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SEMESTER FOUR!! Nursing 214 > Coronary Artery Disease (CAD)/Acute Myocardial Infarction(AMI) - EXAM 4 > Flashcards

Coronary Artery Disease (CAD)/Acute Myocardial Infarction(AMI) - EXAM 4 Flashcards

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1
Q

HDL: good or bad

A

Good. Want high HDL. Carries lipids away from arteries to the liver. Increases with exercise. Associated with lower risk for CAD.

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2
Q

LDL: good or bad?

A

Bad. Contains the most cholesterol. High levels correlate with CAD. Sticks to artery walls.

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3
Q

How do you decrease serum cholesterol levels?

A
  1. Achieve normal weight
  2. Diet that is low in fat, high in fiber, high in monounsaturated fat, plant sterol or stanol esters
  3. Management of Diabetes
  4. Control of BP
  5. Quit smoking
  6. Alcohol in moderation
  7. Medications
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4
Q

How do you increase serum HDL levels?

A
  1. Exercise for 30 minutes or more (aerobic) at least 5 times per week
  2. Quit smoking
  3. Achieve normal triglyceride level of less than 150 if elevated
  4. Diet low in fat, high in monounsaturated fat, high in whole grains, fruits, vegetables
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5
Q

What medications can be taken to decrease serum cholesterol levels?

A
  1. Bile acid sequestering agents (cholestyramine)
  2. Satins (Lipitor)
  3. Fibrates (gemfibrozil)
  4. Nicotinic Acid (Niacin)
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6
Q

atorvastatin (Lipitor)

A

Classification: Antilipemic agent

Mechanism of Action: Blocks synthesis of cholesterol and reduces LDL and triglyceride production. Increases HDL plasma levels

Use: Adjunct to diet therapy for decreasing LDL, cholesterol, triglycerides

Side/Adverse Effects: Mild GI disturbance, elevated liver enzymes, may increase digoxin levels

Nursing Implications:

  1. Do not take if liver disease
  2. Monitor liver function test
  3. Monitor digoxin toxicity
  4. Minimize alcohol intake
  5. Report any neuromuscular changes
  6. Teach patient importance of compliance
  7. Cholesterol med usually taken in the evening because the liver does the most work at night
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7
Q

aspirin (ASA, ECASA)

A

Classification: antiplatelet

Mechanism of Action: Inhibits platelet aggregation and inflammation

Use: Suspected AMI = 4 81mg chewable tablets or 1 325mg tablet to be chewed. Administer ASAP. Used also to prevent recurrences of MI, prophylaxis in unstable angina. 81mg or 325mg

Side/Adverse Effects: Gastric upset, GI bleeding, anaphylaxis

Nursing Implications: give with meal or full glass of liquid

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8
Q

morphine sulfate

A

Classification: narcotic analgesic

Mechanism of Action: binds endogeous opiod receptors. Reduces pre and afterload due to vasodilation

Use: pain of AMI, relieves dyspnea in HF/pulmonary edema, decrease anxiety

Side/Adverse Effects: resp.depression, orthostatic hypotension, constipation

Nursing Implications: Avoid valsalva post AMI, CNS depressant safety issues, monitor VS especially respiration and LOC

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9
Q

isosorbide mononitrate (Imdur)

A

Classification: nitrate vasodilator

Mechanism of Action: vasodilation (relax SM), decrease afterload, decrease venous return to the heart d/t venous pooling, decrease preload, decrease myocardial O2 consumption

Side/Adverse Effects: HA, syncope, flushing, hypotension, orthostatic changes, tachycardia

Nursing Implications: changes positions slowly, given PO, assess for angina/pain, monitor VS, do not break or crush

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10
Q

nitroglycerin

A

Classification: nitrate vasodilator, IV, SL (tab/spray), PO, transdermal spray

Mechanism of Action: Potent vasodilator - relaxes vascular smooth muscle, both arterial and venous. Promotes peripheral pooling of blood, decreases venous return, decrease SVR, decrease pre and afterload, HTN, angina, MI/CHF, decrease cardiac workload

Side/Adverse Effects: HA, Decrease BP, Palpitations, Syncope

Nursing Implications: CHECK SBP BEFORE GIVING THIS MED

IV: To manage HTN crisis, monitor for change in VS/LOC and relief of symptoms. May be used for angina unrelieved from NTG X 3 and morphine.

SL: Assess for signs of HA. Tingling sensation under the tongue, is normal with SL use. Store SL tabs in original bottle, sealed. Dose = 1 tab or 1 spray for angina. If symptoms unchanged after 5 minutes, call 911. May repeat SL q5minutes X 3 doses.

Transdermal: Avoid any bony prominences and an overly hairy location, rotate sites

  • Hold if SBP: less 90mmHg
  • Slowly change position
  • Contraindicated within 24 hours of erectile dysfunction meds
  • May relieve pain in 3 minutes
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11
Q

What is the troponin lab test?

A

Proteins are released following an acute MI, highly specific biochemical markers for cardiac damage.

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12
Q

What are the nursing considerations for troponin?

A

Simple blood test with normal = 0.03ng/mL. Patients will have levels drawn q8hours X3. Activity level significantly reduced until there are 2 negative troponin levels, meaning AMI is ruled out.

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13
Q

What is angina?

A

Chest pain is the clinical manifestation of reversible myocardial ischemia.

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14
Q

What is Prinzmetal’s Angina?

A

Often occurs at rest, usually in response to spasm of a major coronary artery.

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15
Q

What is stable angina?

A

This refers to chest pain that occurs intermittently over a long period of time with the same, perdictable pattern of onset, duration, and intensity of symptoms

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16
Q

What is an acute myocardial infarction (AMI)?

A

Occurs because of sustained cardiac ischemia causing irreversible myocardial cell death

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17
Q

What is an acute coronary syndrome (ACS)?

A

Cardiac ischemia is prolonged and not immediately reversible. Associated with the deterioration of a once stable atherosclerotic plaque.

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18
Q

Why does pain happen with AMI?

A

Severe, immobilizing ischemic chest pain not relieved by rest, position change or nitrate. Usually persists more than 20 minutes

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19
Q

What is the reason for nausea and vomiting with an AMI?

A

Can result from reflex stimulation of the vomiting center by the severe pain

20
Q

What is the reason for diaphoresis with AMI?

A

Due to catecholamine release, epinephrine and norepinephrine, resulting in vasoconstriction of peripheral blood vessels.

21
Q

What is the reason for shortness of breath in AMI?

A

Response to catecholamine release. CO will be initially elevated and then decrease with decreased myocardial contractility. Will see pulmonary crackles with left ventricle dysfunction.

22
Q

What is the reason for fatigue with AMI?

A

Ventricular dysfunction and decreased myocardial contracility with poor perfusion of tissues

23
Q

What is the reason for low grade fever with AMI?

A

Increase in temperature is a systemic manifestion of the inflammatory process caused by myocardial cell death.

24
Q

What is the physiology of coronary artery disease?

A

Risk factors lead to:

  1. Fatty streak formation
  2. CAD
  3. Plaque rupture
  4. Platelet aggregation
  5. Thrombus
25
Q

What is unstable angina and how is it treated?

A

AKA Acute Coronary Syndrome (ACS)

Chest pain is new in onset, occurs at rest, or has worsening pattern.

Unpredictable

Easily provoked by minimal or no exertion

Women: occurs more frequently, unusual symptoms of fatigue, SOB, indigestion, and anxiety

26
Q

What is an acute myocardial ischemia/infarct (AMI) and how is it treated?

A

Angina means transient chest pain r/t myocardial ischemia

Irreversible cellular injury with prolonged myocardial ischemia

Chest pain longer than 20 minutes

27
Q

What are the clinical manifestations of AMI?

A
  • Pain
  • Nausea and Vomiting
  • Diaphoresis
  • SOB
  • Fatigue
  • Low grade fever
  • 25% of patients have silent or painless AMI
  • Infarction pain lasts longer than 20 minutes
28
Q

What is the diagnostic workup for AMI?

A
  • Hx and physical examination
  • 12 lead EKG
  • Cardiac troponin, chemistry profile, CBC
  • Chest X-ray
  • Coronary angiogram
  • Echocardiogram
29
Q

What is the significance of supply and demand imbalance in AMI?

A

Primary problem is tha tthe patient’s cardiac demand for oxygen is not being met. This could be due to paitent’s excessive cardiac workload or inadequate supply of O2 to heart due to coronary artery plaque.

30
Q

How might you decrease the workload on the heart?

A

Decrease demand and increase supply

31
Q

How might you help to increase the supply of oxygen to the heart?

A

Decrease SNS, decrease temperature changes

32
Q

What medications are used for AMI?

A
  1. Lipid lowering agents (prevention)
  2. Antiplatelet medication (ASA)
  3. Nitroglycerin (vasodilation)
  4. Morphine Sulfate (chest pain, decrease workload)
  5. Beta Blockers
  6. Calcium Channel Blockers
33
Q

What is the treatment for ACS/unstable angina?

A

Thrombolytics

  1. Restores blood flow to the myocardium by dissolving the thrombus in the coronary artery
  2. Limited window of opportunity in treating AMI
  3. Baseline coagulation studies
  4. Assess for contraindications
  5. Assess for S/Sx of bleeding
34
Q

What is preload?

A

Preload is pressure in the heart caused by volume. The nitrates effectively move part of this blood out of the heart and into the blood vessels, thereby decreasing preload or filling prssure.

35
Q

What is afterload?

A

Afterload is the SVR (systemic vascular resistance) or force the ventricles must push against to deliver blood to the body. A decreased afterload will decrease the work of the heart, thereby reducing myocaridal oxygen demand.

36
Q

How to nitrates/nitrites reduce the work of the heart?

A

Reduce preload by venodilation - causing relaxation of smooth muscle that surrounds veins and also causing dilation of coronary arteries.

37
Q

How do beta adrenergic blockers reduce the work of the heart?

A

Decrease myocardial work (contractility) and slow the heart rate. This decreases myocardial need for oxygen, because a decreased HR consumes less oxygen.

38
Q

How do calcium channel blockers decrease the workload of the heart?

A

Decrease BP through vasodilation by blocking calcium channels in the vascular smooth muscles and the heart itself, thus reducing cardiac contractility. This decreases SVR and decrease afterload. Within the heart these medications also decrease AV conduction and the refractory period thereby controlling atrial arrhythmias.

39
Q

How do antiplatelets reduce the workload of the heart?

A

Prevent clot formation by preventing platelet aggregation/adhesion. They are used for MI prophylaxis and after stent placement.

40
Q

What is the goal for treating AMI?

A

Goal is to reperfuse ischemic tissue and prevent or minimize irreversible cellular myocardium death. Cardiac cells can withstand ischemia for about 20 minutes before necrosis occurs.

41
Q

What is the action of thrombolytics?

A

Convert plasminogen to plasmin. Plasmin digests fibrin and fibrinogen, thus dissolving clots. Agents such as t-PA should be initiated within six hour of first symptoms unless contraindicated.

42
Q

What is the action of antianginal agents?

A

Used for chest pain

  • Nitrates/nitrites
  • beta blockers
  • calcium channel blockers
  • antiplatelet agents
43
Q

What is the action of morphine sulfate?

A

Use in AMI, relieves pain and decreases contractility of myocardium, thereby reducing oxygen demand

44
Q

What is the action of antidysrhythmics?

A

Generally used to suppress or control cardiac arrhythmias. Exact mechanisms of action vary depending on the group used. The therapeutic goal is to increase hemodynamic performance and decrease symtpoms. Nursing responsibilities include monitoring pulse, BP, and ECG, taking an apical pulse before administration of oral doses, withholding dose and notifying prescriber if Hr is less than 50bpm, administering medication with a full glass of water and medication specific patient teaching

45
Q

What is the action of ACE inhibitors?

A

Useful to control BP and treat complication of heart failure.

Reduces afterload by preventing the breakdown of the vasodilating substance bradykinin and formation of angiotensin II (resulting in vasodilation and decreased SVR)

Reduce preload by blocking the release of aldosterone and preventing sodium and water reabsorption in the kidney resulting in decreased blood volume

SEMESTER FOUR!! Nursing 214 (52 decks)

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