Chapter 19TheHeart

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Cardiology

• Is that branch of medicine which deals with the diagnosis and treatment of heart diseases.

• Cardiologists investigate patients with suspected heart disease by taking a very careful, extensive history of the patient's condition, and performing a complete physical examination.

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Cardiologist

• Cardiology is classified as an internal medicine subspecialty. Knowledge of internal medicine and other specialties is required to obtain certification.

• 4 years medical school• 3 years internal medicine residency• 3 years cardiovascular disease medicine• Cardiology sub specialty (extra years)

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Circulatory System: The Heart

• Gross anatomy of the heart• Overview of cardiovascular system• Cardiac conduction system and cardiac

muscle• Electrical and contractile activity of heart• Blood flow, heart sounds, and cardiac cycle• Cardiac output

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Circulatory System: The Heart• Circulatory system

– heart, blood vessels and blood• Cardiovascular system

– heart, arteries, veins and capillaries

Two major divisions:• Pulmonary circuit - right side of heart

– carries blood to lungs for gas exchange• Systemic circuit - left side of heart

– supplies blood to all organs of the body, including itself and lungs.

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Pulmonary & Systemic CircuitsRight side of the heart serves the pulmonary circuit.

- receives deoxygenated & under nourished blood;

- picked up carbon dioxide and other wastes.

Blood is carried to the pulmonary arteries, which lead to the lungs. To pick up oxygen and release CO2 and waste.

Pulmonary & Systemic Circuits

Left side of the heart serves the systemic circuit.- blood leaves heart by way of the aorta;- arteries are given off that lead to the head,

neck and upper extremities.- arteries are given off as the aorta passes

down the body to organs.

After circulating around the body the now deoxygenated blood returns to the right side of the heart by way of Superior and Inferior Vena Cava.

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Position, Size, and Shape• Located in mediastinum,

between lungs• Base - broad superior

portion of heart attachment of great vessels;

• Apex - inferior end, tilts to the left, tapers to point

• 3.5 in. wide at base, 5 in. from base to apex and 2.5 in. anterior to posterior; weighs 10 oz

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Heart Position

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Heart Position

Pericardium

Is a double walled sac.Contains:

* Outer wall called the parietal pericardium (pericardial sac).

- superficial layer of dense irregular CT- deep, thin serous layer

* Inner wall called the visceral pericardium (epicardium), covering the heart surface.

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PericardiumIn between the parietal and visceral

pericardium is the pericardial cavity.

Pericardial fluid is given off by the serous layer (5 – 30 mL).

Fluid Function:- lubricates membranes, reduces friction;- isolates heart from other thoracic organs;- allows heart room to expand, yet resists excessive expansion.

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Pericarditis

• Inflammation of pericardium• Membranes may become dry and cause

painful friction rub with each heart beat.• Cause:

– Infection– Kidney failure– Medications– Radiation therapy– Metastatic disease

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Pericarditis

• Diagnosis– Pain on breathing, improving with change of

position– pericardial rub – ECG elevated ST segments

• Treatment– anti-inflammatory agents– NSAID’s

The Heart Wall

Consist of 3 layers:

1. Epicardium

2. Myocardium

3. Endocardium

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Heart Wall

• Epicardium (a.k.a. visceral pericardium)– serous membrane covers heart

• Myocardium– In between layer, thickest due to cardiac muscle

development;– Size of muscle is proportionate the workload;– Muscle spirals around the heart, resulting in a

twisting or wringing motion.

Heart Wall

• Endocardium – – smooth inner lining, simple squamous

epithelium;– Continuous with the valve surfaces and

endothelium of blood vessels.

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Fibrous SkeletonCollagenous and elastic fibers.Functions:

1. provides structural support

- esp. around valves & opening of great vessels;2. anchors myocytes and gives them something to pull on;

3. non-conductor of electricity; insulator between the atriums and ventricles;4. provides elastic recoil to aid in heart refilling

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Heart Chambers• 4 chambers

– right and left atria • receive blood returning

to heart from lungs via pulmonary veins.

• Auricle (earlike)

– right and left ventricles • two inferior chambers• pump blood to the body.

On the surface , the chambers are marked by three sulci (grooves):1. Coronary (atrioventricular) sulcus : separates atria, ventricles;

2. Anterior interventricular sulcus3. Posterior interventricular sulcus; BOTH separate the right and left ventricles.

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External Anatomy - Anterior

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External Anatomy - Posterior

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Heart Chambers - Internal• Interatrial septum

– wall that separates atria (which have thin walls)• Pectinate muscles

– internal ridges of myocardium in right atrium and both auricles

• Interventricular septum– wall that separates ventricles

• Trabeculae carneae– internal ridges in both ventricles

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Internal Anatomy - Anterior

Heart ValvesTo provide proper pumping of blood the heart

will need the valves that promote one-way flow.

Location of valves:- valves between each atria and ventricle,- valves between the each ventricle and great vessel.

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Heart Valves

1. Atrioventricular (AV) valves– right AV valve has 3 cusps (tricuspid valve)– left AV valve has 2 cusps (mitral, bicuspid valve)– chordae tendineae - cords connect AV valves to

papillary muscles (on floor of ventricles)

2. Semilunar valves – controls flow into great vessels.

2 types:– Pulmonary V: right ventricle into pulmonary trunk– Aortic Valve: from left ventricle into aorta

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Heart Valves

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Heart Valves

Valve Mechanism

Opening and closing of heart valves is the result of pressure gradients.

• Ventricles relax their pressure is low = both AV valves hang open (limp) → blood flow freely from atria to ventricle (even before atria contract).

• Ventricles now contract = increase pressure in ventricles close the AV valves (chordae tendinae prevent inversion of valves) = blood forces open the semilunar valves forcing blood out into great vessels = pressure is now low in ventricles and higher in vessels = slight back flow closing the semilunar valves.

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Operation of Atrioventricular Valves

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Operation of Semilunar Valves

Valvular Insufficiency

Refers to any failure of a valve to prevent reflux (regurgitation).

Valvular Stenosis – insufficiency caused by stiffening of the cusps and opening is constricted by scar tissue resulting from Rheumatic Fever.

Regurgitation of blood back through the incompetent valve = heart murmur.

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Mitral Valve Prolapse

• Insufficiency of mitral valve(s) causing the cusps to bulge into atrium during ventricular contraction.

• 1 out of 40, hereditary

• No serious dysfunction, in some it can cause chest pain, fatigue, shortness of breath.

• Incompetent valves will could eventually lead to heart failure.

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Blood Flow Through Heart

Coronary CirculationBeats 80years → 75 bpm = 3 billion total beats & pump

200 million liters of blood.Has its own blood supply, can not rely on diffusion from

the chambers.

Inside the aorta, immediately after the aortic semilunar valve are the openings to the coronary circulation.

The two openings lead to the:Left Coronary ArteryRight Coronary Artery

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Coronary Circulation

• Left coronary artery (LCA):– Travels around the coronary sulcus & divides into:

– anterior interventricular branch• supplies blood to interventricular septum and anterior

walls of ventricles– circumflex branch

• passes around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventricle.

• Gives rise to the left marginal branch (supplies left vent.)

Coronary Circulation• Right coronary artery (RCA):

– Supplies the sinoatrial node (pacemaker); & atrioventricular node

Gives rise to:

– right marginal branch • supplies lateral R atrium and ventricle

– posterior interventricular branch• supplies posterior walls of ventricles

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Coronary Vessels - Anterior

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Coronary Vessels - Posterior

Coronary Circulation

The energy demand on the heart is so great that the slightest interruption of blood supply to any part of the myocardium = MyocardiaI Infarction

Some protection: Anastomoses – point where two arteries come together and combine blood flow. This alternative route of blood flow is called collateral circulation.

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Angina and Heart Attack

• Angina pectoris – partial obstruction of coronary blood flow can

cause chest pain – pain caused by ischemia, often activity dependent

• Myocardial infarction

– complete obstruction causes death of cardiac cells in affected area

– pain or pressure in chest that often radiates down left arm

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Venous Drainage of Heart

• 20% of coronary blood drains directly into right atrium and ventricle via thebesian veins

• 80% returns to right atrium via:

– great cardiac vein • Found in anterior interventricular sulcus and drains the anterior

aspect of heart.– middle cardiac vein (aka posterior interventricular vein)

• Found in posterior sulcus- drains the posterior aspect of heart.– left marginal vein – drains the apex on left side & dumps into the …

– coronary sinus • collects blood and empties into right atrium

Venous Drainage

Venous Drainage

Before we go on!

1. Name the three layers of the heart and describe their structural differences.

2. What are the functions of the fibrous skeleton?

3. Trace the blood flow through the heart, naming each chamber and valve in order.

4. What are the three principal branches of the left coronary artery? Where are they located on the heart?

Cardiac Conduction System & Cardiac Muscle

Vertebrate heart beat is myogenic. Originates within the heart.

Contracts in regular intervals (rhythmicity).

Take heart out of the body – still beats!Cut it into little pieces and each piece will

continue to pulsate rhythmically.

Heart is not dependent on the NS, because it has its own pacemaker and electrical system.

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Nerve Supply to Heart

Even though the has it own pacemaker it is still innervated by SNS & PNS:

• Sympathetic nerves - ↑ heart rate – Lower cervical & upper thoracic spinal cord– Efferent fibers travel to cervical ganglia, cardiac nerves

arise from the cervical ganglia and innervate the ventricular myocardium thus

– ↑ the force of contraction.– can raise heart rate to 230 bpm

Nerve Supply to the Heart

• Parasympathetic nerves - ↓ heart rate– Pathway is through

– right vagal nerve innervates the electrical center of the heart called the SA node (sinoatrial);

– vagal tone – normally slows heart rate to 70 - 80 bpm. Without vagas n. influence the heart would have a resting heart rate of about 100 bpm.

Vagus N. (CN X);Vagus N. (CN X);

Cardiac Conduction System

Controls the route and timing of electrical conduction to ensure that the four chambers are coordinated with each other.

Conduction of electrical signals travels:

*SA node → AV node→ AV bundle→ R/L bundle branches→ purkinje fibers

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Cardiac Conduction System• SA node: pacemaker, modified myocytes that initiates

heartbeat, sets heart rate, signals spread throughout the atria.

• fibrous skeleton insulates atria from ventricles

• AV node: (located near the R-AV valve); electrical gateway to ventricles.

• AV bundle (Bundle of His): pathway for signals from AV node, this bundle splits into…

• Right and left bundle branches: enter interventricular septum & descend toward the apex;

• Purkinje fibers: upward from apex spread throughout ventricular myocardium. Distribute the electrical excitation to the myocytes.

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Cardiac Conduction System

Structure of Cardiac Muscle

Purkinje fibers do not reach every cardiac myocyte (cardiocyte).

Cardiocytes pass the electrical impulse to each other through special attachment sites.

This is what coordinates the heartbeat.

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Structure of Cardiac Myocyte• Short, branched cells, one central nucleus• Intercalated discs join myocytes end to end• 3 Distinctive features

– interdigitating folds – the plasma membrane is folded like the bottom of an egg carton = surface area and interlocks cells.

– mechanical junctions two types:• Fascia adherens – extensive, actin of the thin filaments is

anchored to plasma membranes, and via transmembrane proteins, one cell is linked to the other.

• Desmosomes – mechanical junctions, prevents the cells from pulling apart with every contraction.

Structure of Cardiac Myocytes

• electrical junctions - gap junctions allow ions to flow, thus allow the myocyte to electrically stimulate its neighbors.

• Thus both atria contract in unison, as if it was one chamber, as does the ventricles, but not at the same time as the atria.

Metabolism of Cardiac Muscle

Depends upon aerobic respiration to make ATP.

Cardiac muscle is very susceptible oxygen deficiency.

Makes little use of anaerobic fermentation, thus it is not prone to fatigue.

This is important to maintain rhythm and of course keep us alive.

Before We Go On1. Why does the heart have a nerve supply, since it

continues to beat even without one?2. What is the timing mechanism that normally sets off the

heartbeat and regulates its rhythm?

3. What organelle(s) are less developed in cardiac muscle than in skeletal muscle? What one(s) are more developed? What is the function significance of these differences between muscle types?

4. What component of an intercalated disc enables one cardiac myocyte to directly stimulate another? What component keeps them from pulling apart when the muscle contract?

Electrical & Contractile Activity of the Heart

Examine how the electrical events in the heart produce its cycle of contraction and relaxation.

Systole = contraction, ie atrial or ventrical systole

Diastole = relaxation

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Cardiac Rhythm

Sinus rhythm– Normal heart beat set by SA node at 60 – 100 bpm– adult at rest is 70 to 80 bpm (vagal inhibition)

Hypoxia, electrolyte imbalance, stimulants, stress, etc. can cause other parts of the conduction system to fire before the SA node setting off an extra heart beat:

Called premature ventricular contraction (PVC) or extrasystole.

Any region of spontaneous firing other than the SA node is called an ectopic focus.

Cardiac Rhythm

If SA node is damaged an ectopic focus may take over the control of the heart rhythm.

Most common ectopic focus in his case is the AV node, = slower heart beat of 40-50 bpm, called nodal rhythm.

If SA or AV node is not functioning, other ectopic foci fire at rates of 20-40 bpm. (need artificial pacemaker)

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Cardiac Rhythm

• Arrhythmia – any abnormal cardiac rhythm– One cause is a heart block: failure of any part of

the conduction system to transmit signals, usually result of disease and degeneration of conduction fibers.

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Cardiac Arrhythmias

• Three common types:

1. Artial Flutter2. Premature ventricular contractions3. Ventricular fibrillation

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Artial Flutter

• Extra contractions in the atria, atria beats 200 – 400 /minute.

• The atria beat regularly and faster than the ventricles.

• It is most commonly seen in hypertensive, heart artery (coronary) and valvular disease especially in the setting of heart failure (poor heart muscle function).

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Premature Ventricular Contractions

• Extra heartbeat

• Occur singly or in bursts as a result of an ectopic focus (Any region of spontaneous firing other than the SA node.)

• Due to irritation of the heart by stimulants, emotional stress, or lack of sleep.

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Ventricular Fibrillation• Serious arrhythmia caused by electrical signals

arriving at different regions of the myocardium at widely different times.

• Ventricles resemble “bag of worms”

• No coronary perfusion due to lack of blood leaving the ventricles, results in ischemia to myocardium.

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Ventricular Fibrillation

• Defibrillation is the emergency procedure in which the heart is given a strong electrical shock.

• Commotio Cordis

Electrocardiogram schematic tracing, showing the period of vulnerability to stretch-induced ventricular fibrillation which occurs in commotio cordisThe following factors increase the chance of commotio cordis:

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Pacemaker Physiology• SA node cells have an unstable RMP. The RMP is

-60mV and drifts upward, gradually causing depolarization = pacemaker potential (slow influx of Na+ without compensating K+ outflow).

• Action potential – occurs at threshold of -40 mV (fast calcium channels open)Depolarizing phase

• Occurs when fast Ca2+ channels open, (Ca2+ in) to 0mv

Repolarizing phase• K+ channels open, (K+ out)• at -60 mV K+ channels close, pacemaker potential starts over

• Each depolarization creates one heartbeat

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Impulse Conduction to the Myocardium

• SA node signal travels at 1 m/sec through atria• AV node slows signal to 0.05 m/sec

– thin myocytes with fewer gap junctions– delays signal 100 msec, allows ventricles to fill

• AV bundle and purkinje fibers– speeds signal along at 4 m/sec to ventricles

• Ventricular systole begins at apex, progresses up– spiral arrangement of myocytes twists ventricles slightly

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Contraction of Myocardium

• Myocytes have stable resting potential of -90 mV• Depolarization (very brief)

– stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly

– action potential peaks at +30 mV – Na+ gates close quickly

• Plateau - 200 to 250 msec, sustains contraction– slow Ca2+ channels open, Ca2+ binds to fast Ca2+

channels on SR, releases Ca2+ into cytosol: contraction• Repolarization - Ca2+ channels close, K+ channels

open, rapid K+ out returns to resting potential

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Action Potential of Myocyte

1) Na+ gates open2) Rapid

depolarization3) Na+ gates close4) Slow Ca2+

channels open5) Ca2+ channels

close, K+ channels open

Electrocardiograph

Detect electrical currents in the heart. ECG amplifies the signals and produces an electrocardiogram.

Electrodes attached to the wrist, ankles, and six other locations.

ECG is a composite of all action potentials.

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Electrocardiogram (ECG or EKG)

Shows three Shows three principle deflections principle deflections above and below above and below the base line the base line called:called:

1.1.P waveP wave2.2.QRS complexQRS complex3.3.T waveT wave

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ECG

• P wave– SA node fires, atrial depolarization– PQ segment = time required for impulses to

travel from the SA node to the AV node (160 msec).

ECG

• QRS complex– Produced when signal from AV node spreads through

the ventricle myocardium. (ventricular depolarization)

– atrial repolarization and diastole also occurs during this phase but is not recorded due the electrical activity of the muscular ventricals.

ECG

• T wave– ventricular repolarization and diastole;– Major characteristic is the rounded peak.

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1) atrial depolarization begins

2) atrial depolarization complete (atria contracted)

3) ventricles begin to depolarize at apex; atria repolarize (atria relaxed)

4) ventricular depolarization complete (ventricles contracted)

5) ventricles begin to repolarize at apex

6) ventricular repolarization complete (ventricles relaxed)

Relationship

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Diagnostic Value of ECG• Invaluable for diagnosing abnormalities in

conduction pathways, MI, heart enlargement and electrolyte and hormone imbalances

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ECGs, Normal and Abnormal

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ECGs, Abnormal

Extrasystole : note inverted QRS complex, misshapen QRS Extrasystole : note inverted QRS complex, misshapen QRS and T and absence of a P wave preceding this contraction.and T and absence of a P wave preceding this contraction.

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ECGs, Abnormal

Arrhythmia: conduction failure at AV nodeArrhythmia: conduction failure at AV node

No pumping action occursNo pumping action occurs

Blood Flow, Heart Sounds, Cardiac Cycle

Principle of Pressure & Flow

Fluid Dynamics principles of fluid movement: 2 main variables:

1. Pressure – which causes fluid to flow;

2. Resistance – which opposes flow.

Measurement of Pressure

Pressure is observed by measuring how high it can push a column of mercury (Hg) up a tube (manometer).

Sphygmomanometer (SFIG-mo-ma-NOM-eh-tur) is used to measure the blood pressure.

Pressure Gradients and Flow

Any fixed quantity of fluid, its pressure depends upon the volume of space it occupies.

The greater the volume = less pressure, The less volume = greater the pressure.

With blood circulation we are concerned with flow, this is in response to a pressure gradient.

Fluid will flow from higher pressure gradient to a lower pressure gradient

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Left Ventricle – as the ventricle expands it is increasing in volume = lower pressure;

If AV valve is open, blood will flow in from the atria above;

When the ventricle contracts it decreases volume = increase pressure;

When aortic semilunar valve opens blood is ejected out..

Pressure Gradients and Flow

Pressure Gradients and Flow

• Positive blood pressure in the aorta (great vessels) produces a resistance that opposes flow.

– ventricular pressure must rise above this resistance for blood to flow into great vessels

Heart Sounds

Auscultation is listening to sound made by the body.

The cardiac cycle will produce two or three audible sounds, easily picked up by the stethoscope.

1st heart sound – characterized as S1 “lubb”- louder and longer

2nd heart sound – characterized as S2 “dubb”- a little softer and sharper

Heart Sounds

Uncertain, but the theory = S1 and S2 sounds occur in conjunction with the closing of the valves (mitral and tricuspid valves).

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Phases of the Cardiac Cycle

• One complete contraction and relaxation of all 4 chambers of the heart

• Atrial systole, Ventricle diastole• Atrial diastole, Ventricle systole• Quiescent period (all four chambers are in

diastole).

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Rate of Cardiac Cycle

• Atrial systole, 0.1 sec• Ventricular systole, 0.3 sec• Quiescent period, 0.4 sec

– All four chambers in diastole• Total 0.8 sec, heart rate 75 bpm

Phases of the Cardiac Cycle

There are 4 phases of the cardiac cycle:

1. Ventricular Filling2. Isovolumetric contraction3. Ventricular ejection4. Isovolumetric relaxation

1. Ventricular FillingDuring diastole, the ventricles expand and their pressure

drops → AV valves open → blood flows in causing ventricular pressure to rise.

Ventricular filling occurs in three phases:1a. Rapid ventricular filling;1b. Diastasis, slower, P wave occurs at the end of diastsis, marking the end of atria deplorization;1c. Atrial systole occurs completing the filling process.

Now each ventricle contains an end-diastolic volume (EDV) about 130mL

2. Isovolumetric ContractionAtria repolarize, relax and remain in diastole for the rest of the

cardiac cycle;

Ventricles depolarize→generate QRS complex→ pressure increases in ventricles → blood pushes back on the cusps of valves, forcing them closed;

This forceful closing produces the S1 heart sound “lubb”;

Called isovolumetric because the ventricles contract but do not eject blood (no change in volume);

This is due to the pressure in the aorta and pulmonary trunk is greater then the pressure in the ventricles, forcing the semilunar valves closed.

3. Ventricular EjectionEjection occurs when the pressure in the ventricles exceeds

the pressure it the aorta and pulmonary trunk, forcing the semilunar valves open.

Flow of blood out of the ventricles is faster in the beginning due to the increase pressure, but then flow begins to slow as pressure decreases (Like a soda bottle).

Ventricles do not expel all its blood. Remember each ventricle contains EDV of 130mL, they EJECT about 70mL, this is called stroke volume (SV).

The percentage of EDV ejected (54%) is called the ejection fraction.

3. Ventricular Ejection Continued

The blood remaining in the ventricles after contraction (60mL), is called End-Systolic Volume (ESV).

EDV – SV = ESV

In exercise the ejection fraction could be as high as 90%;

Ejection fraction is an important measure of cardiac health, diseased heart may only eject 50% of blood.

4. Isovolumetric RelaxationEarly ventricular diastole (relaxation), T wave ends and

ventricles begin to expand (like squeezing a rubber ball and it recoils);

This recoil cause the ventricle pressure to drop, sucking blood into the ventricles;

Blood in the aorta and pulmonary trunk back flow and force the semilunar valves close;

Resulting in S2 heart sound.

Called isovolumetric because semilunar valves are closed and the AV valves have not opened.

4. Isovolumetric relaxation continued

When AV valves open, ventricular filling begins again (phase 1).

S3 (if present) is thought to be the result sudden filling of the ventricle

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Ventricular Volume Changes at Rest

End-systolic volume (ESV) 60 mlPassively added to ventricle

during atrial diastole+30 mlAdded by atrial systole +40 mlEnd-diastolic volume (EDV) 130 mlStroke volume (SV) ejected

by ventricular systole -70 mlEnd-systolic volume (ESV) 60 mlBoth ventricles must eject same amount of blood

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Cardiac Output (CO)

• Amount ejected by each ventricle in 1 minute• Cardiac Output = Heart Rate (beats/min)(HR)

x Stroke Volume (mL/beat) (SV)• HR x SV = CO, 75 bpm x 70mL/beat =

5250mL/min– about 4 to 6L/min at rest – vigorous exercise CO to 21 L/min for fit person and up to 35 L/min for

world class athlete

• Cardiac reserve: difference between a persons maximum and resting CO with fitness, with disease

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Heart Rate

• Pulse = surge of pressure in artery (radial, carotid arteries)– infants have HR of 120 bpm or more– young adult females avg. 72 - 80 bpm– young adult males avg. 64 to 72 bpm– HR rises again in the elderly

• Tachycardia: resting adult HR above 100– stress, anxiety, drugs, or body temp, ↓SV.

• Bradycardia: resting adult HR < 60– in sleep and endurance trained athletes

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Chronotropic Effects

Factors that affect Heart Rate (HR):• Positive chronotropic agents HR • Negative chronotropic agents HR

Chronotropic Effects of the ANS

NS does not initiate the heart beat but modulates the rhythm and force.

Medulla Oblongata contains the cardiac center:

Contains two neural pools:1. cardioacceleratory center 2. cardioinhibitory center

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Cardioacceleratory Center

• Cardioacceleratory center– Sends signals by way of sympathetic cardiac

nerves to SA node, AV node and myocardium– these nerves secrete norepinephrine, which

have a positive chronotropic effect;– Sympathetic NS can HR up to 230 bpm

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Cardioinhibitory Center

• Cardioinhibitory center sends signal via vagus nerves (CN ?)– To the SA and AV nodes;– secretes ACH (acetylcholine) which opens K+

channels thus having a negative chronotrophic effect;

• cells hyperpolarized, HR slows

– vagal tone: background firing rate holds HR to sinus rhythm of 70 to 80 bpm;

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Other influences on Cardiac Center• Higher brain centers affect HR

– cerebral cortex, limbic system, hypothalamus • sensory or emotional stimuli (rollercoaster, IRS audit, Love)

• Input from receptors to Cardiac center affect HR– Proprioceptors (muscles and joints)

• inform cardiac center about changes in physical activity, HR before metabolic demands arise;

– Baroreceptors (pressoreceptors)• aorta and internal carotid arteries send constant signals

to cardiac center monitoring blood pressure.– pressure , signal rate drops, cardiac center HR– if pressure , signal rate rises, cardiac center HR

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Other influences on Cardiac Center• Chemoreceptors

– sensitive to blood pH, CO2 and oxygen;– Located in aortic arch, carotid arteries and medulla

oblongata; – primarily respiratory control, may influence HR– Circulation to tissues moves too slow to remove

CO2, it accumulates in the blood and CSF produces a state of Hypercapnia;

– CO2 + H20 → HCO3- + H+, thus ↓pH;

– Hypercapnia and acidosis stimulates cardiac center to HR.

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Chronotropic Effects of Chemicals• Affect heart rate• Neurotransmitters - cAMP 2nd messenger

– cAMP activates an enzyme that phosphorylates a Ca2+

channel.– catecholamines (NE and epinephrine)

• potent cardiac stimulants• Drugs

– caffeine inhibits cAMP breakdown– nicotine stimulates catecholamine secretion

• Hormones– TH adrenergic receptors in heart, sensitivity to

sympathetic stimulation, HR

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• Electrolytes– K+ has greatest effect

• hyperkalemia – myocardium less excitable, HR slow and irregular

• hypokalemia – cells hyperpolarized, requires increased stimulation

– Calcium• hypercalcemia

– decreases HR• hypocalcemia

– increases HR

Chronotropic Effects of Chemicals

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Stroke Volume (SV)

• A factor of Cardiac Output• Governed by three factors:

1. preload2. contractility 3. afterload

• Example preload or contractility causes SV afterload causes SV

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Preload

• Amount of tension in ventricular myocardium before it contracts

preload causes force of contraction– exercise venous return, stretches myocardium (

preload) , myocytes generate more tension during contraction (length-tension relationship),if ventricles contact more forcefully = expels more blood, CO matches venous return

• Frank-Starling law of heart - SV EDV– ventricles eject as much blood as they receive

• more they are stretched ( preload) the harder they contract

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Contractility• How hard the myocardium contracts for a

given period of preload (more responsive to stimulation);

• Factors that contractility are called– Positive inotropic agents

• hypercalcemia, catecholamines, glucagon, digitalis

• Factors that contractility are– Negative inotropic agents

• hyperkalemia, hypocalcemia

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Afterload

• Pressure in arteries above semilunar valves opposes opening of valves;

afterload SV– Hypertension afterload; – any impedance in arterial circulation afterload;

• Continuous in afterload (lung disease), causes hypertrophy of right ventricle myocardium, may lead it to weaken and fail:

• Cor pulmonale – Rt ventricle failure due to obstructed pulmonary circulation.

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Exercise and Cardiac Output• Exercise makes ♥ work harder = CO

• HR at beginning of exercise due to signals from proprioceptors in the joints, muscles to cardiac center;

• Muscular activity venous return HR and SV cause CO to compensate for the

venous return;• Exercise produces ventricular hypertrophy

SV allows heart to beat more slowly at rest;– Allows ♥ to beat more slowly while still maintaining a

normal CO.

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Heart Disease• Diseases That Affect the Heart and Cardiovascular System• Cardiovascular disease includes a number of conditions

affecting the structures or function of the heart. They can include:

• Coronary artery disease (including heart attack) • Abnormal heart rhythms or arrythmias • Heart failure • Heart valve disease • Congenital heart disease • Heart muscle disease (cardiomyopathy) • Pericardial disease • Aorta disease and Marfan syndrome • Vascular disease (blood vessel disease)

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Coronary Artery Disease

• (CAD) is atherosclerosis, or hardening of the arteries that provide vital oxygen and nutrients to the heart.

• Heart disease is the No. 1 killer in America affecting more than 13 million Americans.

• Your coronary arteries are hollow tubes. Inside, they are smooth and elastic, allowing blood to flow freely.

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Coronary Artery Disease

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Coronary Artery Disease

• Before your teen years, fat starts to deposit in the blood vessel walls. As you get older, the fat builds up.

• Over time, the inside of the arteries develop plaques of different sizes.

• The plaque builds up and narrows the artery (atherosclerosis).

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CHD Symptoms

• The most common symptom is angina or "angina pectoris”.

• Other symptoms that can occur with coronary artery disease include: – Shortness of breath – Palpitations (irregular heart beats, skipped beats

or a "flip-flop" feeling in your chest) – A faster heartbeat – Weakness or dizziness – Nausea – Sweating

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Coronary Artery Disease Treatment

• reducing your risk factors, • taking medications, • possibly undergoing invasive and/or

surgical procedures and • seeing your doctor for regular health care

follow up visits.

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Risk Factors CAD

• Some are controllable, others are not. • Uncontrollable risk factors include:

• Male sex • Older age • Family history of heart disease • Post-menopausal • Race (African Americans, American Indians, and

Mexican Americans are more likely to have heart disease than Caucasians)

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Risk Factors CAD

• Controllable risk factors include: • Smoking. • High LDL, or "bad" cholesterol and low HDL, or

"good" cholesterol. • Uncontrolled hypertension (high blood pressure). • Physical inactivity. • Obesity (more than 20% over one's ideal body

weight). • Uncontrolled diabetes. • Uncontrolled stress and anger.

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Congestive Heart Failure

• CHF– Results from failure of either ventricle to eject

blood effectively;• Causes: MI, chronic hypertension, valvular

insufficiency, or congenital defects of cardiac structures.

• LF ventricle fails to contract, blood backs up in lungs (pulmonary edema)

• RT ventricle fails to contract, blood backs up in venae cavae (systemic edema)

• Overall failure of one ventricle leads to increase work load of the other, which will eventually fail.