Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharmacology > CV Pharmacology 2 > Flashcards

CV Pharmacology 2 Flashcards

1
Q

Arrhythmia

A

Heart condition with disturbances in

  • Pacemaker impulse formation
  • Contraction impulse conduction
  • Combo of those 2

-Insufficient rate/timing of heart contraction to maintain normal CO

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

Ventricular Arrythmia

A

Most common cause of sudden death

-Meds that decrease incidence of VA, don’t decrease risk of sudden death

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

Electrophysiology-Resting Potential

A

Interior is more negative compared to outside

Na and Ca are higher outside the cell, K+ is higher inside the cell

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

Cardiac Action Potential Phases

A
  • Phase 4: Resting phase, diastole
  • Phase 0: Opening of Na+ channels/rapid depolarization
  • Phase 1: Initial rapid depolarization, close of fast Na channels. R and S waves
  • Phase 2: Plateau: balance between inward Ca and outward K. ST segment
  • Phase 3: repolarization. T wave
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mechanisms of Cardiac Arrhythmias

A

Disorders of impulse formation/conduction

-Causes include: ischemia, excess discharge to transmitters, toxic substance exposure (includes drugs), unknown

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Disorder of Impulse formation

A
  • No signal from pacemaker site
  • ectopic pacemaker
  • Oscillatory after-depolarizations: spontaneous activity in non-pacemaker tissues, can be due to drugs used to treat other cardio pathologies

Can result in Bradycardia (AV Block), Tachycardia (reentrant circuit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Types of Arrhythmias (locations)

A

Sinus, Supraventricular, AV Junctions, Conduction, Ventricular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Anti-arrhythmic Drugs

A

These drugs can cause arrhythmias.

  • Sodium Channel Block
  • Beta-adrenergic receptor block
  • prolong repolarization
  • Calcium channel block
  • Adenosine and Digitalis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Classification of Anti-arrhythmics

A

Based on MOA

  • Class 1: Blocks fast Sodium Channels
  • -Subclass 1a: Quinidine
  • -Subclass 1b: Lidocaine, Phenytoin
  • -Subclass 1c: Flecainide, propefenone
  • Class 2: B-adrenergic blockers: Propanalol, the other “-lols”
  • Class 3: K+ Channel Blockers: developed because people died from Na channel blockers; Amiodarone, Ibultide, Bretylium
  • Class 4: Calcium Channel Blockers: Verapamil; S/E: excessive bradycardia, peripheral vasodilation-> dizzy, headache
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pacemakers

A

Surgical implantation of electrical leads to a pulse generator. Generator can sense electrical activity generated by heart and delivers impulses when needed. Only speeds up heart for bradycardia, can’t do anything for tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Rehab considerations for anti-arrythmics

A

S/E of agents: change in nature of arrhythmias/increased potential for them,

Monitor ECG, Presence of faintness/dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CHF

A
  • Heart cannot provide adequate perfusion of peripheral organs to meet metabolic requirement.
  • Fluid accumulates in peripheral tissues since heart can’t maintain proper circulation.
  • Peripheral edema, decreased tolerance for physical activity, dyspnea/SOB

Classification: 1= asymptomatic, 2= mild, 3= moderate, 4= severe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Factors contributing to CHF

A

Ischemic heart disease, CAD (less blood flow to heart), MI, Hypertension, Diabetes, Lung Disease, Cardiomyopathies (Dilated, Hypertrophic), Abnormal heart valves, congenital heart defects, severe anemia, hyperthyroidism, cardiac arrhythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of Heart Failure

A

Left Ventricular: Most common, systolic: can’t contract, diastolic: can’t relax

Right Ventricular: Occurs after LV failure, less blood received causes damage, less pumping by right, venous pooling in legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Onset of Disease for CHF

A

Chronic: can take years

Endogenous Compensatory Mechanisms: size enlargement, increase muscle mass, increased heart rate, narrow blood vessels/increase BP, blood flow diversion, increase SNS output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

CHF Symptoms

A

SOB: blood pooling in pulmonary veins, fluid in lungs, occurs during rest, activity, sleep.

Persistent cough/wheeze

Edema

Tiredness/fatigue (lack of O2)

Lack of appetite/nausea

Confusion/impaired thinking

increased heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Therapeutic Overview for CHF

A

Problems include:

  • reduced contractionf roce
  • decreased CO
  • Increased TPR
  • inadequate organ perfusion
  • edema
  • decreased exercise tolerance
  • ischemic heart disease
  • sudden death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Drug Therapies for CHF

A

Chronic:
-ACE inhibitors, Beta Blockers, ATII antagonists, aldosterone antagonists, digoxin, diuretics

Acute:
-Diuretics, PDE inhibitors, Vasodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Cardiac Glycosides: MOA, Electrophysiology, Overall Effect, Therapeutic Uses, PK

A

From Plants

  • increase force of myocardial contraction, has toxic S/Es
  • Digoxin most common

MOA: Inhibits Na-K Pump

Electrophysio effects: Spontaneous Depolarization of atrial cells

Overall Effect: Increase CO, increase efficiency, decrease HR, decrease cardiac size

Therapeutic Uses: oral inotropic agent, doesn’t stop disease progression

PK: long 1/2 life, metabolized in liver, excreted in kidneys

20
Q

Cardiac Glycosides Side effects

A

Low therapeutic index, effects caused by Na-K pump inhibition.

CNS: Malaise, confusion, depression, vertigo

GI: anorexia, nausea, cramping, diarrhea

Cardia: bradycardia. arrhythmias

Hypercalcemia= increase toxicity

K+: Hypokalemia: increase toxicity, Contraindicated for patients using K+ depleting diuretics

Vision: Yellow Tinted vision

21
Q

PDE Inhibitors MOA, Therapeutic Use

A

used for management of acute heart failure

+ inotropy, increase rate of myocardial relaxation, decrease TPR and afterload

MOA: increased cardiac contraction, relaxes vascular smooth muscle

Therapeutic Uses: Amrinone/Milrinone: doesn’t stop disease progression/prolong life, prescribed when other therapies don’t work

22
Q

PDE Inhibitors Side Effects

A

Sudden death secondary to ventricular arrhythmias

Hypotension, thrombocytopenia

23
Q

Beta Blockers MOA, Therapeutic Use

A

Standard therapy for CHF, cheap, reduce sudden death caused by other drugs

Propranolol, Carvedilol

MOA: unclear, prevents development of arrhythmias

Therapeutic Use: Oral, given with other therapies (ACE, digoxin), effective for Class 2/3

24
Q

Beta Blockers Side Effects

A

Cardiac decomp, bradycardia, hypoglycemia, cold extremities, fluid retention, fatigue

25
Q

Direct acting sympathomimetics (Dopamine,dobutamine, Nor/Epi) MOA, therapeutic Uses

A

causes immediate increase in inotropy, used for acute CHF, goal to increase CO w/o affecting TPR

MOA:

  • Nor/Epi: increase CO/TPR
  • Dopamine: vasodilation (dopamine receptors) and increase CO (beta receptors)
  • Dobutamine: peripheral vasodilation

Therapeutic Uses
Given IV
-Dopamine: used in cardiogenic, traumatic,hypovolemic shock
-Dobutamine: used for patients with low CO, don’t use in hypotensive patients

26
Q

Direct acting sympathomimetics Side Effects

A

Restlessness, tremor, headache, cerebral hemorrhage, cardiac arrhythmias, caution in patients with beta blockers, can develop dobutamine tolerance

27
Q

ACE Inhibitors/AT1 receptor antag. Drug names, Therapeutic Uses

A

Goal: reduce afterload/preload, reduce workload

Positive cardiac inotropy, used for chronic CHF

ACE: Captopril, Enalopril

AT1: Losartan, Valsartan

Therapeutic Uses: drug of choice in heart failure, increase survival in long-term CHF
-ACE: slow progression Left Vent. Dyfunction

-AT1 antag: More effective than ACE, used in conjunction with ACE for increased effectiveness

28
Q

ACE/AT1 Side Effects

A

ACE: Cough, angioneurotic edema, hypotension, hyperkalemia

Both ACE and AT1 are teratogenic

29
Q

Vasodilators

A

Reduce TPR without large decrease in BP
Reduce Preload/afterload, relieve symptoms, increase exercise tolerance

Drugs:
-Nitroglycerin: acute iscemia/heart fialure, orally active, quick onset for relief

  • Isosorbide dintrate/hydralizine: chronic admin for long-term relief, IV
  • Nesiritide/Natrecor: recomb brain-natriuretic peptide (BNP), vasodilator, inhibit remodeling, suppresses aldosterone secretion. Adverse effects= hypotension, renal failure
30
Q

Diuretics

A

Used in CHF to reduce ECF Volume, used for acute CHF with volume overload

Goal= reduce preload/afterload

OD= excessive reduction in preload/overreduction in stroke volume

Thiazide/loop diuretics (furesomide) used as adjunct therapies

31
Q

Aldosterone Antagonists

A

Aldosterone promotes: Sodium retention, Magnesium and Potassium loss, increase SNS, decrease PSNS, myocardial fibrosis

32
Q

Aldosterone Antagonists Side effects

A

Hyperkalemia, agranulocytosis, anaphylaxis, hepatotoxicity, renal failure

Spironolactone (alactone)= gynecomastia, sexual dysfunction

Eplerenone (inspra)= arrhythmia, MI

33
Q

Rehab Considerations for CHF drugs

A

Be alert to signs of CHF like dyspnea, rales, cough,

Digitalis toxicity signs- dizziness, confusion, nausea, arrhythmias

Patients on diuretics sometimes exhibit fatigue/weakness due to fluid/electrolyte depletion

Vasodilators: hypotension, postural hypotension

34
Q

Coagulation/Circulatory Disorders

A

Drugs are used to maintain/preserve/restore circulation

Anti-coagulants: prevent clot formation that inhibit circulation

Anti-platelets: prevent platelet aggregation

Thrombolytics: Clot busters

Antilipemics: decrease lipid concentration

Peripheral Vasodilators: promote dilation of vessels

35
Q

Anticoagulants

A

Inhibit clot formation, prevent new blots

Venous: DVT and Pulmonary Embolism

Arterial: Coronary Thrombosis (MI), Artificial Heart Valves, CVA

36
Q

Heparin

A

Natural substance in liver that prevents clot formation

Primary use is to prevent venous thrombosis that can lead to pulm embolism/stroke.

Poor absorption through GI, Given SQ/IV

Prolongs Clotting time: partial thromboplastin time, and activated partial thromboplastin time.

Used for DVT, PE, CVA, heart valved prosthesis, DV surgery, post op, hemodialysis.

Low dose: prophylaxis

Full dose: treat thromboembolism, promote neutralization of activated clotting factors= prevention of emboli formation

37
Q

Heparin Side Effects

A

Decreased Platelet Count= Thrombocytopenia

Hemorrhage

Drug Interactions: Increased effect with ASA, NSAIDs, thrombolytics; decreased effect with NTG

38
Q

Low Molecular Weight Heparin (LMWH)

A

prevent venous thromboembolism

Enoxaprin/Lovenox and Dalteparin Sodium (Fragmin)
-more stable, lower risk of bleeding

Use: prevent DVT after hip/knee replacement surgery, abd. surgery

Can be given at home, SW, BID

Given in abdomen

RX is 7 to 14 days

Dont take antiplatelet drugs during therapy

39
Q

Warfarin/Coumadin

A

Inhibits activity of vitamin K required for activation of clotting factors.

Use: prophylactically to precent venous thrombosis, A. Fib, PE, coronary occlusion, thrombophlebitis.

Prolongs clotting time, and monitored by Prothrombin time and INR

INR is 1.3-2.0, therapeutic levels on coumadin = 2-3

INR replaces prothrombin time, INR is more accurate.

well absorbed through GI tract, food decreases absorption.

Long 1/2 life, watch for petetchiae, ecchymosis, tarry stool. hematemesis.

Vit. K= antagonist for Warfarin.

40
Q

Dabigatran

A

Prophylaxis and treatment of venous thromboembolism and PE

No specific antidote: use activated prothrombin complex concentrate, activated charcoal

41
Q

Rivaroxaban

A

Stroke prevention in patients with non-valvular atrial fib.

Acute treatment of DVT/PE, secondary prevention of DVT/PE

NO specific antidote, Prothrombin complex concentrate

42
Q

Apixaban

A

Prophylaxis in patients with non-valvular atrial fib, CVA, Embolism
Treatment/prophylaxis for recurrent DVT and PE
Prophylaxis for post-op DVT for total hip replacement

No specific antidote: use Prothrombin complex concentrate, activated charcoal

43
Q

Edoxaban

A

Prophylaxis for nonvalvular atrial fib, CVA, embolism, Treats DVT and PE

44
Q

Anti-platelet Drugs

A

Aspirin, Dipyridamole, Ticlopidine, Abciximab, Tirofiban

Prevents thrombosis in arteries by suppressing platelet aggregation.

Prevention of MI/Stroke for clients with family history
Prevention of repeat stroke, stroke in clients having TIAs

45
Q

Thrombolytics

A

Thromboembolism: occlusion of an artery or vein caused by thrombus or embolus; results in ischemia that causes necrosis of the tissue distal to obstructed area

Thrombolytics promote fibrinolytic mechanism (plasminogen into plasmin and destroy fibrin in clot)

Use for acute MI; w/in 4 hours to dissolve clot/unblock artery
Also pulmonary embolism, DVT, Non-coronary occlusion

Streptokinase, urokinase, tissue plasminogen activator, anisoylated plasminogen streptokinase activator complex

46
Q

Thrombolytics Side effects/misc

A

Hemorrhage, allergic rxns, vascular collapse

Onset/peak rapid, duration 12 hours

tPa most expensive

Aminocaproic acid used to stop bleeding by inhibiting plasminogen activation

Pharmacology (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions