The Heart Chapter 20. Function of the Heart Pumping the red stuff Anatomy of the Heart Location – mediastinum, slightly to the left of center Size – about.

The Heart

Chapter 20

Function of the Heart• Pumping the red stuff

Anatomy of the Heart• Location – mediastinum, slightly to the left

of center

• Size – about that of your fist

• Mass – 250 – 300 g

Organization of the

Cardiovascular System

Location

Tissues of the Heart

Coverings of the Heart: Anatomy

• Pericardium – a double-walled sac around the heart composed of:– A superficial fibrous pericardium– A deep two-layer serous pericardium

• The parietal layer lines the internal surface of the fibrous pericardium

• The visceral layer or epicardium lines the surface of the heart

• They are separated by the fluid-filled pericardial cavity

Coverings of the Heart: Physiology

• The pericardium:– Protects and anchors the heart– Prevents overfilling of the heart with blood– Allows for the heart to work in a relatively

friction-free environment

Serous pericardium

General Anatomy

Heart Wall

• Epicardium – visceral layer of the serous pericardium

• Myocardium – cardiac muscle layer forming the bulk of the heart

• Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue

• Endocardium – endothelial layer of the inner myocardial surface

• Vessels returning blood to the heart include:– Superior and inferior venae cavae– Right and left pulmonary veins

• Vessels conveying blood away from the heart include:– Pulmonary trunk, which splits into right and left

pulmonary arteries– Ascending aorta (three branches) – brachiocephalic,

left common carotid, and subclavian arteries

External Heart: Major Vessels of the Heart (Anterior View)

• Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries

• Veins – small cardiac, anterior cardiac, and great cardiac veins

External Heart: Vessels that Supply/Drain the Heart (Anterior View)

Surface features of the heart

Cardiac Muscle CellsFigure 20–5

• Vessels returning blood to the heart include:– Right and left pulmonary veins– Superior and inferior venae cavae

• Vessels conveying blood away from the heart include:– Aorta– Right and left pulmonary arteries

External Heart: Major Vessels of the Heart (Posterior View)

Posterior view

Atria of the Heart

• Atria are the receiving chambers of the heart

• Each atrium has a protruding auricle

• Pectinate muscles mark atrial walls

• Blood enters right atria from superior and inferior venae cavae and coronary sinus

• Blood enters left atria from pulmonary veins

Deep in your heart of hearts…

Ventricles of the Heart

• Ventricles are the discharging chambers of the heart

• Papillary muscles and trabeculae carneae muscles mark ventricular walls

• Right ventricle pumps blood into the pulmonary trunk

• Left ventricle pumps blood into the aorta

Note the differences in wall thickness

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 the ventricles

The heart valves

Function of the bicuspid valve

Valve functions

Heart Sounds

Where to go to listen to heart sounds

Some heart valve disorders• Stenosis (narrowing) – the inability of a valve to

open fully

• Insufficiency (incompetence) – failure of the valve to prevent back flow or close properly– Mitral valve prolapse – one or both of the flaps

blows back into the atrium during systole (contraction) of the ventricle allowing backflow into the atrium.

– The aortic semilunar valves can also suffer from stenosis or insufficiency, allowing backflow into the ventricle.

Pathway of Blood Through the Heart and Lungs

• Right atrium tricuspid valve right ventricle

• Right ventricle pulmonary semilunar valve pulmonary arteries lungs

• Lungs pulmonary veins left atrium

• Left atrium bicuspid valve left ventricle

• Left ventricle aortic semilunar valve aorta

• Aorta systemic circulation

Systemic & pulmonary circuits

Blood flow

Coronary Circulation

• Coronary circulation is the functional blood supply to the heart muscle itself

• Collateral routes ensure blood delivery to heart even if major vessels are occluded

Coronary Circulation

(arterial)

Coronary Circulation

(venous)

Cardiac histology & physiology• Cardiac muscle is made of short, branched

fibers

• Striated

• Uninucleate

• There is now some evidence that it has limited mitotic capability (it is likely that regeneration is from migration of stem cells from the blood)

• 99% are contractile

• 1% are “autorhythmic” or “pacemaker” cells

Cardiac Muscle Tissue

Cardiac Muscle Cells

• Intercalated discs:– interconnect cardiac muscle cells– secured by desmosomes – linked by gap junctions– convey force of contraction – propagate action potentials

Characteristics of Cardiac Muscle Cells

1. Small size

2. Single, central nucleus

3. Branching interconnections between cells

4. Intercalated discs

Cardiac Cells vs. Skeletal Fibers Table 20-1

The intrinsic conduction system

• Sinoatrial node: the primary pacemaker – has an intrinsic firing rate of about 100 bpm but kept at 60 – 80 by parasympathetic tone

• Generates pacemaker potentials from leakage of Ca++

• Depolarization spreads via gap junctions in intercalated disks

• Rate can be adjusted by ANS

Intrinsic conduction system • Signals from SA node travel to the

Atrioventricular Node via the internodal pathway

• The AV node has its own intrinsic firing rate of 40 – 60 bpm. In absence of SA node function it can establish a “junctional rhythm” that keeps the ventricles working

The conducting pathways

• The signal is delayed about 0.1 s and then transmitted down the …

• Bundle of His or AV bundle and the left & right bundle branches to the apex

• And from there the depolarization is distributed by the Purkinje fibers

Fig. 20.10a

Contraction of cardiac muscle fibersand the cardiac cycle

The ElectrocardiogramFigure 20–14b

NSR:Normal Sinus

Rhythm

Prolonged contraction of cardiac muscle

Features of an ECG

• P wave:

– atria depolarize

• QRS complex:

– ventricles depolarize

• T wave:

– ventricles repolarize

Resting Potential

• Of a ventricular cell:

–about —90 mV

• Of an atrial cell:

–about —80 mV

3 Steps of Cardiac Action Potential

1.Rapid depolarization:

» voltage-regulated sodium channels (fast channels) open

3 Steps of Cardiac Action Potential

2. As sodium channels close:

– voltage-regulated calcium channels (slow channels) open

– balance Na+ ions pumped out

– hold membrane at 0 mV plateau

3 Steps of Cardiac Action Potential

3. Repolarization:

– plateau continues

– slow calcium channels close

– slow potassium channels open

– rapid repolarization restores resting potential

The Refractory Periods

• Absolute refractory period:

– long

– cardiac muscle cells cannot respond

• Relative refractory period:

– short

– 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

ElectricalActivity and the Cardiac Cycle

Calcium and Contraction

• Contraction of a cardiac muscle cell is produced by an increase in calcium ion concentration around myofibrils

2 Steps of Calcium Ion Concentration

1. 20% of calcium ions required for a contraction:

– calcium ions enter cell membrane during plateau phase

2 Steps of Calcium Ion Concentration

2. Arrival of extracellular Ca2+:– triggers release of calcium ion reserves from

sarcoplasmic reticulum

Intracellular and Extracellular Calcium

• As slow calcium channels close:– intracellular Ca2+ is absorbed by the SR– or pumped out of cell

• Cardiac muscle tissue:– very sensitive to extracellular Ca2+

concentrations

The Cardiac Cycle

• 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

Phases of the Cardiac CycleFigure 20–16

Cardiac output

• CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)• CO = 5250 ml/min (5.25 L/min)

Cardiac output

• 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

Pressure and

Volume in the

Cardiac Cycle

Figure 20–17

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

Factors Affecting Stroke Volume

• Changes in EDV or ESV

Figure 20–23 (Navigator)

Frank-Starling Law of the Heart

• Preload, or degree of stretch, of cardiac muscle cells before 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

Extrinsic Factors Influencing Stroke Volume

• 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

Factors Affecting Heart Rate and Stroke Volume

Extrinsic Factors Influencing Stroke Volume

• Agents/factors that decrease contractility include:– Acidosis– Increased extracellular K+

– Calcium channel blockers

Contractility and Norepinephrine

• Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system

Figure 18.22

Regulation of Heart Rate

• Positive chronotropic factors increase heart rate

• Negative chronotropic factors decrease heart rate

• 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, slowing heart rate and causing vagal tone

Regulation of Heart Rate: Autonomic Nervous System

Autonomic Innervation

Autonomic Pacemaker Regulation

Autonomic Pacemaker Regulation (1 of 3)

• Sympathetic and parasympathetic stimulation:– greatest at SA node (heart rate)

• Membrane potential of pacemaker cells:– lower than other cardiac cells

Autonomic Pacemaker Regulation (2 of 3)

• Rate of spontaneous depolarization depends on:– resting membrane potential– rate of depolarization

Autonomic Pacemaker Regulation (3 of 3)

• ACh (parasympathetic stimulation):– slows the heart

• NE (sympathetic stimulation):– speeds the heart

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

CNS and ANS controls of Cardiac output

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

InterActive Physiology®: Cardiovascular System: Cardiac OutputPLAYPLAY

Factors Involved in Regulation of Cardiac Output

How the heart starts

Examples of Congenital Heart Defects

Congestive Heart Failure (CHF)

• Congestive heart failure (CHF) is caused by:– Coronary atherosclerosis– Persistent high blood pressure– Multiple myocardial infarcts– Dilated cardiomyopathy (DCM)

Arteriosclerosis

Fig. 20.20

Age-Related Changes Affecting the Heart

• Sclerosis and thickening of valve flaps

• Decline in cardiac reserve

• Fibrosis of cardiac muscle

• Atherosclerosis