Lecture 5

Question 1

What does this EKG show?

Answer 1

• tachycardia
• inverted T waves (ischemia)
• pronounced Q waves (irreversible death)
• ST elevations (injury)

Question 2

What is infarction?

Answer 2

• When myocardium undergoes a necrotic process due to ischmemia (lack of oxygen).

Question 3

Baroreceptors in the body and their locations:

Answer 3

1. High-pressure: carotid sinus and wall of aortic arch
2. Low-pressure: atria and pulmonary arteries
3. Renal: perfusion pressure: afferent arterioles

Question 4

Chemoreceptors in the body and their locations:

Answer 4

1. Peripheral: carotid and aortic bodies
2. Central: medulla

Question 5

What do chemoreceptors detect/measure?

Answer 5

partial pressure of CO2 (PCO2).

Question 6

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

Answer 6

CN 9 and CN 10

Question 7

Functions and origins of angiotensin II and aldosterone:

Answer 7

• Kidneys: angiotensin II.
• Adrenal cortex: aldosterone.
• Both are vasoconstrictors and help conserve sodium.
  
  • Sodium conservation increases intravascular volume by holding water.

Question 8

Both angiotensin II and aldosterone increase:

Answer 8

1. total peripheral resistance (vasoconstriction)
2. intravascular volume (sodium conservation/water retention)

Question 9

Neurotransmitters/hormones controlling inotropy and chronotropy and their origins:

Answer 9

1. Norepinephrine (SNS)
2. epinephrine (adrenal medulla)
3. ACh (PSNS)

Question 10

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

Answer 10

1. arginine vasopressin (AVP); hypothalamus
2. angiotensin II (AII); kidneys
3. aldosterone; adrenal cortex
4. norepinephrine; SNS
5. epinephrine; andrenal medulla

Question 11

Neurotransmitters/hormones controlling intravascular volume and their origins:

Answer 11

1. arginine vasopressin (AVP); hypothalamus
2. angiotensin II (AII); kidneys
3. aldosterone; adrenal cortex

Question 12

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

Answer 12

1. heart rate
2. left ventricular contractile force
3. vasomotion (vasodilation and vasoconstriction)
4. blood plasma volume

Question 13

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

Answer 13

• hypothalamus
• regulates urine output and intravascular volume.

Question 14

Systolic BP is due to/mostly dependent on:

Answer 14

• cardiac output.
  
  • CO = SV x BPM

Question 15

Diastolic BP is due to/mostly dependent on:

Answer 15

vascular resistance.

Question 16

Blood pressure (MAP) equation:

Answer 16

BP/MAP = CO x TPR

Question 17

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

Answer 17

• 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)

Question 18

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

Answer 18

150/90

Question 19

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

Answer 19

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).

Question 20

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

Answer 20

angiotensin II produced by the kidneys

Question 21

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

Answer 21

140/90

Question 22

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

Answer 22

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)

Question 23

Effect of elevated MAP on kidneys:

Answer 23

• pressure natriuresis
• (increase in urine output by kidneys)

Question 24

Hypothesized cause of essential hypertension disease:

Answer 24

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

Question 25

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

Answer 25

1. **concentric LVH** * chronic systolic wall stress; pressure overload 2. **eccentric LVH** * chronic diastolic wall stress; volume overload

Question 26

Concentric left ventricular hypertrophy leads to:

Answer 26

* New sarcomeres grow in parallel. * Left ventricles forming thick walls and a relatively small chamber.

Question 27

Eccentric left ventricular hypertrophy leads to:

Answer 27

* new sarcomeres grow in series. * left ventricle walls become thin and dilate.

Question 28

How is left ventricular hypertrophy beneficial early on?

Answer 28

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

Question 29

Physiologic left ventricular hypertrophy occurs in response to:

Answer 29

* EPISODIC pressure or volume overload (i.e. it only occurs when working out).

Question 30

Pathologic left ventricular hypertrophy occurs in response to:

Answer 30

CHRONIC pressure or volume overload.

Question 31

Steps in the development of pathologic LVH:

Answer 31

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.

Question 32

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

Answer 32

* eccentric LVH. * correlated with increased venous return, causing a condition of intracardial volume overload during diastole.

Question 33

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

Answer 33

* concentric LVH. * causes cardiac pressure overload.

Question 34

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

Answer 34

* 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.

Question 35

Primary differences between pathologic and physiologic left ventricular hypertrophy:

Answer 35

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