FNH 161

What are the 3 Main important components of the cardiovascular system?

**1. Heart -** pushes blood out to the body 

**2. Blood vessels -** carry blood throughout the body

**3. Blood -** contains nutrients, O2, CO2, etc.

How does the cardiovascular system contribute to homeostats?

The circulatory system is a **transportation system** 

→ Transports O2, CO2, nutrients, wastes (send to kidneys to be removed), and hormones (secreted from endocrine glands and travel through the blood to bind to target cells) 

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Moves white blood cells + platelets (important for blood clotting)  to sites of injury 

→ These work together to stop bleeding and repair damage 

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Regulate body temperature 

→ Cold: body directs blood toward your core and away from surface, hot: body directs blood to surface thus heat dissipates

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**Note:** Key function of the cardiovascular system is transposition thus we require heart which acts as the motor to pump blood into blood vessels; blood vessels act as highways for blood to flow through the body, and blood consists of nutrients, gases, wastes, etc 

What are the 2 circulatory routes in the cardiovascular system**?**

There are 2 circulatory routes in the cardiovascular system**:** 

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**1. Pulmonary** - Blood goes from heart to lung and back 

**2. Systemic** - Blood goes from heart to body organs and back

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**Arteries Vessels** - Carry blood away from heart 

**Veins Vessels**  - Carry blood back to heart

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In **pulmonary** circulation, pulmonary __arteries are oxygen-poor__ and pulmonary __veins are oxygen-rich__

In **systemic** circulation, systemic __arteries are oxygen-rich__ and systemic __veins are oxygen-poor__ 

What is the anatomy of the heart, how is it protected, and draw the heart with labels.

The heart is a hollow-muscular muscle 

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→ The size of a fist

→ Protected by sternum (chest bone) and spine bone which allows for chest compression as a way to pump blood across someone's body when the heart stops   

How is the blood pumped in the heart?

**Heart as a Dual Pump** 

Right & left sides contract at the same time

Both sides of the heart simultaneously pump **equal** amounts of blood thus they pump as one b/c it is a closed system 

How does the heart pump equal amount of blood through the right and left pump?

***Comparison of Right & Left Pumps***

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**→ Pulmonary circuit (right side)** is low-pressure, low-resistance as it only pumps blood to lungs

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**→ Systemic circuit (left side)** is a high-pressure, high-resistance as it must move through the entire body. This is achieved by this left side containing more muscle to pump blood throughout

What are heart valves and why are they important?

Valves are doorways that separate the heart chambers

→ Separate the atrium from ventricle

→ Separate ventricle from arteries 

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Important for pumping blood in a one-way direction 

→ When pressure is greater behind the valve, it opens. When pressure is great in front of valve, it closes. Note 

that when pressure is greater in front of valve, it doesn't open in opposite direction; that is, it’s a one-way valve 

What are the 2 types of valves?

**1. Atrioventiru lar (AV) Valves**              **2. Semilunar Valves**           

→ Right AV valve (tricuspid)       → Aortic or pulmonary valve

→ Left AV valve (bicuspid)      

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⇒ separate atrium from ventricles ⇒ separate ventricles from arteries

What valves are missing? Why do you think these are not there?

There are no valves between veins and atria; this is b/c the pressure in atria never exceeds pressure in the veins (blood doesn’t flow back into the veins) thus it is simply not required 

What is the heart made up of and how are they arranged in the heart?

Heart is made up of cardiac muscle fibres 

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These fibres are arranged in a unique way, they spiral around the ventricle to “wring” the blood out during contraction which is a more efficient contraction motion to get blood out

Describe the cardiac muscle fibers, what does it consist of?

Looking closely at these cardiac muscle fibres, these are individual cells; these muscle cells are joined together to intercalated disks 

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At intercalated disks, there are 2 key junctions**:**

**1. Desmosome** - Holding cells together 

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**2. Gap junction -**  The window between 2 cells 

→ This allows for **ex.** Electrolytes (Na+) pass from one cell to another 

→ This allows for our heart to function as one unit thus one cell is stimulated, all other cells will be stimulated 

Contraction of cardiac muscles is stimulated by:

→ Calcium binding to troponin & revealing binding sites on actin

What is the electrical activity of the heart?

Heartbeats rhythmically as a result of self-induced action potentials thus doesn't require anything to stimulate it

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Two specialized types of cardiac muscle cells\*\*:\*\*

**1. Contractile cells (99%) -** cells that contract

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**2. Autorhythmic cells (~1%) -** pacemaker cells

→ These automatically induce APs which spreads throughout the whole heart and contractile cells

How can autorythmatic cells self-induce AP?

→ These cells are auto-rhythmic due to containing specialized channels called funny channels; these only open when mV is negative (-60mV)

What is Pacemaker Activity of Cardiac Autorhythmic Cells?

1\. Funny channels open at low membrane potentials (-60mV) and allow Na+ to enter the cell. ICa T (T-type Ca+ channels) also allows some Ca+ to leak in. Cell slowly depolarizes 

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2\. At threshold, ICa L (voltage-gated Ca+ channels) open permitting rapid influx of Ca+ and rapid depolarization then close

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3\. Opening of voltage-gated K+ channels allows K+ to leave the cell causing repolarization 

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4\. Once cell is -60, Funny and ICa T channels open again causing depolarization and cycle repeats

What is the Excitation – Contraction Coupling in Cardiac Contractile Cells activity?

Contractile and autorhythmic cells have different ways of being stimulated; we just went out how autorhythmic (pacemaker) cells allow contraction to occur, now let’s look at contractile cells 

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Contractile cells don’t have pacemaker potentials thus they must be stimulated by something. At rest, these cells have a resting potential of -90mV which is the equilibrium potential of K+ which is due to some K+ channels being open at rest. When a neighbouring cell undergoes pacemaker autorhythmic AP and depolarizes, this cell will also depolarize and undergo AP thus rapid influx of Na+ into cell. These channels then close and K+ channels open and enter cell which causes cell to be slightly negative. Then Ca+ will also open up and enter the cell while K+ remains open but begin to leave the cell. Movement of (+) charges in both directions causes membrane potential to not change and plateau. Ca+ channels then close and since K+ channels remain open, the cell returns back to -90mV.

 In autorhythmic cells, slow depolarization occurs due to:

**→ Opening of funny channels that allow Na+ to enter the cell**

In contractile cells, the action potential (spike) occurs due to:

→Opening of voltage-gated Na+ channels

In the plateau phase of cardiac contractile cell action potentials:

→ Ca+ enters, which ultimately stimulates muscle contraction (the Ca+ that enters the cell during the plateau will bind to troponin and cause the muscle contraction)

Are autorythmic cells dispersed or found in certain areas? explain

Autorhythmic cells aren’t dispersed, they are concentrated in certain regions 

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These regions are: SA node fibres, AV node fibres, Bundle of His and Purkinje fibres 

On their own, how many AP can SA node , AV node , and Bundle of His and Purkinje fibres fire per min?

When they are left on their one**:**

→ SA node (normal pacemaker) fires 70-80 AP/min

→ AV node fires 40-60 AP/min

→ Bundles of His and Purkinje fibres fire 20-40 AP/min

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Since SA node is the normal pacemaker, it determines the rate of firing for the whole heart thus as it fires AP, it travels throughout the entire heart and to those certain areas (AV node, BOF and PF) to make them go at a faster rate than it would on their own

What heart rate would you expect if someone had damage to their SA node?

→40-60 as AV node would take over

How does Spread of Cardiac Excitation occur in the heart?

SA node fires 70-80 AP/min and spread through the atria. There’s a layer of nonconductive tissue separating atrium and ventricles thus for AP to travel throughout the heart, it will go through the AV node, to the Bundles of His then Purkinje fibres and into the ventricles. 

Action potentials are briefly delayed at the AV node. What is the purpose of this? Is this beneficial to cardiac contraction?

**→ Allows atria to contact before the vehicles thus allowing ventricles to fill before contracting this coordination is important as, without the coordinating, this doesn't allow the blood to be pumped effectively**

What is ECG?

**The ECG (electrocardiogram) = R**ecording of the electrical activity that occurs through the heart

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electrical activity = depolarization of atrium and ventricles

What does the ECG record?

**It records the electrical activity that reaches body surface (skin)**

→ Not direct recording of actual electrical activity of heart

→ Compares the movement & direction of current at **two different body points**, not the actual potential

Explain what we will see in an Electrocardiogram Waveforms in Lead II (right arm to right leg)

→ We start with SA node which fires AP thus atria depolarize **(P wave)**

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→ As we pass the AV node, there will be an AV nodal delay which is significant to allow allow atria to contact before the vehicles **(PR segment)**

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→ After we pass the Av node, Bundles of His and Purkinje fibers, we enter the ventricles which depolarize and simultaneously the atria’s will repolarize **(QRS complex)**

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→ Ventricles then contract and empty out the blood into arteries **(ST segment)**

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**→** The ventricles then repolarize **(T wave)**

**Q.** Shortening/lengthening of the PR segment indicates:

**→ Less delay in conduction from atria to AV node**

**→ More delay in conduction from atria to AV**

What can we predict using ECG?

We can predict the abnormalities in rates and rhymes using ECG

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**Rate** - Beats per minute (normal between 60-100)

**→ Tachy-cardia:** A rapid heart rate of more than 100 beats per minute

**→ Brady-cardia:** A slow heart rate of less than 60 beats per minute

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**Rhythm -** Spacing of ECG waves (P QRS T — P QRS T — P QRS T …)

**→ Ar-rhythmia:** Variation from normal rhythm and sequence of excitation of heart (not a nice PQRST)

**Ex.**  ventricular fibrillation

What happens during complete heart block?

**→ Loss of synchronization between atria and ventricles (P is firing but QRS isn’t)**

Explain the Cardiac Cycle along with the how the volume of blood changes

**Diastole -** cardiac muscles __relaxing__ and chambers filling with blood (filling)

**Systole -** cardiac muscles __contracting__ and pushing out blood (emptying)

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**End diastolic volume (EDV):** Volume of blood in the left ventricle before ventricles contract 

**End systolic volume (ESV):** Volume of blood in the left ventricle after contraction 

**Stroke volume: EDV (-) ESV (amount of blood pushed out of the heart)**

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**1st phase: Atrial and ventricular diastole**

Atria and ventricles are relaxed and blood flows from the veins, into the atria and ventricles on both sides. Volume of blood in ventricles slowly increases

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**2nd phase: Atrial Systole**

Atria depolarize and contract and push the last bit of blood into the ventricles. Volume of blood in ventricles reaches the maximum **(End diastolic volume (EDV))**

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**3rd phase: Isovolumetric ventricular contraction (systole)**

When ventricles first contract, the pressure in there increases which results in AV valves to close and at some point, the semilunar valves will also be shut; this is to allow for ventricles to build up pressure thus no blood is moving in or out. Volume of blood in ventricles doesn’t change

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**4th phase: Ventricular Systole**

Pressure build up and opens semilunar valves thus blood rush into arteries. Volume of blood in ventricles decreases and reached minimum **(End systolic volume (ESV))**

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**5th phase: Isovolumetric ventricular relaxation (diastole)**

When ventricles first relax, semilunar and AV valves are both closed until pressure builds up in the atria’s **.** At this point, ventricle valves are closed. Volume of blood in ventricles does not change

The following volumes are observed in a normal cardiac cycle: Volume of blood in left ventricle (ventricular diastole) after atrial contraction: 120 mL Volume of blood in left ventricle at the end of ventricular systole: 50 mL What is the stroke volume?

→ Subtract EDV with ESV to get 120-50=70

What are the two major heart sound?

**Two major heart sounds** 

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1\.  First is low-pitched and soft “lub”

→ Closure of AV valves 

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2\. Second is higher-pitched “dup”

→ Closure of the aortic + pulmonary valves

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**Note:** What we are actually hearing is the backsplash of the blood when the valves close

What do we exactly hear these heart sounds during the heart cycle?

1. The “lub” is heard during Isovolumetric ventricular contraction (systole)

→ This is where the ventricle just begins to contract and the closure of AV valves result in “lub” sound

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2. The “dup” is heard during Isovolumetric ventricular relaxation (diastole)

→ This is where the ventricle just begins to relax and the closure of semilunar valve result in “dub” sound

The name for an abnormal heart sound is:

**→ Murmur (reflect difference in ventricle closing)**

What occurs immediately after the P wave?

**→ Atrial contraction; after atrial depolarize, atrial will contract**

A decrease in the time of the ST segment indicates:

**→ At ST, ventricles contract and pump blood, thus there will be shorter ventricular systole**

What is the stroke volume in the figure below?

→ EDV(135) - ESV(65) = 70

what is cardiac outputs and how is it controlled?

Cardiac output: Volume of blood ejected by *each* ventricle per minute

→Again, both ventricles eject the same volume of blood

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**Cardiac output** (CO) - **To determine how much blood the heart is pumping per minute we use the heart rate and/or stroke volume**

heart rate × stroke volume = 70 beats/min × 70 ml/beat = **4900 ml/min** **or 5 litres/min (at rest)** \\n

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To change cardiac output we must increase/decrease either heart rate or stroke volume (or both)

The sympathetic nervous system releases ______, which causes heart rate to _________

→ Norepinephrine & epinephrine, increase

How do we control cardiac output by changing heart rate?

**Heart Rate (speed of beat)**

Heart rate is varied by altering balance of **parasympathetic (rest and digest)** and **sympathetic (flight or fight)** influence on **SA node**

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→ Parasympathetic stimulation slows the heart rate

* By delaying the slow depolarization

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→ Sympathetic stimulation speeds it up

* By speeding up depolarization

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***Autonomic Control of SA Node Activity and Heart Rate***

The pacemaker on SA node(dotted line), on its own, it beats this rate (slowly depolarize, AP and repeat)

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When parasynthetic sys acts on SA node, it makes SA node slowly depolarize, reach AP and repeat; heart rate is low

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When sympathetic sys acts on SA node, it makes SA node rapidly depolarize, reach AP and repeat; heart rate is high

How do we control cardiac output by changing stroke volume?

**Stroke Volume (volume of blood of each beat)**

Volume of blood ejected from the left ventricle per heartbeat

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Influenced by three factors**:** 

1\. Preload - amount of blood entering heart from veins

2\. Afterload - resistance that needs to be overcome to eject blood from heart 

3\. Contractility - heart contraction

How does Preload factor change stroke volume?

***1. Preload: Frank-Starling Law of the Heart***

Law of the heart: The more the heart is filled (**preload**) the more it will be **stretched** and greater **stretch** leads to greater **force of contraction**, which leads to greater **stroke volume**

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→ Larger preload leads to larger stroke volume

→ Smaller preload leads to smaller stroke volume

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**Q.** The volume of the ventricle at its maximum filling capacity is also called the:

**→ End Diastolic Volume**

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**Frank-Starling Curve**

For any increase EDV (x-axis A to B), there will be a corresponding increase in stroke volume (y-axis A to B)

How does Arfterload factor change stroke volume?

**2. Afterload**

The resistance that the heart must overcome to open the aortic valve

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This is influenced by pressure in the arteries**:**

→ High blood pressure (hypertension) in arteries = harder to open valves

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→ Athero-scler-osis**:** build-up of plaques in arteries = high blood pressure thus harder to open valves

How does Contractility factor change stroke volume?

**3. Contractility**

Sympathetic stimulation affects heart rate and **heart contraction** but **increases strength of heart contraction**

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→ Increase in strength of heart contraction = stroke volume

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→ Increases Ca+ influx to cells allowing more myosin cross-bridges to form with actin

Summary Control of Cardiac Output

How can we estimate the efficiency of cardiac contraction?

**Ejection Fraction** 

Efficiency of cardiac contraction can be estimated by calculating an **ejection fraction**

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Ejection fraction tell us the percentage of blood pumped from the left ventricle each cycle 

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→ Normal \~ 50-70% but decreases if there is heart failure

Complete this table

What is the key concept Vascular System?

Key concept: Two **“closed loops”**

→ Vessels (arteries and veins) do not open at the ends

What does parallel Blood flow indicate, what does it ensure?

**Parallel Blood Flow**

Same volume of blood is pumped into pulmonary (right) as into systemic (left) circulation

**Ex.** If SV = 70 ml, 70 ml going into lungs and 70 ml going into systemic 

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Parallel system of blood flow **ensures** all organs receive **same quality** of oxygenated blood, without it, this will cause for digestive system to take most blood, along with liver, and less to other organs

What is the exception of the parallel Blood flow?

**Exception:** Portal circulation

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**Portal veins** connect two organs (not including the heart) 

**Ex.** Hepatic portal circulation connects small intestine to liver where newly absorbed nutrients are processed

What is the key point regarding the vascular system?

Exchange of material occurs at capillaries and all adjustments to blood flow work to ensure that the capillaries of body organs receive the correct amount of blood

How does our body adjust blood flow?

**The Physics of Blood Flow**

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**F =** flow rate of blood through a vessel

→ Volume of blood passing through a vessel per unit of time

→ This is adjusted by 2 factors\*\*:\*\* pressure and resistance

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**ΔP =** pressure gradient (pressure from beginning to end of vessel)

**R =** resistance of blood vessels

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The rate of blood flow through a vessel is directly proportional to the **pressure gradient** and inversely proportional to **vascular resistance** (increase resistance, less flow)

How does pressure play as a factor in flow of blood through a vessel?

Pressure is the force exerted by blood on the blood vessels and pressure gradient is directly proportional to blood flow

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Blood flows from an area of higher pressure (less space)  to an area of lower pressure (more space)

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→ **Pressure gradients** are the **driving force** for moving blood forward through the vascular system (difference in pressure)

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**Pressures throughout the Systemic Circulation**

Blood flows from high to low pressure

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→ From the beginning, the pressure increase rapidly and decreases rapidly twice in the heart 

→ Pressure then continues to decrease from arteries, to capillaries, and finally veins

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→ The line that goes down signifies the rate of blood flow gradually decreasing as pressure decreases

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**Relationship of Flow to the Pressure Gradient in a Vessel**

The blood in any vessels always flow down the pressure gradient  

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→ In the first blood vessel, blood flows from 50mmHg to 10mmHg; the change of pressure is 40mmHg whereas in the second blood vessle, blood flows from 90mmHg to 10mmHg; the change of pressure is 80mmHg

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→ The pressure gradient in blood vessel #2 is 2 times greater than blood vessel #1 thus there is more flow of blood

If the pressure down vessel 1 decreases from 120 mmHg to 90 mmHg and pressure in vessel 2 decreases from 100 to 40 mmHg, how will this affect flow rate?

→ Vessel 1: ∆P=30 and Vessel 2: ∆P=60; Flow will be 2x lower in Vessel 1 than Vessel 2

How does resistance play as a factor in flow of blood through a vessel?

**Resistance -** Measure of opposition to blood flow through a vessel

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Flow is inversely related to resistance

→ Greater resistance = lower blood flow

→ Lower resistance = higher blood flow

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Major determinant of resistance to flow is **vessel radius (radius describes size of vessel)**

→ Resistance is inversely proportional to radius (R is proportional to 1/r4)

→ Because F to 1/R, and R ⍺ 1/r4, we can rewrite this as F ⍺ r4 OR **flow is directly proportional to the vessel radius**

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→ Big radius/vessel = lower resistance (blood flows easily)

→ Smaller radius/vessel = higher resistance (blood flows harder)

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**Relationship of Resistance and Flow to the Vessel Radius**

Both blood vessels have same pressure gradient but different radius/size

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→ Blood vessel #1 is 1mm in size whereas blood vessel #2 is 2mmin size thus its radius is 2 times larger 

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→ Resistance in blood vessel #2 is 1/16 higher than blood vessel #1

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→ Flow is blood vessel #2 is 16 times larger than in blood vessel #1

If vessel 1 has a 3 mm radius and vessel 2 has a 1 mm radius, how will this affect flow rate?

→ Since F∝ r4, flow will be F∝ 34=81 thus flow will be 81x higher through vessel #1 than vessel #2

What are the key points regarding pressure and resistance?

**Pressure gradients** are the main driving force pushing blood through the vascular system

→ Blood flows from an area of higher pressure to lower pressure

→ A greater pressure gradient = greater flow

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**Resistance** opposes blood flow. Blood vessel radius is the main determinant of resistance

→ Larger radius = less resistance = greater flow

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If we want more blood to flow to muscles, blood vessels dilate 

If we want less blood to flow to muscles, blood vessels constrict 

What are the types of vessels in human body?

**Arteries -** Carry blood from heart to tissues

→ High-pressure

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**Venules -** Formed when capillaries rejoin

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**Veins -** Venules region; return blood to heart

→ Volume reserves

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**Arterioles -** Arteries branch into arterioles; main site of resistance, control blood flow to organs/capillaries 

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**Capillaries -** Arterioles branch into capillaries; smallest of vessels across which all exchanges are made with surrounding cells

What is the anatomy of blood vessels?

All vessels (except capillaries) have an endothelium, basement membrane, smooth muscle, and connective tissue layer

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**Arteries** - Have additional elastic tissue to enable stretching during ventricular systole

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**Capillaries** - Only thin layer of endothelium (epithelial cells) and basement membrane; allows for transfer of material in and out of capillaries at tissues 

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**Veins** - Also has additional elastic tissue and contain Venous valves to prevent backflow of blood as pressure is lowest is veins 

What are the functions of arteries?

Specialized for two functions

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→ Serve as **rapid-transit** **passageways** for blood from heart to organs

* Due to large radius, arteries offer little resistance to blood flow (thus higher blood flow)

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→ Act as **pressure reservoir/supply** to provide driving force for blood when heart is relaxing

* When heart is in diastole, elastic recoil of arteries continues to push blood forward

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*Arteries as a Pressure Reservoir*

→ As heart contract, arteries **expand** to provide flow of blood into smaller blood vessels

→ As heart relax, arteries **contract** to continue flow of blood into smaller blood vessels thus constant flow of blood

Explain Arterial Blood Pressure

**Systolic pressure - Ventricles contracting**

→ Peak pressure exerted by ejected blood against vessel walls during cardiac systole, averages 120 mmHg

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**Diastolic pressure - Ventricles relaxing**

→ Minimum pressure in arteries when blood is draining off into vessels downstream, averages 80 mmHg

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**Pulse Pressure:** Difference in systolic and diastolic blood pressures, imporant to determine mean pressure

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**Mean arterial pressure:** Average pressure driving blood forward into tissues throughout cardiac cycle 

→ Mean arterial pressure = diastolic pressure + ⅓ pulse pressure

→ We are mainly in diastolic pressure than systolic pressure

What is the pulse pressure in the figure? What is the mean arterial pressure in the figure?

→ SP(120) - DP( 80) = 40

→DP + ⅓PP = 80 +⅓(40) = 93

Explain Pressures throughout the Systemic Circulation

→ Once again, we see ventricles contracting and relaxing twice in the heart and how pressure rapidly increases and decreases 

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→ Arteries will also have high pressure; as they contract, there will be systolic pressure and as they relax, there will be diastolic pressure 

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→ The mean pressure for normal person is 93mmHg

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→ As we branch into arterioles, there is a rapid decrease in pressure as these vessels are main resistance vessels due to branching into different organs and a continued decrease in pressure

What are arterioles and its special trait?

Branches of arteries at major organs

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Trait: Major resistance vessels

Why does the size of arterioles must be adjusted?

Radius supplying individual organs can be adjusted independently to\*\*:\*\*

→ distribute cardiac output among systemic organs, depending on body’s momentary needs

→ help regulate blood pressure

**How do arterioles change their radius/size to alternate resistance?**

**Arteriolar Vasoconstriction and Vasodilation**

Smooth muscles hold vascular **tone**

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**Arteriolar Vasoconstriction:** Narrowing/constriction of vessel to ↑resistance and ↓flow

**Arteriolar Vasodilation:** Widening/dilation of vessel to ↓resistance and ↑flow

What are the factors that can influence arteriolar radius?

**Factors Influencing Arteriolar Radius**

**Local Effects -** influence blood flow to specific organs

→ Chemical influences

* Local metabolic change
* Releasing of chemical (**Ex.** Histamine release)

→ Physical influences

* Local application of heat or cold

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**External Effects -** influence total peripheral resistance (blood pressure)

→ Comes from using the sympathetic NS 

→ Important for regulating blood pressure 

How does Local Metabolic Changes play as a factor in influencing arteriolar radius?

How does Releasing of chemical, such as histamine play as a factor in influencing arteriolar radius?

→ Compound released from connective tissues and white blood cells in response to tissue injury or allergic response

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→Promotes vasodilation of arterioles and increased blood flow to the area (redness and swelling on injured areas)

How does Local application of heat or cold play as a factor in influencing arteriolar radius?

Cold causes **vasoconstriction** 

→ When injured, swelling and increase blood flow occur in those areas; we place cold objects to contract vessels and reduce blood flow

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Heat causes **vasodilation** 

→ When undergoing heat therapy, we place hot objects to dilate vessels and increase blood flow 

**The main force driving blood through the vascular system is:**

→ Mean arterial pressure

Control of blood flow to organs occurs mainly through:

→ Vasoconstriction and dilation of arterioles

What are capillaries main function and how does this effect its anatomy?

Main function: Sites of exchange between blood and inter-stitial fluid surrounding cells

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Since capillaries must exchange materials, they are made up of thin-walled, have small-radius, and are extensively branched

→ Consist of endothelium and basement membrane only

What is the control of capillary blood flow?

Since capillaries are extensively branched, body can’t afford to have full blood flow through all capillaries thus body must control how much flows to each capillary blood to ensure adequate blood is received in each tissue. **Arterioles vasoconstriction and vasodilation** is one mechanism, another is capillaries containing **preca-pillary sphincters**

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Capillaries surrounded by precapillary sphincters

→ Contraction of sphincters reduces blood flowing into capillaries in an organ; relaxation of sphincters has opposite effect

→ Precapillary sphincters and arterioles have complementary actions

When a capillary bed needs more blood flow**:**                              

→ Arterioles dilate                                                         

→ Precapillary sphincters open          

→ Increased blood flow through capillary

When a capillary bed needs less blood flow**:**

→ Arterioles constrict

→ Precapillary sphincters close

→ Decreased blood flow through capillary

What is the Capillary Exchange Mechanisms

Since capillaries are composed of a single layer of endothelial cells, there are 3 ways materials can get through a capillary wall:

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1\. Lipid-soluble + gases - simple diffusion

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2\. H2O and water-soluble substances (**Ex.** electrolytes (Na+ and K+), glucose, and amino acids) - water-filled pores

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3\. Proteins - vesicular transport

→ when necessary

What drives movement across capillaries?

Movement of substances between blood and surrounding tissues across capillary walls is driven by two factors**:**

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→ **Passive diffusion** down \[ \] gradients, __primary__ mechanism for exchanging individual solutes

→ **Bulk flow** net movement of fluid through capillary walls

In an exercising muscle, we would likely see net diffusion of ____ from the capillary into the interstitial fluid

→ Oxygen and glucose to feed cells during exercise

How does passive diffusion drive movement across capillaries?

Solutes cross primarily by diffusion down concentration gradients

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→ O2 and Glucose will travel down their \[ \] gradient into interstitial fluid and

to tissue cells 

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→ CO2 and wastes increase in cells and travel from interstitial fluid and back to blood

How does bulk flow drive movement across capillaries?

**Bulk Flow:** Net movement of fluid through capillary wall

→ regulate the distribution of fluid between plasma and interstitial fluid

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Fluid movement is determined by the balance of inward and outward pressures/forces

→ When outward pressure from capillary exceeds inward pressure, fluid is pushed out through pores **(filtration)**

→ When inward-driving pressures exceed outward pressures, fluid moves from interstitial fluid into capillaries **(reabsorption)**

What are the Forces Influencing Bulk Flow?

Main forces:

__Capillary blood pressure (Pc) - Outward pressure__

→ Fluid or hydrostatic pressure exerted by blood tends to force fluid out of capillary walls

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__Plasma-colloid osmotic pressure (Plasma oncotic pressure) (π) - Inward pressure__

→ Oncotic pressure caused by colloidal dispersion of plasma proteins and it encourages fluid movement into capillaries

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Minor forces:

__Interstitial fluid hydrostatic pressure - Inward pressure__

→ Pressure exerted by interstitial fluid and it tends to force fluid into capillaries, but is very low

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__Interstitial fluid–colloid osmotic pressure (Interstitial oncotic pressure) - Outward pressure__

→ Plasma proteins in interstitial fluid but it’s very low and doesn’t contribute significantly to bulk flow

What is the Net Forces Influencing Bulk Flow

At the arterial end:

→ Capillary blood pressure (Pc) outward force exceeds inward force from the oncotic pressure of plasma (⫪p)

→ Fluid is pushed out of capillary (net filtration)

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At the venous end:

→ Osmotic pressure of plasma (⫪p) inward force exceeds the outward force of capillary blood pressure (Pc)

→ Fluid moves back into capillary (net reabsorption)

Some fluid out of the capillaries will be left behind. What will pick them up and how?

The Lymphatic System

Extensive network of one-way vessels which provides a route by which fluid can be returned from interstitial spaces back to blood

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Unlike the circulatory system being one continuous loop, lymphatic system begins as small, blind-ended terminal lymph vessels

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These blind-ended lymph vessels have overlapping endothelial cells that when pressure/interstitial fluid build-up, these overlaps open up and pick up the extra fluid These then converge to form lymph vessels which empty the extra fluid into venous system near where blood enters right atrium

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Without the lymph system, 3L/day of this fluid will leave the blood and be deposited into tissues 

**In addition to returning excess filtered fluids to the blood, the lymphatic system is important for:** 

→ Defense against disease (lymph nodes produce WBC); Transport of absorbed fat (during digestion)

If someone has very high blood pressure, and the capillary blood pressure does not decrease from the arterial to venous ends, how would this affect bulk flow of fluids?

→ Net filtration occurs through whole vessel thus ↓fluid in blood and it accumulates in tissue

 If someone had very low intakes of protein and their plasma protein concentration dropped severely, how would this influence bulk flow of fluids?

→ Net filtration occurs through whole vessel thus ↓fluid in blood and it accumulates in tissue

What is the condition called that occurs when there’s a lot of fluid in tissues?

Swelling of tissues occurs when too much interstitial fluid accumulates

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Causes of oede-ma:

→ Increased venous pressure

→ Reduced concentration of plasma proteins

→ Blockage of lymph vessels (lymph sys picks up additional fluid)

What is the vascular system and what are veins characteristics?

Venous system transports blood back to heart

→ Capillaries drain into venules

→ Venules converge to form small veins that exit organs

→ Smaller veins merge to form larger vessels

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 Vein

→ Large radius offers little resistance to blood flow

→ Serves as blood reservoir (hold a lot of blood)

What is venous return?

Amount of blood returning to the heart from the veins

→ Since viens hold extra blood, body can adjust the amount of blood returning to the heart which influences end-diastolic volume, which then influences stroke volume and cardiac output

End diastolic volume (EDV) is the _____

→ Maximum of amount of blood in the filled ventricle

**Stroke volume is the amount of blood ejected from the heart each cycle/beat. Stroke volume is influenced by:**

**→ End diastolic volume/Preload(the more heart fills, the more heart stretches thus more blood ejection; Afterload; Contractility**

Cardiac output is calculated as:

→ HR x SV or (EDV-ESV = SV) x HR

Explain Pressures throughout the Systemic Circulation

As stated before, blood flows from high pressure to low pressure

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We can observe that blood pressure decrease as we get into the veins

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Pressure is what drives blood forwards and since blood must return back to the heart, there must be other mechanisms to push blood from veins to the heart

What are Factors That Facilitate Venous Return

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1. **Blood Volume in Venous system**

Increase in Venous pressure = increase in pressure gradient

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Influenced by: Bulk flow shift of fluid from interstitial fluid into plasma (into capillaries) and salt + water retention

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2. **Respiratory Pump**

Respiratory pump\*\*:\*\* Change of pressure from breathing

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When breathing in, chest cavity expands and reduces pressure in chest cavity

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This results in veins in chest cavity having low blood pressure thus blood moves from higher pressure to lower pressure, this forces blood in veins to be pumped to the heart

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3. **Skeletal Muscle Pump**

Veins are surrounded by skeletal muscle

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When skeletal muscle contract, they cause veins to contract thus pushes blood back to the heart

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4. **Venous Valves**

Veins are the only blood vessels that have venous valves

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Venous allow for flow of blood in one-direction back to the heart thus blood can’t flow backwards; they work with skeletal muscle to pump the blood in one direction

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5. **Increase Sympathetic vasocontraction**

Constriction of veins result in high pressure in veins thus blood can only be returned to lower pressure area in the heart

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6. **Cardiac Contraction**

Since the circulatory system in a closed loop, the pressure from arteries expands into the veins to push blood into heart

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7. **Cardiac Suction**

Since blood moves from high to low blood pressure, the low pressure in the heart sucks the blood from veins to return to heart

What is blood pressure, and where is it highest at?

Blood pressure is the force exerted by blood on vessels

→ Blood flows from an area of higher pressure to an area of lower pressure (flows down its \[ \] gradient)

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Arteries are the main pressure vessels in the circulatory system (hold most pressure)

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Mean arterial pressure (**MAP**, blood pressure) is the main force driving blood flow through circulatory system (heart is the cause of blood pressure whereas pressure in arteires drives blood flow)

What is the physics behind Blood Flow & Blood Pressure through the Entire Circulatory System

This formula applies to blood flow through a single vessel but we can also use this to describe flow through the entire circulatory system and regulation of MAP

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F = cardiac output (CO, mL/min) 

ΔP = mean arterial pressure (MAP) 

       → Pressure gradient is high pressure - low pressure thus MAP - VP but VP ≈ 0

       → Thus, pressure gradient will equal MAP

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R = total peripheral resistance (TPR), resistance through all blood vessels of the system

What determines blood pressure?

The two main determinants of MAP are **cardiac output (CO)** and **total peripheral resistance (TPR)**, if either increases, blood pressure (MAP) also increases

What determines mean arterial blood pressure?

Mean arterial blood pressure (MAP) is determined by **cardiac output (CO)** and **total peripheral resistance (TPR**) 

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**CO is determined by heart rate and stroke volume** 

→ Heart rate is determined by parasympathetic and sympathetic inputs 

→ Stroke volume is determined by contractility (which is increased by sympathetic stimulation), venous return, and afterload 

→ Venous return is enhanced by the respiratory pump, skeletal muscle pump, sympathetic nervous system, cardiac pressure (moves blood forward in one direction), cardiac suction effect, and blood volume 

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**TPR is influenced by arteriolar radius and blood viscosity (thickness)**

→ Arteriolar radius is determined by local metabolic control (control blood flow into tissues) and extrinsic vasoconstriction/vasodilation control (control all arteries in system) 

→ Blood viscosity is usually constant and thus can be ignored