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Cardiovascular > MIS/Cardiogenicshock/aneurysms > Flashcards

MIS/Cardiogenicshock/aneurysms Flashcards

1
Q

What are DRGs

A

hospitals doing their best to prevent readmissions of patients… if they are readmitted then the insurance companies will not pay for stay

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2
Q

this risk factors for CAD are just

A

risk factors! they are not known to cause CAD

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3
Q

ACS refers to what?

A

unstable angina
NSTEMIS
STEMIS

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4
Q

what happens to people with unstable angina

A

put in observation bed for 24 hours

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5
Q

define after load

A

the pressure that the ventricles must over come in order to push blood out of the aorta

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6
Q

what is angina pectoris?

A

pain caused by ischemia due to poor blood flow caused by clogged up veins

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7
Q

what can cause chest pain

A 
aortic disection 
cholecystisis 
anxiety and depression 
muscle strain 
costochondritis 
esophegeal spasm 
PE 
herpes zoster 
GERD 
pericarditis 
pneumonia 
pneumothorax 
pulmonary hypertension 
pancreatisis
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8
Q

questions to ask about chest pain (the 5 Ws)

A 
what does it feel like 
where is it located 
what makes it worse 
what causes it 
what makes it better
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9
Q

also ask about

A 
quality 
location 
duration 
intensity 
accompanying symptoms
aggravating and relieving factors (ask about exercise to rule out any ischemic causes of pain)
ask family and self history 
age (CAD is more common the older you get)
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10
Q

factor associated with chest pain

A

cold (men over 50 cover mouth when cold outside)
eating heavy
stress
physical exertion

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11
Q

stable angina

A

predictable and persistant angina relieved by rest or nitroglycerin

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12
Q

unstable angina

A

preinfarction/crescendo angina- caused by ischemia, may or may not be relieved with nitro/rest

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13
Q

how much nitro can you give

A

3 5 minutes apart, if not relieving chest pain call the doctor

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14
Q

variant angina

A

pain at rest that causes an ST elevation, thought to be caused by coronary vasospasm

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15
Q

clinical manifestations of an MI

A 
impending sense of death 
apprehension
neck 
jaw 
shoulders 
innerportion of arm (normally left arm) 
tightness 
heavy choking 
strangling feeling like a vice 
diabetic neuropathy may be blunt pain 
women have symptoms like indigestion
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16
Q

silent ischemia

A

clinical manifestations of an MI but patient reports no pain

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17
Q

gender role in chest pain

A

more common in women over 50 and men over 40

chest pain is different in women

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18
Q

signs and symptoms of mis that women experience

A

fatigue, tiredness, sleep disturbances before a cardiac event

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19
Q

red flags in the VS of a cardiac event

A 
abnormal vital signs 
bradycardia or tachycardia 
tachypnea 
hypertension
hypotension
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20
Q

red flag symptoms of an MI/ unstable angina

A 
pallor 
sweating 
dyspnea 
nausea 
productive cough (caused by remodeled LV which means fluid backing into lungs, which means pt is going into HF)
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21
Q

assessment and diagnostic findings of CAD

A 
ECG 
Twave inversion 
Cardiac biomarkers 
echocardiogram 
halter monitor 
cardiac catheterization 
nuclear scan
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22
Q

medical management of CAD

A

pharmacological therapy

reperfusion such as PTCA (percutaneous transluminal coronary angioplasty)

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23
Q

Treating angina

VIP slide

A

if pt has pain or prodromal symptoms (indegestion, choking, heaviness, weakness) take immediate action
stop all activity and bed rest in semi fowlers
measure vs
12 lead ecg
ST and T wave changes
Nitro sublingual tabs, give up to 3 times or as stated by provider
assess VS after each administation of nitro
give oxygen by 2 L of o2

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24
Q

identifying types of MIs

A 
Nstemi
stemi 
anterior wall 
inferior wall 
posterior wall 
lateral wall 
point in time 
acute 
evolving 
old
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25
Q

sign of an old MI

A

Q wave

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26
Q

RCA/PDA occlusion

A

RV/RA infarct front and back
alters lung perfusion
may act as hypovolemic since it can’t return blood to the heart

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27
Q

LAD/Circumflex occlusion

A

LA/LV circumflex occlusion - front to back

Alters perfusion to the rest of the body

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28
Q

Left main occlusion

A 
"widow maker" 
most critical- feeds the LV 
many never make it to the hospital (fatal rhythm) 
emergent CABG 
cannot stent
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29
Q

acute inferior wall mi

A

leads II, III, and AvF represent ECG changes in ST elevation developing Q waves and T wave inversions

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30
Q

anterior wall MI

A

more serious and worst prognosis

ST segment elevation and leads I, aVL and precordial leads overlying the anterior lateral surfaces of the heart

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31
Q

clinical manifestations of MI

A 
some prodromal symptoms 
chest pain 
SOB 
Indigestion 
nausea 
anxiety 
cool, pale, moist skin
elevated HR and RR
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32
Q

assessment and diagnostic findings in cardiovascular system of an MI

A

chest pain not relieved by nitro, palpitations, heart sounds, s3, s4, and new onset murmur
palpitations
heart sounds such as S3, S4
BP may be elevated or decreased (depends on sympethetic stimulation could be elevated, could be decreased because of impending cardiogenic shock or medications) irregular pulse may indicate a fib

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33
Q

respiratory findings in MI

A

SOB
Dyspnea
Tachypnea
crackles if MI had caused pulmonary congestion

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34
Q

Gi findings in an MI

A

nausea, indigestion, vomiting

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35
Q

Skin findings during MI

A

cool, clammy, diaphoretic, pale

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36
Q

neurologic findings during MI

A

anxiety, restlessness, lightheadness

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37
Q

psychological findings during MI

A

fear of impending death or thinking that nothing is wrong

38
Q

medical management of an MI

A 
ecg 
medications 
evaluate for reperfusion therapy 
(PTCA, Thrombolytic therapy) 
therapy like IV LMWH, or heparin, plavix, glycoprotien inhibitor, bedrest for 12 to 24 hours
39
Q

medications for MIs

A 
oxygen
nitroglycerin 
morphine 
aspirin 
beta blockers 
ace inhibitors with in 24 hours 
anticoagulation with heparin
40
Q

when there is an mi what must happen with the ecg

A

it must be be read with in 10 minutes

41
Q

what does a Qwave represent?

A

a hx of an mi

42
Q

how does the ecg evolve over time?

A

t wave inversion (repolarization is altered)
st segment elevation (injured cardiac cells repolarize faster)
q wave after the epsiode
development of tachycardia, bradycardia, or other dysrhythmias

43
Q

how far does the st segment raise during an mi

A

about 1mm

44
Q

what is troponin

A

released during an mi

can be raised for 3 weeks after an episode

45
Q

CK-MB (cardiac muscle)

A

NOT CK-BB and CK-MM

elevated indicates an acute mi elevated in a couple hours and peaks 24 hours after event

46
Q

myoglobin

A

not very specific but negative results can rule out an MI

starts to increase 1-2 hrs after event and peaks 12hrs after onset of symptoms

47
Q

cardiogenic shock

A

decreased CO make decreased perfusion, body responds the same way it does during hypovolumic shock

48
Q

cycle of events in cardiogenic shock

A

heart failure dt ischemia, producing forward and backward failure, circle of events just keeps getting worse

49
Q

when does cardiogenic shock occur?

A 
following an MI when a large area of the myocardium becomes ischemic and hypokinetic 
end stage HF 
cardiac tamponade
PE 
cardiomyopathy 
dysrhythmias
50
Q

what type of MI puts people at the greatest risk for cardiogenic shock

A

anterior wall mi

51
Q

What can cause cardiogenic shock other than cardiac issues

A

SLE
COPD
RF
Multiple trauma

52
Q

clinical manifestations of cardiogenic shock

A

HF
Low BP, CO+CL, SVR high, PVR high
tachycardia w dysrhythmias
Tachypnea, shallow, poor saturation, ARD
Changes in LOC (CVA)
decreased peristalsis leads to bowel infarc/ischemia
skin pale, cool, cyanotic, clammy
abnormal lab values with all organ systems

53
Q

pharmacological management of cardiogenic shock

A

based on

preload, afterload, contractility, goal is to restore cardiac funciton

54
Q

first line of trx in shock

A 
o2
pain control 
ECG and hemodynamic monitoring (a-line, Pulmonary artery catheter) 
lab monitoring (CK-MB, BNP, cTn-1)
fluid therapy (watch for overload)
55
Q

first line medications for cardiogenic shock

A

diuretics, positive inotropic drugs, vasopressors, anticoagulants

56
Q

mechanical assist devices for cardiogenic shock

A

Intra-aortic balloon pumps

57
Q

aim of vasoactive therapy

A

improve cardaic contractiity
decrease preload and afterload
stabilize heart rhythm

58
Q

two drugs often used together in cardiogenic shock

A

inotropic medications and vasodilators

59
Q

nursing management of cardiogenic shock

A 
prevent cardiogenic shock 
monitor hemodynamic status 
administering medications (IV fluids) 
maintaining intra-aortic balloon counter pulsation
ensuring comfort and saftey
60
Q

what is an intra-aortic balloon pump?

A

inflates at the begging of diastole
results in increased perfusion of coronary arteries and peripheral arteries
deflates just before systole which results in decrease in afterload therefore a decrease in resistance which makes a increase in coranary artery perfusion

61
Q

what position do you put someone in in cardiogenic shock

A

reduce venous return to prevent pulmonary edema

high fowlers with legs down

62
Q

saccular aneurysm

A

projects from only one side of the vessel, most common kind of aneurysm

63
Q

fusiform aneurysm

A

entire arterial segment becomes dialated

64
Q

mycotic aneurysm

A

very small aneurysm due to localized infection

65
Q

true aneurysm

A

involves all three layers of the vessel wall

66
Q

psuedoaneurysm (false)

A

involves a dissruption in vessel walls and can lead to disection or tear (always involves a damaged media layer)

67
Q

risk factors for an anyuerism is

A

genetic predisposition
HTN
Tobacco use

68
Q

signs and symptoms of AAA

A

asymptomatic till they expand or rupture
expanding causes sudden severe and constant low back, flank, abdominal or groin pain
palpable pulsating mass is the number one sign- only found in 1/2 of the cases

69
Q

presentation of a ruptured AAA

A

frank shock- cyanosis, molting, AMS, tachycardia, hypotension, sudden pain, may be very dramatic, VS can be normal bc of the retroperitonal containment of hematoma

70
Q

number 1 sign of ruptured AAA

A

back pain w HTN
abd pain
diarrhea

71
Q

Clinical manifestations of AAA

A

pain in back, may only occur when pt is supine
dyspnea due to the pressure of the pressure on the trachea, main bronchi, or the lungs its self
cough
bloody diarrhea
hoarsness
stridor
weakness/complete loss of voice resulting from pressure against the laryngeal nerve

72
Q

assessment diagnostic findings

A

80% of masses can be palpated
may hear a systolic bruit duplex or CTA(ct with dye injected into the aorta to see the size of the mass) is used to determine size. length. and location,

73
Q

when aneurysm is small whats the plan of trx

A

ultrasounds every 6mos

can remain stable for years

74
Q

treatment for AAA is based on

A 
symptoms 
rate it is expanding at 
what tis is caused by 
if it contains a discetion or not 
involved branch vessels
75
Q

what do you want to do with patients with AAA

A

keep BP low, systolic under 120 -90

76
Q

abd aa

A 
most common anuyerism 
common cause is artheriosclorosis 
affects men 2 to 6 times more often then women 
more common in caucasians 
age has a factor 
most occur below renal arteries
77
Q

thoracic aa

A 
discovered unexpectedly normally 
less common 
caused 85% by artherosclerosis 
often grow to the point they rupture
men 50-70 
thoracic area is the most common for dissecting aneurysm 
1/3 die from ruputure
78
Q

medications used for anyeruisms

A

based on clinical studies and images
significant when diameter of aorta reaches larger than 3 cm
preoperatively the systolic pressure is maintained at 90 to 120
use beta blockers such as esmolol or metoproplol
anti-hypertensives such as hydralazine
soduim nitroprusside may be used as a continuous drip to emergantly decrease pressure

79
Q

surgical interventions for aneurysms

A

3 to 4 percent chance of developing paraplegia
goal is to restore vascular continuity with a vascular graft
intensive monitoring is required after surgery

80
Q

gerentological considerations of AAA

A

most occur between ages 60-90

consider r/f death vs r/f surgical complications (may not be a candidate for surgery)

81
Q

rupture is likely when?

A

coexisting HTN and an aneurysm greater than 6cm

82
Q

moderate risk for rupture and how large does it need to be to be repaired

A

5 cm

83
Q

great risk for rupture at

A

6cm

84
Q

signs and symptoms of complications of AA

A 
changes in pulses 
cool extremities 
white or blue extremities or flanks 
sever pain 
abdominal distention 
VS deteration
85
Q

endovascular graphs

A

places around AA and decrease complications
maybe be placed during gore tex or PTFE material reinforced w titanuim stents
inserted vis the brachial or femoral sites

86
Q

nursing management of endovascular repair

A

supine for 6 hrs
HOB elevated 45 degrees after 2 hrs
VS and doppler assessments of periphiral pulses every 15 minutes then progressively longer intervals (if they remain stable)
assess for bleeding, pulsation, swelling, pain, hematoma formation, skin changes in lower extremities
temp every 4 hours
any signs of post implantation syndrome should be reported

87
Q

signs of impeding rupture

A

back or abd pain (severe)
pain localizes in the middle or lower abd left of the midline
rupture into the peritioneal cavity is rapidly fatal
retroperitoneal cavity results in hematomas in the scrotum, perinuem, flanks, or penis
symtoms of HF and a large bruit
bloody diarrhea (bc bowel ischemia)

88
Q

dissecting aorta

A

tear in the media or intima degenerate
occur in aortic arch (highest mortality rate)
arterial dissections are assoicaited with uncontrolled htn
blunt chest trauma
cocaine use

89
Q

clinical manifestations of dissecting aorta

A

sudden
severe persistant pain described as ripping
pain is anterior chest or back and extends to the shoulders, epigastric area, or abdomen
aortic dissection is mistaken for an acute MI
pale, diaphoretic, tachycardic
elevated BP
BP may be different in one arm vs the other

90
Q

assessment and diagnostics of dissecting aorta

A

arteriography

duplex ultra sound

91
Q

intraaortic balloon pumps inflate during

A

Diastole and increase cardiac output

Cardiovascular (5 decks)

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