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Pathophysiology > Exam 2: Ch 20 Heart Failure > Flashcards

Exam 2: Ch 20 Heart Failure Flashcards

1
Q

to meet the body’s needs, the heart adjusts its…

A

cardiac output

increased with exercise

decreased with sleep

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2
Q

calculate CO (cardiac output)

A

SV x HR

SNS can increase both SV and HR

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3
Q

calculate SV (stroke volume)

A

EDV - ESV

end diastolic volume - end systolic volume

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4
Q

calculate EF (ejection fraction)

A

SV/EDV

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5
Q

preload

A

EDV: increased EDV –> increased SV within limits

in HF EDV is very high and SV is low

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6
Q

afterload

A

SVR (systemic vascular resistance): high SVR –> increased work and/or low SV

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7
Q

contractility

A

ability of the heart to eject (SV at any EDV): low EF in HF

calcium from SR and ECF

L-type calcium channels opened by catecholamine binding to receptor

cardiac glycocides inhibit Na/K pump

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8
Q

athletes have a higher __ and lower __

A

SV, HR

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9
Q

heart failure definition

A

heart fails to pump the blood that it receives

veins of lungs and peripheral organs become congested

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10
Q

systolic HF

A

reduced EF: heart contracts poorly

often caused by ischemic heart disease, HBP, aortic stenosis

high EDV

low SV

EF less than 40%

Peripheral venous congestion

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11
Q

disatolic HF

A

preserved EF: heart relaxes and fills poorly

aggravated by tachycardia

low EDV, ESV, SV, CO

hypertrophic cardiomyopathy

Pulmonary congestion

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12
Q

right sided HF

A

high RVEDP –> high RAP –> high peripheral venous pressure

extremities and viscera become conjested –> peripheral edema & ascites

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13
Q

causes of right sided HF

A

Rt sided valve problems or MI

severe pulmonary disease

severe pulmonary HTN

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14
Q

left sided HF

A

low CO

high LVEDP –> high LAP –> high pulmonary venous pressure

lungs become congested and body tissues are inadequately perfused

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15
Q

causes of left sided HF

A

MI

HTN

left sided valve dysfunction

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16
Q

high output HF vs. low output HF

A

high output: CO is elevated but still inadequate

low output: pumping ability of the heart is decreased

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17
Q

Frank-Starling mechanism

A

low CO triggers Na + H2O retention to increase EDV & SV

HF –> high EDV at rest, nearly normal SV

compensatory mechanism partially exhausted so ability to exercise is limited

high LVEDP –> pulmonary congestion

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18
Q

______ are commonly helpful in HF

A

diuretics

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19
Q

SNS activity in HF

A

SNS nerve activity and catecholemine levels high in early HF

maintains CO and vital organ perfusion

downside is increased afterload –> low SV or increased work

down regulates beta receptors

more arrythmias

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20
Q

RAA system

A

stimulated by low renal blood flow or pressure

kidney secretes renin

renin turns renin substrate into angiotensin I

A I –> A II by ACE in lung capillaries

A II increases ADH/Aldo release

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21
Q

ADH/Aldo/A II

A

ADH: increases H2O retention

Aldo: increases Na retention

A II: vasoconstrictor, helps tissue remodeling

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22
Q

naturetic peptides

A

increased in HF

ANP (atrial natriuretic peptide), brain NP

ANP released when atria overstretched

BNP (brain) released from ventricles when stretched

both –> natriuresis (Na excretion by kidneys)

23
Q

endothelins

A

vasoconstrictors released by endothelial cells

cause cardiac tissue hypertrophy and remodeling

24
Q

is hypertrophy an initially helpful compensation for HF?

A

yes

eventually decreases cardiac pump function though

25
Q

stimuli for hypertrophy

A

mechanical stress

A II, ANP, endothelin

ACEI

26
Q

3 types of hypertrophy

A

symmetric

concentric

eccentric

27
Q

symmetric hypertrophy

A

muscle length and wall thickness is increased (athletes)

28
Q

concentric hypertrophy

A

wall thickens too much due to HTN

increased afterload

systolic function initially preserved, then leads to ischemia

29
Q

eccentric hypertrophy

A

muscle length is increased (dilated cardiomyopathy)

decreased wall thickness

increased preload

30
Q

6 manifestations of HF

A

edema and fluid retention

respiratory symptoms

fatigue and confusion

cachexia

cyanosis

arrhythmias and sudden death

31
Q

edema and fluid retention

A

high capillary hydrostatic pressure causes edema

right sided failure –> peripheral edema

left sided failure –> pulmonary edema

nocturia

oliguria

32
Q

nocturia

A

early in HF laying down

high venous return

low urine output

33
Q

oliguria

A

late in HF

low CO and renal perfusion

low urine output

34
Q

respiratory symptoms of HF

A

pulmonary congestion causes dyspnea

worst on exertion, when flat (orthopnea), and at night

cardiac asthma: stimulation of stretch receptors

35
Q

fatigue and confusion is due to

A

decreased organ perfusion

36
Q

cachexia (loss of weight)

A

GI involvement and general fatigue

37
Q

cyanosis

A

arterial desaturation

pulmonary edema or O2 removal

38
Q

arrhythmias and sudden death

A

AF (atrial fibrilation)

VT/VF (ventricular tachycardia/ventricular fibrillation)

39
Q

acute HF syndromes

A

gradual or rapid change in HF signs and symptoms

worsening of chronic HF that responds to Rx

new onset HF from MI

worsening of end-stage HF that is refractory to Rx

40
Q

acute pulmonary edema

A

dramatic and life-threatening symptom of AHFS and complication of left sided HF

severe dyspnea, cyanosis, confusion, frothy blood-tinged sputum

Rx: lower preload and afterload, increase contractility, give O2

41
Q

case of a 51 yro male with SOB: PA chest radiograph demonstrates bilateral parahilar infiltrates resembling batswing o butterfly in which the hilum or medulla of the lungs are mainly involved with sparing of the periphery or cortex

A

pulmonary edema

“bats-wing” pattern

42
Q

2 classification systems for diagnosing HF

A

functional classification of severity by NYHA

or ACC-AHA staging

43
Q

Dx of HF: H&P, Labs, Echo, CXR

A

H&P: ask about dyspnea, nocturia, fatigue, cough, edema

Labs: BNP levels, electrolytes

echo: look at EF, hypertrophy, valve action, distinguish between systolic vs. diastolic failure

CXR: shows cardiac enlargement

44
Q

functional classification system by NYHA

A

class 1 is best, no limitation of physical activity

class 4 is worst, can’t perform any physical activity without discomfort; symptoms present at rest

45
Q

ACC-AHA staging

A

stage A: high risk for HF, no abnormalities yet

Stage B: no symptoms but developed structural heart disease that may lead to HF

Stage C: symptomatic HF associated with structural disease

Stage D: advanced structural heart disease, signs of HF at reset despite max therapy

46
Q

pharmacologic treatment of HF goals

A

treat causes, reduce risk factors

slow or reverse dysfunction, relieve symptoms, improve quality of life

lower edema with Na restriction and diuretics

surgical repair of cardiac defects

47
Q

pharmacology of HF treatment

A

diuretics: improve position of Starling curve
digitalis: poison Na/K pump, lower HR and up contractility

ACEI: lower afterload and aldosterone, slow remodeling

A II receptor blockers: similar as above

beta blockers: lower SNS activation to decrease mortality

vasodilators: isosorbide, hydralazine

48
Q

Swan-Ganz catheter (invasive monitoring)

A

inserted in large vein (goes with flow)

when wedged (PCWP) ~ LVEDP

prolonged inflation causes pulmonary infarct

measures CO: thermodilution

measures MV O2

49
Q

non pharmacologic treatments of HF

A

exercise program

Na/H2O restriction

O2 therapy

cardiac resynchronization

mechanical support

heart transplantation

50
Q

O2 therapy

A

increases O2 saturation

CPAP - constant positive airway pressure

51
Q

cardiac resynchronization

A

use of pacing leads in Rt and Lt ventricles

coordinates activity

52
Q

mechanical support VAD

A

ventricular assist device

implanted percutaneously or open

augment pumping action of LV

53
Q

heart transplantation

A

orthotopic technique: donor heart attached to retained posterior atrial walls of recipient

required continued immunosuppressants

5-yr survival rate is 2/3 –> 3/4

Pathophysiology (24 decks)

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