Physiology Lecture 5 -- Blood Pressure Control Systems Flashcards
Equation for pulse pressure
Pulse P = Systolic P - Diastolic P
Effect of stroke volume on pulse pressure
Increase SV = Increase Pulse P
Effect of arterial compliance on pulse pressure
Decrease arterial compliance = increase pulse pressure
3 equations for MAP
MAP = Diastolic P + 1/3 pulse pressure MAP = CO x TPR MAP = HR x SV x TPR
Normal MAP
100 mm Hg
LVP pressure curve: where is diastolic pressure located?
When the intraventricular pressure just exceeds the pressure in the aorta
Equation for perfusion pressure
Perfusion P = Arterial BP - Venous P
Equation for flow
Flow = Perfusion Pressure / TPR
The most important variable in the CV system and why
Systemic arterial blood pressure since this is the driving force that pushes blood through each of the organs
3 ways to regulate blood pressure
1) Adjust flow according to need (by R)
2) Keep flow constant despite Pa fluctuations (organs autoregulate)
3) Minimize fluctuations in Pa (neuro-hormonal control)
Normal perfusion pressure
90 mm Hg
Normal venous pressure
10 mm Hg
Define total peripheral resistance in words
The resistance experienced by the left ventricle
2 other ways to refer to TPR
Peripheral vascular resistance (PVR)
Systemic vascular resistance (SVR)
Equation of TPR
TPR = MAP/CO
NOTE: is actually [MAP - RAP]/CO, but RAP usually 0
How to change MAP
Changing any of the 3 variables:
Heart rate
Stroke volume
Total peripheral resistance
What variables of the MAP equations can be measured?
MAP and CO
TPR can only be calculate from the other two
Relationship between CO and VR
CO = VR (unless there is a leak at some point in the system)
Relationship between RAP and CVP
RAP is approximately equal to CVP
Normal CVP
5 - 10 mm Hg
What systems regulate blood pressure?
Negative feedback systems
Range of BP for the CNS ischemic response
Very strong reflex that is a last ditch effort to preserve cerebral circulation = only when Pa falls to a very low level (i.e. <60 mm Hg)
Range of BP for baroreceptors
Average daily pressures (bell curve 50 - 225 mm Hg)
Location of baroceptors
Carotid sinus
Arch of the aorta
What nerves carry the baroreceptor afferent information?
Glosspharyngeal nerve –> Vagus nerve
What part of the CNS does afferent information from baroceptors go to?
Brain stem
Relationship between action potentials from the baroreceptors and blood pressure
Increased BP = increased number of action potentials
Baroreceptor: receptor type
Mechanoreceptor (perceives stretching of carotid artery and aorta)
4 system responses to BP falling
Increased heart rate
Increased contraction
Increased arteriolar constriction
Increased venoconstriction
Effect of increasing contractility (that will lead to an increase in BP)
Increase SV
Effect of increasing arteriolar constriction (that will lead to an increase in BP)
Increase TPR
Effect of increasing venoconstriction (that will lead to an increase in BP)
Increased VP and MSFP
Starling’s Law –> Increased EDV = increased SV = increased BP
Controlled variable of the cardiovascular negative feedback control systems
MAP
Effect of removing baroreceptors
Increase of the lability of MAP (beat-to-beat variability)
Another name for the baroreceptor reflex and why
Buffer reflex because it keeps MAP in a narrow range
How can the carotid sinus or its nerves be injured?
During neck surgery or by radiation delivered to the neck (i.e. due to a tumor resection)
Name of condition involving labile MAP
Baroreflex failure
Medical device for treatment of drug-resistant hypertension
Carotid sinus stimulator
Explain how a carotid sinus stimulator works
Stimulates the baroreceptors in the carotid sinus by exciting action potentials to fool the cardiovascular centers in the brain into thinking that BP is higher than it actually is, thus inducing a baroreceptor response
What is essential hypertension?
Hypertension without a known cause (idiopathic)
Renin function
Convert angiotensinogen to angiotensin I
Angiotensin I function
Convert into angiotensin II in the lung
Angiotensin II functions
1) Constrict arterioles
2) Stimulate pituitary gland to release ADH
3) Stimulate adrenal glands to release aldosterone
Effect of ADH
Decrease water extraction from blood in the kidney = increase blood volume = increased VR = increased SV = increased MAP
Effect of Aldosterone
Water retention and decrease Na excretion
?Where is renin secreted from?
Juxtaglomerular cells of the kidneys
When is renin released?
When the pressure in the renal artery falls
Location of angiotensinogen production
Liver
How is angiotensin I converted to angiotensin II?
ACE (located in lungs)
4 types of hypertension drugs affecting the renin-angiotensin-aldosterone (RAA) system
Aldosterone receptor antagonists
ACE inhibitors
AT-II receptor blockers
Renin inhibitor
Effect of aldosterone receptor antagonists
Block aldosterone binding = decrease water and salt retention
Effect of ACE inhibitor
Decrease angiotensin II levels
Effect of AT-II receptor blockers
Block angiotensin II binding = no vasoconstriction and ADH/aldosterone secretion
Effect of renin inhibitor
Decrease angiotensin I
Relationship between urine volume and arterial pressure (give name to phenomenon)
Increase Pa = increase urine V
“Pressure Diuresis”
How determine equilibrium value of Pa using a pressure diuresis curve
Intersect the water and salt intake curve with the renal output of water and salt (urine volume curve)
Difference between the pressure diuresis curve of an isolated kidney versus an intact animal
Intact animal slope is MUCH steeper
Why is the slope of the pressure diuresis curve in an intact animal steeper than that of an isolated kidney?
Contribution of the RAA system and the influence of the sympathetic nervous system on the kidney
What is the significance of the steep pressure diuresis slope?
The body will accommodate itself to a very wide range of water intakes without much effect on MAP since any change in MAP will be negated by a change in level of diuresis (and thus blood V)
Difference between parasympathetic and sympathetic response of the sinoatrial node
Parasympathetic (vagal) response = slow down HR; rapid response
Sympathetic = increase HR; slower onset and much slower decay
Post-ganglionic neurotransmitter of parasympathetic system to sinoatrial node
Muscarinic acetylcholine
Post-ganglionic neurotransmitter of sympathetic system to sinoatrial node
Norepinephrine
Reason for difference in response rates of sinoatrial node due to parasympathetic vs. sympathetic stimulation
Parasympathetic is fast because ACh binds to a receptor that is directly coupled to an ionic channel
Sympathetic is slower because NE binds to a receptor which then instigates a second-messenger intracellular cascade
Reason for difference in decay rates of sinoatrial node due to parasympathetic vs. sympathetic stimulation
Parasympathetic is fast because ACh in cleft is rapidly hydrolyzed by cholinesterase
Sympathetic NE reuptake from synaptic cleft is slower
Define sinus bradychardia
<60 beats per minute HR
Effect of atropine
Muscarinic antagonist = block effect of vagal stimulation to increase HR
Effect of cholinesterase inhibitors
Decrease heart rate
Name of effect of an agent that increases heart rate
Positive chronotropic effect
Name of effect of an agent that decreases heart rate
Negative chronotropic effect
What ionic channel are muscarinic ACh receptors coupled to at the sinoatrial node?
Potassium channels (hyperpolarizes membrane when open)
Type of receptor at sinoatrial node for sympathetic stimulation
B1-adrenergic receptor
Effect of propranolol
B-adrenergic blocker = slow down HR
Effect of isproterenol
B-adrenergic agonist/sympathomimetic agent = tend to increase HR
Chemical effect of sympathetic system
Release of NE from nerve terminals in the heart
Increase in circulating levels of catecholamines (epinephrine and NE)
Use of adrenaline administration in a cardiac arrest
Increase the rate of a subsidiary pacemaker that has taken over the pacing of the heart, or provoke the emergence of such a pacemaker
Define vagal tone
Resting parasympathetic tone
Compare vagal tone to resting sympathetic tone in sinoatrial node
Vagal tone > resting sympathetic tone
How can you tell that the vagal tone greater than the resting sympathetic tone in the sinoatrial node?
Simultaneous blockade of both ANS branches results in a heart rate (“intrinsic heart rate”) that is typically about 100 bpm (higher than resting)
Effect of massaging carotid sinus regularly and in hypersensitive individuals
Stimulate baroreceptor reflex
In some hypersensitive individuals, may cause sinus arrest and syncope
Major physiologic controller of cardiac contractility
Sympathetic nervous system
Location of B1-receptors for sympathetic control of contractility
Ventricular myocytes
Effect of sympathomimetic agents
Increase SV, CO, BP
Poisseuille’s Law
R ~ 1/r^4
Define resting tone of arterioles
Usually partially constricted
Purpose of arteriolar resting tone
Allows them to either increase or decrease their diameter to either increase or decrease the resistance to flow, thus increasing or decreasing blood flow (according to Poisseuille’s Law)
Two components of resting tone of arterioles
Basal tone
Neurogenic tone
Define basal tone
A component intrinsic to the smooth muscle surrounding arterioles
Define neurogenic tone
An additional component due to the resting activity of the ANS
What determines the overall sympathetic tone
Pressor and depressor centres in the brainstem
Neurotransmitter released post-ganglionically to sympathetically control blood vessels
Norepinephrine
Sympathetic receptors on blood vessels
alpha and beta adrenergic receptors
Effect of sympathetic nerve stimulation on blood vessels
a1-adrenergic effect –> arteriolar constriction –> increased resistance + decreased blood flow
a1-adrenergic effect –> venule constriction –> decreased blood volume present in tissue
Define shock
A situation in which tissue perfusion is inadequate to supply the metabolic demands of the tissue
Important factor in shock
Constriction of both arterioles and veins
Effect of increase arteriolar resistance in shock
Maintain the mean systemic arterial blood pressure (since MAP = CO x TPR)
Effect of venoconstriction in shock
Shunts blodo out of organs where it is not needed (i.e. skin, skeletal muscle, gut) = help increase mean circulatory pressure, VR, CO = preserve Pa
Receptor type on vessels in organs
B2-receptors
Effect of adrenal-originated epinephrine binding to B2-receptors of vessels in organs
Works towards producing dilation
Effect of parasympathetic innervation on blood vessels in organs
Vasodilation
Effect of sympathetic stimulation on adrenal medulla
Release of epinephrine and norepinephrine
When do circulating catecholamines have a significant effect?
Usually less important under normal circumstances. Become significant in patients with transplanted hearts, who have a surgically induced autonomic denervation = increased sensitivity to circulating catecholamines (denervation hypersensitivity) –> good cardiac response to exercise
What is pheochromocytoma
Tumor of adrenal medulla
Effect of pheochromocytoma
Secretion of abnormally large amounts of catecholamines; often have hypertension
