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Flashcards in More Physio Deck (29)
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How does increased metabolism lead to vasodilation?

Metabolic waste products are potent vasodilators.
-adenosine, potassium, CO2, histamine, hydrogen ions, adenosine phosphate


Main nutrient that regulates vasodilation in the "nutrient lack" theory.

-lack of oxygen leads to vasodilation
(exception in the lungs, where blood vessels constrict in hypoxia)


What does a thiamine deficiency do to blood flow and blood pressure?

Thiamine is needed for ATP production. A lack of ATP production leads to an accumulation of adenosine which is a vasodilator. Vasodilation increases blood flow and decreases blood pressure.

(neurologically thiamine is used to synthesize GABA. Def. leads to Wernicke or Korsakoffe)


What is reactive hyperemia?

Hyperemia: increase of blood flow to different tissues in the body

Reactive hyperemia: blood flow is occluded to tissues in a certain region (ex. tourniquet). Vasodilator metabolites accumulate and cause vasodilation. Blood flow is returned and occurs at a high level due to the vasodilation. Leads to flushing seen on skin. Eventually the vasodilator metabolites are "washed out" and vessel diameter returns to normal.


What is active hyperemia?

Hyperemia: increase of blood flow to different tissues in the body

Active Hyperemia: increase blood flow to specific tissues due to increased metabolism and nutrient requirement (ex. during exercise)..


Two metabolites that the brain senses leading to vasodilation in the cerebral vasculature.

CO2 and H+


Most important endothelial derived vasoactive mediator. What stimulates its formation and how does it cause vasodilation?

Nitric Oxide
-stimulates by shear stress on the endothelium from increased blood flow
-the gas diffuses from the endothelium to the vascular smooth muscle stimulating cGMP.
-cGMP causes smooth muscle relaxation and vasodilation


Function of endothelin.

Vasoconstrictor released from damaged endothelial cells due to chronic hypertension. Stops bleeding from the damaged area to prevent blood loss.


Most cations and anions cause vasodilation. Which causes vasoconstriction?



What can override neuronal control of vascular smooth muscle?

Local control: metabolites and ions


Most important neural regulator of the cardiovascular system.

Sympathetic Autonomic Nervous System (SANS)


How does the SANS affect the heart?

Innervates the nodes: affects heart rate

Innervates the cardiac muscle: affects contractility

(increased SANS stimulation increases both)


How does the Parasympathetic Autonomic Nervous System (PANS) affect the heart?

Only innervates the nodes: affects heart rate

(increased PANS stimulation decrease heart rate)


What is the mechanism of vasovagal syncope?

Intense emotions stimulate the SANS to vasodilate skeletal muscle vasculature without exercise. This results in a much lower blood pressure accompanied by decreased HR. Less blood flow gets to the brain and the patient faints


What happens to blood pressure (both sys, and dias.) during exercise.

Systolic: slightly elevates--> resistance decreases which drops the blood pressure, however, the increase in flow "overpowers" the decrease in resistance and pressure increases.

Diastolic: decreases---> vasodilation of blood vessels decreases total peripheral resistance


How does atherosclerosis lead to poor blood pressure regulation?

The stretch receptors in the carotid sinus and aortic arch require distension in order for afferent nerves to detect higher blood pressure. If they cannot distend due to plaque buildup then no vagal stimulation can be sent to the heart to slow HR to decrease BP.


How is blood pressure maintained during hemorrhage?

Blood loss leads to lower volume and lower BP. The relaxation of the vessels in the low BP decreases afferent signals from the carotid sinus and aortic arch so the PANS stops sending inhibitory vagal efferents to the heart.

Without the PANS, the SANS takes over and constricts blood vessels, increases HR and increases contractility to raise blood pressure.


What is the Bainbridge Reflex?

Response to atrial wall stretching from increased volume in the chambers. Vagal afferents sense the stretch and signals are sent up to the medulla. The efferent response from the medulla is mediated by the SANS and increases HR and contractility.

This reflex has the most importance on the left side of the heart because it helps to prevent congestion of blood in the lungs. It also works on the right side with peripheral blood flow but is not as important.


Describe the CNS ischemic response.

Normally if blood flow to the brain decreases (ex. obstruction), the brain vasodilates to decrease pressure creating a larger pressure gradient between the periphery and brain so blood gets up to the brain more easily. If that doesn’t work, the sympathetic nervous system is activated to increase peripheral pressure to force blood into the brain.


Describe the Cushing Reaction.

Hypertension with Bradycardia

Increased intracranial pressure (equal to or greater than blood pressure) compresses blood vessels in the brain and cuts off blood supply. This initiates the CNS ischemic response increasing peripheral blood pressure to "open up" the compressed brain vessels and restore blood supply.

The baroceptors located in the aorta and carotid sinus, however, only detect the increased peripheral blood pressure and don't care what's going on in the brain so they respond with vagal stimulation and slow down the heart rate.


What happens to HR during inhalation and exhalation.

Inhalation: HR increases
Exhalation: HR decreases

-during inhalation, intrathoracic pressure and alveolar pressure decreases (become more negative) which decreases the pulmonary blood pressure. This decreases the pulmonary venous return so the heart increases its rate to maintain flow thru the lungs. The opposite affect happens during exhalation.


What two general mechanisms do kidneys use to maintain blood pressure.

1. Volume Control
2. Electrolyte Control


Describe salt insensitive and salt sensitive people and how the kidneys regulate chronic high blood pressure.

Terminology is tricky here:

Salt Insensitive---> the blood pressure in these patients is not heavily influence by salt intake so they are salt insensitive. This is because their kidneys are very sensitive to salt fluctuation and adapt rapidly.

Salt Sensitive---> blood pressure highly affected by salt intake in these individuals because their kidneys are NOT very sensitive to salt fluctuation. Adaptation is much slower.

Salt sensitivity does not refer to the kidneys' response to salt. It refers to the blood pressure change from salt intake.


Which has a larger effect on increasing blood pressure: increasing fluid intake, or salt intake and explain why.

Salt Intake

Fluid intake makes the vascular fluid hypoosmotic. This directs the fluid into the tissues and out of the vasculature so overall the increase in volume is minimal and therefore so is the pressure.

Salt Intake increases osmolarity in the blood. Not only is fluid leaving the tissues and entering the blood, but this high osmolarity is sensed by the posterior pituitary which releases ADH increasing volume retention in the kidneys.


Chronic hypertension decreases life expectancy by three very general mechanisms. Name them.

1. Increased cardiac work (heart failure)
2. Damage to blood vessels (aneurysms)
3. Injury to kidneys


Describe the Renin-Ag-Aldosterone System for BP regulation.

1. Low BP decreases flow thru the nephron. Cells in the macula densa portion of the nephron sense low sodium chloride.

2. The macula densa cells are in contact with cells in the afferent arterioles called Juxtaglomerular Cells which, when signaled by the macula densa due to low NaCl, release Renin.

3. Renin travels thru the blood and enzymatically activates Angioteninogen (a protein made by the liver and sent out into the blood). This forms Angiotensin I.

4. Ag I goes to the lungs when Angiotensin Converting Enzyme (ACE) converts it to Angiotensin II.

5. Ag II acts directly on receptors of vascular smooth muscle to cause vasoconstriction increasing blood pressure. It also stimulates kidneys to retain sodium and water.

6. Ag II also stimulates release of aldosterone from the adrenal medulla. Aldosterone acts directly on the kidneys to reabsorb sodium and water.


Why does coarctation of the aorta result in decreased HR even though the peripheral blood pressure is low?

Coarctations usually occur just distal to the brachiocephalic, L. common carotid, and L. subclavian arteries. Blood pressure is high in this proximal region of the aorta as well as in the head and upper limbs. The baroceptors are located in these regions so they decrease HR. Distal to the stenotic area there is low pressure resulting in an overall low blood pressure.


Treatment for pre-Eclampsia.

Magnesium Sulfate


What is essential hypertension?

Primary HTN which has an unknown origin.
-may be due to increased weight and/or sedentary lifestyle.

(Guyton and Hall pg. 225 has great explanation)