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Transcript of Cardiac drugs
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NAME OF DRUG INDICATION MECAHNISM OF ACTION
CONTRAINDICATION
Side Effects NURSING RESPONSIBILITY
1.Telmisartan (Micardis)80 mgODOral
Hypertension
Blocks constricting and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the angiotensin I receptor in many tissues, such as vascular smooth muscle and the adrenal gland.
Hypersensitivity to drug and its components.
diarrhea,angioedema,sinusitis,pharyngitis,backpain
Monitor patient for hypotension after starting drug.
Closely monitor blood pressure. Patients undergoing dialysis may develop orthostatic hypotension.
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PharmacologyPharmacologyPharmacologyPharmacology
Drugs that Affect the Cardiovascular System
Drugs that Affect the Cardiovascular System
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TopicsTopicsTopicsTopics
• Electrophysiology
• Vaughn-Williams classification
• Antihypertensives
• Hemostatic agents
• Electrophysiology
• Vaughn-Williams classification
• Antihypertensives
• Hemostatic agents
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Cardiac FunctionCardiac FunctionCardiac FunctionCardiac Function
• Dependent upon– Adequate amounts of ATP– Adequate amounts of Ca++
– Coordinated electrical stimulus
• Dependent upon– Adequate amounts of ATP– Adequate amounts of Ca++
– Coordinated electrical stimulus
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Adequate Amounts of ATPAdequate Amounts of ATPAdequate Amounts of ATPAdequate Amounts of ATP
• Needed to:– Maintain electrochemical gradients– Propagate action potentials– Power muscle contraction
• Needed to:– Maintain electrochemical gradients– Propagate action potentials– Power muscle contraction
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Adequate Amounts of CalciumAdequate Amounts of CalciumAdequate Amounts of CalciumAdequate Amounts of Calcium
• Calcium is ‘glue’ that links electrical and mechanical events.
• Calcium is ‘glue’ that links electrical and mechanical events.
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Coordinated Electrical Coordinated Electrical StimulationStimulationCoordinated Electrical Coordinated Electrical StimulationStimulation• Heart capable of automaticity
• Two types of myocardial tissue– Contractile– Conductive
• Impulses travel through ‘action potential superhighway’.
• Heart capable of automaticity
• Two types of myocardial tissue– Contractile– Conductive
• Impulses travel through ‘action potential superhighway’.
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A.P. SuperHighwayA.P. SuperHighwayA.P. SuperHighwayA.P. SuperHighway
• Sinoatrial node• Atrioventricular
node• Bundle of His• Bundle Branches
– Fascicles
• Purkinje Network
• Sinoatrial node• Atrioventricular
node• Bundle of His• Bundle Branches
– Fascicles
• Purkinje Network
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ElectrophysiologyElectrophysiologyElectrophysiologyElectrophysiology
• Two types of action potentials– Fast potentials
• Found in contractile tissue
– Slow potentials• Found in SA, AV node tissues
• Two types of action potentials– Fast potentials
• Found in contractile tissue
– Slow potentials• Found in SA, AV node tissues
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Fast PotentialFast PotentialFast PotentialFast Potential
-80
-60
-40
-20
0
+20
RMP-80 to 90 mV
Phase 1
Phase 2
Phase 3
Phase 4
controlled by Na+
channels = “fast channels”
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Fast PotentialFast PotentialFast PotentialFast Potential
• Phase 0: Na+ influx “fast sodium channels”
• Phase 1: K + efflux
• Phase 2: (Plateau) K + efflux – AND Ca + + influx
• Phase 3: K+ efflux
• Phase 4: Resting Membrane Potential
• Phase 0: Na+ influx “fast sodium channels”
• Phase 1: K + efflux
• Phase 2: (Plateau) K + efflux – AND Ca + + influx
• Phase 3: K+ efflux
• Phase 4: Resting Membrane Potential
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Cardiac Conduction CycleCardiac Conduction CycleCardiac Conduction CycleCardiac Conduction Cycle
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Slow PotentialSlow PotentialSlow PotentialSlow Potential
-80
-60
-40
-20
0
Phase 4 Phase 3
dependent upon Ca++ channels = “slow channels”
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Slow PotentialSlow PotentialSlow PotentialSlow Potential
• Self-depolarizing– Responsible for automaticity
• Phase 4 depolarization– ‘slow sodium-calcium channels’– ‘leaky’ to sodium
• Phase 3 repolarization– K+ efflux
• Self-depolarizing– Responsible for automaticity
• Phase 4 depolarization– ‘slow sodium-calcium channels’– ‘leaky’ to sodium
• Phase 3 repolarization– K+ efflux
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Cardiac Pacemaker Cardiac Pacemaker DominanceDominanceCardiac Pacemaker Cardiac Pacemaker DominanceDominance• Intrinsic firing rates:
– SA = 60 – 100 – AV = 45 – 60– Purkinje = 15 - 45
• Intrinsic firing rates:– SA = 60 – 100 – AV = 45 – 60– Purkinje = 15 - 45
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Cardiac PacemakersCardiac PacemakersCardiac PacemakersCardiac Pacemakers
• SA is primary– Faster depolarization rate
• Faster Ca++ ‘leak’
• Others are ‘backups’– Graduated depolarization rate
• Graduated Ca++ leak rate
• SA is primary– Faster depolarization rate
• Faster Ca++ ‘leak’
• Others are ‘backups’– Graduated depolarization rate
• Graduated Ca++ leak rate
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Potential TermsPotential TermsPotential TermsPotential Terms
APD
ERP
RRP relative refractoryperiod
effective refractory period
action potential duration
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Dysrhythmia GenerationDysrhythmia GenerationDysrhythmia GenerationDysrhythmia Generation
• Abnormal genesis– Imbalance of ANS stimuli– Pathologic phase 4 depolarization
• Ectopic foci
• Abnormal genesis– Imbalance of ANS stimuli– Pathologic phase 4 depolarization
• Ectopic foci
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Dysrhythmia GenerationDysrhythmia GenerationDysrhythmia GenerationDysrhythmia Generation
• Abnormal conduction
• Analogies:– One way valve
– Buggies stuck in muddy roads
• Abnormal conduction
• Analogies:– One way valve
– Buggies stuck in muddy roads
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Reentrant CircuitsReentrant CircuitsReentrant CircuitsReentrant Circuits
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Warning!Warning!Warning!Warning!
• All antidysrhythmics have arrythmogenic properties
• In other words, they all can CAUSE dysrhythmias too!
• All antidysrhythmics have arrythmogenic properties
• In other words, they all can CAUSE dysrhythmias too!
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AHA Recommendation AHA Recommendation ClassificationsClassificationsAHA Recommendation AHA Recommendation ClassificationsClassifications• Describes weight of
supporting evidence NOT mechanism
• Class I• Class IIa• Class IIb • Indeterminant• Class III
• Describes weight of supporting evidence NOT mechanism
• Class I• Class IIa• Class IIb • Indeterminant• Class III
• View AHA definitions• View AHA definitions
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Vaughn-Williams Vaughn-Williams ClassificationClassificationVaughn-Williams Vaughn-Williams ClassificationClassification• Class 1
– Ia– Ib– Ic
• Class II• Class III• Class IV• Misc
• Class 1– Ia– Ib– Ic
• Class II• Class III• Class IV• Misc
• Description of mechanism NOT evidence
• Description of mechanism NOT evidence
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Class I: Sodium Channel Class I: Sodium Channel BlockersBlockersClass I: Sodium Channel Class I: Sodium Channel BlockersBlockers• Decrease Na+ movement in phases 0 and 4
• Decreases rate of propagation (conduction) via tissue with fast potential (Purkinje)– Ignores those with slow potential (SA/AV)
• Indications: ventricular dysrhythmias
• Decrease Na+ movement in phases 0 and 4
• Decreases rate of propagation (conduction) via tissue with fast potential (Purkinje)– Ignores those with slow potential (SA/AV)
• Indications: ventricular dysrhythmias
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Class Ia AgentsClass Ia AgentsClass Ia AgentsClass Ia Agents
• Slow conduction through ventricles
• Decrease repolarization rate– Widen QRS and QT
intervals• May promote Torsades
des Pointes!
• Slow conduction through ventricles
• Decrease repolarization rate– Widen QRS and QT
intervals• May promote Torsades
des Pointes!
• PDQ:– procainamide
(Pronestyl®)
– disopyramide (Norpace®)
– qunidine
– (Quinidex®)
• PDQ:– procainamide
(Pronestyl®)
– disopyramide (Norpace®)
– qunidine
– (Quinidex®)
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Class Ib AgentsClass Ib AgentsClass Ib AgentsClass Ib Agents
• Slow conduction through ventricles
• Increase rate of repolarization
• Reduce automaticity– Effective for ectopic
foci
• May have other uses
• Slow conduction through ventricles
• Increase rate of repolarization
• Reduce automaticity– Effective for ectopic
foci
• May have other uses
• LTMD:– lidocaine (Xylocaine®)
– tocainide (Tonocard®)
– mexiletine (Mexitil®)
– phenytoin (Dilantin®)
• LTMD:– lidocaine (Xylocaine®)
– tocainide (Tonocard®)
– mexiletine (Mexitil®)
– phenytoin (Dilantin®)
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Class Ic AgentsClass Ic AgentsClass Ic AgentsClass Ic Agents
• Slow conduction through ventricles, atria & conduction system
• Decrease repolarization rate
• Decrease contractility• Rare last chance drug
• Slow conduction through ventricles, atria & conduction system
• Decrease repolarization rate
• Decrease contractility• Rare last chance drug
• flecainide (Tambocor®)
• propafenone (Rythmol®)
• flecainide (Tambocor®)
• propafenone (Rythmol®)
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Class II: Beta BlockersClass II: Beta BlockersClass II: Beta BlockersClass II: Beta Blockers
• Beta1 receptors in heart attached to Ca++ channels– Gradual Ca++ influx responsible for
automaticity
• Beta1 blockade decreases Ca++ influx– Effects similar to Class IV (Ca++ channel
blockers)
• Limited # approved for tachycardias
• Beta1 receptors in heart attached to Ca++ channels– Gradual Ca++ influx responsible for
automaticity
• Beta1 blockade decreases Ca++ influx– Effects similar to Class IV (Ca++ channel
blockers)
• Limited # approved for tachycardias
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Class II: Beta BlockersClass II: Beta BlockersClass II: Beta BlockersClass II: Beta Blockers
• propranolol (Inderal®)
• acebutolol (Sectral®)
• esmolol (Brevibloc®)
• propranolol (Inderal®)
• acebutolol (Sectral®)
• esmolol (Brevibloc®)
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Class III: Potassium Channel Class III: Potassium Channel BlockersBlockersClass III: Potassium Channel Class III: Potassium Channel BlockersBlockers• Decreases K+ efflux during repolarization• Prolongs repolarization• Extends effective refractory period• Prototype: bretyllium tosylate (Bretylol®)
– Initial norepi discharge may cause temporary hypertension/tachycardia
– Subsequent norepi depletion may cause hypotension
• Decreases K+ efflux during repolarization• Prolongs repolarization• Extends effective refractory period• Prototype: bretyllium tosylate (Bretylol®)
– Initial norepi discharge may cause temporary hypertension/tachycardia
– Subsequent norepi depletion may cause hypotension
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Class IV: Calcium Channel Class IV: Calcium Channel BlockersBlockersClass IV: Calcium Channel Class IV: Calcium Channel BlockersBlockers• Similar effect as ß
blockers
• Decrease SA/AV automaticity
• Decrease AV conductivity
• Useful in breaking reentrant circuit
• Prime side effect: hypotension & bradycardia
• Similar effect as ß blockers
• Decrease SA/AV automaticity
• Decrease AV conductivity
• Useful in breaking reentrant circuit
• Prime side effect: hypotension & bradycardia
• verapamil (Calan®)• diltiazem (Cardizem®)
• Note: nifedipine doesn’t work on heart
• verapamil (Calan®)• diltiazem (Cardizem®)
• Note: nifedipine doesn’t work on heart
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Misc. AgentsMisc. AgentsMisc. AgentsMisc. Agents
• adenosine (Adenocard®)– Decreases Ca++ influx & increases K+ efflux via
2nd messenger pathway• Hyperpolarization of membrane
• Decreased conduction velocity via slow potentials
• No effect on fast potentials
• Profound side effects possible (but short-lived)
• adenosine (Adenocard®)– Decreases Ca++ influx & increases K+ efflux via
2nd messenger pathway• Hyperpolarization of membrane
• Decreased conduction velocity via slow potentials
• No effect on fast potentials
• Profound side effects possible (but short-lived)
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Misc. AgentsMisc. AgentsMisc. AgentsMisc. Agents
• Cardiac Glycocides
• digoxin (Lanoxin®)– Inhibits NaKATP pump– Increases intracellular Ca++
• via Na+-Ca++ exchange pump
– Increases contractility– Decreases AV conduction velocity
• Cardiac Glycocides
• digoxin (Lanoxin®)– Inhibits NaKATP pump– Increases intracellular Ca++
• via Na+-Ca++ exchange pump
– Increases contractility– Decreases AV conduction velocity
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PharmacologyPharmacologyPharmacologyPharmacology
AntihypertensivesAntihypertensives
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Antihypertensive ClassesAntihypertensive ClassesAntihypertensive ClassesAntihypertensive Classes
• diuretics
• beta blockers
• angiotensin-converting enzyme (ACE) inhibitors
• calcium channel blockers
• vasodilators
• diuretics
• beta blockers
• angiotensin-converting enzyme (ACE) inhibitors
• calcium channel blockers
• vasodilators
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Blood Pressure = CO X PVRBlood Pressure = CO X PVRBlood Pressure = CO X PVRBlood Pressure = CO X PVR
• Cardiac Output = SV x HR
• PVR = Afterload
• Cardiac Output = SV x HR
• PVR = Afterload
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BP = CO x PVRBP = CO x PVR
Key:
CCB = calcium channel blockers
CA Adrenergics = central-acting adrenergics
ACEi’s = angiotensin-converting enzyme inhibitors
cardiac factors circulating volume
heart rate
contractility
1. Beta Blockers2. CCB’s3. C.A. Adrenergics
salt
aldosterone
ACEi’s
Diuretics
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BP = CO x PVR
Hormones
1. vasodilators2. ACEI’s3. CCB’s
Central Nervous System
1. CA Adrenergics
Peripheral SympatheticReceptors
alpha beta
1. alpha blockers 2. beta blockers
Local Acting1. Peripheral-Acting Adrenergics
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AlphaAlpha11 Blockers BlockersAlphaAlpha11 Blockers Blockers
Stimulate alpha1 receptors -> hypertension
Block alpha1 receptors -> hypotension
Stimulate alpha1 receptors -> hypertension
Block alpha1 receptors -> hypotension
• doxazosin (Cardura®)
• prazosin (Minipress®)
• terazosin (Hytrin®)
• doxazosin (Cardura®)
• prazosin (Minipress®)
• terazosin (Hytrin®)
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Central Acting AdrenergicsCentral Acting AdrenergicsCentral Acting AdrenergicsCentral Acting Adrenergics
• Stimulate alpha2 receptors – inhibit alpha1 stimulation
• hypotension
• Stimulate alpha2 receptors – inhibit alpha1 stimulation
• hypotension
• clonidine (Catapress®)
• methyldopa (Aldomet®)
• clonidine (Catapress®)
• methyldopa (Aldomet®)
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Peripheral Acting AdrenergicsPeripheral Acting AdrenergicsPeripheral Acting AdrenergicsPeripheral Acting Adrenergics
• reserpine (Serpalan®)
• inhibits the release of NE
• diminishes NE stores
• leads to hypotension
• Prominent side effect of depression– also diminishes serotonin
• reserpine (Serpalan®)
• inhibits the release of NE
• diminishes NE stores
• leads to hypotension
• Prominent side effect of depression– also diminishes serotonin
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Adrenergic Side EffectsAdrenergic Side EffectsAdrenergic Side EffectsAdrenergic Side Effects
• Common– dry mouth, drowsiness, sedation & constipation– orthostatic hypotension
• Less common– headache, sleep disturbances, nausea, rash &
palpitations
• Common– dry mouth, drowsiness, sedation & constipation– orthostatic hypotension
• Less common– headache, sleep disturbances, nausea, rash &
palpitations
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Angiotensin I
ACE
Angiotensin II
1. potent vasoconstrictor
- increases BP
2. stimulates Aldosterone
- Na+ & H2O
reabsorbtion
ACE Inhibitors ACE Inhibitors ACE Inhibitors ACE Inhibitors .
RAAS
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Renin-Angiotensin Renin-Angiotensin Aldosterone SystemAldosterone SystemRenin-Angiotensin Renin-Angiotensin Aldosterone SystemAldosterone System• Angiotensin II = vasoconstrictor• Constricts blood vessels & increases BP• Increases SVR or afterload• ACE-I blocks these effects decreasing SVR &
afterload
• Angiotensin II = vasoconstrictor• Constricts blood vessels & increases BP• Increases SVR or afterload• ACE-I blocks these effects decreasing SVR &
afterload
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ACE InhibitorsACE InhibitorsACE InhibitorsACE Inhibitors
• Aldosterone secreted from adrenal glands
cause sodium & water reabsorption
• Increase blood volume
• Increase preload
• ACE-I blocks this and decreases preload
• Aldosterone secreted from adrenal glands
cause sodium & water reabsorption
• Increase blood volume
• Increase preload
• ACE-I blocks this and decreases preload
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Angiotensin Converting Angiotensin Converting Enzyme InhibitorsEnzyme InhibitorsAngiotensin Converting Angiotensin Converting Enzyme InhibitorsEnzyme Inhibitors• captopril (Capoten®)
• enalapril (Vasotec®)
• lisinopril (Prinivil® & Zestril®)
• quinapril (Accupril®)
• ramipril (Altace®)
• benazepril (Lotensin®)
• fosinopril (Monopril®)
• captopril (Capoten®)
• enalapril (Vasotec®)
• lisinopril (Prinivil® & Zestril®)
• quinapril (Accupril®)
• ramipril (Altace®)
• benazepril (Lotensin®)
• fosinopril (Monopril®)
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Calcium Channel BlockersCalcium Channel BlockersCalcium Channel BlockersCalcium Channel Blockers
• Used for:
• Angina
• Tachycardias
• Hypertension
• Used for:
• Angina
• Tachycardias
• Hypertension
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CCB Site of ActionCCB Site of ActionCCB Site of ActionCCB Site of Action
diltiazem & verapamil
nifedipine (and otherdihydropyridines)
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CCB ActionCCB ActionCCB ActionCCB Action
• diltiazem & verapamil
• decrease automaticity & conduction in SA & AV nodes
• decrease myocardial contractility
• decreased smooth muscle tone
• decreased PVR
• nifedipine
• decreased smooth muscle tone
• decreased PVR
• diltiazem & verapamil
• decrease automaticity & conduction in SA & AV nodes
• decrease myocardial contractility
• decreased smooth muscle tone
• decreased PVR
• nifedipine
• decreased smooth muscle tone
• decreased PVR
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Side Effects of CCBsSide Effects of CCBsSide Effects of CCBsSide Effects of CCBs
• Cardiovascular
• hypotension, palpitations & tachycardia
• Gastrointestinal
• constipation & nausea
• Other
• rash, flushing & peripheral edema
• Cardiovascular
• hypotension, palpitations & tachycardia
• Gastrointestinal
• constipation & nausea
• Other
• rash, flushing & peripheral edema
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Calcium Channel BlockersCalcium Channel BlockersCalcium Channel BlockersCalcium Channel Blockers
• diltiazem (Cardizem®)
• verapamil (Calan®, Isoptin®)
• nifedipine (Procardia®, Adalat®)
• diltiazem (Cardizem®)
• verapamil (Calan®, Isoptin®)
• nifedipine (Procardia®, Adalat®)
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Diuretic Site of ActionDiuretic Site of ActionDiuretic Site of ActionDiuretic Site of Action
.
loop of Henle
proximaltubule
Distal tubule
Collecting duct
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MechanismMechanismMechanismMechanism
• Water follows Na+
• 20-25% of all Na+ is reabsorbed into the blood
stream in the loop of Henle
• 5-10% in distal tubule & 3% in collecting ducts
• If it can not be absorbed it is excreted with the
urine
Blood volume = preload !
• Water follows Na+
• 20-25% of all Na+ is reabsorbed into the blood
stream in the loop of Henle
• 5-10% in distal tubule & 3% in collecting ducts
• If it can not be absorbed it is excreted with the
urine
Blood volume = preload !
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Side Effects of DiureticsSide Effects of DiureticsSide Effects of DiureticsSide Effects of Diuretics
• electrolyte losses [Na+ & K+ ]
• fluid losses [dehydration]
• myalgia
• N/V/D
• dizziness
• hyperglycemia
• electrolyte losses [Na+ & K+ ]
• fluid losses [dehydration]
• myalgia
• N/V/D
• dizziness
• hyperglycemia
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DiureticsDiureticsDiureticsDiuretics
• Thiazides:
• chlorothiazide (Diuril®) & hydrochlorothiazide
(HCTZ®, HydroDIURIL®)
• Loop Diuretics
• furosemide (Lasix®), bumetanide (Bumex®)
• Potassium Sparing Diuretics
• spironolactone (Aldactone®)
• Thiazides:
• chlorothiazide (Diuril®) & hydrochlorothiazide
(HCTZ®, HydroDIURIL®)
• Loop Diuretics
• furosemide (Lasix®), bumetanide (Bumex®)
• Potassium Sparing Diuretics
• spironolactone (Aldactone®)
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Mechanism of VasodilatorsMechanism of VasodilatorsMechanism of VasodilatorsMechanism of Vasodilators
• Directly relaxes arteriole smooth muscle
• Decrease SVR = decrease afterload
• Directly relaxes arteriole smooth muscle
• Decrease SVR = decrease afterload
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Side Effects of VasodilatorsSide Effects of VasodilatorsSide Effects of VasodilatorsSide Effects of Vasodilators
• hydralazine (Apresoline®)– Reflex tachycardia
• sodium nitroprusside (Nipride®)– Cyanide toxicity in renal failure– CNS toxicity = agitation, hallucinations, etc.
• hydralazine (Apresoline®)– Reflex tachycardia
• sodium nitroprusside (Nipride®)– Cyanide toxicity in renal failure– CNS toxicity = agitation, hallucinations, etc.
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VasodilatorsVasodilatorsVasodilatorsVasodilators
• diazoxide [Hyperstat®]
• hydralazine [Apresoline®]
• minoxidil [Loniten®]
• sodium Nitroprusside [Nipride®]
• diazoxide [Hyperstat®]
• hydralazine [Apresoline®]
• minoxidil [Loniten®]
• sodium Nitroprusside [Nipride®]
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PharmacologyPharmacologyPharmacologyPharmacology
Drugs Affecting HemostasisDrugs Affecting Hemostasis
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HemostasisHemostasisHemostasisHemostasis
• Reproduce figure 11-9, page 359 Sherwood • Reproduce figure 11-9, page 359 Sherwood
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Platelet AdhesionPlatelet AdhesionPlatelet AdhesionPlatelet Adhesion
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Coagulation CascadeCoagulation CascadeCoagulation CascadeCoagulation Cascade
• Reproduce following components of cascade:– Prothrombin -> thrombin
• Fibrinogen -> fibrin
– Plasminogen -> plasmin
• Reproduce following components of cascade:– Prothrombin -> thrombin
• Fibrinogen -> fibrin
– Plasminogen -> plasmin
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Platelet InhibitorsPlatelet InhibitorsPlatelet InhibitorsPlatelet Inhibitors
• Inhibit the aggregation of platelets
• Indicated in progressing MI, TIA/CVA
• Side Effects: uncontrolled bleeding
• No effect on existing thrombi
• Inhibit the aggregation of platelets
• Indicated in progressing MI, TIA/CVA
• Side Effects: uncontrolled bleeding
• No effect on existing thrombi
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AspirinAspirin AspirinAspirin
– Inhibits COX• Arachidonic acid (COX) -> TXA2 ( aggregation)
– Inhibits COX• Arachidonic acid (COX) -> TXA2 ( aggregation)
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GP IIB/IIIA InhibitorsGP IIB/IIIA InhibitorsGP IIB/IIIA InhibitorsGP IIB/IIIA Inhibitors
GP GP IIIIb/b/IIIIIIaaInhibitorsInhibitors
Fibrinogen
GP GP IIIIb/b/IIIIIIaaReceptorReceptor
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GP IIB/IIIA InhibitorsGP IIB/IIIA InhibitorsGP IIB/IIIA InhibitorsGP IIB/IIIA Inhibitors
• abciximab (ReoPro®)
• eptifibitide (Integrilin®)
• tirofiban (Aggrastat®)
• abciximab (ReoPro®)
• eptifibitide (Integrilin®)
• tirofiban (Aggrastat®)
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AnticoagulantsAnticoagulantsAnticoagulantsAnticoagulants
• Interrupt clotting cascade at various points– No effect on platelets
• Heparin & LMW Heparin (Lovenox®)
• warfarin (Coumadin®)
• Interrupt clotting cascade at various points– No effect on platelets
• Heparin & LMW Heparin (Lovenox®)
• warfarin (Coumadin®)
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HeparinHeparinHeparinHeparin
• Endogenous– Released from mast cells/basophils
• Binds with antithrombin III• Antithrombin III binds with and inactivates excess
thrombin to regionalize clotting activity.– Most thrombin (80-95%) captured in fibrin mesh.
• Antithrombin-heparin complex 1000X as effective as antithrombin III alone
• Endogenous– Released from mast cells/basophils
• Binds with antithrombin III• Antithrombin III binds with and inactivates excess
thrombin to regionalize clotting activity.– Most thrombin (80-95%) captured in fibrin mesh.
• Antithrombin-heparin complex 1000X as effective as antithrombin III alone
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HeparinHeparinHeparinHeparin
• Measured in Units, not milligrams
• Indications:– MI, PE, DVT, ischemic CVA
• Antidote for heparin OD: protamine.– MOA: heparin is strongly negatively charged.
Protamine is strongly positively charged.
• Measured in Units, not milligrams
• Indications:– MI, PE, DVT, ischemic CVA
• Antidote for heparin OD: protamine.– MOA: heparin is strongly negatively charged.
Protamine is strongly positively charged.
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warfarin (Coumadinwarfarin (Coumadin®®))warfarin (Coumadinwarfarin (Coumadin®®))
• Factors II, VII, IX and X all vitamin K dependent enzymes
• Warfarin competes with vitamin K in the synthesis of these enzymes.
• Depletes the reserves of clotting factors.
• Delayed onset (~12 hours) due to existing factors
• Factors II, VII, IX and X all vitamin K dependent enzymes
• Warfarin competes with vitamin K in the synthesis of these enzymes.
• Depletes the reserves of clotting factors.
• Delayed onset (~12 hours) due to existing factors
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ThrombolyticsThrombolyticsThrombolyticsThrombolytics
• Directly break up clots– Promote natural
thrombolysis
• Enhance activation of plasminogen
• ‘Time is Muscle’
• Directly break up clots– Promote natural
thrombolysis
• Enhance activation of plasminogen
• ‘Time is Muscle’
• streptokinase (Streptase®)
• alteplase (tPA®, Activase®)
• anistreplase (Eminase®)• reteplase (Retevase®)• tenecteplase (TNKase®)
• streptokinase (Streptase®)
• alteplase (tPA®, Activase®)
• anistreplase (Eminase®)• reteplase (Retevase®)• tenecteplase (TNKase®)
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Occlusion MechanismOcclusion MechanismOcclusion MechanismOcclusion Mechanism
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tPA MechanismtPA MechanismtPA MechanismtPA Mechanism
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Cholesterol MetabolismCholesterol MetabolismCholesterol MetabolismCholesterol Metabolism
• Cholesterol important component in membranes and as hormone precursor
• Synthesized in liver– Hydroxymethylglutaryl coenzyme A reductase– (HMG CoA reductase) dependant
• Stored in tissues for latter use• Insoluble in plasma (a type of lipid)
– Must have transport mechanism
• Cholesterol important component in membranes and as hormone precursor
• Synthesized in liver– Hydroxymethylglutaryl coenzyme A reductase– (HMG CoA reductase) dependant
• Stored in tissues for latter use• Insoluble in plasma (a type of lipid)
– Must have transport mechanism
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LipoproteinsLipoproteinsLipoproteinsLipoproteins
• Lipids are surrounded by protein coat to ‘hide’ hydrophobic fatty core.
• Lipoproteins described by density– VLDL, LDL, IDL, HDL, VHDL
• LDL contain most cholesterol in body– Transport cholesterol from liver to tissues for use
(“Bad”)
• HDL move cholesterol back to liver– “Good” b/c remove cholesterol from circulation
• Lipids are surrounded by protein coat to ‘hide’ hydrophobic fatty core.
• Lipoproteins described by density– VLDL, LDL, IDL, HDL, VHDL
• LDL contain most cholesterol in body– Transport cholesterol from liver to tissues for use
(“Bad”)
• HDL move cholesterol back to liver– “Good” b/c remove cholesterol from circulation
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Why We Fear CholesterolWhy We Fear CholesterolWhy We Fear CholesterolWhy We Fear Cholesterol
• Risk of CAD linked to LDL levels• LDLs are deposited under endothelial surface and
oxidized where they:– Attracts monocytes -> macrophages
– Macrophages engulf oxidized LDL• Vacuolation into ‘foam cells’
– Foam cells protrude against intimal lining• Eventually a tough cap is formed
– Vascular diameter & blood flow decreased
• Risk of CAD linked to LDL levels• LDLs are deposited under endothelial surface and
oxidized where they:– Attracts monocytes -> macrophages
– Macrophages engulf oxidized LDL• Vacuolation into ‘foam cells’
– Foam cells protrude against intimal lining• Eventually a tough cap is formed
– Vascular diameter & blood flow decreased
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Why We Fear CholesterolWhy We Fear CholesterolWhy We Fear CholesterolWhy We Fear Cholesterol
• Plaque cap can rupture
• Collagen exposed
• Clotting cascade activated
• Platelet adhesion
• Thrombus formation
• Embolus formation possible
• Occlusion causes ischemia
• Plaque cap can rupture
• Collagen exposed
• Clotting cascade activated
• Platelet adhesion
• Thrombus formation
• Embolus formation possible
• Occlusion causes ischemia
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Lipid DepositionLipid DepositionLipid DepositionLipid Deposition
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Thrombus FormationThrombus FormationThrombus FormationThrombus Formation
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Platelet AdhesionPlatelet AdhesionPlatelet AdhesionPlatelet Adhesion
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Embolus FormationEmbolus FormationEmbolus FormationEmbolus Formation
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Occlusion Causes InfarctionOcclusion Causes InfarctionOcclusion Causes InfarctionOcclusion Causes Infarction
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Antihyperlipidemic AgentsAntihyperlipidemic AgentsAntihyperlipidemic AgentsAntihyperlipidemic Agents
• Goal: Decrease LDL– Inhibition of LDL
synthesis
– Increase LDL receptors in liver
• Target: < 200 mg/dl• Statins are HMG
CoA reductase inhibitors
• Goal: Decrease LDL– Inhibition of LDL
synthesis
– Increase LDL receptors in liver
• Target: < 200 mg/dl• Statins are HMG
CoA reductase inhibitors
• lovastatin (Mevacor®)• pravastatin (Pravachol®)• simvastatin (Zocor®)• atorvastatin (Lipitor®)
• lovastatin (Mevacor®)• pravastatin (Pravachol®)• simvastatin (Zocor®)• atorvastatin (Lipitor®)