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ExPhys > RCQ CH 5 / Exam 2 SG > Flashcards

RCQ CH 5 / Exam 2 SG Flashcards

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
Q

how is the myocardium affected in STEMI? what variables affect this change?

A

change in shape, size, thickness

size of infarct, ventricular load, patency of affected artery

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26
Q

what chemicals are elevated in a NSTEMI

A

troponin I or T

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27
Q

how to distinguish between stable and unstable angina

A

stable - develops with exertion and decreases with nitroglycerin

unstable - chest discomfort is at rest and won’t respond to NG

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28
Q

characteristics of pericarditis

A

pain at rest, not relieved with nitroglycerin
responds to anti-inflammatory meds

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29
Q

how are pulmonary and bronchospasm pains differentiated

A

pulmonary - with breathing
broncho - exertional related, extreme difficulty breathing

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30
Q

definition of atherosclerosis

A

progressive hardening and narrowing of arteries

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31
Q

Right and Left ventricular pressures during systole

A

R - 15 to 25 mmHg
L - 120 or more

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32
Q

when does myocardial perfusion occur? how does it work?

A

diastole is when the O2 gets perfused

during systole, blood is pushed into the CA when blood is sent through the aorta

33
Q

general kidney responses to HF

A

retention of sodium –> retention of water –> tries to increase BP

34
Q

explain how kidneys respond to HF

A

renal and extra renal sensors detected decreased CO

altered a-adrenergic neural activity catecholamines are circulated
increased angiotensin II released

35
Q

generally how does the blood respond to HF

A

polycythemia
anemia
thrombocytopenia

36
Q

explain why polycythemia occurs in response to HF

A

hypoxic state indicates an increase in erythropoietin production in hopes to have more RBC for O2 and thicker blood

37
Q

what happens to the deoxyhemoglobin curve when in an anemic state

A

rightward shift
critical point of O2 saturation moves to 70mmHg

38
Q

how does the liver respond to HF

A

hepatic venous congestion
subsequent hypoxemia

39
Q

what is the result of hepatic venous congestion

A

inadequate perfusion of O2 to tissue that can lead to hypoxemia

40
Q

when the liver is in a hypoxic state, what occurs

A

cirrhosis that leads to

  • central lobular necrosis
  • atrophy
  • extensive fibrosis
  • sclerosis of hepatic veins
41
Q

what is the skeletal muscles response to HF

A

myopathy

42
Q

pancreatic response to HF

A

impaired insulin secretion
impaired glucose tolerance

–> stomach and intestinal abnormalities / malnutrition can occur

43
Q

what does RGC chemical do

A

regulates myocardial contractility

44
Q

difference between a1 and a2-adrenergic receptors

A

stimulation of
a1 = increased inotropy

a2 = decreased inotropy

45
Q

stimulation of b2-adrenergic receptors causes

A

vasodilation of capillary beds
muscle relaxation of bronchial tracts

46
Q

stimulation of b1-adrenergic receptors leads to

A

increased HR and myocardial force of contraction

47
Q

how does HF affect b1 and b2 receptors

A

ratio of b1 to b2 decreases

48
Q

what is capillary wedge pressure used for? how is this done? what is a normal value?

A

estimation of left atrial pressure

sticking a catheter into a branch of the pulmonary artery

8-12 mmHg

49
Q

where is NT-proBNP made? what does it do

A

cardiac tissues
relaxes isolated arteries

– will have increased levels with CHF

50
Q

what produced ANP/BNP

A

arterial/cardiac myocytes

51
Q

what to ANP/BNP respond to

A

increased stretch due to increased filling pressures

high arterial pressures

cardiac dilation

52
Q

how do ANP/BNP work

A

bind to aorta and vascular smooth muscle

reduce blood volume by supression of renin and aldosterone

53
Q

when will ANP or BNP secretions increase

A

ANP - LVENT EDV backing up into atrium or increased atrial pressure

BNP - increased plasma levels in those with ACS or HF

54
Q

how does LVENT filling pressure affect the Frank-Starling Mechanism

A

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
Q

what is pulmonary HTN defined by?

A

mean pulmonary artery pressure

56
Q

what values are significant for pulmonary HTN

A

25 mmHg or greater = abnormal
20 mmHg or greater = abnormal in those w COPD

57
Q

what does increased pulmonary artery pressure lead to

A

right ventricular dysfunction and failure

58
Q

what can cause pulmonary HTN

A

damaged or failing left heart

59
Q

types of pulmonary edema

A

cardiogenic (hemodynamic)
noncardiogenic (pulmonary capillary membrane)

60
Q

explain stage 1 pulmonary edema

A

increased lymph flow without net gain of interstitial fluid

  • can improve gas exchange slightly due to pulmonary vessels distending
61
Q

explain stage 2 pulmonary edema

A

liquid accumulation compromises small airway lumina

ventilation/perfusion mismatch

hypoxemia and wasted ventilation

tachypnea

62
Q

what is the relationship between hypoxemia and capillary wedge pressure? what is this related to?

A

direct

increase in hypoxemia increases capillary wedge pressure

stage 2 pulmonary edema

63
Q

explain stage 3 pulmonary edema

A

severe hypoxemia and hypercapnia resultant of increased capillary wedge pressure

64
Q

s/s of stage 3 pulmonary edema

A

Filling of large airways with blood colored foam
Reductions in lung volumes
Right to left intrapulmonary shunt
Hypercapnia with acute respiratory acidosis

65
Q

aging effects of cardiovascular system

A

decreased vascular elasticity
decreased adrenergic responsiveness
decreased rate of Ca released
decreased CO
increased systolic arterial pressure
diastolic dysfunction
increased NE levels

66
Q

result of decreased vascular elasticity

A

increased BP

67
Q

result of decreased adrenergic response

A

decreased exercise HR

68
Q

result of decreased rate of Ca

A

weaker, less sustained contraction of myocardium

69
Q

why does systolic arterial pressure increase? what does that result in?

A

decreased distensibility of arteries

could lead to ventricular hypertrophy and diastolic dysfunction

70
Q

what can cause CMD

A

coronary artery disease
cardiac arrythmia
renal insufficiency

71
Q

what is cardiomyopathy

A

contraction and relaxation of myocardial muscle fibers are impaired

72
Q

primary vs secondary cardiomyopathy

A

primary = resultant of pathological process in the heart

secondary = resultant of systemic disease

73
Q

types of cardiomyopathy

A

dilated
hypertrophic
restrictive

74
Q

what causes dilated cardiomyopathy

A

alcohol abuse
HTN
infection
smoking
carnitine deficiency

75
Q

explain dilated cardiomyopathy

A

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
Q

explain hypertrophic cardiomyopathy

A

due to diastolic dysfunction
– increased LVENT diastolic pressure, leading to hypercontractile LV

77
Q

what is the result of hypertrophic cardiomyopathy

A

rapid ventricular ejection and high EF

78
Q

explain restrictive cardiomyopathy

A

diastolic dysfunction and unimpaired contractile function

79
Q

what can restrictive cardiomyopathy result in

A

myocardial fibrosis
hypertrophy
infiltration
impaired myocardial relaxation

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