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Heart
 The heart is about the size of a clenched fist
 Four chambers
Structure of the heart wall
3 distinct layers
1. epicardium- visceral pericardium, forms the external surface of the heart
2. myocardium- multiple layers of cardiac muscle tissue with associated CT, blood vessels and nerves
3. Endocardium- inner surface including valves made up of simple squamous epithelium.
Cardiac muscle tissue
 Cardiocytes-cardiac muscle cells, small with a centrally placed nucleus, contains myofibrils and
alignment of sarcomeres produces striations
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Differs from skeletal muscle:
1. Totally dependent on aerobic respiration, energy reserves are maintained in the form of glycogen
and lipid inclusions
2. T tubules do not form triads with sarcoplasmic reticulum
3. More circulatory supply
4. Contract w/o instructions from the nervous sytem
5. cardiac muscle cells interconnected by intercalated discs.
Orientation and superficial anatomy
 Lies to the left of the midline in the mediastinum
 In the pericardial cavity surrounded by pericardium
 Sits at an angle to the longitudinal axis
 Rotated toward the left side
 Base- the broad superior portion of the heart where it attaches to major arteries and veins of
the pulmonary and systemic circuits
 Apex- the inferior rounded tip which points laterally at an oblique angle.
Auricle- the expanded extension of an atrium
Coronary sulcus- deep groove that marks the border between the atria and ventricles
Anterior and posterior interventricular sulci- the boundary lines (shallow depression) between the left and right
ventricles. The sulci are usually covered in fat.
Internal Anatomy and Organization of the heart
 Atria are separated by the interatrial septum
 Venticles by the interventricular septum
 Each atria communicates with the ventricles of the same side.
 Valves are folds of endocardium that extend into the openings between the atria and ventricles
Rt. Atrium
 Rt. Atrium receives poor venous blood from systemic circulation via the superior and inferior vena cava.
 The Superior Vena Cava opens into the posterior, superior portion of the rt atrim, delivering venous
blood from the head, neck, upper limbs, and chest.
 The Coronary veins also empty into the rt atrium via the coronary sinus.
The interatrial septum from week 5 of developing embryo, the foramen ovale allows blood to flow directly
while the lungs are developing and non functional. In the adult it becomes the fossa ovalis- small depression.
Rt ventricle
O2 poor blood from the rt atrium enters through an opening with flaps or cusps Rt. Atrioventricular
valve or tricuspid valve held by fibers, chordae tendonae.
Blood is ejected from the rt ventricle through the pulmonary semilunar valve into the pulmonary trunk
which branches into left and rt. Pulmonary arteries to the capillaries of the lung.
Lft atrium
From the pulmonary capillaries, the blood now O2 rich goes through the left and rt pulmonary veins
empties into the left atrium through the left AV valve or bicuspid (mitral) valve into the left ventricle.
Blood leaves the left ventricle by passing through the aortic semilunar valve into the ascending aorta on
through the aortic arch into the descending aorta
Structural Differences of the rt and lft venrtricles
CIRCULATION= 2 networks
1. Pulmonary circuit- carries O2 rich blood to the gas exchange surfaces of the lungs and returns O2 rich
blood to the heart.
2. Systemic circuit- transports O2 rich blood to the rest of the body’s cells, returning CO2 rich blood
back to the heart
Arteries- transport blood away from the heart
Veins- return blood to the heart
Capillaries- small thin walled vessels that interconnect veins and arteries
Coronary Circulation
 The heart uses 5% of the ciculating blood to meet its own metabolic requirements
 Blood vessels of the heart constitute coronary circulation ~ 250ml of blood/min.
Arterial supply
 Immediately after the aorta leaves the left ventricle, it gives off right and left coronary arteries
 The left coronary passes under the left auricle and divides into 2 branches:
1. anterior interventricular artery (left anteriror descending (LAD) artery)- travels down
interventricular sulcus toward the apex
2. circumflex artery- supplies left atrium and posterior wall of the left ventricle
The right coronary artery supplies the right atrium continues along the coronary sulcus under the right auricle
and then gives off 2 branches:
1. marginal artery- supplies the lateral aspect of the right atrium and ventricle
2. posterior interventricualr artery- travels down the corresponding sulcus and supplies the posterior walls
of both ventricles.
Myocardial infarctionVenous Drainage
 Refers to the route by which blood leaves an organ
 After flowing through the cappllaries of the myocardium, about 20% of coronary blood empties
directly from small veins into the right ventricle. The other 80% returns by :
1. great cardiac vein- collects blood from the anterior aspect of the heart and travels along the
anterior interventricular artery. Carries blood from the apex toward the atrioventricular
sulcus
2. middle cardiac vein- in the posterior sulcus, collects blood from the posterior aspect from
the apex upward.
3. Coronary sinus- collects blood from these and smaller cardiac veins, crosses the posterior
aspect in the coronary sulcus and empties into the right atrium.
Cardiac Conduction System
 Myogenic-signal originates within the heart itself (pacemaker cells)
 Cardiac myocytes are autorhythmic- depolarize spontaneously at at regular time intervals
 Some myocytes lose the ability to contract and become specialized for generating action potentials
forming the cardiac conduction system- coordinates action of all four chambers.
 Conduction system components:
1. sinoatrial node (SA)- right atrium under epicardium near superior vena cava.- pacemaker- initiates
heart beat and determines heart rate.
2. atrioventricular node (AV)- near right AV valve at lower end of inter atrial septum. An electrical
gateway- prevents currents from getting to the ventricles by another route.
3. atrioventricular (AV) bundle (Bundle of His)- pthway by which signals leave the AV node
4. Right and Left bundle branches-divisions of the AV bundle that enter the interventricular septum and
descend toward the apex.
5. Purkinje fibers- nerve like processes that come from the bundle branches near the apex and turning
upward throughout the ventricular myocardium.- Distribute electrical excitationto the ventricles.
SA nodeAV nodeAV bundleRt & lft bundle branchesPurkinje fibers
Cardiac Rhythm
Sinus rhythm- normal heartbeat triggered by the SA node ~ 70-80 beats/min (bpm)
Stimuli such as, hypoxia, electrolyte imbalances, caffeine, nicotine and other drugs can cause other parts
of the conduction system to fire before the SA node does, seting off an extra heartbeat (extrarasystole).
Ectopic focus- any region of spontaneous firing other than the SA node.
Most common ectopic focus is the AV node- produces a slower heart beat of ~ 40-50 bpm- nodal
rhythm.
Arrhythmia- any abnormal cardiac rhythm
Heart block- failure of any part of the cardiac conduction system to transmit signals.
Physiology of the SA node
No stable resting membrane potential (-60mV and up)
Gradual depolarization- pacemaker potential. Possible due to slow inflow of Na without compensating
outflow of K.
Action potential of a ventricular myocyte
1. voltage gated sodium channels open
2. Na inflow depolarizes the membrane and triggers opening of more Na channels creating a
positive feedback cycle and rapidly rising membrane voltage
3. Na channels close when the cell depolarizes and voltage peaks at nearly +30mV
4. Ca entering through slow calcium channels prolongs depolarization of the membrane,
creating a plateau
5. Ca channels close and Ca is transported out of the cell K channels open and rapid K outflow
returns membrane to its resting potential. (Repolarization)
Electrocardiogram
A recording of electrical currents generated by action potentials produced by the heart.
Amplifies the heart’s electrical signals and produces 12 tracings from the leads on the limbs and chest
It is possible to determine:
1. if the conducting pathway is abnormal
2. if the heart is enlarged
3. if certain regions of the heart are damaged
3 recognizable waves appear with each heartbeat
o P wave- small upward deflection- atrial depolarization- spreads from SA node through
contractile fibers in both atria
o QRS complex- begins as downward deflection, continues as a large upright triangular wave and
ends as a downward wave.- rapid ventricular depolarization- action potential spreads through
ventricular contractile fibers
o T wave- 3rd wave- ventricular repolarization- occurs as ventricles are starting to relax
o Flat- plateau period of steady depolarization
Enlarged P- enlargement of atrium
Enlarged Q- myocardial infarction
Enlarged R- enlarged ventricles
Elevated T- hyperkalemia (high blood potassium levels)
Flatter T- insufficient oxygen- coronary artery disease
o P-Q interval- time required for the action potential to travel through the atria, atrioventricular
node and the remaining fibers of the conduction system
o S-T segment- time when ventricular contractile fibers are depolarizing during plateau phase of
action potential. (ventricle contract and eject blood)
o Elevated in acute myocardial infarction (above baseline)
o Depressed when heart muscels receives insufficient oxygen.
o Q-T interval-beginning of ventricular repolarization to end of ventricular repolarization.
o Can be lengthened by myocardial ischemia (decreased blood flow) or conduction
abnormalities.
The Cardiac Cycle
A single cardiac cycle includes all events associated with one heart beat- complete contraction and
relaxation of all 4 heart chambers
Activity of the heart
Systole- contraction
Diastole- relaxation
Heart Sounds- Auscultation
 Blood turbulence caused by the closing of valves.
 4 heart sounds during cardiac cycle but only S1 and S2 are heard in a normal heart.
 S1- lubb associated with blood turbulence of AV valve closure after ventricular systole begins
 S2- dupp closure of SL valves at the beginning of ventricular diastole
 S3-blood turbulence during rapid ventricular filling
 S4- blood turbulence during atrial systole
Phases of the Cardiac cycle
1. Ventricular filling
Diastole
 Ventricles expand
 Pressure drops in atria
 AV valves open
 Blood flows in causing ventricular pressure to rise and atrial pressure to fall
 3 phases
1. rapid ventricular filling
2. diastasis
3. atrial systole
At the end of ventricular filling, each ventricle contains an end-diastolic volume (EDV)= 130 ml of
blood
2. Isovolumetric contraction
 Atria repolarize, relax and remain in diastole for remaining of cardiac cycle.
 Ventricle depolarize, generate QRS complex and begin to contract
 Pressure in ventricles rises sharply and reverses the pressure gradient
 AV valves close as ventricular blood surges back against the cusps.
 Isovolumetric-ventricles contract but do not eject blood
3. Ventricular ejection
Begins when ventricular pressure exceeds arterial pressure and forces the semilunar valves to open.
In an average resting heart the amount of blood ejected is ~ 70ml = stroke volume (SV) ejection
fraction is 54%
 The blood remaining behind is called end-systolic volume (ESV) EDV-SV=ESV
 Diseased hearts may eject less than 50% of the blood contains.
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4. Isovolumetric relaxationEarly ventricular diastole
Blood from the aorta and pulmonary trunk briefly flows backward theough the semilunar valves
Backflow fills the cusps closing the valves
Blood rebounds from the closed semilunar valves and the ventricles expand
Isovolumetric because the semilunar vlaves are closed, the AV valves have not yet opened- ventricles
not yet taking in blood.
*As a chamber of the heart contracts, blood pressure within it increases
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Congestive heart failure
Cardiac Output
 Cardiac Output (CO) the volume of blood ejected from the ventricle into the aorta or pulmonary
trunk each minute (ml/min)
CO= SV x HR
SV- stroke volume- the volume of blood ejected by the ventricle during each contraction (ml/beat
HR- heart rate- the number of heartbeats per min (beats/min)
Cardiac Reserve= the ratio between a persons maximum cardiac output and cardiac output at rest. 4-5x
the resting value is normal
Regulation of stroke volume
3 factors regulate stroke volume and ensure that the left and right ventricles pump equal volumes of
blood
1. preload- the degree of stretch in the heart before it contracts
2. contractility- the forcefulness of contraction of individual muscle fibers
3. afterload- the pressure that must be exceeded if ejection of blood from the ventricles is to occurcauses SL valves to open.
1. Frank-Starling Law of the heart- within limits, the more the heart is filled during diastole, the greater
the force of the contraction during systole
2. Substances that increase contractitlity = positive inotropic agent
Substances that decrease contractility = negative inotropic agents
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Positive inotropic agents promote Ca+ inflow during cardiac action potentials which strengthens
the force of muscle contraction
Stimulation of the sympathetic division of the autonomic nervous system, hormones (epin. And
norepin.), high levels of Ca in the extracellular fluid and the drug digitalis all have positive
inotropic effects.
Inhibition of sympathetic division of the ANS, anoxia, acidosis, some anesthetics and high K
levels have negative inotropic effects
Ca channel blockers reduce Ca inflow and decrease the strength of the heart beat.
3. At any given preload, an increase in afterload causes stroke volume to decrease and more blood
remains in the ventricles at the end of systole
Conditions that increase afterload
Hypertension- high bp
Artherosclerosis- narrowing of the arteries