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MedSurg Test 1 > Chapt 34/ CAD & ACS > Flashcards

Chapt 34/ CAD & ACS Flashcards

1
Q

What is the most common type of Cardiovascular Disease?

A

Coronary Artery Disease (CAD)

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2
Q

What is CAD?

A

Blood vessel disoorder caused by atherosclerosis. Takes a long time to develope. This is why it is important to catch it early and detect high risk patients.

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3
Q

What is ACS?

A

Acute Coronary Syndrome. It has the same s/s (full or almost complete blockage of artery) of CAD but includes unstable angina (UA) and mycardial infarction (MI).

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4
Q

How prevelant is an MI in ACS?

A

70-80% because of thrombus formation.

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5
Q

When in angina seen in CAD?

A

Not until approx 75% the the vessel is occluded. Turbulent flow is what breaks off the occlusion= thrombous

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6
Q

During an MI how long does it take the heart to have full necrotic damage with Collateral circulation?

A

6 hours

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7
Q

What is collateral circulation

A

Angiogenesis and the presence of chronic ischemia. Promotes blood flow to comprised areas

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8
Q

Is collateral damange good or bad?

A

good

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9
Q

If a patient has a rapid onset of CAD will they have collatreral circulation?

A

No, because there is no time for development of angiogenesis.

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10
Q

Dose Angiogenesis prevent MI’s?

A

No, but it does lessen the severity.

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11
Q

What is the value for HTN

A

140/90

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12
Q

What does Pre HTN DX/CKD stand for?

A

A modifable risk factor for CAD. Prehypertension (130/80) with DM2 or Chronic Kideny Disease.

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13
Q

What is metabolic syndrome?

A

A modifable risk factor for CAD. Your body becomes insulin resistent and damages nerves and vessels.

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14
Q

In what way are homocysteine levels related to CAD?

A

The break down our vasculature system

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15
Q

What are the leveds for serum Lipids?

A 
High Cholesterol (>200)
Fasting triglycerides (>150)
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16
Q

Why is tobacco a modiable risk factor CAD.

A

Because nictoine releases catacholemines (Epi, NorEpi) which decreases blood flow and constricts the plaqy vessels.

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17
Q

FITT

A 
Risk Prevention for CAD/ Physical Activity/Promoting weight loss and a decrease in insuline resistance.
F=Frequency (at least 5X/week)
I=Intensity (moderate)
T-Type (Isotonic)
T=Time (30 minutes)
~ Add resistance 2days/week.
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18
Q

If you are at a high risk for CAD what should your overall nutrition look like?

A

Decrease in saturated fats
Increase in Fiber
30% of calories come from mono/poly unsaturated fats
Reduce or eliminate alcohol/simple sugars
Increase omega 3 fatty acids

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19
Q

What age should you start complete lipid profiles?

A

20 years old and then every 5 years

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20
Q

How do you lower your cholesterol?

A
  1. Diet and Exercise (Diet therapy first!) (Reassess after 6 weeks if no change then move to medications)
  2. Medication
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21
Q

What are the 5 groups of Cholesterol Lowering Drugs

A
  1. Statins
  2. Niacin
  3. Fibric Acid Derivative
  4. Bile Acid Sequesterants
  5. Cholesterol ABsorption Inhibitors
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22
Q

What is the mechanism of Action for Statin Drugs

Simvastatin, Atorvastatin, Rosuvastatin

A 
Inhibit cholesterol synthesis in the liver
You haev to take them at night 
Serious side effects
-rhabdomyolysis (muscle breakdown)
-Liver damage 
        ~ Monitor SLT,ALT
-No grapefruit Juice, dig toxicity.
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23
Q

What is the mechanism of Action for Niacin?

A 
Inhibits Cholesterol Synthesis
Many adverse side effects 
-Severe flushing (take tylenol)
-Itching
-GI problems
-orthostatic hypotension
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24
Q

What is the mechanism of Action for Fibric Acid Derivatives ( Gemibrozil, Fenofibrate) ?

A
  • Do not effects LDL’s, Target VLDL’s
  • Take 2 hours before all other medications becuase this drug competes for binding sites. Medication is active when not bound. Therfore can cause toxicities.
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25
Q

What is the mechanism Actions for Bile Acid Sequesterants (chlestyramine, Colesevelam) ?

A

Increases conversion of cholesterol to bile acid

Needs to be given 2 hours apart from other medication

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26
Q

what is the mechanism of action for Cholesteral Absorption Inhibitor (Ezetimibe) ?

A

Inhibits absorption of dietary and billary cholesterol.
Often used with diet changes for primary hypercholesterolemia.
Works really well when combined with statins.

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27
Q

What two cholesterol lowerind drugs need to be taken two hours before any other medications?

A

Fibric Acids Derivatives

Bile Acid Sequesterants

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28
Q

What two cholesterl lowering drugs work really well when combined?

A

Statins and Cholesteral Absorption Inhibitors

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29
Q

What is the standart antiplatelet therapy for CAD?

A

Low dose ASA (81 mg)

-baby ASA lowers the risk of GI bleeds

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30
Q

What are symptoms of a GI bleed?

A

Dark Tary stools

Change in LOC

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31
Q

How do you treat the gerontologic community with CAD?

A

Aggressively treat HTN and hyperlipidemia
Stop smoking
Planned physical activity.

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32
Q

What is prinzmetals’s Angina?

A

Chest pain at rest

Pt with migranes and Raynaud’s

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33
Q

What is angina?

A

Temporary imblalance between oxygen supply and the hearts demand. Anaeroblic metabolism=lactic acid irritates nerves.

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34
Q

What are the usual causes of angina?

A

Stable, atherosclertoic plaque.

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35
Q

Precipitating Factors of Angina

A 
Physical Exertion (Supply and demant)
Temp extremes (cold, vasoconstrict)
Strong emotions (catacholamines)
Eating a heavy meal (shunting blood flow to gut)
Tobacco Use (catacholamines)
Sexual Activity
Stimulants 
Disrupt in circadian rhythm (early morning)
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36
Q

Can Nitrates be taken prophylactically?

A

Yes

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37
Q

Describe Chronic Stable Angina

A
  • Plaque build up in the coronary a.
  • Chest pain occurs intermittently over a long period witht he same patter of onset, duration, and intensity.
  • Pain lasts 5-15 minutes
  • Usu controlled with rest or meds to provide peak effects when angina occurs.
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38
Q

What are Holter Monitors?

A

Heart monitors what go home with the pt and monitor for 24 hours.

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39
Q

Silent ischemia

A

ischemai without symptoms. Often seen in pt’s with diabetes because of nerve damage.

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40
Q

Nocturnal Angina

A

Occurs only at night

41
Q

How do you treat Prinzmetal’s Angina?

A

Calcium Channel Blockers and or Nitrates

42
Q

When do you used a 12- lead ECG

A

Electrical conduction issues

43
Q

CXR

A

Chest X ray for enlargements or calcifications

44
Q

What diagnostic test confirm CAD?

A

Cholesterol Lipid Profile

45
Q

If the pt has already been diagnosed with CAD what diagnostic test would you do?

A
  • Echo to check for decreased ventricular functions. Normal Echo is 60-70%
  • Stress test: ST changes on the ECG= Chronic Stable Angina
46
Q

What is the drug therapy for Angina?

A 
Short-Acting Nitrates
Long-Acting Nitrates
Beta Blockers
ACE Inhibitors
Calcium Channel Blockers
47
Q

To give a nitrate what is the range for BP?

A

> 100

48
Q

What are common side effects for Nitrates?

A 
Tingling
Headache= vasodilation of cerebral a.
Increased HR= systemic vasodilation
Dizziness
Flushing
49
Q

When should you never give a pt Nitrate?

A

When the pt is on viagra!

50
Q

Regime for Short Acting Nitrate

A
  • Onset of Angina
  • Take 1 NTG; if symptoms dont change call EMS and take a second NTG.
  • Take 2 NTG b/c symptoms improved but not gone; take another NTG. Symptoms dont improve. Call EMS
  • Take 3 NTG b/c symptoms improved but not gone. Symptom are not 0=Call EMS
51
Q

When do we use Long Acting Nitrates (Imdur, Isordil)?

A

Used to reduce the incident of Angina attacks. Chronic Stable Angina.

  • Pt can develop a tolerance, take off at night
  • Comes in past or patch
  • Make pt aware of orthostatic hypotension
52
Q

What is the treatment goal for Chronic Stable Angina

A

Shift from demand to supply

53
Q

Beta Blockers are the perferred drug for

A

Chronic Stable Angina
Following an MI
b/c of cardio protective actions

54
Q

To give a BB what doe the pulse need to be?

A

> _ 60

55
Q

What type of pts are prohibited from BB

A

Pts with asthma

56
Q

When do we give our patient an ACE inhibitor?

A

if at a high risk for a cardiac event
Echo if 40% or less
Side effect: Cough

57
Q

What are Calcium Channel Blocker prescribed for?

A

Prinzmetal’s Angina caused by vascular spasms
Use only for Angina not after an MI
Watch out for Dig Toxicity
has no cardio protective affects

58
Q

If I have Angina I treat with _

A

Nitrates

59
Q

If I have Chronic Stable Angina or at High Risk I am prescribed _

A

ACE Inhibitor/ Prevent reverse remodeling of the heart tissue. Vasodilate and decrease blood volume

60
Q

If I have a history of MI’s and L Ventricular dsyfunction I am prescribed __

A

Beta Blockers.

Dec Contractility, HR,SVR, BP

61
Q

If I have Prinzmetal’s Angina I am prescribed__

A

Calcium Channel Blocker

62
Q

What is Unstable Angina (UA)

A

New chest pain, pain that occurs at rest, or pain that has a worsening pattern (Unpredictable)
EMERGENCY

63
Q

Acute Coronary Sydrome has two outcomes, what are they?

A
  1. Partially Occluded Vessel
    - UA
    - NSTEMI
  2. Total Occluded Vessel
    - STEMI
64
Q

What are the hallmarks of a MI

A

Severe chest pain not relieved by

  1. Rest
  2. Nitrate
65
Q

Define Acute Myocaridal Infarction (AMI)

A

Sustained ischemia >20min causing irreversible myocardial cell death.
Mostly due to a thrombus
Severity can depend of Collateral Circulation

66
Q

During an MI, how long before you have necrosis of heart tissue?

A

10 minutes

67
Q

What are S/S of AMI?

A 
Severe immobilizing chest pain
More common in the early am
Last longer than 20 minutes
Sweaty, Ashen, Clammy
Increased BP and HR (drops) later.
Crackles (fluid in left ventricle)
JVD (Blood backing in the periphery)
n/v
Temp=Inflammation
High gluecose
Holosystolic murmur=damage to tissue affect valves
dysrhythmias
68
Q

What does an inverted t wave represent

A

Ischemia

69
Q

During a STEMI what would an ECG show

A
  1. Pathological Q wave
  2. Elevated ST
  3. Inverted T wave.
70
Q

During a NSTEMI what would an ECG show?

A
  1. ST Depression

2. Inverted T wave

71
Q

What is a pathological Q wave indicative of?

A

STEMI

MI

72
Q

During a MI what would the ECG show?

A

Pathological Q wave

Inverted Twave

73
Q

What is the healing process of the heart?

A
  1. Dead cardiac cells release enzymes (Epi, NorEpi)
  2. Leukocytes infiltration and cardiac wall thins
  3. Glucose and fatty acids are released (Stress response used for energy)
  4. Can see the necrotic zone with ECG changes
  5. 10-14 days after a weak scar develops, very fragile
  6. 6 wekks after healed but the scarred area is less compliant.
  7. Normals cells will hypertrophy and dilated=ventricular remodedling=HF
74
Q

How do you diagnose and UA and MI?

A

Coronary Angiography

75
Q

What portion of the heart does the LAD supply?

A

Left Ant Descending supplies the Ant. portion

76
Q

What portion of the heart does the RCA supply?

A

Right Carotid Artery supply the Inf. portion of the heart.

77
Q

What portion of the heart does the circumflex a supply?

A

Post and latertal portion of the heart.

78
Q

What arteries are involved in an anterior lateral MI?

A

LAD

Circumflex

79
Q

What is the general treatment for an MI

A
  1. Establish an IV
  2. Oxygen (2-4 L NC) upright position
  3. 12 lead ECG
  4. Chewable ASA, SL NTG
  5. Treat dysrhythmias
  6. VS with pulse oz frequently
  7. Bedrest for 12-24 hours
80
Q

How do you treat an UA or NSTEMI without cardiac markers?

A
  • ASA
  • Heparin
  • Coronary Angiogram with PTCA once stabilized and agina controlled
81
Q

How do you treat STEMI or NSTEMI with cardiac markers.

A

Reperfusion Therapy

  • emergent PTCA
  • Fibrinolytics
  • coronary surgical revascularization
82
Q

What is Percutaneous Trasnluminal Coronary Angioplasty (PTCA)

A

Frist line treatment with confirmed MI
A stent opens occlusion a pushes the clot to the side of the artery
Requires and antiplatlet drug

83
Q

What is the time goal for a PTCA?

A

Open the artery within 90 minutes of arriving to the hospital.

84
Q

What is the recovery time for a PTCA

A

Walking w/in 24 hours
home in 1-3 days
Work in 1 week

85
Q

What is fibrinolytics?

A

Only done if the facility dose not have a cath lab

Goal is to stop the infarction process by dissolving the thrombus and reperfusing the myocardium.

86
Q

What is the time frame for fibrinolytics?

A

Idealy given with/in 1 hour of systems but cannot be given after 6.

87
Q

What is a common complication with fibrinolytics

A

Bleeding

-ex. Gums

88
Q

What are the different types of coronary surgery revascularization

A

1) MIDCAB- Minimally Invasice Direct Coronary Artery Bypass: Through the ribs
2) OPCAB-Off Pump Coronary Artery Bypass: Beta blockers
3) Coronary Artery Bypass Graft
4) Transmycoardial revascularization

89
Q

Explain the process of CABG

A

CABG is done for pts who fail medical managment., have left main coronary a. or 3 vessel disease and are not candidates for PTCA.

90
Q

What artery is most commonly used for CABG?

A

Internal mammary artery (IMA)

91
Q

What is the nursing care after a CABG?

A 
PA cathater,
arterial line
Chest tubes
Continous ECG monitoring
Epicardial pacing wires (prophylatic for conduction issues)
Urinary Catheter
NGT
92
Q

What is postop cognitive dsyfunction, “Pump Head”

A

Post op cognitive dsyfunction assoiated with CABG surgery. Pumping blood into a machine and back into the patient.

93
Q

Initailly what medications would you be prescribed for a MI.

A

-IV Nitroglycerin
-Morphine
-Dual antiplatlet therapy/ prevent further occlusions
ASA
Slopidogrel (Plavix)
-LMWH to stop compromised a. build up

94
Q

24 Hours after an MI, what medications would you anticipate a pt to be one.

A
  • Beta adrenergic Blocker: Cardio protective
  • ACE Inhibitors: Stop Ventricular remodeling
  • Antidysrhthmics: Targets blockage preventing conduction
  • Lipid lowering drugs: stop the build up
  • Stool Softner: Pt is not ambulating and on high medications you odnt want your patient to bear down.
95
Q

What are some complications after an Acute MI from Coronary Arter Disease

A

1) Dsyrhythmias- Very common because of the K+ released from dead tissue
2) HF: Pulmonary Congestion
3) Cardiogenic Shock- Heart is not perfusing the body. Pt would need an IABP
4) Papillary Muscle Dsyfunction-Damage to the valves/ Mitral regurgitation leads to fluid backing up into the lunngs
5) Ventricular Aneurysm
6) Pericarditis- Chest pain worse with inspriaton
7) Dresslers Syndrome

96
Q

When is pericarditis common after an acute MI

A

2-3 days

97
Q

What is Dresslers Syndrome?

A

Pericarditis with effusion and fever developing 4-6 weeks after MI or cardiac sx.

98
Q

What is Sudden Cardiac Death?

A

Death that usu occurs with/in 1 hour of symptoms with no warning signs.
- Acute Ventricular dysrhythmias

MedSurg Test 1 (6 decks)

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