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Adults 2 > Exam 2 Cardiac > Flashcards

Exam 2 Cardiac Flashcards

1
Q

mitral stenosis

A

narrowing of the mitral valve (left side of heart) reducing blood flow to the left ventricle

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2
Q

effects of mitral valve stenosis

A

reduced blood flow to left ventricle; reduced cardiac output; increased pressure in left atrium; left atrium hypertrophy and pulmonary congestion

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3
Q

mitral valve regurgitation

A

allows blood flow from the left ventricle back into the left atria; causes decrease in cardiac output and left ventricular hypertrophy as it tries to pump harder

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4
Q

aortic stenosis

A

narrowing of the aortic valve causing left ventricle hypertrophy

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5
Q

aortic regurgitation

A

blood travels back into the left ventricle from the aorta and causes reduced blood flow out through the aorta

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6
Q

pulmonary hypertension

A

can be caused by mitral stenosis

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7
Q

clinical manifestations of pulmonary hypertension

A

shortness of breath, fatigue, racing heart, decreased appetite, right abdominal pain

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8
Q

interventions for pulmonary hypertension

A

meds consist of sildenafil and veletri

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9
Q

mitral valve prolapse

A

part of one or both valve leaflets collapse back into the left atrium

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10
Q

clinical manifestations of mitral valve prolapse

A

palpitations, chest pain, fatigue, dizziness, shortness of breath

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11
Q

valvuloplasty

A

valve repair and reconstruction; minimally invasive procedure

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12
Q

types of valvular replacement

A

replacements done when unable to do valvuloplasty prosthetic consist of mechanical, biological, homograft

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13
Q

mechanical valve replacement

A

long term disability; risk for thrombi and emboli; risk for infection; requires life-long anticoagulation

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14
Q

biologic valve replacement

A

durability of <10 years

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15
Q

homograft valve replacement

A

comes from deceased human valve; limited availability

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16
Q

purpose of hemodynamic monitoring…

A

early detection, identification, and treatment of life threatening conditions such as HF or cardiac tamponade; used to evaluate pt immediate response to medications; used to evaluate cardiovascular function like cardiac index and output

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17
Q

arterial line

A

IV pressure catheter in an artery (radial or femoral); continuous BP monitoring; transducer has to be at phelbostatic axis (midaxillary line or 4th intercostal space)

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18
Q

indications for arterial line

A

intubation to monitor ABG and have lab access; shock; critical patients on vasopressor medications

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19
Q

central venous pressure

A

measures preload because it is influenced by venous return

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20
Q

indications for central venous pressure

A

assess the circulating blood volume and allows for a guide for fluid therapy; allows assess right ventricular function and venous blood return

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21
Q

central venous pressure limitations

A

does not always reflect true fluid volume; not a reliable indicator of left ventricular function or preload of the left side of heart

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22
Q

pulmonary artery catheter

A

measures the only artery that carries blood away from the heart and is deoxygenated; normal pressure is 30/15; travels in the superior vena cava and through the RA then RV then through pulmonary valve to artery; aka Swan ganz catheter

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23
Q

pulmonary wedge

A

when the pulmonary artery catheter is advanced and balloon is inflated; we then measure a wedge pressure which is the inadvertent pressure of the left side of heart; wedge pressure usually 12

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24
Q

commissures

A

repair of stenosed mitral valve; fused commissures are incised

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25
Q

assessment valvular disorders

A

decreased cardiac output and cerebral perfusion; syncope with exertion; pulmonary edema (crackles), dyspnea and tachypnea; tachycardia; chest pain

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26
Q

risks of valve replacement

A

bleeding, stroke, perforation, infective endocarditis

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27
Q

new meds after valve replacement

A

aspirin- antiplatelet; clopidogrel (plavix)- antiplatelet; warfarin (coumadin)- vitamin k antagonist; heparin- thrombin inactivater

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28
Q

central line

A

IV in large vein such as internal jugular vein, subclavian vein; catheter is advanced into cavoatrial junction; can provide continuous central venous pressure monitoring

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29
Q

angina

A

cardiac pain caused by imbalance of O2 demand and O2 supply; stble is predictable. unstable is preinfarction; prinzmetal is coronary artery spasm

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30
Q

stable angina

A

predictable; occurs with exertion

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31
Q

unstable angina

A

preinfarction state; occurs at rest and more frequently

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32
Q

prinzmetal/variant angina

A

pain at rest with reversible ST elevation

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33
Q

medications for angina

A

nitrates, beta blockers, calcium channel blockers, antiplatelet, oxygen, morphine

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34
Q
A
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35
Q

calcium channel blockers

A
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36
Q

S1 heart sound

A

tricuspid and mitral valves closing; “lub”; beginning of systole; ventricles are contracting; best heard at the apex

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37
Q

S2 heart sound

A

aortic and pulmonic valves are closing; beginning of diastole; “dub”; best auscultated at bases

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38
Q

S3 heart sound

A

heard just after S2; low pitched sound that is best heard with the bell; caused by rapid filling of ventricle likely due to HF

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39
Q

S4 heart sound

A

4th heart sound heard at end of diastole; low pitched that is best heard with the bell; produced during atrial contraction; caused by decreased ventricular compliance

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40
Q

electrical conduction through the heart

A

begins in SA node (primary) in right atrium which initiates atrial activation; then moves to AV node (backup) which causes atria depolarization and slows the impulse; then atrial contraction begins and traves to heart apex; then bundle of his and bundle branches (going down septum); then to purkinje fibers through the ventricular myocardium which then causes ventricular contraction

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41
Q

depolarization on 12 lead

A

negative to positive; moving from the top of the heart down to the apex; heart goes from negative at rest to positive as it depolarizes (creates positive deflection)

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42
Q

acute coronary syndrome

A

caused by blocked or decreased blood flow to the heart muscle angina-warning but no damage results; unstable warning occurs at rest; NSTEMI is a partial occlusion that is reversible; STEMI is a complete occlusion that is irreversible

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43
Q

signs and symptoms of acute coronary syndrome

A

chest pain is most common; arm shoulder jaw back or upper abdominal pain; other symptoms are SOB, cool clammy skin, nausea, lightheadedness, anxiety, indigestion

44
Q

difference between STEMI and NSTEMI

A

STEMI shows EKG changes associated with the infarction whereas NSTEMI does not show EKG changes

45
Q

management of acute coronary syndrome

A

morphine to decrease pain and cardiac workload by vasodilating; oxygen to increase PaO2 in blood and reach ischemic tissue; nitrates to dilate vessels; aspirin as an antiplatelet

46
Q

why nitrates used during angina or acute coronary syndrome

A

vasodilation of veins and large arteries to increase O2; dilates coronary arteries; improves blood flow to heart muscle and decreases workload which decreases O2 demand; decreases preload and afterload; can admin up to 3 doses 5 min apart as long as BP is adequate

47
Q

side effects of nitrate use

A

headache, dizziness, weakness, hypotension, flushing, pallor, increased perspiration, tachycardia, nausea

48
Q

prior to administering nitrates… (contraindications)

A

hepatic/renal disease, hypotension, hypovolemia, increased cranial pressure, ED medication within past 24 hours

49
Q

chest pain protocol

A

VS, height, weight, cardiac monitor; EKG and call cath lab; portable CXR; start 2 IVs and draw labs (troponin, glucose, INR, rainbow); undress shave pt, allens test; assess pain using OPQRST, PMH allergies and meds; drug or alcohol use, admin meds (NS, pain meds, zofran, pressors, atropine/amio, electrolytes)

50
Q

cardiac catheterization

A

coronary angiography to view where occlusion is and open up; stent is placed

51
Q

cardiac cath complications

A

bleeding, hemorrhage, hematoma, retroperitoneal bleed, thrombus/emboli, LOC changes, arrythmia, tamponade, MI, restenosis, reaction to dye used, infection, pulmonary edema, infection

52
Q

coronary artery bypass graft (CABG)

A

can be schedule or be emergent; indications are angina not controlled by medication and data from cath lab

53
Q

complications caused by pump during cardiac surgery

A

neuro-cognitive changes, ischemic hypo perfusion, micro-emboli, renal failure, renal hypo perfusion, arrhythmias, coagulopathy

54
Q

indications for cardiac transplant

A

severe disease that would result in death in a year if untreated; cardiomyopathy; end stage cardiac disease

55
Q

P wave

A

atrial contraction; depolarization;

56
Q

PR segment

A

movement of electrical activity from atria to ventricles; isoelectric or flat line from P wave to q wave is electricity being held in AV node; from end of P wave to beginning of QRS

57
Q

QRS complex

A

ventricle contraction; depolarization; positive deflection; 0.06-0.12s; from beginning of Q wave to end of S wave

58
Q

ST segment

A

time between ventricular depolarization and repolarization; end of S wave to beginning of T wave

59
Q

QT interval

A

from beginning of Q wave to end of T wave; start of ventricular contraction to repolarization; < 0.40s

60
Q

T wave

A

ventricle relaxing (repolarizing)

61
Q

TP interval

A

time from end of T wave to beginning of next P wave

62
Q

measuring EKG strips

A

each strip is 6 seconds; each small box is 0.04s; each large box is 0.20s; 5 large boxes are 1.0s

63
Q

interpreting EKG 8 step process

A

measure rate; examine R-R interval ad decipher if regular or irregular; examine P wave and identify if upright, constant, and one for every QRS; measure P-R interval to decide if prolonged; is the p followed by QRS complex; examine and measure QRS complex; measure QT interval; identify the rhythm

64
Q

sinus bradycardia

A

rate of 60 or below; R-R interval is regular; P wave is regular, upright, and matches all QRS; P-R interval is 0.18-0.2; P preceds QRS; QRS complex is 0.08; QT interval is 0.40; Sinus bradycardia

65
Q

treatment of sinus bradycardia

A

atropine 0.5mg and dopamine; pacemaker

66
Q

Sinus tachycardia

A

rate 100-140; R-R interval is regular; P wave is regular upright and matching

67
Q

treating cause of sinus tachycardia

A

fluids, O2, fever, pain, rest; treat with meds BB; antianxieties, antipyretics, CCB, BB, vagal stim, carotid artery massage, pain relief

68
Q

Sinus rhythm

A

60-100; R-R interval is regular; P wave is upright and precedes each QRS

69
Q

Atrial fibrillation

A

atrial rate is unable to be calculated; R-R interval is irregular; P wave is undistinguishable; PR interval cannot be calculated; cannot identify if a P wave precedes each QRS

70
Q

concern with atrial fibrillation

A

loss of atrial kick and blood stasis; increased risk for blood clots; increased risk of hypotension; increased or decreased rate; decreased CO; need blood thinners for life

71
Q

atrial fibrillation RVR

A

atrial fibrillation with a ventricular rate above 110

72
Q

atrial fibrillation medications to convert

A

beta blockers, calcium channel blockers, digoxin all used to slow conduction from SA node to AV node; amiodarone not as commonly used; cardioversion

73
Q

atrial flutter

A

one spot of atria is misfiring; can see sawtooth P wave with regular R-R interval; cannot distinguish P wave due to sawtooth; PR interval cannot be calculated

74
Q

concerns with atrial flutter

A

loss of atrial kick; blood stasis; NOT as dangerous as Afib due to ore regularity

75
Q

Supraventricular tachycardia

A

fast and skinny; cannot distinguish between P and T waves (p and t smushed together); R-R regular; cannot calculate PR interval; cannot distinguish if P wave precedes each QRS;

76
Q

treatment of SVT

A

want to convert and slow; use vagal maneuver, meds to slow rates, cardioversion, adenosine

77
Q

adenosine

A

1st line med used to convert SVT to sinus rhythm when vagal is ineffective; pushed rapidly over 1-2s; temporarily inhibits AV node conduction and blocks retry leading to reset HR

78
Q

premature atrial contraction (PAC)

A

feels like a palpitation; temporarily lose cardiac output; Pr interval may be normal or prolonged with normal QRS

79
Q

treatment of PAC

A

may not be treated if asymptomatic; reduce caffeine, alcohol, smoking; give beta blocking meds

80
Q

treatment of atrial flutter

A

beta blocker, calcium channel blocker, cardioversion

81
Q

ventricular tachycardia

A

can have a pulse or be pulseless; very wide QRS complex; unable to identify atrial rate; regular R-R interval; undistinguishable P wave; no P-R interval; no p wave preceding each QRS

82
Q

treating Vtach with a pulse

A

oxygen, antiarrhythmics such as amiodarone, synchronized cardioversion

83
Q

synchronized cardioversion

A

shock delivered in sync with QRS complex

84
Q

treating unstable Vtach (pulseless)

A

CPR, follow ACLS protocol for defibrillation, intubation, drug therapy like epi, vaso, and amiodarone

85
Q

ventricular fibrillation

A

no pulse present; complete loss of contraction; no atrial rate or ventricular rate; R-R interval is undeterminable; no P wave present; P-R interval is undistinguishable; no P wave before QRS

86
Q

treating Vfib

A

CPR, then defibrillate, meds such as epi and amiodarone; no cardiac output present

87
Q

asystole

A

complete cessation of electrical impulses in the heart; unconscious and pulseless

88
Q

treating asystole

A

CPR and meds such as epi, bicarb; cannot shock due to no electrical activity present

89
Q

Pulseless electrical activity (PEA)

A

electrical activity on EKG but no pulse is present

90
Q

treatment of PEA

A

CPR, treat underlying causes, administer meds like epinephrine

91
Q

etiology of PEA

A

H’s and T’s; hypovolemia, hypoxia, hydrogen ion (acidosis), hypo or hyperkalemia, hypoglycemia, toxins, tamponade, tension pneumo., thrombosis (coronary or pulmonary), trauma

92
Q

premature ventricular contraction

A

3 in a row is considered vtach; can be completely normal; can be electrical or actual contraction but does not add to cardiac output; no p wave present before QRS

93
Q

cardioversion

A

administration of electrical current synchronized with patients heart rhythm to treat SVT, AF, Aflutter, Vtach with pulse; beware of R on T phenomenon

94
Q

R on T phenomenon

A

cardioverting on T wave instead of QRS which can cause lethal arrhythmia

95
Q

nursing considerations for cardioversion

A

informed consent with pt timeout, sedation (propofol), ACLS equip., 12 lead to confirm rhythm, NPO, electrolyte in normal limits, pt connected to pads, TEE done prior to assess for clot, anticoagulated (INR > 2); successful 12 lead and gag reflex prior to transfer

96
Q

defibrillation

A

used to treat vfib or vtach without a pulse; unsynchronized shock of 360 joules for example; CPR, pads applied, “all clear”, resume CPR after shock, assess for rhythm, admin epi

97
Q

transcutaneous pacing

A
98
Q

antidysrhythmic classes

A
  1. sodium channel blockers (lidocaine) to slow impulses in atria ventricles and bundle of his (used for ventricular arrhythmias; 2. beta blockers; 3. potassium channel blockers; 4. calcium channel blockers; 5. non classed drugs
99
Q

class 2. beta blockers like metoprolol

A

used to treat SVT and PVCs; decreases HR, cardiac excitability, and cardiac output); slows conduction through AV node and prolongs AV node repolarization

100
Q

side effects of beta blockers

A

hypotension, bradycardia, AV block, bronchospasm, dyspnea, loss of libido, decreased exercise tolerance

101
Q

class 3. potassium channel blocker

A

first line management for vfib; prolongs electrical impulses in all heart cells; blocks potassium channels and slow outward movement of K during phase 3 of action potential and prolongs; example is amiodaronesi

102
Q

side effects of potassium channel blockers

A

decreased HR, lung damage, visual impairment

103
Q

class 4. calcium channel blockers

A

ex. verapamil and diltiazem; slows SA node automaticity, delays AV conduction, reduces myocardial contractility; block calcium ions across the cell membrane and depresses generation of action potentials

104
Q

side effects of calcium channel blockers

A

decreased HR, AV block, HF, hypotension, constipation

105
Q

digoxin

A

inotropic effect meaning squeezes harder; inhibits NA-K ATPase and calcium accumulates in myocytes, competes with K for binding sites; negative dromotropic effects; meaning it slows AV node impulses; negative chronotropic effects meaning beats slower

106
Q

parameters of blood pressure

A
107
Q

transcutaneous pacing

A

electrical shocks to increase HR if goes below certain amount; done via placing pads; temporary; sedate because pt will be getting shocks

Adults 2 (7 decks)

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