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Pathophys - Nat > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

varicose veins are the result of ___ ___

A

valve incompetency

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2
Q

the SA node provides stimulus for heart to pump at what rate?

A

60-100 bpm

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3
Q

“neurohumoral” refers to what?

A

renin-angiotensin-aldosterone system

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4
Q

most of the blood entering the right ventricle enters (actively/passively)

A

passively

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5
Q

cause of increased right atrial pressure

A

right ventricular congestion (due to left ventricular insufficiency)

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6
Q

result of increased right atrial pressure

A

peripheral edema

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7
Q

right side of heart is (low/high) pressure

A

low

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8
Q

cause of increased left atrial pressure

A

left ventricular congestion (due to HTN, injury, etc)

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9
Q

result of increased left atrial pressure

A

pulmonary edema/congestion

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10
Q

purpose of chordae tendonae

A

prevent valvular prolapse (of AV valves) –> ensure one-way blood flow

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11
Q

purpose of sinuses of Valsalva

A

protect right and left coronary arteries from excessive increases in pressure/volume

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12
Q

location of sinus of Valsalva

A

surrounding leaflets of semilunar valves

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13
Q

rate of ventricular automaticity

A

20-30 bpm

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14
Q

rate of AV node automaticity

A

40-60 bpm

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15
Q

rhythmicity def

A

regularity of impulse generation by cardiac automatic cells

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16
Q

conductivity def

A

ability to transmit an electrical impulse across a distance

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17
Q

excitability def

A

ability to respond to a stimulus (i.e. catecholamines)

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18
Q

arteries have a (low/high) volume, (low/high) pressure flow

A

low volume, high pressure

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19
Q

where in circulation does regulation of blood pressure occur?

A

alpha and beta (1) receptors on arterioles

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20
Q

___ are the major site of exchange in circulation, due to their ___

A

capillaries, fenestrae

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21
Q

laminar flow properties

A

unidirectional, smooth, fastest in the center of vessel, some frictional resistance along sides

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22
Q

veins have a (low/high) volume, (low/high) pressure flow

A

high volume, low pressure

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23
Q

function of skeletal muscle pump

A

facilitating venous return by massaging the veins with muscular movement; forces blood to flow away from wherever the vein is being sqeezed, but it can only go in the direction that the venous valves allow: towards the heart

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24
Q

function of thoracic pull

A

movement of diaphragm creates a vacuum, assisting in “pulling” blood towards thoracic cavity

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25
Q

which coronary artery is most often affected by disease

A

left anterior descending artery (?)

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26
Q

lymphatic vessels empty into the

A

super vena cava

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27
Q

pulmonary circulation is ___ pressure, ___ volume, and ___ resistance

A

low, low, low

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28
Q

pulmonary hypertension leads to right ventricular ___

A

hypertrophy

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29
Q

cor pulmonale def

A

right ventricular hypertrophy caused by pulmonary hypertension; most often the result of left heart failure but can also be caused by chronic lung disease

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30
Q

stimulation of beta 1 receptors (norepinephrine) of heart

A

increased heart rate, increase stroke volume, vasoDILATION of coronary arteries; increase conduction through AV node

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31
Q

sympathetic response is stimulation of ___ receptors

A

adrenergic (beta and alpha)

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32
Q

describe cascade of cellular effects of beta 1 receptor stimulation in heart muscle

A

norepi binds to b1 receptor, a g-protein linked receptor; activation of adenylyl cyclase; formation of cAMP –> increase in inotropy, lusitropy, and chronotropy

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33
Q

inotropy def

A

strength of cardiac contraction, affected by # of Ca 2+ ions and adrenergic stimulation

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34
Q

lusitropy def

A

relaxation of contracted cardiac muscle

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35
Q

chronotropy def

A

rate of cardiac contraction

36
Q

parasympathetic response is carried out by the ___ nerve

A

vagus

37
Q

type of receptors that create a parasympathetic response

A

cholinergic/acetylcholine

38
Q

ACh ___ heart rate

A

decreases

39
Q

ADH effects (2)

A

water reabsorption in kidneys and vasoconstriction –> increase BP

40
Q

factors that stimulate release of renin

A

drop in BP (detected by JGA); decreased serum NaCl; beta-adrenergic stimulus (norepi); decreased angiotensin II; decreased serum K+

41
Q

angiotensin II effects

A

vasoconstriction; stimulates release of aldosterone and ADH; promotes growth of cardiovascular tissues; increased sympathetic output (catecholamines)

42
Q

purpose and MOA of ACE inhibitors

A

for managing HTN; inhibits the action of angiotensin converting enzyme (ACE) in converting ang I to ang II

43
Q

true or false: chronic elevation of aldosterone is independently damaging to cardiac tissues

A

true

44
Q

Poiseuille’s law

A

Resistance is dependent on: viscosity of the blood, the length of the vessel; it is inversely proportional to the fourth power of the lumen’s radius –> small changes in radius create BIG changes in resistance

45
Q

cardiac output formula and normal range

A

CO = SV x HR; normally about 5 L/min

46
Q

stroke volume determinants and normal range

A

SV = (end-diastolic volume) - (end-systolic volume); or
SV = preload - afterload
normal is 50-70 mL

47
Q

ejection fraction formula

A

EF = (end-systolic volume) / (end-diastolic volume)

48
Q

cardiac index formula and normal range

A

CI = CO/surface area
normal CO = 5L/min, normal surface area = 1.78 m^2
(5 L/min) / (1.78 m^2) = 2.8 L/min/m^2
normal is 2.8-3.6 L/min/m^2

49
Q

Starling’s law

A

the volume of blood in the heart at the end of diastole (the length of its muscle fibers) is directly related to the force of contraction during the next systole –> preload and contractility affect SV and therefore CO

50
Q

sinus of Valsalva allows blood to enter the coronary arteries during what cardiac phase?

A

left ventricular diastole

51
Q

beta 1 receptor stimulation causes vaso-___

A

DILATION (think “beta makes it bigger”)

52
Q

alpha receptor stimulation causes vaso-___

A

CONSTRICTION (think “a is to c as b is to d”)

53
Q

cardiac reserve def

A

the degree to which the heart is able to increase CO in response to increased activity

54
Q

tissue ischemia causes vaso-___

A

dilation

55
Q

ischemia def

A

inadequate perfusion of tissues (not enough blood flow)

56
Q

ischemia is (reversible/irreversible)

A

reversible

57
Q

pathogenesis of coronary artery disease

A

atherosclerosis of coronary arteries causes cardiac ischemia

58
Q

pathophysiology of atherosclerosis

A
  1. endothelial injury (can be caused by HTN, diabetes, etc.)
  2. platelets adhere to site of injury
  3. macrophages enter site and eat lipids of tunica intima, forming foam cells
  4. build up of foam cells creates protrusive fatty streak
  5. protrusion interrupts laminar flow –> turbulent flow
  6. turbulent flow causes further injury to endothelium
  7. fatty streaks continue to grow together forming fibrous plaques, result of collagen destruction and LDL oxidation
59
Q

modifiable risk factors for CAD/atherosclerosis

A

hyperlipidemia, obesity, hypertension, smoking, stress

60
Q

cardiac markers

A

CPK, LDH, MB-CK, troponin

61
Q

viral pericarditis patho

A

decreases cardiac conductibility

62
Q

preload def

A

degree of myocardial stretch at the end of ventricular diastole

63
Q

afterload def

A

amount of force necessary for ventricles to eject blood; determined by systolic pressure, ventricular wall thickness, and radius of aorta/pulm arteries

64
Q

forward vs backward heart failure

A

forward: poor ventricular contractility
backward: poor ventricular filling

65
Q

two hormones that directly contribute to ventricular remodeling

A

ang II and aldosterone

66
Q

thrombus vs embolus

A

thrombus is the blood clot; when it dislodges, it is an embolus

67
Q

atherosclerotic lesions tend to develop at what areas in the arteries?

A

points of branching, where there is more turbulent blood flow

68
Q

arterial occlusion will present with ___, while venous occlusion will present with ___

A

pain (claudication), edema (local)

69
Q

arterial aneurysm pathogenesis

A

medial layer of artery deteriorates, causes dilation/ballooning of weakened arterial wall

70
Q

aortic aneurysms most commonly occur at:

A

places below the renal arteries

71
Q

function of pericardial fluid (2)

A

suspension, lubrication

72
Q

why is a slower heart rate more efficient?

A

the slower the heart rate, the more time per beat the sinus of Valsalva is open, allowing more blood to perfuse the coronary arteries

73
Q

the dicrotic notch is caused by:

A

the aortic valve snaps shut at the end of ventricular systole, the elastic force of the aortic walls recoiling after being pumped full of blood briefly increases pressure

74
Q

assess the health/efficacy of the AV node with ___ on EKG

A

P-R interval

75
Q

EKG changes with 1st degree AV block

A

AV node is delaying conduction –> long P-R interval, but still one P wave per QRS

76
Q

EKG changes with 2nd degree AV block

A

AV node is intermittently blocking conduction –> some long P-R intervals, some “lonely” P waves that are not followed by QRS; causes atrial flutter

77
Q

EKG changes with 3rd degree AV block

A

AV node totally obstructs conduction –> no SA node control of ventricular beats. Marching P waves at SA rhythm (60-100 bpm), but no QRSs; ventricular beats elicited by Perkinje fibers, so very slow HR

78
Q

what makes the SA node the “pacemaker”?

A

the cells of the SA node have the fastest automatic depolarization/repolarization cycles, and all other cells depolarize according to the rate of the fastest cells

79
Q

In coronary artery disease, smooth muscle cell apoptosis or macrophage apoptosis may lead to development of:

A

calcification

80
Q

ventricular septal defects are most often found in (membranous/muscular) septum, and people with genetic ___ are at high risk of developing them

A

membranous; trisomies

81
Q

most common cause of abdominal aortic aneurysm

A

arteriosclerosis (smoking is a HUGE risk factor)

82
Q

Tetralogy of Fallot

A

VSD, pulmonary valve stenosis, misplaced aorta, right ventricular hypertrophy

83
Q

rheumatic heart disease most often affects which valve?

A

mitral (left AV)

84
Q

serous pericarditis is/is not usually a big problem

A

is not

85
Q

Marfan’s syndrome characteristics

A

floppy mitral valve; long, thin chordae tendonae; mid-systolic click

Pathophys - Nat (6 decks)

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