Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ADULT 2 > Exam One > Flashcards

Exam One Flashcards

1
Q

Acute Coronary Syndrome (general)

A

Reduction/occlusion in the coronary arteries and degree of damage to the myocardium (heart muscle). This includes NSTEMI, STEMI, and unstable angina. All three types start with some sort of damage to the endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

STEMI

A

ST elevation myocardial infarction… the most dangerous of myocardial infarctions because it indicated complete occlusion of the artery!!!! Heart muscle is blocked off from oxygen = necrotic cardiomyocytes

Transmural infarction (across the whole myocardium)

Can lead to rupture of papillary muscles which can lead to further complication of mitral regurgitation or mitral prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Non STEMI (NSTEMI)

A

Does not involve the presence of ST elevation on a 12 lead EKG… rather you see an ST segment depression

Characteristic finding = subendocardial infarction/ST segment depression

There is no elevation in cardiac markers/enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Non modifiable risk factors for plaque build up

A

Aging, male sex, family history, caucasian

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

unstable angina vs stable angina

A

Unstable angina - you have chest pain even when you’re resting (a lot more serious). Pain usually lasts longer than 20 min and is unrelieved by nitroglycerin.

Stable angina - chest pain that goes away when resting - usually lasts 3-5 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Modifiable risk factors for NSTEMI/myocardial infarction

A

Smoking, hypertension, dyslipidemia, obesity, poor diet, diabetes, sedentary lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Is acute coronary syndrome a medical emergency?

A

Yes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute Coronary Syndrome Clinical Presentation

A

Central chest pain (“crushing” “heaviness” “tightness”)

Pain radiates to neck, jaw, left arm

Diaphoresis (bc sympathetic activation)

Feeling of impending doom (anxiety)

N/V

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Troponin and CK-MB during STEMI/NSTEMI

A

Elevated

They get released into the blood stream when the heart muscle becomes necrotic.. so we measure to see if heart muscle has died :-)

Troponin is released very fast, hits high peak at day 2 after chest pain and then decreases

CK-MB is also released fast (but not as high as troponin) and then decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which heart marker (enzyme) is most important to measure for STEMI/NSTEMI?

A

Troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How do heart enzyme levels change during stable/unstable angina?

A

They don’t. They stay the same. Troponin and CK-MB only rise during STEMI/NSTEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patient shows up to ER with major chest pain radiating to left arm. What do you do first?

A

Investigate! Start 12 lead EKG, get full blood count, EUC, check glucose and lipid profiles, cardiac enzymes (TROPONIN !!, CK-MB)

X-ray to rule out other differentials if suspected

DO NOT DELAY TREATMENT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ECG Changes in ACS - unstable angina

A

20% may be normal initially
Usually don’t see any ECG changes
Normal or sometimes T wave inversion (depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Unstable angina physiology

A

1st hits the left anterior descending artery (which supplies anterior wall and septum)

2nd hits the right coronary artery (supplies right wall and posterior wall)

3rd hits the left circumflex artery (which supplies lateral wall of heart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which artery is most affected during myocardial infarction/”heart attack” ?

A

The left anterior descending artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

STEMI ECG Changes

A

ST elevation

Also need to look for new left bundle branch block (WILLIAM)

Widened QRS
V1 = W shape
V6 = M shape

New left bundle branch block may suggest infarction of hear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Initial management of all ACS - MOAN

A

Morphine (IV Opioids)
Oxygen (if < 93%)
Aspirin (+ lopiridil)
Nitrates (to reduce <3 workload and increase O2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

STEMI Definitive Managment

A

Emergency Reperfusion

1st choice = PCI = primary percutaneous coronary intervention. Angiogram is performed. Dilated balloon/stent inserted to clear blockage.

2nd choice = fibrinolytic therapy = thrombolysis. Use streptokinase, alteplase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Unstable Angina/NSTEMI Definitive Management

A

High Risk Patient = start on anti platelets, anticoagulants, beta blockers. Consider glycoprotein inhibitors and revascularisation.

Low Risk/Intermedate Patients = continuous monitoring of cardiac enzymes (TROPONIN) and ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Ongoing Management of all ACS

A

Lifestyle modification!!!

Quit smoking
Reduce alcohol intake
Eating healthy
Exercise
Lose weight 
Pharm (BAAAS)
Beta Blockers - BP, HR
Aspirin - Prevent clots from forming
ACE Inhibitors/Angiotensin Receptor Antagonist - help reduce BP/workload
Statins - help reduce cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Myocardial Infarction Definition

A

limited blood supply to the myocardial tissue that causes it to die/become necrotic

22
Q

Myocardial Infarction Causes

A

Blockage in coronary artery due to CAD (most common)

Coronary spasm/constriction from drug usage (cocaine)

HTN

Damage to artery due to coronary artery dissection (tear in inner layer of artery “tunica intima” which causes it to leak into “tunica media”)

23
Q

Cardiac output is the amount of

A

blood ejected by the heart in 1 minute and is measured in liters.

24
Q

What determines cardiac output?

A

Hr and stroke volume and is controlled by both

25
Q

Stroke volume is the volume of

A

blood ejected during systole per minute.

26
Q

Filling pressure of the right ventricle is based on

A

the right atrial pressure

27
Q

Filling of the left ventricle is based on

A

the left atrial pressure

28
Q

How to calculate Cardiac Output

A

SV x HR

29
Q

Decreased HR and increased SV cause

A

an increase in CO

30
Q

Increased HR and increased SV cause

A

an increase in CO

31
Q

Normal CO for an adult is

A

4 - 7 L/min

32
Q

3 factors affect SV

A

preload, after load, contractility

33
Q

Preload

A

amount of blood returning to the heart from the pulmonary vessels (left side) and the venous return (right side).

34
Q

Afterload

A

the resistance that the heart must overcome to pump blood through the valves and aorta to the peripheral circulation

35
Q

Contractility

A

the amount of force generated by the myocardium to eject blood into circulation.

36
Q

Increasing cardiac output

A

increased preload - blood returns to the right atrium

Increased contractility occurs

Decreased afterload - decreases pressure that the heart must pump against.

37
Q

Factors affecting HR

A

HR affects the cardiac output by causing a decrease or increase in SV

HR is controlled by baroreceptors in the aortic arch, which are sensitive to changes in the BP

Stimulation of the parasympathetic nervous system (vagus nerve) decreases the HR

Stimulation of the sympathetic nervous system increases the HR

38
Q

Atherosclerois is

A

A type of arteriosclerosis. It is a soft intraarterial build up of fat and fibrin that eventually thickens and hardens the arterial walls through several ways.

Atherosclerosis is NOT a single disease or problem. It is a process that affects the entire arterial vascular system and is the leading cause of coronary artery and cerebrovascular disease.

39
Q

Causes of atherosclerosis

A

Consumption of high fat and LDL foods

HTN, smoking, + obesity (inhibits the oxidation of LDL)

Diabetes, hyperlipidemia

Increased C-reactive protein, insulin resistance, infection and periodontal disease (have been found to damage endothelium)

40
Q

Atherosclerosis nursing teachings

A

Encourage intake of enriched fortified cereals that contain folic acid, vitamin B, + fresh veggies

Discourage meals high in LDL (red meats, eggs, food fried in saturated fats)

Exercise + weight management

Diabetes - control glucose

41
Q

Cardiac ischemia is

A

Partial or temporary loss of blood flow/tissue oxygenation

42
Q

Ischemia in the heart is called

A

Angina - chest pain that occurs when the myocardium does not get enough blood.

43
Q

In a severe ischemic environment cardiac cells remain viable for

A

approx. 20 minutes

44
Q

Can myocardial ischemia be asymptomatic?

A

Yes, it can be “silent” with no chest pain

45
Q

Q Wave

A

0.04 seconds wide OR 1/3 height of the R wave

May take 8-48 hours to show up on the ECG

Never goes away.

46
Q

Transmural injury on ECG

A

Marked ST elevation with hyper acute T wave changes

47
Q

Necrosis on ECG

A

Pathologic Q waves, less ST elevation, terminal T wave inversion

48
Q

Ischemia ECG

A

ST depression

49
Q

Northwest Deviation ECG

A

Emphysema
Hyperkalemia
Ventricular Tachycardia

50
Q

Verticle Axis ECG

A

1 small square = 1mm
1 large square = 5mm
2 large squares = 1mV

51
Q

Horizontal Axis ECG

A

1 small square = 0.04s
1 large square = 0.2s
5 large squares = 1s

ADULT 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions