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Cardio Sem 2 > Cardio Exam 3 > Flashcards

Cardio Exam 3 Flashcards

1
Q

EKG lead locations

A

V1 - 4th intercostal space to the right of the sternum
V2 - 4th intercostal space to the left of the sternum
V3 - directly between V2 & V4
V4 - 5th intercostal space at midclavicular line
V5 - level with V4 @ left anterior axillary line
V6 - level with V5 @ left midaxillary line (under the armpit

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2
Q

electrical impulses generates heart beat and is affected by which electrolytes

A

sodium, potassium, magnesium, calcium

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3
Q

normal rate of SA node

A

60-100 BPM

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4
Q

Normal rate of AV node

A

40-60 BPM

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5
Q

Normal rate of bundle of his

A

20-40 BPM

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6
Q

cardiac conduction system pathway

A

SA -> interatrial -> internodal bundles ->AV -> bundle of his -> purkinje

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7
Q

what EKG finding is indicative of SA node firing? What does it mean? How should they look?

A

P-wave

atrial depolarization

rounded

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8
Q

PR interval

What could it indicate if it’s prolonged?

A

time it takes for impulse to travel from SA node to AV node

a block

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9
Q

Normal PR interval

A

0.12 - 0.20

3-5 small squares

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10
Q

QRS complex

A

ventricular depolarization and atrial repolarization

time for electrical impulse to travel from AV node through ventricles

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11
Q

Normal QRS complex

A
  1. 06-0.10

1. 5-2.5 little boxes

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12
Q

T-wave

A

follows the QRS complex

ventricular repolarization (resting state)

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13
Q

ST segment

A

time from completion of contraction to recovery

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14
Q

how to calculate HR from EKG

A

count number of complexes in a 6 second strip x10

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15
Q

Normal sinus rhythm EKG

A 
regularity of rhythm
HR
P wave (present for every QRS)
PR interval
QRS interval
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16
Q

Cardio-selective beta blockers

A

MANBABE

metoprolol, metoprolol ER, atenolol, nebivolol, bisoprolol, acebutolol, betaxolol, esmolol

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17
Q

non-cardioselective beta blockers

A

propranolol, nadolol, labetalol, carvedilol, sotalol

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18
Q

causes of premature atrial contraction

A

hypoxia, cigarette smoking, heart failure, electrolyte imbalances, caffeine, alcohol, meds, fatigue, anxiety, stress

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19
Q

what is atrial fibrillation

A

electrical impulses initiated randomly from ectopic sites = atria quiver

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20
Q

is a PAC intermittent or continuous?

A

can be both

constant = increased risk for emboli

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21
Q

Afib RVR

A

(unstable Afib)

ventricular HR >100

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22
Q

Afib s/sx

A

hypotension, dizziness, pulse deficit, chest pain, palpitations, fatigue

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23
Q

Afib treatments

A 
anticoags (warfarin, eliquis, xarelto)
control rate and rhythm (BB, CCB, Dig)
cardioversion
cardiac ablation
surgery
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24
Q

digoxin functions

A

strengthen ventricular contraction, decreases conduction through the SA and AV node

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25
Q

digoxin normal range

A

0.5-2.0

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26
Q

s/sx digoxin toxicity

A

N/V/D, arrhythmias, vision changes, decreased appetie, confusion

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27
Q

what do you monitor while on digoxin

A

potassium (hypokalemia increases dig toxicity)
calcium (hypercalcemia increases risk for dig toxicity)
magnesium (hypomagnesemia increases for dig toxicity)

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28
Q

nursing implications for digoxin

A

monitor apical pulse for 1 full minute
hold if <60 bpm
monitor EKG during IV administration and 6hr after each dose

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29
Q

A flutter

a-flutter risks

A

coordinated electrical activity in the atria
not every atrial impulse goes into the ventricle

sawtooth pattern
no PR interval

risk = incomplete contraction -> blood stasis -> risk for stroke/embolism

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30
Q

A-flutter EKG

A

rhythm = atria is regular, ventricles could be regular or irregular
HR: atrial 250-350 bpm, ventricle depends on the underlying rhythm
P-waves: rapid coordinated, sawtooth pattern
PR interval: unable to determine
QRS: less then or equal to 0.1

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31
Q

PVC

A

premature ventricular contraction

very common

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32
Q

ventricular tachycardia

A

ventricles become the pacemaker instead of the SA node

33
Q

V-tach ekg

A 
rhythm: regular
HR: 150-250
Pwaves: absent
PR interval: unable to determine
QRS: >0.1, wide, bizarre looking
34
Q

Vtach treatment with a pulse

A

synchronized cardioversion
ICD (intracardiac defib)
ablation
meds: lidocaine, adenosine, beta blocker, amiodarone, diltiazem

35
Q

vtach treatment w/o pulse

A

CPR
Defibrillate
meds: epi, lidocaine, amiodarone

36
Q

v-fib

A

ventricles quivering with no discernable waves

no pulse present

37
Q

causes of v-fib

A

hyperkalemia, hypomagnesemia, CAD, MI, electrocution, VTACH

38
Q

vfib treatments

A

CPR -> epinephrine, amiodarone, lidocaine

39
Q

what is arteriosclerosis

A

thickening, loss of elasticity, and calcification of arterial walls (part of aging process)

40
Q

what is atherosclerosis

A

formation of plaque within arterial wall -> injury to endothelial cells -> growth of muscle cells which secrete collagen and fibrous proteins -> lipids platelets, and clotting factors accumulate

41
Q

diagnosing atherosclerosis

A

lipid panel, c-reactive protein, blood glucose levels

42
Q

lipid profile normal ranges

A

total cholesterol: <200
triglycerides: <150 (critical: >400)
LDL: <100
HDL: >45 men, >55 women

43
Q

c-reactive protein

A

1.0-3.0
>3.0 = low grade inflammation

can indicate if something else is causing blockage

44
Q

blood glucose levels

A

elevated levels can increase the risk for atherosclerosis

45
Q

atherosclerosis therapeutic measurements

A

DASH diet, smoking cessation, exercise, low-dose aspirin, statins
** statins may take up 4-6 weeks

46
Q

what is angina

A

chest pain due to ischemia

47
Q

Stable angina

A

occurs in a pattern familiar to patient, only lasts a few minutes, goes away with rest/nitro

48
Q

unstable angina

A

increases unpredictably in frequency
occurs at rest and/or during sleep
NOT RELIEVED BY MEDS OR REST
treat as an emergency

49
Q

prinzmetal angina

A

aka variant or vasospastic
caused by coronary artery spasms
cyclical pattern
lasts longer than stable

50
Q

microvascular angina

A

spasms in walls of tiniest arteries

pain may be more severe

51
Q

angina treatment

A

nitroglycerin

52
Q

things to know about nitro

A

dilates arteries = reduced workload

assess BP and pain (hold if BP is low)

given sublingual = faster absorption (acts in 1-2 minutes, lasts 30-40 minutes)

1 Q5min x3

53
Q

nitro side effects

A

hypotension, headache

54
Q

STEMI

A

ST Elevation Myocardial Infarction: most serious, effects full thickness of heart

necrosis has probably occured

55
Q

NSTEMI

A

Non ST Elevation Myocardial Infarction: less serious, blockage is usually partial, can be reversed and necrosis can be avoided

56
Q

which part of the heart is effected during an MI

A

depends on the effected coronary artery

57
Q

how long does it take for an ischemic injury to result in necrosis

A

it may take hours, but can be prevented if caught in time

58
Q

when should meds be given for MI

A

within the hour

**time is muscle

59
Q

necrosis can lead to scar tissue causing what

A

decreased muscle contraction and heart failure

60
Q

S/sx of myocardial infarction

A

heaviness, pressure, tightness, burning, constriction, crushing pain (elephant sitting on my chest)
fatigue, weakness, SOB, anxiety, SNS is activated (low BP, high HR, clammy and gray skin)
N/V

**pain may radiate!

61
Q

MI diagnostic tests

A

troponin: <0.04 is normal
myoglobin and CK-MB: not as sensitive - takes longer to elevate
EKG: Look at ST segment
magnesium and potassium: vital for heart function

62
Q

MI treatments (surgeries)

A

Cardiac catheterization: balloon angioplasty, percutaneous coronary intervention (PCI)

Coronary Artery Bypass Graft (CABG): vessel usually taken from the leg to bypass blockage

63
Q

Post MI medications

A 
beta blockers: metoprolol, Carvedilol
ACE inhibitors: lisinopril, ramipril
STATINS: crestor, lipitor
antiplatelet: plavix, brilinta
vasodilators: isosorbide mononitrate
64
Q

Peripheral Arterial Disease (PAD)

A

narrowing of arteries that leads to occlusions or obstructions

65
Q

which part of the body is usually effected by PAD

A

lower extremities

66
Q

causes/risk factors for PAD

A

Any other cardiovascular disease

67
Q

S/sx of PAD

60-75% of blockage

A 
intermittent claudication
paresthesia
thin, shiny, and taut skin
loss of hair on the lower legs
diminished or absent pedal, popliteal, or femoral pulses
pallor of extremity when elevated, reddish-purple when dependent
cool skin
thickened toenails
dry, flaky, scaly skin
decreased sensation
pain at rest
68
Q

PAD complications

A

atrophy of the skin and underlying muscles
delayed healing = risk for infections, gangrene
wound infection
tissue necrosis
arterial ulcers (defined borders, painless)
amputation

69
Q

aneurysms

A

balloon-like bulge in the vessel

70
Q

types of aortic aneurysms

A

aortic arch, thoracic aorta, abdominal aorta (AAA)

71
Q

normal diameter of the aorta?

diameter of aorta that requires treatment

A

<3cm

> 5cm

72
Q

Aortic aneurysm s/sx

A

Thoracic: asymptomatic, SOB, SP pain that radiates to back
AAA: asymptomatic, pulsatile mass, bruit, back or flank pain, abdominal pain/feeling of fullness

73
Q

aneurysm diagnostic tests

A

abdominal US, CT, MRI, Aortography (arteriogram)

74
Q

aneurysm treatments

A

lifestyle changes: wt loss, diet, smoking cessation, decreased BP
surgery: removal of dilated section - graft placed
endovascular aneurysm repair (EVAR): catheter threaded through femoral artery to place stent

75
Q

aortic aneurysm complications

A

aortic dissection rupture

76
Q

aortic dissection

A

tear in the inner wall and blood will pool between the inner and outer wall = increased risk for rupture

77
Q

rupture

A 
#1 complication
into retroperitoneal space - can tamponade surrounding structures 
into thoracic or abdominal cavity - blood can compress lungs, heart, or abdominal organs -> massive hemorrhage = death
78
Q

aortic dissection

A

tear -> blood between inner and middle layer -> systolic pulsation increases pressure on damaged area -> further dissection -> may occlude major branches of aorta

Cardio Sem 2 (3 decks)

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