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Year 3: Clinical Medicine and Pathophysiology > Lecture 3: Heart Failure and Cardiomyopathy > Flashcards

Lecture 3: Heart Failure and Cardiomyopathy Flashcards

1
Q

what is heart failure

A

impaired ventricular contractility, increased after load, or impaired filling of the ventricles that leads to systolic or diastolic dysfunction

systemic compensations occur including
- increased SNS activity
- increased hormone circulation
- vasoconstriction
- ventricular remodeling

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2
Q

what are CO and SV

A

CO = volume of blood ejected from LV per minute (normal = 4-5L/min)

SV = volume of blood ejected per contraction

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3
Q

factors that affect CO

A

preload

contractility

afterload

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4
Q

what is preload

A

degree heart mm can stretch before contraction

correlated to end diastolic volume (max amount of blood returning to heart)

directly proportional to SV ( more blood returns to heart, the greater volume can leave)

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5
Q

frank starling law and relation to HF

A

greater volume of blood is ejected when greater volume of blood returns to heart

HF results in lower SV at given level of ventricular filling

if less blood is returned to heart, less is ejected

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6
Q

what is contractility

A

ability of ventricles to contract to send blood to lungs and periphery

increased HR = increased contractility

in HR > 120 there is an increase in Ca to result in stronger contraction

reflected by ejection fraction

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7
Q

what is ejection fraction

A

best indicator of cardiac function

ratio of volume ejected vs volume received prior to contraction

some blood must remain in the ventricles to maintain a certain degree of stretch

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8
Q

what is after load

A

force that resists contraction

pressure within the arterial system during systole

expressed as systemic vascular resistance or total peripheral resistance

increased after load = decreased SV = decreased CO

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9
Q

HF statistics

A

6.7 million in US

900,000 new cases/year

> 12 million medical visits per year due to HF related complaints

responsible for 14% all deaths

56.3% of HF deaths = women

over $30.7 billion per year

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10
Q

etiology of HF

A

loss of contractile tissues resulting from MI, mm dysfunction, or cardiomyopathy

arrhythmias

increased preload associated with fluid overload

increased after load from HTN

most common cause of HF is CAD with a previous MI

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11
Q

what are the systemic compensations for HF

A

increased blood volume to improve preload

increased sympathetic activation

increased HR

increased anti-diuretic hormone

increased RAAS activation to increase blood volume and SVR

decreased vagal/parasympathetic activation

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12
Q

EF abbreviation meaning

A

ejection fraction

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13
Q

HFeEF abbreviation meaning

A

heart failure with reduced EF

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14
Q

HRmrEF abbreviation meaning

A

heart failure with mildly reduced EF

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15
Q

HFpEF abbreviation meaning

A

heart failure with preserved EF

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16
Q

HF classifications I-IV

A

I = no limits in PA; PA doesn’t cause undue breathlessness, fatigue, or palpitations

II = slight limit PA; comfortable at rest; ordinary PA results in undue breathlessness, fatigue, or palpitations

III = marked limit in PA; still comfortable at rest but less than ordinary PA causes isses

IV = S&S present at rest; unable to complete PA without discomfort; discomfort increases with PA

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17
Q

describe L HF

A

LV fails to pump effectively

blood backs up into lungs

systolic failure

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18
Q

describe R HF

A

RV fails to pump effectively

back up of blood to R atrium then periphery

diastolic failure

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19
Q

describe Bilateral HF

A

LV and RV fail to pump effectively

LV fails to pump; blood backs up to lungs

pulmonary aa pressure rises

RV has increased resistance in lungs and fails

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20
Q

common S&S of L HF

A

restlessness
confusion
orthopnea
tachycardia
exertion dyspnea
fatigue
cyanosis

paroxysmal nocturnal dysnpnea

elevated pulmonary capillary wedge pressure

pulmonary congestion
- cough
-crackles
- wheezes
- blood tinged sputum
- tachypnea

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21
Q

common S&S of R sided HF

A

fatigue
increased peripheral venous pressure
ascites
enlarged spleen/liver

may be secondary to chronic pulmonary problems

distended jugular vein

anorexia

GI distress

weight gain

dependent edema

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22
Q

dyspnea is a result of what in HF

A

poor gas transport between lungs and cells of body

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23
Q

what is paroxysmal nocturnal dyspnea/orthopnea

A

SOB worse in recumbent positions and at night

result of ventilation/perfusion mismatch and tendency for worse pulmonary edema in dependent portions of lungs

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24
Q

what weight gain amount is indicative of HF exacerbation

A

> 3lb per day

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25
respiratory patterns for HF
fast/shallow breaths common not caused by hypoxemia but by stimulation of receptors at the alveolar membrane from fluid increase and pressure
26
what heart sound is a hallmark sign of HF
S3
27
what causes peripheral edema in HF patients
results of fluid retention from kidneys and hearts inability to pump blood from the periphery
28
what causes jugular dissension
fluid overload and back up into venous vasculature
29
what causes poor perfusion to extremities with HF
pale, cool, cyanotic limbs results from increased sympathetic activation causing vasoconstriction and decreased peripheral BF
30
why do HF patients experience sinus tachycardia
it is a negative compensation for decreased CO
31
what are rales/crackles
abnormal breath sounds caused by increased fluid in the alveoli
32
poor exercise tolerance in HF pts causes what
early onset anaerobic metabolism causing decrease in peak O2 consumption
33
lab findings for HF pts
increased BNP increased BUN/Cr decreased Na
34
characteristics of compensated HF
heart function is good enough to prevent obvious S&S initial response to HF is to compensate by raising HR or SV NYHA stage I-II
35
characteristics of decompensated HF
heart function has deteriorated so much that S&S are present S&S can be present at rest with severe decompensation typically requires medical attention and likely hospitalization NYHA stage III-IV
36
what is cardiomyopathy
impaired heart contraction and relaxation primary causes result from pathology of the heart mm itself secondary causes result from systemic disease
37
what is dilated CM
ischemic CM- mitochondrial dysfunction cause lack of energy needed for function dilation of heart chambers and wall thinning, especially LV weakened LV causes decreased CO, SV, EF, and contractility
38
causes of dilated CM
CAD ETOH HTN pregnancy smoking chemo myocarditis
39
what is hypertrophic/obstructive CM
opposite of dilated CM chamber wall thickening, LV especially diastolic dysfunction with impaired ventricular filling nonischemic EF stays normal
40
what causes hypertrophic/obstructive CM
autosomal dominant trait high risk of sudden cardiac death
41
describe restrictive CM
stiffness of myocardium resulting in diastolic dysfunction with impaired ventricular filling LV hypertrophy, fibrosis, thickening nonischemic EF stays normal or mildly reduced can be well treated with beta blockers to decreased HR
42
causes of restrictive CM
rare connective tissues diseases chemo/radiation genetic mutations cardiac tissue tumors
43
valvular disease is more common on what side
L side of heart
44
risk factors for valvular disease
congenital heart defects genetics smoking high BMI HTN CAD/HF autoimmune disorders IV drug use age
45
what is stenosis/S&S
narrowing of valve/leaflets causes increased pressure and blood accumulation in chamber behind stenotic valve symptoms based on which valve is dysfunctional but related to impaired CO can hear loudest murmur during systole
46
what is regurgitation
abnormal blood flow in both directions through incompetent valve incomplete closing from thickened or stretched leaflets increased volume of pumped blood increased dilation of chamber either behind or ahead to accommodate added volume
47
what is lymphedema
inability of lymphatic system to handle the fluid demands placed on it results in accumulation of protein rich interstitial edema increased blood capillary filtration decreased blood capillary reabsorption
48
what is transport capacity of the lymphatic system
max ability to transport lymph fluid
49
what is lymphatic load
amount of lymph transported
50
lymphatic system is under control of what nervous system
SNS
51
describe large lymphatic vessels
largest lymphatic vessels have valves and thick smooth mm to move fluid around
52
R lymphatic duct drains to
subclavian vein
53
thoracic (L lymphatic) duct drains to
IVC largest lymph vessel in the body drains largest surface area
54
describe dynamic insufficiency of the lymphatic system
lymphatic load exceeds transport capacity high fluid volumes result in pitting edema HF, venous insufficiency, immobility, and pregnancy can cause
55
describe mechanical insufficiency of the lymphatic system
impaired transport capacity lymphatic load exceeds impaired transport capacity results in true lymphedema
56
describe combined insufficiency of the lymphatic system
reduced transport capacity abnormally high lymphatic load prolonged elevated lymphatic load damages lymphatic valves
57
describe primary lymphedema
as lymphedema progresses, vessels dilate and valves become incompetent results in lymphostasis, protein rich fluid stuck in interstitium excess weight worsens lymphatic vessel damage as they are crushed, resulting in lymphedema
58
describe secondary lymphedema
results from unknown insult to lymphatic system impaired transport capacity
59
stage 0 lymphedema
latency no clinical edeam tissue and skin appear normal lymph transport capacity already reduced
60
stage 1 lymphedema
reversible soft pitting edema present edema reverses with elevation edema worsens with standing/activity tissue and skin will still appear normal
61
stage 2 lymphedema
irreversible progresses to non pitting "brawny/firm" edema edema does not reverse with elevation positive stemmer sign tissue is fibrosclerotic; proliferation of adipose frequent infections
62
stage 3 lymphedema
lymphostatic elephantiasis all of stage 2 signs plus: - non pitting brawny firm edema present at all times - severe skin changes (papillomas, skin folds, warty, protrusions, hyperkeratosis, etc)
63
negative vs positive stemmer sign
negative = fold of skin at base of second toe can be gently pinched and lifted (normal) positive = fold of skin at base of second toe cannot be pinched and lifted (lymphedema)

Year 3: Clinical Medicine and Pathophysiology (8 decks)

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