N402 1. Angina is caused by insufficient O2 to part of the myocardium Therefore, angina is relieved...
-
Upload
pierce-scearce -
Category
Documents
-
view
223 -
download
1
Transcript of N402 1. Angina is caused by insufficient O2 to part of the myocardium Therefore, angina is relieved...
1
N402
Pharmacology for the Cardiovascular and Respiratory Systems
2
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….
4
β-Blockers
Organic
Nitrates
Ca Chann
el Blocke
rs
Classes of antianginals
5
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…
6
Slow the heart rate and decrease contractilityTherefore, afterload is decreasedUsed to treat both hypertension and anginaNot effective on Prinzmetal’s angina
β-Blockers
7
Relax arteriolar smooth muscle to decrease BP
Therefore, decrease afterloadAlso dilate coronary smooth muscleUseful in treating Prinzmetal’s angina
Ca Channel Blockers
8
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
9
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
10
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
11
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
12
Anticoag.ASA/clopidogrel
AntianginalNitrates
ACEIPain Mgt
MS
↓ O2 demandΒ-Blockers
Pharmacologic management after MI
13
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
14
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
15
Commonly associated drugs:Antibiotics—especially PCNs, cephalosporins,
sulfonamidesNSAIDS—ASA, ibuprofen, naproxenACEIsOpioids Iodine based contrast media
Anaphylaxis (anaphylactic shock)
16
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
17
Major categories
Cardiac dysrhythmias
Atrial
Ventric-ularBlocks
18
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
19
Atrial fibrillation
20
Ventricular fibrillation
21
Heart block
22
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
23
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
24
Prevent depolarizationAction potential slowsEctopic pacemaker activity suppressed
Procainamide May produce new dysrhythmiasHypotension
Class I: Sodium Channel Blockers
25
Decrease conduction through the AV nodeAutomaticity is reducedDysrhythmias can be stabilized
Propanolol (Inderal)Watch for laryngospasmBradycardiaSerious dysrhythmiasMyocardial ischemia
Class II: β-Blockers
26
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
27
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
28
Remember?
COPD includes:Chronic bronchitisEmphysema
And asthma is off in its own category….
And finally…the Respiratory System!
29
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….
30
Broncho-
spasm
Inflam-mation Asthma
Asthma is combined of 2 components
31
Bronchodilators address muscle spasm of the respiratory tree:
Medications are directed at each component
β-adrenergic agonists
Methly-xanthines
Anti-cholinergi
cs
32
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
33
Alternative for patients who cannot tolerate β-adrenergic agonists
Block the parasympathetic nervous systemPrevent vasoconstriction
Ipratropium (Atrovent) HeadacheCough Dry mouthParadoxical bronchospasmPharyngitis
Anticholinergics
34
Older drugsLong term management of persistent asthmaNarrow margin of safetyRelated to caffeine
Theophylline (Theo-Dur)TremorsTachycardiaDysrhythmiasHeadache Respiratory arrest
Methlyxanthines
35
Cortico-steroids
Mast cell stabilizers
Lelukotriene
modifiers
Decreasing inflammation for the asthma patient
36
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
37
Alternative drugsInhibit release of leukotrienes
EdemaInflammationbronchoconstriction
Zafirkulast (Acolate)Headache, nauseaThroat painIncreased suicidal ideation
Leukotriene modifiers
38
Inhibit release of histamine from mast cellsTaken dailyNot effective for acute events
Cromolyn (Intal)Sneezing, nasal stingingThroat irritationAngioedemaBronchospasm
Mast cell stabilizers
39
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
40
β-blockers which cause bronchoconstrictionRespiratory depressants (MS, barbiturates)
Most importantly…smoking cessation!
COPD patients should NOT receive