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Cardiovascular > ECG/Dysrhythmias > Flashcards

ECG/Dysrhythmias Flashcards

1
Q

Left main

A

Left main (widow maker, CABG, cannot do angiography)

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2
Q

Left anterior descending artery

A

feeds anterior wall

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3
Q

Circumflex artery

A

lateral left wall of the heart

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4
Q

Right coronary artery

A

feeds inferior wall of the heart

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5
Q

posterior descending artery

A

posterior wall of the heart

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6
Q

cholesterol

A

less than 200

increases risk for CAD

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7
Q

LDL

A

Less than 160
main method of transport of cholesterol and triglycerides into the cell
Harmful effects in the deposition into cell walls

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8
Q

HDL

A

Transport cholesterol away from the tissues and cells of the artery wall to the liver for excretion
inverse relationship of elevated HDLs and CAD

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9
Q

BNP and what is it used for

A

Neurohormone that helps reduce BP and fluid volume
Secreted in the ventricles in response to increased preload and afterload in elevated ventricular pressure
BNP increases as the ventricular walls expand from increased pressure so it is helpful to monitor heart failure
obtained quickly used effectively in the ER
Can also indicate a PE, MI, Ventricular Hypertrophy
higher than 100= likely heart failure

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10
Q

C reactive protien and hemocystine

A

Produced in the liver in response to systemic inflammation
inflammation has a role in the development of artherosclerosis
predicts CVD risk
people with high hs-crp levels (3 or higher) are at an increased risk for CVD
Amino acid linked to the development of arteriosclerosis because it damages endothelial lining and promotes thrombus formation
An elevated blood level of hs is thought to increase r/f CAD, CVA, PVD, but not an independent predictor of CAD

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11
Q

Coagulation studies

A

injury to the vessel wall initiates the formation of thrombus
coagulation cascade is activated
complex factor interactions among phospholipid , calcium, clotting factors that convert prothrombin to thrombin
coagulation studies are routinely preformed before invasive procedures such as cardiac cath, electrophysiology, cardiac catheterization

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12
Q

nursing interventions after cardiac catheterization

A

fast 8-12 hrs before procedure
can not drive home
IV meds given but will be on hard table for 1-2 hrs
explain about palpitations
cough and deep breathing
Valvsa manuvar
observe site for bleeding and hematoma
check dorsal pedis and posterior tibalis q15 minutes 1hr, 30min 1 hr, q4 till discharge
assess bp, HR evaluate temp, color, capillary refill of effected extremity
dysrythmia after wards
bed rest 2-6 hours

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13
Q

CVP and what is it used for ?

A 
central venous pressure 
pressure measured in the right atrium or vena cava 
equal at the end of diastole 
normal in 2 to 6 mmHg 
main reason for monitoring= hypovolemia
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14
Q

normal CVP

A

2 to 6 mmHg

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15
Q

Cardiac action potential (depolarization)

A

depolarization = electrical activation of cell caused by influx of sodium into the cell while the potassium exits the cells

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16
Q

Repolarization

A

where the return of cell resting state caused by the reentry of potassium unto the cell while the sodium when the cell exits

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17
Q

refactory period

A

phase in which cells are incapable of depolarizing

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18
Q

relative refactory period

A

phase which cells require stronger than normal action potential

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19
Q

vectors

A

each person has a different mean vector deviated

has an axis deviated to the right or the left

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20
Q

equation for regular heart beats

A

count small blocks, divde into 1500

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21
Q

equation for irregular heart beats

A

6 second strips

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22
Q

causes of sinus brady

A

lower BMR, needs vagal nerve stimulation, athletic training, hypothyroidism, sleep medications, calcium channel blockers, increased ICP, sinus node dysfunction, ca channel blockers, CAD

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23
Q

sinus brady can happen what type if MI?

A

inferior wall MI

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24
Q

trx of sinus brady

A

atropine 0.5mg of IV bolus q 3 to 5 minutes, max dosage of 3 grams

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25
Q

causes of sinus tachycardia

A

stress, blood loss, anemia, hypovolemia, heart failure, fever, catecholamines, aminophylline, atropine, caffeine nicotine, enchanced automacity of the SA node
autonomic dysfunction- spinal cprd injured dt postural orthostatic tachycardia
may cause syncope
ablation of SA node that causes abnormality if there is issues with quality of life

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26
Q

what happens to BP and CO with tachycardia

A

they can decrease which may cause syncope.. if chronic this may cause pulmonary edema

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27
Q

treatment of sinus tachycardia

A 
Narrow QRS: 
Adenosine 
Beta blockers 
Ca Channel blockers 
Wide QRS: 
Procainamide
amioderone 
sortalol
28
Q

if someone with sinus tachy is hemodynaimically unstable what is the trx of choice?

A

cardioversion

29
Q

why do runners get a fib?

A

hypertrophy of the left ventricle

30
Q

causes of A fib

A 
structural cardiac defects 
anemia
age
kidney disease 
valvular heart disease 
cardiomyopathy 
hypertension 
DM
Hyperthyroidism 
obstructive sleep apnea
31
Q

signs of a fib

A

light headness, chest pain, dizziness, fatigue, breathlessness

32
Q

address what modifiable risk factors for people with a fib

A

smoking cessation
exercise
weight management
ETOH or drug abuse

33
Q

stroke prevention

A

untreated a fib can cause thromboembolism
anticoags are used to prevent stroke
Coumadin- assess for bleeding

34
Q

CHADS 2

A

which stands for CHF, HTN, age 75 or older DM, prior CVA/TIA, clinical prediction to rule out assessing the risk of stroke in patients with nonvalvular a fib and with our significant aortic or mitral valve disorders
The higher the chads score, the higher the stroke risk, anticoags will still be given even if the a fib converts to NSR

35
Q

anticoags used to treat a fib

A

coumadin
jantoven
unfractionated heparin
LMW Heparin

36
Q

New thrombin and factor Xa inhibitors

A

antiplatelet drugs, such as clopidorgel (plavix)

37
Q

asprin alone

A

no longer reccomended to treat a fib

38
Q

electrical cardioversion for a fib

A

conversion to NSR is shown to decrease symptoms
used in new onset a fib
younger patients
antiarythmic, electrical cardioversion, transesophegeal echocardiogram, patient may be on warfarin for 4wks post procedure
does not work for everyone, for the people with serious lifestyle changes

39
Q

medications used to treat persistant A fib

A

Av conduction blocker
Digoxin, cardizem
Beta blocker
propanolol, atenolol, metoprolol, esmolol
calcium channel blockers
diltizem, verapamil, do not use if pt has impaired ventricular function

40
Q

COPD

A

no beta blockers

41
Q

P wave and T wave in patients with a flutter

A

P wave has a saw tooth pattern

T wave is hidden in the sawtooth pattern

42
Q

medical management of atrial flutter

A

use vagal manuver
administration of adenosine which causes sympathetic block slowing the conduction of the AV node
this may eliminate the tachycardia

43
Q

max shock for some one in shock w a flutter

A

250 joules

44
Q

causes of a PVC

A

nicotine, caffinee, alchohol

cardiac ischemia, infarction, increased work load, digitalis toxicity, hypoxia, acidosis or hypokalemia

45
Q

trxx of continuous pvcs

A

amioteriol or sortalol

46
Q

criteria to treat PVCs

A

multifocal
polymorphic
occur on the t wave

47
Q

treatment of VT

A

antiarrythmic medication
antitachycardia pacing
direct cardioversion or fibrillation
procainamuide for those with stable vt and are not having an MI
amioderione for pt with impaired cardiac function
cardioversion for monophasic VT in a symptomatic patient

48
Q

treatment of choice in v tach with out a pulse

A

defibrillation

49
Q

if EF is less than 35 % then what in vt pt

A

implantable cardioverter defibrilator

50
Q

if EF is more than 35 % then what in vt pt

A

managed by amioderone

51
Q

what is used if a pace maker is needed but their insurance refuses to cover it

A

a zole life vest

Provides defibrillation if absolutely needed

52
Q

causes in vt

A

more than 100 bpm
pt w large mis
pt unresponsive and pulseless
tickling ventricles in cardiac cath lab

53
Q

if pt has afib or a flutter and is in vt or vf then what

A

the p waves are unrecognizable because the contractions in the ventricle are so strong

54
Q

what is a PAC and what does it look like?

A

p wave comes early on the ECG, the rest of the beat follows

55
Q

characteristics and treatment of of V fib

A

abscence of heart beat palpabel pulse and abscent respirations death is immanent
early defib is critical for survival
do CPR
Epi after 1st unsucessful defib and every 3 to 5 minutes afterwards
vasopressin may be given if cardiac arrest continues
mild hyperthermia occurs

56
Q

treatment of asystole

A 
CPR 
intubate
IV access 
bolus IV epi in 3-5 minute intervals 
vasopressin 
hypothermia 
transfer to higher level of care
57
Q

nursing care of a patient with a dysrythmia

A 
causes 
assess CO and o2 
accurate Hx due to previous condition 
meds OTCs included 
patients "perception of dysrhythmia" 
drugs, nicotine, caffine, ETOH, OTCs 
any life stycle changes
58
Q

physical assessment of someone with a dysrythmia

A 
skin is pale and cool 
signs of fluid retention 
ex. JVD, lung congestion 
decreased CO (LOC is first to change) 
rate, rhythm of apical, pulses 
heart sounds 
BP and Pulse pressure
59
Q

turn patient one what side helps w dysrhythmias and heart function

A

Left side

60
Q

AV block, PR intervals is outside the limits of what?

A

0.2-0.12seconds

61
Q

a small block equals how many seconds?

A

0.04 seconds

62
Q

A large box (5 little boxes)

A

0.2 seconds

63
Q

watch youtube video on heart blocks

A

https: //www.youtube.com/watch?v=XXu36p56ybg
https: //www.youtube.com/watch?v=HBChhz-_xz0

64
Q

normal PR interval

A

0.8-0.20 seconds

65
Q

normal QRS complex

A

0.08-0.10 seconds

66
Q

normal QT interval

A

0.4-0.43 seconds

Cardiovascular (5 decks)

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