cardiovascular physiology 246 part 2 (2013)

8/12/2019 Cardiovascular Physiology 246 Part 2 (2013)

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Eric P. Widmaier Boston University

Hershel Raff Medical College of Wisconsin

Kevin T. Strang University of Wisconsin - Madison

Chapter 12

Part 2

Cardiovascular Physiology

Asad ZeidanOffice DTS 2-55

[email protected]

American University of Beirut

Dept. of Anatomy, Cell Biology and

Physiology



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- What is the "normal" pacemaker of heart?

- Trace the conduction system in the heart.

SA node-> internodal pathway->AV node-> Bundle of his/AVbundle->right and left bundle branches->Purkinje fibers.



The prolonged refractory period of cardiac muscle prevents

tetanus, and allows time for ventricles to fill with blood prior to

pumping.

Figure 12-18

Refractory Period of the Heart



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6

• S1 - 1st sound (lub)

• Closing of the AV valves.• Louder and longer than the

second sound.

• Beginning of ventricular systole

• S2 - 2nd sound (dup) • Closing of the semilunar valves.

• Short, sharp sound.

• End of ventricular systole.

• Murmur - an abnormal sound of the heart;

sometimes a sign of abnormal function of the

heart valves

Heart Sounds (lub-dup)



Cardiac Cycle

The cardiac cycle is a term referring to allor any of the events related to the flow or

blood pressure that occurs from the

beginning of one heartbeat to the

beginning of the next

• Systole is the contraction phase.

• Diastole is the relaxation phase.



- The contraction of the heart muscle of the left and right atria.

- Normally, both atria contract at the same time.

- 80% of the blood flows passively down to the ventricles, sothe atria do not have to contract a great amount

Atrial systole



The contraction of the muscles of the left and right ventricles.

Ventricular systole



Preload and Afterload

• Afterload is the pressure that the ventricles must overcome

to force open the aortic and pulmonary valves. Afterload = pressure or resistance the heart has to overcome to eject blood.

• Preload is proportional to the amount of ventricularmyocardial fiber stretch just before systole (End-Viastolic

volume (EDV)).

• Anything that increases systemic or pulmonary arterial

pressure can increase afterload.

(ex. Hypertension)



Define preload.degree of stretch of the cardiac muscle fibers at the end of diastole

*End diastolic volume distending the ventricle*

Define Afterloadthe amount of resistance to ejection of blood from the ventricle

*Pressure the ventricular myocardium must overcome to

eject blood during systole*



Systole: Ventricles contracting

Figure 12-19

Afterload is the pressure that

the ventricles must overcome

to force open the aortic andpulmonary valves.



Stroke volume = amount of blood pumped from

ventricles with each contraction

Cardiac output = amount of blood pumped with eachstroke volume over a given period (1 min)

So... just to make it simple to see the relationship....

if you pump 1mL with each stroke --> and your heart rate

is 65 bpm --> your cardiac output would be 65 mL perminute

Stoke Volume and Cardiac Output relationship



How many L/min is pumped out of the heart

(Cardiac Output)?

5-6 L/min



Figure 12-19

Diastole: Ventricles relaxed



Pressure and volume changes in

the left heart during a contraction

cycle.

Figure 12-20



Pressure changes in the right heart during a contraction cycle.

Figure 12-21

Pulmonary Circulation Pressures



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Cardiac Output

•

Cardiac output is the amount of blood pumped out ofeach ventricle in one minute.

• Each time the heart beats, a volume of blood is

ejected stroke volume (SV).

• It is the product of heart rate (HR)

and stroke volume (SV).

• CO=HR x SV

• Normal cardiac output is 5.25 L/min.



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Regulation of Heart Rate

• In a healthy system SV is fairly constant. If blood volume

drops or if the heart weakens, then SV declines and CO ismaintained by increasing HR.

• CO= SV x HR

• Things that increase HR are positive chronotropic factors.

• Things that decrease HR are negative chronotropic factors.

• Heart rate is also controlled by the input from the nervoussystem:

- SNS increases heart rate;

- PSNS decreases heart rate.



Figure 12-22

Curve b: by increasing sodium and calcium influx into the

pacemaker cells, sympathetic signals those cells to

reach threshold for an action potential more rapidly.

Control of Heart Rate



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The ventricles are maximally filled at a time just before theheart contracts called end diastole.

When the ventricles are maximally emptied (there is still some

blood remaining in them) this period is referred to as end

systole.

End Diastolic Volume - End Systolic Volume

= Stroke Volume

Stroke Volume



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Stroke Volume

• Anything that increases EDV or increases the force

of the ventricular contraction can increase SV.

• The ventricles are never completely empty of

blood, so a more forceful contraction will expelmore blood with each pump.

• Extrinsic controls of SV include:

! Sympathetic drive to ventricular muscle fibers

! (NE at Beta1 receptors in cardiac muscle cells)

! Hormonal control

! (Thyroid hormones can increase the force of contraction)



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Starlings Law

• Starlings law says that the critical factor controlling stroke

volume is preload.

• Preload is the degree to which the cardiac muscle cells are

stretched before they contract.

• The most important factor in causing stretch is the amount of blood in the ventricles. The amount of blood in the ventricles is

controlled by venous return.

• This controls the end diastolic volume (EDV).

• Anything that increases venous return or slows heart rate

increases EDV.

EDV



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Frank-Starling Mechanism

Fig. 12-24

To increase the hearts stroke volume:

fill it more fully with blood. The increased stretch of the ventricle will align itsactin and myosin in a more optimal pattern of overlap.



To further increase the stroke volume:

Fill it more fully with blood

AND

deliver sympathetic signals (norepinephrine and epinephrine);

it will also relax more rapidly, allowing more time to refill.

Figure 12-25

Fi 12 25



Sympathetic signals (norepinephrine and epinephrine) cause a stronger

and more rapid contraction and a more rapid relaxation.

Figure 12-25



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Node Cells

Pumping cells

To increase the volume of blood pumped per stroke



deliver the sympathetic hormone, epinephrine, and/or

release more sympathetic neurotransmitter (norepinephrine).

Figure 12-27

To increase the volume of blood pumped per stroke

To speed up the heart rate



To speed up the heart rate:

• deliver the sympathetic hormone, epinephrine, and/or

• release more sympathetic neurotransmitter (norepinephrine), and/or

• reduce release of parasympathetic neurotransmitter (acetylcholine).

Figure 12-23

To speed up the heart rate



Figure 12-28

To increase SV, increase:

1. end-diastolic volume

2. norepinephrine delivery from

sympathetic neurons

3. epinephrinedelivery from the

adrenal medulla.

delivery fromadrenal medulla

3. reduce

parasympathetic.

M t f C di F ti



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Measurement of Cardiac Function• Human cardiac output can be measured by a variety of methods.

• Echocardiography: Echocardiography is a noninvasivetechnique that uses ultrasonic waves.

- This technique can detect the abnormal functioning of cardiac

valves or contractions of the cardiac walls.

• Cardiac angiography: requires the temporary threading of a thin,

flexible tube called a catheter through an artery or vein into the

heart. A liquid containing radio-opaque contrast material is then

injected through the catheter during high-speed x-ray

videography.

- This technique is useful for evaluating cardiac function and for

identifying narrowed coronary arteries

Echocardiography



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Echocardiography

Cardiac angiography



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Cardiac angiography



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The Vascular System



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The Vascular System

• The vascular system are the pipes that carry the blood. The

arteries and veins both have vascular smooth muscle cells,endothelial cells, and advential fibroblasts, but the

composition of each type varies in amounts.

• The types of structures involved are:• Arteries

" Elastic arteries

" Muscular arteries

" Arterioles

" Capillaries

• Veins

" Venules

A t i



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Arteries

Fig. 12-30

Arteries are often calledpressure reservoirs because

of the elastic recoil. They arenot as compliant as veins.

Compliance = !volume/ ! pressure

The higher the compliance of a

structure, the more easily it canbe stretched.

El ti A t i



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Elastic Arteries

• Near the heart which carry blood for circulation.

• The major example of an elastic artery is the aorta.

• These are large lumen vessels (low resistance) that contain moreelastin than the muscular arteries.

• This allows them to be pressure reservoirs "" they expand andcontract (recoil) as blood is ejected by the heart. This allows blood flow to be continuous.

•

Atherosclerosis and arteriosclerosis affect the ability tofunction properly.

• Furthermore, if pressure becomes too great over time, the wallseither remodel or weaken. If they weaken they can burst.



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Muscular Arteries

• These arteries deliver blood to specific organs

(mesenteric artery, renal artery etc.).

• They have proportionally the thickest media (most

smooth muscle) and are very active in vasoconstriction.

• These arteries can play a large role in the regulation of

blood pressure. " For example, the mesenteric artery carries ~25 % of the CO, so

alterations in its diameter would have a large effect.



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Pressures

• The average blood pressure is considered to be

120/80 mm Hg.

• Blood pressure of about 140/90 mm Hg is

considered hypertensive.

• Hypertension is a disease that affects millionsof patients.

I t th l til t ti f th h t



Figure 12-29

In response to the pulsatile contraction of the heart:

pulses of pressure move throughout the vasculature,decreasing in amplitude with distance

A

o r t a



Pulse Pressure



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Pulse Pressure

• The difference between systolic pressure and diastolic pressure

(120 – 80 = 40 mmHg in the example) is called the pulse pressure.

• It can be felt as a pulsation or throb in the arteries of the wrist or

neck with each heartbeat.

• The most important factors determining the magnitude of the pulse pressure are:

(1) Stroke volume

(2) Speed of ejection of the stroke volume

(3) Arterial compliance

• A decrease in arterial compliance occurs in arteriosclerosis

(stiffening of the arteries).

Measurement of Systemic Arterial Pressure



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Measurement of Systemic Arterial Pressure

Fig. 12-32

Stethoscope

Sphygmomanometer



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Arterioles and blood flow

Arteriolar blood flow



Arteriolar blood flow

• Local controls

- Active hyperemia

- Reactive hyperemia (Flow autoregulation)

• Extrinsic controls

1. Sympathetic: Norepinephrine2. Hormones : Epinephrine

- Hyperemia (increase in blood flow)

- Vasodilation (arteriolar dilation) = increase blood flow

Local controls of blood flow



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Local controls of blood flow

Fig. 12-34Local control in response to(a) increases in metabolic activity: leads to Active hyperemia

(b) decreases in blood pressure: leads to Flow autoregulation

Extrinsic Controls Fig. 12-35



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Extrinsic Controls g

Sympathetic stimulation of alpha-adrenergic receptors cause

vasoconstriction to avert blood away from that location.

Sympathetic stimulation of beta-adrenergic receptors lead to

vasodilation to cause a bigger blood blast at that location.

Note: a given setof arterioles will

likely have eitheralpha- or beta-

type receptors.

Endothelial Cells and Vascular



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Endothelial Cells and Vascular

Smooth Muscle

• Endothelial cells secrete several paracrineagents that diffuse to the adjacent vascular

smooth muscle and induce either relaxation or

contraction.

• One of the most important is nitric oxide (NO).

• NO causes vasodilation and is critical to propervessel tone.



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Capillaries

Figure 12-38



Capillaries lack smooth muscle, but contraction/relaxation of circular smooth

muscle in upstream metarterioles and precapillary sphincters determine the

volume of blood each capillary receives.

interstitial fluid (ISF)

Capillaries: Exchange



Capillaries: Exchange

• Capillaries have the thinnest walls

– Single layer of flattened endothelial cells

– Supported by basal lamina

• Plasma and cells exchange materials across

thin capillary wall

• Capillary density is

related to metabolic

activity of cells

Two Types of Capillaries



Two Types of Capillaries



• Bone marrow, liver and spleen do not have

typical capillaries but sinusoids (incomplete

basement membrane)

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Precapillary Sphincters



Figure 15-15a





Figure 15-15b


Velocity of Blood Flow



Velocity of Blood Flow

Velocity of flow depends on total cross-sectional

area of the vessels

Velocity is slowest

in the capillarybeds because

they have a

greater cross-

sectional area.



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There are many, many capillaries, eachwith slow-moving blood in it, resulting in

adequate time and surface area for

exchange between the capillary blood andthe ISF.

Capillary Exchange



Capillary Exchange

• Exchange by

1- paracellular pathway (between cells)

2- transendothelial transport (transcytosis)

• Small dissolved solutes and gasses by diffusion isdetermined by concentration gradient

• Large solutes and proteins by vesicular

transport (transcytosis)

Figure 12-41



Movement of fluid and solutes into the blood is called absorption.

Absorption

Filtration

Movement of fluid and solutes out of the blood is called filtration.



O ti P



67

Osmotic Pressure

• Colloid osmotic pressure is the force that

opposes the hydrostatic pressure.

• It is created by the large nondiffusible

molecules, like plasma proteins.

• It does not vary from one end of the capillaries

to the other, like hydrostatic force.

N t Filt ti P



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Net Filtration Pressure

• NFP=(HPc –HPif ) – (OPc- OPif )

• So if HP exceeds OP, then fluid leaves the

capillaries (filtered). If OP is greater than HP, itenters the capillaries (reabsorbed).

• Generally the amount of fluid lost and notregained is about 1.5 ml/min. This is picked up bythe lymph system and returned to the circulation.



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70

Veins



Figure 12-44

Veins



At rest, most of the

blood volume is in

the veins.Sympathetically

mediated

venoconstriction can

substantially increase

venous return to the

heart.

Veins



Varicose Veins



Venous Pressure



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• Blood pressure in veins is ~15 mm Hg. This is not sufficient to

move blood back to the heart. So there are the pumps:

1. Muscular pump: When muscles contract they squeeze

the veins. This results in blood moving forward and

being prevented from backflow by the veins. This

moves blood toward the heart.

2. Respiratory pump: Pressure

changes in the central cavity due to

the pressure changes due tobreathing. This helps to propel blood

back to the heart.

Venous Pressure

Figure 12-45

Venous Pressure



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The smooth muscle in the veins is under SNS control

and contract when stimulated, similar to the arterial

smooth muscle. This causes contraction and anarrowing of the lumen.

Venous Pressure

Venous return



Alterations in venous return alter end-diastolic volume (EDV);

increased EDV directly increases stroke volume and cardiac output.

Figure 12-46

Figure 12-52



Blood loss causes a

reduction in MAP, which, ifleft unchecked, would result

in rapid and irreversible

damage to the brain and the

heart.

= MAP



The Lymphatic System



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The Lymphatic System

• The lymphatic system is made up of lymphatic

vessels and lymphatic tissue.

• Function:

1- Collect the fluid lost from the capillaries and

return it to the circulation and

2- House the phagocytes and lymphocytes that play

a role in the immune system.



Figure 12-47



Lymphatic fluid, formed by

the slight mismatch

between filtration and

absorption in thecapillaries, returns to the

blood in the veins.



84

CO = HR x SV

SV = EDV-ESV

cardiovascular physiology 246 part 2 (2013)

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