Regulation of Arterial Pressure Flashcards Preview

Cardiovascular > Regulation of Arterial Pressure > Flashcards

Flashcards in Regulation of Arterial Pressure Deck (24)
Loading flashcards...

short term regulation of AP

correction achieved in at least 1-2 hours, usually within a few minutes

affects AP through changes in TPR and CO


long-term regulation of AP

corrections take place over horus to days

affects AP through blood volume and CO 


arterial baroreflex

innervation of carotid sinus and aortic arch

efferent pulses through vagus and sympathetic nerve fibers

glossopharyngeal (IX) and vagus (X) nerves for carrying impoulses to the brain stem, where they synapse to the medulla


stimulus for arterial baroreflex

radio distntion by the difference between intravascular pressure and extramural pressure

threshold pressure is about 60 mmHg and the maximum discharge rate occurs at about 200 mmHg


What happens to blood pressure if the baroreceptors are lost to the system (denervated)?

the mean pressure does not change appreciably

the distribution of pressure is larger for a 24 hour period in the denervated group


brainbridge reflex

lower rates lead to increased right atrial filling

causes an increase in heart rate

only seen at very low sinus rates due to direct contention with baroreceptor reflex


atrial stretch receptors

stretch receptors in atrial walls, afferent fibers in sympathetic nerves and vagus nerve

sensitive to filling and atrial contraction

cardiac preload and blood volume are affected

activation produces effects similar to arterial baroreceptor stimulation with involvement of altered renal excretion of water and sodium


ventricular baroreceptors and chemoreceptors

stretch receptor on anterior wall of LV

pressor reflex when stretched (increased HR and TPR)

stretch receptor on posterior wall of LV - depressor reflex when stretched (decreased HR and TPR)


Bezold-Jarisch Reflex

stretch and chemoreceptors

receptors in the atria, great veins, and LV

activation or stimulation in case of ischemia may result in activation of vagal afferents and efferents

leads to hypotension, nausea,vomiting, and decreased CO


effects of high CO2 or low O2 levels on the brain stem CV centers

decreased venous capacitance, increased TPR, coronary dilation, increased heart rate


pulmonary mechanoreceptors

stimulation of the lung mechanoreceptors by increased rate and depth of breathing results in a net decrease in cardiac vagal efferent discharges (withdrawal)


central chemoreceptor reflex

receptors on the ventral surface of the brainstem

stimuli iinclude hypercapnia, fall in pH, cerebral hypoxia, fall in cerebral perfusion pressure

response is a pressor reflex


fight or flight response

heart rate and contractility increases

cardiac output increases

circulating epinephrine dilates blood flow to skeletal muscles

increased sympathetic activity decreases kidney and splanchnic flow

splanchnic cpacitance vessels are constricted


neurocardiogenic response (vasovagal syncope)

sudden slowing of the heart due ot increased vagal activity and a skeletal muscle vasodilation because of decreased sympathetic output and increased cholinergic output

causes an abrupt fall in blood pressure


diving reflex

intense slowing of the heart due to the parasympathetic nervous system and peripheral vasoconstriction when the face is submerged in cold water


somatic afferent cardiovascular reflexes

mechanoreceptors in skeletal muscle tendons help icnrease sympathetic drive during exercise


visceral afferent reflexes

activation of abdominal visceral afferents induces a reflex response

remain intact after cervical cord transection

ex. gall bladder and urinary bladder distension raises TPR by sympathoexcitation and increased AMP


Cushing response

increase in intracranial pressure

threshold: intracranial and intra-arterial rpessure difference of 30-50 mmHg


CNS reflex response

generalized increase in sympathetic vasoconstriction to return cerebral blood flow back to normal


complications of severe hemorrhage

arterial pressres drop to below 60 mmHg

cerebral ischemia leads to vasoconstriction and tachycardia

fall in blood flow through carotid and aortic bodies leads to vasoconstriction and bradycardia

loss of more than 30% blood volume for more than 1 hours leads to irreversible hypotension and death


rapid resposne to hemorrhage

activation of sympathetics

increase heart rate and contractility

increase constriction of resistance and capacitance vessels

augmented venous tone increases venous return to heart


slow resposne to hemorrhage

re-establish plasma volume through renal vasoconstriction, reduced urine formation

renin and angitensin II leadss to aldosterone release and vasopressin release

reduced salt water loss from renal tubules

thirst develops to get more water input


cardiovascular shock

condition characterized by multiple organ failure secondary to inadequate tissue perfusion

extreme hypotension and reduced coronary flow leads to reduced AP and tissue hypoxia and eventually ischemia


response to weightlessness