Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PCOL > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

a measurement, expressed as a percentage, of how much blood the left ventricle pumps out with each contraction

A

Ejection Fraction

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

50-70% is pumped out during each contraction (comfortable during activity)

A

NORMAL Ejection Fraction

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

41-49% is pumped out during each contraction (sx may be noticeable during activity)

A

BORDERLINE Ejection Fraction

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

<_ 40% is pumped out during each contraction (sx ate noticeable even during rest)

A

REDUCED Ejection Fraction

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

T/F:
it is also possible to have a diagnosis of heart failure with a seemingly normal (or preserved) ejection fraction of greater than or equal to 50%

A

TRUE

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

•Occurs when cardiac output is inadequate to provide the oxygen needed by the body

• The heart cannot meet the metabolic requirements of the peripheral systems

• Heart’s inability to fill or empty the left ventricle properly

A

Heart Failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

S/Sx: of Heart Failure
DetPePue TaShoCa

A

• Decreased exercise tolerance
• Peripheral edema
• Pulmonary edema
• Tachycardia
• Shortness of breath
• Cardiomegaly

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

Neurohumoral Compensatory Mechanism
(RaSyEnNat)

A

• Renin-angiotensin-aldosterone system (Angiotensin II)
• Sympathetic stimulation (NE, Epi)
• Endothelin release
• Natriuretic peptides (Brain Natriuretic Peptide)

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

Neurohumoral Compensatory Mechanism
a.va=
b.pro=

A

a. vasoconstriction=↑afterload
b. Prolongedβ-activation=caspases = apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Enlargement of myocardial cells due to chronic and increased stress on the heart (release of caspases)

A

Myocardial Hypertrophy

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

• thickening of heart walls/muscle
• can lead to ischemic changes, impairment of diastolic filling, and alterations in ventricular geometry

A

Myocardial Hypertrophy

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

• dilation (other than that due to passive stretch) and other slow structural changes that occur in the stressed myocardium

A

Remodeling

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

Pathophysiology of Cardiac Performance
(PACH)

A

a. Preload
b. Afterload
c. Contractility
d. Heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Patho

•is usually increased in heart failure because of increased blood volume and venous tone
• Increased blood volume and venous tone increases fiber length or filling pressure, and increases oxygen demand in the myocardium.

A

Preload

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

Patho

• Reduced by diuretics and venodilators

A

Preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Decreased CO in chronic failure results to reflex increased in SVR (__) mediated by:

•increased sympathetic outflow and circulating catecholamines (baroreceptor reflex)
•activation of the renin-angiotensin system § endothelin

A

Afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Reduced by drugs that reduces arteriolar tone

A

Afterload

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

Chronic heart failure demonstrates a reduction in_____
• Decreased ___result in:

•decreased velocity of muscle shortening
•decreased rate of intraventricular pressure development
•reduced stroke output

A

Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Inotropic drugs increase contractility

A

Contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

• Major determinant of cardiac output
• First compensatory mechanism that comes into play to maintain cardiac output
• _______(2) limits diastolic filling time and coronary flow, further stressing the heart

A

Heart rate

Tachycardia

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

drugs may benefit patients with high heart rates

A

Bradycardic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Classification of HF

• aka left-sided HF or left ventricular HF
• Reduced mechanical pumping action (contractility) of the heart
• reduced CO and significantly reduced EF
• Resulting from myocardial ischemia/infarction
• Responds with inotropic agents

A

SYSTOLIC HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Classification
Symptoms:
•pulmonary symptoms (dyspnea, orthopnea, tachypnea, paroxysmal nocturnal dyspnea, Cheyne-stokes respiration),
•S3 gallop or third heart sound
•cardiomegaly

A

SYSTOLIC HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Classification:
• aka right-sided HF or right ventricular HF
• Stiffening and loss of adequate ventricular relaxation to permit normal filling and cardiac output
• CO is reduced, EF may be normal
• Resulting from hypertrophy and stiffening of myocardium
• Does not respond with inotropic agents

A

DIASTOLIC HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Symptoms:
•peripheral edema
•neck-vein engorgement
•hepatomegaly

A

DIASTOLIC HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Cardiac output is below the normal range, but demand for blood flow is normal

A

Low output HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

• the demands of the body for blood is unusually high, that even increased CO is insufficient
• result from hyperthyroidism, beriberi, anemia, and arteriovenous shunts
• responds poorly to drugs, thus, management is by correcting the underlying cause

A

High Output HF

28
Q

Causes of high output HF
SaHyArfBerPa

A

Severe anemia
Hyperthyroidism
Arteriovenous fistula
Beriberi
Paget’s disease

29
Q

Blood contains too few oxygen-carrying bv

A

Severe anemia

30
Q

Thyroid gland produces too much thyroid hormone.

A

Hyperthyroidism

31
Q

An abnormal connection between an artery and a vein

A

Arteriovenous fistula

32
Q

Deficiency of thiamine (vitamin B1)

A

Beriberi

33
Q

Abnormal breakdown and regrowth of bones, which develop an excessive amount of blood vessels

A

Paget’s disease

34
Q

New York Heart Association Functional Classification

Patients with cardiac disease but resulting in no limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnea or anginal pain.

A

Class l

35
Q

New York Heart Association Functional Classification

Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnea or anginal pain.

A

Class ll

36
Q

New York Heart Association Functional Classification

Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity
causes fatigue, palpitation, dyspnea or anginal pain.

A

Class lll

37
Q

New York Heart Association Functional Classification

Patients with cardiac disease resulting in inability to carry on any physical activity without discomfort. Symptoms of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken, discomfort increases.

A

Class IV

38
Q

American College of Cardiology/American Heart Association classification

Px are high risk for HF but w/o structural hdx or sx of Hf

A

Stage A

39
Q

American College of Cardiology/American Heart Association classification

Px w/ structural hdx but w/o s/sx of hf

A

Stage B

40
Q

American College of Cardiology/American Heart Association classification

Px w/ structural hdx w/ prior or current sx of hf

A

Stage C

41
Q

American College of Cardiology/American Heart Association classification

Px w/ refractory hf requires specialized intervention

A

Stage D

42
Q

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium

reduces the actions of cardiac glycosides; increased cardiac automaticity is inhibited

A

Hyperkalemia

43
Q

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium

enhances the actions of cardiac glycosides; increases risk of digoxin toxicity

A

Hypokalemia

44
Q

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium

enhances the actions of cardiac glycosides; increases risk of digoxin toxicity

A

Hypokalemia

45
Q

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium

increases the risk of a digitalis-induced arrhythmia

A

Hypercalcemia

46
Q

Interactions of Cardiac Glycosides with Potassium, Calcium & Magnesium

increases risk of digoxin toxicity

A

Hypomagnesemia

47
Q

Management of Digoxin Toxicity
Administration of antiarrhythmics for

ventricular and atrial arrhythmias

A

Phenytoin

48
Q

Management of Digoxin Toxicity
Administration of antiarrhythmics for

ventricular tachyarrhythmias

A

Lidocaine and procainamide

49
Q

Management of Digoxin Toxicity
Administration of antiarrhythmics for

ventricular and supraventricular tachycardia but not in the presence of AV block

A

Propranolol

50
Q

Management of Digoxin Toxicity
Administration of antiarrhythmics for

Sinus bradycardia and various degrees of AV block

A

Atropine

51
Q

Management of Digoxin Toxicity
Administration of Digoxin-specific antibody fragment for

• Life-threatening digoxin or digitoxin overdosage
• Patients exhibiting shock or cardiac arrest, ventricular arrhythmias, progressive bradyarrhythmias, or severe hyperkalemia

A

DigiFab & DigiBind

52
Q

MOA: inhibits phosphodiesterase isozyme 3 (PDE3) leading to ↑cAMP → Protein kinase A (PKA) activation → ↑influx of Ca2+ into the cell = (+) inotropy, chronotropy and dromotropy

A

Bipyridines

53
Q

• Increase contractility and promote vasodilation
• Used only intravenously
• Only for acute heart failure or severe exacerbation of chronic heart failure

A

Bypiridines

54
Q

Adverse Effects of specific bypitiridines

nausea and vomiting, arrhythmias,
thrombocytopenia, hepatoxicity = already withdrawn

A

Inamrinone

55
Q

Adverse Effects of specific bypitiridines

arrhythmias; less likely to cause thrombocytopenia and hepatoxicity

A

Milrinone

56
Q

Adverse Effects of specific bypitiridines

arrhythmias; less likely to cause thrombocytopenia and hepatoxicity

A

Milrinone

57
Q

MOA: stimulates β1-receptors = ↑cAMP → Protein kinase A (PKA) activation → ↑influx of Ca2+ into the cell = (+) inotropy, chronotropy and dromotropy

A

β1-receptor Agonists

58
Q

B1 receptor agonist

increaseinCO,decreaseinventricularfillingpressure

A

Dobutamine (β1-selective)

59
Q

B1 receptor agonist

acuteheartfailure,ifthereisaneedtoraisebloodpressure

A

Dopamine (non-selective)

60
Q

Investigational Positive Inotropic Drugs
IsLeOm

A

Istaroxime
Levosimendan
Omecamtiv mecarbil

61
Q

Investigational Positive Inotropic Drugs

• steroid derivative that inhibits Na+/K–ATPase
• in addition, appears to facilitate sequestration of Ca2+ by the SR =
less arrhythmogenic than digitalis

A

Istaroxime

62
Q

Investigational Positive Inotropic Drugs

• sensitizes the troponin system to Ca2+ and inhibits phosphodiesterase

A

Levosimendan

63
Q

Investigational Positive Inotropic Drugs

• parenteral agent that activates cardiac myosin and prolongs systole without increasing oxygen consumption of the heart

A

Omecamtiv mecarbil

64
Q

Agents With No Positive Inotropic Effects
DiAcArVBb

A

Diuretics
Ace/Arbs
Vasodilators
Beta blockers

65
Q

Agents With No Positive Inotropic Effects

• Reduce left ventricular filling pressure and decrease left ventricular volume and myocardial wall tension (lower oxygen demand)
• Reduce salt and water retention, edema, and symptoms

A

Diuretics

66
Q

Agents With No Positive Inotropic Effects

“balanced unloaders”
• Arteriolar vasodilation = ↓ SVR = ↓ afterload
• Venous vasodilation = ↓ venous return/ventricular filling pressure = ↓ preload
• reduce salt and water retention = ↓ preload

A

ACE/ARBs

67
Q

Specific vasodilators

• Used in patients who cannot tolerate ACE inhibitors
• African Americans respond better than with ACEis and
ARBs
• Balanced unloader if combined

A

Isosorbide dinitrate
Hydralazine

PCOL (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions