Unit 4- CVS Flashcards

1
Q

Structure of the heart

A

4 chambers, need patent blood vessels for optimal flow, need competent valves for one way flow

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2
Q

A functoining heart has

A

optimum flow, healthy vessels.

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3
Q

Plaque build up

A

fatty streak, established legions,

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4
Q

Coronary artery disease

A

coronary arteries deliver constant supply of blood to the heart muscle. Start to develop fatty plaque which leads to restriction of blood flow to the heart. Eventuality that restriction is what causes a MI.

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5
Q

atherosclerosis develops in 3 phases

A

fatty streak, fibrous plaque, complicated lesion. Takes years to develop.

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6
Q

Chronic endothelial injury

A

caused by hypertension, tobacco use, hyperlipidemia, diabetes, infection, damage to endothelium

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7
Q

Fatty streak

A

lipid accumulate and migrate into smooth muscle cells

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8
Q

Fibrous plaque

A

collagen covers the fatty streak, vessel lumen is narrowed blood slow is reduced, fissure can develop

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9
Q

complicated lesion

A

plaque rupture, thrombus formation, further narrowing or total occlusion of vessel

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10
Q

non modifiable risk factors for CAD

A

age, genetics, sex, family

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11
Q

modifiable risk faactors for CAD

A

metabolic syndrome, hyperlipidemia, hypertension, heart failure, smoking, sedentary lifestyle, obesity, elevated lifestyle, elevated BMI, Diabetes, Stress, cocain and meth, elevated homocysteine

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12
Q

Subjective questions

A

fatigue, indigestion, leg swelling, poor wound healing, smoking, drinking, med Hx, fam hx, diet, VS

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13
Q

Lab test to do for CAD

A

Diabetes, LDL/HDLm C-reactive protein, stress test, ECHO, ECG, LIpids, CBC, THyroudm CRP, Hemoglobin A1C

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14
Q

HDL

A

good cholesterol for healthy, high portion of protein, transports cholesteril to liver for excretion, beneefits effect on arterial wall. Can be increased by physical exercise. Benefits on arterial wall

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15
Q

LDL

A

Bad or lousy cholesterol. Low portion of protein to lipid ratio, harmful effects, affinity to arterial wall

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16
Q

Homocysteine

A

an amino acid. Vit B12-3 and folate break down and other chemical in the body. High level could mean deficiency. Without treatment it puts people at risk for homocysteine, increased risk for dementia, heart disease, stroke. Can damage arterial walls.

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17
Q

stress test AKA the treadmill stress test

A

Excerise treadmill test evaluates the Cardiovacular response to physical vital signs, continous ECG, physican present

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18
Q

What are you looking for in a treadmill test

A

HR, BP, MI, expertise duration, Symptoms pronlong, arrythmias

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19
Q

Nuclear stress test

A

uses radioactive dye and an imaging machine to create picture showing the blood flow to your heart. sjowing areas of blood flow or damaging in your heart. The test usually involves injecting radioactive dye, then taking two sets of images of your heart.

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20
Q

Cardiac ECHO

A

shape, size, movement of heart walls, fluid, valve disease, HF, invasive

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21
Q

ECG

A

The cardiac cycle (PQRST) captures electrical activity of the heart from different angles

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22
Q

P wave

A

atria are depolarizing (contracting)

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23
Q

QRS

A

Ventricles are depolarizing (contracting) atria are repolarizing (recharging) can not see that

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24
Q

ST segment

A

Should be isoelectric (flat)

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25
Q

T wave

A

Ventricles are depolarizing (recharing)

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26
Q

Depolarization

A

The movement of ions across the cell membrane, sodium, potassium and calcium channels, casuses contraction of the cardiac cells/muscles

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27
Q

Depolarization

A

Cardiac cells are at rest, no electrical activity, relaxation of cardiac cells/muscles

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28
Q

Pharm therapy for CAD

A

Atrovastatin (lipitor) Metoprolol, SAS

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29
Q

disease process of Angina

A

vasospasm, fixed stenosis thrombus, decreased coronary blood flow.

Increased heart rate, contracility, afterload, preload, increased oxygen consumptoms

When the O2 demand is greater then O2 supply

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30
Q

What makes Oxygen demands higher

A

CIA, HTN, Med, Genes, smoking, alcohol

31
Q

Stable angina

A

caused by isthmi, chest pain, relieved by rest
-Chronic, same pattern, brief, usually exercise induced, goes away with rest

32
Q

Unstable angina

A

Ischmia: chest pain, 1st episode, change in pattern
-Chronic that changes, occurs at rest, dosen’t always go away at rest, may need meds

33
Q

Subjective data

A

heart burn, preessure, substernal ache, squeezing, suffocating, choking

34
Q

Location of pain during angina

A

Midternal, left shoulder and down the arms, neck and arms, Under jaw, down left arm, epigastric radiating to neck, jaw, and arms, intrascapular

35
Q

Nursing management for angina

A

O2 sats over 95, Meds, monitor pain and BP, Diagnostic tests

36
Q

Diagostic tests for angina

A

12-lead ECG, Echo, Chest X ray, exercise stress test, CTA

37
Q

Angina chnages in an ECG

A

decreased blood flow due to narrowing of the coronary arteries by artherosclerosis. Pain subsides hwen the precipitating factos is released.

38
Q

for ischmia to occur

A

the artery is usually 75% or more stenosed

39
Q

If an ECG shows ST segment depression then it is

40
Q

Cardiac catherization coronary angiography

A

diagnostic.. PCI. balloon angioplasty, stent

41
Q

First line med for angina

A

Nitrates, causes bvasodilation improving blood flwo through the vessels

42
Q

How to take nitroglycerine

A

1st dose, wait 5 mins, 2nd wait 5 mins, 3rd dose wait 5 mins. No releif call 911. Proper delivery is important. Ensure client is sitting when taking nitro or their BP may drop. Make sure to monitor BP between so they dont bottom out.

43
Q

Nitro patch

A

worn 12 hours if angina occurs daily apply in am, if nightly apply pm. Client can take spray before exercise. Can cause headaches, dizziness, hypotension

44
Q

What meds should you stay away from when taking nitro

A

erectile disfunction

45
Q

Second most common med used for angina

A

Beta Blocker. Decreases BP, Decreases myocardial contractility, HR, and BP, therefore decreasing the myocardinal oxygen demands. ex. Metoprolol, atenolol, carvedilol.

46
Q

third line for angina

A

CCB: for people who can’t handle BB Decreases O2 demand (decreased peripheral resistnace, after load and decrease HR) and increase O2 supply
ex. Amlodipine or verapamil

47
Q

4th line med for BB

A

ASA, Plavix (need a higher dose for stent)

48
Q

What is acute coronary syndrome

A

When ischmia is prolonged and is not immedietly reversible, acute coronary syndrome develops. Unstable angina, Non ST segment-elevation myocardial infarction, ST segment elevation MI

49
Q

Disease process of acute coronary syndrome

A

deterioration of a once stable plaque, stimulates platelet aggregation and thrombus formation NSTEMI
Results in:
1.Partial occlusion of coronary artery
2. total occlusion of coronary artery STEMI

50
Q

MI

A

Results of sustained ischmia causing irreversible myocardinal cell death (necrosis)

51
Q

how long does it take for necrosis full thickness to occur

52
Q

Objective assessmet for MI

A

ABC, Vitals, cardiac, respiratory, PVS

53
Q

risk for MI

A

Sex, genetics, fam hx, smoking, exercise, weight/diet/high BMI, HYperlipidemia, hypertension, uncontrolled diabetes

54
Q

Nursing management for MI

A

M:morphine
O:oxygen
N: nitrates
A:asprin
-monitor sats, IV access, 12-lead ECG, baseline blood work, cardiac markers

55
Q

Nursing managment for MI (clotting)

A

Antiplatelet, anticoagulant, Aspirin/plavix/together, heparin, fibrinolytic, rTPA, TNK

56
Q

Nursing managemnet diagnostic tests

A

Bloodwork, ECG, Angiogram, angioplasty, stent

57
Q

Signs and symptoms of cardiac ischmia

A

ACS, ST elevation, Biomarkers, STEMI

No ST elevation
Biomarkers
unstable angina
Biomarkers
NSTEMI

58
Q

What happens to ST in stable angina

A

ST depression

59
Q

What happens to ST in NSTEMI

A

No ST elevation, +/- ECG changes

60
Q

What happens to ST in STEMI

A

ST elevation

61
Q

what are Cardiac markers

A

protein are relased from necrotic heart, proteins that are released when there is cell death, lytes, Na, K

62
Q

What are the cardiac markers

A

troponin I and T, CKMB, Myoglobin, C reactive protein CRP

63
Q

Cardiac troponin

A

Most commonly used fpr biomarkers. It has the highest known sensitivity. It enter through your blood stream soon after a heart attack. It also stays in your blood stream days after.

64
Q

Creatinine kinsase

A

This enzyme can also be measured several times over a 24 hour period. It will usually at least double if youve had a heart attack. But because levels of CK can go up in many other condition (this is not specific)

65
Q

CK-MB

A

Subtype of CK. It is more sensitive for heart attack. Rises 4-6 hours after a heart attack. But goes back to normal 4-6 days after. IT helpful when a healthcare provider is trying to figure out whther your recent chest pain was a heart attack.

66
Q

myoglobin

A

This is a small protein that stores oxygen it is measured occasionally. Myoglobin is sometimes measured in addition to tropinin to help diagnose

67
Q

Thrombolysis

A

Enzymatic digestion of thrombus to open lumen

68
Q

Percutaneous transluminal coronary angioplasty

A

physical disruption of plaque to open lumen. Placement of a stent to prevent reocclusion

69
Q

Coronary artery bypass grafting (CABG)

A

Surgicala placement of a new conduit to bypass occlusion. Reduces chest pain, heart attacks

70
Q

Surgical revascularization

A

new pathway from aorta to myocardium

71
Q

Heart healthy diet

A

low sodium, low fat, high fibre

72
Q

Nursing managemnet cardiac rehab

A

exercise, sex, return to work

73
Q

Nursing management health teaching

A

A: anti platelet, abtianginal, ACE
B: Beta Blocker, blood pressure
C: Cholestrol, cigarettes
D: Diet, diabetes
E: Education, exercise
F: Flu vaccine

74
Q

Women and MI

A
  1. uncomfortable pressure, fullness, lasting or go and some
  2. Pain or discomfort in one or both arms, the back, jaw or stomach
  3. Shortness of breath or without discomfort
  4. Other signs such as breaking out in a cold sweat, nausea, lighheaded
    WOmen are more likely to experience back pain, SOV, n and vomiiting, jaw pain