FL-K24 Cardiovascular System

8/12/2019 FL-K24 Cardiovascular System

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Copyright 2004 Pearson Education, Inc., publishing as Benjamin Cummings

Human Anatomy & Physiology, Sixth Edit ion

Elaine N. Marieb

PowerPointLecture Slides prepared by Vince Austin, University of Kentucky

The Cardiovascular System:


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Heart Anatomy

Figure 18.1


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Pericardial Layers of the Heart

Figure 18.2


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External Heart: Anterior View

Figure 18.4b


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Gross Anatomy of Heart: Frontal Section

Figure 18.4e


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Pathway of Blood Through the Heart and Lungs

Figure 18.5



Coronary Circulation: Arterial Supply

Figure 18.7a



Coronary Circulation: Venous Supply

Figure 18.7b



Heart Valves

Heart valves ensure unidirectional blood flow

through the heart

Atrioventricular (AV) valves lie between the atria

and the ventricles

AV valves prevent backflow into the atria when

ventricles contract

Chordae tendineae anchor AV valves to papillary

muscles



Heart Valves

Aortic semilunar valve lies between the left

ventricle and the aorta

Pulmonary semilunar valve lies between the right

ventricle and pulmonary trunk

Semilunar valves prevent backflow of blood into theventricles


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Heart Valves

Figure 18.8c, d


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Atrioventricular Valve Function

Figure 18.9


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Semilunar Valve Function

Figure 18.10


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Microscopic Anatomy of Heart Muscle

Cardiac muscle is striated, short, fat, branched, andinterconnected

The connective tissue endomysium acts as both

tendon and insertion

Intercalated discs anchor cardiac cells together and

allow free passage of ions

Heart muscle behaves as a functional syncytium

I nterActive Physiology:

Cardiovascular System: Anatomy Review: The HeartPLAY
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Microscopic Anatomy of Heart Muscle

Figure 18.11


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Cardiac Muscle Contraction

Heart muscle:

Is stimulated by nerves and is self-excitable

(automaticity)

Contracts as a unit

Has a long (250 ms) absolute refractory period

Cardiac muscle contraction is similar to skeletal

muscle contraction


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Heart Physiology: Intrinsic Conduction System

Autorhythmic cells:

Initiate action potentials

Have unstable resting potentials called pacemakerpotentials

Use calcium influx (rather than sodium) for rising

phase of the action potential


Cardiovascular System: Cardiac Action PotentialPLAY
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Pacemaker and Action Potentials of the Heart

Figure 18.13


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Heart Physiology: Sequence of Excitation

Sinoatrial (SA) node generates impulses about 75

times/minute

Atrioventricular (AV) node delays the impulse

approximately 0.1 second

Impulse passes from atria to ventricles via theatrioventricular bundle (bundle of His)


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AV bundle splits into two pathways in the

interventricular septum (bundle branches)

Bundle branches carry the impulse toward the apex

of the heart

Purkinje fibers carry the impulse to the heart apex

and ventricular walls


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Figure 18.14a


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Heart Excitation Related to ECG

Figure 18.17


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Extrinsic Innervation of the Heart

Heart is stimulated

by the sympathetic

cardioacceleratory

center

Heart is inhibited by

the parasympathetic

cardioinhibitorycenter

Figure 18.15


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Heart Sounds

Heart sounds (lub-dup) are associated with closing

of heart valves

First sound occurs as AV valves close and signifies

beginning of systole

Second sound occurs when SL valves close at the

beginning of ventricular diastole


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Ph f h C di C l


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Phases of the Cardiac Cycle

Ventricular filling mid-to-late diastole

Heart blood pressure is low as blood enters atria

and flows into ventricles

AV valves are open, then atrial systole occurs

Ph f th C di C l


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Ventricular systole

Atria relax

Rising ventricular pressure results in closing of AVvalves

Isovolumetric contraction phase

Ventricular ejection phase opens semilunar valves

Ph f th C di C l


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Isovolumetric relaxation early diastole

Ventricles relax

Backflow of blood in aorta and pulmonary trunkcloses semilunar valves

Dicrotic notch brief rise in aortic pressure caused

by backflow of blood rebounding off semilunarvalves


Cardiovascular System: Cardiac CyclePLAY

Ph f th C di C l
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Figure 18.20

C di O t t (CO) d R


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Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each ventricle

in one minute

CO is the product of heart rate (HR) and stroke

volume (SV)

HR is the number of heart beats per minute

SV is the amount of blood pumped out by a

ventricle with each beat

Cardiac reserve is the difference between resting

and maximal CO

C di O t t E l


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Cardiac Output: Example

CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)

CO = 5250 ml/min (5.25 L/min)

R l ti f St k V l


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Regulation of Stroke Volume

SV = end diastolic volume (EDV) minus end

systolic volume (ESV)

EDV = amount of blood collected in a ventricle

during diastole

ESV = amount of blood remaining in a ventricle

after contraction

F t Aff ti St k V l


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Factors Affecting Stroke Volume

Preload amount ventricles are stretched by

contained blood

Contractility cardiac cell contractile force due to

factors other than EDV

Afterload back pressure exerted by blood in the

large arteries leaving the heart

Frank Starling La of the Heart


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Frank-Starling Law of the Heart

Preload, or degree of stretch, of cardiac muscle cellsbefore they contract is the critical factor controlling

stroke volume

Slow heartbeat and exercise increase venous return

to the heart, increasing SV

Blood loss and extremely rapid heartbeat decrease

SV

Preload and Afterload


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Preload and Afterload

Figure 18.21

Extrinsic Factors Influencing Stroke Volume


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Contractility is the increase in contractile strength,

independent of stretch and EDV

Increase in contractility comes from:

Increased sympathetic stimuli

Certain hormones

Ca2+and some drugs



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Agents/factors that decrease contractility include:

Acidosis

Increased extracellular K+

Calcium channel blockers


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Regulation of Heart Rate


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Regulation of Heart Rate

Positive chronotropic factors increase heart rate

Negative chronotropic factors decrease heart rate

Regulation of Heart Rate: Autonomic Nervous


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Sympathetic nervous system (SNS) stimulation is

activated by stress, anxiety, excitement, or exercise

Parasympathetic nervous system (PNS) stimulation

is mediated by acetylcholine and opposes the SNS

PNS dominates the autonomic stimulation, slowingheart rate and causing vagal tone

Regulation of Heart Rate: Autonomic Nervous

System

Atrial (Bainbridge) Reflex


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Atrial (Bainbridge) Reflex

Atrial (Bainbridge) reflex a sympathetic reflex

initiated by increased blood in the atria

Causes stimulation of the SA node

Stimulates baroreceptors in the atria, causing

increased SNS stimulation

Chemical Regulation of the Heart


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Chemical Regulation of the Heart

The hormones epinephrine and thyroxine increase

heart rate Intra- and extracellular ion concentrations must be

maintained for normal heart function


Cardiovascular System: Cardiac OutputPLAY
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BLOOD PRESSURE

Tekanan yang dibentuk oleh darah terhadap

dinding pembuluh darah

Sistole: pada saat jantung kontraksi

Diastole: pada saat jantung relaksasi

Tekanan Darah = Cardiac Output x Total

Peripheral Resistance

ESH 2003 & JNC VII(2003)

JNC 7


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ESH 2003 & JNC VII(2003)ESH-ESC 2003

BP Classification

BP BP JNC VII(2003)

Bp Classification

Optimal 110

Isolated Systolic

Hypertension

Isolated Systolic

Hypertension> 140 < 90

ESC 2003

JNC 7

2003


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Capillaries


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Capillary Beds

SlideCopyright 2003 Pearson Education, Inc. publishing as Benjamin Cummings

Capillary bedsconsist of two

types of vesselsVascular shunt

directly connects an

arteriole to a venule

Figure 11.10


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Capillary Beds


True capillaries exchange vessels

Oxygen and

nutrients cross tocells

Carbon dioxide

and metabolicwaste productscross into blood

Figure 11.10


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Diffusion at Capillary Beds


Figure 11.20


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FL-K24 Cardiovascular System