Introduction to Abnormal Blood Pressure Flashcards
Mean Arterial Pressure
MAP- determines blood flow through the organs; average pressure over time
MAP = (CO * SVR) + CVP OR MAP = (CO*SVR) + RAP
Central venous pressure (CVP) = R atrial pressure (RAP); majority of time want it to be close to or at 0
If reduce CO by 50% but double SVR then the MAP remains the same
Systemic vascular resistance or peripheral vascular resistance = SVR
Factors Affecting Mean Arterial Pressure
MAP = (CO * SVR) + CVP
Local factors: factors produced by endothelium; affects SVR
Vascular Anatomy affects SVR
Neurohumoral Factors: HR affects CO Inotropy affects SV Venous Compliance affects Preload Renal Na+ and H2O Handling affects Blood Volume
MAP and Systolic/Diastolic Pressure Relationship
MAP = Pdias + 1/3(Psys-Pdias)
Thus, if normal 120/80:
MAP = 80 + 1/3(120-80) = 93mmHg
Closer to diastolic because during HR the heart cycle stays longer in diastole than systole
Not necessarily a normal value for MAP because changes throughout the system depending on where you measure it; at least 65mmHg to adequately perfuse the tissues
This is an average
Arterial (Aortic) Pulse Pressure
Calculated by Psys-Pdias
Determined by SV and compliance (acute vs. chronic)
Compliance – elasticity of vessel determines relationship between pressure and volume
As we age, the arteries harden and lose compliance
Long term increase in PP is caused by loss of compliance from disease or age; elderly has a higher PP than someone in their 20s
More elastin fibers – less resistance
More collagen fibers – more resistance
Vascular Anatomy and Function
Aorta is a distributing vessel; it does not have a lot of constriction and very compliant
Large arteries are for distribution and don’t have a role in regulating pressure on a regular basis
Small arteries and arterioles do regulate pressure and are controlled by sympathetic system and have receptors for hormones and tissue factors that affect resistance
Capillaries: exchange vessels and not constricting or dilation because no smooth muscle
Veins and venules: collection of capacitance and are blood reservoirs
Anatomic Determinants of Arterial Pressure: Equation
Poiseuille’s Law: F = (change in P * r^4) / (viscosity * length)
Length and viscosity tend to remain constant, therefore radius(diameter) is the most important factor
Small changes in vessel diameter can lead to large changes in resistance
This equation only applies to a single vessel at a time, but be applied to any vessel
0.4 to 0.8 radius (increasing) which decreases the resistance and flow increases by a factor of 16
If you reduce the radius of renal arterial in kidney by 50% the resistance of that vessel will go up 16 fold
Series vs. Parallel Arrangement of Vasculature
Series – Rtotal = R1+ R2 + R3 + R4…..
Parallel – 1/Rtotal = 1/R1 + 1/R2 + 1/R3 + 1/R4….
Distribution of BP
High BP from aorta and then decreases through system
As we move from heart the pressure decreases
Pressure and MAP will differ depending on where the measurement is being taken
Greatest pressure change is along small arteries and arterioles
2/3 of SVR is arteriolar resistance
Relationship Between Vessel Diameter, Cross-Sectional Area, MAP, and Velocity
Order: Elastic Arteries (aorta), Muscular Arteries, Arterioles, Capillaries, Venules, Veins, and Vena Cava
Vessel Diameter: greatest at elastic arteries then decreases then greatest again at vena cava
Average BP: greatest at elastic arteries then decreases
Total Cross Sectional Area: bell curve where capillaries are greatest
Velocity of Blood Flow: greatest at elastic arteries then decreases and then rises slightly starting at veins
The Windkessel Effect
Elasticity or Distensibility of the arteries
Dampens the pulsatile nature of blood flow
Responsible for continuous blood flow
Refers to elasticity of the arteries
Ability of aorta to dampen the pulse that is coming out
Only about 50% of blood immediately shoots through the aorta, but the other 50% is stored in the “pouch” of aorta and then the ejection of it is slow and continuous (dampens pulses) until next rapid ejection
Clinical Relevance of the Windkessel Effect
Increasing the stiffness of the aorta (reducing compliance)
Increases systolic pressure
Increases diastolic pressure, pulse pressure, and systolic velocity
Increases left ventricular afterload
Reduces subendocardial blood supply during diastole
Increase stiffness of aorta by decreasing compliance you increase pressure; heart must work harder to overcome the pressure
This graph looks at pulse and age
Vessels of Greatest Resistance
Resistance is greatest in the small arteries and arterioles making them primarily responsible for controlling arterial blood pressure and blood flow to organs
Distribution of Blood Volume
60-80% is normally within the venous vessels
Altered by changes in venous tone
Can affect MAP
Can lose about 20% of blood volume, but because of storage in veins it helps reduce the effects that result from the loss of volume since veins keep 60-65% of blood
Increase vasocontriction then decrease amount of blood in veins but increase in arterial system and vice versa
Gravity: has effect of where greatest blood volume is
Vascular Tone
Degree of vasoconstriction under a given physiologic state
Differs among organs
Factors that Detemine Constriction and Dilation:
Extrinsic: come from outside the blood system; neural and humoral
Intrinsic: come from endothelial or tissue directly surrounding the vessel; tissue metabolites, local hormones, myogenic, and endothelial factors
Tissue and Vascular Factors Affecting SVR and Arterial Pressure
The vasodilator theory: ↑ metabolism or ↓ O2/nutrients causes ↑ production of vasodilators
Adenosine is usually very low, but if hypoxic then ATP is being used and adenosine is increased
Increased metabolism increases CO2
Depolarization causes K+ is being lost and if very fast then can cause the pumps not to keep up and excess K+ causes hyperpolarization
Paracrine hormone: released from one cell and acts on nearby cells
Histamine and bradykinin (both cause vasodilation); bradykinin causes NO and prostacyclin release for this; ACE inhibition causes decrease in breakdown of bradykinin to allow for more vasodilation
Endothelial Factors
Nitric oxide (NO): vasodilator; released in response to shear stress created by blood flow and paracrine hormones
Chronic hypertension or atherosclerosis
Nitrate containing drugs
Endothelin: vasoconstrictor; increased in injured vessels; can be a vasodilator or vasoconstrictor depending on which receptor it interacts with; regulatory mechanism
Prostacyclin (PGI2): vasodilator; synthesis stimulated by adenosine and NO; inhibits platelet aggregation
Myogenic Mechanisms
Stretch induced contraction
High arterial pressure stretches vessel – reactive vasoconstriction
Low arterial pressure reduces stretch – reactive vasodilation
Stretch induced vascular depolarization
Brain Regions and Autonomic Control
Cerebral Cortex: higher center influences; has effect on BP; stress, anxiety, anger changes BP through hypothalamus by modulating control
Hypothalamus: integrative control
Medulla: location of sympathetic and parasympathetic (vagal) neurons and receives sensory input; cell bodies in sympathetic and para are located; unconscious control center; receiving sensory input from baroreceptors
Spinal cord: sympathetic efferents
*All are working together
Autonomic Nerves
Sympathetic: Increases resistance to flow Increases heart rate and contractility Vasoconstrictor tone Effects mediated by norepinephrine
Parasympathetic:
Decreases heart rate
Effects mediated by acetylcholine
Effect of Sympathetic Activation on Arterial Pressure
↑ SVR (vasoconstriction): α-adrenergic receptors coupled to Gq
↑ CO (HR x SV):
β1-adrenergic receptors coupled to Gs
↑ blood volume (RAA mediated)
↑ cardiac preload
Activation of sympathetic nerves:
↑ pressure during physical activity
Stress
Heart failure - reflex response via baroreceptors
Shock (circulatory and cardiogenic): decrease in BP to stimulate reflexes to increase pressure
Effects of Parasympathetic Activation on Arterial Pressure
Direct vasodilation:
Only some tissues (erectile tissue)
Ach binds to muscarinic receptors
Results in NO production
Indirect actions:
↓ HR leading to ↓CO
Stimulates production of vasodilator substances, eg. Bradykinin
Does not play a significant role in regulation of SVR and arterial pressure!
Vasovagal syncope: fear or emotion causes activation to get bradycardia and decreased sympathetic tone and fainting
Summary of Sympathetic vs. Parasympathetic Activation
Chronotropy = rate; sympathetic +, parasympathetic - Ionotropy = contractility; sympathetic +, parasympathetic - Dromotropy = conduction velocity; sympathetic +, parasympathetic -
Vessels = vasoconstriction: Resistance = arteries, arterioles; sympathetic +, parasympathetic only certain organs Capacitance = veins, venules; sympathetic +, parasympathetic none
Circulating Catecholamines
Sources: Primary: Adrenal medulla Epinephrine – 80% Norepinephrine – 20 % Secondary: Sympathetic nerves
Cardiac effects:
Increased cardiac output
Cardiac β-adrenergic receptors
Increased blood volume (renal β1-adrenergic receptors) and cardiac preload
E has higher affinity for beta receptors so more function in the heart
NE has higher affinity for alpha so majority of actions are in blood vessels
Have affinity for beta and alpha for both, but just has one that it favors
Catecholamines: Vascular Effects and Increased Activation
Vascular effects:
Vasodilation (β2 receptors)
Vasoconstriction (α1 & α2 receptors)
Circulating catecholamines are increased by:
Increased physical activity
Stress
Heart failure
Shock (circulatory and cardiogenic)
Pheochromocytoma: benign tumor of adrenal gland
NOTE: These are the same events that increase SYMPATHETIC activity!
Baroreceptor Regulation
Provide feedback regulation of autonomic nerves
Carotid Sinus: innervated by sinus (Hering’s) nerve – joins the Glossopharyngeal nerve (CN IX)
Aortic Arch Receptors: innervated by the Vagus nerve (CN X)
Baroreceptor Firing
Baroreceptor firing is increased by:
Increased mean arterial pressure
Increased arterial pulse pressure
Increase in pressure in aorta causes aorta to stretch and cause firing or baroreceptor afferents to medulla; baroreceptors are constantly giving feedback
Firing only during increases
As rate of pressure changes get greater firing
Threshold for carotid sinus receptor activation is ~60 mm Hg. Maximal firing at 180 mm Hg. Maximal sensitivity – normal MAP (not fixed! Can change) = 95mmHg so at 50% firing rate, but remember MAP changes and is not fixed; aortic arch has a higher threshold for activation and less sensitive to changes
Medullary Connections
Afferents synapse in the nucleus tractus solitarius (NTS) in medulla, which have interneurons
Interneurons project to cardiovascular centers:
Enhances vagal efferent activity
Decreases sympathetic efferent activity
Say increase in pressure you activate inhibitory interneurons for sympathetic NS and decrease sympathetic efferent activity to overall decrease the pressure
Enhance vagal activity to by decreasing HR for example to decrease pressure
Hypothalamus modulates the medullary centers
Baroreceptors: Decrease in MAP
Fall in BP you decrease firing rate of baroreceptors and inhibiting parasympathetic NS and increasing sympathetic NS
A drop in aortic pressure initiates a baroreceptor reflex. Resistance vessels constrict to limit outflow from the arterial system.
Venoconstriction/ venous system capacity is reduced and blood is squeezed out.
LV preload increases: venous blood arrives back at the heart and EDP increases.
Inotropy increases: myocardium contracts with increased force
HR increases to move blood returning from veins back into arterial system
MAP is restored by increasing CO and SVR
Baroreceptor Resetting and Adaptation
Rapidly adapting; 1-2 days: short term regulation
In hypertension, baroreceptor firing curve shifts to the right (less sensitive)
If increase MAP for a couple of days, this will reset the baroreceptors
Only useful for short term regulation
As we increase BP to HTN and maintain the HTN it will increase threshold for baroreceptor firing
Baroreceptor Function Can be Altered By
Exercise: medullary and hypothalamic centers modulate autonomic responses; reset arterial pressure to higher level
Pain
Chronic hypertension
Chronic heart failure
Arterial vascular disease: carotid arteries become less compliant (stretch less)
Renin-Angiotensin-Aldosterone System
Kidneys are stimulated to release renin by:
Sympathetic stimulation (β1-adrenoceptors)
Renal artery hypotension
Decreased Na+ in distal tubules
Renin is an enzyme that is stimulated by sympathetics
Renin is released and goes into systemic system and causes conversion from angiotensinogen to angiotensin I then flows to lungs and acted upon ACE and converted by angiotensin II, which stimulates aldoesterone release by the adrenal glands
Causes increased Na2+ reabsorption to pull more water back into blood vessels and thus increasing CO, preload, and MAP
RAAS is for increasing pressure
Angiotensin II
Increases blood volume (Increase CO):
Stimulates renal reabsorption of Na+ and H2O
Stimulates aldosterone release to increase Na+ and H2O retention
Stimulates ADH release from posterior pituitary
Stimulates thirst centers
Increase SVR and decrease venous compliance
Augments sympathetic activity:
Faciltiates NE release
Inhibits NE reuptake
AT1 receptors in RVLM increases sympathetic activity
Cardiac and vascular hypertrophy
Hemorrhaging and RAAS
In this situation, arterial pressure is at 100 and hemorrhage drops it to 50 and over several minutes can increase the pressure but not always back to normal
If no RAAS cannot recover from these situations
Normally functioning kidneys are assumed in this
MAP does not change much when Na+ is increased
When RAAS is functioning normally arterial pressure is maintained even with a 100-fold increase in salt intake or a decrease to 1/10 normal intake
Blocking formation of Ang II causes blood pressure to drop when salt intake decreases
Preventing suppression of Ang II causes dramatic increase in pressure
Anti-Diuretic Hormone (ADH) or Vasopressin or Arginine Vasopressin (AVP)
Primary actions:
↑ renal reabsorption of water = ↑ blood volume
Acts on kidney via V2 receptors
Secondary actions:
Vasoconstriction via V1 receptors, ↑ SVR
Only occurs at high circulating concentrations (hypovolemic shock, heart failure)
Natriuretic Peptides
Atrial natriuretic peptide (ANP): synthesized and released by atria
Release stimulated by:
Atrial stretch (hypervolemia and congestive heart failure)
Sympathetic stimulation
Angiotensin II (AII)and endothelin (ET-1)
Brain natriuretic peptide (BNP): synthesized and released by ventricles Release stimulated by: Ventricular dilation (heart failure) Sympathetic stimulation AII and ET-1 Diagnostic marker for heart failure
*Both lower BP
Natriuretic Peptides Mechanism
Counter the RAAS – regulatory mechanism
Increased pressure / blood volume causes atrial distension to get release of ANP to increase GFR and turn off production RAAS to get back to normal from release Na+ and water into urine to decrease pressure and volume
Therefore, natriuretic peptides decrease BP
Venous Pressure
Central venous pressure (CVP):
Pressure in thoracic vena cava near right atrium
Determinant of filling pressure and preload of right ventricle
Δ CVP = ΔV/ Cv (V=volume and Cv=compliance)
CVP is increased by:
- Increased venous volume -volume shifts (standing to supine) and renal Na+ reabsorption
- Decreased venous compliance (increased venous tone)- the smaller veins outside the thorax, sympathetic activation, circulating vasoconstrictors, and external compression/muscle contraction
Hypotension with Causes
Abnormally low arterial pressure (
Consequences of Hypotension
Reduced blood flow and O2 delivery to organs
Loss of consciousness
Metabolic acidosis
Organ dysfunction and death
