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Pharmacology > Cardiac Medications > Flashcards

Cardiac Medications Flashcards

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1
Q

Background of angina pectoris

A
  • Chest pain due to ischemic heart disease: caused by O2 demand/supply mismatch & can be predicted/exacerbated by physical exertion
  • Very high prevalence in US: many patients receiving PT may suffer from this disease state
  • Can be sudden & described as intense compression & tightness of the chest that can sometimes radiate to the jaw or left arm
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2
Q

Describe EKG anomalies

A
  • Gives info about electrical activity in the heart
  • Well established template where anomalies can be detected & help to determine what is happening to the heart muscle
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3
Q

Describe the parts of the EKG heart beat wave

A
  • QRS: ventricle depolarization/contraction
  • T: ventricle repolarization/relaxation
  • ST segment: interval b/w depolarization & repolarization (elevation or depression or T wave inversion is often due to ischemia
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4
Q

Pharmacologic treatments for angina pectoris

A
  • Nitrates
  • Bete blockers
  • Calcium channel blockers
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5
Q

Describe organic nitrates

A
  • Prodrugs that are converted to nitric oxide (NO) within vascular smooth muscle
  • Nitric oxide increases cGMP which inhibits smooth muscle contraction
  • Produces general vasodilation -> decreases preload & afterload
  • Reduces workload on the heart (decreased oxygen demand)
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6
Q

List organic nitrate drugs

A
  • Nitroglycerin
  • Isosorbide dinitrate
  • Isosorbide mononitrate
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7
Q

Describe nitroglycerin (Nitrobid, Nitrostat)

A
  • Used for acute Tx of anginal attacks
  • Sublingual administration is preferred in acute attacks due to rapid absorption (therapeutic effects begin within 2 min; bypasses 1st pass effect)
  • Can also be administered ar an aerosol, ointment, patch, or oral tablet (patch must be removed for 10-12 hrs due to development of tolerance)
  • Used as a powerful explosive: this feature is inactivated by diluting with lactose, alcohol, or propylene glycol
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8
Q

Describe isosorbide dinitrate

A
  • Used for Tx of acute episodes of angina & for prevention of future attacks
  • Longer effects
  • Sublingual, buccal, chewable, or oral tablets
  • Primarily used as preventive medication
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9
Q

Describe isosorbide mononitrate

A
  • Primarily used as preventive medication
  • Similar to Isosorbide dinitrate but longer acting
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10
Q

Adverse effects of organic nitrate drugs

A
  • Headache
  • Dizziness
  • Orthostatic hypotension
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11
Q

Describe beta blockers

A
  • Drugs: Metoprolol, Labetalol, Carvedilol
  • MOA: antagonist to beta1 receptors on the myocardium; decrease HR & myocardial contraction force; decreases O2 demands
  • Adverse effects: nonselective agents may cause bronchoconstriction in pts with asthma; otherwise well tolerated; watch for excessive cardiac depression
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12
Q

Describe calcium channel blockers

A
  • Drugs: Diltiazem, Verapamil, Amlodiopine, Nifedipine
  • MOA: affects vascular smooth muscle cells causing vasodilation (systemic vasodilation causes decreased myocardial O2 demand); mediates coronary vasodilation (increases O2 supply)
  • Adverse effects: peripheral vasodilation (headache, flushing, dizziness); peripheral edema; reflex tachycardia (-ipine)
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13
Q

Describe stable angina

A
  • Myocardial O2 demand > supply
  • Typically brought on by physical exertion
  • Acute Tx: sublingual nitroglycerin
  • Prevention: beta blockers or long acting nitrate
  • Chest pain/discomfort can occur with physical exertion
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14
Q

Describe variant angina

A
  • Coronary vasospasm causes a decrease in myocardial O2 supply
  • Tx: calcium channel blocker
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15
Q

Describe unstable angina

A
  • Myocardial O2 supply decreases at the same time O2 demand increases
  • Due to atherosclerotic plaque rupture within coronary arteries
  • Chest pain/discomfort can occur during physical exertion or rest
  • Tx: requires further evaluation & a combination of pharmacologic & interventional therapies
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16
Q

Non-pharmacologic management of angina pectoris

A
  • Pharmacologic agents only treat the symptoms not the condition
  • Lifestyle changes: exercise, weight loss, smoking cessation, stress management
  • Angina related to plaque build up or thrombosis can be addressed with cardiac catheterizations & subsequent intervention or coronary artery bypass surgery of needed
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17
Q

What type of patients require special sternal precautions to be aware of during PT

A
  • CABG patients have a scar down their chest & require special sternal precautions
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18
Q

Key points for PT related to angina pectoris

A
  • Ensure patient has PRN nitroglycerin if needed
  • Beta blockers & calcium channel blockers may blunt the myocardial response to exercise
  • All of these drugs can cause hypotension: may be exaggerated upon sudden sitting to standing
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19
Q

Background of arrhythmias

A
  • Arrhythmia: any significant deviation from normal cardiac rhythm
  • Untreated arrhythmias can result in impaired cardiac function & may be associated with CVA, heart failure, & fatalities
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20
Q

Normal cardiac rhythm/electrical conduction pathway

A
  • Sinoatrial node (SA)
  • Atrioventricular node (AV)
  • Bundle of His
  • Left/Right bundle branches
  • Purkinje Fibers
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21
Q

Classification of Antiarrhythmic drugs

A
  • Class I: Sodium channel blockers
  • Class II: Beta blockers
  • Class III (drugs that prolong repolarization): K+ channel blockers
  • Class IV: Calcium channel blockers
  • Others: Digoxin
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22
Q

List class I sodium channel blockers

A
  • Class IA: Quinidine, Procainamide
  • Class IB: Lidocaine, Mexilatine
  • Class IC: Flecainide, Propafenone
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23
Q

MOA and adverse reactions of class I sodium channel blockers

A
  • MOA: control the rate of Na entry; control excitation/conduction to stabilize the cardiac cell membrane
  • Adverse effects: increased arrhythmias, dizziness, visual disturbance, N/V, diarrhea
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24
Q

List class II beta blocker drugs

A
  • Atenolol
  • Esmolol
  • Metoprolol
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25
MOA and adverse effects of class II beta blockers
- MOA: decrease excitatory effects of the sympathetic NS; slows conduction through the myocardium (blocks AV node) - Adverse effects: Non-selective = increased bronchoconstrictionn; bradycardia, orthostatic hypotension
26
List class III K+ channel blockers
- Amiodarone - Dofetilide - Dronedarone
27
MOA and adverse effects of class III K+ channel blockers
- MOA: prolong the effective refractory period; slows & stabilizes the HR - Adverse effects: torsades de pointes (pro-arrhythmic); amiodarone = pulmonary, thyroid, liver toxicity
28
List class IV calcium channel blockers
- Verapamil - Diltiazem
29
MOA and adverse effects of CLass IV calcium channel blockers
- MOA: block calcium influx which alters the excitability & conduction; decrease the rate of discharge of the SA node & inhibit velocity through the AV node - Adverse effects: excessive bradycardia, peripheral vasodilation = dizziness & headache
30
Non-pharmacologic treatment of arrhythmias
- Drugs do not resolve cause of arrhythmia - Implantable devices: pacemakers, defibrillators - Interventions: ablations
31
Key points for PT for arrhythmias
- Be aware of the various side effects of these agents (commonly dizziness, hypotension) - May play a role in early detection - Potential for increased arrhythmias with many medications & with activity - If no EKG is available, palpation of pulse for rate & regularity may be useful
32
Background of congestive heart failure (CHF)
- Heart is unable to pump a sufficient quantity of blood - Fluid accumulates in the lungs & peripheral tissues because the heart is unable to maintain proper circulation
33
Pathophysiology of congestive heart failure (CHF)
- Cardiac lesion -> decreased cardiac performance -> neurohumeral compensation -> increased cardiac workload -> myocardial cell changes -> decreased cardiac performance - Vicious cycle
34
Systolic dysfunction of CHF
- Cardiac output is reduced - Neurohumeral compensation activates further worsening dysfunction - Increased preload & after load due to vasoconstriction & sodium & water retention - Cardiac remodeling
35
Diastolic dysfunction of CHF
- 50% of patients have normal systolic function & cardiac output - Left ventricle is stiff & unable to relax -> unable to fill & increased pressure - Progressive changes in cellular function & impaired cardiac function
36
Signs and symptoms of CHF
- Pulmonary edema - Pleural effusion - Distended neck veins - Enlarged liver & spleen - Ankle edema
37
Difference between left and right sided heart failure
- Left: volume backs up in the lungs - Right: volume backs up in peripheral tissues
38
Pharmacotherapy for CHF
- Inotropes (improve pumping ability of the heart): Digitalis, Phosphodiesterase inhibitors, and Dobutamine/Dopamine - Decrease cardiac workload: ACE inhibitors/ARBs, beta blockers, loop diuretics, and vasodilators
39
MOA and adverse effects of Digoxin
- MOA: increase intracellular Ca facilitates interaction b/w myosin & actin filaments; directly inhibits sympathetic NS - Adverse effects: GI distress (N/V/D); CNS disturbances (drowsiness, fatigue, confusion, visual disturbances); arrhythmias
40
MOA and adverse effects of phosphodiesterase inhibitors: Milrinone
- MOA: inhibit phosphodiesterase which breaks down cGMP allowing more calcium to enter the cells (increases force of contraction); vasodilates (reduces preload & afterload) - Adverse effects: Hypotension and arrhythmias
41
Describe Milrinone
- IV infusion medication - Used in more severe advanced heart failure or short term for decompensated heart failure
42
MOA and adverse effects of Dobutamine & Dopamine
- MOA: stimulate beta1 receptors on the myocardium which increases contractility - Adverse effects: Hypotension and arrhythmias
43
Describe Dobutamine & Dopamine
- IV infusion medication - Used in more severe advanced heart failure or short term for decompensated heart failure
44
List ACE inhibitors and ARBs drugs
- ACE inhibitors: Lisinopril, Enalapril, Ramipril - ARBs: Losartan, Valsartan
45
MOA and adverse effects of ACE inhibitors and ARBs
- MOA: block production or activity of angiotensin II which also reduces production of aldosterone - Adverse effects: ACE inhibitors = cough; hypotension, acute kidney injury
46
List beta blockers
- Metoprolol succinate - Carvedilol - Bisoprolol
47
MOA and adverse effects of beta blockers
- MOA: attenuate excessive sympathetic activity contributing to the vicious cycle - Adverse effects: bradycardia and hypotension
48
List loop diuretics
- Furosemide - Bumetanide - Torsemide
49
MOA and adverse effects of loop diuretics
- MOA: increase excretion of sodium & water = reduces preload - Adverse effects: volume depletion and electrolyte imbalances = hyponatremia, hypokalemia
50
List vasodilators
- Hydralazine - Nitrates
51
MOA and adverse effects of vasodilators
- MOA: reduce peripheral vascular resistance to decrease amount of blood returning to the heart (preload) and pressure the heart must pump against (afterload) - Adverse effects: headache, dizziness, hypotension, orthostatic hypotension, reflex tachycardia
52
Key points for PT related to congestive heart failure (CHF)
- Exercise programs for these patients result in improved exertion tolerance, endurance, & improved quality of life - Must remain alert for signs of acute HF: cough, difficulty breathing, abnormal respiratory sounds - Watch for signs of adverse drug events especially orthostatic hypotension
53
Background of coagulation disorders & hyperlipidemia
- Hemostasis: balance between too much and too little blood coagulation - Restoration of hemostasis involves pharmacologic methods: excessive clotting = anti platelets, anticoagulants, fibrinolytics; inadequate clotting = replacing missing clotting factors
54
Describe anticoagulants
- Control the function & synthesis of certain clotting factors - Prevent clot formation in the venous system - 4 classes: heparin, warfarin, direct thrombin inhibitors, factor Xa inhibitors
55
List heparin agents
- Unfractionated heparin - Low molecular weight heparin (enoxaparin)
56
MOA and adverse effects of heparin agents
- MOA: potentiates the activity of antithrombin - binds to several clotting factors & renders them inactive - Adverse effects: heparin induced thrombocytopenia (HIT)
57
MOA and how to monitor warfarin
- MOA: interferes with Vit. K metabolism in the liver & impairs the synthesis of several clotting factors - Monitoring: periodic INR checks
58
List direct thrombin inhibitors and their MOA
- Dabugatran (Oral); Bivalirudiin, Argatroban (IV) - MOA: bind directly to the active site on thrombin & inhibit its ability to convert fibrinogen to fibrin
59
List factor Xa inhibitors and their MOA
- Fondaparinux (SQ); Rivaroxaban, Apixaban (PO) - MOA: inhibit factor Xa which is the combination of the intrinsic & extrinsic pathways
60
Describe antiplatelets
- Inhibit abnormal platelet activity & prevent aggregation in arteries - Help reduce incidence of myocardial infarction & ischemic stroke
61
MOA and adverse effects of aspirin
- MOA: suppresses platelet aggregation by inhibiting the synthesis of prostaglandins & thromboxane - Adverse effects: GI irritation, liver and kidney toxicity
62
Uses for aspirin
- Limits progression of platelet induced occlusion thereby reducing the extent of damage to the myocardium in an acute MI - Stroke - After certain interventions: grafts, valve replacements
63
List ADP receptor blockers
- Clopidogrel - Prasugrel - Ticagrelor
64
MOA and uses of ADP receptor blockers
- MOA: inhibit ADP on the platelet membrane which decreases platelet activity - Uses: myocardial infarction (MI), ischemic stroke
65
Describe fibriinolytics
- Facilitate destruction of blood clots - Used to reestablish blood flow through vessels that have been occluded by thrombi: MI, ischemic stroke, and DVT/PE - IIV médications used in emergency situations
66
List fiibrinolytics
- Alteplase - Tenecteplase - Reteplase
67
Adverse effects of antithrombotics
- Bleeding
68
Describe hemophilia
- Hereditary disease - Unable to synthesize a specific clotting factor - Tx: replace clotting factor either prophylactically or during acute events ($$$)
69
Describe vitamin K deficiency
- Insufficient ingestion or inadequate absorption - Tx: administer exogenous vitamin K
70
Describe hyperlipidemia
- Chronic & excessive increase in plasma lipids - Deposited on arterial walls forming plaque like lesions which can occlude the artery - Rupture of these lesions leads to thrombosis & infarction
71
List HMG-CoA reductase inhibitors (Statins)
- Atorvastatin, Rosuvastatin - Simvastatin, Lovastatin, Prevastatin
72
MOA and adverse effects of HMG-CoA reductase inhibitors (Statins)
- MOA: inhibit HMG-CoA reductase which catalyzes one of the early steps in cholesterol synthesis; decrease LDL & triglycerides; increases HDL - Adverse effects: myalgias
73
List fabric acids (Fibrates)
- Fenofibrate - Gemfibrozil
74
MOA and adverse effects of fabric acids (Fibrates)
- MOA: binds to a receptor to affect the transcription of genes that affect lipid metabolism; primarily decreases triglycerides - Adverse effects: Rhabdomolysis = particularly in combination with other agents
75
Describe bile acid sequestrants
- Cholestyramine, colesevelam, colestipol - Bind to bile acids within the GI tract & increase fecal excretion which accelerates cholesterol breakdown
76
Describe Niacin
- Decreases LDL and triglycerides; increases HDL - Adverse effects: flushing
77
Describe Ezetimibe
- Inhibits cholesterol absorption in the GI tract - Primarily decreases LDL
78
Key points for PTs related to coagulation disorders & hyperlipidemia
- Any procedure or technique which may induce bleeding should be done cautiously for patients on antithrombotics - Intrajoint hemorrhage is common with hemophilia & rehab of the affected joints is necessary - PTs can help design & implement exercise programs for weight loss to assist with hyperlipidemia therapy

Pharmacology (12 decks)

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