Regulation of Blood Pressure and Cardiac Function Flashcards
Responsible for Vascular Adjustments?
Change in tone of smooth muscle tissue
Vasodilators work on Arterioles, Veins, or Both?
Only on Arterioles
Sympathetic nerves release?
Norepinephrine
Receptors for Norepinephrine
Alpha-1 Adrenergic Receptors
Effect of Norepinephrine on Vascular Smooth Muscle
Vasoconstriction
The Brain, Heart, and Skeletal Muscles blood flow closely follow what?
Metabolic Rate
Skin and Kidney blood flow is regulated by?
Sympathetic Nerves (Rather than metabolic rate as the others are)
Functions of Blood Flow (6)
- Delivery of Oxygen
- Delivery of Nutrients (Glucose)
- Removal of CO2
- Removal of H Ions
- Maintenance of Proper Concentration of other Ions
- Transport of Hormones
Local Blood Flow Regulation is regulated by? In organs, these are regulated by?
- Muscular arteries and large arterioles
2. In organs by metarterioles and endothelial cells of capillaries
Vasodilator Theory
Endothelial tissue produce a vasodilator substance in response to availability of O2 and Nutrients
Oxygen Lack Theory
Oxygen is required to allow muscle contraction, lack of this causes local arterioles and metarterioles to relax and dilate
Reactive Hyperemia
Transient increase in blood flow following a period of ischemia
Active Hyperemia
Increase in blood flow associated with increased metabolic activity (Such as in exercise)
Vasoconstrictor Agents (4)
Norepinephrine and Epinephrine
Angiotensin II
Vasopressin
Endothelin
Vasodilator Agents (2)
Bradykinin
Histamine
Increase in Calcium (Constrict or Dilate)
Vasoconstriction
Increase in Potassium (Constrict or Dilate)
Vasodilation
Increase in Magnesium (Constrict or Dilate)
Powerful Vasodilation
Low pH (Constrict or Dilate)
Dilatation of Arterioles
Acetate and Citrate (Constrict or Dilate)
Mild Vasodilation
Increase in CO2 (Constrict or Dilate)
Moderate Dilation in other Parts (Especially in the Brain)
Which Vessels are Not INnervated by the Sympathetic Nervous System?
Capillaries
Pre-capillary Sphincters
Metarterioles
Most Important Part for Regulation of Circulation
Why?
Sympathetic Nervous System
Most blood vessels do not have parasympathetic innervations
What can pass the Blood-Brain Barrier
Glucose and CO2
Heart is Innervated By?
Sympathetic and Parasympathetic Nerves
Parasympathetic Nerves (Vagi) effect on the Heart?
Lowers BPM
If Heart is De-Innervated, Will it Beat Faster or Slower?
It will beat faster, unlike abrupt termination of response to vagal activity; effects of sympathetic stimulation will only slow gradually after stimulation is stopped
Location of Vasomotor Center
Medulla and Upper Pons
Vasomotor Center Transmits What Impulses
- Vagus Nerve
- Spinal Cord
- Parasympathetic
2. Sympathetic
Vasovagal Reflex
Compression of Carotid Arteries slows down HR
Chemoreceptors Location
Carotid and Aortic Bodies
Chemoreceptors Sensitive To? (3)
- O2 Lack
- CO2 Excess
- H+ Excess
Volume Reflex
Stretch in Atria causes Diuretic Effect
Increase in GFR -> Increased Urine Output -> Decrease in BP
Bainbridge Reflex
Increase in HR in response to atrial stretch
Prevents damming of blood to the veins
Chemoreceptor Reflex
Decreases flow in artery as result of hypoxic conditions
CNS Ischemic Response (a.k.a.?)
Cushing Reflex
Intense vasoconstrictor stimulation
When is the Cushing Reflex stimulated?
When is it maximal?
BP < 60mmHg
BP < 15-20mmHg
Abdominal Compression Reflex
Effect
Stimulation of the baroreceptor/chemoreceptor reflex causes stimulation o the skeletal muscles, especially in the abdomen
Pushes blood back to the heart
Renal Function Curve
What happens when too much ECF?
Arterial pressure rises causing the kidney to excrete more urine
Infinite Feedback Gain
Water and salt output must equal intake
Chronic Hypertension:
What happens to
- Peripheral Resistance
- Cardiac Output
- Fluid Volume Levels
Increased peripheral resistance
Cardiac output eventually returns to normal
Return to normal fluid volume over time
Angiotensin II Functions (3)
- Vasoconstriction
- Decreased secretion of salt and water
- Raises BP halfway to normal after sudden Hypotension
How long for Angiotensin II to be fully active?
20 Minutes
Angiotension II Pathway resulting from Decreased Arterial Pressure
Decreased Pressure -> Renin -> Angiotensinogen -> Angiotensin -> Angiotensin II -> Vasoconstriction + Renal Retention of Salt and Water -> Increased Arterial Pressure
Factors Causing Hypereffectivity
- Nervous Excitation
2. Hypertrophy
Hypoeffective Heart
Increased venous return with no accompanying increase in cardiac output
Factors Causing Hypoeffectivity (6)
- Inhibition of Nervous Excitation
- Abnormal Rhythm or Rat eof Heart
- Valvular Disease
- Congenital Heart Disease
- Myocarditis
- Cardiac Anoxia
Beri-Beri
Lack of thiamine diminishes cell’s ability to use nutrients
Cells send signal to heart to beat faster to deliver more nutrients
Arteriovenous Fistula
Abnormal connection between major artery and vein
Diminishes peripheral resistance (Bypasses microcirculation)
Hyperthyroidism
Increased BMR
Anemia
Diminished oxygen delivery and viscosity (Hypoviscosity)
Pathologically High Cardiac Outputs (4)
- Beri-beri
- Arteriovenous Fistula
- Hyperthyroidism
- Anemia
Pathologically Low Cardiac Output (2)
- Decreased Pumping Effectiveness of heart
2. Decreased Venous Return
Normal External Pressure
-4 mmHg
Cardiac Tamponade
Accumulation of fluid in the pericardium around the heart
Goldblatt Hypertension
Results from compression/obstruction of renal arteries or its branches
Integrated System that Acts Within Seconds
- Baroreceptors
- Chemoreceptors
- CNS Ischemic REsponse
Integrated System That Acts Within Minutes
- Renin-Angiotensin System
- Stress Relaxation of Vasculature
- Capillary Fluid Shift Mechanism
Cardiac Output
Amount of blood pumped into aorta each minute by the heart
Venous Return
Quantity of blood flowing from veins into right atrium each minute
Cardiac Output should equal?
Venous Return
Improving cardiac output must be accompanied with improved venous return
Normal CO for Men, For Women?
5.6 liters/min; 10-20% less for women
Primary Controller of Cardiac Output
Various factors of Peripheral Circulation that Affect Venous Return
Frank-Starling Law of the Heart
Increased blood flow into heart stretches out cardiac chambers
Additional stretch causes muscle fibers to contract with increased force
Heart pumps out all the additional blood
Factors Affecting Venous Return (3)
- Right Atrial Pressure
- Mean Systemic Filling Pressure
- Resistance to Blood Flow
Effect of Increased RA Pressure on Venous Return
Lowers Venous Return
When does Venous Return Decrease to 0?
When the RA Pressure reaches 7mmHg (Mean Systemic Filling Pressure)
Greater Mean Systemic Filling Pressure effect on Venous Return Curve
Shifts Upward and Right
Greater Difference Between RA and Mean Systemic Filling Pressure
Greater Venous Return
Compensation for Acute Failure By Sympathetic Reflexes
Pumps more vigorously
Increased tone of vasculature, Increased RA pressure
Chronic Stages of Failure
Renal Retention of Fluids and Increase in Blood Volume
Fluid Retention in Heart Failure
Fall in cardiac output causes fall in urine output
Treatment of Decompensation (3)
- Strengthening of Heart (Digitalis, Inotropes)
- Administering Diuretics
- Reducing Water and Salt Intake
Decompensated Heart Failure
Low CO prevents kidney from excreting necessary daily amounts of fluid and salt, leading to edema
Cardiogenic Shock
Heart is too damaged, unable to pump enough blood to keep body alive