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