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The Cardiovascular System: The Heart

• Heart pumps over 1 million gallons per year

• Over 60,000 miles of blood vessels

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Heart Location• Heart is located in the

mediastinum

• 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

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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)

• Epicardium– visceral layer of serous

pericardium

• Myocardium – cardiac muscle layer is the

bulk of the heart• Endocardium

– chamber lining & valves

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Myocardium – cardiac muscle

• shares structural and functional characteristics with skeletal and muscle

• striated• thin filaments contain troponin and tropomyosin – regulates cross-bridge

formation• possess a definitive tension-length relationship• plentiful mitochondria and myoglobin• well-developed T-tubule structure

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Myocardium – cardiac muscle

• shares structural and functional characteristics with smooth muscle

• calcium entry from the ECF triggers its release from the SR• displays pace-maker activity – initiates its own APs without external

influence• interconnected by gap junctions (intercalated discs) – enhance the

spread of APs• innervated by the ANS

• unique – cardiac muscle fibers are joined in a branching network– action potentials last longer than skeletal before repolarization

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Heart Anatomy Review

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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

– separates right atrium from right ventricle

– has three cusps

Right Ventricle

• Forms most of anterior surface of heart• Papillary muscles are cone shaped &

raised bundles of cardiac muscle• Chordae tendineae: cords linking

valve cusps to papillary muscles• Interventricular septum: partitions

ventricles• Pulmonary semilunar valve: blood

flows through this valve into pulmonary trunk

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Left Atrium

• Forms most of the base of the heart• Receives blood from lungs - 4 pulmonary

veins (2 right + 2 left)• Bicuspid valve: separates left atrium

from 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 • Aortic semilunar valve:

– blood passes through this valve into the ascending aorta

– just above valve are the openings to the coronary arteries

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• A-V valves open and allow blood to flow from atria into ventricles when ventricular blood pressure is lower than atrial pressure– occurs when ventricles are

relaxed, chordae tendineae are slack and papillary muscles are relaxed

Atrioventricular Valves

• A-V valves close when ventricular blood pressure is higher than atrial pressure• chordae tendinae of the AV valves prevent backflow of blood

into atria• 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• SL valves open with ventricular

contraction/increased ventricular blood pressure– allow blood to flow into

pulmonary trunk and aorta• SL valves close with ventricular

relaxation– prevents blood from returning to

ventricles

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Blood Circulation• 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 found 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 via the

two vena cava

• 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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SVC/IVC Right Atrium (tricuspid valve) Right Ventricle

Lungs

Left Atrium

Pulmonary Artery

Pulmonary Vein

Aorta Left Ventricle(aortic semilunar valve)Body

Body

bicuspid (mitral) valve

(pulmonary semilunar valve)

Passage of Blood through the Heart

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Conduction System of Heart

• two types of cardiac muscle cells– 1. contractile cells

• 99% of cardiac muscle cells• Do mechanical work of pumping by contracting• Normally do not initiate own action potentials

– 2. autorhythmic cells• Do not contract• Specialized for initiating and conducting action potentials responsible for

contraction of working cells

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• intercalated discs – region that joins two cardiac cells– site of intermembrane junctions– two types of membrane junctions:

• a. desmosomes – abundant in tissues under considerable stress

– formation of a protein-rich plaque on the PM surface of each cardiomyocyte

– plaques link to the underlying cytoskeleton

– plaques are joined to each other by adhesion proteins – cadherins (require calcium for interaction)

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– two types of membrane junctions:• b. gap junctions – two PMs are

connected by a “channel” made of specific proteins = connexons

– two connexons join end to end to connect the cells & allow a free flow of materials from cell to cell

– allow for the spread of electricity within each atrium and ventricle

– no gap junctions connect the atrial and ventricular contractile cells – block to electrical conduction from atria to ventricle!!!

– also a fibrous skeleton the supports the valves – nonconductive

– therefore a specialized conduction system must exist to allow the spread of electricity from atria to ventricles

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Conduction System of Heart• SA node = 1.

– cluster of cells in wall of Rt. Atria– begins heart activity that spreads

to both atria– excitation spreads to AV node

• AV node = 2.– in atrial septum, transmits signal

to bundle of His• AV bundle (bundle of His) = 3.

– the connection between atria and ventricles

• Bundle branches = 4. – for conduction of action potential

through the interventricular septum

• Purkinje fibers = 5.– large diameter fibers that conduct

signals quickly

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• 1. atrial conduction system/interatrial pathway – spread of electricity from right to left atrium ending in the LA– through gap junctions of the contractile cells

• 2. internodal pathway – spread of electricity to the AV node via autorhythmic cells– slow spread through the AV node allows for complete filling of the ventricles before they

are induced to contract = AV nodal delay• 3. ventricular conduction system (Purkinje system) – Bundles, Purkinje fibers,

ventricular muscle– simultaneous contraction of all ventricular cells– BUT the PFs do not connect with every ventricular contractile cell– so the impulse spreads via gap junctions through the ventricle muscle

Conduction Pathways

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Rhythm of Conduction System• various autorhythmic cells have different rates of depolarization to

threshold – so the rate of generating an AP differs– SA node fires spontaneously 70-100 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

blockage of transmission from SA through the AV node

failure of SA node

• contraction rate is driven by the SA node – fastest autorhythmic tissue• AV node is necessary to link the atrial rate to ventricular rate• in some cases – the normally slowest Purkinje fibers can become overexcited = ectopic

focus– premature ventricular contraction (PVC)– occurs upon excess caffeine, alcohol, lack of sleep, anxiety and stress, some organic conditions

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Cardiac excitation• efficient cardiac function requires three criteria:• 1. atrial excitation and contraction should be

complete before ventricular excitation and contraction

• 2. cardiac fiber excitation should be coordinated to ensure each chamber contracts as a unit

• 3. atria and ventricles should be functionally coordinated (atria contract together, ventricles contract together)

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• pacemaker potential of the autorhythmic cells• provided by the SA node

– Autorhythmic cells do NOT have voltage- gated Na+ channels !!!!!– two important events:– 1. decreased outward K+ current

• coupled to constant inward leak inward of Na+ is a decreased leak of K+ outward• as the K+ outflow decreases – membrane constantly drifts toward threshold (doesn’t

balance out the Na+ inward flow)

Cardiac muscle action potentials

Autorhythmic Cells

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– 2. increased inward Ca+ current• T-type Ca+ channels (voltage-gated) open as the membrane drifts toward

threshold• brief influx of Ca increases the depolarization – reach threshold• at threshold – L-type Ca channels open – longer lasting voltage-gated

channels• big influx of calcium – so the influx of calcium (rather than Na) is what

drives the membrane potential of a cardiac cell toward positive• resets through the closing of these Ca channels and the opening of voltage-

gated K+ channels

Cardiac muscle action potentials

Autorhythmic Cells

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• action potentials in the contractile cells of the myocardium are initiated by the SA node and spread via gap junctions – induces an AP in the contractile cells

Cardiac muscle action potentialsContractile cells

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Cardiac muscle action potentialsContractile cells

• but the AP mechanism differs from that of the autorhythmic cells– 1. almost “instantaneous” rising phase of depolarization – activation of Na+ entry

through voltage-gated channels (similar to neurons) = “fast” Na+ channels– 2. Na+ permeability then rapidly plummets to its resting level – this could cause

repolarization but IT DOESN’T

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Cardiac muscle action potentialsContractile cells

– 2. Na+ permeability then rapidly plummets to its resting level – this could cause repolarization but IT DOESN’T

– 3. BUT the membrane potential instead of rapidly returning to negative is held a positive for an extended period of time = plateau phase

• activation of the “slow” L-type channels PLUS a delay in the opening of voltage-gated K+ channels = delays repolarization

• prolongs the positivity inside the cell– 4. rapid falling phase results – inactivation of Ca+ channels

and eventual opening of voltage-gated K+ channels • results in a sudden opening of K+ channels and a rapid

repolarization

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The AP and contraction

• the “slow” L-type Ca+ channels are found within the T-tubules

• triggers the opening of Ca+ channels within the adjacent lateral sacs of the SR (foot proteins) –

• this “Ca-induced Ca release” triggers a very large release of Ca+ from the SR

• burst of Ca+ = Ca+ sparks• together with the slow removal of Ca+ - results in a

long sustained contraction of heart muscle

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AP and contraction

• Ca+ triggers the same series of events as seen in skeletal muscle – troponin-tropomyosin “shift”– BUT – the amount of Ca+ release can

directly affect the number of cross-brides formed in cardiac muscle and can directly affect the strength of the contraction!

– elevated ECF Ca+ can increase the strength of contraction

• refractory period of cardiac muscle is longer than skeletal muscle (250msec)– allows for the emptying of the chambers

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Electrocardiogram---ECG or EKG

• electrical currents generated by the heart are also transmitted through the body fluids

• can be measured on the surface of the chest

• therefore the EKG is not a direct measurement of the actual electrical conductivity of the heart itself

• represents the overall spread of activity through the heart during depolarization – sum of all electrical activity

• measured through the placement of 6 leads on the chest wall (V1 – V6) PLUS 6 limb leads (I, II, III, aVR, aVL and aVF)

• it's usual to group the leads according to which part of the left ventricle (LV) they look at.

– AVL and I, as well as V5 and V6 are lateral, while II, III and AVF are inferior.

– V1 through V4 tend to look at the anterior aspect of the LV

• see EKG lab on the website

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Electrocardiogram---ECG or EKG

http://www.ecglibrary.com/ecghist.htmlhttp://www.anaesthetist.com/icu/organs/heart/ecg/Findex.htm

• P wave (80msec) = atrial depolarization– SA to AV node and right atrium to left

atrium– absence: atrial fibrillation and SA blocks– increased amplitude = hypokalemia (low

K+)• PR (PQ) interval (120-200msec) = SA

node through the AV node and into ventricles

– AV node function and coordination between atrial and ventricular conduction systems

– long interval –AV block

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Electrocardiogram---ECG or EKG

• QRS complex (80-120msec) = rapid depolarization of ventricles– used to diagnose: cardiac arrhythmias,

conduction abnormalities, ventricular hypertrophy and myocardial infarctions

• QT interval = depolarization and repolarization of the ventricle– measures electrical conduction/activity of

the entire ventricle– lengthened QT interval could be a sign of

sudden cardiac death• ST segment (80-120msec) = end of QRS to the start of the T wave

-period when ventricles are depolarized

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Cardiac Cycle – for Anatomists

Atrial andventricular diastole

Atrial systole and ventricular diastole

Ventricular systole and atrialdiastole

0.1sec

0.4sec

0.3 sec

2

1

3

• diastole – rest period– chambers are filling with blood

• systole – pumping period– cardiac muscle contraction forces blood

out under pressure• 1. Atrial and ventricular diastole

– atria and ventricles are filling with blood– muscle is relaxed

• 2. Atrial systole/ventricular diastole– contraction of atria forces blood into

ventricles• 3. Ventricular systole/atrial diastole

– ventricular contraction forces blood out of lungs and body

– atria start to fill again

Here’s your cardiac cycle!

AHHHH!

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Cardiac cycle• 1. Midventricular diastole

– during most of the ventricular diastole, the atrium is also in diastole = TP interval on the EKG

– as the atrium fills during its diastole, atrial pressure rises and exceeds ventricular pressure (1)

– the AV valve opens in response to this difference and blood flows into the right ventricle

– the increase in ventricular volume rises before the onset of atrial contraction (2)

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Cardiac cycle• 2. Late ventricular diastole

– SA node reaches threshold and fires its impulse to the AV node = P wave (3)

– atrial depolarization results in contraction – increases the atrial pressure curve (4 – green line)

– corresponding rise in ventricular pressure (5 – red line) occurs as the ventricle fills & ventricular volume increases (6)

– the impulse travels through the AV node

– the atria continue to contract filling the ventricles

Cardiac cycle

• 3. End of ventricular diastole– once filled the ventricle will start to

contract and enter its systole phase– ventricular diastole ends at the onset

of ventricular contraction– atrial contraction has also ended– ventricular filling has completed– ventricle is at its maximum

volume (7) = end-diastolic volume (EDV), 135ml

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Cardiac cycle• 4. Start of ventricular systole

– at the end of this contraction is the onset of ventricular excitation (8) = QRS complex

– the electrical impulse has left the AV node and enters the ventricular musculature = ventricular contraction

– ventricular pressure will begin to rise rapidly after the QRS complex (red line)

– this increase signals the onset of ventricular systole (9)

– atrial pressure is at its lowest point as its contraction has ended and the chamber is empty (green line)

– the ventricular pressure now exceeds atrial – AV valve closes

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Cardiac cycle• E. isovolumetric ventricular

contraction– just after the closing of the AV and

opening of the SL valves is a brief moment where the ventricle is a closed chamber (10) = isovolumetric contraction

– ventricular pressure continues to rise (red line) but the volume within the ventricle does not change (11)

– ventricular pressure opens the semilunar valves

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Cardiac cycle• F. Ventricular ejection

– ventricular pressure will now exceed aortic pressure as the ventricle continues is contraction (12)

– the aortic SL is forced open and the ventricle empties

– this volume of blood – stroke volume (SV)

– the ejection of blood into the aorta increases its pressure (aortic pressure) and the aortic pressure curve rises (13 – purple line)

– ventricular volume now decreases (14 – blue line)

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Cardiac cycle• F. End of ventricular systole

– the ventricular volume drops – BUT ventricular pressure continues to

rise for a short period of time as the contraction increases its force (red line)

– pressure then starts to decrease as blood begins to be ejected

– at the end of the systole there is a small volume of blood that remains in the ventricle – end-systole volume (ESV), 65ml (15)

– EDV-ESV = SV (point 7 – point 15)

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Cardiac cycle• G. Ventricular

repolarization– T wave – (16)– as the ventricle relaxes –

ventricular pressure falls below aortic and the aortic SL closes (17)

– this closure produces a small disturbance in the aortic pressure curve – dicrotic notch (18)

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Cardiac cycle• H. Isovolumetric

ventricular relaxation – Start of Ventricular Diastole– all valves are closed

because ventricular pressure still exceeds atrial pressure – isovolumetric relaxation (19)

– chamber volume remains constant (20) but ventricular pressure drops sharply (19)

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• I. Ventricular filling/MidVentricular Diastole– as the atria fills from blood from the

pulmonary veins (lungs) it increases atrial pressure

– as atrial pressure exceeds ventricular pressure – the AV valve opens again (21)

– ventricular filling starts again increasing ventricular volume (blue line)

– with the AV valve open this blood fills the ventricle rapidly (23)

– then slows down (24) as the blood drains the atrium

– during this period of reduced filling, blood continues to come in from the pulmonary veins – goes directly into the ventricle

– cycle starts again with a new SA depolarization

– a new SA depolarization

Cardiac cycle

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• Heart sounds Auscultation• Stethoscope• Sounds of heartbeat are from

turbulence in blood flow caused by valve closure

– first heart sound (lubb) is created with the closing of the atrioventricular valves

– second heart sound (dupp) is created with the closing of semilunar valves

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Cardiac Output• Amount of blood pushed into aorta or pulmonary trunk by a

ventricle• Determined by stroke volume and heart rate• CO = SV x HR• Cardiac reserve is the ratio of the maximum output to normal

cardiac output at rest– average is 4-5 while athlete is 7-8

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Stroke volume• SV = end-diastolic volume - end-systolic

volume SV = EDV- ESV– ESV –amount of blood left in a ventricle after

systole)• measured by EKG – end of the T wave

– EDV –amount of blood in a ventricle after filling • measured using MRI, CT scan or a ventriculography

(catheter in the ventricle and injection of an X-ray visible dye)

Stroke volume• two components influence SV:• 1. intrinsic control: heart’s inherent ability to vary SV

– as more blood returns to the heart, the heart pumps out more blood

– blood returning to the heart = Venous Return– as VR increases so does EDV

Starling’s LawStroke volume isdependent uponVenous Return

– 1. intrinsic control: as more blood returns to the heart, the heart pumps out more blood– WHY? depends on the length-tension relationship of cardiac muscle– for skeletal muscle –when muscle length is less than or greater than optimal length/l o– muscle

contraction is weak because of the effect on cross-bridge #– for cardiac muscle – resting cardiac muscle length is already less than lo

• SO – stretching cardiac muscle length moves the fiber towards lo & increases contractile tension

• therefore filling the ventricle with more blood stretches the cardiac muscle and increases the resultant force of contraction

• as the cardiac cell is stretched - myofilaments are pulled closer together• allows more cross-bridge formation

Stroke volume• 2. extrinsic control

– sympathetic and parasympathetic control– sympathetic impulses increase force of contraction

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EXTRINSIC

EXTRINSIC+INTRINSIC

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• Nervous control from the cardiovascular center in the medulla oblongata– OUTPUT: 1. Sympathetic impulses increase heart rate and force of contraction– 2. Parasympathetic impulses decrease heart rate through the vagus – INPUT : 1. Chemoreceptors detect changes in blood chemistry– 2. Proprioceptors monitor changes in body activity– 3. Baroreceptors (pressure receptors) detect changes in BP

Regulation of Heart Rate

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Regulation of Heart Rate

– Heart rate is also affected by hormones and ions– epinephrine & norepinephrine from adrenal medulla, thyroid hormones– ions (Na+, K+, Ca2+)– age, gender, physical fitness, and temperature

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– Sympathetic impulses increase heart rate & force of contraction

• supplies the atrial and ventricular musculature PLUS the SA and AV nodes

• speeds up contraction rate by• 1. speeding up the rate of depolarization of the autorhythmic cells of the

SA node– decreases K+ permeability by inactivating K+ channels– swifter drift towards threshold

• 2. reduces the AV delay – by activating L-type Ca channels

• 3. speeds the rate of conduction through the Bundles and Purkinje fibers– in autorhythmic cells - release of norepinephrine from ANS binds to 1

adrenergic receptors and produces a faster depolarization rate– in contractile cells, NE increases contractile strength by increasing Ca+

permeability and intensifies the cross-bridge formation between actin and myosin

Sympathetic Regulation of Heart Rate

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Parasympathetic Regulation of Heart Rate

– parasympathetic impulses decrease heart rate through the vagus nerve

• primarily supplies the SA and AV nodes – no musculature• little effect on ventricular conduction system or ventricular

contractile cells• 1. hyperpolarizes the SA node – slows APs - release of AcH

by the vagus binds to muscarinic receptors on the autorhythmic cells of the SA node

• 2. decreases the excitability of the AV node – increases AV delay (hyperpolarizes the AV node)

• in contractile cells of the atria – reduces the inward Ca+ flow shortening the plateau phase – weakened atrial contraction

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