THE CARDIOVASCULAR SYSTEM: THE HEART

THE CARDIOVASCULAR SYSTEM: THE HEART

Heart pumps over 1 million gallons per year. Over 60,000 miles of blood vessels

ANATOMY OF THE HEART

Principles of Human Anatomy and Physiology, 11e

ANATOMY OF THE HEART

HEART LOCATION

Principles of Human Anatomy and Physiology, 11e

Heart is located in the mediastinum

area from the sternum to the vertebral column and between the lungs

HEART ORIENTATION

Heart has 2 surfaces: anterior and inferior, and 2 borders: right and left

PERICARDIUM

Fibrous pericardium dense irregular CT protects and anchors the heart, prevents overstretching Serous pericardium thin delicate membrane contains parietal layer-outer layer 7 pericardial cavity with pericardial fluid visceral layer (epicardium)

LAYERS OF HEART WALL

Epicardium

visceral layer of serous pericardium cardiac muscle layer is the bulk of the heart chamber lining & valves
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Myocardium

Endocardium

MUSCLE BUNDLES OF THE MYOCARDIUM

Cardiac muscle fibers swirl diagonally around the heart in 9 interlacing bundles

CHAMBERS AND SULCI OF THE HEART

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

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CHAMBERS AND SULCI

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Anterior View

CHAMBERS AND SULCI

Posterior View

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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

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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 14 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 15 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 16 just above valve are the openings to the coronary arteries

MYOCARDIAL THICKNESS AND FUNCTION

Thickness of myocardium varies according to the function of the chamber Atria are thin walled, deliver blood to adjacent ventricles Ventricle walls are much thicker and stronger right ventricle supplies blood to the lungs (little flow resistance) left ventricle wall is the thickest to supply systemic 17 circulation

THICKNESS OF CARDIAC WALLS

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Myocardium of left ventricle is much thicker than the right.

FIBROUS SKELETON OF HEART

Dense CT rings surround the valves of the heart, fuse and merge with the interventricular septum

Support structure for heart valves (Valves open and close in response to pressure changes as the heart contracts and relaxes.) Insertion point for cardiac muscle bundles Electrical insulator between atria and ventricles 19

prevents direct propagation of APs to ventricles

ATRIOVENTRICULAR VALVES OPEN

A-V valves (bicuspid/mitral & tricuspid) 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 20

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
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SEMILUNAR VALVES (AORTIC & PULMONARY)

SL valves open with ventricular contraction

allow blood to flow into pulmonary trunk and aorta

prevents blood from returning to ventricles, blood fills valve cusps, tightly closing the SL valves 22

SL valves close with ventricular relaxation

VALVE FUNCTION REVIEW

Atria contract, blood fills ventricles through A-V valves

Ventricles contract, blood pumped into aorta and pulmonary trunk through SL 23 valves

BLOOD CIRCULATION : SYSTEMIC

Two closed circuits, the systemic and pulmonary 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

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BLOOD CIRCULATION : PULMONARY

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

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BLOOD CIRCULATION

Blood flow
blue = deoxygenated red = oxygenated

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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 It delivers oxygenated blood and nutrients to and removes carbon dioxide and wastes from the myocardium Many anastomoses

connections between arteries supplying blood to the same region, provide alternate routes if one artery becomes occluded
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ANTERIOR VIEW

L. Coronary artery

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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. 29 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
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CARDIAC MUSCLE AND THE CARDIAC CONDUCTION SYSTEM

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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 They also exhibit branching. 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.

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CARDIAC MUSCLE HISTOLOGY

Branching, intercalated discs with gap junctions, involuntary, striated, single central nucleus per cell 33

Principles of Human Anatomy and Physiology, 11e

CARDIAC MYOFIBRIL

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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 tissue. Treatment may involve injection of thrombolytic agents, coronary angioplasty, or coronary artery bypass grafts.
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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.

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CONDUCTION SYSTEM OF HEART

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Coordinates contraction of heart muscle.

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) 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.

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CONDUCTION SYSTEM OF HEART

Autorhythmic Cells

Cells fire spontaneously, act as pacemaker and form conduction system for the heart cluster of cells in wall of Rt. Atria begins heart activity that spreads to both atria excitation spreads to AV node in atrial septum, transmits signal to bundle of His the connection between atria and ventricles divides into bundle branches & purkinje fibers, large diameter fibers that conduct signals quickly

SA node

AV node

AV bundle of His

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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

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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 fibersallows atria to fully contract filling ventricles before ventricles contract In 50 msec excitation spreads through both ventricles simultaneously

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ACTION POTENTIAL AND CONTRACTION OF

CONTRACTILE FIBERS An impulse in a ventricular contractile fiber is characterized by rapid depolarization, plateau, and repolarization The refractory period of a cardiac muscle fiber (the time interval when a second contraction cannot be triggered) is longer than the contraction itself .Therefore tetanus cannot occur in myocardial cells.

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CONDUCTION SYSTEM OF THE HEART

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PHYSIOLOGY OF CONTRACTION

Depolarization,

plateau, repolarization

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Principles of Human Anatomy and Physiology, 11e

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
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ACTION POTENTIAL IN CARDIAC MUSCLE

Changes in cell membrane permeability.

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Principles of Human Anatomy and Physiology, 11e

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.

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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.

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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
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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)

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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.

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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.

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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

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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

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CARDIAC CYCLE

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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.

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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.

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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?

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CARDIAC OUTPUT
Since the bodys need for oxygen varies with the level of activity, the hearts 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
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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 athletes is 7-8x

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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

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STROKE VOLUME AND HEART RATE

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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.
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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.

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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.

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REGULATION OF HEART RATE

Cardiac output depends on heart rate as well as stroke volume. Changing heart rate is the bodys principal mechanism of short-term control over cardiac output and blood pressure. Several factors contribute to regulation of heart rate.

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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

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REGULATION OF HEART RATE

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Principles of Human Anatomy and Physiology, 11e

AUTONOMIC REGULATION OF THE HEART

Nervous control of the cardiovascular system stems from the cardiovascular center in the medulla oblongata 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.

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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.

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EXERCISE AND THE HEART

A persons cardiovascular fitness can be improved with regular exercise. Aerobic exercise (any activity that works large body muscles for at least 20 minutes, preferably 3 5 times per week) increases cardiac output and elevates metabolic rate. Several weeks of training results in maximal cardiac output and oxygen delivery to tissues Regular exercise also decreases anxiety and depression, controls weight, and increases fibrinolytic activity. Sustained exercise increases oxygen demand in muscles As a heart fails, a persons mobility decreases. Heart transplants may help such individuals. Other possibilities include cardiac assist devices and surgical procedures.

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