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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
What is the treatment for atrial flutter?
CCBs, BBs, cardioversion, antidysrythmic drugs, radio catheter ablation.
26
What do beta blockers do to the heart?
Decrease automaticity of SA node, decrease velocity of conduction through AV node, decreased myocardial contractility.
27
What are the therapeutic indications for BBs?
Dysrhythmias, supraventricular tachydysrythmias, suppression of excessive discharge, slowing V rate.
28
What are the AE of BBs?
Heart block, HF, AV block, sinus arrest, hypotension, bronchospasm.
29
What is quinidine's effects on the heart and ECG?
- Blocks Na channels - Slows impulse conduction - Delays repolarization - Blocks vagal input to the heart. - Widens QRS complex - Prolongs QT interval
30
What are the therapeutic uses for quinidine?
Used for supraventricular and ventricular dysrythmias.
31
What are the AE of quinidine?
Diarrhea, cinchonism, cardiotoxicity, atrial embolism, alpha-adrenergic blockade, hypersensitivity reactions.
32
What is atrial fibrillation?
Disorganization of atrial electrical activity due to multiple ectopic foci, resulting in loss of effective atrial contraction. Most common dysrhythmias.
33
What are clinical associations with a-fib?
- Rheumatic heart disease - CAD - Cardiomyopathy - Hypertension - Throtoxicosis - Alcohol intoxication - Caffeine use - Electrolyte disturbances - Stress - Cardiac surgery - HF - Pericarditis
34
What is the clinical significance of a-fib?
Decreases CO, may cause thrombi, embolus may develop and cause stroke.
35
What is the treatment for a-fib?
- Decrease V rate and prevent embolic events. - Drugs: CCBs, BBs, anticoagulant therapy. - Cardioversion.
36
What are junctional dysrythmias?
Dysrhythmias that start in the AV node. SA node fails or has been blocked at the AV node.
37
What are the clinical associations for junctional rhythms?
CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, rheumatic heart disease, digoxin, amphetamines, caffeine, nicotine.
38
What is the treatment for junctional dysrythmias?
Atropine, hold digoxin if caused by digoxin, BBs, CCBs, amiodarone for rate control for junctional tachycardia.
39
What is digoxin?
Drug used for HF and SVTs. Shorten's QT interval. AE: Cardiotoxicity. Increases risk of hypokalemia.
40
What is a first-degree AV block?
Every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged.
41
What are the clinical associations of a first degree AV-block?
MI, CAD, rheumatic fever, hyperthyroidism, vagal simulation, digoxin, BBs, CCBs, flecainide.
42
How are first degree AV blocks treated?
Check meds, monitor.
43
What is a second degree AV block type 1?
Lengthening of PR interval due to prolonged AV conduction.
44
What are the clinical associations with 2nd degree AV block type 1?
Associated with digoxin and BBs and sometimes CAD.
45
What is the clinical significance of 2nd degree AV blocks type 1?
Result of myocardial ischemia/ infarction. Transiant and well tolerated.
46
What is the treatment for 2nd degree AV Block Type 1?
Symptomatic- atropine, temp pacemaker. | Asymptomatic- monitor w/ transcutaneous pacemaker on standby.
47
What is a second degree AV block type 2?
P wave not conducted w/o antecendent PR lengthening. Occurs when a block in one bundle branch is present.
48
What are the clinical associations for a second degree AV block Type 2?
Rheumatic heart disease CAD Anterior MI Digitalis toxicity
49
What is a third degree AV heart block?
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
What are the clinical associations for a 3rd degree heart block?
Severe heart disease, systemic diseases, digoxin, BBs, CCBs.
51
What are premature ventricular contractions?
Premature contraction in the ventricles, causes wide distorted QRS complex.
52
what are clinical associations with PVCs?
Stimulants, electrolyte imbalances, hypoxia, fever, MI, mitral valve prolapse, HF, CAD.
53
What is the clinical significance of PVCs?
Usually benign in normal heart, PVCs may decrease CO and cause angina and HF.
54
What is the treatment for PVCs?
O2 therapy for hypoxia, electrolyte replacement, treatment according to cause.
55
What is ventricular tachycardia?
Run of 3 or more PVCs.
56
What are the clinical associations of V-tach?
MI, CAD, electrolyte imbalance, cardiomyopathy, mitral valve prolapse, long QT syndrome, digitalis toxicity, CNS disorders, fibrillation.
57
What does sustained VT cause?
Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest.
58
How are monomorphic VTs treated?
hemodynamically stable: IV amiodarone | hemodynamically unstable: IV amiodarone and cardioversion.
59
What is accelerated idioventricular rhythm?
Happens when the intrinsic pacemaker rate becomes less than the ventricular ectopic pacemaker.
60
What are the clinical associations of AIVR?
Acute MI, reperfusion of myocardium after thrombolytic therapy or angioplasty.
61
How is AIVR treated?
Temp pacing may be required. Don't use drugs.
62
What does lidocaine do to the heart?
Blocks Na channels, slows conduction in the atria, ventricles, and His-Purkinje system, reduces automaticity in the ventricles and His-Purkinje system.
63
What are the adverse effects of lidocaine?
Drowsiness, confusion, paresthesias
64
What is ventricular fibrillation?
Severe fuckery of the heart rhythm. No contraction really. Heart goes bingo bongo.
65
What are the clinical associations of V-Fib?
Acute MI, CAD, cardiomyopathy, accidental electric shock, hyperkalemia, hypoxia, acidosis, drug toxicity.
66
What is the treatment of V Fib?
CPR, resucitation.
67
What is pulseless electrical activity?
Electrical activity evident on ECG, no mechanical activity evident. Pt is pulseless.
68
What is defibrillation?
Restart heart button. Shocks heart to make the SA node do its job.
69
What is synchronized cardioversion?
Used for hemodynamically unstable ventricular/ supraventricular tachydysrythmias. Delievers shock on R wave of QRS complex.
70
What are implantable cardioverter-defibrillator used for?
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
What are pacemakers used for?
Used to pace heart when the normal conduction. For anditbradycardia pacing and overdrive pacing and tachycardias.
72
What is radiofrequency catheter ablation therapy?
Electrode-tipped ablation catheter 'burns' accessory pathways or ectopic sites in the atria, AV node and ventricles.
73
What is radiofrequency catheter ablation therapy used for?
AV nodal reentrant tachycardia, reentrant tachy r/t accessor bypass tracts, control of ventricular response of certain tachydysrythmias.
74
What ECG changes are associated with acute coronary syndrome?
- Ischemia - ST segment depression/ T wave inversion - ST segment depression significant
75
What is a STEMI?
MI w/ ST elevation. Causes ischemia and necrosis.
76
How is a STEMI managed?
O2, aspirin, morphine, betablockers, nitroglycerin, reperfusion therapy.
77
What drugs are used for MI?
- Fondaparinux (selective factor Xa inhibitor) - Bivalirudin (direct thrombin inhibitor) - Antiplatelet drugs - Thrombolytic drugs
78
What is PCI?
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
What is fibrinolytic therapy?
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
What are the complications of STEMIs?
Ventricular dysrythmias, cardiogenic shock, ventricular dysrythmias, cardiogenic shock, HF, cardiac rupture.
81
What is syncope?
Kennedy. | Jk. Caused by vasovagal syncope or dysrythmias, hypoglycemia, hysteria, seizure.

NURS 3560 (4 decks)

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