Exam 2: Ch 20 Heart Failure Flashcards

(53 cards)

1
Q

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

A

cardiac output

increased with exercise

decreased with sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

calculate CO (cardiac output)

A

SV x HR

SNS can increase both SV and HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

calculate SV (stroke volume)

A

EDV - ESV

end diastolic volume - end systolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

calculate EF (ejection fraction)

A

SV/EDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

preload

A

EDV: increased EDV –> increased SV within limits

in HF EDV is very high and SV is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

afterload

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

athletes have a higher __ and lower __

A

SV, HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

heart failure definition

A

heart fails to pump the blood that it receives

veins of lungs and peripheral organs become congested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

disatolic HF

A

preserved EF: heart relaxes and fills poorly

aggravated by tachycardia

low EDV, ESV, SV, CO

hypertrophic cardiomyopathy

Pulmonary congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

right sided HF

A

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

extremities and viscera become conjested –> peripheral edema & ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

causes of right sided HF

A

Rt sided valve problems or MI

severe pulmonary disease

severe pulmonary HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

causes of left sided HF

A

MI

HTN

left sided valve dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

______ are commonly helpful in HF

A

diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ADH/Aldo/A II

A

ADH: increases H2O retention

Aldo: increases Na retention

A II: vasoconstrictor, helps tissue remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
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