Blood Pressure Regulation Flashcards
Cardiac Output Formula
CO=HRxSV
Regular Cardiac Output
5000mL
72bpmx70mL
Stroke Volume Formula
SV=EDV-ESV
70mL=120mL-50mL
Frank Sterling Law
heart has intrinsic ability to change SV in response to input (venous return)
the heart pumps what it recieves
Preload
filling of the ventricle
increases SV
direct result of venous return
Contractility
heart contracts more or less forcefully
increases SV
Afterload
pressure the heart must overcome to eject blood
decreases SV
blood pressure
Ejection Fraction
SV/EDV
normally 60%-70%
Positive Inotropes
increase contractility, increase Ca++ flow, increases cAMP
examples are Epinephrine, Caffiene, and digitalis
Chronotropes
increase cardiac rate
Sympathetic Chronotropes
positive inotropes, increases cardiac rate,
Epinephrine, Norepinephrine
Parasympathetic Chromotropes
negative inotropes, decreases cardiac rate
Vagus Nerve via ACh
Atropine blocks ACh, stimulating cardiac rate
Max Heart Rate Formula
- Old Formula: 220-age in years
- New Formula: 208-(0.7xage in years)
CO in Tachycardia
in a heart rate over 170bpm CO is decreased die to insufficient filling time
Digitalis
enhances Ca++ entry, increases contractility
antidepressant
Nitroglycerin
cardiac vasodilator, increases preload
Ca++ channel blockers
smooth muscle antagonist, dilates smooth muscle, lower BP
decreases afterload, negative inotrope
Fick Principle
used to estimate Cardiac Output in living subjects, application of law of conservation of mass
can be estimated knowing O2 consumption, with arterial pulmonary and venous valves for O2
Fick Principle
C.O. (Q) formula
(O2 consumption(mL/min))/(O2 arterial - O2 venous)
Fick Principle Thermodilution
cold saline is used instead of dye and thermal identification is used
Fick Principle Thermodilution
C.O. formula
(mg of dye injectedx60 sec)/(avg dye conc.(mg/L)xduration of curve in seconds)
atherosclerosis
hardening of arteies due to gradual plaque buildup
treated by beta blockers, calcium channel blockers, and anti-clotting medications
Angina Pectoris
squeezing, heaviness, tightness, or pain in the chest
caused by reduced blood flow to the heart muscle (ischemia)
Coronary Bypass
surgical procedure to treat coronary artery disease
reroutes blood flow from clogged coronary arteries to arteries and veins harvested from elsewhere, utilizes a bypass machine
Angioplasty
minimally invasive procedure meant to widen narrowed or obstructed arteries and veins
uses guide wire, catheter, and a balloon
The Sounds of Korotkoff
the sounds heard during the measurement of blood pressure
Pulse Pressure Formula
Systolic-Diastolic=Pulse Pressure
120mmHg-80mmHg=40mmHg
Mean Arterial Pressure
Effectivness of the heart as a pump, resistance to blood flow, distribution of blood between arterial and venous blood vessels
Mean Arterial Pressure Formulas
MAP=(1/3)Pulse Pressure + Diastolic Pressure
MAP=(1/3)(2Diastolic Pressure + Systolic Pressure)
MAP=COxTPR(total peripheral resistance)
Formulas for Flow
DeltaP/R
MAP/Resistance
Resistance to flow = 1/(radius)^4 or MAPx(radius^4)
Arterioles
Resistance vessels in system
pressure flow regulators
small in diameter
Venuoles and Veins
capacitance vessels
volume storage
54% of blood volume is in venous system
Capillaries
exchange vessels (O2, CO2, hormones)
largest area
5 liters or blood but 8-10 liters of capillary space
shunting example
increased blood flow to the digestive system after eating, reducing blood to other systems
Which organ requires the most blood?
the kidney requires the most blood per gram
Continuous Capillary
body capillaries with confluent lining
Fenestrated Capillaries
capillary endothelium has windows or pores called fenestra
in kidneys and intestines
Sinusoidal Capillaries
wide clefts between endothellial cells
in liver, bone marrow, and lymphatic system
Law of Laplace Formula
Pressure = Wall Tension / radius
T/r
Batista Procedure (Brazil)
removes part of the ventricular wall of an enlarged heart, reducing the radius, then less tension is required to mantain blood pressure
Bernoulli Principle
sum of kinetic energy and flow energy in a closed system is constant, when fluid moves from a wide to narrow tube, potential energy falls as velocity increases and kinetic energy increases
lower pressure in smaller diameter tube with faster velocity
Blood Pressure Regulators
- Autonomic Nervous System
- Baroreceptors
- Renal Mechanisms
- Role of Venous Return
- Role of Hormones
- Autoregulation
- Chemoreceptors
- Effect of Temperature
ANS
Sympathetic BP Regulation
increase heart rate, force of contraction, Alpha Receptors Vasoconstrict w/ NE
Beta 1 receptors increase heart rate and force of contraction
ANS
Parasympathetic BP Regulation
decrease heart rate via vagus nerve, ACh, no effect on contraction force
ANS
Acetylcholine and BP regulation
ACh is a vasodilator, but usually not a force in blood flow regulation
ANS
Medullary Ischemia
ischemia to the medulla oblongata triggers body wide vasocontriction, increased HR and contractility
Most Important Flow Regulator
vasocontriction
will restrict flow to nonessential organs
Baroreceptors
most important short term regulator, rapid acting
located in the carotid sinus and aortic body
Effect of increased BP on Baroreceptors
- BP increase
- Baroreceptors increase firing
- Excites vagal nerve (decreased HR)
- Inhibits Medullary vasocontriction centers
Decrease is the opposite
Baroreceptors long term
not good at long term BP regulation as they reset after several days with a prevailng BP
Orthostatic Hypotension
pressure compensation from lying to standing
Renal Mechanisms
Very important long term regulator
Renal Angiotension Aldosterone System (RAAS)
hormone system that regulates blood pressure
when renal blood flow is reduced Angiotension is released, which vasocontricts
J-G Apparatus
contains renin producing cells
RAAS Steps
- Macula Densa of DCT senses decrease in Renal BP
- Increase in Renin release by J-G apparatus is signaled
- Renin acts on Angiotensinogen making Angiotensin 1,
- Angiotensin 1 is altered by Angiotensin Converting Enzyme(ACE)
- Angiotensin 2(vasocontrictor) is made
- Angiotensin 2 triggers Aldosterone release
- Aldosterone increases sodium and water reabsorbtion by distal tubule, increasing blood volume and blood pressure
- Angiotensin 3 acts as a vasoconstrictor
Factors of Venous Return
- Venous Valves
- Skeletal Muscle Pump
- Thorasic Pump Inhalation
Venous Valves
???
Skeletal Muscle Pump
When skeletal muscles contract and squeeze veins, pushing more blood toward the heart.
Thoracic Pump Inhalation
venous return is increased during to inhalation due to increased pressure on abdoninal veins and decreased pressure on throracic veins
Endothelium Derived Relaxing Factor (EDRF)
Endothelium derived relaxing factor, relaxes vascular smooth muscle
Nitroglycerin, Viagra
Bradykinin
vasodilator, increases vascular permeability,
Histamine
vasodilator, constricts EDHF to produce vasodilating agents
Epinephrine
dilator in heart , liver, skeletal muscle, B2 receptor activation
Atrial Natriuretic Peptide/Factor (ANP/ANF)
- Released by an increase in BP
- Causes Vasodilation
- Opposite action of Aldosterone
Vasodilates by increasing kidney sodium secretion by DCT, water excretion, less volume, less BP
prostocyclin
inhibits platelet aggregation, vasodilator
Thromboxane
platelet aggregator, vasocontrictor
aspirin
cyclooxygenase inhibitor, inhibits platelet aggregation
Autoregulation
Myogenic Theory and Metabolic Theory
Myogenic Theory
smooth muscles reaction to stretch is contraction as BP increases, vessel wall contracts, flow “autoregulates”
Metabolic Theory
tissues produce vasodilators,
decrease in flow -> vasodilators accumulate
increase in flow -> vasodilators wash away
Active Hyperemia
metabolic demand of tissue causes vasodilation
skeletal muscle, digestive tract
Reactive Hyperemia
transient increase in organ blood flow following a brief period of ischemia
Chemoreceptors
more important at lower pressures,
Chemoreceptor vasodilation
increase PCO2, H+
decrease in pH
decrease PO2
Effect of temperature
increase: vasodilation
decrease: vasoconstrict
Four Starling Forces
determine fluid movement in capillaries
Pc, Pi, pic, pii
Pc
hydrostatic pressure in capillary(filtration force)
primary outward force
tends to force fluid out of the capillary
Pi
hydrostatic pressure of interstitial fluid(0 or filtration force)
weak force
zero to negative in value
pic
oncotic pressure of capillary plasma proteins(reabsorbtion force)
tends to force fluid into the capillary
pii
oncotic pressure of interstitial fluid proteins(filtration force)
tends to force fluid out of the capillary
Net filtration rate formula
L[(Pc-Pi)-(pic-pii)]
arterial side of capillaries
have a net outward force (filtration)
venous side of capillaries
have a net inward force (reabsorbtion)
summation of both arterial and venous capillaries
yields a net outward force (filtration)
2mL/min
Lymphatic system funciton in fluid accumulation
lymphatic system shunts fluid and proteins back into circulation from the area around the capillaries
Edema Causes
high capillary permeability(blood pressure), low blood protein(starvation), lymphatic blockage(mastectomy, cancer), increased capillary permeability
High Blood Pressure
140/90 mmHg
Primary or Essential Hypertension
Hypertension from an undetermined cause
treatment of hypertension
- Diuretics
- Beta Blockers
- Calcium Channel Blockers
- Ace inhibitors
- ARB(s)
Diuretics
decrease fluid absorbtion by kidney
fluid loss = blood volume loss = blood pressure drop
Beta Blockers (B1 receptors)
decrease heart rate, contractility due to B1 receptrors blocking
blood pressure drop due to decreased heart pump functions
Calcium Channel Blockers
block calcium entry into muscle, esp smooth muscle of vasculature
blocks vasoconstriction
ACE inhibitors
blocks Angiotensin Converting Enzyme “ACE”, less Angiotenin 2 and Aldosterone production,
less vasoconstriction and less Na+ and volume recovery by Kidney
ARB(s)
Angiotensin Receptor Blockers, blocks Angiotensin receptor at the target tissue level
blocks vasoconstriciton and adrenal release of Aldosterone
Alpha 1 receptors
stimulates contraction of smooth muscles, increases IP3
Alpha 2 receptors
same as A1 receptors, also inhibits smooth muscle contraction of the GI system, decrease cAMP
Alpha receptors
greater affinity for NE
Adrenergic Receptors
Alpha and Beta Receptors
Beta 1 receptors
stimulates heart rate, contractility, increase cAMP
Beta 2 receptors
inhibits smooth muscle, increase cAMP, esp in lung, heart, skeletal muscle blood vessels
Beta 3 receptors
fat exclusively, lipolysis, increase cAMP