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Cardiovascular > Newman: Questions for CV disease and CAD > Flashcards

Newman: Questions for CV disease and CAD Flashcards

1
Q

What are the determinants of BP?

A

P = Q x R

*altering flow and resistance

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2
Q

the ability of the arterioles to clamp down ro relax

A

resistance

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3
Q

What substances can increase vascular resistance?

A

Norepi
Epi
Angiotensin II

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4
Q

What substances decrease vascular resistance

A

NO

prostacylin

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5
Q

T or F: Flow = Cardiac Output

A

True

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6
Q

CO =

A

SV x HR

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7
Q

quantity (CCs) of blood ejected from the left ventricle into the aorta every cardiac cycle

A

stroke volume

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8
Q

What are the determinants of SV?

A

preload, afterload, contractility

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9
Q

the volume of the left ventricle at the end of diastole

A

preload (EDV)

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10
Q

T or F: An increase in preload will increase blood pressure

A

T

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11
Q

Why would you insert a pulmonary artery catheter?***

A

to measure preload: ballon inflates in the (left ventricle?) and the preload can be measured (left ventricular end diastolic pressure)

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12
Q

A bigger left ventricle (dilation) will (increase or decrease) the afterload.

A

increase

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13
Q

The inherent ability of the heart to contract–is independent of preload and afterload

A

contractility

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14
Q

SV / EDV =

A

ejection fraction

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15
Q

A pt has an ejection fraction of 30%, is that good or bad?

A

bad

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16
Q

A pt has an ejection fraction of 70%, is that good or bad

A

good

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17
Q

renin is secreted fron JG apparatus in response to ____

A

dec Q, CO, SV

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18
Q

Angiotensin I goes thru the ____ and is converted to ang II by_____

A

lungs

converting enzyme

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19
Q

What 2 important things does angiotensin II do?

A
  1. potent vasoconstrictor (inc resistance)

2. stimulates the secretion of aldo from the adrenal glands

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20
Q

An decrease in the amount of angiotenisn II would (inc or dec) BP

A

decrease

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21
Q

What does aldosterone do?

A

causes reabs of Na and excretion K+

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22
Q

Would a person in HF want to have high or low levels of aldosterone?

A

low – do not was to reabsorb any more Na/H2O

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23
Q

A pt presents to you with chest pain only upon exertion and is relieved by rest.
What would a treadmill test tell you?
What would a cardiac catherterization tell you?
What pharm

A

treadmill: will increase HR and SBP, which exacerbate the exertional chronic stable angina

cardiac cath will tell you how blocked he is, but I don’t think he’s a candidate for this?

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24
Q

A pt has severe chest tightness which wakes him from sleep

normal ECG

A

acute coronary syndrome

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25
Q

You have 3 vessel coronary disease. What do you do now?

A

bypass–STAT!

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26
Q

pt presents to the ED with severe chest pain. the ECK reveals ST elevation in leads 2, 3, and avF what do you do?

A

cath?

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27
Q

3 syndromes of coronary disease

A

chronic stable angina
Acute coronary syndrome
ST elevation MI

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28
Q

62 yr old male walks his dog and gets tightness in chest with SOB. He sits down and the pain goes away.
Dx

A

chronic stable angina

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29
Q

Man carrying bag of groceries upstairs and it got better when he sat down.
Dx

A

chronic stable angina

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30
Q

tighness/contrictoion in chest + SOB + gets better when sits down/at rest

A

chronic stable angina

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31
Q

exertional symptoms

A

chronic stable angina

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32
Q

inadequate supply of blood to myocardium (heart blockages) and increased demand relative to the supply

A

chronic stable angina

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33
Q

2 major determinates of myocardial demand

A

systolic BP

HR

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34
Q

Effect of exercise on HR and systolic pressure

A

inc HR and inc systolic pressure

35
Q

What reduces supply in chronic stable angina?

A

arthlerosclerosis

36
Q 
Wakes up with elephant sitting on chest
pale
sweating
breathing hard
*this is not dependent upon exertion
A

acute coronary syndrome

37
Q

pathophys of acute coronary syndrome

A

arthlerosclerotic plaque narrown lumen –> ruptures–>

  1. increased constriction/resistance
  2. thrombotic state in which blood clots form at area of rupture
38
Q

T or F: acute coronary syndrome is a problem of supply and demand

A

false

*there is no inc demand on the heart, just a problem with supply

39
Q

What is the diff btwn MI and acute coronary syndrome?

A

in MI, there is ZERO perfusion/supply = CA is 100% occluded

Has ECG changes!

40
Q

problem of supply and demand–inc demand will not lead to a proportinal inc supply

A

chronic stable angina

41
Q

O2 supply is a function of ____

A

coronary blood flow

42
Q

arthleroscloerotic plaque causes

A

inadeqate supply

43
Q

Myocardial demand is a function of

A

systolic BP and HR

44
Q

blockage restricts O2 supply when it takes up ___% of CA lumen

A

70%

45
Q

heart pains are always more than _____mins and never more than ____mins (time)

A

5 mins; 30 mins

46
Q

Heart pains assc with activities is better or worse prognosis

A

better prognosis

47
Q

Chronic stable angina is assc with (inc or dec) catecholamines

A

inc catecholamins –> skin gets pale

= over sympathetic activity

48
Q

angina pectoris/chronic stable angina assc with

A

diaphoresis

sense of breathlessness

49
Q

T or F: heart pains almost always makes a person alter their activities

A

true

50
Q

angina pectoris is a consequence of myocardial oxygen demand exceeding _____

A

myocardial oxygen supply

51
Q

can replicates syndrome (see if gets pale, breaks out in sweat, pain, see EKG)

A

treadmill test

52
Q

At the microscopic level in chronic stable angina, what is happening at microscopic level?

A

ishemia

53
Q

etiologic factors other than artherlosclerosis that can cause an MI

A

injury

emboli

54
Q

pt that woke up in middle of the night with an elephant on chest with normal ECG

A

acute coronary syndrome

*lack of complete occlusion of artery

55
Q

pathophys of ACS

A

artherlosclerotic CA –> rupture –> platelets move in –> TXA2 made –> momentary vasoconstriction –> decrease in O2 supply/ischemia

56
Q

artherlosclerosis –> ______ –> rupture –> _______

A

chronic stable angina

acute coroney syndrome

57
Q

What causes the arthlerosclerotic plaque rupture in ACS?

A 
endothelial activation 
smoking
cytokines
elevated glc (AGE)
HTN

lead to
-vasoconstrion and platelet aggrgation –> rupture

58
Q

vulnerable plaque vs stable plaque

A

vulterable have large lipid core, thin cap

stable: more smooth muscle cells and is more well formed

59
Q

role of platelets in ACS

A

rupture of plaque –> paltelets rush in –> TXA2 produced –> vasoconstriction –> fibrin deposition

60
Q

In ACS the ____ is the culprit

A

vessel

platelets are the 2nd most important part

61
Q

rupture –> thrombus

A

ACS

62
Q

What is the Tx of ACS

A

blood thinners (heparin)

63
Q

MI and ACS presents similarly, what is the only distinguishing factor

A

ECG

64
Q

severe prolong contriction of chest (may last an hour or 2)
very pale
very diaphortetic
difficulty breathing

A

acute MI

65
Q

Complications of acute MI

A 
syncope
arrythmia
LHF
cardiogenic shock
sudden death
66
Q

Describe the heart pain in an acute MI

A

30 mis to several hour of chest pain

pain radiates to arm, neck, jaw

67
Q

MI ECG changes

A

ST elevation

68
Q

ST elevation means

A

the vessel has been 100% occulded (by thrombus)

69
Q

locations of ST elevation on ECG determines _____

A

location of MI on heart

70
Q

as myocytes die the secrete enzymes….

A

CK
SGOT
LDH
troponin

71
Q

_____ is a predictor of ischemic event

A

troponin

72
Q

more than 1 p wave for every QRS

A

heart block (casues arrhythmia?)

73
Q

Tx of heart block

A

pacemaker

74
Q

ventricualr fibrillation

A

know ECG for it

75
Q

complication of MI

A

myocardial rupture

-blow hole in wall of ventricle, IV septum, papilary muscle

76
Q

fluid in lungs due do abnormal accumulation of Na and H2O

A

HF (fluid in alveoli)

77
Q

What to do when person has MI and there is no cath lab

A

get rid of clot to reperfuse

-streptokinase

78
Q

treateent of choice for a pt with ST elevation MI

A

put in mesh balloon/stent at area of occlusion = angioplasty

79
Q

take veins from leg, anastomose to proximal aorta and anastomose to area distal to CA blockage

A

bypass surgery

80
Q

What has a positive effect on SV?

Negative?

A

positive:
- inc length of myocardial fibers by increasing preload (EDV)

negative:
- inc afterload decreases the contractility (dialated left ventricle); inc systolic BP

81
Q

Formula to calculate ejection fraction

A

SV / EDV

82
Q

arthlerosclerotic plaque narrown lumen –> ruptures–>

  1. increased constriction/resistance
  2. thrombotic state in which blood clots form at area of rupture
A

ACS

83
Q

How are heart pains (in chronic stable angina) distinguished from other pains?

A

longer than 5 mins and less than 30mins

make a person alter their activities

84
Q

T or F: in ACS the coronary artery is 100% occluded

A

False, not 100%

This is why the EKG is unremarkable*

Cardiovascular (31 decks)

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