Brainscape's Knowledge GenomeTM

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


See full index

CP1.06_Cardio_ZACHOW > Lecture 5 > Flashcards

Lecture 5 Flashcards

1
Q

What does this EKG show?

A
  • tachycardia
  • inverted T waves (ischemia)
  • pronounced Q waves (irreversible death)
  • ST elevations (injury)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is infarction?

A
  • When myocardium undergoes a necrotic process due to ischmemia (lack of oxygen).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Baroreceptors in the body and their locations:

A
  1. High-pressure: carotid sinus and wall of aortic arch
  2. Low-pressure: atria and pulmonary arteries
  3. Renal: perfusion pressure: afferent arterioles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Chemoreceptors in the body and their locations:

A
  1. Peripheral: carotid and aortic bodies
  2. Central: medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do chemoreceptors detect/measure?

A

partial pressure of CO2 (PCO2).

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

All information from chemoreceptors and baroreceptors in the body travel on what afferents to the medulla?

A

CN 9 and CN 10

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

Functions and origins of angiotensin II and aldosterone:

A
  • Kidneys: angiotensin II.
  • Adrenal cortex: aldosterone.
  • Both are vasoconstrictors and help conserve sodium.
    • Sodium conservation increases intravascular volume by holding water.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Both angiotensin II and aldosterone increase:

A
  1. total peripheral resistance (vasoconstriction)
  2. intravascular volume (sodium conservation/water retention)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Neurotransmitters/hormones controlling inotropy and chronotropy and their origins:

A
  1. Norepinephrine (SNS)
  2. epinephrine (adrenal medulla)
  3. ACh (PSNS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Neurotransmitters/hormones controlling vascular smooth muscle tone (vasoconstriction) and their origins:

A
  1. arginine vasopressin (AVP); hypothalamus
  2. angiotensin II (AII); kidneys
  3. aldosterone; adrenal cortex
  4. norepinephrine; SNS
  5. epinephrine; andrenal medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Neurotransmitters/hormones controlling intravascular volume and their origins:

A
  1. arginine vasopressin (AVP); hypothalamus
  2. angiotensin II (AII); kidneys
  3. aldosterone; adrenal cortex
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ultimately, feedback from baroreceptors and chemoreceptors lead to changes in:

A
  1. heart rate
  2. left ventricular contractile force
  3. vasomotion (vasodilation and vasoconstriction)
  4. blood plasma volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

The osmoregulatory center of the brain (detects plasma sodium) is located where?

A
  • hypothalamus
  • regulates urine output and intravascular volume.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Systolic BP is due to/mostly dependent on:

A
  • cardiac output.
    • CO = SV x BPM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Diastolic BP is due to/mostly dependent on:

A

vascular resistance.

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

Blood pressure (MAP) equation:

A

BP/MAP = CO x TPR

17
Q

Total peripheral resistance (i.e. blood pressure) is determined by:

A
  • vascular smooth muscle function and intravascular volume:
    1. SNS (vasoconstrict)
    2. AVP (vasoconstrict and water retention)
    3. angiotensin II (vasoconstrict and water retention)
    4. aldosterone (vasoconstrict and water retention)
18
Q

>60 years of age, BP should be less than:

A

150/90

19
Q

Steps in body raising blood pressure in response to low blood pressure:

A
  1. low pressure baroreceptors and chemoreceptors activated.
  2. information sent to medulla via CN9 and CN10.
  3. SNS tone increased; PSNS tone decreased.
  4. norepi causes increased HR (β1 receptors) and vascular resistance (α1 receptors).
  5. hypothalamus releases arginine vasopressin (AVP; vasoconstriction).
  6. kidneys release angiotensin II (vasoconstrictor).
  7. Angiotensin II causes aldosterone release from adrenal cortex (vasoconstrictor).
20
Q

What stimulates the secretion of the steroid hormone aldosterone from the adrenal cortex?

A

angiotensin II produced by the kidneys

21
Q

<60 years of age, BP should be less than:

A

140/90

22
Q

Steps in body’s normal response to high blood pressure:

A
  1. high pressure baroreceptors activated.
  2. information sent to medulla via CN9 and CN10.
  3. PSNS tone increased; SNS tone decreased.
  4. ACh binds to CM2 receptors in heart tissue. HR slows.
  5. Vasodilation since SNS tone shut off.
  6. Pressure natriuresis (increase in urine output by kidneys)
23
Q

Effect of elevated MAP on kidneys:

A
  • pressure natriuresis
  • (increase in urine output by kidneys)
24
Q

Hypothesized cause of essential hypertension disease:

A
  • high pressure baroreceptor desensitization.
  • SNS tone maintained at higher blood pressures than normal.
25
Q

The two types of left ventricular hypertrophy (LVH) and their causes:

A
  1. concentric LVH
    • chronic systolic wall stress; pressure overload
  2. eccentric LVH
    • chronic diastolic wall stress; volume overload
26
Q

Concentric left ventricular hypertrophy leads to:

A
  • New sarcomeres grow in parallel.
  • Left ventricles forming thick walls and a relatively small chamber.
27
Q

Eccentric left ventricular hypertrophy leads to:

A
  • new sarcomeres grow in series.
  • left ventricle walls become thin and dilate.
28
Q

How is left ventricular hypertrophy beneficial early on?

A
  • Normalizes wall stresses and tensions in the left ventricle.
  • Hypertrophies in order to maintain the same cardiac output against greater stress.
29
Q

Physiologic left ventricular hypertrophy occurs in response to:

A
  • EPISODIC pressure or volume overload (i.e. it only occurs when working out).
30
Q

Pathologic left ventricular hypertrophy occurs in response to:

A

CHRONIC pressure or volume overload.

31
Q

Steps in the development of pathologic LVH:

A
  1. Chronic pressure (systole) or chronic volume overload (diastole) leads
  2. to sarcomere proliferation to compensate for increased stress.
  3. Increased apoptosis, interstitial fibrosis, and endothelial cell dysfunction occurs.
  4. RAAS (aldosterone and angiotensin II) cause changes in gene expression, rendering unfavorable remodeling irreversible.
32
Q

Isotonic exercise (e.g., running) may result in what type of left ventricualr hypertrophy?

A
  • eccentric LVH.
  • correlated with increased venous return, causing a condition of intracardial volume overload during diastole.
33
Q

Isometric exercise (e.g., strength training) may result in what type of left ventricualr hypertrophy?

A
  • concentric LVH.
  • causes cardiac pressure overload.
34
Q

What is hypothesized to lead to heart failure in patients with pathologic LVH?

A
  • sarcomere growth associated with fibrosis, endothelial cell dysfunction, and apoptosis.
  • RAAS pathway (aldosterone and angiotensin II) cause changes in gene expression, which renders unfavorable remodeling irreversible.
35
Q

Primary differences between pathologic and physiologic left ventricular hypertrophy:

A
  • physiologic LVH is:
    • caused by episodic, not chronic, stress.
    • not associated with RAAS (therefore reversible).
    • not associated with fibrosis, apoptosis, or endothelial cell dysfunction.

CP1.06_Cardio_ZACHOW (10 decks)

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