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CV > Newman_HighYield > Flashcards

Newman_HighYield Flashcards

1
Q

BP =

A

CO x PVR

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2
Q

constrictors?

A

NE, Epi, Ag2, TxA2

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3
Q

dilators?

A

PGI2, NO

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4
Q

stretch of myocardial fibers measures?

A

preload

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5
Q

what are afterload determinants?

A

size of dilation of the LV

systolic BP of the LV

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6
Q

what is contractility?

A

the inherent ability of the heart to contract irrespective of preload and afterload

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7
Q

EF =

A

SV / LV EDV

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8
Q

What is considered a good Ejection Fraction (EF)?

A

anything over 50%

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9
Q

What are the 3 syndromes of coronary disease?

A

Chronic stable angina (angina pectoris)
Acute Coronary syndrome
MI

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10
Q

chest pain upon exertion, think?

A

chronic stable angina

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11
Q

myocardial oxygen demand is a function of what?

A

systolic BP

HR

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12
Q

chest pain without exertion, think?

A

acute coronary syndrome

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13
Q

what is seen on ECG with MI?

A

ST elevation

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14
Q

what percentage of the coronary artery is occluded in acute coronary syndrome?

A

~80%

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15
Q

what percentage of the coronary artery is occluded in MI (STEMI)?

A

100%

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16
Q

what can distinguish acute coronary syndrome from MI?

A

ECG (MI has ST elevation)

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17
Q

what are markers of MI?

A

CK-MB, SGOT, LDH, Troponin I

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18
Q

features of a vulnerable plaque?

A

large lipid core
many inflammatory cells
low smooth muscle count
thin fibrous cap

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19
Q

features of stable plaques?

A

more smooth muscle cells

well formed

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20
Q

what do vulnerable plaques typically lead to?

A

acute coronary syndrome

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21
Q

what do stable plaques typically lead to?

A

stable angina

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22
Q

myocardial O2 supply is a function of?

A

coronary blood flow

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23
Q

tx options for MI?

A

streptokinase (clot buster)
angioplasty and stent placement
bipass surgery

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24
Q

what is the ideal tx for MI with ST elevation?

A

angioplasty and stent placement

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25
Q

what are the two main valvular diseases?

A

stenosis

regurgitation

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26
Q

aortic regurgitation occurs during?

A

diastole

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27
Q

mitral regurgitation occurs during?

A

systole

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28
Q

what is the cardiac pathophysiological adaptation in stenosis? results from?

A

concentric hypertrophy (sarcomeres in parallel)

results from increased pressure

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29
Q

what is the cardiac pathophysiological adaptation in regurgitation? results from?

A

eccentric hypertrophy (sarcomeres in series)

results from increased volume

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30
Q

describe changes in concentric hypertrophy

A

increased thickness of muscle, normal volume and size

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31
Q

describe chances in eccentric hypertrophy

A

normal thickness, increase mass and dilation

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32
Q

what is the thickness of a normal interventricular septum?

A

2 cm

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33
Q

in the assessment of murmurs, what indicates stenosis? regurgitation?

A

turbulent flow

inappropriate timing

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34
Q

What does Echo allow you to do?

A

study blood flow

identify diseased valves

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35
Q

What are two factors involved in the assessment of stenosis?

A 
the gradient (pressure drop bw LV and LA)
flow (cardiac output)
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36
Q

What are two main causes of mitral stenosis?

A 
rheumatic fever (most common)
HTN
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37
Q

What are causes of mitral regurgitation?

A

MVP (most common)
LV dilatation
Rheumatic Fever

38
Q

What happens to SV and EF in mitral regurg?

A

both increased

39
Q

What helps distinguish acute mitral regurg from chronic mitral regurg?

A

lack of eccentric hypertrophy in acute

40
Q

what are signs of aortic stenosis?

A

concentric hypertrophy
delayed arterial pulse (tardus)
weakened arterial pulse (parvus)

41
Q

what 2 things are needed in IE?

A

bacteremia (bugs in the blood)

diseased valve

42
Q

complications of IE?

A

valve destruction
embolization
immune complex deposition

43
Q

What is the most common cause of sudden cardiac death?

A

ventricular fibrillation

44
Q

P-wave represents

A

depolarization of atria

45
Q

PR interval is…

A

conduction through the AV node

46
Q

Q wave

A

depolarization of septum

47
Q

RS complex

A

depolarization of ventricles

48
Q

ST segment

A

period in which the ventricles are depolarized

49
Q

T wave

A

ventricular repolarization

50
Q

if the axis of the electrode is parallel (in the same direction) to the axis of the heart: ____ deflection

A

positive

51
Q

if the axis of the electrode is perpendicular to the axis of the heart: ____ deflection

A

no deflection, straight line

52
Q

if the axis of the electrode is parallel and in the opposite direction to the axis of the heart: ____ deflection

A

negative

53
Q

slow APs (SA and AV nodes) are driven by ___

A

Ca2+

54
Q

fast APs are driven by ___

A

Na+

55
Q

where is the absolute refractory period located?

A

bw phases 0 and 3

56
Q

where is the relative refractory period located?

A

bw phases 3 and 4

57
Q

What are the 2 common mechanisms of dysrhythmias?

A

altered (enhanced) automaticity

Reentry

58
Q

how does enhanced automaticity occur?

A

altered phase 4 (resting state) diastolic depolarization of the AP such that threshold potential is reached out of order/more easily

59
Q

what factors can lead to increased automaticity?

A 
autonomic (increased SNS activity)
metabolic (low O2, high CO2, low pH, inc T)
mechanical (stretch)
drugs (digitalis, NE, Epi)
electrolytes (low K, high Ca)
60
Q

what 3 things does reentry need

A
  1. contiguous pathway that forms a loop circuit
  2. unidirectional block (refractory tissue)
  3. slow conduction in the alternate pathway (different conduction velocity)
61
Q

what is the most common cause of stroke?

A

atrial fibrillation

62
Q

pericardial disease disrupts the elasticity of the heart during _____

A

diastole

63
Q

what can cause acute pericarditis?

A 
anything that causes inflammation:
infection
trauma
autoimmune (SLE)
metabolic (kidney failure, thyroid disease)
64
Q

symptoms of acute pericarditis?

A

chest pain, worse when supine, relieved when leaning forward

65
Q

main sign of acute pericarditis?

A

pericardial friction rub

66
Q

what do you see on echo with pericardial effusion?

A

large clear halo surrounding heart

67
Q

pericardial effusion leads to ____dysfunction

A

diastolic

68
Q

hallmark of pericardial effusion?

A

all chambers have equal pressure during diastole → cardiac tamponade → EDV decreases bc the heart cannot fill up enough → C.O. decreases → BP decreases

69
Q

hallmark of cardiac tamponade?

A

pulsus paradoxus

70
Q

what is pulsus paradoxus?

A

exaggerated decrease in systolic BP and pulse wave amplitude during inspiration

71
Q

what are the 2 major determinants of afterload?

A

size of the LV

Systolic BP

72
Q

what 4 drugs/classes can save lives in tx of chronic HF?

A

ACE inhibitors (“prils”)
ARBs (“sartans”)
B-Blockers (“lols”)
Spironolactone (aldosterone antagonist)

73
Q

what are the 3 neurohumoral systems activated in HF?

A

SNS
RAAS
natriuretic peptides

74
Q

what are some contraindications to heart transplant?

A

systemic disease

>65 age

75
Q

define acute HF

A

when oxygen delivery to the heart is inadequate relative to oxygen requirement

76
Q

most common cause of acute HF? other causes?

A

acute MI

exacerbation of chronic HF
post-op complication

77
Q

if you see a low EF on exam, think?

A

heart failure

78
Q

normal tissues extract around ___ % of oxygen delivered to them

A

25%

79
Q

normally, about ___% of the oxygen delivered to tissues is returned to the heart

A

75%

80
Q

Normal CO is ____ L/min. What happens to O2 extraction if CO decreases? Venous O2 saturation/return to heart?

A

5 L/min
tissue O2 extraction increases
venous O2 return decreases

81
Q

In HF, RAAS and SNS are activated. What are the effects?

A

vasoconstriction of peripheral vessels (increased TPR) which maintains perfusion to the brain at the expense of decreased perfusion to kidneys (increased renin, creatinine), gut, and skin (pallor, cool extremities)

82
Q

what measures preload?

A

pulmonary artery catheter

83
Q

what are tx goals in HF?

A 
raise cardiac index (CO)
raise mixed venous O2 concentration
reduce LV filling pressure (preload)
reduce TPR
maintain MAP
84
Q

chronic HF is a syndrome of?

A

salt and water retention dictated by RAAS

85
Q

in chronic HF, what factors affect the RAAS?

A
  • RBF (decreased RBF increases renin)
  • amount of Na+ in diet (reduced Na+ intake will reduce aldosterone levels)
  • thermal stress (increased heat will increase aldosterone)
  • body position (supine with elevated legs will turn off RAAS and decrease renin)
86
Q

what ratio can differentiate bw decompensated and compensated HF?

A

urinary Na+:K+ ratio

1 in compensated

87
Q

what are signs/symptoms of HF?

A

low C.O.
abnormal retention of Na and water
pulmonary congestion (crackles, orthopnea)
systemic congestion (ascites, edema, JVD)

88
Q

dangerous side effect of ACE inhibitors?

A

hyperkalemia

89
Q

how does chronic HF related to systemic disease?

A
  • cachexia (wasting of muscles)
  • increased oxidative stress
  • elevated pro-inflammatory cytokines (TNFa, IL6)
90
Q

how do you measure increased intravascular volume?

A

measure JVD

91
Q

T or F: diuretics are less effective when supine

A

F, diuretics are more effective when supine

CV (4 decks)

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