Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pharmacology > Cardiac Medications > Flashcards

Cardiac Medications Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pharmacologic treatments for angina pectoris

A
  • Nitrates
  • Bete blockers
  • Calcium channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

List organic nitrate drugs

A
  • Nitroglycerin
  • Isosorbide dinitrate
  • Isosorbide mononitrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe isosorbide mononitrate

A
  • Primarily used as preventive medication
  • Similar to Isosorbide dinitrate but longer acting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Adverse effects of organic nitrate drugs

A
  • Headache
  • Dizziness
  • Orthostatic hypotension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe variant angina

A
  • Coronary vasospasm causes a decrease in myocardial O2 supply
  • Tx: calcium channel blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Normal cardiac rhythm/electrical conduction pathway

A
  • Sinoatrial node (SA)
  • Atrioventricular node (AV)
  • Bundle of His
  • Left/Right bundle branches
  • Purkinje Fibers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

List class I sodium channel blockers

A
  • Class IA: Quinidine, Procainamide
  • Class IB: Lidocaine, Mexilatine
  • Class IC: Flecainide, Propafenone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

List class II beta blocker drugs

A
  • Atenolol
  • Esmolol
  • Metoprolol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

MOA and adverse effects of class II beta blockers

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

List class III K+ channel blockers

A
  • Amiodarone
  • Dofetilide
  • Dronedarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

MOA and adverse effects of class III K+ channel blockers

A
  • MOA: prolong the effective refractory period; slows & stabilizes the HR
  • Adverse effects: torsades de pointes (pro-arrhythmic); amiodarone = pulmonary, thyroid, liver toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List class IV calcium channel blockers

A
  • Verapamil
  • Diltiazem
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA and adverse effects of CLass IV calcium channel blockers

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Non-pharmacologic treatment of arrhythmias

A
  • Drugs do not resolve cause of arrhythmia
  • Implantable devices: pacemakers, defibrillators
  • Interventions: ablations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Key points for PT for arrhythmias

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Background of congestive heart failure (CHF)

A
  • 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
Q

Pathophysiology of congestive heart failure (CHF)

A
  • Cardiac lesion -> decreased cardiac performance -> neurohumeral compensation -> increased cardiac workload -> myocardial cell changes -> decreased cardiac performance
  • Vicious cycle
34
Q

Systolic dysfunction of CHF

A
  • Cardiac output is reduced
  • Neurohumeral compensation activates further worsening dysfunction
  • Increased preload & after load due to vasoconstriction & sodium & water retention
  • Cardiac remodeling
35
Q

Diastolic dysfunction of CHF

A
  • 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
Q

Signs and symptoms of CHF

A
  • Pulmonary edema
  • Pleural effusion
  • Distended neck veins
  • Enlarged liver & spleen
  • Ankle edema
37
Q

Difference between left and right sided heart failure

A
  • Left: volume backs up in the lungs
  • Right: volume backs up in peripheral tissues
38
Q

Pharmacotherapy for CHF

A
  • 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
Q

MOA and adverse effects of Digoxin

A
  • 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
Q

MOA and adverse effects of phosphodiesterase inhibitors: Milrinone

A
  • 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
Q

Describe Milrinone

A
  • IV infusion medication
  • Used in more severe advanced heart failure or short term for decompensated heart failure
42
Q

MOA and adverse effects of Dobutamine & Dopamine

A
  • MOA: stimulate beta1 receptors on the myocardium which increases contractility
  • Adverse effects: Hypotension and arrhythmias
43
Q

Describe Dobutamine & Dopamine

A
  • IV infusion medication
  • Used in more severe advanced heart failure or short term for decompensated heart failure
44
Q

List ACE inhibitors and ARBs drugs

A
  • ACE inhibitors: Lisinopril, Enalapril, Ramipril
  • ARBs: Losartan, Valsartan
45
Q

MOA and adverse effects of ACE inhibitors and ARBs

A
  • MOA: block production or activity of angiotensin II which also reduces production of aldosterone
  • Adverse effects: ACE inhibitors = cough; hypotension, acute kidney injury
46
Q

List beta blockers

A
  • Metoprolol succinate
  • Carvedilol
  • Bisoprolol
47
Q

MOA and adverse effects of beta blockers

A
  • MOA: attenuate excessive sympathetic activity contributing to the vicious cycle
  • Adverse effects: bradycardia and hypotension
48
Q

List loop diuretics

A
  • Furosemide
  • Bumetanide
  • Torsemide
49
Q

MOA and adverse effects of loop diuretics

A
  • MOA: increase excretion of sodium & water = reduces preload
  • Adverse effects: volume depletion and electrolyte imbalances = hyponatremia, hypokalemia
50
Q

List vasodilators

A
  • Hydralazine
  • Nitrates
51
Q

MOA and adverse effects of vasodilators

A
  • 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
Q

Key points for PT related to congestive heart failure (CHF)

A
  • 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
Q

Background of coagulation disorders & hyperlipidemia

A
  • 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
Q

Describe anticoagulants

A
  • 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
Q

List heparin agents

A
  • Unfractionated heparin
  • Low molecular weight heparin (enoxaparin)
56
Q

MOA and adverse effects of heparin agents

A
  • MOA: potentiates the activity of antithrombin - binds to several clotting factors & renders them inactive
  • Adverse effects: heparin induced thrombocytopenia (HIT)
57
Q

MOA and how to monitor warfarin

A
  • MOA: interferes with Vit. K metabolism in the liver & impairs the synthesis of several clotting factors
  • Monitoring: periodic INR checks
58
Q

List direct thrombin inhibitors and their MOA

A
  • Dabugatran (Oral); Bivalirudiin, Argatroban (IV)
  • MOA: bind directly to the active site on thrombin & inhibit its ability to convert fibrinogen to fibrin
59
Q

List factor Xa inhibitors and their MOA

A
  • Fondaparinux (SQ); Rivaroxaban, Apixaban (PO)
  • MOA: inhibit factor Xa which is the combination of the intrinsic & extrinsic pathways
60
Q

Describe antiplatelets

A
  • Inhibit abnormal platelet activity & prevent aggregation in arteries
  • Help reduce incidence of myocardial infarction & ischemic stroke
61
Q

MOA and adverse effects of aspirin

A
  • MOA: suppresses platelet aggregation by inhibiting the synthesis of prostaglandins & thromboxane
  • Adverse effects: GI irritation, liver and kidney toxicity
62
Q

Uses for aspirin

A
  • 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
Q

List ADP receptor blockers

A
  • Clopidogrel
  • Prasugrel
  • Ticagrelor
64
Q

MOA and uses of ADP receptor blockers

A
  • MOA: inhibit ADP on the platelet membrane which decreases platelet activity
  • Uses: myocardial infarction (MI), ischemic stroke
65
Q

Describe fibriinolytics

A
  • 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
Q

List fiibrinolytics

A
  • Alteplase
  • Tenecteplase
  • Reteplase
67
Q

Adverse effects of antithrombotics

68
Q

Describe hemophilia

A
  • Hereditary disease
  • Unable to synthesize a specific clotting factor
  • Tx: replace clotting factor either prophylactically or during acute events ($$$)
69
Q

Describe vitamin K deficiency

A
  • Insufficient ingestion or inadequate absorption
  • Tx: administer exogenous vitamin K
70
Q

Describe hyperlipidemia

A
  • 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
Q

List HMG-CoA reductase inhibitors (Statins)

A
  • Atorvastatin, Rosuvastatin
  • Simvastatin, Lovastatin, Prevastatin
72
Q

MOA and adverse effects of HMG-CoA reductase inhibitors (Statins)

A
  • MOA: inhibit HMG-CoA reductase which catalyzes one of the early steps in cholesterol synthesis; decrease LDL & triglycerides; increases HDL
  • Adverse effects: myalgias
73
Q

List fabric acids (Fibrates)

A
  • Fenofibrate
  • Gemfibrozil
74
Q

MOA and adverse effects of fabric acids (Fibrates)

A
  • 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
Q

Describe bile acid sequestrants

A
  • Cholestyramine, colesevelam, colestipol
  • Bind to bile acids within the GI tract & increase fecal excretion which accelerates cholesterol breakdown
76
Q

Describe Niacin

A
  • Decreases LDL and triglycerides; increases HDL
  • Adverse effects: flushing
77
Q

Describe Ezetimibe

A
  • Inhibits cholesterol absorption in the GI tract
  • Primarily decreases LDL
78
Q

Key points for PTs related to coagulation disorders & hyperlipidemia

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions