Download Cardiovascular Agents Primary Factors Responsible for Blood

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Cardiovascular Agents
Unit 7
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Hypertension Risk Factors
• Advancing age
• Weight gain – esp. around the hips and thighs
• Race
– Most in blacks
– Least in Mexican Americans
• Males more than females
• Heredity
• Tobacco use
• High-fat diets
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Primary Factors Responsible for Blood Pressure
• Cardiac output
– volume of blood pumped per min.
• Peripheral resistance
– resistance in arteries increases due to constriction
• Blood volume
– increase in amount of blood
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Classification of HTN in Adults
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Non Pharmacological Methods for treating HTN
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Normal - SBP < 120 and DBP < 80
Prehypertension - SBP 120–139 or DBP 80–89
Stage I hypertension - SBP 140–159 or DBP 90–99
Stage II hypertension - SBP > 160 or DBP >100
Weight reduction
Stop tobacco use
Limit salt intake
Limit alcohol consumption
Exercise
Reduce stress
HTN Therapy
• Selection of antihypertensive drug depends on severity of disease
• Trial period on med of about 2-4 weeks then recheck to evaluate
• If hypertension not improved, may change drug, increase dose or implement
stepped care.
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“Stepped Care” Principles - Pertaining to Antihypertension Drugs
• Use two drugs from different classes to control hypertension
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Allows lower doses of each drug
Lower doses produce fewer side effects
Better patient compliance
Combination drugs - patient can take one pill instead of 2
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Renin-Angiotensin Pathway Modifiers Block the Renin-Angiotensin
Pathway and Decrease Blood Pressure
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ACE Inhibitors
• ACE inhibitors “prils”- block angiotensin-converting enzyme (ACE) that blocks formation of
angiotensin II resulting in vasodilation and decrease reabsorption of sodium by kidneys
resulting in more urine excreted resulting in decreased blood volume which decrease BP
• Primary uses – hypertension
• Important side effects – persistent dry non productive cough, hypotension, Increased K+
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Nursing considerations
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Angiotensin receptor blockers
• Angiotensin receptor blockers “sartans” - block angiotensin receptors in arteriolar
smooth muscle and adrenal glands- leading to arteriolar dilation and increase
renal sodium excretion which decreases BP
• Primary uses – hypertension
• Side effects: - headache, hypotension
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Nursing considerations
• Monitor BP, I/O, daily wt.
• Monitor serum K+ levels, renal function
• Examples : Diovan (valsartan)
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Beta Blockers
• Beta Blockers- “olols”
• Mechanism of action - bind to block b1 and b2 receptors, decreasing heart contractility,
decrease SA node firing (heart rate)
• Therapeutic effects: decrease HR, decrease angina, decrease angiotensin II formation.
• Primary uses: hypertension, angina, cardiac arrhythmias , migraine headaches
• Side effects: bradycardia, heart failure, bronchospasm, fatigue, depression, impotence
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Nursing considerations
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Monitor BP, HR, I/O, daily wt
Focused assessment : cardiac, pulmonary
Contraindicated in some dysrhythmias, heart failure, some lung diseases
Examples: inderal (propranolol), Lopressor (metoprolol), Tenormin (atenolol)
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Calcium Channel Blockers
• Mechanism of action - block calcium channels in plasma membrane which
causes vasodilation of arteriole which decreases BP
• Primary use - angina, hypertension
• Important side effects – bradycardia, peripheral edema, headache, dizziness
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Nursing considerations
• Monitor BP, heart rate, I/O, daily weight and side effects
• Focused assessment – cardiac and pulmonary
• Examples
– Calan (verapamil)
– Cardiazem (diltazem)
– Norvasc (amlodipine)
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Diuretics
• Mechanism of action - increase the amount of urine produced by the kidneys which
increases excretion of water and electrolytes (Na, Ca, CL, K) which decreases blood volume
which decreases BP
• Primary use - mild to moderate hypertension
• Important side effects - electrolyte imbalances (especially loss of K)
• Example - hydrochlorothiazide (HydroDIURIL), furosemide (Lasix)
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Types of Diuretics
• Loop- Inhibit sodium and chloride reabsorption (Lasix)
– Monitor K+ levels
• Thiazide and Thiazide-like – inhibit sodium reabsorption (Hydrochlorothhiazide)
– Monitor K+ levels
• Potassium sparing
– Inhibits sodium- potassium exchange in distal tubles (aldactone)
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Nursing Considerations for Diuretics
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Monitor I/O closely
Monitor BP prior to dosing
Monitor Electrolytes (especially K+)
Monitor Kidney function
Direct-Acting Vasodilators
• Mechanism of action - direct relaxation of arteriolar smooth muscle leading to vasodilation
which decreases BP
• Primary use - severe hypertension, hypertensive crisis
• Important side effects - reflex tachycardia, sodium and fluid retention, diziness
• Examples: Apresoline (hydralazine)
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• Nursing considerations: Monitor HR, BP
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Angina Pectoris
• Reduced blood flow to the heart muscle is called myocardial ischemia
• Decreased blood flow in the coronary arteries results in decreased oxygen to the
heart muscle
• Lack of oxygen to the myocardium causes chest pain or angina pectoris
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Classic Presentation of Angina Pectoris
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Sharp pain in the heart region
Moving to left side of neck and lower jaw and down left arm
Preceded by physical exertion or emotional excitement
Angina pain may closely mimic myocardial infarction (MI)
Stable Angina
• Subsides with rest
• Predictable in frequency and duration
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Unstable Angina
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Lifestyle Changes
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Can occur with rest
Occurs more frequently or severely
Signifies an increased risk of myocardial infarction (MI)
Requires aggressive medical treatment
Tobacco cessation
Limit sodium intake and eat foods rich in potassium and magnesium
Limit alcohol consumption
Implement an exercise plan
Reduce stress levels
Reduce dietary saturated fats
Keep weight at optimal level
Treat hyperlipidemia and/or hypertension if present
Surgical Procedures
• Coronary artery bypass graft (CABG)
• Percutaneous transluminal coronary angioplasty (PTCA)
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Antianginal Drugs
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Reduce Myocardial Demand for Oxygen
Slowing heart rate
Reducing blood flow into the heart (reduce preload) by dilating veins
Reducing contractility
Lowering blood pressure (reducing afterload)
Antianginal drugs only relieve symptoms, they do not cure the underlying disorder
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Classes of Antianginal Drugs
• Organic nitrates
• Beta-adrenergic blockers
• Calcium channel blockers
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Organic Nitrates - Vasodilation
• Relieve anginal pain by dilating both venous and arterial smooth muscle
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Organic Nitrates - Decrease Workload of the Heart
• Dilatation of the veins reduces preload - less blood in the heart
• Less blood in the heart decreases afterload - decreased cardiac output
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Organic Nitrates - Dilation of Coronary Arteries
• Primary mechanism is to treat variant angina
• Spasm of a coronary artery
• Nitrates relax spasms
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Two Types of Organic Nitrate
• Short-acting is taken sublingually - nitroglycerin
• Long-acting is taken orally or transdermally - isosorbide dinitrate
– Tolerance often develops
– Reduce symptoms of heart failure
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Adverse Effects of Nitrates
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Reduction in blood pressure with possible dizziness
Tachycardia and palpitations
Headache
Flushing of the skin
Can cause life-threatening hypotension and cardiovascular collapse when used
within 24 hours of taking Viagra
Drug Profile - Organic Nitrate, Vasodilator
• Nitroglycerin (Nitrostat, Nitrobid, Nitro-Dur), short-acting nitrate
• Actions- vasodilation
• Adverse effects-headache, hypotension
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Beta-Adrenergic Blockers to Relieve Angina
• Decrease oxygen demands on the heart
– Slow heart rate and decrease contractility
• Used for angina prophylaxis
• Interactions:
– Cardiac suppression when used with ca+channel blockers
– Heart block when used with digitalis
• Example : tenormin (atenolol)
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Calcium Channel Blockers (CCBs) To Relieve Angina
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Left-Sided Heart Failure
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Relax arterial smooth muscle - lowers peripheral resistance and reduces blood pressure
Decreases myocardial oxygen demand
Useful in treating variant angina
Example: cardizem (diltazem)
Decrease Cardiac Output
Skin cyanotic and clammy, which leads to decreased oxygen supply
Anxiety/restlessness leads to decreased oxygen to the brain
Upright posture/leaning forward/persistent cough leads to blood backing into the lungs
Rapid breathing leads to decreased oxygen to the body
Right-Sided Heart Failure
• Decrease Blood to Lungs
• Edema of lower limbs leads to blood backing up in venous circulation
• Fast heart rate leads to the body not getting enough oxygen
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Nonpharmacological Methods for Controlling Heart Failure
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Stop using tobacco
Limit salt (sodium) intake and eat foods rich in potassium and magnesium
Limit alcohol consumption
Implement a medically supervised exercise plan
Learn and use effective ways to deal with stress
Reduce weight to an optimum level
Limit caffeine consumption
First-Choice Drugs for CHF
• ACE Inhibitors and Diuretics
• Given first
• Reduce most symptoms of mild to moderate heart failure
– Diuretics reduce volume
– ACE inhibitors –unload (decrease afterload)
• Fewer side effects
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Second-Choice Drugs to Treat CHF
• Phosphodiesterase inhibitors, vasodilators, and beta-adrenergic blockers
• Used in severe heart failure
• First-choice drugs not effective
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Three Basic Steps to Hemostasis
• Injured vessel constricts to slow blood flow
• Platelets adhere to injured area and aggregate, plugging damaged vessel
• Coagulation cascade occurs thus forming insoluble fibrin strands which slows
blood flow more
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Coagulation Cascade
• Series of Complex Steps
– Injured cells release prothrombin activator
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– Prothrombin activator changes prothrombin to thrombin
– Thrombin changes fibrinogen to fibrin
– Fibrin forms an insoluble web over injured area which stops blood flow
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Coagulation-Modifier Drugs
• Anticoagulants
• Thrombolytics
• Hemostatics
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Anticoagulants
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Prevent the Formation of Clots and Enlargement of Clots
Inhibiting specific clotting factors in the coagulation cascade
Diminishing the clotting action of platelets
Both ways increase the time to form clots
Anticoagulants
• Mechanism of action - inhibit specific clotting factors which interfere with coagulation
cascade in order to prevent formation or enlargement of clot
• Primary use - thromboembolic disease; prevent formation of clots in veins
• Adverse effects - abnormal bleeding
• Examples - heparin (Heplock), warfarin (Coumadin)
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Antiplatelet Agents
• Prolong Bleeding Time by Interfering with Platelet Aggregation
• Mechanism of actions
– Aspirin: inhibits thromboxane2, which prevents aggregation of platelets
– ADP receptor blockers: interfere with platelet plasma membrane, which prevents platelet aggregation
– Glycoprotein IIb/IIIa inhibitors: glycoprotein IIb/IIIa enzyme inhibited which prevents platelet aggregation
• Example – Asprin (acetylsalicylic acid), dipyridamole (persantine)
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Antiplatelet Agents
• Primary uses - prevent clot formation in arteries
• Adverse effects - abnormal bleeding; reduce number of neutrophils
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Thrombolytics
• Used to Dissolve Existing Clots
• Given IV
• Adverse effects - abnormal bleeding; contraindicated in patients with active
bleeding or recent trauma
• Example - alteplase (Activase)
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Cardiac Glycosides
• Positive inotropes
• Increase the Force of Myocardial Contraction
• Mechanism of action - 1) positive inotropic effect: more blood ejected per beat leads to
increased cardiac output in order to meet, the metabolic demands of tissues; 2) slow
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electrical conduction through the heart, which creates fewer beats per minute and
decreases heart rate
• Example - digoxin (Lanoxin)
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Cardiac Glycosides (cont’d)
• Primary use - heart failure
• Administration:
– Loading
• Generally 1mg over 24 hrs in divided doses orally or IV
– Maintenance
• 0.125mg- 0.25mg orally daily
• Monitor serum digoxin levels, K+ level
• Important adverse effects –bradycardia, loss of appetite, vomiting, diarrhea, headache, drowsiness,
confusion, visual disturbances (yellow halos)
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Nursing considerations
• Monitor HR
– When would you hold a dose?
• Monitor renal function
– Cannot be dialyzed out
• Client ed: teach signs of dig. Toxicity
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Beta-Adrenergic Blockers
• Used in Combination with Other Drugs to Slow Progression of Heart Failure and to Prolong Patient
Survival
• Mechanism of action - blocks beta1, beta2, and alpha1 receptors, which decreases heart rate and
blood pressure, decreases afterload, and reduces the workload on the heart
• Primary use - slow progression of heart failure and increased exercise tolerance when combined
with other heart failure drugs
• Important adverse effects - can worsen heart failure
• Example - carvedilol (Coreg)
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Natriuretic Peptides
• First New Drugs to Treat Heart Failure in More than 10 Years
• Mechanism of action - acts on kidney, which increases excretion of sodium and water,
thereby lowering blood pressure; also causes vasodilation, which reduces preload
• Primary use - severe heart failure
• Important adverse effects - severe hypotension
• Example - nesiritide (Natrecor)
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Dysrhythmias
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Heart chambers are not contracting in a synchronized manner
Can Seriously Affect Cardiac Output
Both atria contract simultaneously
Followed by contraction of both ventricles
Dysrhythmias Based on Location and Conduction Abnormality
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• Atrial dysrhythmias
– Premature atrial contractions lead to ectopic foci in atria, producing impulse
– Atrial tachycardia - atria contracting at greater than 150 bpm
– Atrial flutter and/or fibrillation - very rapid, uncoordinated contractions of atria
• Sinus bradycardia - SA node producing impulses at less than 50 bpm
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Dysrhythmias Based on Location and Conduction Abnormality (con’t)
• Ventricular dysrhythmias
– Premature ventricular contractions (PVC) - ectopic foci in ventricles producing impulses
– Ventricular tachycardia - ventricles contract at greater than 150 bpm
– Ventricular flutter and/or fibrillation - very rapid, uncoordinated contractions of ventricles
• Heart block - area where impulse is prevented either partially or completely from passing
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Ion Channels in the Plasma Membrane of Myocardial Cells Open and Close
• Sodium ion channels open, allowing sodium ions to rush into cell and produce
depolarization
• Calcium ion channels open, allowing calcium ions to enter the cell which are responsible for
cardiac muscle contraction
• Potassium ion channels open, allowing potassium ions to leave the cell, after which the cell
is polarized
• Cells in the SA and AV nodes result in calcium ions that produce the depolarization
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Pharmacotherapy of Dysrhythmias
• Block potassium, sodium, or calcium ion channels
• Prolong the refractory period
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Nonpharmacological Treatment of Dysrhythmias
• Cardioversion (defibrillation) - for more serious types of dysrhythmias
– Electrical shock momentarily stops all electrical impulses in the heart
– Allows SA node to return conduction to normal sinus rhythm
• Catheter ablation - identification and destruction of myocardial cells responsible for the
abnormal conduction
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Nonpharmacological Treatment of Dysrhythmias (con’t)
• Insertion of cardiac pacemaker - for dysrhythmias that cause the heart to beat too slowly
• Implantable cardioverter defibrillator (ICD)
– Paces the heart to normal sinus rhythm or
– Gives an electrical shock when dysrhythmia occurs
– Stores information regarding heart rhythm
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Basic Mechanisms of Antidysrhythmics
• Block ion channel
– Sodium ion channels
– Potassium ion channels
– Calcium ion channels
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• Block beta-adrenergic receptors in the heart
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Sodium Channel Blockers (Class I)
• Mechanisms of action - blocks Na+ channels, slowing rate of impulse conduction through
heart
• Primary use - many types of dysrhythmias; some more specific - only for life-threatening
ventricular dysrhythmias
• Important adverse effects - creates new dysrhythmias or worsens existing ones,
hypotension, dizziness, fainting
• Example –Xylocaine (lidocaine), Quinidex (quinidine)
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Beta-Adrenergic Blockers (Class II)
• Mechanisms of action - block beta receptors in the heart, which slows the heart rate and
decreases conduction velocity through the AV node
• Primary use - atrial dysrhythmias associated with heart failure
• Important adverse effects - bradycardia, hypotension with dizziness and fainting,
bronchospasms if they block beta2 receptors
• Example - propranolol (Inderal)
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Potassium Channel Blockers (Class III)
• Mechanism of action - block potassium ion channels in myocardial cells,
prolonging the refractory period of the Heart
• Primary use - resistant ventricular tachycardia, atrial dysrhythmias with heart
failure
• Important adverse effects - can worsen dysrhythmias, bradycardia, hypotension
• Example –Cordarone (amiodarone)
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Calcium Channel Blockers (Class IV)
• Mechanisms of action - block calcium channels in myocardial cells, which leads to reduced
automaticity in SA node and slows impulse conduction through the AV node, which prolongs
the refractory period
• Primary use - supraventricular tachycardia
• Important adverse effects - bradycardia, hypotension
• Monitor BP and HR prior to administering
• Example – Calan (verapamil), Cardizem (diltiazem)
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