CV Physiology 7-9 Flashcards
where are high and low pressure baroreceptors located in the heart, respectively?
high pressure baroreceptors - aortic arch, carotid sinus
low pressure baroreceptors - right atrium/vena cava and left atrium/pulmonary vein regions
where are chemoreceptors located within the heart? what do they sense?
chemoreceptors and high pressure baroreceptors are both found in aortic body and carotid sinus
chemoreceptors are very sensitive to changes in PCO2 (and decreased blood pH), less sensitive to PO2
when PCO2 rises, chemoreceptors are activated to augment SNS cardiovascular activity (to remove deoxygenated blood quicker)
how do baroreceptors respond to chronic elevation in BP?
baroreceptors are designed to correct only acute changes in BP
when BP is chronically elevated (such as unmanaged HTN), baroreceptors become desensitized and reset to a new set point
high pressure baroreceptors activate fibers within afferent ____ and ____ tracts
high pressure baroreceptors activate fibers within afferent VAGAL and GLOSSOPHARYNGEAL tracts
these tracts terminate in medulla and coordinated actions dampen SNS activity to heart and vascular smooth muscle, while increasing PSNS activity in heart (via R/L efferent vagal tracts)
[though recall there is no PSNS activity innervating vasculature smooth muscle! mechanism is simply turning down SNS activity]
differentiate the action of angiotensin II (AII) when it binds its receptors AT1 vs AT2
AT1: predominant AII receptor, mediates vasoconstriction (vascular smooth muscle)
AT2: counter-modulatory function to AT1
name 4 ways by which angiotensin II increase TPR (total peripheral resistance), and therefore BP
- vasoconstriction of vascular smooth muscle (potent)
- block high pressure baroreceptors signaling
- simulates aldosterone secretion from adrenal cortex (—> Na+ reabsorption/subsequent H2O retention + direct vasoconstriction)
- stimulate release of norepinephrine from post-ganglionic SNS fibers (—> vasoconstriction)
name 5 types of drugs that can be used to treat hypertension
- ACE inhibitors: dampen angiotensin II (AII) activity
- AT1 antagonists (predominant receptor for AII)
- beta-blockers: antagonists of beta1 adrenergic receptors in heart
- Ca2+ channel blockers: impair influx of Ca2+ in vascular smooth muscle and/or cardiac muscle
- diuretics: lower blood volume by blocking effects of aldosterone (cause increase in urine)
what is the cause of concentric vs eccentric left ventricle hypertrophy (LVH)
concentric LVH: increase in systolic wall stress (HTN, aortic stenosis, pressure overload) - new sarcomeres form in parallel —> thick walls, small cavity
eccentric LVH: increase in diastolic wall stress (aortic insufficiency, volume overload) - new sarcomeres form in series —> thin walls, dilated LV
explain how epinephrine/norepinephrine affect capillary pressure to raise BP
epi/norepi cause increase in arteriolar TPR (total peripheral resistance) —> this causes greater drop in pressure in capillaries
reduced capillary pressure establishes gradient that favors H2O reabsorption from ECF —> this increases venous return —> increased CO —> increased BP
put CO, TPR, and MAP in an equation together and explain why it makes sense
CO = MAP/TPR
where MAP = mean arterial pressure
and TPR = total peripheral resistance
basically, the arterial pressure that can be created by cardiac output will be smaller if there is a lot of peripheral resistance the heart is working against
remember that TPR is the difference between arterial and venous pressures
what are the 2 general mechanisms that underly the pathophysiology of cardiac ischemia?
- fixed vessel narrowing (e.g. atherosclerosis)
- abnormal vascular tone
what causes chronic stable angina pectoris?
angina = severe and constricting pain
chronic stable angina: results from fixed narrowing of 1+ coronary vessels, usually due to atheromatous plaque formation - O2 supply cannot meet cardiac demand
symptoms can be alleviated with vasodilator, beta blocker
what is the effect of chronically elevated epinephrine levels on beta2 adrenergic receptors?
chronically elevated epi concentrations activate beta2 receptors, which are coupled to release of norepi
effect is that in extreme SNS activity (or pathology of adrenal medulla), both epi and norepi stimulate vasoconstriction to markedly increase TPR (total peripheral resistance)
what is the driving factor of colloid osmotic pressure (aka oncotic pressure)?
colloid osmotic/oncotic pressure is driven by concentration of charged serum proteins (mostly albumin)
high oncotic pressure pulls fluid into capillaries (to dilute concentration of proteins) - esp. at venous end of capillary bed
where does filtration vs absorption (reabsorption) occur in capillary bed
filtration at arterial end - fluid leaves capillaries driven by hydraulic pressure
reabsorption at venous end - fluid sucked into capillaries driven by oncotic pressure (albumin)
*note lymphatics reabsorb excess fluid from interstitium to prevent edema (able to do so because it has a discontinuous basement membrane)
