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BSNC 2000 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Mean Arterial Pressure

A

average pressure in the systemic circulation.

indicator of how much force needed to move blood around the body

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2
Q

Intrathoracic Pressure & Venous return

A

Intrathoracic Pressure impedes venous return to the heart as it increases opposing pressure on veins and can occlude vessels

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3
Q

Systolic blood pressure

A

arterial blood pressure during ventricular contraction

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4
Q

Diastolic blood pressure

A

arterial blood pressure during ventricular relaxation

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5
Q

Cardiac output

A

total volume of blood ejected from the left ventricle per minute

determined by: stroke volume x heart rate

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6
Q

Stroke Volume

A

total volume of blood ejected from left ventricle per contraction

determined by preload, afterload, and contractility

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7
Q

Frank-Starling Mechanism

A

states that within limits, increased preload (stretch) increases contractility.

this is due to the optimal arrangement of sarcomeres when stretched

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8
Q

Preload

A

wall tension placed on the ventricular at the end of diastolic filling.

determined by central venous volume
increased preload = increased stroke volume

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9
Q

Contractility

A

force of contraction during systole.

increases stroke volume independent of preload/afterload

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10
Q

Afterload

A

force heart has to work against during systolic contraction.

determined by peripheral vascular resistance and ventricular wall tension.
increased afterload = decreased stroke volume

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11
Q

End Systolic Volume

A

blood volume remaining in ventricles after systole.

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12
Q

End Diastolic Volume

A

blood volume in ventricles at the end of diastolic filling.

end systolic volume + diastolic filling
determines preload

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13
Q

Heart rate and Preload

A

Increased heart rate decreases amount of diastolic relaxation between contractions

Reduced end diastolic volume causes reduced preload

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14
Q

Wall Tension & Wall Thickness

A

wall tension = opposing force of the wall of a blood vessel
wall thickness = diameter of the vessel wall

there is an inverse relationship between wall tension & wall thickness.
increased thickness = decreased tension

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15
Q

Determinants of muscle contraction

A

Calcium
ATP
Oxygen
Na+/K+ pump

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16
Q

Electrical Conduction System

A

SA Node –> AV Node (delayed) –> AV Bundle (delayed) –> Purkinje Fibers

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17
Q

Atrial Kick

A

during atrial contraction, the atria eject the remaining bit of blood from atrial chambers –> ventricles

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18
Q

Cardiac performance

A

affected by work demand of heart and ability of coronary perfusion to meet metabolic demand

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19
Q

Inotropy Factors

A

factors that alter muscle contraction

can be positive (promote contraction) or negative (inhibit contraction)

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20
Q

Vasoconstrictors

A

Angiotensin II
Catecholamines (mainly norepinephrine)
ADH
Prostaglandins - released by arachidonic pathway
Serotonin - released by clotting platelets

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21
Q

Vasodilators

A 
Nitric Oxide - released by endothelial cells
Natriuretic Peptides 
Histamine - mast cells + basophils
Bradykinin
Ace-i
ARB
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22
Q

Common Causes of Heart Failure

A 
Coronary Artery Disease
Hypertension
Myocardial Infarction
Dilated Cardiomyopathy
Valvular Heart Disease
Pulmonary disorders (Right-sided HF)
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23
Q

Ejection Fraction

A

percentage of blood ejected from the heart during systole

calculated by stroke volume / end diastolic volume

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24
Q

Heart Failure EF

A

equal to or under 40%

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25
Q

Heart Failure Definition

A

functional or structural impairment of the heart causing inadequate cardiac output to meet metabolic demand

caused by heart not pumping properly or filling properly

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26
Q

HF Compensatory Mechanisms

A 
Frank-Starling Law --> increased preload
SNS activation
RAAS activation
Natriuretic peptides 
Myocardial remodeling
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27
Q

Pathology of Ventricular Hypertrophy

A

initially is effective as a compensatory mechanism.
concentric hypertrophy over time decreases contractility due to arrangement of sarcomeres + reduces ventricular lumen
increased wall thickness = decreased wall tension therefore reducing contractility and increases metabolic demand of heart

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28
Q

Angiotensin II functions

A 
vasoconstrictor
stimulates adrenal medulla to rls aldosterone
stimulates PPG to rls ADH
stimulates rls of norepinephrine
increase thirst response
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29
Q

Aldosterone functions

A

Increase sodium reabsorption –> increase water retention
Increase potassium excretion
stimulate fibroblast activity in myocardium

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30
Q

Antidiuretic Hormone functions

A

aka vasopressin

increases water reabsorption
vasoconstrictor

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31
Q

Natriuretic Peptides

A

ANP –> rls by atrial cells
BNP –> rls by ventricular cells. biomarker for heart failure

released in response to stretch
promote excretion of sodium and water
vasodilator

32
Q

Types of Heart Failure

A 
Right-side vs. Left-side
Diastolic vs. Systolic
Reduced Ejection Fraction vs. Preserved Ejection Fraction
Acute vs. Chronic
Biventricular
33
Q

S/S of Left Sided HF

A 
Wet cough 
Reduced ejection fraction
Hemoptysis 
SOB 
Dizziness, light-headedness 
Fatigue - gets worse throughout day 
Hypoxemia --> hypoxic tissue injury
Orthopnea
Proxysmal Nocturnal Dyspnea 
Inspiratory crackles
34
Q

S/S of Right Sided HF

A 
Distended Jugular Vein
Peripheral edema
Upper abdominal pain 
Hepatomegaly, splenomegaly 
Reduced appetite
Nocturia
35
Q

Normal BNP levels

A

<100 pg/Ml

36
Q

Normal EF

A

> 50%

37
Q

Pleural Effusion

A

fluid build in in the pleural cavity

38
Q

Calcium Efflux mechanisms

A

1) Active calcium pump (req ATP)

2) Sodium-calcium exchanger

39
Q

Medication classes used for heart failure

A

Diuretics
Ace-i
Angiotensin II Receptor Blockers (ARB)
Cardiac Glycosides

40
Q

Spironolactone

A

potassium sparing diuretic

onset: unknown
peak: 2-3 days
duration: 2-3 days

41
Q

Spironolactone mechanism

A

competitive antagonist
blocks aldosterone receptors on the distal convoluted tubule
prevents reabsorption of sodium while saving potassium and hydrogen ions

42
Q

Captopril

A 
ace inhibitor 
side fx: chronic dry cough 
onset: 15-60 min
peak: 60-90 min
duration: 6-12 hours
43
Q

Captopril mechanism

A

antagonist?
inhibits ACE-i activity thereby preventing the conversion of angiotensin I to angiotensin II
promotes vasodilation, decreased sodium reabsorption, decreased release of aldosterone

44
Q

Angiotensin II effects

A

major vasoconstrictor -> increases blood pressure
promotes release of ADH from PGH
promotes release of aldosterone from adrenal medulla
increase sodium reabsorption in the kidneys
increases thirst sensation
decreases baroreceptor sensitivity

45
Q

Losartan

A 
angiotensin II receptor blocker
used when ACE-i are contraindicated 
onset: 6 hours
peak: 3-4 weeks
duration: 24 hours
46
Q

Losartan Mechanism

A

prevents angiotensin II from binding to receptors on smooth muscle –> promotes vasodilation
lowers blood pressure

47
Q

Bisoprolol

A

selective beta-1 blocker

onset: 1-4 hours
peak: 2-4 hours
duration: 24 hours

48
Q

Andrenergic receptors

A

cell membrane receptors that bind with catecholamines

49
Q

Beta-1 Receptor Locations

A

heart
kidneys
fat cells

50
Q

Bisoprolol Mechanism

A

prevents epinephrine from binding with beta-1 receptors on the myocardium
reduces contractility, decreases heart rate, promote diastolic filling, reduce O2 demand
reduces cardiac output (decrease work of heart)
decreases renin production by juxtaglomerular cells

51
Q

Digoxin

A 
cardiac glycoside 
requires a loading dose
onset: 50min-2 hours
peak: 2-6 hours
duration: 2-4 days
52
Q

Digoxin mechanism

A

beta-1 agonist
inhibits the sodium-potassium pump, increasing sodium –> increasing intracellular calcium
promotes increased contractility –> increased cardiac output
increases refractory period at sa/av nodes –> decreased heart rate

53
Q

Inotropy

A

agent that affects the force of muscular contractions. can be positive or negative
positive = increase contraction
negative = decrease contraction

54
Q

Positive inotropic agents

A

Digoxin

Calcium

55
Q

BNP

A 
brain natriuretic peptide
released from ventricular cells in response to overstretching
biomarker of heart failure
<100 = normal
>400 = heart failure likely
56
Q

Normal hemoglobin levels for women

A

117-155 g/L

57
Q

Normal hemoglobin levels in men

A

140-173 g/L

58
Q

Heart Failure Treatment

A 
fluid restrictions (1.5 L/day)
daily weigh-ins
restrict salt
restrict fatty food
exercise with rest periods 
medication 
tertiary prevention
59
Q

Recommended Salt for HF Patients

A

2000 mg/day

60
Q

Recommended activity levels

A

30 min of moderate activity daily

61
Q

Acute cardiac symptoms

A

chest pain
shortness of breath
dizziness/light-headedness

62
Q

HF Weight guidelines

A

no more than 4 lbs in 2 days or 5 lbs in 1 week

63
Q

Aim of Heart Failure Medication Treatment

A

Increase preload
Increase contractility
Decrease remodeling
Decrease afterload

64
Q

Which kidney cell produces renin

A

juxtaglomerular cells

65
Q

First Line HF treatment

A 
vasodilators (ACE-i, BNP, ARB)
diuretics 
b-1 antagonists 
diuretics
HCN blockers
66
Q

Second Line HF treatment

A 
Cardiotonic agents (digoxin)
positive inotropic agents
67
Q

Calcium efflux

A

sodium-calcium exchanger (3 Na+ for 1 Ca++)
exchange depends on voltage of plasma membrane
positive = more calcium ENTERS cell
negative = more calcium EXITS cell

68
Q

Proxysmal nocturnal dyspnea

A

SOB that occurs during sleeping due to fluid accumulation in lungs –> wakes up the patient

69
Q

HF Diagnostics

A 
Blood tests - check for BNP levels 
Chest Xray - look at heart size
ECG 
Exercise stress test
Angiogram 
Echo - measures EF
70
Q

5 Areas of HF

A 
Coronary (Perfusion)
Valvular
Percardium
Myocardium
Electrical
71
Q

Types of cyanosis

A

Central

Peripheral

72
Q

Central cyanosis

A

caused by hypoxemia

decreased O2 in arterial blood

73
Q

Peripheral cyanosis

A

caused by tissue consumption of O2

reduced cardiac output, vasoconstriction

74
Q

Types of cardiomyopathies

A

dilated
hypertrophy
restrictive

75
Q

Dilated cardiomyopathy

A

all four heart chambers dilate
impacts systolic and diastolic function
ventricle walls thin –> decreased contractility
diluted lumen –> excessive preload

76
Q

Hypertrophic cardiomyopathy

A

concentric hypertrophy –> narrows lumen
impairs contractility due to overcrowding of sarcomeres
decreases diastolic filling due to narrow ventricular lumen

77
Q

Restrictive cardiomyopathy

A

fluid in pericardium/fibrosis decreases cardiac compliance

impairs diastolic filling

BSNC 2000 (9 decks)

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