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RCQ CH 5 / Exam 2 SG Flashcards

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1
Q

cor pulmonale

A

right sided HF due to issue in lungs

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2
Q

where will blood back up to in right sided HF

A

anywhere venous blood gets taken from to go to the heart

atrium, liver, abdomen, bilateral ankle/hands
lungs

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3
Q

where will left sided HF back up blood to

A

left atrium
pulmonary capillaries
lungs

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4
Q

s/s of forward sequelae of right HF

A

palpitations and fatigue due to increased CO2 levels

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5
Q

s/s backward sequelae of right-sided HF

A

LE congestion
jugular vein distension
weight gain
increase urination

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6
Q

s/s of left-sided HF forward sequelae

A

palpitations
fatigue
decreased urine production

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7
Q

s/s of left-sided HF backward sequelae

A

weight gain
orthopnea
lung congestion
dyspnea
pink foamy mucous

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8
Q

systolic dysfunction will cause

A

impaired contraction of ventricles
–> decreases SV

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9
Q

what happens to ejection fraction with systolic dysfunction

A

it is reduced

Ejection Fraction is <40%
increased EDV
HFrEF

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10
Q

ejection fraction formula

A

ESV / EDV

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11
Q

diastolic dysfunction causes

A

inability of ventricles to accept blood ejected from atria in rest or diastole

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12
Q

what causes diastolic dysfunction

A

ventricular wall hypertrophy

reduction in ventricular compliance

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13
Q

what happens with ejection fraction in diastolic dysfunction? what is the EF?

A

HFpEF
EF > 50%

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14
Q

how does CO get affected by r or pEF

A

rEF - more significant decreased CO
pEF - EF maintains, but CO decreases overall

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15
Q

what are the treatments for HF

A

implantable cardiac defibrillator
pacemaker
dialysis and ultrafiltration
ventricular assisted device
intra-aortic balloon pump

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16
Q

what is the effect of HTN on exercise?

A

exercise capacity is reduced by 15-30%

peak HR is lowered and CO is reduced

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17
Q

what does long term exercise do to HTN values

A

systolic pressure dec by 10 mmHg
diastolic pressure dec by 8 mmHg

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18
Q

HTN sequelae

A

increased arterial pressure
left ventricular hypertrophy
increased afterload
increased metabolic cost

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19
Q

how does increased afterload affect the myocardial fibers

A

overstretches them
–> less effective pumping

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20
Q

how does angiogenesis related to ventricular hypertrophy

A

it does not happen in a proportional manner

muscle builds without adequate blood vessels to supply that muscle

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21
Q

what medications are prescribed for HTN

A

ACE inhibitors
calcium-channel blockers
diuretics
beta-blockers

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22
Q

ECG characteristics of STEMI

A

ST elevation
Q wave development

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23
Q

ECG characteristics of NSTEMI

A

ST depression
no Q wave

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24
Q

what infarction occurs during STEMI vs NSTEMI

A

STEMI = transmural
–> distal to occluded coronary artery

NSTEMI = subendocardial
–> coronary arteries are not blocked

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25
how is the myocardium affected in STEMI? what variables affect this change?
change in shape, size, thickness size of infarct, ventricular load, patency of affected artery
26
what chemicals are elevated in a NSTEMI
troponin I or T
27
how to distinguish between stable and unstable angina
stable - develops with exertion and decreases with nitroglycerin unstable - chest discomfort is at rest and won't respond to NG
28
characteristics of pericarditis
pain at rest, not relieved with nitroglycerin responds to anti-inflammatory meds
29
how are pulmonary and bronchospasm pains differentiated
pulmonary - with breathing broncho - exertional related, extreme difficulty breathing
30
definition of atherosclerosis
progressive hardening and narrowing of arteries
31
Right and Left ventricular pressures during systole
R - 15 to 25 mmHg L - 120 or more
32
when does myocardial perfusion occur? how does it work?
diastole is when the O2 gets perfused during systole, blood is pushed into the CA when blood is sent through the aorta
33
general kidney responses to HF
retention of sodium --> retention of water --> tries to increase BP
34
explain how kidneys respond to HF
renal and extra renal sensors detected decreased CO altered a-adrenergic neural activity catecholamines are circulated increased angiotensin II released
35
generally how does the blood respond to HF
polycythemia anemia thrombocytopenia
36
explain why polycythemia occurs in response to HF
hypoxic state indicates an increase in erythropoietin production in hopes to have more RBC for O2 and thicker blood
37
what happens to the deoxyhemoglobin curve when in an anemic state
rightward shift critical point of O2 saturation moves to 70mmHg
38
how does the liver respond to HF
hepatic venous congestion subsequent hypoxemia
39
what is the result of hepatic venous congestion
inadequate perfusion of O2 to tissue that can lead to hypoxemia
40
when the liver is in a hypoxic state, what occurs
cirrhosis that leads to - central lobular necrosis - atrophy - extensive fibrosis - sclerosis of hepatic veins
41
what is the skeletal muscles response to HF
myopathy
42
pancreatic response to HF
impaired insulin secretion impaired glucose tolerance --> stomach and intestinal abnormalities / malnutrition can occur
43
what does RGC chemical do
regulates myocardial contractility
44
difference between a1 and a2-adrenergic receptors
stimulation of a1 = increased inotropy a2 = decreased inotropy
45
stimulation of b2-adrenergic receptors causes
vasodilation of capillary beds muscle relaxation of bronchial tracts
46
stimulation of b1-adrenergic receptors leads to
increased HR and myocardial force of contraction
47
how does HF affect b1 and b2 receptors
ratio of b1 to b2 decreases
48
what is capillary wedge pressure used for? how is this done? what is a normal value?
estimation of left atrial pressure sticking a catheter into a branch of the pulmonary artery 8-12 mmHg
49
where is NT-proBNP made? what does it do
cardiac tissues relaxes isolated arteries -- will have increased levels with CHF
50
what produced ANP/BNP
arterial/cardiac myocytes
51
what to ANP/BNP respond to
increased stretch due to increased filling pressures high arterial pressures cardiac dilation
52
how do ANP/BNP work
bind to aorta and vascular smooth muscle reduce blood volume by supression of renin and aldosterone
53
when will ANP or BNP secretions increase
ANP - LVENT EDV backing up into atrium or increased atrial pressure BNP - increased plasma levels in those with ACS or HF
54
how does LVENT filling pressure affect the Frank-Starling Mechanism
too much or not enough leads to decreased LVENT performance too much = increased stretch during diastole and decreased pump efficiency not enough = decreased stretch and decreased pump efficiency
55
what is pulmonary HTN defined by?
mean pulmonary artery pressure
56
what values are significant for pulmonary HTN
25 mmHg or greater = abnormal 20 mmHg or greater = abnormal in those w COPD
57
what does increased pulmonary artery pressure lead to
right ventricular dysfunction and failure
58
what can cause pulmonary HTN
damaged or failing left heart
59
types of pulmonary edema
cardiogenic (hemodynamic) noncardiogenic (pulmonary capillary membrane)
60
explain stage 1 pulmonary edema
increased lymph flow without net gain of interstitial fluid - can improve gas exchange slightly due to pulmonary vessels distending
61
explain stage 2 pulmonary edema
liquid accumulation compromises small airway lumina ventilation/perfusion mismatch hypoxemia and wasted ventilation tachypnea
62
what is the relationship between hypoxemia and capillary wedge pressure? what is this related to?
direct increase in hypoxemia increases capillary wedge pressure stage 2 pulmonary edema
63
explain stage 3 pulmonary edema
severe hypoxemia and hypercapnia resultant of increased capillary wedge pressure
64
s/s of stage 3 pulmonary edema
Filling of large airways with blood colored foam Reductions in lung volumes Right to left intrapulmonary shunt Hypercapnia with acute respiratory acidosis
65
aging effects of cardiovascular system
decreased vascular elasticity decreased adrenergic responsiveness decreased rate of Ca released decreased CO increased systolic arterial pressure diastolic dysfunction increased NE levels
66
result of decreased vascular elasticity
increased BP
67
result of decreased adrenergic response
decreased exercise HR
68
result of decreased rate of Ca
weaker, less sustained contraction of myocardium
69
why does systolic arterial pressure increase? what does that result in?
decreased distensibility of arteries could lead to ventricular hypertrophy and diastolic dysfunction
70
what can cause CMD
coronary artery disease cardiac arrythmia renal insufficiency
71
what is cardiomyopathy
contraction and relaxation of myocardial muscle fibers are impaired
72
primary vs secondary cardiomyopathy
primary = resultant of pathological process in the heart secondary = resultant of systemic disease
73
types of cardiomyopathy
dilated hypertrophic restrictive
74
what causes dilated cardiomyopathy
alcohol abuse HTN infection smoking carnitine deficiency
75
explain dilated cardiomyopathy
lack of energy necessary for proper heart function increases left vent End diastolic Volume and pressure -- leads to dilated left ventricle -- will empty slower and eject less
76
explain hypertrophic cardiomyopathy
due to diastolic dysfunction -- increased LVENT diastolic pressure, leading to hypercontractile LV
77
what is the result of hypertrophic cardiomyopathy
rapid ventricular ejection and high EF
78
explain restrictive cardiomyopathy
diastolic dysfunction and unimpaired contractile function
79
what can restrictive cardiomyopathy result in
myocardial fibrosis hypertrophy infiltration impaired myocardial relaxation

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