Cardiovascular Flashcards

1
Q

is a condition that occurs when perfusion of the myocardium is compromised due to some imbalance between myocardial oxygen supply and/or demand

A

Ischemia

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

is regulated by the patency or size of the lumen of the coronary vessel, the ability of the ventricular wall to compress and the amount of time the ventricle spends in diastole

A

Oxygen supply

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

is dependent upon myocardial contractility, HR, and amount of ventricular stress

A

Demand

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

an abrupt or acute reduction in blood flow to the myocardium caused by thrombus, coronary vasospasm or platelet aggregation.

A

Supply ischemia

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

an increase in need for oxygen and nutrients due to exercise or stress

A

Demand ischemia

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

3 common causes of ischemia?

A
  • blockage of coronary artery (thrombus)
  • spasm of coronary artery
  • coronary artery obstruction (formation of plaque)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

It only takes ___ mins to progress to necrosis if the flow to the myocardium is not restored

A

20 mins

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

is a continuum that begins with plaque rupture within a coronary artery and results in infarction of myocardial tissue if perfusion is not restored in good time.

A

acute coronary syndrome

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

3 phases of acute coronary syndrome

A
  • unstable angina
  • NSTEMI
  • STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Formation of fatty fibrous lesion with a lipid core and fibrous cap

A

stable angina

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

Rupture of fibrous cap allows leaking of lipids and platelet aggregation

A

unstable angina

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

Clot formation

A

NSTEMI

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

Thrombus causes occlusion of vessel

A

STEMI

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

The T wave represents

A

ventricular repolarization

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

is often seen on an ECG as ST segment depression and T wave inversion during the period of pain.

A

unstable angina

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

necrosis of myocardial tissue occurs, but because the full thickness of the ventricle is not involved, electrical activity is not disrupted and there are no obvious changes on the ECG.

A

non-STEMI

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

is an enzyme found in the heart, brain, and skeletal muscle and is released when these cells are damaged.

A

Creatinine Kinase (CK)

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

CK-MM

A

skeletal muscle

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

CK-BB

A

brain tissue

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

CK-MB

A

myocardial tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q
  • a protein found in skeletal and cardiac muscle

- increases earlier, more quickly, and stays elevated longer than CK

A

Troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

arterial occlusion is complete, resulting in necrosis of the full thickness of the ventricle, which alters electrical conduction.

A

STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

seen as ST elevation on the ECG and cardiac biomarkers are elevated

A

STEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

cell death and necrosis has occurred; seen as pathological Q waves on the ECG; cells replaced with scar tissue.

A

zone of infarct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

injured but potentially viable tissue, surrounding the area of infarct; seen as ST segment elevation on the ECG

A

zone of injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

outer region of the infarcted area; cells are still viable; manifests as T wave inversion on the ECG.

A

zone of ischemia

27
Q

is depicted by the flipped or inverted T wave

A

ischemia

28
Q

depicted by the elevated ST segment

A

injury

29
Q

depicted by a pathological Q wave (deep or wide)

A

infarct

30
Q

are often caused by movement to anaerobic metabolism in the presence of ischemia without manufacture of enough ATP

A

Dysrhythmias

31
Q

decreases afterload through vasodilation

A

morphine

32
Q

vasodilates vascular smooth muscle, decreases afterload and myocardial oxygen demand and improves coronary and artery blood flow.

A

nitroglycerin

33
Q

prevents platelet aggregation; should be chewed

A

ASA

34
Q

decrease workload of the heart by decreasing contractility and heart rate

A

beta-blockers

35
Q

prevents activation of the glycoprotein IIIb/IIIa complex required for platelet aggregation

A

Adenosine Diphosphate Receptor Antagonist (Clopidogrel)

36
Q

accelerates action of anti-thrombin, which inactivates thrombin to prevent formation of thrombus

A

Anticoagulant (Heparin)

37
Q

fibrinolysis is achieved with tenecteplase (TNK) to re-establish artery patency.

A

Reperfusion therapy

38
Q

A balloon tipped catheter is used to open occluded arteries in the catherization lab; a stent may be inserted to keep the artery open

A

PCI- percutaneous coroniary intervention

39
Q

A surgical technique where the patient’s own blood vessels are harvested from a distant site, and used to bypass an occluded artery.

A

CABG- coronary artery bypass grafting

40
Q

Decreases thrombus formation by making platelets less “sticky” so that risk of clot formation is decreased.

A

Glycoprotein IIIb/IIIa inhibitors

41
Q

Results in relaxed vessels and decreased LV workload

Prevents conversion of angiotensin I to angiotensin II

A

ACE-I

42
Q

Prevents angiotensin from attaching to receptors, which inhibits vasoconstriction and ultimately decreases LV workload

A

ARB (angiotensin receptor blocker)

43
Q

Inhibit HMG-CoA Reductase, the enzyme needed for cholesterol synthesis, reducing LDL levels

A

Statins

44
Q

Due to fluid shifting from capillaries, the individual develops congestion of peripheral tissues, including the liver, GI tract and distant periphery such as the ankles

A

right sided HF

45
Q

Pulmonary congestion occurs, as fluid leaks into pulmonary tissues

A

left sided HF

46
Q

what is a normal ejection fraction?

A

50-75%

47
Q

the amount of volume in the ventricle at the end of diastole

A

preload

48
Q

the amount of resistance the ventricle is up against as it tries to contract

A

afterload

49
Q

the ability of the muscle to stretch and contract, like an elastic

A

contractility

50
Q

refers to the patient for whom normal daily falls to produce symptoms

A

class I

51
Q

refers to those whose normal daily activities initiates symptoms but the patient controls them with rest

A

class II

52
Q

is reserved for those in whom minimal activity produces symptoms, but they remain symptom free at rest

A

class III

53
Q

is attributed to those for whom any activity precipitates symptoms

A

class IV

54
Q

____ balances arterial and venous vasodilation reducing BP, permitting the LV to eject more efficiently, raising the CO and decreasing serum levels of NE and aldosterone, and blunting activation of the RAA system

A

Nesiritide (a synthetic BNP)

55
Q

is a unique form of pacemaking that helps to re-establish normal coordinated contractions between the atria and ventricles of the heart

A

Cardiac resynchronization therapy (CRT)

56
Q

are medications that improve contractility, decrease afterload

A

inotropes

57
Q

reduce volume and thus, pressures by inducing sodium and water excretion

A

diuretics

58
Q

Increase contractility, but also increase oxygen consumption and should be used with caution

A

beta adrenergic agonists

59
Q

also improves contractility through inotrope effects but also acts as a negative chronotrope, reducing heart rate and thus myocardial workload

A

cardiac glycosides (ex. Digoxin)

60
Q

improve contractility, vasodilate, increase CO and reduce BP, given IV and in the short term

A

phosphodiesterase inhibitors

61
Q

Prevents angiotensin II activity as well as that of aldosterone; improves hemodynamic function; decreases afterload and MV02

A

ACE-I

62
Q

increase venous capacity, reducing afterload

A

vasodilators

63
Q

have negative chronotropic and inotropic activity, decreasing the overall workload of the heart

A

Beta blockers