Autonomic control of cardiovascular function

Question 1

(Cardiovascular regulation) What is the sympathetic NS responsible for?

Answer 1

Kicks in when there’s too little perfusion

Question 2

What is the parasympathetic NS responsible for?

Answer 2

Kicks in when there’s too much perfusion

Question 3

What are 3 mechanisms of regulating tissue perfusion?

Answer 3

Change cardiac output (CO = SV - stroke volume x HR)

Change blood vessel tone (arteriolar resistance) - vasoconstriction = increased pressure

Change preload (venous return to the heart)

Question 4

Baroreceptors are ___ located in the walls of ___ and ___

There are 2 categories of baroreceptors. What are they and where are they located?

Answer 4

Baroreceptors are stretch receptors located in the walls of heart and blood vessels

Baroreceptor types: high and low pressure receptors:

High pressure: carotid sinus, aortic arch

Low pressure: right and left atria

Question 5

Describe the Bezold-Jarisch reflex

Answer 5

Stimulation of cardiac receptors (spec ventricular vagal C fibers) leads to triad of bradycardia, hypotension and apnea (aka Bezold-Jarisch reflex)

**note that this is mediated by chemo receptors throughout the heart: atria, ventricles great veins, pulmonary art, juxtacapillary region of alveoli**

Question 6

What is the function of mechanoreceptors in cardiovascular regulation?

Answer 6

Mechanoreceptors decrease sympathetic tone/increase vagal tone in response to increased blood pressure (in the left ventricle)

Question 7

Arterial baroreceptors are more sensitive to changes in blood pressure aka pulse pressure. What are the effects of an increase in pulse pressure (3 things)?

Answer 7

***Remember that your pulse pressure is the difference between your systolic and diastolic BP***

Arterial baroreceptors are more sensitive to changes in blood pressure (so changes in systolic and diastolic pressure)

Increased pulse pressure (or pressure difference) >>increased baroreceptor firing >>inhibition of sympathetic tone, activation of vagal tone in the heart (the point is to lower the pressure back to normal)

Question 8

Since phenylephrine is an alpha agonist, how does it lower heartrate?

Answer 8

Phenylephrine lowering heartrate by affecting baroreceptor firing (RR interval depicts heartrate. The shorter RR interval = faster heartrate, wider RR interval = slower heartrate)

**indirect effect of phenylephrine - normally phenylephrine increased vasoconstriction of peripheral vasculature but here it lowers heartrate by decreasing sympathetic tone**

Question 9

Define the following:

Chronotropy

Dromotropy

Inotropy

Lusotropy

What is the effect of sympathetic stimulation on each of the above?

What is the effect of sympathetic stimulation on vagal parasympathetic stimualtion?

Answer 9

**see below**

**increased HR, contractility etc**

**inhibits vagal PS stimulation**

Question 10

What is the effect of parasympathetic stimulation on cardiac function?

What are the effects of atropine on cardiac function?

Answer 10

Parasympathetic innervation counters the effects of sympathetic stimulation (decrease HR, contractility)

Atropine – parasympatholytic – blocks parasympathetic stimulation >> excessive sympathetic stimulation

Question 11

What are the effects of sympathetic innervation to the vasculature?

What are the effects of sympathetic stimulation of arteries in skeletal muscle?

Answer 11

**see below**

Sympathetic innervation to vasculature: vasoconstriction (more in arterioles, a little in veins - mostly splanchnic veins)

Effects on skeletal muscle arteries is actually vasodilation (makes sense b/c you need increased perfusion>>O2 to those working muscles)

Question 12

What are the physiologic effects of baroreceptor discharge (5)?

Answer 12

Arterial vasodilation

Venodilation

Decreased blood pressure, heart rate and cardiac output

Question 13

How does shock develop?

Answer 13

Shock: inadequeate tissue perfusion >> tissue hypoxia >> hypotension >> multi-organ failure

*don’t know what happens first tho**

Question 14

The ANS response to shock is ___

Answer 14

The ANS response to shock is a pressor response resulting in increased mean arterial pressure

Blood will move from venous reserve into the arterial system to increase preload in the heart

Increase vascular resistance/tone in arterioles/peripheral resistance vessels

Question 15

What is the role of the sympathetic nervous system in exercise?

Answer 15

The main goal of the sympathetic NS in exercise is to increase perfusion to the muscles

**

increased heart rate, contractility

increased venous tone >> increased blood from venous system to arterial system >> increased preload

Question 16

Describe the valsalva maneuver

What are the effects of the valsalva on ANS feedback loops?

Answer 16

Question 17

What is neurocardiogenic syncope?

Answer 17

It’s basically when you have an increase in parasympathetic stimulation that results in fainting

Question 18

There are 3 types of presentations of neurocardiogenic syncope, namely ___, vasodepressor and ___

Answer 18

There are 3 types of presentations of neurocardiogenic syncope, namely cardioinhibitory, vasodepressor and mixed response

Question 19

Describe cardioinhibitory presentation of syncope. What heart condition (tachycardia/bradycardia) is this most often ass’d with?

Answer 19

Increased parasympathetic tone; ass’d with bradycardia

Question 20

Describe the vasodepressor presentation of neurocardiogenic syncope

Answer 20

Decreased sympathetic tone >> hypotension

Question 21

Describe the mixed response presentation of neurocardiogenic syncope

Answer 21

Both decreased heart rate and blood pressure

Question 22

How does neurocardiogenic syncope occur? (i.e. describe the pathogenesis)

Answer 22

Inappropriately high (exaggerated) vagal afferent activity coming to the medullary center (nucleus tractus solitarius) results in:

Sympathetic withdrawal – [vasodepressor] and/or

Increased parasympathetic tone- [cardioinhibitory]

Question 23

Name 3 other triggers of vagal efferents

Answer 23

Pain

Visual and temporal lobe stimuli

Noxious stimuli

Question 24

Which exogenous catecholamine can exacerbate/elicit neurocoardiogenic syncope?

Answer 24

Isoproterenol (used to induce this response during tilt table test)

Question 25

Fill in the blanks with the definitions of hypertension below

Answer 25

\*\*see below\*\*

Question 26

At what systolic and diastolic blood pressures is a pt considered to be in a hypertensive crisis?

Answer 26

SBP \> 180mmHg, DBP \> 120mmHg

Question 27

There are multiple components of hypertensive crisis, including retinal hemorrhages or papilledema w/ visual loss, \_\_\_, ___ and angina

Answer 27

Components of hypertensive crisis (or things that suggest hypertensive crisis): Retinal hemorrhages, papilledema with visual loss Renal failure LV failure and angina

Question 28

If a patient has a coarctation of the aorta, what will the BP readings look like in the upper vs lower extremities?

Answer 28

If a pt has an aortic coarction, they will have high blood pressure in the upper extremities but low BP in the lower extremities

Question 29

Fill in the blanks

Answer 29

\*\*see below\*\* Basically normotensve is normal BP, measured and in real life Sustain HTN is hypertension in both the doc's office and in real life Masked HTN is the pt is NOT hypertensive at the doc's office but is hypertensive in real life White Coat hypertension is when the pt only is hypertensive coz they're nervous to be in the doc's office (or something)

Question 30

Describe the observations in the graph below. What is the relationship between age and blood pressure?

Answer 30

Systolic blood pressure increases with age, but diastolic blood pressure drops around age 50-55, then rises again

Question 31

Explain what's happening in the graph below What is nocturnal hypertension?

Answer 31

Nocturnal drop in blood pressure: 10mmHg drop in BP when we’re sleeping is normal. People with stiffened vessels due to age or vascular disease or something lose this drop in BP \>\> correlates with bad prognosis

Question 32

Name 5 predictors of mortality

Answer 32

Widened pulse pressure Loss of nocturnal drop in blood pressure when sleeping Masked hypertension Elevated systolic pressure Elevated diastolic pressure\*\* (this is not an independent predictor of mortality bt rather it makes you reach a widened pulse pressure sooner)

Question 33

Describe the graph below. How do the contributions of cardiac output and peripheral resistance to hypertension change with increasing age?

Answer 33

With increasing age, there’s a higher contribution of cardiac output to BP earlier in time but as you get older, that contribution decreases and peripheral resistance has a higher contribution \*\*Hyperkinetic phase of hypertension: vigorous cardiac output contributing to hypertension\*\*

Question 34

There are 2 groups of regulators of blood pressure, chronic and acute. What 3 organs/factors are chronic regulators of BP? What factor(s) is/are an acute regulator of BP?

Answer 34

Chronic BP regulators: heart, blood vessels (tone), kidneys Acute BP regulators: reflexes (baroreceptor and chemoreceptor reflexes)

Question 35

The two types of hypertension are __ and \_\_

Answer 35

The two types of hypertension are **primary** and **secondary hypertension**

Question 36

What is the difference between primary hypertension and secondary hypertension?

Answer 36

Primary hypertension is hypertension with **no identifiable cause**, whereas secondary hypertension which **occurs secondary to some preexisting condition/identifiable cause**

Question 37

What factors can contribute to primary hypertension? (\*\*see below\*\*)

Answer 37

Abnormal vasoconstriction + high venous return Too much renin release Impaired salt/water handling Inappropriately high cardiac output Too much sympathetic outflow

Question 38

Renal disease is critically related to secondary hypertension. The most common form of 2nday hypertension is \_\_\_

Answer 38

The most common form of secondary hypertension arises from people with intrinsic kidney disease (scarring in the kidney) - occurs due to loss of renal mass/functional nephrons

Question 39

How does kidney damage contribute to secondary hypertension? (hint: its a vicious cycle)

Answer 39

Damaged kidneys \>\> fewer functional nephrons available \>\> more work on the fewer nephrons \>\> development of intraglomerular hypertension \>\> more kidney damage \>\> systemic HTN etc etc

Question 40

Besides instrinsic kidney disease, renovascular disease can also cause secondary HTN. Explain what this is

Answer 40

Renovascular disease, unlike intrinsic kidney disease, involves damage to renal vasculature that leads to kidney disease in a previously healthy kidney \>\> hypertension \*\*renovascular disease is the least common of the two\*\*

Question 41

Review the renin-angiotensin-aldosterone system

Answer 41

Question 42

How do you treat (i.e. medically manage) pts with renovascular disease?

Answer 42

Pts are treated the same way as folks with coronary artery disease: aspirin, antihypertensive therapy, improved glycemic control

Question 43

Draw and describe how primary aldosteronism develops/the downstream effects on blood pressure

Answer 43

\*\*see below\*\*

Question 44

In a pt with hypertension, increased serum and urine levels of of which ion will clue you into primary hyperaldosteronism?

Answer 44

Very high potassium in the urine and serum in cases of primary hyperaldosteronism compared to primary hypertension

Question 45

What are two ways to manage adrenal hypertension due to adenoma? How do you manage hypertension due bilateral adrenal hyperplasia?

Answer 45

For treating adenoma \>\> surgical excision or lower aldosterone release using spironolactone or eplerenone For bilateral adrenal hyperplasia: manage with the above drugs

Question 46

3 other causes of monogenetic hypertension include gain of function mutations, ___ and \_\_\_

Answer 46

3 other causes of monogenetic hypertension include gain of function mutations, hormone deficiencies and excessive aldosterone synthesis

Question 47

Describe Liddle's syndrome and Gordon's syndrome and how they contribute to HTN

Answer 47

Liddle’s Syndrome – increased ENaC activity Gordon’s Syndrome – increased NaCl transporter

Question 48

Name 2 adrenal hormone deficiency types that can lead to HTN

Answer 48

Congenital adrenal hyperplasia Apparent mineralocorticoid excess

Question 49

Describe the scenario below

Answer 49

So the levels of hormone are normal but there’s increased activity on the mineralocorticoid receptor because the hormone precursors aren’t broken down

Question 50

Describe glucocorticoid remediable hypertension

Answer 50

Low renin HTN where aldosterone secretion mainly controlled by ACTH and not Ang II \*\***suppression of aldosterone** by exogenous glucocorticoids (dexamethasone) is the difference between this and the mineralocorticoid excess condition\*\*

Question 51

What is the mechanism through which glucocorticoid remediable HTN occurs? How do you treat this condition?

Answer 51

There's crossover between the 2 genes for cortisol release + aldosterone release such that any time ACTH acts on the new gene, there's aldosterone secretion \*\*see below\*\* Rx: treat with steroids to block the ACTH \>\> dexamethasone; alternative Rx is to block aldosterone release with spironolactone

Question 52

Outline the process for screening for 2ndary HTN involving the RAAS

Answer 52

Question 53

What is pheochromocytoma?

Answer 53

Pheochromocytoma: neuroendocrine tumor of the medulla of the adrenal glands (originates in chromaffin cells)

Question 54

A previously healthy 28 year old female comes to your office presenting with a headache, sweats and palpitations and a very high blood pressure (200/100). Symptoms developed rapidly (over 3 days) and the pt's blood panel showed elevated plasma metanephrines, catecholamianes and VMA. Pt now has to be intubated. What cancer is on your differential? How would you treat this?

Answer 54

Pheochromocytoma Rx for pheo: 1. Blood Pressure: Alpha blockers 2. Tachyarrhythmia: Beta Blockers (after alpha blockers) 3. Catecholamine release: Alpha methyl p-tyrosine

Question 55

Another cause of 2ndary HTN is ___ (you Rx it w/ a CPAP)

Answer 55

Obstructive sleep apnea

Question 56

What are examples of organ damage that can occur due to HTN?

Answer 56

Question 57

What is the natural history of HTN?

Answer 57

Most folks will die of heart attacks, some with a stroke/CNS change, more will develop renal disease and there's a 4x increase in dementia

Question 58

Of the drugs below, which drugs should you choose as 1st line therapy for uncomplicated HTN? Ace Inhibitors Angiotensin Receptor Blockers Beta blockers Calcium channel blockers Diuretics Which ones do Caucasians/African Americans respond to better?

Answer 58

All of them can be used as first line Clinical Caveat\* Caucasians generally respond better to ACE/ARB/BB African Americans have better response to CCB/diuretics

Question 59

For the following conditions/patient groups, which drugs would you use? Heart failure Post-MI pts High risk coronary artery disease Proteinuria

Answer 59

\*\*see below\*\* Basically ACE inhibitors feature for every disease The only time you won’t use BBs is with proteinuria