the heart and cardiovascular system muse 2440 lecture #2 1/19/11

The Heart and Cardiovascular systemMuse 2440 Lecture #2 1/19/11

Overview of today’s lesson

- Blood flow thru the heart- Conduction system (SA and AV nodes- Cardiac cycle- Hormone control of heart- Innervation control of heart- Stroke volume control- Blood vessels- Cardiovascular pathologies

Introduction to Cardiovascular System

The Pulmonary Circuit

Carries blood to and from gas exchange surfaces of

The Systemic Circuit

Carries blood to and from the body

Blood alternates between pulmonary circuit and

systemic circuit

Three Types of Blood Vessels

Arteries

Carry blood away from heart

Carry blood to heart

Capillaries

Networks between arteries and veins

Exchange materials between blood and tissues

Figure 20–1 An Overview of the Cardiovascular System.

Four Chambers of the Heart

Right atrium

Collects blood from systemic circuit

Right ventricle

Pumps blood to pulmonary circuit

Left atrium

Collects blood from pulmonary circuit

Left ventricle

Pumps blood to systemic circuit

Anatomy of the Heart

Figure 20–3b The Superficial Anatomy of the Heart

Figure 20–2c

The Pericardium

Double lining of the pericardial cavity

Parietal pericardium

Outer layer

Forms inner layer of pericardial sac

Visceral pericardium

Inner layer of pericardium

The Pericardium

Pericardial cavity

Is between parietal and visceral layers

Contains pericardial fluid

Pericardial sac

Fibrous tissue

Surrounds and stabilizes heart

Figure 20–2b The Location of the Heart in the Thoracic Cavity

Superficial Anatomy of the Heart

Thin-walled

Expandable outer auricle (atrial appendage)

rt auricle has some endocrine function

Coronary sulcus: divides atria and ventricles

Anterior interventricular sulcus and posterior interventricular

sulcus:

– separate left and right ventricles

– contain blood vessels of cardiac muscle

Figure 20–3a The Superficial Anatomy of the Heart

Blood flow through the heart

Deoxygenated blood enters right atrium from superior vena cava,passes from rt. atrium into rt ventricle thru the tricuspid valve. Getspumped out of right ventricle into pulmonary artery to go to lungs. Backflow is prevented by semilunar valves. Oxygenated blood returns from lungs through pulmonary veins and enters left atrium.The blood flows into the left ventricle through the mitral (bicuspid) valve. From the left ventricle, it is pumped into the aorta and out to the body.

Remember: left-leaves

Figure 20–3a The Superficial Anatomy of the Heart

The Heart Wall Epicardium (outer layer)

Visceral pericardium

Covers the heart

Myocardium (middle layer) Muscular wall of the heart

Concentric layers of cardiac muscle tissue

Atrial myocardium wraps around great vessels

Two divisions of ventricular myocardium

Endocardium (inner layer) Simple squamous epithelium

Figure 20–4 The Heart Wall

Cardiac Muscle Tissue

Intercalated discs

Interconnect cardiac muscle cells

Secured by desmosomes

Linked by gap junctions

Convey force of contraction

Propagate action potentials

Figure 20–5 Cardiac Muscle Cells

Figure 20–6a-b The Sectional Anatomy of the Heart.

The Right Ventricle Free edges attach to chordae tendineae

from papillary muscles of ventricle

Prevent valve from opening backward

Right atrioventricular (AV) Valve Also called tricuspid valve

Opening from right atrium to right ventricle

Has three cusps

Prevents backflow

The Right Ventricle

Trabeculae carneae

Muscular ridges on internal surface of right (and

left) ventricle

Includes moderator band:

– ridge contains part of conducting system

– coordinates contractions of cardiac muscle cells

The Pulmonary Circuit

Conus arteriosus (superior end of right ventricle)

leads to pulmonary trunk

Pulmonary trunk divides into left and right

pulmonary arteries

Blood flows from right ventricle to pulmonary trunk

through pulmonary valve

Pulmonary valve has three semilunar cusps

The Left Atrium

Blood gathers into left and right pulmonary

Pulmonary veins deliver to left atrium

Blood from left atrium passes to left ventricle

through left atrioventricular (AV) valve

A two-cusped bicuspid valve or mitral valve

The Left Ventricle Holds same volume as right ventricle

Is larger; muscle is thicker and more powerful

Similar internally to right ventricle but does not have

moderator band

Systemic circulation Blood leaves left ventricle through aortic valve into

ascending aorta

Ascending aorta turns (aortic arch) and becomes

descending aorta

Figure 20–6c The Sectional Anatomy of the Heart.

Figure 20–7 Structural Differences between the Left and Right Ventricles

The Heart Valves

Two pairs of one-way valves prevent backflow

during contraction

Atrioventricular (AV) valves

Between atria and ventricles

Blood pressure closes valve cusps during ventricular

contraction

Papillary muscles tense chordae tendineae: prevent valves

from swinging into atria

Figure 20–8

The Heart Valves

Semilunar valves

Pulmonary and aortic tricuspid valves

Prevent backflow from pulmonary trunk and aorta

into ventricles

Have no muscular support

Three cusps support like tripod

Figure 20–8

Aortic Sinuses

At base of ascending aorta

Sacs that prevent valve cusps from sticking to

Origin of right and left coronary arteries

Figure 20–8a Valves of the Heart

Figure 20–8b Valves of the Heart

Figure 20–8c Valves of the Heart

The Coronary Arteries

Left and right

Originate at aortic sinuses

High blood pressure, elastic rebound forces

blood through coronary arteries between

contractions

Right Coronary Artery

Supplies blood to

Right atrium

Portions of both ventricles

Cells of sinoatrial (SA) and atrioventricular nodes

Marginal arteries (surface of right ventricle)

Posterior interventricular artery

Left Coronary Artery

Supplies blood to

Left ventricle

Left atrium

Interventricular septum

Two main branches of left coronary artery

Circumflex artery

Anterior interventricular artery

Arterial Anastomoses

Interconnect anterior and posterior interventricular

arteries

Stabilize blood supply to cardiac muscle

The Cardiac Veins

Great cardiac vein

Drains blood from area of anterior interventricular artery into

coronary sinus

Anterior cardiac veins

Empties into right atrium

Posterior cardiac vein, middle cardiac vein, and

small cardiac vein

Empty into great cardiac vein or coronary sinus

Figure 20–9a Coronary Circulation

Figure 20–9b Coronary Circulation

Figure 20–9c Coronary Circulation

Figure 20–10 Coronary Circulation and Clinical Testing

The Conducting System

The Cardiac Cycle

Begins with action potential at SA node

Transmitted through conducting system

Produces action potentials in cardiac muscle cells

(contractile cells)

Electrocardiogram (ECG)

Electrical events in the cardiac cycle can be recorded on an

electrocardiogram (ECG)

Figure 20–11 An Overview of Cardiac Physiology

A system of specialized cardiac muscle

Initiates and distributes electrical impulses

that stimulate contraction

Automaticity

Cardiac muscle tissue contracts automatically

Structures of the Conducting System

Sinoatrial (SA) node - wall of right atrium

Atrioventricular (AV) node - junction

between atria and ventricles

Conducting cells - throughout myocardium

Prepotential

Also called pacemaker potential

Resting potential of conducting cells

Gradually depolarizes toward threshold

SA node depolarizes first, establishing heart

Figure 20–12 The Conducting System of the Heart

Heart Rate

SA node generates 80–100 action potentials

per minute

Parasympathetic stimulation slows heart rate

AV node generates 40–60 action potentials

per minute

The Sinoatrial (SA) Node

In posterior wall of right atrium

Contains pacemaker cells

Connected to AV node by internodal pathways

Begins atrial activation (Step 1)

Figure 20–13 Impulse Conduction through the Heart

The Atrioventricular (AV) Node

In floor of right atrium

Receives impulse from SA node (Step 2)

Delays impulse (Step 3)

Atrial contraction begins

The AV Bundle

In the septum

Carries impulse to left and right bundle

branches

Which conduct to Purkinje fibers (Step 4)

And to the moderator band

Which conducts to papillary muscles

Purkinje Fibers

Distribute impulse through ventricles (Step 5)

Atrial contraction is completed

Ventricular contraction begins

Abnormal Pacemaker Function

Bradycardia: abnormally slow heart rate

Tachycardia: abnormally fast heart rate

Ectopic pacemaker

Abnormal cells

Generate high rate of action potentials

Bypass conducting system

Disrupt ventricular contractions

Electrocardiogram (ECG or EKG)

A recording of electrical events in the heart

Obtained by electrodes at specific body

locations

Abnormal patterns diagnose damage

Figure 20–14b An Electrocardiogram: An ECG Printout

Time Intervals Between ECG Waves

P–R interval

From start of atrial depolarization

To start of QRS complex

Q–T interval

From ventricular depolarization

To ventricular repolarization

Figure 20–14a An Electrocardiogram: Electrode Placement for Recording a Standard ECG

Figure 20–14b An Electrocardiogram: An ECG Printout

Contractile Cells

Purkinje fibers distribute the stimulus to the

contractile cells, which make up most of the

muscle cells in the heart

Resting Potential

Of a ventricular cell: about –90 mV

Of an atrial cell: about –80 mV

Figure 20–15 The Action Potential in Skeletal and Cardiac Muscle

Refractory Period

Absolute refractory period

Cardiac muscle cells cannot respond

Relative refractory period

Response depends on degree of stimulus

Timing of Refractory Periods

Length of cardiac action potential in

ventricular cell

250–300 msecs:

– 30 times longer than skeletal muscle fiber

– long refractory period prevents summation and tetany

The Role of Calcium Ions in Cardiac

Contractions

Contraction of a cardiac muscle cell is

produced by an increase in calcium ion

concentration around myofibrils

The Energy for Cardiac Contractions

Aerobic energy of heart

From mitochondrial breakdown of fatty acids and

glucose

Oxygen from circulating hemoglobin

Cardiac muscles store oxygen in myoglobin

The Cardiac Cycle

Phases of the Cardiac Cycle

Within any one chamber

Systole (contraction)

Diastole (relaxation)

The Cardiac Cycle

Figure 20–16 Phases of the Cardiac Cycle

The Cardiac Cycle

Blood Pressure

In any chamber

Rises during systole (ventricular compression) 120

Falls during diastole (vessel elasticity) 60

Blood flows from high to low pressure

Controlled by timing of contractions

Directed by one-way valves - not perfect seals

The Cardiac Cycle

Cardiac Cycle and Heart Rate

At 75 beats per minute

Cardiac cycle lasts about 800 msecs

When heart rate increases

All phases of cardiac cycle shorten, particularly

diastole

The Cardiac Cycle

Figure 20–17 Pressure and Volume Relationships in the Cardiac Cycle

The Cardiac Cycle

Heart Sounds

Loud sounds Lub

Produced by AV valves

Loud sounds Dub

Produced by semilunar valves

S3, S4

Soft sounds often missed

Blood flow into ventricles and atrial contraction

The Cardiac Cycle

Heart Murmur

Sounds produced by regurgitation through

valves

Example - mitral valve prolapse

The Cardiac Cycle

Figure 20–18 Heart Sounds

Cardiodynamics

Cardiac Output

CO = HR X SV

CO = cardiac output (mL/min)

HR = heart rate (beats/min)

SV = stroke volume (mL/beat)

Cardiodynamics

Factors Affecting Cardiac Output

Cardiac output

Adjusted by changes in heart rate or stroke volume

Heart rate

Adjusted by autonomic nervous system or hormones

Stroke volume

Adjusted by changing EDV or ESV

Cardiodynamics

Factors Affecting the Heart Rate

Autonomic innervation

Cardiac plexuses: innervate heart

Vagus nerves (X): carry parasympathetic preganglionic fibers

to small ganglia in cardiac plexus

Cardiac centers of medulla oblongata:

– cardioacceleratory center controls sympathetic

neurons (increases heart rate)

– cardioinhibitory center controls parasympathetic

neurons (slows heart rate)

Cardiodynamics

Autonomic Innervation Cardiac reflexes

Cardiac centers monitor:– blood pressure (baroreceptors)– arterial oxygen and carbon dioxide levels

(chemoreceptors)

Cardiac centers adjust cardiac activity Autonomic tone

Dual innervation maintains resting tone by releasing ACh and NE

Fine adjustments meet needs of other systems

Cardiodynamics

Figure 20–21 Autonomic Innervation of the Heart

Cardiodynamics

Effects on the SA Node Sympathetic and parasympathetic stimulation

Greatest at SA node (heart rate)

Membrane potential of pacemaker cells Lower than other cardiac cells

Rate of spontaneous depolarization depends on Resting membrane potential Rate of depolarization

ACh (parasympathetic stimulation) Slows the heart

NE (sympathetic stimulation) Speeds the heart

Cardiodynamics

Figure 20–22 Autonomic Regulation of Pacemaker Function

Cardiodynamics

Hormonal Effects on Heart Rate

Increase heart rate (by sympathetic

stimulation of SA node)

Epinephrine (E)

Norepinephrine (NE)

Thyroid hormone

Cardiodynamics

Factors Affecting the Stroke Volume

The EDV: amount of blood a ventricle contains at the

end of diastole

Filling time:

– duration of ventricular diastole

Venous return:

– rate of blood flow during ventricular diastole

Cardiodynamics

The Frank–Starling Principle

As EDV increases, stroke volume increases

Physical Limits

Ventricular expansion is limited by

Myocardial connective tissue

The cardiac (fibrous) skeleton

The pericardial sac

Cardiodynamics

End-Systolic Volume (ESV)

The amount of blood that remains in the

ventricle at the end of ventricular systole is

the ESV

Cardiodynamics

Effects of Autonomic Activity on Contractility

Sympathetic stimulation

NE released by postganglionic fibers of cardiac nerves

Epinephrine and NE released by suprarenal (adrenal)

medullae

Causes ventricles to contract with more force

Increases ejection fraction and decreases ESV

Cardiodynamics

Effects of Autonomic Activity on

Contractility

Parasympathetic activity

Acetylcholine released by vagus nerves

Reduces force of cardiac contractions

Cardiodynamics

Hormones

Many hormones affect heart contraction

Pharmaceutical drugs mimic hormone actions

Stimulate or block beta receptors

Affect calcium ions (e.g., calcium channel

blockers)

Cardiodynamics

Heart Rate Control Factors

Autonomic nervous system

Sympathetic and parasympathetic

Circulating hormones

Venous return and stretch receptors

Cardiac Reserve

The difference between resting and maximal cardiac output

Classes of Blood Vessels

Arteries Carry blood away from heart

Arterioles Are smallest branches of arteries

Capillaries Are smallest blood vessels

Location of exchange between blood and interstitial fluid

Venules Collect blood from capillaries

Veins Return blood to heart

Blood Vessels

The Largest Blood Vessels

Attach to heart

Pulmonary trunk

Carries blood from right ventricle

To pulmonary circulation

Carries blood from left ventricle

To systemic circulation

Blood Vessels

The Smallest Blood Vessels

Capillaries

Have small diameter and thin walls

Chemicals and gases diffuse across walls

Blood Vessels

The Structure of Vessel Walls

Walls have three layers:

Tunica intima

Tunica media

Tunica externa

Blood Vessels

The Tunica Intima

Is the innermost layer

Includes

The endothelial lining

Connective tissue layer

Internal elastic membrane:

– in arteries, is a layer of elastic fibers in outer margin of

tunica intima

Blood Vessels

The Tunica Media

Is the middle layer

Contains concentric sheets of smooth muscle in loose

connective tissue

Binds to inner and outer layers

External elastic membrane of the tunica media

Separates tunica media from tunica externa

Blood Vessels

The Tunica Externa Is outer layer Contains connective tissue sheath Anchors vessel to adjacent tissues in arteries

Contain collagen Elastic fibers

In veins Contains elastic fibers Smooth muscle cells

Vasa vasorum (“vessels of vessels”) Small arteries and veins In walls of large arteries and veins Supply cells of tunica media and tunica externa

Blood Vessels

Figure 21–1 Comparisons of a Typical Artery and a Typical Vein.

Blood Vessels

Differences between Arteries and Veins Arteries and veins run side by side

Arteries have thicker walls and higher blood pressure

Collapsed artery has small, round lumen (internal

space)

Vein has a large, flat lumen

Vein lining contracts, artery lining does not

Artery lining folds

Arteries more elastic

Veins have valves

Structure and Function of Arteries

Arteries and Pressure Elasticity allows arteries to absorb pressure waves

that come with each heartbeat

Contractility Arteries change diameter

Controlled by sympathetic division of ANS

Vasoconstriction:

– the contraction of arterial smooth muscle by the ANS

Vasodilatation:

– the relaxation of arterial smooth muscle

– enlarging the lumen

Vasoconstriction and Vasodilation

Affect

Afterload on heart

Peripheral blood pressure

Capillary blood flow

Arteries

From heart to capillaries, arteries change

From elastic arteries

To muscular arteries

To arterioles

Elastic Arteries

Also called conducting arteries

Large vessels (e.g., pulmonary trunk and

aorta)

Tunica media has many elastic fibers and few

muscle cells

Elasticity evens out pulse force

Muscular Arteries

Also called distribution arteries

Are medium sized (most arteries)

Tunica media has many muscle cells

Arterioles Are small

Have little or no tunica externa

Have thin or incomplete tunica media

Artery Diameter Small muscular arteries and arterioles

Change with sympathetic or endocrine stimulation

Constricted arteries oppose blood flow

– resistance (R):

» resistance vessels: arterioles

Aneurysm

A bulge in an arterial wall

Is caused by weak spot in elastic fibers

Pressure may rupture vessel

Figure 21–2 Histological Structure of Blood Vessels

Figure 21–3 A Plaque within an Artery

Structure and Function of Capillaries

Capillaries

Are smallest vessels with thin walls

Microscopic capillary networks permeate all active

tissues

Capillary function

Location of all exchange functions of cardiovascular system

Materials diffuse between blood and interstitial fluid

Capillary Structure

Endothelial tube, inside thin basal lamina

No tunica media

No tunica externa

Diameter is similar to red blood cell

Continuous Capillaries

Have complete endothelial lining

Are found in all tissues except epithelia and

cartilage

Functions of continuous capillaries

Permit diffusion of water, small solutes, and lipid-

soluble materials

Block blood cells and plasma proteins

Specialized Continuous Capillaries

Are in CNS and thymus

Have very restricted permeability

For example, the blood–brain barrier

Fenestrated Capillaries

Have pores in endothelial lining

Permit rapid exchange of water and larger solutes

between plasma and interstitial fluid

Are found in

Choroid plexus

Endocrine organs

Kidneys

Intestinal tract

Sinusoids (sinusoidal capillaries) Have gaps between adjacent endothelial cells

Liver Spleen Bone marrow Endocrine organs

Permit free exchange Of water and large plasma proteins Between blood and interstitial fluid

Phagocytic cells monitor blood at sinusoids

Figure 21–4 Capillary Structure

Arteriovenous Anastomoses

Direct connections between arterioles and

venules

Bypass the capillary bed

Capillary Sphincter

Guards entrance to each capillary

Opens and closes, causing capillary blood to

flow in pulses

Vasomotion

Contraction and relaxation cycle of capillary

sphincters

Causes blood flow in capillary beds to

constantly change routes

Structure and Function of Veins

Collect blood from capillaries in tissues and organs

Return blood to heart

Are larger in diameter than arteries

Have thinner walls than arteries

Have lower blood pressure

Vein Categories

Venules Very small veins Collect blood from capillaries

Medium-sized veins Thin tunica media and few smooth muscle cells Tunica externa with longitudinal bundles of elastic fibers

Large veins Have all three tunica layers Thick tunica externa Thin tunica media

Venous Valves

Folds of tunica intima

Prevent blood from flowing backward

Compression pushes blood toward heart

Figure 21–6 The Function of Valves in the Venous System

Blood Vessels

The Distribution of Blood

Heart, arteries, and capillaries

30–35% of blood volume

Venous system

60–65%:

– 1/3 of venous blood is in the large venous networks of the liver,

bone marrow, and skin

Blood Vessels

Figure 21–7 The Distribution of Blood in the CardiovascularSystem

Blood Vessels

Capacitance of a Blood Vessel

The ability to stretch

Relationship between blood volume and blood

pressure

Veins (capacitance vessels) stretch more

than arteries

Blood Vessels

Venous Response to Blood Loss

Vasomotor centers stimulate sympathetic

nerves

Systemic veins constrict (venoconstriction)

Veins in liver, skin, and lungs redistribute venous

reserve

Pressure and Resistance

Pressure (P)

The heart generates P to overcome resistance

Absolute pressure is less important than pressure

gradient

The Pressure Gradient (P)

Circulatory pressure = pressure gradient

The difference between

Pressure at the heart

And pressure at peripheral capillary beds

Force (F)

Is proportional to the pressure difference (P)

Divided by R

Measuring Pressure

Blood pressure (BP)

Arterial pressure (mm Hg)

Capillary hydrostatic pressure (CHP)

Pressure within the capillary beds

Venous pressure

Pressure in the venous system

Turbulence

Swirling action that disturbs smooth flow of

liquid

Occurs in heart chambers and great vessels

Atherosclerotic plaques cause abnormal

turbulence

Figure 21–12 Forces Acting across Capillary Walls

Fluid Recycling Water continuously moves out of capillaries, and back

into bloodstream via the lymphoid system and serves

to Ensure constant plasma and interstitial fluid communication

Accelerate distribution of nutrients, hormones, and dissolved

gases through tissues

Transport insoluble lipids and tissue proteins that cannot

cross capillary walls

Flush bacterial toxins and chemicals to immune system

tissues

Cardiovascular Regulation

Figure 21–13 Short-Term and Long-Term Cardiovascular Responses

Reflex Control of Cardiovascular Function

Cardiovascular centers monitor arterial blood

Baroreceptor reflexes:

– respond to changes in blood pressure

Chemoreceptor reflexes:

– respond to changes in chemical composition, particularly

pH and dissolved gases

Baroreceptor Reflexes Stretch receptors in walls of

Carotid sinuses: maintain blood flow to brain

Aortic sinuses: monitor start of systemic circuit

Right atrium: monitors end of systemic circuit

When blood pressure rises, CV centers Decrease cardiac output

Cause peripheral vasodilation

When blood pressure falls, CV centers Increase cardiac output

Cause peripheral vasoconstriction

Figure 21–14 Baroreceptor Reflexes of the Carotid and Aortic Sinuses

Hormones and Cardiovascular Regulation

Hormones have short-term and long-term

effects on cardiovascular regulation

For example, E and NE from suprarenal

medullae stimulate cardiac output and

peripheral vasoconstriction

Antidiuretic Hormone (ADH)

Released by neurohypophysis (posterior lobe of

pituitary)

Elevates blood pressure

Reduces water loss at kidneys

ADH responds to

Low blood volume

High plasma osmotic concentration

Circulating angiotensin II

Angiotensin II

Responds to fall in renal blood pressure

Stimulates

Aldosterone production

ADH production

Thirst

Cardiac output

Peripheral vasoconstriction

Erythropoietin (EPO)

Released at kidneys

Responds to low blood pressure, low O2

content in blood

Stimulates red blood cell production

Natriuretic Peptides

Atrial natriuretic peptide (ANP)

Produced by cells in right atrium

Brain natriuretic peptide (BNP)

Produced by ventricular muscle cells

Respond to excessive diastolic stretching

Lower blood volume and blood pressure

Reduce stress on heart

Figure 21–16a The Hormonal Regulation of Blood Pressure and Blood Volume.

Figure 21–16b The Hormonal Regulation of Blood Pressure and Blood Volume.

Cardiovascular Adaptation

The Cardiovascular Response to Exercise

Light exercise Extensive vasodilation occurs:

– increasing circulation

Venous return increases:

– with muscle contractions

Cardiac output rises:

– due to rise in venous return (Frank–Starling principle)

and atrial stretching

The Cardiovascular Response to Exercise

Heavy exercise Activates sympathetic nervous system

Cardiac output increases to maximum:

– about four times resting level

Restricts blood flow to “nonessential” organs (e.g., digestive system)

Redirects blood flow to skeletal muscles, lungs, and heart

Blood supply to brain is unaffected

Short-Term Elevation of Blood Pressure

Carotid and aortic reflexes

Increase cardiac output (increasing heart rate)

Cause peripheral vasoconstriction

Sympathetic nervous system

Triggers hypothalamus

Further constricts arterioles

Venoconstriction improves venous return

Short-Term Elevation of Blood Pressure

Hormonal effects

Increase cardiac output

Increase peripheral vasoconstriction (E, NE,

ADH, angiotensin II)

Long-Term Restoration of Blood Volume

Recall of fluids from interstitial spaces

Aldosterone and ADH promote fluid retention

and reabsorption

Thirst increases

Erythropoietin stimulates red blood cell

production

Vascular Supply to Special Regions

Through organs with separate mechanisms to

control blood flow

Blood Flow to the Brain

Is top priority

Brain has high oxygen demand

When peripheral vessels constrict, cerebral

vessels dilate, normalizing blood flow

Stroke

Also called cerebrovascular accident (CVA)

Blockage or rupture in a cerebral artery

Stops blood flow

Heart Attack

A blockage of coronary blood flow

Can cause

Angina (chest pain)

Tissue damage

Heart failure

Fetal and Maternal Circulation

Cardiovascular Changes at Birth Newborn breathes air

Lungs expand Pulmonary vessels expand

Reduced resistance allows blood flow

Rising O2 causes ductus arteriosus constriction

Rising left atrium pressure closes foramen ovale

Pulmonary circulation provides O2

Fetal Pulmonary Circulation Bypasses

• Foramen ovale: Interatrial opening

Covered by valve-like flap

Directs blood from right to left atrium

• Ductus arteriosus:

Short vessel

Connects pulmonary and aortic trunks

Figure 21–33a Fetal Circulation: Blood Flow to and from the Placenta

Figure 21–33b Fetal Circulation: Blood Flow Through the Neonatal Heart

Figure 21–34 Congenital Cardiovascular Problems

Aging and the Cardiovascular System

Cardiovascular capabilities decline with

Age-related changes occur in

Blood vessels

Three Age-Related Changes in Blood

Decreased hematocrit

Peripheral blockage by blood clot (thrombus)

Pooling of blood in legs

Due to venous valve deterioration

Five Age-Related Changes in the Heart

Reduced maximum cardiac output

Changes in nodal and conducting cells

Reduced elasticity of cardiac (fibrous) skeleton

Progressive atherosclerosis

Replacement of damaged cardiac muscle cells by

scar tissue

Three Age-Related Changes in Blood Vessels

Arteries become less elastic

Pressure change can cause aneurysm

Calcium deposits on vessel walls

Can cause stroke or infarction

Thrombi can form

At atherosclerotic plaques

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