11. cardiac drugs -dr. firman
DESCRIPTION
asddTRANSCRIPT
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Cardiac Drugs
Firman DullahSMF Ilmu Penyakit Jantung &
Pembuluh DarahRS Bahteramas Kendari
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OVERVIEW
Autonomic nervous system review
Cardiac Drug`s
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Autonomic NervousSystem
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Autonomic Nervous System
Also known as the Visceral Nervous System and Involuntary Nervous System.Is a division of peripherial nervous system system that influences the function of internal organs.
It is regulated within the brain by the Hypothalamus.
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Autonomic Nervous System
Functions– Regulation of cardiac function– Temperature regulation– Fluid & electrolyte balance– Metabolism– Digestion– Excretion
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Autonomic Nervous System
SympatheticFight or flight response
ParasympatheticRelaxation response
NorepinephrineEpinephrine --- released fromadrenal medulla
Acetylcholine
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Actions of autonomic drugs
• Increase the amount of neurotransmitters• Inhibit or augment the breakdown of
neurotransmitters in the synaptic cleft• Interact with post-synaptic receptors
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Receptor Types
AlphaReceptor
Beta
Receptor
Vasoconstrictionureteral contraction
Beta-1----- Increased myocardial contractility & rate
Beta-2-----Vasodilation, bronchodilation Stimulated by norepinephrine & epinephrine 8
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Sympathetic Stimuli
• Stress• Hypoglycemia• Postural hypotension• Exercise
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Receptor Types: Parasympathetic
• Decreased heart rate, increased GI motility, relaxation of bladder sphincter– Stimulated by acetylcholine & baroreceptors
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CARDIAC DRUG`S
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CARDIACDRUG`S
* Alpha blockers* Beta blockers
* Nitrates
* ACE Inhibitors (ACE-I)* Angiotensin Receptor
Blockers (ARB)* Calcium Channel Blockers (CCB)
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Alpha blockersDoxazosin (Cardura), Terazosin (Hytrin)
• Action: block alpha-1 receptors smooth muscle relaxation
• Uses:– Prostate enlargement– Hypertension
• Side effects– Orthostatic hypotension • First dose at bedtime• Change position carefully
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Beta blockersBisoprolol(Concor),Propanolol(Inderal), Atenolol(Tenormin), metoprolol (Fapressor), Carvedilol
(VBloc)
• Action: Blocks sympathetic nervous system stimulation – lowers heart rate, BP– reduces myocardial work, lowering oxygen consumption
• Uses: – Blood pressure control– Control of angina– Prolongs survival after MI (prevents arrhythmias)– Prolongs survival in heart failure– Treatment of certain abnormal heart rhythms– Prevention of Migraines
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Beta Blockers
• Cautions:– Worsening heart failure in acute CHF– Bradycardia when combined with calcium channel
blockers • (often combined in angina)
– Diabetics: masking of hypoglycemia– Exacerbation of wheezing in asthmatics
• Adverse effects– Symptomatic bradycardia– Hypotension– Fatigue
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Implications
• Check pulse and BP prior to administration– Goal for pulse in patient with CAD often 50-60, as
tolerated• Patient education– Check pulse– Make sure they know why they are taking it!– Diabetics: hypoglycemia issue
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NITRATE
• Isosorbid Mononitrate, Isosorbid Dinitrate, Isosorbid Trinitrate, Nitroglycerin(NTG).
• Provide an exogenous source of Nitrit Oxide (NO) ---- cAMP ---- Vasodilator.
• Venous dilation predominates.
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Implications
• Beware of nitrat tolerance.• Education and Self monitoring patient`s
needed.• Side Effect : Headache, Flushing and rash,
Dizziness, Postural hypotension and reflex tachycardia.
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ACE InhibitorsCaptopril, Ramipril, Enalapril (Vasotec), Lisinopril (Zestril)
• Blocks conversion of Angiotensin I to Angiotensin II– Blocks vasoconstriction effects of Angiotensin II– Blocks sodium retention effect of Aldosterone• Effects: reduced peripheral vascular resistance, less
fluid retention
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ACE inhibitors
• Uses– Management of heart failure, prolongs survival• Decreases preload and afterload
– Control of high blood pressure• Diabetics: protective effect on kidneys• Works well with HCTZ
– Prolongs survival in MI with LV dysfunction• Prevents enlargement during remodeling phase of
recovery
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ACE Inhibitors
• Adverse effects– Cough ( increase of bradykinin)• Substitute Angiotensin receptor blocker
– Lightheadedness, hypotension– Hyperkalemia– Kidney dysfunction in bilateral renal artery
stenosis• Watch renal function when first started
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Implications
• Check BP prior to giving– Note: in heart failure goal systolic BP may be 85-
90, • it may not decrease BP in these patients• Always check with MD before holding dose
• Monitor creatinine, potassium• Patient education:– Patient must know why it is being taken– Stopping ACE in CHF can cause worsening, leading
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Angiotensin receptor blockers (ARB’s)
• Also called Angiotensin II inhibitors• Losartan (Cozaar), Valsartan (Diovan),
Irbesartan, Telmisartan, Candesartan.• Blocks Angiotensin II effects --/-- the AT1
receptor`s.• No effects on bradykinin no cough
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Angiotensin receptor blockers
• Uses:– Substitute for ACE, when not tolerated due
to cough• Heart failure management• Hypertension
–Adverse effects similar to ACE, no cough–Generally well-tolerated
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Calcium Channel BlockersAmlodipine (Norvasc), Diltiazem (Cardizem), Nifedipine (Procardia),
Verapamil (Calan)
• Action: Blocks calcium entry into cells, decreasing the strength of contraction– Relaxation of smooth muscle– Decreased heart work– May slow heart rate
• Uses– Blood pressure control– Angina Control– Heart rate control in atrial arrhythmias
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Calcium Channel Blockers
• Several types of CCB• Adverse effects– Verapamil: constipation– Dizziness, flushing, peripheral edema
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Diuretics
• Prevent sodium reabsorption and facilitates fluid excretion in kidneys.Prevent sodium reabsorption and facilitates fluid
excretion in kidneys.
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Loop diureticsFurosemide (Lasix), Bumetanide (Bumex)• Very potent• Used for fluid overload, especially CHF• Larger doses needed with renal dysfunction • Frequent dose adjustments made• Adverse effects: – potassium and magnesium wasting• Monitor potassium levels with dosage change • Potassium supplements
– Dehydration, hypotension, lightheadedness• Reduce dose, replace fluids
– Ototoxicity with rapid IV administration29
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Diuretics• Thaizide Diuretics–Hydrochlorothiazide (HCTZ) –Milder than loop diuretics–Used for hypertension, edema• Often combined with other
antihypertensives for synergistic effect• Adverse effects: potassium and magnesium
loss
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Potassium-sparing Diuretics
• Spironolactone, triamterene• Mild diuretics• Used in combination with other diuretics to
prevent potassium wasting• Side effects: – hyperkalemia
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Implications : diuretics
• DAILY WEIGHTS!– Weights are most accurate indicator of fluid status
changes
• Monitor electrolyte levels– Check potassium level before giving potassium
supplements
• Patient education:– Daily weights– May do sliding scale diuretic doses in CHF management
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Antithrombotic
Platelet Inhibitors
Anticoagulant
Fibrinolytics
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Platelet Inhibitors
PAR receptors
Respond to thrombin and TXA2 to activate Platelets
Aspirin (aspilet, thromboaspilet)
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Platelet Inhibitors
P2Y1, PY12 receptors
Respond to ADP Receptors to activate Platelets
Clopidogrel(Plavix,Vaclo), Prasugrel,Ticlopidine, Ticagrelor
(Brilinta)
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Platelet Inhibitors
GpIIBIIIA receptors
Binds Fibrinogen and and vWF to form platelet
Abciximab,Tirofiban, Eptifibatide
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Anti-coagulant
CLOTTING BLEEDING
Anticoagulants tip the balance towards bleeding
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Anticoagulant
Heparin• Unfractional Heparin(UFH)• Inhibits Factors Xa & the thrombin also
coagulation protease.• Drugs : Inviclot.
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Low Molecular Weight Heparin(LMWH)• One third of the molecular weight of heparin.• Greater bioavailability and a longer plasma
half life than heparin.• Same action with heparin.• Simple and single use but high cost.• Drugs : Fondaparinux(Arixtra),
Enoxaparin(Lovenox), Parnaparin, Dalteparin.
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Warfarin(Vitamin K Antagonist/VKA)• Oral anticoagulant.• Inhibits/inactivation of Vitamin K in hepatic
microsomes.• Needs monitoring and self-guided warfarin
therapy.• Depends on Index Normalized Ratio (INR)
Level.
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Direct Thrombin Inhibitor• Its acyl gluronides are competitive and cause
thrombin enable the conversion fibrin to fibrinogen.
• Dabigatran etexilate (Pradaxa)• No need Monitoring but high in cost
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Anti X-a Agents• Directly inhibits of factor X• Rivaroxaban (Xarelto), Apixaban• No Need Monitoring
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Fibrinolytic
• Thrombolytic/Reperfusion therapy• The generation of plasmin ---plasminogen that
binds to the clot surface to lyse the clot• Needs special preparation and checklist• Be careful of allergic paients --- rare case• Drugs : Streptokinase, Urokinase
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Fibrinolytic
• Tissue Plasminogen Activator (tPA)• Is a naturally occuring enzyme that binds to
fibrin with a greater afinity than streptokinase/urokinase.
• Needs special preparation and checklist• Drugs : Alteplase, Reteplase, Tenecteplase
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AntiArrhytmia
• Divided by Vaughan Wiiliams Class.Class I --- IA, IB & ICClass IIClass IIIClass IV
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Anti-arrhythmic Agents– Classification of anti-arrhythmic agents with the
Vaughan-Williams system (Classes I, II, III and IV) • Based on their effects on certain ion channels and/or
receptors• Class I agents further divided into subclasses IA, IB and IC
based one electrophysiological effects• Class I agents –Mechanism of Action: block Na+ channels, slow
conduction velocity, prolong refractoriness, decrease automaticity of sodium-dependent tissues– Subclasses due to differences in effect on repolarization
(recovery)» Subclass IA – block K+ channels (prolonged recovery phase)
resulting in QRS widening and QT prolongation» Subclass IB – do not block K+ channels but shorten repolarization
phase» Subclass IC – no effect on repolarization phase but profoundly
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–Subclass indications:»Class IA – Atrial and ventricular
arrhythmias»Class IB – Ventricular arrhythmias»Class IC - Atrial and ventricular
arrhythmias• Class II agents– Mechanism of Action: Beta-adrenergic antagonist
with decreased heart rate– Indications:»Slow ventricular rate in Atrial
Flutter/Fibrillation and Paroxysmal SupraVentricular Tachycardia (PSVT)»Symptomatic Premature Ventricular
Contractions (PVC)48
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Anti-arrhythmic Agents
–Classification of anti-arrhythmic agents with the Vaughan-Williams system (Classes I, II, III and IV) continued:• Class III agents –Mechanism of Action: block K+ channels leading to
prolonged repolarization and QT prolongation– Indications:» Amiodarone – Atrial and ventricular arrhythmias» Bretylium – Ventricular arrhythmias » Sotalol – Ventricular arrhythmias» Butilide and dofetilide – conversion of atrial
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• Class IV agents–Mechanism of action: Ca+2 channel blockers
decreasing the heart rate– Indications: slow ventricular rate in atrial
flutter/fibrillation and PSVT
•Misc. Agents–Digoxin - slow ventricular rate in atrial
flutter/fibrillation and PSVT–Adenosine – endogenous hormone that
slows conduction through cardiac tissue, used to treat PSVT
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Anti Arrhytmia Drug ClassesClass Channel Effect Repolarization Time Drugs
IA Sodium Block Effect ++ Prolongs QuinidineDisopiramideProcainamide
IB Sodium Block Effect + Shortens LidocainePhenitoinMexiletineTocainide
IC Sodium Block Effect +++ Unchanged FlecainidePropafenone
II A pacemaker and Depolarizing current; indirect Ca Channel Block
Unchaged Beta Blocker
III Repolarizing K currents Markedly Prolongs AmiodaroneSotalolIbutilideDofetilide
IV Av Nodal Ca Block Unchaged VerapamilDiltiazem
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Cardiac glycosides
• Definitions--preload, afterload, inotrope, chronotrope, cardiac output
• Clinical effects--increase myocardial contractile force, the positive inotropic action increases CO, RBF and diuresis; decreases preload
• Uses--CHF, arrhythmias (afib and aflutter)
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Cardiac glycosides--Digoxin
• Mechanism of action-inhibition of the Na-K pump and increasing intracellular sodium to activate the Na-Ca carrier to increase calcium concentration inside the cell
• Results in an increase in the force of contraction of myocardial muscle fibers and increase in SV and CO
• Blood volume decreases, venous pressures and EDV decreases and distended heart returns to normal
• Decrease in sympathetic stimulation-renal elimination of sodium and water improves secondary to improved renal perfusion, heart rate decreases (decrease AV conduction)
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Digoxin
• Adverse effects--digitalis intoxication, electrolyte disturbances, cardiac arrhythmias, GI symptoms, visual disturbances, fatigue
• Heart rate must be checked prior to digoxin administration and must be >60 bpm
• Treatment is drug discontinuation and treat symptoms. Check dig.level to be between 0.5 to 2.0 ng/ml
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