There is a systemic and pulmonary circuits that is in series. 

In the systemic circuit: The right side of the heart pumps blood to the lungs and the left side of the heart pumps blood to the systemic circulation. 

parallel

are independent (better to have more paths)

decreases

Arteries has the highest

Then capillaries

Veins have the lowest

120/80

2-7

(The pressure across the wall x radius)/ wall thickness

T = (Ptm x R)/ (M)

Big vessels that have a large diameter

Aorta

inversely

lower

1/3

2/3

Longitudinal

Circular

Stretch and Recoil

Distribute

Circular smooth muscle

resistance

exchange

fluid flux

Longitudinal VSM

Compliance

Refers to the total quantity of blood that can be stored in a given portion of the circulation for each mm rise in pressure.

C= Volume change/ Pressure change

A pressure gradient

From high pressure to a low pressure

from arteries to veins

Ohm's Law

Flow = Q

Q = ΔP/R

where P = pressure

R= resistance to flow

R ∞ η/r⁴

So Resistance increases as the viscosity increases.

And if the radius was to increase, this will decrease the resistance by a factor of 10^4.

Wider

If you increase r then you decrease the resistance.

ΔP = Cardiac output x Total resistance

ΔP = P aorta - P Vena cava

ΔP  = CO x TPR

(where TPR is the total peripheral resistance)

Increase the pressure in the arteries

or

decrease the resistance in the arteriole

By pumping a volume of blood against arterial pressure

if you increase either the pressure or volume pumped by the heart you have more work

Capillaries

1 single celled endothelial used for exchage/fluid flux

Hydrostatic pressure

Oncotic pressure

1. Flux occurs down a hydrostatic pressure gradient

2. Flux occurs into the area with High oncotic P

3. Flux depends on permeability

NFP = (P_c-P_if) - (∏_p-∏_if)

Pc = pressure in capillary

Pif = pressure in intersitial fluid

where P is the change in hydrostatic pressure

And ∏ is the change in oncotic pressure

out

+ NFP

When there is an increase in interstitial fluid pressure.

If more fluid flows out of the capillaries

and if there is an elevated capillary pressure

They contract surrounding muscles (this increases the pressure)

Pulsate adjacent arteries

And compress the tissues

Filtration coefficient (Fc)

permeability

Liver

Brain

You can constrict arterioles which lowers Pc

This makes more fluid enter the capillaries from the Interstitium.

If you lower the # of protein then you decrease your ∏p which makes more fluid leave the capillaries and create Edema.

Atria

ventricles

pressure (will increase if the chamber size decreases)

they have to pump blood out of the heart.

They do additional work

Mitral valve

left side

atrial

right

Systole

Diastole

1. The mitral valve closes (makes first heart sound)

sn. the other valves are also closed for a short period of time

2. Ventricular pressure rises abruptly because all the valves are closed

3. Ventricles continue to contract until the left ventricular pressure is slightly higher than aortic pressure and right ventricular pressure is higher than pulmonary artery pressure.

4. Mitral valve open and signals the ejection period.

1. The ventricles relax

2. This causes a steep fall in intraventricular pressure

3. The blood from the large arteries wants to flow back towards the ventricles but this causes the Aortic and Pulmonic valves to snap shut.

4. Aortic closure of valves causes the 2nd heart sound

5. The ventricular volume remains the same but the pressure drops as the valves stay closed.

1. Ventricular filling occurs

2. When ventricular presure is less than atrial pressure, the AV vlaves open

2. Blood flows from the atria into ventricles

3. Most blood is fileld during the first thrid of diastole which is aka rapid filling period.

4. Middle third of diastole the inflow is at a standstill.

5. the last third of diastole is marked bny atrial contraction which gives an additional thrust to ventricular filling.

End diastolic Volume

50 mL (end systolic volume)

Stroke volume = EDV - ESV

End diasolic volume - the end systolic volume

120-50 = 70 ml

ejection fraction is the fraction of diastolic volume that is ejected from the heart during systole.

Ejection fraction  = SV/EDV

Stroke volume/ End diastolic volume

it determines the pump efficiency

Mitral valve prolapse

Mitral Valve Regurgitation

1. It can be Asymptomatic-- meaning no symptoms. Dont know they have it until they get a check up.

2. Could have midsystolic clicks

3. Could have late systolic murmurs

4. Can have chest pains (arrhythmias)

Can lead to regurgitation by rupture of the chordae.

Lead to infective endocarditis

Can form an emboli

lead to atrial/ventricular arrhythmias

1. rupture of chordae tendina

2. Rheumatic heart disease

3.Hypertrophic myopathy

4. Left ventricle enlargement

5. Infective endocarditis

6. Abnormality in valves/papillary muscles

7. Ischemic heart disease (CAD)

The volume overload of the left ventricle and atrium can lead to:

1. atrial arrhymthmias

2. pulmonary edema

3. left side heart failure

4. enlargement of LV which leads to S3

1. Thickening and calcification of the valves

2. Shortening/thickening of the chordae tendinae caused by Rheumatic fever and Strep

left ventricle

left atrium

diastole

(sn: a opening snap may preced the murmur as a result of the incrase in LA pressure)

there is a pressure overload int he atrium that can lead to

1. LA enlargement

2. Atrial arrhythmias

3. Right heart failure due to pulmonary edema

4. thrombus formation

Decreased

increased

Rheumatic fever

Congenetial valve malformations

Senile calcification

Late Systolic ejection murmur

4th sound

aortic pressure

left ventricle pressure

It is a pressure overload in the ventricles that can lead to:

1. chest pain

2. angina, syncope (Fainting)

3. Left side heart failure

4. dizzy when exercise

5. Dyspnea

6. Cyanosis

Floppy valve leaflets or deformed aortic roots that are caused by:

1. Rheumatic disease

2. congential valve defect

3. aortic root dilation

4. hypertension

5. endocarditis

1. LV dilation ventricular arrhythmias

2. fatigue, exercise intolerance

3. Angina

4. Pulmonary edema

5. Dyspnea

SA node

Sinoatrial node

1. SA node

2. Internodal = from SA to AV

3. Bachmann bundle = SA to LA

4. AV node = 2nd pacemaker

5. Bundle of His

6. Purkinje fibers = impulse to ventricles

Phase 0 = rapid D.P

Phase 1 = Early R.P.

Phase 2 = Plateau

Phase 3 = final Rapid R.P.

Phase 4 = Diastolic D.P.

Phase 0 = Na+ gates open and causes a D.P

Phase 1 = Na+ channels become inactive due to efflux of  K or influx of Cl.

Phase 2 = Plateau occurs cuz K+ permeability is low so cell stays D.P. And Ca influx into cell via L-type Ca channels.

Phase 3= Final rapid R.P. Channels close and Ca and Na influx stop. K moves out

phase 4 = membrane resting potential

It has a spontaneous phase 4 depolarization

aka

automaticity