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N202 > Cardiac > Flashcards

Cardiac Flashcards

0
Q

Automaticity

A

The ability to spontaneously initiate an electrical impulse

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1
Q

Causes of dysthymia’s

A

Acid, autonomic nervous system, electrolyte imbalances, ischemia, injury, hypoxia, unhealthy heart, drugs

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2
Q

Excitability

A

The ability to respond to an electrical impulse

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3
Q

Conductivity

A

The ability to transmit the impulse to another cardiac cell

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4
Q

Contractility

A

The ability to contract after receiving a stimulus

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5
Q

What cells in the heart can spontaneously initiate an electrical impulse

A

Any cell

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6
Q

What move in cells when ventricles contract

A

Sodium and calcium

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7
Q

What enters the cells when ventricles repolarize

A

Potassium

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8
Q

Depolarization

A

Contraction or systole

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9
Q

Repolarization

A

Relaxation or diastole

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10
Q

What is the primary pacemaker

A

SA node

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11
Q

SA node

A

Primary pacemaker, located in right atrium, 60-100 bpm

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12
Q

AV node

A

Located in lower right atrium, delays conduction, gatekeeper so it allows time for the atria to contract and the ventricles to fill

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13
Q

Bundle of HIS

A

2 branches (left and right bundle), 30-40 bpm

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14
Q

Purkinje fibers

A

Where the bundle branches terminate in a network of fibers, 20-40 bpm

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15
Q

can the electrical system exist without the mechanical contraction

A

yes

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16
Q

can the mechanical exist without the electrical activity

A

no

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17
Q

what does the autonomic nervous system control

A

rate of impulse formation
speed of conduction
strength of contraction

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18
Q

what does the parasympathetic nervous system control

A

vagus nerve: decreaes rate, slows impulse conduction, decreases force of contraction

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19
Q

what does the sympathetic nervous system control

A

incrase rate incrases force of contraction

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20
Q

absolute refractory period

A

heart cells cant respond to stimulus, starts at Q wave to 1st 1/3rd of the T wave

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21
Q

relative refractory period

A

cardiac cells respond to a strong stimulus usually with a unorganized response, later 2/3 rds of the T wave

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22
Q

supernormal period

A

cardiac cells can respond to a weaker tan normal stimulus, @ the end of the T wave

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23
Q

refractory period

A

period between depolarizations

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24
Q

isoelectric line

A

base line of te EKG

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25
Q

P Wave

A

SA node firing, the right and left atria are contracting/systole/deplarization, it is a positive defelectino in lead II

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26
Q

PR interval

A

time from the begining of the P wave to the begining of the Q wave, duration is 0.12-0.2 seconds, represents the electrical impulse spread through the atria, AV node, bundle of HIS, BB, purkinje

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27
Q

QRS complex

A

contraction/systole/depolarization of the ventricles, duration is less than 0.10, measure from the begining of the Q to the end of the S wave, a positive deflection in lead I is normal, a negative deflection is normal in lead V1

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28
Q

ST segment

A

ventricular walls relax/diastole/repolarization, measure from end of S wave to begining of T wave
elevation of 2mm or higher or depression

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29
Q

ST segment depression or elevation is a sign of

A

MI, pericarditis, pulmonary emboli, electrolyte imbalance

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30
Q

T wave

A

ventricular repolarization/relaxation/diastole, follows the QRS wave and ST segment, typically rounded and smooth

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31
Q

an inverted T wave coud represent what

A

ischemia

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32
Q

a peaked T wave respresents what

A

hyperkalemia

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33
Q

QT interval

A

represents the time required for ventricular depolarizationand repoalrization to occur, starts at begining of Q to the end of the T wave

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34
Q

length of the QT interval

A

less than alf the distance between consecutive R waves (R-R interval) when the rhythm is regular

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35
Q

normal PR interval

A

0.12-0.2 seconds

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36
Q

normal QRS complex

A

less than 0.1 seconds

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37
Q

normal QT interval

A

half of the R-R interval

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38
Q

sinus rhythm

A

60-100 bpm, regular, pacemaker site is SA node, PR interval is 0.12-0.2 seconds, QRS is less than 0.1 seconds

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39
Q

sinus bradycardia

A

less than 60 bpm,

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40
Q

what can cause bradycardia

A

acute MI, CAD, SA node disease, CCB, BB, hyperkalemia, digitalis

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41
Q

clinical Sz of bradycardia

A

hypotension, pale, cool skin, weakness, angina, dizziness, confusion, shortness of breath

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42
Q

Tx for bradycardia

A

atropine, pacemaker, dopamine if BP is decreased

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43
Q

sinus tachycardia

A

100 bpm or more, pacemaker sire is SA node, p wave usually normal but may be slightly taller can be buried in the preceding T wave

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44
Q

causes of tachycardia

A

CHF, MI, pericarditis, cardiogenic shock, anxiety exercise, fever, infection, pain, hemorrhage, pulmonary embolis, hypovolemia, ingestion of stimulus, pharmacologics: atropine, caffeine, cocaine, nicotine….-ine

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45
Q

Sx of tachycardia

A

dizziness, hypotension

sinus tachycardia is frequently a COMPENSATORY MECHANISM

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46
Q

what does sinus tachycardia do the the oxygen demands

A

it increases the oxygen demands,

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47
Q

Tx for sinus tachycardia

A

Tx underlying cause

*if hypovolemic give fluids

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48
Q

sinus arrhythmia

A

60-100 bpm, may increase during inspiration and decrease during expiration, regularly irregular (R-R interval greater than or = to squars difference

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49
Q

what Tx is there for sinus arrhythima

A

none

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50
Q

premature atrial contraction (PAC)

A

contraction originating from ectopic (abnormal position) focus in atrium in location other than SA node, represents irritable atrial tissue

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51
Q

PAC can lead to what

A

a flutter or a fib

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52
Q

Tx for PAC

A

Tx underlying cause (emotional stress, COPD, electrolyte imblances), beta blockers are used

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54
Q

atrial tachycardia

A

140-250 bpm, pacemaker site is ectopic (not SA node), P wave may be hidden in T wave,

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55
Q

paroxsymal atrial tachycardia

A

atrial tachycardia that starts and dtops suddenly

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56
Q

supraventricular tachycardia (SVT)

A

umbrella term that can mean a fib or a flutter or atrial tach

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57
Q

what rhythm do you have if you have more than 3 PACs in a row

A

PAT paroxsymal atrial tachycardia

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58
Q

causes of atrial tachycardia

A

stress, anxiety, caffeine, alcohol, stimulants, chronic lung disease, dig toxicity

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59
Q

Tx of atrial tachycardia

A

depends on the pt tolerance of the rhythm
* stable: O2, diltiazem or BB or amiodarone
*unstable: O2, amiodarone or diltiazem
12 lead EKG

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60
Q

a flutter

A

recurring, regular sawtooth shaped flutter waves, originates from a single ectopic focus, atrial HR 250-400, ventricular HR 60-150

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61
Q

what keeps the ventricles from increasing HR although the atria are beating 250-400 bpm

A

AV node (gatekeeper)

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62
Q

Cause of a flutter

A

CAD, HTn, mitral valve disorders, pulmonary embolis, cardiomyopathy, digoxin, quinidine,epi

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63
Q

what are you at risk for after a flutter

A

stroke because of a possible thrombus formation in the atria

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64
Q

Tx of a flutter

A

slow ventricular responses by increasing AV block (CCB, BB), electrocardioversion, cardiozem, if there is no thrombi, to be put on a heparin drip to prevent clots then cardiozem, if the Rxs dont work, cardioversion is needed

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65
Q

what will be done if a pt has multiple episodes of flutter

A

they will get an ablation

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66
Q

a fib

A

atrial HR of 400 or more, ventricle HR greater than 100 is uncontrolled, less than 100 is controlled, PR interval is unable to be measured, pacemaker has multiple ectopic sites in the atira

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67
Q

cause of a fib

A

heart disease (rheumatic), CAD, cardiomyopathy, HF, pericarditits

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68
Q

what can happen if a fib is not tx

A

thrombi can form in the atria as a result from blood stasis, embolus may develop and travel to the brain, cauing a stroke

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69
Q

Tx of a fib

A

goal: decrease ventricular response, prevent embolic stroke
give CCb, CBB, digoxin
long term coumadin

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70
Q

what do you do if the duration of the arrhythmia has lasted longer than 48 hours

A

begin heparin, TEE, cardioversion, anticoag

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71
Q

junctional dysrhytmia

A

originates in the area of the AV node, SA node has failed to fire or has been blocked by the AV node, P wave may be absent, or premature with negative deflection

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72
Q

cause of premature junctional contraction (PJC)

A

acute inferior myocaridal infarction, rheumatic heart disease, valvular disease, excessive caffeine intake

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73
Q

Tx of premature junctional contractions

A

tx the cause

hold digoxin, restrict caffeine intake

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74
Q

junctional rhythum

A

HR 40-60, pacemaker is Av node, negative deflection of P wave

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75
Q

Tx for junctional dysrhythmias

A

is symptomatic (brady): atropine
tachy: BB, CCB, amiodarone used for rate control (when not caused by dig toxicity
CARDIOVERSION IS CONTRAINDICATED

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76
Q

first degree AV block

A

PR interval is prolonged greater than 0.2 seconds

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77
Q

Tx for first degree block

A

check medications, continue to monitor, usually no Tx

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78
Q

second degree AV block Type 1

A

gradual lengthening of PR interval then a QRS complex that is blocked (missing), more p waves than R waves

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79
Q

Tx for sencond degree AV block type 1

A

usually no Tx, if symptomatic: atropine or a temporary pacemaker

80
Q

second degree AV block type 2

A

have 2 or 3 p waves before each QRS complex, PR interval remains constant (may be normal or prolonged),

81
Q

what is the clinical significance of a sencond degree AV block type 2

A

can progress to third degree AV block and isassociated with a poor prognosis

82
Q

Tx for second degree AV block type 2

A

if symptomatic: (hypotension, angina), temporary pacemaker, epi for HR, dopamine for BP permanent pacemaker

83
Q

tird degree AV block

A

HR 20-40, no association between atria and ventricles, PT interval varies greatly

84
Q

Tx of third degree AV block

A

if symptomatic (syncope, bradycardia): pacemaker, epiniphrine, atropine

85
Q

premature ventricular contractions (PVC)

A

contraction originating in ectopic areas of the ventricles, wide distorted QRS complex (greater than 0.12), R opposite T reflection, PR interval is not measureable

86
Q

Tx for PVC

A

usually not treated when isolated/infrequent, oxygen therapy for hypoxia, electrolyte replacement, BB, CCB, amiodarone

87
Q

ventricular tachycardia

A

run of 3 or more PVCs, HR 140-250, no p waves associated with V tach, non measureable PR interval, QRS complex is wide ( 0.12 seconds or greater), considered life threatening because of the decreased CO and the possibility of deterioration ventricular fibrillation

88
Q

a pt who has v tach with a pulse what is the tx

A

cardioversion with sedation (versed), if BP is stable

89
Q

a pt who has v tach without a pulse what is the tx

A

CPR and rapid defibrillation, epi if defibrillation is unsuccessful

90
Q

PTorsades de pointes

A

give IV magnesium

91
Q

if v tach is not tx what will happen

A

turn into v fib then asystole

92
Q

ventricular fibrillation (v fib)

A

severe derangement of the heart rythm characterized by irregular undulations of varying contour and amplitude

93
Q

Tx of v fib

A

CPR, ACLS, defibrillation

94
Q

asystole

A

represents total absence of ventricular electrical activity, no CO occurs because no depolarization occurs, may have occasional P

95
Q

pulsesless electrical activity (PEA)

A

electrical activity can be observed on the EKG but there is no mechanical activity of the ventricles and the pt has no pulse

96
Q

tx for PEA

A

CPR followed by intubation and IV epi, defibrillation

97
Q

defibrillation

A

passage of electrical shock through the heart to depoalrize the cells of the myocardium to allow the SA node to resume the role of pacemaker

98
Q

what do we defibrillate

A

V fib and pulseless V tach

99
Q

biphasic defibrillators

A

deliver succeful shocks at lower energies and with fewer post shock EKG abnormalities

100
Q

synchronized cardioversion

A

synchronized circuit delivers a countershock on the R wave of the QRS complex

101
Q

what do we cardiovert

A

rapid a fib, rapid a flutter, PAT, V tach with pulse

102
Q

sodium

A

135-145, stimulates reactions within nerve and muscle tissue, important for depolarization

103
Q

SE of sodium

A

hyponatremia: HA, N/V, anxiety, weak, confused, anorexia
hypernatremia: dry mucous membranes, fatigue, restlessness, agitation, convulsions

104
Q

potassium

A

3.5-5, regulates cardiac electrical activity, important for replarization and stable polarized state,

105
Q

hypokalemia

A

ventricular arhythmias (PVCs), muscle weakness, U ave, lef cramps, anorexia, N/V

106
Q

hyperkalemia

A

confusion, diarrhea, peasked T wave, blocks, asystole

107
Q

hyponatremia

A

HA, N/V, anxiety, weakness, confused, anorexia

108
Q

hypernatremia

A

dry MM, fatigue, restlessness, weakness, agitation, convulsions

109
Q

calcium

A

8.5-10.5, transmits electrical impulses in the heart, important for initiation and propagation of electrical impulse for myocardial contraction

110
Q

pulsesless electrical activity (PEA)

A

electrical activity can be observed on the EKG but there is no mechanical activity of the ventricles and the pt has no pulse

111
Q

tx for PEA

A

CPR followed by intubation and IV epi, defibrillation

112
Q

defibrillation

A

passage of electrical shock through the heart to depoalrize the cells of the myocardium to allow the SA node to resume the role of pacemaker

113
Q

what do we defibrillate

A

V fib and pulseless V tach

114
Q

biphasic defibrillators

A

deliver succeful shocks at lower energies and with fewer post shock EKG abnormalities

115
Q

synchronized cardioversion

A

synchronized circuit delivers a countershock on the R wave of the QRS complex

116
Q

what do we cardiovert

A

rapid a fib, rapid a flutter, PAT, V tach with pulse

117
Q

sodium

A

135-145, stimulates reactions within nerve and muscle tissue, important for depolarization

118
Q

SE of sodium

A

hyponatremia: HA, N/V, anxiety, weak, confused, anorexia
hypernatremia: dry mucous membranes, fatigue, restlessness, agitation, convulsions

119
Q

potassium

A

3.5-5, regulates cardiac electrical activity, important for replarization and stable polarized state,

120
Q

hypokalemia

A

ventricular arhythmias (PVCs), muscle weakness, U ave, lef cramps, anorexia, N/V

121
Q

hyperkalemia

A

confusion, diarrhea, peasked T wave, blocks, asystole

122
Q

hyponatremia

A

HA, N/V, anxiety, weakness, confused, anorexia

123
Q

hypernatremia

A

dry MM, fatigue, restlessness, weakness, agitation, convulsions

124
Q

calcium

A

transmits electrical impulses in the heart

125
Q

hypocalcemia

A

prolonged QT interval, numbness, tingling, tetany, bleeding

126
Q

hypercalcemia

A

AV block, weak, abdominal cramps, confused

127
Q

magnesium

A

1.2-2.5, transmission of electrical activity in the heart, a decrease in Mg will increase intracellular K which increases cellular membrane excitability

128
Q

hypomagnesemia

A

prolonged QT interval, ventricular arrhythimas

129
Q

hypermagnesemia

A

tremors, vasodilation, bradycardia, weak, impaired respirations, heart block, arrest

130
Q

lidocaine/rythmol

A

NA channel blocker, slow down depolarization, suppress conduction of electrical impulse, CLASS 1

131
Q

Se of lidocaine/rythmol

A

dissiness, confusion, altered mental status, seizure, arrythmias, hypotension

132
Q

Na channel blockers treat what

A

PVC, V tach, V fib

* NOT used for MI

133
Q

Atenolol, metoprolol

A

Beta adrenegic receptor blockers, CLASS 2, reduce SA node automaticity and conduction through AV node, decrease renin secretion by kidney, prevents remodeling

134
Q

SE of BB

A

decrease HR, BP, fatigue, weakness, depression, bronchospasm, AV node block, 2nd degree heart block

135
Q

BB tx what

A

SVTs (PSVT, PAT, AT), a flutter, a fib, ischemia, ACS (MI & unstable angina), PVCs

136
Q

amiodarone

A

CALSS 3, lengthen refractory period, prolong or delay repolarization (relaxation), inhibit Na channels

137
Q

SE of amiodarone

A

decrease Hr, BP, arrhthimas, heart failure, pulmonary fibrosis, weakness, prolongs QT interval, angioedema

138
Q

what does amiodarone tx

A

atrial and ventricular arrhytmias

*need glass bottle or polyolefin bag and special tubing

139
Q

cardizem, verapamil

A

CLASS 4, CCB, inhibit Ca channels within SA & AV nodes, decreases automaticity of SA node, decrease HR, BP, and contractility

140
Q

Se of cardizem and verapamil

A

decrease BP, HR, arrhythimas, fatigue, HA, edema, nausea

141
Q

what does cardizem and verapmil tx

A

SVT (PSVT, AT, PAT), a fib, a flutter

verapimil also txs PVC

142
Q

adenosine

A

CLASS 5, decreases SA node automaticity and ACV node conduction, slows conduction through AV node and interrupts AV node pathways

143
Q

SE of adenosine

A

flushing, dyspnea, HA, heart block, transient asystole (common), use caution in asthma pts

144
Q

adenosine is used to Tx

A

primarily for Dx of underlying rhythm, SVTs, and Wolff parkinson white syndrome

145
Q

atropine

A

CLASS 5, increases sinus rate, accelerates AV conduction by blocking vagus nerve (effects acetylcholine)

146
Q

SE of atropine

A

tachycardia, dry mouth, urinary hesitancy, drowsiness

147
Q

wat is atropine used to Tx

A

symptomatic sinus bradycardia

148
Q

digoxin

A

CLASS 5, antiarrhythmic, postive inotropic agent, increases CO, decreases HR, increases force of contraction, decreases conduction through SA & AV nodes

149
Q

SE of digoxin

A

anorexia, N/V, visual halos, decrease HR, prolongs PRI, AV block (dont give if pt has any type of AV block)

150
Q

digoxin is used for Tx of

A

SVTs, atrial arrhythmias

151
Q

epinephrine

A

alpha and beta adrenergic receptor stimulation, increases HR (facilitates automaticity), increase blood flow to myocardium, vasoconstriction, increase myocardial O2 consumptionand lactate production

152
Q

Se of epinephrine

A

arrhythmias, increase of BP and HR, palpatations, tremor, restlessness

153
Q

what is epinephrine used to Tx

A

V fib, pulseless v tach, asystole, PEA, symptomatic bradycardia after atropine, pacing
*used to initiate a heart beat

154
Q

dopamine

A

stimulates dopaminergic , beta and alpha receptors, positive inotropic effect, increae BRP, increase CO, increases cardiac contractility

155
Q

SE of dopamine

A

arrhythmias, HTN

156
Q

what is dopamine used as a Tx for

A

hypotension, unless caused by hypovolemia

157
Q

magnesium sulfate

A

necessary for cellular reactions

158
Q

SE of magnesium sulfate

A

ventricular arrhythimas, tremors, bradycardia, impaired respirations, arrest, heart block

159
Q

Magnesium sulfate is used to Tx

A

ventricular arrhythmias (torsades) and PVCs

160
Q

Vasopressin

A

alternative to epinephrine for refractory VF, only used one time, potent vasoconstrictor

161
Q

what medications need to be given via ET tube

A 
NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine
162
Q

What is the Tx for sinus bradycardia

A

O2, atropine, epinephrine, dopamine, pacing (rare)

163
Q

What is the Tx for SVT (AT, PAT, PSVT)

A

vagal stimulation, adenosine, CCB, BB, digoxin (for EF less than 40% after cardioversion), Cardioversion when hemodynamically unstable (cool clammy, increase HR), amiodarone,

164
Q

What is the Tx for a flutter and a fib

A

rate control (CCb, BB, digoxin, sotalol {long term rate control})
rhythm control (amiodarone, propafenone)
less than 48 hours: cardioversion after TEE, convert rhythm after control rate
more than 48 hours: heparin drip, amiodarone, diltiazem or CCB, BB, digoxin
if hemodynamically unstable : cardioversion immediatelyregardless of duration of rhythm

165
Q

what is the Tx for second degree AV block

A

transcutaneous pacemaker
epi
dopamine if hypotension
permanent pacemaker

166
Q

what is the Tx for 3rd degree AV block

A

transcutaneous pacemaker, epi, atropine, dopamine, permanent pacemaker

167
Q

what is the Tx for PVCs

A

treat the cause, BB, amiodarone, lidocaine, rythmol

168
Q

what is the Tx for Stable V tachwith a pulse

A

amiodarone, lidocaine, cardioversion if TRx doesnt convert

169
Q

unstable v tach with a pulse

A

sedate, cardiovert, IV meds as for PVCs, O2

170
Q

what is the Tx for v fib or v tach without a pulse

A

check pulse, call for help, CPR, defibrillate, CPR (5 cycles/2 minutes), IV, intubate, epi orvasopression…etc

171
Q

what is the Tx for ventricular irritability

A

Mg or K supplement

172
Q

what is the Tx for asystole and PEA

A

epi, vasopression, treat underlying cause

173
Q

what are the 2 most common and easily reversible causes of PEA

A

hypovolemia and hypoxia

174
Q

what PVCs are dangerous

A

more than 6 a minute, run of 3, bifocal, multifocal, cuplet

175
Q

Cardiac conduction

A 
SA node
internodal pathways
AV node
Bundle of HIS
Bundle branches
purkinje fibers
176
Q

a standardized performance measure that provides a way to rate the performance of Beebe in comparision to other hospitals

A

quality measure

177
Q

adult CPR

A

30:2

178
Q

sinus rhythm

A

reqular PQRST, rate 60-100

179
Q

sinus bradycardia

A

regular PQRST, rate less than 60

180
Q

sinus tachycardia

A

regular PQRST, rate more than 100

181
Q

sinus arrhythmia

A

irregular PQRST (3 or more squares difference 0.12), rate less than 100

182
Q

P wave may be in previous T wave, PR shortened, PQRST came too soon, no compensatory pause

A

PAC

183
Q

3 or more PACs in a row with rate of greater than 140, PQRST all look the same

A

AT

184
Q

sudden start and end of AT, sudden doubling or tripling of HR

A

PAT

185
Q

saw tooth pattern variable conduction to ventricle, QRS look same

A

a flutter

186
Q

R-R-R intervals are off, wavy baseline, no P wave, irregular irregularity, QRS look the same

A

a fib

187
Q

may refer to AT, PAT, PSVT, junctional tachycardia, rate over 100

A

SVT

188
Q

inverted P before or after QRS, or no P with a QRS, beat came too soon, QRS looks normal, regular rhythm, no compensatory pause

A

PJC

189
Q

QRS greater than 0.12, R opposite T wave, wide bizarre, beat came too soon, complete compensatory pause

A

PVC

190
Q

3 or more PVCs in a row, uniform pattern wide and bizarre

A

V tach

191
Q

irregular waves, chaotic, no pattern no PQRST

A

v fib

192
Q

Stable PR greater than 0.2 seconds

A

first degree AV block

193
Q

gradual prolongation of PR interval until QRS is dropped

A

second degree AV block type 1 (Wenckebach)

194
Q

stable PR when present, Ps without QRS

PR is constant

A

second degree AV block type 2

195
Q

no stable PR interval, atria and ventricles beat independently, HR 20-40

A

third degree AV block

196
Q

blood flow through heart

A 
superior/inferior vena cava
right atrium
tricuspid valve
right ventricle
pulmonary vavle
pulmonary artery
lungs
aveoli (gas exchange)
pulmonary vein
left atrium
mitral valve
left ventricle
aortic valve
aorta
body

N202 (8 decks)

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