Brainscape's Knowledge GenomeTM

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


See full index

Patho > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is cardiac output affected by?

A

Stroke volume and heart rate - SV+HR=CO

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

What affects stroke volume?

A

Contractility and Afterload

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

What affects contractility?

A

preload (think frank starling law) and sympathetic nervous system.

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

What affects afterload?

A

peripheral vasoconstriction, stenosis

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

What affects the heart rate?

A

Sympathetic nervous system (norepi) and parasympathetic nervous system (acetylcholine)

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

What affects preload?

A

heart rate can affect preload (not enough time to fill), venous return, blood volume.

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

What is preload proportional to?

A

End diastolic volume. As more blood enters the heart, the heart muscles (sarcomeres) stretch, and sarcomere length gets greater and contractility increases.

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

What is the Frank Starling Law?

A

The more volume that enters the heart, the harder the heart can contract. Until there’s too much stretch, and then it’s like a loose rubber band.

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

What is afterload?

A

The pressure that the ventricles need to generate to overcome resistance to the ejection of blood. Diastolic BP is a good indicator of afterload.

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

What is low output heart failure?

A

When the CO is below normal, and can’t even meet minimal demands of the body (like even at rest)

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

What is high output heart failure?

A

It’s pretty uncommon but CO is above normal but can’t meet increased demands for oxygenated blood. Example: severe anemia, and hyperthyroidism.

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

What is left sided heart failure

A

When the left ventricle isn’t working properly. Examples: MI, mitral or aortic valve disease, htn. Blood back up into left atrium and pulmonary circulation.

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

What are the effects of left sided heart failure?

A

Decreased cardiac output, increased pulmonary congestion.

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

What are the signs of pulmonary congestion?

A

Dyspnea, exertional dyspnea, orthopnea, resting dyspnea, nocturnal dyspnea, cough, rales, wheezing, hemoptysis as pulmonary vessels break, pallor and cyanosis from hypoxemia

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

Why do some people with left sided heart failure experience orthopnea?

A

Gravitational forces increase venous return and blood flow to the lungs. Relieved by sitting up.

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

Why do some people get paroxysmal nocturnal dyspnea? How is this different than orthopnea?

A

It’s not just the lying down part. Peripheral edema returns to circulation at night and gets taken to lungs. That coupled with respiratory depression at night causes decreased arterial oxygen.

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

How does pulmonary edema affect ventilation and gas exchange?

A

It makes someone hypoxic because there’s too great of a distance for oxygen and co2 to properly exchange. Also, pulmonary edema makes the lungs stiff and that decreases compliance nad makes it harder to inhale.

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

What are some signs of decreased cardiac output?

A

hypotension, insufficient blood being pumped to tissues - fatigue, muscle wekaness, skin pallor, dizziness, confusion, oliguria.

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

Where causes right sided heart failure?

A

Right heart is weakened due to pulmonary htn d/t primary lung disease like cor pulmonale, pulmonary embolism, pulmonary or tricuspid valvular dx, right ventricular infarction.

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

What does blood back up into in right sided heart failure?

A

Goes to right atrium and systemic venous system.

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

What’s cor pulmonale?

A

Chronic bronchitis and emphysema cause the lungs to be hypoxic so the lungs compensate by constricting blood and causing an increase pulmonary BP leading to cor pulmonale.

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

What does right sided heart failure look like?

A

Peripheral edema, swollen ankles, weight gain, hepatomegaly, ascites, RUQ pain, decreased liver fxn, nausea, abdominal discomfort, increased JVP, flushed face, headache.

23
Q

What’s systolic dysfunction?

A

Left ventricle can’t pump enough blood out to the systemic circulation during systole

24
Q

What’s diastolic dysfunction?

A

The left ventricle can’t relax and fill during diastole.

25
Q

What causes systolic dysfunction?

A

1) Myocardial damage that impairs the contractility, 2) volume overload (excessive preload) causing too much stretch 3) pressure overload (too much afterload) and heart’s ability to contract can’t overcome afterload.

26
Q

What causes ischemic cardiomyopathy?

A

If heart hypertrophies faster than what the coronary blood flow can adapt to - the coronary blood flow can’t match the demands of the hypertrophied muscle.

27
Q

When the ventricles aren’t pumping effectively what happens to stroke volume?

A

stroke volume and therefore cardiac output decreases.

28
Q

When the ventricles aren’t pumping effectively, what happens to the end systolic volume?

A

The systolic volume because blood remains in the heart after systole.

29
Q

What happens to preload if the heart’s ventricles aren’t pumping effectively?

A

Preload would increase because the heart isn’t pumping it on and it’s pooling. This initially would increase contractility, until the heart muscle stretches too much and then it will decrease contractility.

30
Q

What is the ejection fraction?

A

The % of blood that’s ejected during systole. It’s equal to stroke volume divided by End diastolic volume. Is a reflection on how well the heart is contracting.

31
Q

What’s a good ejection fraction?

A

60-80%

32
Q

What’s a bad ejection fraction?

A

Less than 40% = “reduced” ejection fracture; greater than 40% is considered a “preserved” ejection fracture. - indicates systolic dysfunction. Measured by an echo, or migi or a muga.

33
Q

What causes diastolic heart dysfunction?

A

1) Decreased compliance (stretch) Like b/c of ventricular hypertrophy from htn and aortic stenosis or scar tissue from an MI or radiation. 2) Obstruction of ventricular filling Mitral valve stenosis, cardiac tamponade, chronic pericarditis from a fibrosed pericardium.

34
Q

What happens to end diastolic volume when the ventricle can’t fill properly?

A

It would decrease because it’s not filling properly

35
Q

What happens to stroke volume when the heart can’t fill properly?

A

Stroke volume would decrease because the heart needs to fill properly in order to contract properly. (decreased volume = decreased contractility)

36
Q

What happens to ejection fracture if ventricular filling is impaired?

A

It’s likely normal because both stroke volume and end diastolic volume are both decreased. As long as that’s proportional.

37
Q

What are three systems that work to compensate for decreased cardiac output?

A

Sympathetic nervous system, RAAS and myocardial remodeling

38
Q

How does the sympathetic nervous system respond to decreased cardiac output?

A

Arterial baroreceptors in the carotid arches and aortic arch detect a decreased stretch which signals to B1 receptors to speed up heart rate and contractility and the alpha 1 receptors constrict venous and arterial vessels

39
Q

What triggers the RAAS system?

A

Decreased blood flow to the kidneys because of decreased extracellular fluid or arterial blood pressure

40
Q

Long story short, what does the RAAS system do to increase cardiac output?

A

Increases blood volume by retaining sodium and therefore water (increased preload) and vasoconstriction

41
Q

What are the steps of the RAAS system?

A

Juxtaglomerular cells notice a decrease in blood volume, which releases renin. Renin goes to the lungs and stimulates release of Angiotensinogen to Angiotensin I. Angiotensin I converts to Angiotensin II which vasoconstricts arterioles and stimulates the adrenal cortex to pump out aldosterone which is responsible for sodium and water retention.

42
Q

What are three things that angiotensin II does?

A

1) Potent arterial vasoconstrictor
2) Stimulates aldosterone release from adrenal gland
3) Stimulates ADH release from posterior pituitary gland.

43
Q

What causes ventricular dilation?

A

Chronic excessive preload because of increased blood volume, increased venous return or end systolic volume.

44
Q

Why does increased preload contribute to ventricular dilation?

A

It stretches ventricular myocardial cells during diastole and stimulates eccentric hypertrophy (when the cells get longer, not bigger. “Proteins arranged in a series”. Eccentric hypertrophy allows them the heart to contract better in the short term. Detrimental in the long term - decreases stroke volume)

45
Q

What does increased ventricular dilation look like?

A

Cardiomegaly - ventricles and the entire heart become more spherical and the lungs get displaced and it looks big on an x-ray

46
Q

What causes ventricular hypertrophy?

A

Chronic excessive afterload (increased blood volume and vasoconstriction) stimulates concentric hypertrophy where the proteins are arranged parallel. The cells are bigger, but not longer. Muscle mass increases to pump blood against increased resistance.

47
Q

What’s good about ventricular hypertrophy?

A

It initially maintains systolic function. But will eventually decrease wall compliance (because of increased wall thickness) and increased oxygen demand.

48
Q

What are three compensatory mechanisms that lead to decompensation?

A

Arterial vasoconstriction, increased blood volume and increased heart rate.

49
Q

How does arterial vasoconstriction lead to decompensated heart failure?

A

Arterial vasoconstriction leads to increased afterload, which increases O2 demands on the heart. It also redistributes blood flow which affects the GI tract, skin, kidneys etc.

50
Q

How does increased blood volume lead to decompensation?

A

It increases the amount of pressure in the heart which causes ventricular dilation.

51
Q

How does increased heart rate affect decompensation?

A

Less diastolic filling time, compromised coronary artery perfusion and increased workload and O2 demand on the heart

52
Q

When does ANP and BMP get released?

A

When there is distension or increased filling pressure in the heart like increased blood volume.

53
Q

What is the purpose of ANP and BMP?

A

They work to vasodilate and stimulate natriuresis to compensate for all that extra volume. It suppresses the effects of the SNS and RAAS (decrease preload and afterload)

Patho (12 decks)

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