Exam 2: Ch 20 Heart Failure Flashcards Preview

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Flashcards in Exam 2: Ch 20 Heart Failure Deck (53):
1

to meet the body's needs, the heart adjusts its...

cardiac output

increased with exercise

decreased with sleep

2

calculate CO (cardiac output)

SV x HR

SNS can increase both SV and HR

3

calculate SV (stroke volume)

EDV - ESV

end diastolic volume - end systolic volume

4

calculate EF (ejection fraction)

SV/EDV

5

preload

EDV: increased EDV --> increased SV within limits

in HF EDV is very high and SV is low

6

afterload

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

7

contractility

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

8

athletes have a higher __ and lower __

SV, HR

9

heart failure definition

heart fails to pump the blood that it receives

veins of lungs and peripheral organs become congested

10

systolic HF

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

11

disatolic HF

preserved EF: heart relaxes and fills poorly

aggravated by tachycardia

low EDV, ESV, SV, CO

hypertrophic cardiomyopathy

Pulmonary congestion

12

right sided HF

high RVEDP --> high RAP --> high peripheral venous pressure

extremities and viscera become conjested --> peripheral edema & ascites

13

causes of right sided HF

Rt sided valve problems or MI

severe pulmonary disease

severe pulmonary HTN

14

left sided HF

low CO

high LVEDP --> high LAP --> high pulmonary venous pressure

lungs become congested and body tissues are inadequately perfused

15

causes of left sided HF

MI

HTN

left sided valve dysfunction

16

high output HF vs. low output HF

high output: CO is elevated but still inadequate

low output: pumping ability of the heart is decreased

17

Frank-Starling mechanism

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

18

______ are commonly helpful in HF

diuretics

19

SNS activity in HF

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

20

RAA system

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

21

ADH/Aldo/A II

ADH: increases H2O retention

Aldo: increases Na retention

A II: vasoconstrictor, helps tissue remodeling

22

naturetic peptides

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

endothelins

vasoconstrictors released by endothelial cells

cause cardiac tissue hypertrophy and remodeling

24

is hypertrophy an initially helpful compensation for HF?

yes

eventually decreases cardiac pump function though

25

stimuli for hypertrophy

mechanical stress

A II, ANP, endothelin

ACEI

26

3 types of hypertrophy

symmetric

concentric

eccentric

27

symmetric hypertrophy

muscle length and wall thickness is increased (athletes)

28

concentric hypertrophy

wall thickens too much due to HTN

increased afterload

systolic function initially preserved, then leads to ischemia

29

eccentric hypertrophy

muscle length is increased (dilated cardiomyopathy)

decreased wall thickness

increased preload

30

6 manifestations of HF

edema and fluid retention

respiratory symptoms

fatigue and confusion

cachexia

cyanosis

arrhythmias and sudden death

31

edema and fluid retention

high capillary hydrostatic pressure causes edema

right sided failure --> peripheral edema

left sided failure --> pulmonary edema

nocturia

oliguria

32

nocturia

early in HF laying down

high venous return

low urine output

33

oliguria

late in HF

low CO and renal perfusion

low urine output

34

respiratory symptoms of HF

pulmonary congestion causes dyspnea

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

cardiac asthma: stimulation of stretch receptors

35

fatigue and confusion is due to

decreased organ perfusion

36

cachexia (loss of weight)

GI involvement and general fatigue

37

cyanosis

arterial desaturation

pulmonary edema or O2 removal

38

arrhythmias and sudden death

AF (atrial fibrilation)

VT/VF (ventricular tachycardia/ventricular fibrillation)

39

acute HF syndromes

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

acute pulmonary edema

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

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

pulmonary edema

"bats-wing" pattern

42

2 classification systems for diagnosing HF

functional classification of severity by NYHA

or ACC-AHA staging

43

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

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

functional classification system by NYHA

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

ACC-AHA staging

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

pharmacologic treatment of HF goals

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

pharmacology of HF treatment

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

Swan-Ganz catheter (invasive monitoring)

inserted in large vein (goes with flow)

when wedged (PCWP) ~ LVEDP

prolonged inflation causes pulmonary infarct

measures CO: thermodilution

measures MV O2

49

non pharmacologic treatments of HF

exercise program

Na/H2O restriction

O2 therapy

cardiac resynchronization

mechanical support

heart transplantation

50

O2 therapy

increases O2 saturation

CPAP - constant positive airway pressure

51

cardiac resynchronization

use of pacing leads in Rt and Lt ventricles

coordinates activity

52

mechanical support VAD

ventricular assist device

implanted percutaneously or open

augment pumping action of LV

53

heart transplantation

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

required continued immunosuppressants

5-yr survival rate is 2/3 --> 3/4