Pharm 5

• Atherosclerosis: disease characterized by deposits of fattyplaques on the inner walls of arteries
• Angina: acute pain in the chest resulting from decreased bloodsupply to the heart muscle
• Pulmonary arterial hypertension (PAH): high blood pressure inthe pulmonary artery (heart to lungs), which can also causechest pain and results in heart failure if not treated
• Beta (β)-blockers: reduce angina, nursing goal monitor pulse

  • treats hypertension (atenolol)
• Calcium channel blockers: act by inhibiting themovement of calcium ions across cell membranes ofcardiac muscle cells
• Calcium channel blockers adverse reaction: severe bradycardia
• *** Nitrates: relax smooth muscle layer of blood vessels, increasing the lumen of the artery or arteriole, increases the amount of blood flowing through the vessels***
• ACE inhibitor drug: captopril
• Antianginal Drugs—Uses

  Used to:

  o Relieve cardiac pain and acute anginal attacks

  o Prevent angina

  o Treat chronic stable angina pectoris
• Antianginal drug

  -If client’s heart rate falls below 50 bpm or if the systolic BPis below 90 mm Hg, hold the drug and notify the provider
• Antianginal drug

  -Teach clients proper administration of nitrates that are prescribed via sublingual or buccal route

  -Dose of sublingual nitroglycerin or spray can be repeated every 5 minutes until pain is relieved or until client has received 3 doses in a 15-minute period; contact provider if angina is not relieved
• Antianginal drug

  • tolerance can occur
  • Apply the patch in the morning and leave in place for 10to 12 hours; remove patch and leave off for 10 to 12hours
• Buccal: space in the mouth between the gum and cheek in either the upper or lower jaw
• prophylaxis: prevention
• Antianginal drug

  • do not rub nitroglycerin ointment into the skin because this will immediately deliver a large amount of the drug through the skin.
• Hemostasis: A complex process by which fibrin forms and blood clots
• Thrombosis: Formation of a blood clot or “thrombus”
• Deep Vein Thrombosis

  
• Anticoagulants: prevent the formation and extension of a thrombus; used prophylactically in clients at risk for clot formation (“blood thinners”) Prevention and treatment of DVT (deep vein thrombosis)
• Oral and Parenteral Anticoagulants:-Low–molecular-weight heparins (LMWHs) or fractionated heparins

  -Interfere with the clotting mechanism of the blood preventing theformation and extension of a thrombus

  Med: enoxaparin (Lovenox)
• Oral and Parenteral Anticoagulants—Adverse Reactions

  -bowel: monitor for blood in the stool (black tarry stools)
• Antiplatelet Drugs:

  *work by decreasing the platelets ability to stick together (aggregate)

  *Antiplatelet drugs decrease the platelets ability to aggregate (orstick together). This reduces the chance of thrombus formation inthe arterial circulation for conditions such as acute coronary syndrome, MI, and stroke
• Thrombolytic Drugs:

  * break down fibrin clots by converting plasminogen to plasmin
• Warfarin: Prioritize assessing PT/INR

  *Optimal therapeutic results—PT is 1.2 to 1.5 times the control value. INR less than 3.0
• Anticoagulant, Antiplatelet, or Thrombolytic

  * Withhold the drug and notify the provider if:

  • The PT exceeds 1.5 times the control value

  • There is evidence of bleeding

  • The INR is greater than 3
• Parenteral Anticoagulants:

  *Protamine is antidote for heparin

  • Perform blood coagulation tests every 4 hours
• Managing Anticoagulant Over dosage:

  *(Anticoagulant antagonist)–Otherwise known as Vitamin K-antidote for warfarin
• Angiotensin II Receptor Antagonists:

  med: Lozartan
• Cardiotonics: improve the myocardial contraction

  *treats heart failure

  * Increases cardiac output through positive inotropic activity (an increase in the force of the contraction)

  * When a cardiotonic is used, the pulse rate is monitored and the drug is held if the client’s heart rate is less than 60 bpm
• Cardiotonic med: Digoxin
• Cardiotonic adverse reaction:

  -Visual disturbances (blurring or yellow halo with digoxin; increased brightness with ivabradine)
• Antiarrhythmic Drugs:

  -Class IA: (Sodium channel blocker) produce moderate slowing of cardiac conduction; prolong the action potential duration
• Antiarrhythmic Drugs:

  * Class IB–Sodium channel blocker: selectively depress cardiac conduction*Decreases diastolic depolarization, decreases automaticity of ventricular cells, and raises the threshold of the ventricular myocardium

  * Class IC–Sodium channel blocker: Depresses fast sodium channels, decreases the height and rate of rise of action potentials, and slows conduction of all areas of the heart
• Antiarrhythmic Drugs:

  *Class II Beta-Adrenergic (β-adrenergic) Blockers-Block β-adrenergic receptors of the heart and kidney, decreasing the excitability of the heart and the release of renin (lowering heart rate and blood pressure)
• Antiarrhythmic Drugs:

  *Class III Potassium Channel Blockers-Prolongs the refractory period and repolarization and increasing the ventricular fibrillation threshold
• Antiarrhythmic Drugs:

  *Inhibit the movement of calcium through channels across the myocardial cell membranes and vascular smooth muscle

  *Rarely–agranulocytosis Pt may present with fever, chills & sore throat and have LOW white blood cell count.
• Antiarrhythmic Drug #1 adverse reaction: Constipation
• Antiarrhythmic Drugs:

  *Depresses myocardial excitability, or the ability of the myocardium to respond to an electrical stimulus.
• Antiarrhythmic Drugs:

  *Quinidine

  -Ringing in the ears

  -Hearing loss

  -Nausea/vomiting

  -dizziness
• Antiarrhythmic Drugs cardiovascular adverse reaction: bradycardia