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Nur 3010 exams > cardiac assessment & conduction abnormalities > Flashcards

cardiac assessment & conduction abnormalities Flashcards

1
Q

review: what are the 3 layers of the heart

A

endocardium, myocardium, epicardium

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2
Q

where does contractility occur in the heart

A

myocardium

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3
Q

4 chambers of the heart

A

R atrium, R ventricle, L atrium, L ventricle

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4
Q

atrioventricular valves (2)

A

tricuspid/mitral

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5
Q

semilunar valves (2)

A

aortic/pulmonic

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6
Q

what are valves connected to

A

cartilage connected to walls of heart via tendons

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7
Q

coronary arteries

A

blood supply of heart
- starts at Aorta -> R coronary artery
- L main (widow maker) -> circumflex and Left anterior descending

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8
Q

conduction of heart sequence

A

SA node -> AV node -> ventricles

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9
Q

Review: depolarization

A

electrical activation of cell caused by influx of sodium into cell while potassium exits cell

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10
Q

review: repolarization

A

return of cell to resting state caused by reentry of potassium into cell while sodium exits -> can’t depolarize again

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11
Q

review: what are the 2 refractory periods

A

effective refractory period
relative refractory period

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12
Q

effective refractory period

A

phase in which cells are incapable of depolarizing

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13
Q

relative refractory period

A

phase in which cells require stronger-than-normal stimulus to depolarize

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14
Q

how is a contraction formed

A

calcium IN -> mycocardial cells -> potassium OUT -> increases positive charge -> depolarizes cell -> allows for contraction

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15
Q

healthy myocardial cells have what 6 properties

A

automaticity, excitability, conductivity, contractility, rhythmicity (pattern), refractoriness (no stimulus)

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16
Q

___________/_________ maker potential changes based on location

A

automaticity/pace

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17
Q

SA node

A

60-100 BPM (innervated by SNS/PNS to increase/decrease rate)
- ex: scared -> catecholamines -> increase HR -> PNS -> signal to slow down -> automaticity -> slower rate

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18
Q

AV node

A

40-60

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19
Q

Bundle of HIS

A

25-40
30-40

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20
Q

Purkinje fibers

A

20-40

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21
Q

what is the cardiac cycle

A

events that occur in heart from beginning of one heartbeat to next
- number of cycles depends on HR
- 3 major sequential events: diastole, atrial systole, ventricular systole

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22
Q

diastole

A

start (relaxation)

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23
Q

atrial systole

A

atria contract first -> blood intro ventricles -> Lub (S1)

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24
Q

ventricular systole

A

ventricles with volume -> fill with blood -> aorta/pulmonic -> valves close -> Dub (S2)

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25
Q

what is cardiac output

A

amount of blood pumped out of the L ventricle in L/min

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26
Q

CO equation & normal amount

A

CO = SV x HR
- normal CO: 4-8L/min

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27
Q

what is stroke volume

A

amount of blood ejected with each beat
- determined by L ventricle

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28
Q

SV: preload?

A

degree of stretch of cardiac muscle fibers at end of diastole

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29
Q

SV: afterload

A

resistance to ejection of blood from ventricle

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30
Q

SV: contractility

A

ability of cardiac muscle to shorten in response to electrical impulse
- TIP: cardiac myocytes can squeeze/shorten if triggered by: calcium

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31
Q

ejection fraction

A

percent of END DIASTOLIC VOLUME ejected from the L ventricle with each heart beat
- normal EF: 50-75%

TIP: R ventricle ejects blood -> Lungs. L ventricle stronger than R ventricle

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32
Q

what are the 2 influencing factors of cardiac output

A

1) control of HR
2) control of SV

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33
Q

how does HR affect CO (2)

A

1) autonomic nervous system: SNS (increases HR r/t increased catecholamines & excess thyroid hormone) /PNS (travels to vagus nerve to slow HR) -> changes in metabolic demand r/t stress, exercise, and illness = changes in CO
2) baroreceptor reflex (homeostasis): nervous system bundles (increase HR r/t blood pressure) -> accommodates changes in pressure by releasing discharge, transmitting impulses to medulla -> initiates PNS -> (elder) decrease HR and BP

TIP: opposite for hypotension = decrease baroreceptor -> increase BP/HR

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34
Q

How does SV affect CO (preload? after load? contractility?)

A

augmented by catecholamines, SNS, medications
- preload: determined by volume status
- afterload: determined by vascular resistance
- contractility

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35
Q

what is contractility decreased with? (5)

A
  • hypoxia
  • hypoxemia
  • acidosis
  • some drugs (beta-blockers - decrease contractility, NOT digoxin - increase contractility)
  • viable heart muscle available, etc.
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36
Q

assessment of cardiovascular system

A

(COLDSPA)
health hx (resp, cardiac, everything)
demographic information (environmental exposures)
family/genetic hx
cultural/social factors
risk factors: modifiable/non-modifiable

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37
Q

what are modifiable risk factors for cardiovascular

A

lack of exercise
diet
obesity
high BP
lipid panels
blood glucose

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38
Q

what are nonmodifiable risk factors for cardiovascular

A

age
family hx
sex (female/male)
ethnic background

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39
Q

common sx of cardiovascular system (6)

A
  • chest pain/discomfort
  • pain/discomfort in other areas of the upper body
  • SOB/dyspnea
  • peripheral edema, wt. gain, abd distentino
  • palpitations (sometimes)
  • unusual fatigue, dizziness, syncope, change in LOC = decrease CO = decrease BF = brain
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40
Q

past health, family, and social hx (8) considerations

A
  • medications
  • nutrition
  • elimination
  • activity/exercise
  • sleep, rest
  • self perception/self concept
  • roles and relationships
  • coping and stress
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41
Q

physical assessment considerations (7)

A
  • general appearance (pale? ashen? diaphoretic? temperature change?)
  • skin and extremities (lack perfusion? bruising?)
  • BP, othrostatic changes (15-30 seconds, teach slow movements)
  • arterial pulses (radial, femoral, DP/PT, carotid)
  • Jugular vein pulsations
  • HR, inspection, palpation, auscultation
  • assessment of other systems

TIP: good central pulse =/= BP

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42
Q

lab tests for cardiovascular

A
  • cardiac biomarkers (troponin HIGH SENSITIVITY, creatine kinase and CK-MB)
  • blood chemistry, hematology, coagulation (electrolytes, renal function - contrast)
  • brain (B-type- natriuretic peptide (BNP)
  • lipid profile: cholesterol (total: <200, HDL-good >60, LDL-bad <100, triglycerides <150)
43
Q

describe troponin high sensitivity

A
  • sustains cardiac injury
  • guides interventions
  • myocardial injury (heart attack) -> body releases troponin (cardiac biomarker) -> decreases blood flow to heart
  • (muscle break down of the heart) or (heart mnucle injury)
44
Q

describe BNP

A
  • chest tightness
  • released when there is cardiac muscle stretch
  • key indicator for HEART FAILURE
    ex: CHF: ventricles stretch d/t increased volume -> increase BNP
45
Q

electrocardiography (describe)

A

12 lead (one point in time, tells us cardiac damage) vs. continuous (hardwire or ambulatory monitoring - heart monitor)
- identifies RATE and RHYTHM
- useful for identifying ST elevation

46
Q

what do leads determine

A

waveforms
- split into 4 sections of 3 seconds (12 total) - 6 seconds on exam (2 sections)

47
Q

cardiac stress test (type (2), patient instruction, meds)

A
  • exercise stress test
  • pharmacologic stress test
  • pt. instructed to AVOID stimulants pre-procedure (coffee, smoking)
  • beta blockers, ca channel blockers, or other rate control drugs may be held (allow us to see more information about heart function)
48
Q

describe exercise stress test

A
  • pt. walks on treadmill with intensity progressing according to protocols
  • ECG, echo, VS, symptoms monitored (chest pain? SOB?)
  • terminated when target HR is achieved
  • if chest pain or 150 HR = patient FAILED
49
Q

describe pharmacologic stress test (what, meds?)

A
  • agents given to mimic exercise if patient cannot handle actual test -> physical impair
  • dobutamine - synthetic sympathomimetic drug
50
Q

describer ECHO (echocardiography)

A

(GOLD STANDARD FOR CARDIAC TEST, q6 months outpatient)
largely noninvasive US test that is used to
- measure ejection fraction
- examine size, shape, and motion of cardiac structures
- identifies valve disease
- easy to perform
most common: transthoracic - against chest wall, tranesophageal (TEE) - same but in esophagus

51
Q

describe cardiac catheterization (what, Left, right)

A
  • what: invasive procedure used to diagnose (and treat) structural and functional diseases of the heart and great vessels (ex: coronary ds.)
  • right heart Cath: pulmonary artery pressure and oxygen saturations may be obtained, biopsy of myocardial tissue may be obtained
  • left heart Cath: involves CONTRAST, identifies blockages that can be treated via percutaneous coronary intervention (PCI) - diseased arteries are “ballooned” and stented with specialized catheters (keep vessels open)
  • usually use femoral artery or radial artery
  • if thin blood -> sheath stays in vessel (one way valve, water tight seal)
52
Q

nursing care post Cath (8)

A
  • observe Cath site for bleeding, hematoma (MOST IMPORTANT)
  • assess peripheral pulses
  • evaluate temp, color, cap refill of affected extremities
  • screen for dysrhythmias
  • maintain BR for 2-6 hours
  • instruct patient to report chest pain, bleeding
  • monitor for contrast induced nephropathy
  • ensure patient safety (Manual pressure Q30 min post Cath)
53
Q

dysrhythmias (what, irregularities, concerns, diagnosed)

A

disorders of formation/conduction (or both) of electrical impulses within heart
- irregularities in: rate, rhythm, or both
- concerning when the alter blood flow and hemodynamics (change BP)
- diagnosed by: ECG waveforms (patient goes in and out rhythm (continuous/12lead)

54
Q

2 types of dysrhythmias

A

atrial
ventricular

55
Q

atrial dysrhythmias type 3

A

premature atrial complex
atrial flutter
atrial fibrillation

56
Q

ventricular dysrhythmias

A

premature ventricular complex
ventricular tachycardia
ventricular fibrillation
ventricular asystole

57
Q

normal conduction pathway

A

SA node
AV node
bundle of HIS
right and left bundle branches
purkinje fibers
- depolarization: stimulation (contraction) = systole
- repolarization: relaxation = diastole

58
Q

components of telemetry (3)

A

electrodes
apply electrodes
5 lead wire system

59
Q

describe electrodes

A
  • disposable disks consisting an adhesive ring with a conductive substance in the center
  • conductive media conducts skin surface voltage changes through color coded wires
60
Q

apply electrodes

A
  • apply on dry skin (no alcohol)
  • remove dead/dry skin before application with rough paper or cloth
  • clip hair
  • place on skin over areas with minimal muscle activity to avoid artifact
  • change as needed or daily
  • change batteries for portable monitors as needed
61
Q

describe 5 lead wire system

A
  • most common set up in acute & critical care
  • white, black, and red electrodes are located in identical positions to the 3 lead set
  • green electrode is located opposite the red electrode
  • brown precordial lead V1 is located to the right of the sternal border at the 4th intercostal space
  • precordial vectors may be moved to translate different sections of the heart
62
Q

what is P wave

A

atrial depolarization

63
Q

what is QRS complex

A

ventricular depolarization

64
Q

what is t wave

A

ventricular repolarization

65
Q

ECG analysis

A

heart rhythm & rate
P wave evaluation
PR interval evaluation
QRS evaluation
QT interval evaluation

step 1: rhythm?
step 2: rate? - calculate heartbeat by 6 second method (count # QRS in 6 sec, multiple by 10)

66
Q

what to do after rate?

A

atrial conduction
- are p waves present
- p waves per QRS?
- p waves before QRS?
- shape of p wave? do they look alike (if not = issues)
- more p waves than QRS? (1:1 ratio)

67
Q

what happens if ectopic beats

A
  • ask if there are abnormal shaped P waves in relationship to these beats? SA node fire independently? extra beats
  • are the p waves buried? no av blocks
68
Q

describe AV conduction

A

allows for atrial kicks - maximize for filling ventricle
- is PR interval normal? 0.12-0.20 (atrial kick)
- are PR intervals the same?
- if PR intervals different, is there a pattern? (specific to AV blocks)

69
Q

describe ventricular conduction

A
  • ORS complexes normal? 0.06-0.12
  • QRS complexes of same duration (1 QRS/ p wave)
  • QRS complexes look the same?
70
Q

describe QT intervals

A
  • looking for elevation or depression
  • timing can be prolonged with drugs (antipsychotics, abx, zofran = taken all together)
  • longer -> longer refractory periods -> dangerous arrhythmias
71
Q

normal sinus rhythm

A
  • rate: 60-100 bpm
  • normal PR interval
  • normal QRS
  • 1 P wave for every QRS complex (t wave)
72
Q

sinus Brady

A
  • rhythm: regular (slow)
  • rate: <60 bpm
  • normal p wave, preceding each QRS
  • normal PR, QRS interval, T wave, QT interval
73
Q

clinical considerations for sinus Brady(3)

A

signs of poor perfusion:
- low BP, decreased LOC, dizziness, syncope, chest pain, dyspnea
possible causes:
- cardiac ischemia, HR slowing meds (digoxin, beta blockers, ca channel blockers, antiarrhythmics like amirodarone and betapace)
non cardiac disorders:
- electrolyte imbalance (hyperkalemia), vagal responses, hypothermia, hypothyroid

74
Q

treatment for sinus Brady

A
  • asses ABC’s
  • assess VS, IV patency
  • Administer O2
  • transcutaneous external pacemaker (sedate: can change rate, painful) (send electrical impulse to heart)
  • IV dopamine got 2-10 mcg/min (1mg in 500 ml 0.9 NS @ 1-5 ml/min)
  • atropine (0.5-1.0 mg every 3-5 minutes to a total of 0.4 mg/kg)

tip: not uncommon for athletes to have slow HR, tx is reserved for sx., SB that occurs with sleep is not abnormal

75
Q

sinus tachycardia

A
  • rhythm: regular atrial and ventricular
  • rate: >100 bpm
  • P waves for of normal size and shape preceding QRS, may be superimposed on preceding t wave with increasing HR
  • PR intervals, ORS complex, T waves normal
  • OT interval usually shortens
76
Q

clinical significance of sinus tachycardia (what, assess?, causes, presence of?, tx?)

A
  • decreases cardiac output by REDUCING DIASTOLE (increase myocardial O2 demand in unhealthy heart)
  • assess: ABCs, VS, chest pain, dyspnea, palpitations
  • causes: hypovolemia, pain, anxiety, physiologic stress (eg. infection, sepsis, anemia, shock states), fever (anything that stimulates SNS)
  • presence of stimulants (caffeine, nicotine, amphetamines, OTC dugs, illicit drugs)
  • tx: treat underlying cause if possible (consider slowing HR w/ beta blockers, calcium channel blockers, be careful d/t compensatory mechanisms) (provide reassurance and reduce fear and anxiety if possible)
77
Q

describe sinus arrhythmia

A
  • GAP
  • irregularity
78
Q

electrocardiography atrial rhythms (PACs)

A
  • extra beats originating in the atria
  • conducted (rhythm -> QRS)/ non-conducted (extra P wave) PACs
  • pathway matters: how do we know if it comes from a different pathway (clue = ds)
  • look at causes: ICU pt may have more PACs than other pts (will increase OT)

TIP: extra P wave, quite common

79
Q

describe atrial fibrillation (rate, what, effects)

A
  • atrial rate of 350-600 times/minute of disorganized chaotic stimulus
  • AV node acts as a buffer zone to the ventricles
  • coordinated atrial emptying during diastole is IMPAIRED
  • effects include: loss of atrial kick (decrease CO 30%), pooling and clotting of blood in atria (subsequent thromboembolism, strokes)
80
Q

diagnostic characteristics of atrial fibrillation (rhythm, rate, pqrst complex)

A
  • rhythm: irregularly irregular
  • atrial rate: indiscernible; often >400/min
  • ventricular rate: <100 - 150/min (regular if given meds, tachycardic with meds = RVR (rapid ventricular response)
  • P waves absent, PR internal indiscernible
  • QRS complex <0.12 sec., T wave and QT interval indiscernible
81
Q

risk factors for AFIB

A
  • HTN
  • advancing age
  • dilated L atrium
  • Valve disease (aortic or mitral)
  • coronary artery disease
  • elevated glucose (uncontrolled)
  • thyroid disease (typically hyper, but also hypo)
82
Q

complications r/t AFIB (3)

A
  • loss of ventricular regulation (too much impulse going towards AV node can cause “rapid ventricular response” RVR, rates exceed normal SR & diminish diastolic filling (decrease SV), tx with rate/rhythm control drugs: beta, calcium, amiodarone)
  • loss of coordinated emptying (tx with DOACs (perdaxa, eliquis) or heparin IV (quicker)
  • loss of atrial systole (30% CO)
83
Q

rate/rhythm control in afib (meds) (3)

A

amiodarone (anti arrhythmic): brings back to SR
diltiazem (calcium channel blocker): control rate (decrease ventricular response)
verapamil (calcium channel blocker: control rate (ventricular response)
- sometimes beta blocker to reduce sympathetic stimulation of the heart (metoprolol)

84
Q

stroke preventions in afib (CHA2DS2VASc)

A

(higher score = more aggressive with anticoagulation)
CHA2DS2VASc scoring system
- C = congestive heart failure
- H = HTN
- A2 = age 75
- D = diabetes
- S2 = stroke
- v = vascular disease
- A = age 65
- Sc = sex category (female)

85
Q

score risk recommendation for LT anticoagulation

A

0 = 1.9% adjusted stroke risk (no therapy indicated)
1 = intermediate (anticoagulation recommended risk vs. benefit discussed with patient, ASA strongly advised at least)
2 or more (3 for women) = anticoagulation highly recommended, high (CHA2Ds2VASc) or intermediate (CHADS2 classic), DOAC unless there are reasons to avoid it OR Coumadin if valvular disease present

86
Q

DOAC vs warfarin

A

warfarin
- slow onset
- variable dosing
- vitamin K affect
- many drug interactions
- requires monitoring
- offset is long
DOAC (apixiban (eliquis), dabigatran (pradaxa), rivaroxaban (xarelto)
- rapid onset
- fixed dosing
- no food affect
- few drug interactions
- no monitoring
- offset is shorter

87
Q

afib treatment (4)

A

1) electrical cardioversion (resets heart rhythm)
- must be on anticoagulation for a minimum 4 wks, with a TEE to r/o clot
2) catheter ablation therapy (similar invasiveness to cardiac Cath)
3) cox maze procedures (requires open heart approach)
4) left atrial appendage occlusion (watchman device) - not candidate for blood thinners, mesh net that sit in atria

88
Q

atrial flutter (rate, pqrst)

A
  • atrial rate: 200-400 bpm, will be treated than ventricular rate (organized atrial rhythm)
  • abnormal p waves referred to as flutter or “saw tooth waves”
  • QRS complex will usually be normal
  • PR interval: atrial regular, ventricular irregular
  • QT: indiscernible

tip: atria tries to stimulate AV node, another impulse fills atria

89
Q

aflutter mangement (4) depends on?

A
  • dependent on ventricular response rate
  • pharmacologic cardioversion: (ibutilide, sotalol, procainamide, amiodarone)
  • pharmacologic rate control: (calcium channel blockers, beta blockers, digoxin)
  • non pharm interventions: cardioversion (electrical), overdrive atrial pacing (set atrial higher, slowly bring down)
  • permanent termination: radiofrequency ablation
90
Q

ventricular arrhythmias

A

PVCs
Vtach
Vfib
Asystole
blocks (not on exam)

91
Q

premature ventricular contractions (PVCs) where, pqrst, tx)

A
  • originate in ventricles below bundle of HIS from different pathway
  • P waves absent d/t no atrial depolarization
  • T waves and QRS complexes deflect in opposite directions
  • QRS complex is wider than normal
  • can be normal with no tx or a warning of ventricular irritability

tip: random contractions decrease AV node, no stimulations

92
Q

managing PVCs (tx)

A
  • assess need for tx
  • assess for sx
  • treat cause: assess for electrolytes, drugs that cause ventricular ectopy
  • pharmacologic management: beta blockers to reduce sympathetic stimulation, antidysrhythymic drugs
93
Q

ventricular tachycardia (VT) (what, rhythm?, rate?, pqrst?)

A
  • 3 or more PVCs in row
  • unable to determine atrial rhythm; ventricular rate >100/min
  • ventricular rhythm may or may not be regular
  • no p waves and unmeasurable PR intervals
  • QRS complex is wide and bizarre with T wave in the opposite direction (varies but usually)
94
Q

Vtach management (stable, unstable, pulseless)

A

dependent upon patient condition
- pulseless VT: life threatening; unsynchronized defibrillation
- unstable VT: electrical cardioversion (AED)
- stable VT: no loss of cardiac output, amiodarone or what? talk, slight palpitation

95
Q

ventricular fibrillation (what, management)

A

life threatening (no contraction at all, no CO)
- mangement: defibrillation, cardiopulmonary resuscitation

96
Q

ventricular fibrillation diagnostics

A
  • chaotic rhythm
  • rate: indeterminate
  • no p waves, immeasurable PR
  • indiscernible t waves
  • waveform may appear as a wavy baseline
  • this is one of the PRIMARY LETHAL ARRHYTHMIAS
97
Q

clinical significance of VT/VF (stable, unstable, pulseless)

A
  • stable patients in VT may convert with Amiodarone 150 mg over 10 minutes
  • unstable patients in VT require cardioversion
  • unresponsive patients in VT require defibrillation
  • in vfib, ventricles are quivering instead of contracting reducing CO to ZERO
  • ABCs are of VITAL important (check pt responsiveness, defibrillate/AED if pt. is pulseless, CPR until defibrillator arrives)
98
Q

asystole (what, evidence, pqrst, etiology)

A
  • cardiac standstill or total absence of ventricular electrical activity
  • evidenced clinically by no pulse or CO
  • no QRS seen on monitor
  • caused by: ischemia, hypoxia, drug OD, electrolyte disturbances, traumatic arrest
  • think about cause as much as treatment (tx with CPR and EPI 1 mg every 2-5 min)
99
Q

pacemakers (types, indication)

A

3 common types: transcutaneous, transvenous, permanent/implanted (can include automated internal cardiac defibrillator AICD)
- indicated for unstable Brady arrhythmias (open heart surgery)

100
Q

external pacing (transcutaneous) pacemaker

A
  • electrodes placed on chest delivers impulses through chest wall
  • chest wall impedance often causes great discomfort or inability to capture
  • location: right upper, left lower, anterior/posterior
101
Q

internal/implanted pacer

A

consists of:
- generator/battery
- pacing leads (stay in place forever)
- somtimes a defibrillator lead (automatic)
- outpatient procedure (battery change)

102
Q

3 functions of pacemakers

A

1) firing or pacing: pacer delivers impulses per programmed rate. seen on monitor by observable spike followed by p wave (f atria stimulated) or QRS (ventricle is target chamber)
- may prolong QRS
- why would we want atrial lead? atrial kick back
2) capture target chamber: successfully depolarizes the target chamber (atria or ventricle) as evidenced by monitor by a p wave or QRS after the spike
- if new pacemaker and no capture, turn pt on L side (make pacers float in vent)
3) sensing: pacers ability to recognize presence of absence of intrinsic electrical activity. (if too sensitive) it will recognize inappropriate internal activity (such as skeletal muscle depolarization) and not fire when necessary (not sensitive) it won’t recognize intrinsic activity and fire on top of one’s own electrical stimulations

103
Q

automated internal cardiac defib (AICD) (what, indicated, in conjunction with)

A
  • allows for detection and termination of life threatening arrhythmias
  • indicated for: post MI w/ severe LV dysfunction, EF less than or equal to 35%, non ischemic dilated cardiomyopathy w/ low EF
  • usually in conjunction with anti-arrhythmic meds to minimize risk of electrical discharge
104
Q

key interventions for arrhythmias (9)

A
  • assess for chest pain
  • evaluate rhythm
  • assess and monitor cardiovascular status
  • complete assessment of peripheral circulation
  • monitor VS frequently
  • evaluate client’s response to dysrhythmias
  • monitor appropriate lab tests (lytes, mg/phos/ca/k, cardiac enzymes (trop vs BNP)
  • administer anti-arrhytmics
  • promote stress reduction

Nur 3010 exams (13 decks)

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