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ACS > General ACS > Flashcards

General ACS Flashcards

1
Q

What are the three terms included under the ACS umbrella?

A

Unstable angina, NSTEMI, STEMI

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2
Q

What is unstable angina? What is the chest pain characteristic?

A

Ischemia for 10-20 minutes. Chest pain at rest.

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3
Q

What are the characteristics of unstable angina? Any ECG changes? Are cardiac biomarkers released?

A

The ischemic event is not severe enough to cause myocardial necrosis. ST elevation is not typically present, but there may be temporary ST segment depression or T-wave inversion. No, cardiac biomarkers are not released.

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4
Q

What is an NSTEMI? What is the chest pain characteristic?

A

Injury to the cardiac muscle for greater than 20 minutes. Severe CP lasting >20 minutes.

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5
Q

What are characteristic of NSTEMI? Any ECG changes? Are cardiac biomarkers released?

A

Ischemic changes. ST segment depression or T-wave inversion persisting after pain is relieved. Yes, biomarkers released.

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6
Q

What is a STEMI? What is the chest pain characteristic?

A

Infarct (cell death) to myocardial tissue. Severe chest pain lasting >30 minutes.

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7
Q

What are the characteristics of STEMI? ECG changes? Are cardiac biomarkers released?

A

Ischemic changes that are associated with ST segment elevation >1 mm. Yes, biomarkers are released.

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8
Q

What is the most common cause of decreased O2 supply to myocardial cells?

A

CAD

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9
Q

Arteries are comprised of what three layers?

A

Intima, media and adventia

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10
Q

Describe how endothelial dysfunction plays a role in atherosclerosis?

A

Chronic inflammatory condition which produces substances that cause cellular adhesion, decreased nitric oxide production and increased release of vasoconstrictor substances.

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11
Q

Men over what age and what characteristic of women are more at risk of development CAD?

A

Men over 55 and women who are post-menopausal

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12
Q

How does tobacco contribute to the development of CAD?

A

Increasing LDL, decreasing HDL, and promoting vasoconstriction and damaging endothelium

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13
Q

Metabolic syndrome contributes to the development of CAD. It’s diagnosis is made when what characteristic are present?

A

Elevated fasting BG, HTN, abdominal obesity

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14
Q

What are examples of modifiable RF for CAD?

A

Smoking, high fat diet, HTN, stress, diabetes, physical inactivity, overweight, a fib, high cholesterol.

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15
Q

What are examples of non-modifiable RF for CAD?

A

Age, genetics/family history, sex, personal situations (lack of access to healthy food, clean water, health care)

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16
Q

Why is diabetes a major RF for the development of CAD?

A

Often undiagnosed/untreated which increases impact on development of CAD, contributes to endothelial dysfunction, it is linked with HTN, obesity, hypercholesterolemia, and their attendant effects on coronary vasculature

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17
Q

What two areas are being researched as RF for CAD?

A

CRP and lipoprotein a

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18
Q

How does obesity contribute to an increased risk for CAD (it is not a direct RF)?

A

Increase insulin resistance, reduce exercise tolerance

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19
Q

What is a key difference in RF between men and women with CAD?

A

First cardiovascular events in women are often fatal

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20
Q

All RF that are associated with the development of CAD are associated with what two things?

A

Inflammation and endothelial dysfunction

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21
Q

What cardiac muscle is supplied by the RCA? What conducting tissue?

A

Right atrium, right ventricle, portion of the posterior and inferior surfaces of the LV. SA node in 55% AV node is 90%

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22
Q

What artery does the LAD arise from? What cardiac muscle is supplied? What conducting tissue is supplied?

A

Left main coronary artery. Portions of anterior left and right ventricles, interventricular septum. Bundle branches.

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23
Q

What artery does the circumflex artery arise from? What cardiac muscle is supplied? What conducting tissue is supplied?

A

Left main coronary artery. Portions of left atrium and left lateral ventricle. SA node in 45%, AV node in 10%.

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24
Q

What are characteristics of endothelium? * 5 things

A

Blood-compatible container, as long as blood is in contact with a healthy endothelial lining it remains a fluid/non-thrombotic state. Selective barrier between vessel lumen and surrounding tissue controlling passage of WBC in/out of bloodstream. Involved in regulation of vascular tone and growth. Plays a role in regulation of thrombosis and fibrinolysis. Plays a role in immune and inflammatory response.

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25
Q

Walk me through the development of a plaque

A

Fats and lipids floating around start to damage endothelium. Lipids get under endothelium and initiate an inflammatory response (WBC start to migrate and attach to intima). Foam cell turns into a fatty streak and secretes pro-inflammatory substances which increase the size of the streak becoming a fatty plaque. The larger the plaque the more pro-inflammatory substances released. Smooth muscle cells move from media to intima and form a fibrous cap. Cap becomes fragile and erratic blood flow can damage cap which causes an inflammatory response. More WBC will enter and increase the size of the plaque and a clot will form over the damaged area. Clot will limit/blood BF in artery.

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26
Q

What is shear stress? What arises from shear stress? What has shear stress been implicated in?

A

Fluid “drag force” exerted by BF against BV wall. Normal BF is “laminar” (no “eddies”, swirls, turbulence. It is streamlined). If flow is not laminar is can lift and damage and promote inflammatory process in endothelial cells. Impact cellular regrowth. Formation of atherosclerosis.

27
Q

In terms of a plaque - what does stable angina, unstable angina, NSTEMI and STEMI relate to?

A

Stable angina - stable fixed atherosclerotic plaque
Unstable angina - unstable plaque
NSTEMI - thrombus on plaque partially occluding artery
STEMI - thrombus on plaque fully occluding artery

28
Q

What type of receptors are activated by ischemia? How do each of these result in pain?

A

Chemoreceptor and mechanoreceptors. Chemoreceptors activate bradykinin which stimulated inflammatory and pain response. Mechanoreceptors stimulated by stretch from edema, altered local contractility or ischemic injury. Both stimulate visceral afferent fibres which conduct pain. Fibres connect with different dermatomes which may change where/how individual experiences pain.

29
Q

Where are common locations for pain related to cardiac ischemia?

A

Chest, back, R/L arm, jaw, neck, epigastric discomfort, fatigue

30
Q

Who is silent ischemia common among?

A

Elderly and diabetics, people with high pain threshold.

31
Q

What are some key points about women and heart disease?

A

Diabetic women are at increased risk, tend to develop CAD ten years later than men, can have atypical symptoms (nausea, SOB, fatigue), increased stress in relation to social supports, increased risk of anxiety and depression.

32
Q

What is the initial treatment of ACS?

A

Nitrates, ASA, O2 if SpO2 <90%

33
Q

What is most important about tasks related to confirmed or suspected ACS?

A

Tasks must be time-sensitive, “time is muscle”. Prompt treatment of chest pain is not to be sacrificed for a complete physical exam.

34
Q

What do nitrates do in the initial treatment of ACS?

A

Dilate large coronary arteries and arterioles, venous dilation (decreases preload), systemic arterial dilation (at higher IV doses - decreased preload), enhances collateral flow (for individuals with long-term heart disease and where this flow has developed)

35
Q

Treatment considerations of nitrates in initial treatment of ACS

A

Use with caution in pt with SBP less than 90 or decrease by 30 from baseline (causes decreased preload therefore decreased CO and BP), those with marked bradycardia <50 or tachycardia >100 as these individuals could have hemodynamic instability relating to their BP and nitro will decrease preload. If patient is taking phosphodiesterase-5 inhibitors within the last 24 hours (48 hr for Cialis), if they have hypertrophic cardiomyopathy or severe aortic stenosis.

36
Q

What two things does the duration of the hypoxic episode reflect?

A

Amount of cardiac damage and the amount of each specific cardiac enzyme released.

37
Q

How are cardiac enzymes measured?

A

According to a very specific protocol that reflects their pattern of release.

38
Q

What is the rationale for using troponin blood test for MI diagnosis?

A

Toponin I and T are two isotopes found in myocardium and are released when myocardial muscle is damaged. Troponin I is found exclusively in the myocardium and has 100% sensitivity for MI.

39
Q

What is the rationale for using creatinine kinase (CK) for MI diagnosis?

A

Enzyme that diffuses from cellular damage.

40
Q

What is the rationale for using glucose in MI diagnosis?

A

Glucose is elevated when endogenous epinephrine is mobilized.

41
Q

What is the rationale for using creatnine in MI diagnosis?

A

Waste product formed during muscle protein metabolism and is a reflection of the excretory function of the kidney. Decreased EOP would result in creatnine to rise.

42
Q

What is the rationale for using GFR in MI diagnosis?

A

Decreased EOP can affect renal function. Furthermore, some drugs used in the treatment of ACS can impair renal function (need to know baseline).

43
Q

Why is aspirin given in the initial treatment of ACS? What is the initial dose of aspirin ususally? Maintenance doses? What does early administration of aspirin reduce?

A

It inhibits platelet aggregation. 160-320 mg of non-coated tablets for patient to chew, and then daily 81 mg or 325 mg of enteric coated tablets. Reduces mortality significantly.

44
Q

Considerations of initial treatment of ACS with oxygen

A

Only use if SpO2 <90%. Too much oxygen can cause coronary artery vasoconstriction, increase coronary vascular resistance, decrease CO, increase free radicals and cause reperfusion arrhythmias.

45
Q

If the area of ischemia is unknown, what are the best leads to use “ST fingerprint” mode in if a continuous 12 lead ECG monitor is unavailable?

A

Leads III and V3

46
Q

Infarction to the right ventricle can occur in conjunction with what other area of the heart?

A

Inferior or posterior wall infarction.

47
Q

What leads view the lateral aspects of the heart?

A

I, aVL, V5, V6

48
Q

List the contiguous leads

A 
I, aVL
II, III, aVF
V1, V2
V3, V4
V5, V6
49
Q

What leads view the inferior aspect of the heart?

A

II, III, aVF

50
Q

What leads view the septal region of the heart?

A

V1, V2

51
Q

What are the anterior leads?

A

V1, V2, V3, V4

52
Q

What leads view the anterior aspect of the heart?

A

V3, V4

53
Q

What might a large anterior wall MI be associated with? What ECG leads would you expect to see changes? What artery is likely affected?

A

Ventricular pump failure, cardiogenic shock, death. V2, V3, V4. Proximal LAD.

54
Q

An inferior wall MI would be seen in which ECG leads? What artery is likely occluded? What might be seen in someone with this type of MI?

A

II, III, aVF. RCA. Conduction disturbances as the RCA supplies blood to the SA node (55%) and AV node (90%). You might see bradydysrhythmias.

55
Q

A lateral wall MI would be seen in which ECG leads? What artery is likely occluded? What other location would you want to look into as being involved? Clinical implications?

A

V5, V6, I, aVL. Left circumflex. Posterior wall as also fed by circumflex. Hemodynamic changes can occur and dysrhythmias related to SA and AV node dysfunction.

56
Q

An anterolateral MI would be seen in which ECG leads? Which artery is likely occluded? Clinical implications?

A

V1 - V6, I, aVL. Left main coronary artery. Hemodynamic compromise, heart failure, pulmonary edema, cardiogenic shock, intraventricular conduction disturbances and intraventricular septal rupture.

57
Q

A septal MI would be seen in which ECG leads? Which artery is likely occluded?

A

V1, V2. LAD.

58
Q

A posterior MI would be seen in which ECG leads? Which artery is most likely occluded? What other area should be evaluated for involvement? Clinical implications?

A

V1, V2. Left circumflex or RCA (reciprocal changes). Lateral wall. Hemodynamic changes, dysrhythmias related to SA and AV node dysfunction.

59
Q

What artery is occluded in a RV infarct? What are clinical implications? Does a standard ECG show this?

A

Proximal RCA. RV ischemia can be identified in 1/2 of inferior wall MI. Hemodynamic effects can be anticipated. If infarct is large enough, cardiogenic shock can occur. No, a right-sided ECG would need to be done to rule out RV infarct (if patient has has inferior wall MI).

60
Q

If you see Q waves on an ECG, what might this indicate?

A

Myocardial necrosis or resolution (old MI if Q wave present with no ST elevation).

61
Q

If a patient is receiving a nitro infusion, and is experiencing nausea, fatigue, and diaphoresis, why might the nurse choose to go up on the infusion even if no pain is present?

A

Nausea, diaphoresis and profound fatigue are all signs of myocardial ischemia and nitro can work to augment the coronary blood flow through vasodilation of the coronary arteries.

62
Q

What is the criteria to diagnose a STEMI?

A

ST elevation in two or more contiguous leads. New LBBB (guidelines have changed).

63
Q

What are reciprocal changes? Where do they show up?

A

Leads opposite to area of infarct can have ST depression. PAILS. Posterior, Anterior, Inferior, Lateral, Septal. Changes will occur in the next letter of the acronym where ST elevation is seen.

ACS (3 decks)

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