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N402

Pharmacology for the Cardiovascular and Respiratory Systems

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Angina is caused by insufficient O2 to part of the myocardium

Therefore, angina is relieved by decreasing O2 to the myocardium! Accomplished by:

Decrease the heart rate…Dilate the veins (decrease preload)…

Decrease contractility… or,Decrease BP (decrease

afterload)

Angina? It’s direct….

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β-Blockers

Organic

Nitrates

Ca Chann

el Blocke

rs

Classes of antianginals

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Requires drugs from 2 classes because each class relieves angina from a different approach…

β-Blockers slow heart rate and decrease contractility…

Ca Channel Blockers decrease afterload…, and

Organic Nitrates decrease preload

Persistent angina…

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Slow the heart rate and decrease contractilityTherefore, afterload is decreasedUsed to treat both hypertension and anginaNot effective on Prinzmetal’s angina

β-Blockers

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Relax arteriolar smooth muscle to decrease BP

Therefore, decrease afterloadAlso dilate coronary smooth muscleUseful in treating Prinzmetal’s angina

Ca Channel Blockers

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Dilation of veins decreases amount of blood returning to heart

Therefore decreases preloadAlso dilates coronary arteriesUseful in treating Prinzmetal’s anginaMay be short acting (NTG) or long acting

(isosorbide)

Organic Nitrates

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Sudden blockage of coronary artery by dislodged plaque

Causes coagulation cascadeResults in:

UNSTABLE ANGINA INFARCTIONIncomplete occlusion Complete occlusionby thrombus by thrombusCauses chest pain Causes

ischemia andnecrosis

Acute Coronary Syndrome

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Goals of treatment:

Acute Coronary Syndrome

Unstable angina

Relief of pain

Prevent clot enlargement

Myocardial infarction

Restore blood supplyPrevent thrombus

enlargement

Decrease O2 demand

Prevent dysrhythmias

Manage pain

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Should be given within first 20 minutes to 12 hours

Risk is excessive bleedingNot everyone is a candidateUse with caution in the elderly

Restoring blood supply through thrombolytics

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Anticoag.ASA/clopidogrel

AntianginalNitrates

ACEIPain Mgt

MS

↓ O2 demandΒ-Blockers

Pharmacologic management after MI

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Occurs when there is insufficient blood supply to vital organs by cardiovascular system

Major types of shock:Hypovolemic Excessive blood loss

Cardiogenic SepticPump failure Toxins in blood

NeurogenicSudden loss of sympathetic

activity

Shock

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Used when fluids alone are ineffectiveRapid onset, short durationGiven by continuous IV until patient is stabilized

Dopamine (Dopastat, Intropin 2-5 mcg/kg/min; up to 20-50 mcg/kg/minNorepinepherine (Levophed) 0.5 mcg/min up to 8-30 mcg/minPhenyephrine (Neo-Synepherine)Epinephrine

Watch closely for adverse effects: BP changes, dysrhythmias, necrosis at infusion/injection site (Regitine)

Treating shock with vasopressors

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Commonly associated drugs:Antibiotics—especially PCNs, cephalosporins,

sulfonamidesNSAIDS—ASA, ibuprofen, naproxenACEIsOpioids Iodine based contrast media

Anaphylaxis (anaphylactic shock)

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Epinephrine 1:1000 subcu or IM initial drug of choice

Antihistamines e.g., diphenhydramineBronchodilator by inhalation, e.g., albuterolHigh flow oxygen (some exceptions)Systemic cortico- steroids

Treatment of anaphylaxis

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Major categories

Cardiac dysrhythmias

Atrial

Ventric-ularBlocks

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SupraventricularOriginate in the atriaAtrial fibrillation is most common SV

dysrhythmiaVentricular

More serious than atrial dysrhythmiasComplete disorganization of contractions

Heart blockBlockage of electrical conduction system

Classification of dysrhythmias

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Atrial fibrillation

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Ventricular fibrillation

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Heart block

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CardioversionDisrupts cardiac rhythm to “reset”Patient may be awake

DefibrillationUses more joules of shockPatient should not be awake!

Implantable cardioverter defibrillators

Respond to sensing of dysrhythmias

Nonpharmacologic treatment of dysrhythmias

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Block flow through Change autonomicion channels activity(conduction) (automaticity)

I Sodium channel blockers II β-blockersIII Potassium channel blockersIV Calcium channel blockers

Mechanism of action of antidysrhythmic drugs –Classes

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Prevent depolarizationAction potential slowsEctopic pacemaker activity suppressed

Procainamide May produce new dysrhythmiasHypotension

Class I: Sodium Channel Blockers

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Decrease conduction through the AV nodeAutomaticity is reducedDysrhythmias can be stabilized

Propanolol (Inderal)Watch for laryngospasmBradycardiaSerious dysrhythmiasMyocardial ischemia

Class II: β-Blockers

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Delay repolarization of the myocardial cellsLengthen refractory periodUsed for serious dysrhythmiasUsed for atrial and ventricular dysrhythmias

Amiodarone May cause new dysrhythmiasHypotensionBradycardia

Class III: Potassium channel blockers

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Slow conduction velocity through AV nodeReduced automaticity in the heartSlows heart rateProlongs refractory period

VerapamilMyocardial infarctionHeart failureMay be given continuous IV for up to 24 hours

Class IV: Calcium Channel Blockers

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Remember?

COPD includes:Chronic bronchitisEmphysema

And asthma is off in its own category….

And finally…the Respiratory System!

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Ventilation is the process of moving air in and out of the lungs

Respiration is the exchange of gases due to diffusion

Perfusion is the flow of blood through the lungs

Some terms you must master….

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Broncho-

spasm

Inflam-mation Asthma

Asthma is combined of 2 components

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Bronchodilators address muscle spasm of the respiratory tree:

Medications are directed at each component

β-adrenergic agonists

Methly-xanthines

Anti-cholinergi

cs

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Activate the sympathetic nervous system (sympathetic = dilation; parasympathetic = constriction)

Cause vasodilationDrugs in this category classified as long-acting or short-

actingShort-acting referred to as rescue-drugs Long-acting cannot relieve acute bronchospasm!

Albuterol (Proventil)TachycardiaDysrhythmiasHypokalemiaParadoxical bronchospasm

β-adrenergic agonists

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Alternative for patients who cannot tolerate β-adrenergic agonists

Block the parasympathetic nervous systemPrevent vasoconstriction

Ipratropium (Atrovent) HeadacheCough Dry mouthParadoxical bronchospasmPharyngitis

Anticholinergics

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Older drugsLong term management of persistent asthmaNarrow margin of safetyRelated to caffeine

Theophylline (Theo-Dur)TremorsTachycardiaDysrhythmiasHeadache Respiratory arrest

Methlyxanthines

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Cortico-steroids

Mast cell stabilizers

Lelukotriene

modifiers

Decreasing inflammation for the asthma patient

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Potent, naturally occurringAllow smooth muscle to become more

sensitive to bronchodilationReduce responsiveness to allergensUsed for preventing asthma attacks

Beclomethasone (Qvar)HoarsenessCough, sore throatOropharyngeal candidiasis

Corticosteroids

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Alternative drugsInhibit release of leukotrienes

EdemaInflammationbronchoconstriction

Zafirkulast (Acolate)Headache, nauseaThroat painIncreased suicidal ideation

Leukotriene modifiers

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Inhibit release of histamine from mast cellsTaken dailyNot effective for acute events

Cromolyn (Intal)Sneezing, nasal stingingThroat irritationAngioedemaBronchospasm

Mast cell stabilizers

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Many of the same drugs are used with the COPD patient

Medications are based on COPD symptoms

The COPD patient….

Broncho-dilators

Mucolytics

Oxygen Antibiotics

Cortico-steroids

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β-blockers which cause bronchoconstrictionRespiratory depressants (MS, barbiturates)

Most importantly…smoking cessation!

COPD patients should NOT receive