Chapter 20
Chapter 20
THE CARDIOVASCULAR SYSTEM: THE HEART
Lecture Outline
INTRODUCTION
• The cardiovascular system consists of the blood, heart, and blood vessels.
• The heart is the pump that circulates the blood through an estimated 60,000 miles of blood vessels.
• The study of the normal heart and diseases associated with it is known as cardiology.
Chapter 20
The Cardiovascular System: The Heart
• Heart pumps over 1 million gallons per year.
• Over 60,000 miles of blood vessels
ANATOMY OF THE HEART
ANATOMY OF THE HEART
Location of the heart
• The heart is situated between the lungs in the mediastinum with about two-thirds of its mass to the left of the midline (Figure 20.1).
• Because the heart lies between two rigid structures, the vertebral column and the sternum, external compression on the chest can be used to force blood out of the heart and into the circulation. (Clinical Application)
Heart Location
• Heart is located in the mediastinum
– area from the sternum to the vertebral column and between the lungs
Heart Orientation
• Apex - directed anteriorly, inferiorly and to the left
• Base - directed posteriorly, superiorly and to the right
• Anterior surface - deep to the sternum and ribs
• Inferior surface - rests on the diaphragm
• Right border - faces right lung
• Left border (pulmonary border) - faces left lung
Heart Orientation
• Heart has 2 surfaces: anterior and inferior, and 2 borders: right and left
Surface Projection of the Heart
• Superior right point at the superior border of the 3rd right costal cartilage
• Superior left point at the inferior border of the 2nd left costal cartilage 3cm to the left of midline
• Inferior left point at the 5th intercostal space, 9 cm from the midline
• Inferior right point at superior border of the 6th right costal cartilage, 3 cm from the midline
Pericardium
• The heart is enclosed and held in place by the pericardium.
– The pericardium consists of an outer fibrous pericardium and an inner serous pericardium (epicardium. (Figure 20.2a).
• The serous pericardium is composed of a parietal layer and a visceral layer.
– Between the parietal and visceral layers of the serous pericardium is the pericardial cavity, a potential space filled with pericardial fluid that reduces friction between the two membranes.
– An inflammation of the pericardium is known as pericarditis. Associated bleeding into the pericardial cavity compresses the heart (cardiac tamponade) and is potentially lethal (Clinical Application).
Pericardium
• Fibrous pericardium
– dense irregular CT
– protects and anchors the heart, prevents overstretching
• Serous pericardium
– thin delicate membrane
– contains
• parietal layer-outer layer
• pericardial cavity with pericardial fluid
• visceral layer (epicardium)
Layers of the Heart Wall
• The wall of the heart has three layers: epicardium, myocardium, and endocardium (Figure 20.2a).
• The epicardium consists of mesothelium and connective tissue, the myocardium is composed of cardiac muscle, and the endocardium consists of endothelium and connective tissue (Figure 20.2c).
• Myocarditis is an inflammation of the myocardium.
• Endocarditis in an inflammation of the endocardium. It usually involves the heart valves.
Layers of Heart Wall
• Epicardium
– visceral layer of serous pericardium
• Myocardium
– cardiac muscle layer is the bulk of the heart
• Endocardium
– chamber lining & valves
Muscle Bundles of the Myocardium
• Cardiac muscle fibers swirl diagonally around the heart in interlacing bundles
Chambers and Sulci of the Heart (Figure 20.3).
• Four chambers
– 2 upper atria
– 2 lower ventricles
• Sulci - grooves on surface of heart containing coronary blood vessels and fat
– coronary sulcus
• encircles heart and marks the boundary between the atria and the ventricles
– anterior interventricular sulcus
• marks the boundary between the ventricles anteriorly
– posterior interventricular sulcus
• marks the boundary between the ventricles posteriorly
Chambers and Sulci
Chambers and Sulci
Right Atrium
• Receives blood from 3 sources
– superior vena cava, inferior vena cava and coronary sinus
• Interatrial septum partitions the atria
• Fossa ovalis is a remnant of the fetal foramen ovale
• Tricuspid valve
– Blood flows through into right ventricle
– has three cusps composed of dense CT covered by endocardium
Right Ventricle
• Forms most of anterior surface of heart
• Papillary muscles are cone shaped trabeculae carneae (raised bundles of cardiac muscle)
• Chordae tendineae: cords between valve cusps and papillary muscles
• Interventricular septum: partitions ventricles
• Pulmonary semilunar valve: blood flows into pulmonary trunk
Left Atrium
• Forms most of the base of the heart
• Receives blood from lungs - 4 pulmonary veins (2 right + 2 left)
• Bicuspid valve: blood passes through into left ventricle
– has two cusps
– to remember names of this valve, try the pneumonic LAMB
• Left Atrioventricular, Mitral, or Bicuspid valve
Left Ventricle
• Forms the apex of heart
• Chordae tendineae anchor bicuspid valve to papillary muscles (also has trabeculae carneae like right ventricle)
• Aortic semilunar valve:
– blood passes through valve into the ascending aorta
– just above valve are the openings to the coronary arteries
Myocardial Thickness and Function
• The thickness of the myocardium of the four chambers varies according to the function of each chamber.
– The atria walls are thin because they deliver blood to the ventricles.
– The ventricle walls are thicker because they pump blood greater distances (Figure 20.4a).
– The right ventricle walls are thinner than the left because they pump blood into the lungs, which are nearby and offer very little resistance to blood flow.
– The left ventricle walls are thicker because they pump blood through the body where the resistance to blood flow is greater.
Myocardial Thickness and Function
• Thickness of myocardium varies according to the function of the chamber
• Atria are thin walled, deliver blood to adjacent ventricles
Thickness of Cardiac Walls
HEART VALVES AND CIRCULATION OF BLOOD
• Valves open and close in response to pressure changes as the heart contracts and relaxes.
Fibrous Skeleton of Heart
• (Figure 20.5). Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum
– Support structure for heart valves
– Insertion point for cardiac muscle bundles
– Electrical insulator between atria and ventricles
• prevents direct propagation of AP’s to ventricles
Atrioventricular Valves Open
• A-V valves open and allow blood to flow from atria into ventricles when ventricular pressure is lower than atrial pressure
– occurs when ventricles are relaxed, chordae tendineae are slack and papillary muscles are relaxed
Atrioventricular Valves Close
• A-V valves close preventing backflow of blood into atria
– occurs when ventricles contract, pushing valve cusps closed, chordae tendinae are pulled taut and papillary muscles contract to pull cords and prevent cusps from everting
Semilunar Valves
• SL valves open with ventricular contraction
– allow blood to flow into pulmonary trunk and aorta
• SL valves close with ventricular relaxation
– prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the SL valves
Heart valve disorders
• Stenosis is a narrowing of a heart valve which restricts blood flow.
• Insufficiency or incompetence is a failure of a valve to close completely.
• Stenosed valves may be repaired by balloon valvuloplasty, surgical repair, or valve replacement.
Valve Function Review
Valve Function Review
Blood Circulation
• Two closed circuits, the systemic and pulmonic
• Systemic circulation
– left side of heart pumps blood through body
– left ventricle pumps oxygenated blood into aorta
– aorta branches into many arteries that travel to organs
– arteries branch into many arterioles in tissue
– arterioles branch into thin-walled capillaries for exchange of gases and nutrients
– deoxygenated blood begins its return in venules
– venules merge into veins and return to right atrium
Blood Circulation (cont.)
• Pulmonary circulation
– right side of heart pumps deoxygenated blood to lungs
– right ventricle pumps blood to pulmonary trunk
– pulmonary trunk branches into pulmonary arteries
– pulmonary arteries carry blood to lungs for exchange of gases
– oxygenated blood returns to heart in pulmonary veins
Blood Circulation
• Blood flow
– blue = deoxygenated
– red = oxygenated
Coronary Circulation
• The flow of blood through the many vessels that flow through the myocardium of the heart is called the coronary (cardiac) circulation; it delivers oxygenated blood and nutrients to and removes carbon dioxide and wastes from the myocardium (Figure 20.8b).
• When blockage of a coronary artery deprives the heart muscle of oxygen, reperfusion may damage the tissue further. This damage is due to free radicals. Drugs that lessen reperfusion damage after a heart attack are being developed .
Coronary Circulation
• Coronary circulation is blood supply to the heart
• Heart as a very active muscle needs lots of O2
• When the heart relaxes high pressure of blood in aorta pushes blood into coronary vessels
• Many anastomoses
– connections between arteries supplying blood to the same region, provide alternate routes if one artery becomes occluded
Coronary Arteries
• Branches off aorta above aortic semilunar valve
• Left coronary artery
– circumflex branch
• in coronary sulcus, supplies left atrium and left ventricle
– anterior interventricular art.
• supplies both ventricles
• Right coronary artery
– marginal branch
• in coronary sulcus, supplies right ventricle
– posterior interventricular art.
• supplies both ventricles
Coronary Veins
• Collects wastes from cardiac muscle
• Drains into a large sinus on posterior surface of heart called the coronary sinus
• Coronary sinus empties into right atrium
CARDIAC MUSCLE AND THE CARDIAC CONDUCTION SYSTEM
Histology of Cardiac Muscle
• Compared to skeletal muscle fibers, cardiac muscle fibers are shorter in length, larger in diameter, and squarish rather than circular in transverse section (Figure 20.9).
• They also exhibit branching (Table 4.4B).
• Fibers within the networks are connected by intercalated discs, which consist of desmosomes and gap junctions
• Cardiac muscles have the same arrangement of actin and myosin, and the same bands, zones, and Z discs as skeletal muscles.
• They do have less sarcoplasmic reticulum than skeletal muscles and require Ca+2 from extracellular fluid for contraction.
Cardiac Muscle Histology
• Branching, intercalated discs with gap junctions, involuntary, striated, single central nucleus per cell
Cardiac Myofibril
Conduction System of Heart
Myocardial ischemia and infarction
• Reduced blood flow through coronary arteris may cause ischemia. Ischemia cuases hypoxia and may weaken the myocardial cells. Ischemia is often manifested through angina pectoris.
– A complete obstruction of flow in a coronary artery may cause myocardial infarction (heart attack).
– Tissue distal to the obstruction dies and is replaced by scar tissur.
– Treatment may involve injection of thrombolytic agents, coronary angioplasty, or coronary artery bypass grafts.
• While it was long thought that cardiac muscle lacked stem cells, recent studies five evidence for replacement of heart cells. It appears that stem cells in the blood can migrate to the heart and differentiate into myocardial cells.
Autorhythmic Cells: The Conduction System
• Cardiac muscle cells are autorhythmic cells because they are self-excitable. They repeatedly generate spontaneous action potentials that then trigger heart contractions.
• These cells act as a pacemaker to set the rhythm for the entire heart.
• They form the conduction system, the route for propagating action potential through the heart muscle.
Conduction System of Heart
Conduction
• Components of this system are the sinoartrial (SA) node (pacemaker), atrioventricular (AV) node, atrioventricular bundle (bundle of His), right and left bundle branches, and the conduction myofibers (Purkinje fibers) (Figure 20.10)
• Signals from the autonomic nervous system and hormones, such as epinephrine, do modify the heartbeat (in terms of rate and strength of contraction), but they do not establish the fundamental rhythm.
Conduction System of Heart
Rhythm of Conduction System
• SA node fires spontaneously 90-100 times per minute
• AV node fires at 40-50 times per minute
• If both nodes are suppressed fibers in ventricles by themselves fire only 20-40 times per minute
• Artificial pacemaker needed if pace is too slow
• Extra beats forming at other sites are called ectopic pacemakers
– caffeine & nicotine increase activity
Timing of Atrial &
Ventricular Excitation
• SA node setting pace since is the fastest
• In 50 msec excitation spreads through both atria and down to AV node
• 100 msec delay at AV node due to smaller diameter fibers- allows atria to fully contract filling ventricles before ventricles contract
• In 50 msec excitation spreads through both ventricles simultaneously
Abnormal Conduction
• Sick sinus syndrome describes an abnormally functioning SA node that initiates irregular heart beats.
• When abnormal pacing of the heart develops, heart rhythm can be restored by implanting an artificail pacemaker, a device that sends out small, regular currents to stimulate myocardial contraction..
Action potential and contraction of contractile fibers
• An impulse in a ventricular contractile fiber is characterized by rapid depolarization, plateau, and repolarization (Figure 20.11).
• The refractory period of a cardiac muscle fiber (the time interval when a second contraction cannot be triggered) is longer than the contraction itself (Figure 20.11). Therefore tetanus cannot occur in myocardial cells.
Conduction System of the Heart
Physiology of Contraction
• Depolarization, plateau, repolarization
Depolarization & Repolarization
• Depolarization
– Cardiac cell resting membrane potential is -90mv
– excitation spreads through gap junctions
– fast Na+ channels open for rapid depolarization
• Plateau phase
– 250 msec (only 1msec in neuron)
– slow Ca+2 channels open, let Ca +2 enter from outside cell and from storage in sarcoplasmic reticulum, while K+ channels close
– Ca +2 binds to troponin to allow for actin-myosin cross-bridge formation & tension development
• Repolarization
– Ca+2 channels close and K+ channels open & -90mv is restored as potassium leaves the cell
• Refractory period
– very long so heart can fill
Action Potential in Cardiac Muscle
ATP production in cardiac muscle
• Cardiac muscle relies on aerobic cellular respiration for ATP production.
• Cardiac muscle also produces some ATP from creatine phosphate
• The presence of creatine kinase (CK) in the blood indicates injury of cardiac muscle usually caused by a myocardial infarction.
Electrocardiogram
• Impulse conduction through the heart generates electrical currents that can be detected at the surface of the body. A recording of the electrical changes that accompany each cardiac cycle (heartbeat) is called an electrocardiogram (ECG or EKG).
• The ECG helps to determine if the conduction pathway is abnormal, if the heart is enlarged, and if certain regions are damaged.
• Figure 20.12 shows a typical ECG.
Electrocardiogram---ECG or EKG
• EKG
– Action potentials of all active cells can be detected and recorded
• P wave
– atrial depolarization
• P to Q interval
– conduction time from atrial to ventricular excitation
• QRS complex
– ventricular depolarization
• T wave
– ventricular repolarization
ECG
• In a typical Lead II record, three clearly visible waves accompany each heartbeat It consists of:.
• P wave (atrial depolarization - spread of impulse from SA node over atria)
• QRS complex (ventricular depolarization - spread of impulse through ventricles)
• T wave (ventricular repolarization).
• Correlation of ECG waves with atrial and ventricular systole (Figure 20.13)
ECG
• As atrial fibers depolarize, the P wave appears.
• After the P wave begins, the atria contract (atrial systole). Action potential slows at the AV node giving the atria time to contract.
• The action potential moves rapidly through the bundle branches, Purkinje fibers, and the ventricular myocardium producing the QRS complex.
• Ventricular contraction after the QRS comples and continues through the ST segment.
• Repolarization of the ventricles produces the T wave.
• Both atria and ventricles repolarize and the P wave appears.
THE CARDIAC CYCLE
• A cardiac cycle consists of the systole (contraction) and diastole (relaxation) of both atria, rapidly followed by the systole and diastole of both ventricles.
• Pressure and volume changes during the cardiac cycle
• During a cardiac cycle atria and ventricles alternately contract and relax forcing blood from areas of high pressure to areas of lower pressure.
• Figure 20.14 shows the relation between the ECG and changes in atrial pressure, ventricular pressure, aortic pressure, and ventricular volume during the cardia cycle.
One Cardiac Cycle - Vocabulary
• At 75 beats/min, one cycle requires 0.8 sec.
– systole (contraction) and diastole (relaxation) of both atria, plus the systole and diastole of both ventricles
• End diastolic volume (EDV)
– volume in ventricle at end of diastole, about 130ml
• End systolic volume (ESV)
– volume in ventricle at end of systole, about 60ml
• Stroke volume (SV)
– the volume ejected per beat from each ventricle, about 70ml
– SV = EDV - ESV
Phases of Cardiac Cycle
• Isovolumetric relaxation
– brief period when volume in ventricles does not change--as ventricles relax, pressure drops and AV valves open
• Ventricular filling
– rapid ventricular filling:as blood flows from full atria
– diastasis: as blood flows from atria in smaller volume
– atrial systole pushes final 20-25 ml blood into ventricle
• Ventricular systole
– ventricular systole
– isovolumetric contraction
• brief period, AV valves close before SL valves open
– ventricular ejection: as SL valves open and blood is ejected
Cardiac Cycle
Atrial systole/ventricular diastole
• The atria contract, increasing pressure forces the AV valves to open.
– The amount of blood in the ventricle at the end of diastole is the End Diastolic Volume (EDV)
• Ventricular systole/atrial diastole
– Ventricles contract and increasing pressure forces the AV valves to close.
– AV and SL valves are all closed (isovolumetric contraction).
– Pressure continues to rise opening the SL valves leading to ventricular ejection.
– The amount of blood in the left ventrical at the end of systole is End Systolic Volume (ESV). Stroke volume (SV) is the volume of blood ejected from the left ventricle SV = EDV-ESV.
Relaxation period
• Both atria and ventricles are relaxed. Pressure in the ventricles fall and the SL valves close. Brief time all four valves are closed is the isovolumetric relaxation. Pressure in the ventricles continues to fall, the AV valves open, and ventricular filling begins.
Ventricular Pressures
• Blood pressure in aorta is 120mm Hg
• Blood pressure in pulmonary trunk is 30mm Hg
• Differences in ventricle wall thickness allows heart to push the same amount of blood with more force from the left ventricle
• The volume of blood ejected from each ventricle is 70ml (stroke volume)
• Why do both stroke volumes need to be same?
Auscultation
• The act of listening to sounds within the body is called auscultation, and it is usually done with a stethoscope. The sound of a heartbeat comes primarily from the turbulence in blood flow caused by the closure of the valves, not from the contraction of the heart muscle (Figure 20.15).
• The first heart sound (lubb) is created by blood turbulence associated with the closing of the atrioventricular valves soon after ventricular systole begins.
• The second heart sound (dupp) represents the closing of the semilunar valves close to the end of the ventricular systole.
Heart Sounds
Murmurs
• A heart murmur is an abnormal sound that consists of a flow noise that is heard before, between, or after the lubb-dupp or that may mask the normal sounds entirely.
• Some murmurs are caused by turbulent blood flow around valves due to abnormal anatomy or increased volume of flow.
• Not all murmurs are abnormal or symptomatic, but most indicate a valve disorder.
CARDIAC OUTPUT
• Since the body’s need for oxygen varies with the level of activity, the heart’s ability to discharge oxygen-carrying blood must also be variable. Body cells need specific amounts of blood each minute to maintain health and life.
• Cardiac output (CO) is the volume of blood ejected from the left ventricle (or the right ventricle) into the aorta (or pulmonary trunk) each minute.
– Cardiac output equals the stroke volume, the volume of blood ejected by the ventricle with each contraction, multiplied by the heart rate, the number of beats per minute. CO = SV X HR
• Cardiac reserve is the ratio between the maximum cardiac output a person can achieve and the cardiac output at rest.
Cardiac Output
• CO = SV x HR
– at 70ml stroke volume & 75 beat/min----5 and 1/4 liters/min
– entire blood supply passes through circulatory system every minute
• Cardiac reserve is maximum output/output at rest
– average is 4-5x while athlete’s is 7-8x
Influences on Stroke Volume
• Preload (affect of stretching)
– Frank-Starling Law of Heart
– more muscle is stretched, greater force of contraction
– more blood more force of contraction results
• Contractility
– autonomic nerves, hormones, Ca+2 or K+ levels
• Afterload
– amount of pressure created by the blood in the way
– high blood pressure creates high afterload
Stroke Volume and Heart Rate
Preload: Effect of Stretching
• According to the Frank-Starling law of the heart, a greater preload (stretch) on cardiac muscle fibers just before they contract increases their force of contraction during systole.
– Preload is proportional to EDV.
– EDV is determined by length of ventricular diastole and venous return.
• The Frank-Starling law of the heart equalizes the output of the right and left ventricles and keeps the same volume of blood flowing to both the systemic and pulmonary circulations.
Contractility
• Myocardial contractility, the strength of contraction at any given preload, is affected by positive and negative inotropic agents.
– Positive inotropic agents increase contractility
– Negative inotropic agents decrease contractility.
• For a constant preload, the stroke volume increases when positive inotropic agents are present and decreases when negative inotropic agents are present.
Afterload
• The pressure that must be overcome before a semilunar valve can open is the afterload.
• In congestive heart failure, blood begins to remain in the ventricles increasing the preload and ultimately causing an overstretching of the heart and less forceful contraction
– Left ventricular failure results in pulmonary edema
– Right ventricular failure results in peripheral edema.
Regulation of Heart Rate
• Cardiac output depends on heart rate as well as stroke volume. Changing heart rate is the body’s principal mechanism of short-term control over cardiac output and blood pressure. Several factors contribute to regulation of heart rate.
Regulation of Heart Rate
• Nervous control from the cardiovascular center in the medulla
– Sympathetic impulses increase heart rate and force of contraction
– parasympathetic impulses decrease heart rate.
– Baroreceptors (pressure receptors) detect change in BP and send info to the cardiovascular center
• located in the arch of the aorta and carotid arteries
• Heart rate is also affected by hormones
– epinephrine, norepinephrine, thyroid hormones
– ions (Na+, K+, Ca2+)
– age, gender, physical fitness, and temperature
Regulation of Heart Rate
Autonomic regulation of the heart
• Nervous control of the cardiovascular system stems from the cardiovascular center in the medulla oblongata (Figure 20.16).
• Proprioceptors, baroreceptors, and chemoreceptors monitor factors that influence the heart rate.
• Sympathetic impulses increase heart rate and force of contraction; parasympathetic impulses decrease heart rate.
Chemical regulation of heart rate
• Heart rate affected by hormones (epinephrine, norepinephrine, thyroid hormones).
• Cations (Na+, K+, Ca+2) also affect heart rate.
• Other factors such as age, gender, physical fitness, and temperature also affect heart rate.
• Figure 20.16 summarizes the factors that can increase stoke volume and heart rate to cause an increase in cardiac output..
Risk Factors for Heart Disease
• Risk factors in heart disease:
– high blood cholesterol level
– high blood pressure
– cigarette smoking
– obesity & lack of regular exercise.
• Other factors include:
– diabetes mellitus
– genetic predisposition
– male gender
– high blood levels of fibrinogen
– left ventricular hypertrophy
Plasma Lipids and Heart Disease
• Risk factor for developing heart disease is high blood cholesterol level.
– promotes growth of fatty plaques
– Most lipids are transported as lipoproteins
• low-density lipoproteins (LDLs)
• high-density lipoproteins (HDLs)
•
