• Delivering O₂ and nutrients to the tissues
• Removing CO₂ waste products from the tissues

• (volume of blood ejected/unit time)
• At steady state Cardiac output=Venous return

• Flow of blood anywhere in the system is the same.
• connected end-to-end

 àRight Atriumà(Tricuspid Valve)Right Ventricleà(Pulmonic Valve)Pulmonary Artery (exception, because it is carrying deoxygenated blood to the lungs)àLungsàCapillaries (Large Cross-sectional area and therefore slow velocity)àPulmonary Vein(exception, because it is carrying oxygenated blood to the heart to be distributed to the rest of the body)àLeft Atriumà(Mitral Valve) Left Ventricleà(Aortic Valve) AortaàOxygenated blood to the rest of the body! 

Pulmonary: deoxygenated blood goes from right ventrical to the lungs to get oxygenated. The blood then returns to left atrium.

Systematic: oxygenated blood goes from left ventrical to the rest of the body and then goes to the right atrium.

ventricles=arteries > capillary > vein > atrium

systematic(left heart) > pulmonary(right heart)

systematic(left) has much more pressure gradient (different possibilities depending on circumstance)

Papillary muscle tighten the Chordea tendineae to prevent backflow of blood through mitral and tricusbid valves. (atrium/ventrical valves)

What are the 2 major groups of vessels? Give an example of each:

• Conduit vessels: transports blood from A to B. example; Aorta
• Resistant vessels: regulate flow and pressure. example; Arteriole

Compliance= (Δ Volume/Δ Pressure)

Means how easily a vessel can be stretched.

• Low compliance: not easily stretched. Has alot of elastin. (arteries, atherosclerosis, vessels in old age)
• High compliance: easily stretched. Has less elastin. (veins)

• Capacity to hold blood.
• High and low are same as compliance

How hard the walls of a vessel are being stretched.

• Tension is DIRECTLY PROPORTIONAL to (Radius x Pressure)
• Aorta has the highest wall tension

• Pressure at A,B, and C are the same
• B has greater radius and thus greater wall tension.
• B is more at risk of dissection (wall tear) than A or C

Q= ΔP/R

Q:blood flow(volume)

ΔP: the pressure difference between the two ends of the vessel. 

R: vascular resistance

• Silent
• molecules adhere to each other towards middle of vessel. Vmax at center.
• Molecules flow in layers/lamina

Turbulant Flow, and what causes it.

• Noisy/Low velocity
• Fluid molecules bouncing around

-Vascular aneurysm

-Stenotic vessel (narrowing)

-AV Fistula (abnormal connection between artery and vein)

-Anemia (low hemoglobin)

Dimensionless # of flow

N_R= (Velocity x Diameter x Density)/ Viscocity

N_R< 2000→ laminar flow

N_R> 2000→ turbulent flow

Velocity= Flow/cross-section area

Velocity(speed): rate of blood displacement with respect to time. (e.g cm/s)

Flow: volume per unit time (e.g ml/s)

Velocity is INVERSELY PROPORTIONAL to cross-sectional area

Aorta has the smallest(fastest velocity)

Capillaries have the largest (slowest velocity)

R= ΔP/Q

Peripheral: use pressure between systematic arteries and veins.

Pulmonary: use pressure difference between pulmonary arteries and veins.

R= (ηL/r⁴)(8/pi)

R=resistance

η=viscosity of blood

L=length of vessel

r=radius of vessel

8/pi=constant

The fourth power of radii of vessels ar the major determinant of vascular resistance.

R is proportional to 1/r⁴

If radius decreases by 1/2 then the resistance with increase by 16 fold.

R_total= R1+ R2 +R3....

• Total resistance is always greater than individual resistance.
• Flow is equal at all points
• Pressure decreases according to the resistance that it has to overcome.

• Hypertension is caused by the constriction of arterioles. That increases Resistance through those vessels.
• All vessels before the arterioles have increased pressure and vessels after have decreased pressure.
• Hypertension treatments vasodilate the arterioles.

Parallel Resistors

1/R_total = 1/R1 + 1/R2 .....

• The reciprical of the total resistance is the sum of the recipricals of individual resistances.
• Total resistance is always smaller than any individual resistances.
• Adding a resistor wil decrease total resistance. However increasing the resistance of a resistor will increase total resistance.
• Flow in individual resistors can be adjusted independantly.
• Vessels in organs and such are arranged in parallel.
• No loss of pressure in parallel arrangement.

• % of blood that is cells. The rest is plasma.
• 40% is normal.
• Too few: Anemia
• Too many: Polycythemia
• Viscocity increase with Hematocrit

Pressure= Force/Area

• Blood pressure: force exerted by blood against any unit area of the vessel wall.
• Systolic Pressure(SP): peak aortic pressure. occurs during ejection of blood from left ventrical.
• Diastolic Pressure(DP): minimum aortic pressure.
• Pulse Pressure: SP-DP
• Mean arteriole pressure(MAP): DP + 1/3(SP)

MAP= CO x TPR

ΔP= Q x R(same thing)

CO: Cardiac Output

TPR: Total peripheral resistance

Pressure ↓

• increase stroke volume
• decrease compliance of arteriole tree

• decrease in total peripheral resistance(TPR)
• MAP= CO x TPR

• Increase stroke volume
• Decrease in compliance of arteriole tree
• Decrease TPR

• The Femoral Artery has lower diastolic pressure which allows it to have a lower mean arteriole pressure.(MAP)

• Hardening of arteries.
• Causes Systolic pressure to rise.

• narrowing of Aorta
• Decreases systolic bloop pressure

• Blood from aorta goes back into pulmonary artery.
• Systolic Pressure increase
• Diastolic pressure decreases

• Aortic valve is damaged.
• Increase in Systolic Pressure
• Decrease in Diastolic Pressure

Decrease in Compliance/Elasticity

• Pressure in the right atrium.
• Normally=0
• Can have back up of blood(weakness of right atrium) or conjection of fluid in veins. Both would raise the pressure and lead to heart failure

• Enlarged or twisted veins
• Due to incompetence of veneous valves.

• degree of distension of neck veins.
• neck vein starts to protrude when the right atrial pressure increases to 10mmHg (heart failure)

• Blood pressure is higher at your feet than it is at your head.

SA node→ AV node→ AV bundle→ right and left bundle branches→ purkinje fibers→ ventricular fibers (from endocardium to epicardium)

Significance: It allowsventricular filling.

Mechanism: Small number of gap junctions

Fibrous tissue between atria and ventricle act as insulator

Purkinje fibers are the fastest.  Allows ventrical to contract fast.

AV node is the slowest.

SA node: 60-100 per minute

AV node: 40-60 per minute

AV bundle/bundle of His: 40 per minute

Purkinje fibers: 15-20 per minute

• Fainting due to lack of blood flow to brain.
• Tachycardia
• Ventricle doesn't have enough time to fill with fluid.
• Cardiac output would be low.

• Abosolute
• Effective
• Relative
• Supranormal

• negative chronotropic effect (decreased heart rate)
• negative dromotropic effect (decreased conduction velocity)
• decreases Na influx via G pathway. (increases length of phase 4)

• positive chronotropic effect (increased heart rate)
• positive dromotropic effect (increased velocity)
• positive inotropic effect (contractility)
• increases Na influx. More posistive resting membrane potential.

• Cause SR pump to store more Ca.

example: Digitalis

• positive inotropic effect.(contractility)
• used to treat people with congestive heart failure.
• It blocks the Na/K pump which increases intracellular Na concentration.
• The Na/Ca counter transport(secondary active transport) slows down which increases the intracellular [Ca].

• the volume of blood ejected from one ventricle in one beat.
• SV= end-diastolic volume - end-systolic volume

EF= (stroke volume)/(end-diastolic volume)

indication of how good contractility is

• Left ventricular end-diastolic volume (LVEDV)
• Left ventricular end-diastolic pressure (LVEDP)
• Left atrial pressure
• Pulmonary venous pressure
• Pulmonary wedge pressure (Swan-Ganz catheter) Indirectly measures left atrium pressure.

Resistance that must be overcome to eject the stroke volume.

• Hypertension increase afterload
• Hypotension decreases afterload
• Aortic stenosis(narrowing) increases afterload.
• BP lets you know how much heart has to work.

wall tension and pressure of heart chamber

P= (2HT)/r

P: pressure of heart chamber

H: thickness of chamber wall

T: wall tension

r: radius

CO= Stroke volume x Heart rate

Stroke volume can be increased by Contractility(ANS) and Preload

Normal CO is 4-6L/min

Blood flow out will increase

flow out= flow in

• What ever the heart recieves, it will pump
• based on length tension curve

• consumes most energy and oxygen
• work= force x distance

Phase I: Period of filling. The atrium pressure is larger than the ventricle pressure so the mitral valve opens. End of this period represents EDV.

Phase II: Period of isovolumic contraction. Mitral valve closes. Left ventrical contracts until pressure is higher than aortic.

Phase III: Period of ejection. Aortic valve opens.

Phase IV: Period of Isovolumic relaxation. Valve closes when aortic pressure drops. This phase represents ESV.

• Increase in sroke volume.

• (hypertension or aortic stenosis)
• Reduced stroke volume
• Increased End-Systolic volume
• Increased Pressure

Effect of increased contractility on pressure-volume loop:

• Increased stroke volume
• Decreased end systolic volume

• Increasing preload
• Decreasing afterload
• Increasing contractility

• Afterload
• Contractility

Aortic valve pathology

• Arotic Stenosis: pressure gradient aorta and ventrical
• Aortic Regurgitation: aorta and ventrical both increase and have same pressure.

Mitral valve pathology

• Mitral Stenosis: happens during Diastole
• Mitral Regurgitation: happens during Systole

Cardiac function curve: shows the CO. Based on Frank-Sterling length-tension relationship.

Vascular function curve: shows the venous return at different right atrium pressures. Shows the Mean Systemic Pressure when venous return = 0.

• The right atrial pressure when the venous return equals zero.
• ↑blood volume in venous pool= ↑MSP
• ↑Compliance of veins= ↓MSP

Rt Atrial Pressure= 2

CO/Venous return: both = 5ml

Positive inotropic effect: Moves CO curve to the left (more steep, and higher)

Negative inotropic effect: Moves CO curve to the right (more shallow, and lower)

Increased blood volume: vascular curve moves to the right and goes higher.

Decreased blood volume: vascular curve moves to the left and goes down.

• Increased TPR: decreases both curves.
• Decreased TPR: increases both curves.

• At rest: 3-4 ml/min/100g of muscle
• During extreem exercise: 50-80 ml/min/100g
• ↑Sympathetic Outflow
• Contriction of arterioles cause less blood to flow.(No reduction of blood to brain or heart)
• ↑Systolic Arterial Pressure

Increase in Cardiac Output: due to sympathetic stimulation which leads to ↑contractility and ↑heart rate.

Inreased Venous Return: due to ↑mean systemic pressure, ↓resistance in all blood vessels in the active muscle, ↑ventilation (thoracic suction pump), Pumping action of contracting muscle.

• The CO drops from around 5 to around 2ml/min. Intersects with venous function curve at a right atrial pressure of about 4(Usally less than 2).
• Sympathetic activity increases alot and the Cardiac function curve shifts to the left. The Venous function curve shifts to the right due to increased venous blood retention. This results in the CO being returned to 5ml/min but the atrial pressure remains high at 4mmHg.
• Simultaneously sympathetic activity decreases to normal and venous blood retention increases. This results in a CO of 5ml/min(normal) but an atrial pressure of 8(really high)