UNIT 4 Cardiovascular System Flashcards
(27 cards)
Arrhythmia: Causes
CHF, CAD, MI, drug therapy
Arrhythmia: Symptoms
mild palpitations, cardiac arrest, asymptomatic, fatigue
Arrhythmia: Types
bradycardia, tachycardia, atrial flutter, atrial fibrillation, ventricular fibrillation, premature atrial contraction, premature ventricular contraction
Antiarrhythmics: Goal
return to a normal sinus rhythm;
does not cure the underlying cause;
affects the membrane and movement ions to improve cardiac function
Cardiac Arrest
heart stops beating suddenly
Antiarrhythmics: Classes
Class I: blocks Na+ channels;
Class II: beta blockers
Class III: blocks K+ channels
Class IV: CCBs
Miscellaneous Antiarrhythmic
Antiarrhythmics: Class I
MOA: block Na+ channels, decrease influx of Na+ during repolarization, decrease rate, decrease conduction, prolong refractory period
USES: ventricular and supraventricular arrhythmias
DRUGS: quinidine (Quinaglute)
procainamide (Pronestyl)
lidocaine (Xylocaine)
PATIENT TEACHING/SIDE EFFECTS: N, D, tremors, restlessness, anorexia
Antiarrhythmics: Class II
Beta-Blockers
MOA: bind to beta-1 receptors, slow down HR, slow down velocity of conduction
USES: increased sympathetic nervous system activity; ventricular and supraventricular tachyarrhythmias
DRUGS: propranolol (Inderal) - non-selective beta blocker
PATIENT TEACHING/SIDE EFFECTS: drowsiness, GI upset, CNS depression, mental depression, monitor serum lipid levels, monitor glucose levels in diabetics, bradycardia, do not use with asthma patients - bronchoconstriction
Antiarrhythmics: Class III
K+ channel blockers
MOA: blocks K+ channels, delays repolarization, prolongs refractory period
USES: ventricular tachycardia, ventricular fibrillation
DRUGS: bretylium (Bretylol)
amiodarone (Cordarone) - potent, while others are not effective, contains iodine, may interfere with thyroid fxn
PATIENT TEACHING/SIDE EFFECTS: may affect thyroid fxn - contains iodine, hypotension, dizziness, GI upset, tremors, skin discoloration
Antiarrhythmics: Class IV
CCBs
MOA: blocks entry of Ca2+ into cells; decreases HR and velocity of conduction, decreases FOC (watch our for CHF patients)
USES: tachyarrhythmias (SVT)
DRUGS: verapamil (Calan)
diltiazem (Cardizem)
PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, xerostomia, facial flushing, HA, constipation
Miscellaneous Antiarrhythmic
MOA: decreases activity Ca2+ in SA and AV nodes, decreases conduction and rate
DRUGS: adenosine (Adenocard) - emergent or acute situations
USES: SVT
PATIENT TEACHING/SIDE EFFECTS: respiratory difficulty/bronchospasm, hypotension
Anemia
insufficient RBCs or Hbg
insufficient levels of O2
Anemia: Symptoms
weakness, fatigue, increased HR, SOB, pallor, irritability
Anemia: Causes
genetic, blood loss, bone marrow suppression, destruction of RBCs, lack of vitamins and minerals, drugs
Anemia: Types
Iron Deficiency Anemia, Vitamin B12 Anemia/Pernicious Anemia, Folic Acid Deficiency Anemia
Iron Deficiency Anemia (Fe+)
lack of iron causing decreased Hgb
DIET: fish, meat, soy, beans, green veggies
-give supplement (Vitamin C to increase intestinal absorption)
DRUGS: ferrous sulfate
ferrous gluconate
ferrous fumarate
PATIENT TEACHING/SIDE EFFECTS: N, constipation, darkened stools, gastric irritation, discoloration of teeth (use a straw or mix with juice)
Vitamin B12 Deficiency Anemia/Pernicious Anemia
DIET: meats, eggs, milk, seafood
not enough in diet (not common); stomach lacks an intrinsic factor for absorption of the vitamin (B12)
may lead to production of megablastic RBCs (too large and have a short lifespan)
Vitamin B12 USES: DNA synthesis, cell division, RBC production, myelin sheath protection
DRUGS: cyanocabalamin (Vitamin B12)
PATIENT TEACHING/SIDE EFFECTS: invasive, injections are for lifetime, monitor injection site for reactions
Folic Acid Deficiency Anemia
USES OF FOLIC ACID: cell growth, cell reproduction, protein synthesis
DIET: leafy greens, fortified cereals, citrus fruits
-may lead to megablastic anemia (RBCs are too large and have a short lifespan)
DRUGS: folic acid
Erythropoietin (EPO)
protein produced by the kidneys that is responsible RBC production
MOA: increases number of RBCs, increases H&H
DRUG: epoietin alpha (Epogen, Procrit)
PATIENT TEACHING/SIDE EFFECTS: N, D, HA, joint pain
Thromboembolism
moving clot becomes lodged
Coagulation
1) Thromboplastin is an enzyme that secreted by platelets (clotting factors); it is a tissue extract (substance released from injured cells)
2) Prothrombin is converted into thrombin with the use of thromboplastin
3) Thrombin converts fibrinogen into fibrin (a mesh responsible for forming a clot; it folds platelets together; is the main component of a clot)
Ca2+ and K+ are required for formation and functioning of clotting factors
4) Plasminogen is converted into plasmin by tissue plasminogen activator (tPA);
plasmin - an enzyme that makes fibrin a more soluble product
5) balance between clot formation and clot breakdown occurs due to homeostasis
Anticoagulants
used against clot formation when the clotting mechanism becomes too active
USES: Deep Vein Thrombosis, Thrombophlebitis, Pulmonary Embolism, Stroke, MI, atrial fibrillation
Anticoagulants: Types
1) High Molecular Weight
2) Low Molecular Weight
3) Oral Vitamin K Antagonist
Anticoagulants: High Molecular Weight
MOA: interferes with platelet aggregation; binds to platelets and thromboplastin, preventing thrombin formation
given IV and SubQ
do not administer IM (hematoma) or orally (too acidic for stomach)
do not cross placenta
antidote: protamine sulfate
DRUGS: heparin
PATIENT TEACHING/SIDE EFFECTS: risk for hemorrhage, alopecia, thrombocytopenia, osteoporosis, fever, petechiae, do not massage the injection site, rotate the injection, do not administer where there is bruising from previous injection, epistaxis, easy bruising
