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NURS 3560 > Week 3: Cardiac Function > Flashcards

Week 3: Cardiac Function Flashcards

1
Q

What are the properties of cardiac cells?

A 
CACE
Contractibility
Automaticity
Conductivity
Excitability
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2
Q

What does the ANS control in the heart?

A

Rate of impulse formation
Speed of conduction
Strength of contraction

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3
Q

What does the parasympathetic nervous system vagus nerve control in the CVS?

A

Decrease rate, slows impulse conduction, decrease force contraction.

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4
Q

What does the sympathetic nervous system control in the CVS?

A

Increase rate, increase force of contraction.

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5
Q

How are dysrhythmias evaluated?

A

Holter monitoring, event recorder monitoring, exercise treadmill testing, signal-averaged ECG, electrophysiological study.

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6
Q

What is sinus bradycardia?

A

Slow heart rate. Less than 60 BPM.

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7
Q

What diseases cause sinus brady?

A

Hypothyroidism, increased ICP, obstructive jaundice, inferior wall MI.

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8
Q

What causes sinus brady occur as a response to?

A

Carotid sinus massage, valsalva manoeuvre, hypothermia, increased intraocular pressure, increased vagal tone, administration of parasympathomimetic drugs.

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9
Q

How is sinus brady treated?

A

Atropine, pacemaker.

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10
Q

What is sinus tach?

A

Increased HR. Over 100 bpm.

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11
Q

what is sinus tach r/t?

A
  • exercise
  • fever, pain
  • hypotension
  • anemia
  • hypoxia
  • hypoglycemia
  • MI
  • HF
  • hyperthyroidism
  • anxiety
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12
Q

How is sinus tach treated?

A

Treat cause. BBs to reduce HR and heart O2 consumption.

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13
Q

What is premature atrial contraction?

A

Contraction originating from ectopic focus in atrium that is not the SA node. DISTORTED P WAVES. Can be stopped, delayed or conducted normally at the AV node.

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14
Q

What is premature atrial contraction caused by?

A

emotional stress, physical fatigue, use of caffeine, tobacco, alcohol, hypoxia, electrolyte imbalances, hyperthyroidism, COPD, CAD.

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15
Q

How are premature atrial contraction’s treated?

A

Dependent on symptoms, BBs. Reduce caffeine intake.

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16
Q

What is paroxysmal supraventricular tachycardia?

A
  • Originates in ectopic focus above bundle of His.
  • Run of premature beats.
  • Paroxysmal means abrupt onset and termination.
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17
Q

What are the clinical associations with PSVT?

A
  • Normal Heart: overexertion, deep inspiration, emotional stress, stimulants.
  • Digitalis toxicity
  • Rheumatic heart disease
  • CAD
  • Cor Pulmonale
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18
Q

What is the clinical significance of PSVT?

A

Prolonged tachycardia
Hypotension
Dyspnea
Angina

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19
Q

How is PSVT treated?

A

Vagal manoeuvres
IV adenosine
DC cardioversion if meds and vagal moves don’t work.

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20
Q

What is adenosine?

A

Decreases automaticity in SA node, slows conduction through the AV node, prolongs PR interval. Used for PSVT

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21
Q

What are the AE of adenosine?

A 
Sinus brady
Dsypnea
Hypotension
Facial flushing
Chest discomfort
LOW and SLOW
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22
Q

What is atrial flutter?

A
  • Sawtooth shaped flutter waves.

- Originates from single ectopic focus.

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23
Q

What are the clinical associations with atrial flutter?

A

CAD, Hypertension, mitral valve disorders, PE, lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism, cardiac drugs.

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24
Q

What is the clinical significance of atrial flutter?

A

Decrease CO and precipitate HF and angina, risk for stroke b/c of thrombus formation in atria.

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25
Q

What is the treatment for atrial flutter?

A

CCBs, BBs, cardioversion, antidysrythmic drugs, radio catheter ablation.

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26
Q

What do beta blockers do to the heart?

A

Decrease automaticity of SA node, decrease velocity of conduction through AV node, decreased myocardial contractility.

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27
Q

What are the therapeutic indications for BBs?

A

Dysrhythmias, supraventricular tachydysrythmias, suppression of excessive discharge, slowing V rate.

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28
Q

What are the AE of BBs?

A

Heart block, HF, AV block, sinus arrest, hypotension, bronchospasm.

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29
Q

What is quinidine’s effects on the heart and ECG?

A
  • Blocks Na channels
  • Slows impulse conduction
  • Delays repolarization
  • Blocks vagal input to the heart.
  • Widens QRS complex
  • Prolongs QT interval
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30
Q

What are the therapeutic uses for quinidine?

A

Used for supraventricular and ventricular dysrythmias.

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31
Q

What are the AE of quinidine?

A

Diarrhea, cinchonism, cardiotoxicity, atrial embolism, alpha-adrenergic blockade, hypersensitivity reactions.

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32
Q

What is atrial fibrillation?

A

Disorganization of atrial electrical activity due to multiple ectopic foci, resulting in loss of effective atrial contraction. Most common dysrhythmias.

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33
Q

What are clinical associations with a-fib?

A
  • Rheumatic heart disease
  • CAD
  • Cardiomyopathy
  • Hypertension
  • Throtoxicosis
  • Alcohol intoxication
  • Caffeine use
  • Electrolyte disturbances
  • Stress
  • Cardiac surgery
  • HF
  • Pericarditis
34
Q

What is the clinical significance of a-fib?

A

Decreases CO, may cause thrombi, embolus may develop and cause stroke.

35
Q

What is the treatment for a-fib?

A
  • Decrease V rate and prevent embolic events.
  • Drugs: CCBs, BBs, anticoagulant therapy.
  • Cardioversion.
36
Q

What are junctional dysrythmias?

A

Dysrhythmias that start in the AV node. SA node fails or has been blocked at the AV node.

37
Q

What are the clinical associations for junctional rhythms?

A

CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, rheumatic heart disease, digoxin, amphetamines, caffeine, nicotine.

38
Q

What is the treatment for junctional dysrythmias?

A

Atropine, hold digoxin if caused by digoxin, BBs, CCBs, amiodarone for rate control for junctional tachycardia.

39
Q

What is digoxin?

A

Drug used for HF and SVTs. Shorten’s QT interval. AE: Cardiotoxicity. Increases risk of hypokalemia.

40
Q

What is a first-degree AV block?

A

Every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged.

41
Q

What are the clinical associations of a first degree AV-block?

A

MI, CAD, rheumatic fever, hyperthyroidism, vagal simulation, digoxin, BBs, CCBs, flecainide.

42
Q

How are first degree AV blocks treated?

A

Check meds, monitor.

43
Q

What is a second degree AV block type 1?

A

Lengthening of PR interval due to prolonged AV conduction.

44
Q

What are the clinical associations with 2nd degree AV block type 1?

A

Associated with digoxin and BBs and sometimes CAD.

45
Q

What is the clinical significance of 2nd degree AV blocks type 1?

A

Result of myocardial ischemia/ infarction. Transiant and well tolerated.

46
Q

What is the treatment for 2nd degree AV Block Type 1?

A

Symptomatic- atropine, temp pacemaker.

Asymptomatic- monitor w/ transcutaneous pacemaker on standby.

47
Q

What is a second degree AV block type 2?

A

P wave not conducted w/o antecendent PR lengthening. Occurs when a block in one bundle branch is present.

48
Q

What are the clinical associations for a second degree AV block Type 2?

A

Rheumatic heart disease
CAD
Anterior MI
Digitalis toxicity

49
Q

What is a third degree AV heart block?

A

Form of AV dissociation where no impulses from the atria are conducted to the ventricles. The atria contracts independently from the ventricles. Ventricle rhythm is an escape rhythm.

50
Q

What are the clinical associations for a 3rd degree heart block?

A

Severe heart disease, systemic diseases, digoxin, BBs, CCBs.

51
Q

What are premature ventricular contractions?

A

Premature contraction in the ventricles, causes wide distorted QRS complex.

52
Q

what are clinical associations with PVCs?

A

Stimulants, electrolyte imbalances, hypoxia, fever, MI, mitral valve prolapse, HF, CAD.

53
Q

What is the clinical significance of PVCs?

A

Usually benign in normal heart, PVCs may decrease CO and cause angina and HF.

54
Q

What is the treatment for PVCs?

A

O2 therapy for hypoxia, electrolyte replacement, treatment according to cause.

55
Q

What is ventricular tachycardia?

A

Run of 3 or more PVCs.

56
Q

What are the clinical associations of V-tach?

A

MI, CAD, electrolyte imbalance, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity, CNS disorders, fibrillation.

57
Q

What does sustained VT cause?

A

Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest.

58
Q

How are monomorphic VTs treated?

A

hemodynamically stable: IV amiodarone

hemodynamically unstable: IV amiodarone and cardioversion.

59
Q

What is accelerated idioventricular rhythm?

A

Happens when the intrinsic pacemaker rate becomes less than the ventricular ectopic pacemaker.

60
Q

What are the clinical associations of AIVR?

A

Acute MI, reperfusion of myocardium after thrombolytic therapy or angioplasty.

61
Q

How is AIVR treated?

A

Temp pacing may be required. Don’t use drugs.

62
Q

What does lidocaine do to the heart?

A

Blocks Na channels, slows conduction in the atria, ventricles, and His-Purkinje system, reduces automaticity in the ventricles and His-Purkinje system.

63
Q

What are the adverse effects of lidocaine?

A

Drowsiness, confusion, paresthesias

64
Q

What is ventricular fibrillation?

A

Severe fuckery of the heart rhythm. No contraction really. Heart goes bingo bongo.

65
Q

What are the clinical associations of V-Fib?

A

Acute MI, CAD, cardiomyopathy, accidental electric shock, hyperkalemia, hypoxia, acidosis, drug toxicity.

66
Q

What is the treatment of V Fib?

A

CPR, resucitation.

67
Q

What is pulseless electrical activity?

A

Electrical activity evident on ECG, no mechanical activity evident. Pt is pulseless.

68
Q

What is defibrillation?

A

Restart heart button. Shocks heart to make the SA node do its job.

69
Q

What is synchronized cardioversion?

A

Used for hemodynamically unstable ventricular/ supraventricular tachydysrythmias. Delievers shock on R wave of QRS complex.

70
Q

What are implantable cardioverter-defibrillator used for?

A

For people who have survived SCD, have spontaneous sustained VT, have syncope w/ inducible ventricular tachycardia, peeps who are at high risk for life-threatening dysrhythmias.

71
Q

What are pacemakers used for?

A

Used to pace heart when the normal conduction. For anditbradycardia pacing and overdrive pacing and tachycardias.

72
Q

What is radiofrequency catheter ablation therapy?

A

Electrode-tipped ablation catheter ‘burns’ accessory pathways or ectopic sites in the atria, AV node and ventricles.

73
Q

What is radiofrequency catheter ablation therapy used for?

A

AV nodal reentrant tachycardia, reentrant tachy r/t accessor bypass tracts, control of ventricular response of certain tachydysrythmias.

74
Q

What ECG changes are associated with acute coronary syndrome?

A
  • Ischemia
  • ST segment depression/ T wave inversion
  • ST segment depression significant
75
Q

What is a STEMI?

A

MI w/ ST elevation. Causes ischemia and necrosis.

76
Q

How is a STEMI managed?

A

O2, aspirin, morphine, betablockers, nitroglycerin, reperfusion therapy.

77
Q

What drugs are used for MI?

A
  • Fondaparinux (selective factor Xa inhibitor)
  • Bivalirudin (direct thrombin inhibitor)
  • Antiplatelet drugs
  • Thrombolytic drugs
78
Q

What is PCI?

A

Uses angioplasty rather than fibrinolytic therapy, stents may be placed. Goal: primary PCI w/90 min of pt contact. Pts should recieve an anticoagulant, antiplatelet drugs, glycoprotein Ilb/Illa inhibitor

79
Q

What is fibrinolytic therapy?

A

Goal: to improve ventricular function, limit size of infarct, reduce mortality. Used to open occluded artery in pts. Better for pts younger than 75.

80
Q

What are the complications of STEMIs?

A

Ventricular dysrythmias, cardiogenic shock, ventricular dysrythmias, cardiogenic shock, HF, cardiac rupture.

81
Q

What is syncope?

A

Kennedy.

Jk. Caused by vasovagal syncope or dysrythmias, hypoglycemia, hysteria, seizure.

NURS 3560 (4 decks)

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