Blood Vessels & Blood Pressure

Hierarchy of BV

Heart—>arteries—>arterioles—>capillaries—>venules—> veins

Arteries

• muscular and elastic tubes that can absorb pressure from heart)

• Lots of high blood pressure moves through them

• distributes blood to body

Arterioles

• Can vasodilate ad vasoconstrict

• Affect pressure in the arteries (Mean arterial pressure)

• affect how much blood enters capillaries

• affects exchange of blood

Arteriole Vasoconstriction

BV constrict making it harder for blood in the arteries to drain downstream, leading to high blood pressure in arteries

Arteriole Vasodilation

BV dilation makes it easier for blood in the arteries to travel downstream, lowering blood pressure in the arteries.

Capillaries

• Thin walls allow for particles and gases within the blood to ppass in/out of tissue.

• walls to thin and easily tear causing leaking of plasma

• EDEMA= localized swelling

Venules

transitional vessels that bridge capillaries to veins in order to bring blood back to heart

Veins

• blood pressure extremely low (less tha 15 mmHG)

• veins consist of smooth muscle to contract blood toward heart

• One-way valves keep blood in one direction like fish ladder

• Vena Cavas can hold blood (capacitance vessels)

Mean Arterial Pressure

MAP= CO x R (Total Resistance)

a regulated variable

Cardiac Output: Low Heart Rate

Decreased HR: potassium binds to SA node decreasing HR

Cardiac Output: High Heart Rate

Increased HR: sodium binds to SA node increasing HR

Cardiac Output: Increasing Stroke Volume

• More venous return results in increased EDV

• More stretch leads to more calcium release and stronger contractions, decreased ESV

Resistance in arterioles (R)

• Vasoconstriction in most tissues

• Vasodilation to heart, liver, and skeletal muscle

Factors that Change Arteriole Diamter: Metabolites

• Local

• During cell metabolism, waste is produced, called metabolites

• Arterioles will DILATE to cleanse and wash away metabolite build-up

Factors that Change Arteriole Diameter: Autonomic Nervous system

• Global

• Will always be in a sympathetic or parasympathetic state. In the parasympathetic state, it is a withdrawal of sympathetic activity

Factors that Change Arteriole Diameter: Histamine

• Local

• Histamine (chemical) Sac is released when tissue is injured

• Causes local arterioles to dilate, causing edema in the tissue

Factors that Change Arteriole Diameter: Temperature

• Local

• Vasodilation in heat

• Vasoconstriction in cold

Factors that Change Arteriole Diamter: Angiotensin II

• Global

• Hormone causes vasoconstriction; released after blood loss to increase MAP

Factors that Change Arteiole Diameter: Nitric oxide

• Local

• Chemical that vasodilates (used to prevent heart attack)

Factors that Change Arteriole Diameter: Caffeine

• Global

• chemical vasoconstrict blood vessels

• Great at treating headaches

• Increases heart rate (tachycardia)

How does Angiotensin II work?

Angiotensinogen stored in liver—> Renin (enzyme) from the kidney turns AT in Angiotensin I—> ACE (enzyme) turns AT I into Angiotensin II—> it increases R, increases thrist and kidneys hold onto water to increase blood volume

Hypovolemic Shock

hypo(low) volemic(volume)

Means an inadequate amount of blood

Hemorrhagic Shock

inadequate blood flow to tissues due to external or internal bleeding

compensation: tachycardia, thirst

Traumatic Shock

Blood leaks into tissue due to crush injuries

Burn Shock

massive plasma loss as it leaks because skin is not present. Leads to build up of hematocrit (rbc)

Distributive Shock

blood volume is normal, but blood is not reaching vital tissues or is being shunted elsewhere.

Fainting

Neurogenic vasodilation of arterioles. brain causes widespread dilation and gravity pulls blood flow downward. Bloodflow does not go to brain

Anaphylaxis

allergic reaction that causes histamine-like response and massive dilation throughout the body. This drastically drops blood pressure

Sepsis

toxins in the blood that cause massive vasodilation to wash awa toxin

Cardiogenic shock

heart is unable to pump blood around

Myocardial infarction (heart attack)

blood clot or blockage which prevents blood flow to myocardium

Congestive heart failure

The left ventricle has weaker contractions, and the atria fill the ventricle, so ESV increases. Blood flows back into the atria, then into the pulmonary veins, then into the pulmonary capillaries in the lungs. This creates trouble breathing

Cardiovascular Receptors

baroreceptors

Cardiovascular effectors: Short term

Sympathetic nervous system for distributive and cardiogenic shock

Cardiovascular effectors: Medium term

replace blood with fluid through IV, thirst, and retaining water in kidney

Cardiovascular effectors: long term

make new blood

Angiotensin II as an Effector

• Vasoconstrict to increase blood pressure (R)

• Create Thirst

• Retain water in the kidneys

Making New Blood: EPO

• Kidney and liver release EPO into blood stream to be delivered to bone marrow

• inside bone marrow it makes red blood cells

Making New Blood: EPI

• SNS release EPi from adrenal gland into blood stream

• binds to liver receptors and stimulate protein synthesis

• albumin and other plasma proteins released into blood stream

Making New Blood: Plasma

drink water, eat food, and have kidney water retention to make plasma