Biology 322 – Human Anatomy

Cardiac Anatomy

•Remember that the cardiovascular system refers to the (1) heart and the (2) blood vessels

•CV system consists of two main divisions based on where the blood is going after leaving the heart

1. Pulmonary circuit - carries blood that is O2-poor/CO2-rich to the lungs so that O2 and CO2 can be exchanged, returning O2-rich/CO2-poor blood back to the heart so it can enter the systemic circuit

2. Systemic circuit – carries O2-rich/CO2-poor blood from the heart out to all of the tissues of the body, THEN carries the O2-poor/CO2-rich blood back to the heart so that it can enter the pulmonary circuit

• The right side of the heart pumps blood through the pulmonary circuit….left side of the heart pumps blood through the systemic circuit

•Heart is located roughly in the center of the thoracic cavity (mediastinum) between the two lungs•The broad, superior portion is the BASE•The narrower inferior portion is the APEX•Heart is angled to the left so that about 2/3 of the heart is to the left of the midsaggital plane (despite what every cartoon would have you think!)

•Several very large blood vessels are attached at the base of the heart (GREAT VESSELS)

1. Aorta – carries oxygenated blood from left ventricle out to systemic circ.

2. Inferior and superior vena cava – returns deoxygenated blood back to the heart from the systemic circ.

Pericardium

•Heart is contained within a double-layered sac known as the PERICARDIUM•PARIETAL PERICARDIUM is the outer layer th

Consists of a outer fibrous layer and an inner serous layer

•VISCERAL PERICARDIUM is the inner layer closest to the heart (also known as the EPICARDIUM)

Basically a continuation of the serous layer of the parietal pericardium

•Between the two layers is the PERICARDIAL CAVITY

Filled with PERICARDIAL FLUID that allows the heart to operate in a low friction environment

Heart Wall

•Three layers 1. Epicardium (visceral pericardium) – a

simple layer of squamous epithelia directly on the surface of the heart

2. Myocardium – thickest layer composed of the cardiac muscle cells that carry out contraction

3. Endocardium – another simple layer of squamous epithelial cells lining the interior of the heart and valves

• These three layers make up the wall of each of the 4 chambers of the heart 2 upper atria, 2 lower ventricles Thickness of the walls will vary

Chambers and valves of the heart

•Atrioventricular (AV) valves prevent backflow of blood from ventricle into atrium

Tendinous cords and papillary muscles prevent valve prolapse

•Pulmonary and aortic valves (“semilunar valves”) and AV valves ensure one-direction blood flow

•Atria are chambers that receive blood from lungs or rest of body•Ventricles are chambers that expel blood to the lungs or rest of body•Atria and ventricles are separated by a muscular wall called a septum

•Faulty valves caused blood to flow back into atria (AV valves) or ventricles (semilunar valves)•Increased pressures in these chambers force heart to contract more forcefully …more strain on heart•Faulty valves often are the cause of heart murmurs (abnormal heart sounds)

Flow of blood through the heart

1. Superior, inferior vena cava2. Right atrium3. Right AV valve4. Right ventricle5. Pulmonary valve6. Pulmonary artery7. LUNGS8. Pulmonary vein9. Left atrium10. Left AV valve11. Left ventricle12. Aortic valve13. Aorta14. REST OF THE BODY

O2-poor blood

O2-rich blood

Coronary circulation

•Coronary arteries and cardiac veins supply blood to the tissues of the heart•Pattern is quite variable from person to person•Most major vessels run along AV sulci and interventricular sulci

•Most coronary venous blood drains into CORONARY SINUS and then into Rt. Atrium•Arterial blood comes from 2 coronary arteries that branch directly off of aorta and then give off multiple branches•Clots in coronary blood vessels cause myocardial infarction!!!

Nerve supply of the heart

•The heart is innervated by both divisions of the autonomic nervous system•Allows us to regulate rate and force of heart contraction

1. Sympathetic division – generally increases force and rate of contraction, as well as increasing blood flow through coronary blood vessels• Important for “fight or flight” response

2. Parasympathetic division – generally reduces heart rate• Main influence is through the VAGUS NERVE (CN X)

•Innervation by ANS is important for REGULATION of rate and force of contraction, BUT heart will still beat even if all innervation is removed

Heart will naturally beat at about 100 beats/min without innervationRegular, rhythmic beating of the heart is stimulated by SINOATRIAL NODE of the

right atrium

Signal conduction through the heart

•Sinoatrial node (SA node) is a patch of cells in the right atrium known as the “pacemaker” of the heart •SA node cells depolarize much easier than other muscle cells and will spontaneously depolarize at regular intervals•Depolarization of SA node triggers depolarization of both atria

Cardiac cells possess GAP JUNCTIONS that allow signals to rapidly pass from one cell to another!!!

•Atrioventricular node (AV node) is another patch of cells lying near the bottom of the interatrial septum

Detects depolarization of atria and sends signal that triggers depolarization of ventriclesBoth divisions of the ANS send nerve fibers

to the SA node – control of rate and force

Signal conduction through the heart

•Fibers from the AV node travel down the interventricular septum and split into right and left bundle branches, then travel up along the surface of both ventricles•These branches give off modified nerves called PURKINJE FIBERS that stimulate the entire ventricle to contract

The depolarization (electrical activity) of different parts of the heart are detected and reported on an ELECTROCARDIOGRAM (ECG)

Cardiac muscle

•Although purkinje fibers carry the electrical signal, not every cell is DIRECTLY stimulated by these fibers

•Cardiac muscle cells (cardiomyocytes) are linked to each other by INTERCALATED DISKS

•These connections are VERY strong and contain gap junctions that allow signals to rapidly pass from one cell to the next

•So…contraction of one cell can trigger contraction of other cells nearby, and so on, and so on….

•Allows the heart to contract in coordinated fashionAllows for efficient ejection of blood from one

chamber to the next

Cardiac muscle metabolism…..

•Cardiac muscle cells rely almost exclusively on AEROBIC RESPIRATION to generate ATP needed for contraction

Lots of myoglobin Lots of large mitochondria Lots of stored glycogen

• Makes heart very resistant to fatigue, BUT very vulnerable when O2 is not available (heart attack)

Cardiac rhythm and contraction

•Coordinated contraction and relaxation of atria and ventricles are essential to efficient pumping of blood through pulmonary and systemic circuits

Prevents overload of circuits – elevated pressures

•SYSTOLE = contraction of chambers, ejects blood•DIASTOLE = relaxation of chambers, allows filling of chambers with blood•All 4 chambers DO NOT contract at same time!!!

BOTH atria contract first, both ventricles contract shortly after

• Depolarization begins at SA node → causes atria to contract first• Signals travel to AV node and then on to the ventricles → delay causes ventricles

to contract shortly after atria ---- about 100 msec after atria contract• This delay is VERY important because it allows ventricles time to fill with blood

Cardiac rhythm and contraction

•Conduction of signal occurs very rapidly across atria…allows atrial tissue to contract uniformly

•Ventricular cardiomyocytes receive signal to contract in one of two ways

1. Signal is received via intercalated disks from a nearby cell (slower)

2. Signal is receive directly from purkinje fibers (faster)

•Ventricles are quite large and thick with many more cells than in atria

Purkinje fibers allow signal to get to most of the ventricle much faster than only by diffusing through intercalated disks

•In reality, the entire ventricular myocardium doesn’t contract at EXACTLY the same time

•Path of signal along bundle branches and purkinje fibers cause apex to contract first and the contraction spreads upward (superiorly)

•This pattern of contraction helps “push” blood up and out through pulmonary or aortic valves

Ventricles sort of wring themselves out to ensure adequate ejection of blood

Ventricular contraction

•In a normal heart rhythm, the contraction is triggered by the SA node, spreads throughout atria → AV node → bundle fibers, purkinje fibers→ spreads throughout ventricle

SINUS RHYTHM

•Damage to conduction system (SA node, AV node, bundle branches, purkinje fibers) alters heart rhythm and is known as HEART BLOCK

•Some electrolyte imbalances, drugs, or damage to the SA node can cause part of heart to depolarize BEFORE SA node fires (either the atria or ventricles)

ECTOPIC FOCUSOften causes FIBRILLATION

•Any heart rhythm where depolarization initiates away from the SA node is an ARRHYTHMIA

•Atrial fibrillation (A-fib) occurs when depolarizations occur at areas other than the AV node•Causes atria to flutter or quiver

•Often goes undetected since adequate amounts of blood often still enter the ventricles

•Normally not life-threatening, episodes can come and go, but can be chronic

•Dramatically increases risk of stroke due to formation of blood clotsClots could eventually get pumped out of the heartMany people with diagnosed A-fib take anticoagulants each day (Coumadin is an

anticoagulant drug)

Atrial fibrillation

Ventricular fibrillation

•Signals are not carried through the conduction system normally (AV node → bundle fibers, purkinje fibers→ rest of ventricle)•Instead, depolarizations o •Causes ventricle to quiver or flutter

Blood is not pumped efficiently →no systemic circulation→ no coronary circulation (myocardium dies quickly)

•Abnormal rhythm can often be corrected in a number of ways:

1. Antiarrhythmic drugs2. Cardioversion – delivery of an electrical

shock at a very specific time of the heartbeat

3. Defibrillation – normally only done in extreme circumstances. Large shock of electricity depolarizes the ENTIRE HEART at the same time• Hope is that normal sinus rhythm will resume – like a “reset” button

Pacemaker physiology

•Cells of the SA node will rhythmically fire action potentials without any nerve stimulation and allows heart to beat about every 0.8 sec……..But how????

•Remember depolarization requires flow of (+) ions into the cell

Normally accomplished by opening of ligand- or voltage-gated ion channels

•SA node cells contain 3 important ion channels : Na+ channel, Ca2+ channel, K+ channel•Some Na+ channels are constantly open (Na+ is flowing into the cell) allowing cell to VERY SLOWLY depolarize•When the cell reaches an electrical threshold, LOTS AND LOTS of voltage-gated Ca2+ channels open and Ca2+ rushes in causing rapid depolarization of the cell•Soon, K+ channels open and K+ quickly leaves the cell allowing it to become repolarized•BUT!! Na+ channels are still open and slowly depolarizing the cell AGAIN!!!

•This cycle allows SA node cells to depolarize routinely without stimulation

The Electrocardiogram (EKG or ECG)

•Depolarizations and repolarizations are really changes in the electrical activity of the heart•An EKG measures electrical activity throughout the cardiac cycle•Electrodes positioned on the wrists, ankles, and chest send info on electrical activity to an electrocardiograph •Each peak on an EKG represents the depolarization or repolarization of a certain portion of the heart

1. P-wave – represents the depolarization of the SA node and subsequent depolarization of the atria

2. QRS complex – represents the depolarization of the AV node and then the ventricles

3. T-wave – represents the repolarization of the ventricles• NOTE – the repolarization of the atria is not seen on an EKG

since the larger QRS complex masks it…

One complete heartbeat or cardiac cycle

Principles of pressure, blood flow, and the cardiac cycle

A little bit of fluid dynamics……•A given amount of fluid will occupy a certain volume at a particular pressure

Assuming there is no outlet to relieve the pressure•As the volume of a space increases, the pressure decreases

Explains why blood is drawn into ventricle when it expands (during relaxation/diastole)•As the volume of a space decreases, the pressure increases

Blood is ejected from ventricles when they contract (i.e., during systole)•PRESSURE GRADIENTS (the difference in fluid pressure between two areas) dictate when and under what pressure a fluid will move between two places

These principles govern how blood moves between chambers and vessels Ex. #1 As the pressure inside the right ventricle increases (contraction) blood is forced into the

lower pressure area of the pulmonary trunk Ex. #2 As the pressure inside the right ventricle decreases (relaxation) blood flows from the area

of higher pressure (atrium) into the area of lower pressure (ventricle)

•Generally, pressure gradients cause fluids to flowBlood from pulmonary or systemic circuits → atria, or atria→ ventricles, or ventricles →

great vessels

•However, AV and semilunar valves prevent this flow even though there is a gradient!!!Positive pressure in RV and LV force the AV valves to close (no flow back into atria)Positive pressure in pulmonary trunk and aorta force semilunar valves closed (no back

flow into ventricles)

Heart Sounds

•Listening to the sounds of the body (heart, lungs, etc…) is known as AUSCULTATION•Important part of a physical exam•Normal adult heartbeat has two sounds ”LUBB….DUBB”•First sound is caused by closing of AV valves during ventricular systole (lubb)•Second sound is caused by closing of semilunar valves during diastole (dubb)

LUBB

DUBB

Abnormal heart sounds often indicate damaged or impaired AV or semilunar valves

Cardiac output

Defined as the amount of blood ejected from the heart each minute

Mathematically: • Stroke volume (SV) X Heart rate (HR) in beats per minute = Cardiac output (CO) • So, for a normal resting person…..

70 mL X 75 beats per minute = 5,250 mL/min

•Since most people have about 5L of blood, all of the blood in the body passes through the ENTIRE pulmonary and systemic circuits every single minute!

•CO will vary slightly from person to person (variations in stroke volume, resting heart rate)

•CO is affected by exercise and condition of individualExercise elevates HR → increased CO (most people can increase CO by ~400%...CARDIAC

RESERVE)Well trained athletes often have increased SV

Balanced ventricular output

•Imbalances in ventricular output lead to abnormal blood pressures in the pulmonary and systemic circuits•If RV output exceeds LV output (i.e, more blood is sent to the lungs than returns to the heart), blood backs up in the lungs → pulmonary edema

Under high pressures fluid escapes from blood vessels and accumulates in tissues

•So, if the RV ejects 60 mL of blood into the lungs, the LV needs to be able to accept 60 mL of blood from the left atrium (which is receiving blood from the lungs

•Pulmonary edema is a serious complication of cardiovascular disease•Often the result of LV failure (less ejection means less filling!)•Patients have extreme difficulty in breathing and cough up blood

Balanced ventricular output

•Similar situation develops if LV output exceeds RV output•LV is ejecting more blood into the systemic circuit than the RV is sending to the lungs•Pressure builds up in systemic circuit → systemic edema

Swelling of legs, feet, and hands can be indicative of heart failure

•Both situations can be caused by damage to the ventricles after a heart attack

A damaged ventricle cannot pump as much blood If one ventricle fails, eventually the other fails too

Heart Rate Regulation

•Easily measured by counting pulsations in a superficial artery (pulse)•“Normal” resting heart rate is around 75 beats/min

•Tachycardia – resting heart rate about 100 beats/minCan be result of stress, drugs, heart disease, etc…Can also compensate for low SV

•Bradycardia – resting heart rate below 60 beats/minCommon during sleep, and in very well trained athletesCan also be caused by some medications (depressants)

•Factors (hormones, drugs, etc..) that change the HR are known as CHRONOTROPIC AGENTSPositive chronotropic agents INCREASE rateNegative chronotropic agents DECREASE rate

Influence of ANS on heart rate

Heart Rate Acceleration – • Sympathetic nerve fibers travel from medulla oblongata to SA node, AV

node, and myocardium• Nerve fibers release norepinephrine that binds to β-adrenergic receptors

Norepinephrine increases HR“Beta-blockers” are often prescribed to treat hypertension – reduces heart rate

and therefore CO and therefore BP

Heart Rate Inhibition – • Parasympathetic nerve fibers (via VAGUS nerve) travel to SA and AV nodes• Nerve fibers release acetylcholine(ACh)

ACh binds to ligand-gated K+ channels causing K+ to flow OUT of S.A. node cells making them HYPERPOLRIZED and very difficult to depolarize

Slows down depolarization of node cells → slows HR• Vagus nerve is always affecting HR

Called VAGAL TONE – reduces HR to normal 75 beats/min (SA node normally fires at rate of about 100 beats/min)

VASOVAGAL SYNCOPE – fainting due to overactivation of vagus nerve

Autonomic control of heart rate

Cardiovascular control centers in the brainstem receive info from various parts of the body and direct appropriate changes in HR • Excellent example of a FEEDBACK LOOP

Proprioceptors – mechanical sensors in joints and muscles tell cardiac center to increase HR (via sympathetic division of ANS) – these sensors detect movement of limbs

Baroreceptors – pressure receptors located in various parts of the body that send info to cardiovascular centers• Elevation in blood pressure causes decrease in HR• Decrease in blood pressure causes increase in HR

Chemoreceptors – receptors that sense levels of CO2, 02, and pH• CO2 in blood gets converted to carbonic acid (lowers blood pH) – need to get rid of CO2

through the lungs → increase in HR• Low O2 levels also increase HR…..need to pump more blood to satisfy tissue needs for O2

Control of stroke volume

Other way to regulate cardiac output is by changing stroke volume

Stroke volume is influenced by three factors:1. Preload – amount of blood in ventricles (EDV) dictates stroke volume

• Remember ventricle needs to eject as much blood as it receives• STARLING LAW OF THE HEART basically says that the more you stretch the

heart (larger EDV), the more forcefully it will contract (TO A CERTAIN LIMIT!!!!)• Unlike skeletal muscle, resting cardiac muscle is not naturally at optimal resting

length…..so some stretching is good for contraction

2. Contractility – describes the force with which the heart contracts for a given PRELOAD• Positive and negative INOTROPIC agents increase or decrease contractility of

heart• Ca2+ and agents that increase Ca2+ levels make the heart muscle cells contract

more forcefully (more myosin heads binding to active sites on actin)

•Elevation in Ca2+ also lengthens the plateau phase of cardiac muscle cell depolarization (longer contraction)

3. Afterload – describes the pressure of blood “after” the heart beats • Basically the amount of blood pressure in the

pulmonary trunk or aorta• A very large afterload limits how much blood the

ventricles will be able to eject into the circulation• Afterload is very high in pulmonary and systemic

hypertension Eventually, ventricles have to beat so hard to

overcome afterload, that they fail