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Pathophys - Nat > Cardiovascular > Flashcards

Cardiovascular Flashcards

(85 cards)

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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
which coronary artery is most often affected by disease
left anterior descending artery (?)
26
lymphatic vessels empty into the
super vena cava
27
pulmonary circulation is ___ pressure, ___ volume, and ___ resistance
low, low, low
28
pulmonary hypertension leads to right ventricular ___
hypertrophy
29
cor pulmonale def
right ventricular hypertrophy caused by pulmonary hypertension; most often the result of left heart failure but can also be caused by chronic lung disease
30
stimulation of beta 1 receptors (norepinephrine) of heart
increased heart rate, increase stroke volume, vasoDILATION of coronary arteries; increase conduction through AV node
31
sympathetic response is stimulation of ___ receptors
adrenergic (beta and alpha)
32
describe cascade of cellular effects of beta 1 receptor stimulation in heart muscle
norepi binds to b1 receptor, a g-protein linked receptor; activation of adenylyl cyclase; formation of cAMP --> increase in inotropy, lusitropy, and chronotropy
33
inotropy def
strength of cardiac contraction, affected by # of Ca 2+ ions and adrenergic stimulation
34
lusitropy def
relaxation of contracted cardiac muscle
35
chronotropy def
rate of cardiac contraction
36
parasympathetic response is carried out by the ___ nerve
vagus
37
type of receptors that create a parasympathetic response
cholinergic/acetylcholine
38
ACh ___ heart rate
decreases
39
ADH effects (2)
water reabsorption in kidneys and vasoconstriction --> increase BP
40
factors that stimulate release of renin
drop in BP (detected by JGA); decreased serum NaCl; beta-adrenergic stimulus (norepi); decreased angiotensin II; decreased serum K+
41
angiotensin II effects
vasoconstriction; stimulates release of aldosterone and ADH; promotes growth of cardiovascular tissues; increased sympathetic output (catecholamines)
42
purpose and MOA of ACE inhibitors
for managing HTN; inhibits the action of angiotensin converting enzyme (ACE) in converting ang I to ang II
43
true or false: chronic elevation of aldosterone is independently damaging to cardiac tissues
true
44
Poiseuille's law
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
cardiac output formula and normal range
CO = SV x HR; normally about 5 L/min
46
stroke volume determinants and normal range
SV = (end-diastolic volume) - (end-systolic volume); or SV = preload - afterload normal is 50-70 mL
47
ejection fraction formula
EF = (end-systolic volume) / (end-diastolic volume)
48
cardiac index formula and normal range
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
Starling's law
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
sinus of Valsalva allows blood to enter the coronary arteries during what cardiac phase?
left ventricular diastole
51
beta 1 receptor stimulation causes vaso-___
DILATION (think "beta makes it bigger")
52
alpha receptor stimulation causes vaso-___
CONSTRICTION (think "a is to c as b is to d")
53
cardiac reserve def
the degree to which the heart is able to increase CO in response to increased activity
54
tissue ischemia causes vaso-___
dilation
55
ischemia def
inadequate perfusion of tissues (not enough blood flow)
56
ischemia is (reversible/irreversible)
reversible
57
pathogenesis of coronary artery disease
atherosclerosis of coronary arteries causes cardiac ischemia
58
pathophysiology of atherosclerosis
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
modifiable risk factors for CAD/atherosclerosis
hyperlipidemia, obesity, hypertension, smoking, stress
60
cardiac markers
CPK, LDH, MB-CK, troponin
61
viral pericarditis patho
decreases cardiac conductibility
62
preload def
degree of myocardial stretch at the end of ventricular diastole
63
afterload def
amount of force necessary for ventricles to eject blood; determined by systolic pressure, ventricular wall thickness, and radius of aorta/pulm arteries
64
forward vs backward heart failure
forward: poor ventricular contractility backward: poor ventricular filling
65
two hormones that directly contribute to ventricular remodeling
ang II and aldosterone
66
thrombus vs embolus
thrombus is the blood clot; when it dislodges, it is an embolus
67
atherosclerotic lesions tend to develop at what areas in the arteries?
points of branching, where there is more turbulent blood flow
68
arterial occlusion will present with ___, while venous occlusion will present with ___
pain (claudication), edema (local)
69
arterial aneurysm pathogenesis
medial layer of artery deteriorates, causes dilation/ballooning of weakened arterial wall
70
aortic aneurysms most commonly occur at:
places below the renal arteries
71
function of pericardial fluid (2)
suspension, lubrication
72
why is a slower heart rate more efficient?
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
the dicrotic notch is caused by:
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
assess the health/efficacy of the AV node with ___ on EKG
P-R interval
75
EKG changes with 1st degree AV block
AV node is delaying conduction --> long P-R interval, but still one P wave per QRS
76
EKG changes with 2nd degree AV block
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
EKG changes with 3rd degree AV block
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
what makes the SA node the "pacemaker"?
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
In coronary artery disease, smooth muscle cell apoptosis or macrophage apoptosis may lead to development of:
calcification
80
ventricular septal defects are most often found in (membranous/muscular) septum, and people with genetic ___ are at high risk of developing them
membranous; trisomies
81
most common cause of abdominal aortic aneurysm
arteriosclerosis (smoking is a HUGE risk factor)
82
Tetralogy of Fallot
VSD, pulmonary valve stenosis, misplaced aorta, right ventricular hypertrophy
83
rheumatic heart disease most often affects which valve?
mitral (left AV)
84
serous pericarditis is/is not usually a big problem
is not
85
Marfan's syndrome characteristics
floppy mitral valve; long, thin chordae tendonae; mid-systolic click

Pathophys - Nat (6 decks)

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