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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
Q

respiratory patterns for HF

A

fast/shallow breaths common

not caused by hypoxemia but by stimulation of receptors at the alveolar membrane from fluid increase and pressure

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26
Q

what heart sound is a hallmark sign of HF

A

S3

27
Q

what causes peripheral edema in HF patients

A

results of fluid retention from kidneys and hearts inability to pump blood from the periphery

28
Q

what causes jugular dissension

A

fluid overload and back up into venous vasculature

29
Q

what causes poor perfusion to extremities with HF

A

pale, cool, cyanotic limbs

results from increased sympathetic activation causing vasoconstriction and decreased peripheral BF

30
Q

why do HF patients experience sinus tachycardia

A

it is a negative compensation for decreased CO

31
Q

what are rales/crackles

A

abnormal breath sounds caused by increased fluid in the alveoli

32
Q

poor exercise tolerance in HF pts causes what

A

early onset anaerobic metabolism causing decrease in peak O2 consumption

33
Q

lab findings for HF pts

A

increased BNP

increased BUN/Cr

decreased Na

34
Q

characteristics of compensated HF

A

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
Q

characteristics of decompensated HF

A

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
Q

what is cardiomyopathy

A

impaired heart contraction and relaxation

primary causes result from pathology of the heart mm itself

secondary causes result from systemic disease

37
Q

what is dilated CM

A

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
Q

causes of dilated CM

A

CAD

ETOH

HTN

pregnancy

smoking

chemo

myocarditis

39
Q

what is hypertrophic/obstructive CM

A

opposite of dilated CM

chamber wall thickening, LV especially

diastolic dysfunction with impaired ventricular filling

nonischemic

EF stays normal

40
Q

what causes hypertrophic/obstructive CM

A

autosomal dominant trait

high risk of sudden cardiac death

41
Q

describe restrictive CM

A

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
Q

causes of restrictive CM

A

rare connective tissues diseases

chemo/radiation

genetic mutations

cardiac tissue tumors

43
Q

valvular disease is more common on what side

A

L side of heart

44
Q

risk factors for valvular disease

A

congenital heart defects
genetics
smoking
high BMI
HTN
CAD/HF
autoimmune disorders
IV drug use
age

45
Q

what is stenosis/S&S

A

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
Q

what is regurgitation

A

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
Q

what is lymphedema

A

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
Q

what is transport capacity of the lymphatic system

A

max ability to transport lymph fluid

49
Q

what is lymphatic load

A

amount of lymph transported

50
Q

lymphatic system is under control of what nervous system

A

SNS

51
Q

describe large lymphatic vessels

A

largest lymphatic vessels have valves and thick smooth mm to move fluid around

52
Q

R lymphatic duct drains to

A

subclavian vein

53
Q

thoracic (L lymphatic) duct drains to

A

IVC

largest lymph vessel in the body

drains largest surface area

54
Q

describe dynamic insufficiency of the lymphatic system

A

lymphatic load exceeds transport capacity

high fluid volumes result in pitting edema

HF, venous insufficiency, immobility, and pregnancy can cause

55
Q

describe mechanical insufficiency of the lymphatic system

A

impaired transport capacity

lymphatic load exceeds impaired transport capacity

results in true lymphedema

56
Q

describe combined insufficiency of the lymphatic system

A

reduced transport capacity

abnormally high lymphatic load

prolonged elevated lymphatic load damages lymphatic valves

57
Q

describe primary lymphedema

A

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
Q

describe secondary lymphedema

A

results from unknown insult to lymphatic system

impaired transport capacity

59
Q

stage 0 lymphedema

A

latency

no clinical edeam

tissue and skin appear normal

lymph transport capacity already reduced

60
Q

stage 1 lymphedema

A

reversible

soft pitting edema present

edema reverses with elevation

edema worsens with standing/activity

tissue and skin will still appear normal

61
Q

stage 2 lymphedema

A

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
Q

stage 3 lymphedema

A

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
Q

negative vs positive stemmer sign

A

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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