoconstriction
Beta 2 stimulators
Dobutamine- systemic vasodilation
STEMI treatment
MONA-DAPT(ASA and P2Y12-I +/-GPIIb/IIIa inhibitor–Anticoag therapy–PCI in<90min
MONA
Morphine- Anti-anxiety /pain relief decrease sympathetic response
Oxygen-Increase available O2 titrate SPO2 >90%
Nitrates-Vasodilation
Aspirin- anti-platelet therapy
P2Y12-I-Dosing in the ACS Pt
Any Pt with ACS
Clopidogrel (Plavix)600mg loading dose, followed by 75mg PO daily x 1 year
Tricagrelor- 190mg loading dose followed by 90mg PO BID x 1 year
Differentiate between non-modifiable and modifiable risk factors for CHD
Modifiable-Smoking, hyperlipidemia, HTN, Obesity, Diet, dibetes, inactivity
Non-modifiably- family Hx, age, gender
Angina Treatment algorithm
chest pain–>EKG–>angina-no–.consider other causes
Angina-yes–>Pt ed, lifestyle modification, daily ASA, NTG —>infrequent episodes relieved-yes–>monitor and reevaluate periodically.
infrequent episodes relieved-no–> Monotherapy with BB–>if not relieved—>add CCB–>if still no relief refer to cardiology
Lisinopril (ACS)
(ACE-Inhibitor)
MOA: Prevent conversion of angiotensin 1 to angiotensin 2 which is a potent vasoconstrictor, it also prevents cardiac remodeling
Indications: Give within 24 hrs to all Pts with ACS who also have HF, DM, or CKD
AE: Scr increase, cough, angioedema
Contraindications: Pregnancy, bilateral renal artery stenosis, Allergy
Special Considerations: May cause Hypotension and reduce renal function
Losartan (ACS)
(ARB) Blocks the binding of Angiotension 2 at the ATI receptor, blocking Vasoconstriction and sympathetic activation. Similar to ACE inhibitors
Indications: Give within 24 hrs to all Pts with ACS who also have HF, DM, or CKD
AE: Scr increase, cough, angioedema
Contraindications: Pregnancy, bilateral renal artery stenosis, Allergy
Special Considerations: May cause Hypotension and reduce renal function- ARB can be given to Pt intolerant of ACE-I
Nitroglycerin (NTG)(ACS)
Class:Nitrates
MOA- causes arterial and venous vasodilation by promoting release of nitric oxide from endothelium. This in turn lowers preload, BP and myocardial demand
Indications: ACS, angina
Dose: 0.4mg SL, can give IV drip and transdermal
AE: reflex tach, flushing, headaches, hypotension
Contra- Recent use of PD-5 inhibitor(Viagra/ Cialis)
ED: Tell Pt to call 911 if taken 3 doses and no still has angina
Metoprolol succinate in ACS
Beta Blocker-succinate-slow
MOA: Competitive blockade of B1 adrenergic receptors decreases HR, myocardial contractility and BP
Indications-Give within 24 hrs of ACS Pt unless contraindicated and continue for 3 years
AE: bradycardia, hypotension, HB, acute HF, block typical hypoglycemia signs
CI: Bradycardia, Hypotension, 2/3rd degree HB and cardiogenic shock
Amlodipine in ACS
Dihydropyridine Calcium Channel blocker
MOA: Stops calcium from entering smooth muscles which dilates arteries, reduces afterload and myocardial contractility
Indication: add on or substitution to BB
AE: Can cause reflex tachycardia
Special-Can be used in combination with BB
Great at reducing coronary spasm (Prinzmetal)
Aspirin (ASA)
Anti-platelet agent
MOA-reduces platelet aggregation by inhibiting COX1
Indication: In ACS-325mg PO, daily after care or before care 81mg daily
No contraindications for ACS, with preventative care GI bleed is contraindication
Stop all other NSAIDs due to increased risk of death
Ranolazine
MOA: Unclear- inhibits late influx of Na+ and decreases intracellular Ca++- decreasing myocardial contraction
Indication- adjunct therapy for Its non responsive to BB and CCB
AE-dizziness, constipation, headache, nausea
Contra-prolonged QT, watch for drug-drug interactions
Special-$$$EXPENSIVE$$$
Unfractionated heparin (UFH)
Anticoagulants
MOA-potentiates the action of antithrombin3, inactivating thrombin and factor Xa- prevents the conversion of fibrinogen to fibrin (stops the coagulation cascade)
Indications: all Pt with ACS.
Dosing- 60 units/kg IV, stop shortly before PCI
AE: Bleeding, HIT
Contra- Hx of HIT, uncontrolled bleeding
Enoxaparin (LMWH) Lovenox
Anticoagulants
MOA- potentiates action of antithrombin 3, mainly working on Factor Xa
Indication- Pt with ACS
Dosing- 1mg/kg SQ q 12 hrs
AE: Bleeding, HIT
Contra- Hx HIT uncontrolled bleeding
Warfarin monitoring
INR between 2-3 for most indications, check daily until in target range then monthly
Treatment for NSTEMI Ischemia guided
MONA- DAPT(ASA and PGY12-I)- Anitcoag Therapy(IV UFH, SQ LMWH, or Bivalirudin)
Treatment for NSTEMI- early invasive strategy
MONA-DAPT(ASA, PGY12-I, +/-GP 2b/3a I)-Anticoag(IV UFH, SQ LMWH, or Bivalirudin)–Need for revascularization-(PCI-or CABG)
CABG Continue ASA stop DAPT 12 hrs emergent-5-7 days elective-
Continue UFH iv for both but discontinue SQ enoxaparin 12 hrs before and Bivalirudin 3 hrs before
Treatment of STEMI
PCI capable facility
MONA-DAPT(ASA and P2Y12-I) and anticoag(IV UFH, or SQ LMWH, Bivalirudin) Door to balloon in 90 min
Amlodipine HTN Class
CCB-Dihydropyridine
Amlodipine HTN MOA
Block intracellular Ca++ influx, decreases smooth muscle contraction, Potent vasodilation(Turns vessel into firehose)
Amlodipine HTN ADR
Tachy, Headache, Dizzy, flushing, edema
Amlodipine HTN CI
AV node dysfunction, Sick SInus Syndrome, HF exacerbation
Amlodipine HTN Dosing, Special consideration and Monitoring
2.5mg-10mg daily, Cheap, monitor BP
Lisinopril HTN-Class
ACE Inhibitor
Lisinopril HTN MOA
Inhibits ACE blocking the conversion angiotensin I to angiotensin II(A potent Vasoconstrictor) causes relaxation of vessels,
Decreases aldosterone decreasing Na+retention
Vasodilates efferent arterioles in kidney(protective with sufficent afferent blood flow)
Stops breakdown of bradykinin causing vasodilation (cough)
Lisinopril HTN ADR
Cough!! Hyper K+, Hypotension, rash, angioedema, Acute renal failure in bilateral renal artery stenosis or dehydration
Lisinopril HTN CI
2nd/3rd trimester of pregnancy, History of Angioedema
Lisinopril HTN Monitoring
K+, Cr(30% bump is acceptable) BP
Lisinopril HTN Dosing
5-40 mg daily
Lisinopril HTN special considerations
Cheap, if cant tolerate cough switch to ARB
Losartan HTN Dosing
25-100 mg daily
Losartan HTN Class
ARB- cousin to ACE I
Losartan HTN MOA
Block Angiotensin II receptor causing vasodilation, decreases aldosterone
Losartan HTN ADR
Hyper K+, Hypotension, rash, angioedema, Acute renal failure in bilateral renal artery stenosis or dehydration
Losartan HTN monitoring
K+, Cr and BP
Losartan HTN Special
Consider if cannot tolerate ACE I
Hydrochlorothiazide HTN Dosing
12.5-25 mg Daily
Hydrochlorothiazide HTN Class
Thiazide diuretic
Hydrochlorothiazide HTN MOA
increases Na+ excretion in distal tubule, decreasing plasma and extracellular volume
Hydrochlorothiazide HTN ADR
Low K+ and Mg++, Hyperglycemia, hypercalcemia, hyperuricemia, mild increase to cholesterol and triglyceride
Hydrochlorothiazide HTN CI
Caution in Hx of Gout, less effective if CrCl<30 use a loop diuretic instead
Hydrochlorothiazide HTN Monitoring
Baseline and recheck in 2 weeks, BMP, BP dehydration and uric acid
Metoprolol Succinate HTN Class
Cardioselective beta blocker
Metoprolol Succinate HTN MOA
Block B1 receptors in heart and kidneys, causing decrease HR/CO causing a decrease in BP
Blocks some B2 blocking at higher doses
decrease in sympathetic stimulation of Renin secretion(RAAS)
Metoprolol Succinate HTN ADR
fatigue, insomnia, nightmares, bradycardia, aggravates PVD, hypoglycemia signs can e masked, decreased HDL, increased TG
Metoprolol Succinate HTN CI
bradycardia, heart blocks, sinus node disease, uncontrolled HR (caution)
Metoprolol Succinate HTN Special considerations and Education
tartrate- immediate release
succinate- delayed release
may aggravate asthma or lung dz,
don’t stop abruptly if IHD (taper doses)
Clonidine HTN Class
Centrally acting Alpha 2 agonist
Clonidine HTN MOA
increase central A2 receptor to decrease peripheral symp activity, decreasing BP
Clonidine HTN ADR
Dry mouth, sedation, fatigue, dizzy, orthostatic hypotension
Clonidine HTN CI
Do not use in pregnancy, use methyldopa instead
Clonidine HTN Special consideration
avoid abrupt d/c can cause severe rebound HTN, Rebound HTN will be worse if also on BB
Spironolactone HTN Class
K+ sparing aldosterone antagonist diuretic
Spironolactone HTN MOA
Aldosterone antagonist-decrease in Na+ and H2O retention
Spironolactone HTN ADR
Hyperkalemia(especially if given w/ K+ supplements, ACE I or if renal insufficiency
gynecomastia
Spironolactone HTN Special considerations
Gynecomastia( use Eplerenone as causes less gynecomastia
Spironolactone HTN Monitoring
BMP, K+, and BP
Terazosin HTN Class
A1 receptor Blocker
Terazosin HTN MOA
Dilates arterioles and veins- relaxation of smooth muscles
Terazosin HTN ADR
Hypotension, orthostatic hypotension, syncope with first dose, vivid dreams, interactions with PDE-5 Inhibitors (viagra)
Terazosin HTN Special considerations and monitoring
Give dose at half strength due to orthostatic hypotension
BP - titrate to standing BP
Hydralazine HTN Class
Direct vasodilation
Hydralazine HTN MOA
arteriolar smooth muscle relaxation
Hydralazine HTN ADR
Fluid retention,
rebound tachycardia
Headaches
Lupus like symptoms
Hydralazine HTN Special
may need concomitant Diuretic and BB
Warfarin class
anticoag
Warfarin MOA
Vitamin K antagonist, decreases synthesis of “1972” factors X, IX, VII, and II
Warfarin ADR
Hemorrhage, skin necrosis, purple toe symptoms
Warfarin CI
Pregnancy, High risk hemorrhage, noncompliance, EtOH abuse, surgery/dental work(may need to stop), spinal anesthesia
Warfarin Special considerations
Onset 36-72 hrs- will need a bridge therapy of UFH or LMWH for 4-5 days
Protein bound drug
CYP metabolite
Caution with Amio, cimetidine, gemfibrozil, omeprazole, bactrim, rifampin, and carbamazepine
Warfarin Education
Diet consistent Vit K intake
EtOH acute vs Chronic effects on INR
Apixaban Class
DOAC- direct oral anticoag
Apixaban MOA
Factor Xa inhibitor
Apixaban ADR
Bleeding
Apixaban CI
Active pathologic bleeding, severe hypersensitivity, prosthetic heart
Apixaban Special considerations
Spendy, reversal agent is available but spendy
Pregnancy Cat B
CYP 3A4
Apixaban monitoring
monitor renal function for need to adjust dose
Clopidogrel Class
Anti platlet
clopidogrel Indication
ischemic stroke(prevention and tx)
VTE prevention
ACS( prevention and stroke)
Stent thrombus prevention
Clopidogrel MOA
P2Y11 inhibitor- inhibits ADP( which promotes platlet binding/aggregation)- decreases platelet aggregation
Clopidogrel ADR
Bleeding and diarrhea
Clopidogrel CI
Major active bleed, PUD, Intracranial hemorrhage
Clopidogrel SPecial considerations
CYP 2C1
Clopidogrel monitoring
Continue taking for 6 months post stent
Apixaban Indications
Throboembolism( stroke) in afib
VTE prevention(post op)
DVT/PE treatment and prevention of reocurrence
Warfarin Indications
VTE (treatment and prophylaxis) TIA stroke AMI Prosthetic heart valves hypercoag state Afib PAD(occlusive)
Heparin indications
VTE (treatment and prophylaxis) CABG HD Unstable angina angioplasty AMI IV flush
Enoxaparin indications
Prophylactic post hip/knee surgery
VTE bridge therapy
Enoxaparin dosing for VTE
1mg/kg SQ q12hrs until INR is theraputic
Metoprolol Succinate HF Dosing
12.5-25 mg daily increasing to 200mg daily
200mg daily is ideal dosing
Beta Blockers effect in HF
Decrease HR, antiarrhythmic
Benefits- Reduce morbidity and mortality
Reduces hospitalization
Causes reverse remodeling of L ventricle(returning heart to normal size, shape and function)
ACE inhibitors in HF impact and benefit
Decrease preload and after load
Reduces morbidity and mortality
Reduces hospitalization in HFrEF
Slows disease progression decreases/prevents remodeling
Angiotensin II receptor blocker in HF benefits/effects
reduces morbidity and mortality in Pt with current or prior HF symptoms
Alternative if Pt cant handle or take an ACE I
ANgiotensin receptor Neprilysin inhibitor (ARNI) in HF
Benefits
Reduce morbidity and mortality in Pt with prior or current HF symptoms
More effective than ACE inhib alone to decrease death or HF hospitalizations
In Pt with chronic symptomatic HFrEF NYHA class 2/3 who tolerate ACE I or ARB replacement by ARNI/ARB is recommended
Aldosterone Antagonist in HF benefits
Decrease preload
Reduces morbidity and mortality
Reduces hospitalization
Aldosterone ANtagonists (Spironolactone) Recommended for
Pt with NYHA class 2-4 who have LVEF<35% Pt following an acute MI who have LVEF<40% with symptoms of HF or DM
Diuretics in HF benefit
Decreases Preload
Decreases symptoms not mortality
Digoxin in HF benefits
Increases myocardial contractility(positive inotrope)
Antiarrhythmic for Pt in Afib
Alleviates six and improves clinical status in Pt with HFrEF decreasing Hospitalizations
No significant effect on survival
Hydralazine in HF benefits and recommendations
Direct acting vasodilator-prevents nitrate tolerance, may interfere with HF progression(antioxidants)
A.A. with class 3-4 on guideline directed med therapy Pt with HFrEF who cannot be given an ACE/ARB LVEF <40% with persistent class 3/4 despite GDMT
Nitrates(long term) in HF benefits and recommendations
Venodilation- decreasing preload, may inhibit ventricular remodeling
Recommended for
A.A. with class 3/4 HFrEF on GDMT
Pt with HFrEF who cannot take ACE/ARB
LVEF <40%with persistent class 3/4 despite GDMT
Ivabradine in HF benefits
Works on funny channel slowing HR w/o decreasing BP
Prevents hospitalization but doesn’t reduce mortality
Lisinopril Dosing in HF
Start at 5mg qday, (10mg if Pt has HTN)
Titrating dose upto 10 mg intervals of 2 weeks reaching goal of 20mg qday(max of 40mg qday)
Lisinopril HTN Caution
Hyperkalemia
Hypotension
Renal dysfunction
Lisinopril in HF Monitor
BP, K+, renal function
ACE inhib recommendations in HF
All Pt’s with reduced EF to prevent HF
All pts with HFrEF unless contraindicated
ACE inhib in CHF alternatives
ARBs, or Hydralazine+Isosorbide for Pts intolerant of ACE I
Losartan in HF dosing
12.5-25 mg qday starting
50-100mg qday-ideal
ARBs in HF monitoring
K+
BP
Renal function
Carvedilol in HF
Class-MOA-AE-CI-Special, monitoring and Pt ED
BB, Given when Pt is stable,
Blocks the beta 1 adernergic receptors
Hypotension, fluid retention, bradycardia
CI in unstable HF Pt
Low starting dose titrations up slowly with close monitoring
BP, HR and fluid status
Teach to take BP, HR and monitor weight
Sacubitril/Valsartan in HF
Class, MOA, Indication, AE, CI, special, monitoring and Pt ED
ARNI/ARB
Increases sodium loss and vasodilation and enhances ARBs efficacy
For Pt with SYstolic HF(HFrEF)
Hypotension, angioedema
Hf of angioedema, concurrent with ACE I or with in last 36 hrs of last ACE I dose due to risk of angioedema
K+, BP and renal function
Furosemide in HF
Class, MOA, Indication, AE, CI, special, monitoring and Pt ed
Loop Diuretic Inhibits sodium reabsorbtion in ascending renal loop, proximal and distal CT, water follows salt Moderate overload-PO Severe overload-IV Dehydration, hypotension Anuria BP, K+ Avoid over diuresis especially in starting ACE I Emphasize Sodium restrictions
Metolazone cautions
Potent thiazide diuretic, inhibits Na+ reabsorption in distal tubule
2.5 mg trial dose
Monitor K+, Weight, UO(urine output)
Cautiously as out Pt treatment PRN based on weight(1-2 times per week)
Stages of HF
A:Pt at High Risk of HF-no structural heart disease no Sx of HF
B:Pt with structural heart disease but no Signs or sX of HF
C: Pt with structural heart disease and current or prior Sx of HF
D: Pt with refractory HF requiring specialized interventions
Classes of HF
I: Pt with cardiac disease but no limitations, ordinary activity doesn’t cause issues
II:Pt with cardiac disease that have slight limitations of activity ordinary physical activity results in fatigue
III: Pt with cardiac disease with marked limitations of physical activity-Pt is comfortable at rest
IV: Pt with cardiac disease-unable to carry on physical activity w/o discomfort, Sx of CHF are present at rest
Goals of HF treatment
Improve quality of Life
Decrease Mortality
Reduce compensatory mechanisms causing Sx
Aldosterone ANtagonists in HF
Monitoring
BP, K+, renal Function(check at baseline, 3 days, 1 week and q3 months for Spironolactone)
Standard First line therapies for HFrEF
ACE I/ ARB/ ARNI-ARB/ Hydralazine+Isosorbide (Lisinopril/Losartan)
Beta Blocker(Metoprolol ER, Carvedilol, Bisoprolol)
Aldosterone Antagonists (Spironolactone)
Diuretics (Thiazide-LooP)
Digoxin
Management of Decompensated HF
Hospitalization
IV loop diuretics( add a thiazide if needed)
IV dobutamine to increase renal blood flow and diuresis
IV NTG if not hypotension