Autonomic control of cardiovascular function Flashcards
(Cardiovascular regulation) What is the sympathetic NS responsible for?
Kicks in when there’s too little perfusion
What is the parasympathetic NS responsible for?
Kicks in when there’s too much perfusion
What are 3 mechanisms of regulating tissue perfusion?
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)
Baroreceptors are ___ located in the walls of ___ and ___
There are 2 categories of baroreceptors. What are they and where are they located?
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
Describe the Bezold-Jarisch reflex
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**
What is the function of mechanoreceptors in cardiovascular regulation?
Mechanoreceptors decrease sympathetic tone/increase vagal tone in response to increased blood pressure (in the left ventricle)
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)?
***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)
Since phenylephrine is an alpha agonist, how does it lower heartrate?
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**
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?
**see below**
**increased HR, contractility etc**
**inhibits vagal PS stimulation**
What is the effect of parasympathetic stimulation on cardiac function?
What are the effects of atropine on cardiac function?
Parasympathetic innervation counters the effects of sympathetic stimulation (decrease HR, contractility)
Atropine – parasympatholytic – blocks parasympathetic stimulation >> excessive sympathetic stimulation
What are the effects of sympathetic innervation to the vasculature?
What are the effects of sympathetic stimulation of arteries in skeletal muscle?
**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)
What are the physiologic effects of baroreceptor discharge (5)?
Arterial vasodilation
Venodilation
Decreased blood pressure, heart rate and cardiac output
How does shock develop?
Shock: inadequeate tissue perfusion >> tissue hypoxia >> hypotension >> multi-organ failure
*don’t know what happens first tho**
The ANS response to shock is ___
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
What is the role of the sympathetic nervous system in exercise?
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
Describe the valsalva maneuver
What are the effects of the valsalva on ANS feedback loops?
What is neurocardiogenic syncope?
It’s basically when you have an increase in parasympathetic stimulation that results in fainting
There are 3 types of presentations of neurocardiogenic syncope, namely ___, vasodepressor and ___
There are 3 types of presentations of neurocardiogenic syncope, namely cardioinhibitory, vasodepressor and mixed response
Describe cardioinhibitory presentation of syncope. What heart condition (tachycardia/bradycardia) is this most often ass’d with?
Increased parasympathetic tone; ass’d with bradycardia
Describe the vasodepressor presentation of neurocardiogenic syncope
Decreased sympathetic tone >> hypotension
Describe the mixed response presentation of neurocardiogenic syncope
Both decreased heart rate and blood pressure
How does neurocardiogenic syncope occur? (i.e. describe the pathogenesis)
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]
Name 3 other triggers of vagal efferents
Pain
Visual and temporal lobe stimuli
Noxious stimuli
Which exogenous catecholamine can exacerbate/elicit neurocoardiogenic syncope?
Isoproterenol (used to induce this response during tilt table test)
Fill in the blanks with the definitions of hypertension below
**see below**
At what systolic and diastolic blood pressures is a pt considered to be in a hypertensive crisis?
SBP > 180mmHg, DBP > 120mmHg
There are multiple components of hypertensive crisis, including retinal hemorrhages or papilledema w/ visual loss, ___, ___ and angina
Components of hypertensive crisis (or things that suggest hypertensive crisis):
Retinal hemorrhages, papilledema with visual loss
Renal failure
LV failure and angina
If a patient has a coarctation of the aorta, what will the BP readings look like in the upper vs lower extremities?
If a pt has an aortic coarction, they will have high blood pressure in the upper extremities but low BP in the lower extremities
Fill in the blanks
**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)
Describe the observations in the graph below. What is the relationship between age and blood pressure?
Systolic blood pressure increases with age, but diastolic blood pressure drops around age 50-55, then rises again
Explain what’s happening in the graph below
What is nocturnal hypertension?
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
Name 5 predictors of mortality
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)
Describe the graph below. How do the contributions of cardiac output and peripheral resistance to hypertension change with increasing age?
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**
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?
Chronic BP regulators: heart, blood vessels (tone), kidneys
Acute BP regulators: reflexes (baroreceptor and chemoreceptor reflexes)
The two types of hypertension are __ and __
The two types of hypertension are primary and secondary hypertension
What is the difference between primary hypertension and secondary hypertension?
Primary hypertension is hypertension with no identifiable cause, whereas secondary hypertension which occurs secondary to some preexisting condition/identifiable cause
What factors can contribute to primary hypertension? (**see below**)
Abnormal vasoconstriction + high venous return
Too much renin release
Impaired salt/water handling
Inappropriately high cardiac output
Too much sympathetic outflow
Renal disease is critically related to secondary hypertension. The most common form of 2nday hypertension is ___
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
How does kidney damage contribute to secondary hypertension? (hint: its a vicious cycle)
Damaged kidneys >> fewer functional nephrons available >> more work on the fewer nephrons >> development of intraglomerular hypertension >> more kidney damage >> systemic HTN etc etc
Besides instrinsic kidney disease, renovascular disease can also cause secondary HTN. Explain what this is
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**
Review the renin-angiotensin-aldosterone system
How do you treat (i.e. medically manage) pts with renovascular disease?
Pts are treated the same way as folks with coronary artery disease: aspirin, antihypertensive therapy, improved glycemic control
Draw and describe how primary aldosteronism develops/the downstream effects on blood pressure
**see below**
In a pt with hypertension, increased serum and urine levels of of which ion will clue you into primary hyperaldosteronism?
Very high potassium in the urine and serum in cases of primary hyperaldosteronism compared to primary hypertension
What are two ways to manage adrenal hypertension due to adenoma?
How do you manage hypertension due bilateral adrenal hyperplasia?
For treating adenoma >> surgical excision or lower aldosterone release using spironolactone or eplerenone
For bilateral adrenal hyperplasia: manage with the above drugs
3 other causes of monogenetic hypertension include gain of function mutations, ___ and ___
3 other causes of monogenetic hypertension include gain of function mutations, hormone deficiencies and excessive aldosterone synthesis
Describe Liddle’s syndrome and Gordon’s syndrome and how they contribute to HTN
Liddle’s Syndrome – increased ENaC activity
Gordon’s Syndrome – increased NaCl transporter
Name 2 adrenal hormone deficiency types that can lead to HTN
Congenital adrenal hyperplasia
Apparent mineralocorticoid excess
Describe the scenario below
So the levels of hormone are normal but there’s increased activity on the mineralocorticoid receptor because the hormone precursors aren’t broken down
Describe glucocorticoid remediable hypertension
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**
What is the mechanism through which glucocorticoid remediable HTN occurs?
How do you treat this condition?
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
Outline the process for screening for 2ndary HTN involving the RAAS
What is pheochromocytoma?
Pheochromocytoma: neuroendocrine tumor of the medulla of the adrenal glands (originates in chromaffin cells)
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?
Pheochromocytoma
Rx for pheo:
- Blood Pressure: Alpha blockers
- Tachyarrhythmia: Beta Blockers (after alpha blockers)
- Catecholamine release: Alpha methyl p-tyrosine
Another cause of 2ndary HTN is ___ (you Rx it w/ a CPAP)
Obstructive sleep apnea
What are examples of organ damage that can occur due to HTN?
What is the natural history of HTN?
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
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?
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
For the following conditions/patient groups, which drugs would you use?
Heart failure
Post-MI pts
High risk coronary artery disease
Proteinuria
**see below**
Basically ACE inhibitors feature for every disease
The only time you won’t use BBs is with proteinuria
