Lecture 5 Flashcards
What does this EKG show?
- tachycardia
- inverted T waves (ischemia)
- pronounced Q waves (irreversible death)
- ST elevations (injury)
What is infarction?
- When myocardium undergoes a necrotic process due to ischmemia (lack of oxygen).
Baroreceptors in the body and their locations:
- High-pressure: carotid sinus and wall of aortic arch
- Low-pressure: atria and pulmonary arteries
- Renal: perfusion pressure: afferent arterioles
Chemoreceptors in the body and their locations:
- Peripheral: carotid and aortic bodies
- Central: medulla
What do chemoreceptors detect/measure?
partial pressure of CO2 (PCO2).
All information from chemoreceptors and baroreceptors in the body travel on what afferents to the medulla?
CN 9 and CN 10
Functions and origins of angiotensin II and aldosterone:
- Kidneys: angiotensin II.
- Adrenal cortex: aldosterone.
-
Both are vasoconstrictors and help conserve sodium.
- Sodium conservation increases intravascular volume by holding water.
Both angiotensin II and aldosterone increase:
- total peripheral resistance (vasoconstriction)
- intravascular volume (sodium conservation/water retention)
Neurotransmitters/hormones controlling inotropy and chronotropy and their origins:
- Norepinephrine (SNS)
- epinephrine (adrenal medulla)
- ACh (PSNS)
Neurotransmitters/hormones controlling vascular smooth muscle tone (vasoconstriction) and their origins:
- arginine vasopressin (AVP); hypothalamus
- angiotensin II (AII); kidneys
- aldosterone; adrenal cortex
- norepinephrine; SNS
- epinephrine; andrenal medulla
Neurotransmitters/hormones controlling intravascular volume and their origins:
- arginine vasopressin (AVP); hypothalamus
- angiotensin II (AII); kidneys
- aldosterone; adrenal cortex
Ultimately, feedback from baroreceptors and chemoreceptors lead to changes in:
- heart rate
- left ventricular contractile force
- vasomotion (vasodilation and vasoconstriction)
- blood plasma volume
The osmoregulatory center of the brain (detects plasma sodium) is located where?
- hypothalamus
- regulates urine output and intravascular volume.
Systolic BP is due to/mostly dependent on:
- cardiac output.
- CO = SV x BPM
Diastolic BP is due to/mostly dependent on:
vascular resistance.
Blood pressure (MAP) equation:
BP/MAP = CO x TPR
Total peripheral resistance (i.e. blood pressure) is determined by:
- vascular smooth muscle function and intravascular volume:
- SNS (vasoconstrict)
- AVP (vasoconstrict and water retention)
- angiotensin II (vasoconstrict and water retention)
- aldosterone (vasoconstrict and water retention)
>60 years of age, BP should be less than:
150/90
Steps in body raising blood pressure in response to low blood pressure:
- low pressure baroreceptors and chemoreceptors activated.
- information sent to medulla via CN9 and CN10.
- SNS tone increased; PSNS tone decreased.
- norepi causes increased HR (β1 receptors) and vascular resistance (α1 receptors).
- hypothalamus releases arginine vasopressin (AVP; vasoconstriction).
- kidneys release angiotensin II (vasoconstrictor).
- Angiotensin II causes aldosterone release from adrenal cortex (vasoconstrictor).
What stimulates the secretion of the steroid hormone aldosterone from the adrenal cortex?
angiotensin II produced by the kidneys
<60 years of age, BP should be less than:
140/90
Steps in body’s normal response to high blood pressure:
- high pressure baroreceptors activated.
- information sent to medulla via CN9 and CN10.
- PSNS tone increased; SNS tone decreased.
- ACh binds to CM2 receptors in heart tissue. HR slows.
- Vasodilation since SNS tone shut off.
- Pressure natriuresis (increase in urine output by kidneys)
Effect of elevated MAP on kidneys:
- pressure natriuresis
- (increase in urine output by kidneys)
Hypothesized cause of essential hypertension disease:
- high pressure baroreceptor desensitization.
- SNS tone maintained at higher blood pressures than normal.
The two types of left ventricular hypertrophy (LVH) and their causes:
-
concentric LVH
- chronic systolic wall stress; pressure overload
-
eccentric LVH
- chronic diastolic wall stress; volume overload
Concentric left ventricular hypertrophy leads to:
- New sarcomeres grow in parallel.
- Left ventricles forming thick walls and a relatively small chamber.
Eccentric left ventricular hypertrophy leads to:
- new sarcomeres grow in series.
- left ventricle walls become thin and dilate.
How is left ventricular hypertrophy beneficial early on?
- Normalizes wall stresses and tensions in the left ventricle.
- Hypertrophies in order to maintain the same cardiac output against greater stress.
Physiologic left ventricular hypertrophy occurs in response to:
- EPISODIC pressure or volume overload (i.e. it only occurs when working out).
Pathologic left ventricular hypertrophy occurs in response to:
CHRONIC pressure or volume overload.
Steps in the development of pathologic LVH:
- Chronic pressure (systole) or chronic volume overload (diastole) leads
- to sarcomere proliferation to compensate for increased stress.
- Increased apoptosis, interstitial fibrosis, and endothelial cell dysfunction occurs.
- RAAS (aldosterone and angiotensin II) cause changes in gene expression, rendering unfavorable remodeling irreversible.
Isotonic exercise (e.g., running) may result in what type of left ventricualr hypertrophy?
- eccentric LVH.
- correlated with increased venous return, causing a condition of intracardial volume overload during diastole.
Isometric exercise (e.g., strength training) may result in what type of left ventricualr hypertrophy?
- concentric LVH.
- causes cardiac pressure overload.
What is hypothesized to lead to heart failure in patients with pathologic LVH?
- 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.
Primary differences between pathologic and physiologic left ventricular hypertrophy:
- physiologic LVH is:
- caused by episodic, not chronic, stress.
- not associated with RAAS (therefore reversible).
- not associated with fibrosis, apoptosis, or endothelial cell dysfunction.
