TOPIC 11

MOVEMENTS IN BODY

1. cell components move within the cell during cell division

2. white blood cells can propel themselves through the body

3. MUSCLE CELLS: contraction specialists involved in events ranging from propulsion of food though GI tract to propulsion of whole body (walking)

TOPIC 11

THREE TYPES OF MUSCLE

1. SKELETAL: striated (alternating light and dark bands) and voluntary (innervated by somatic nervous system)

2. CARDIAC: striated, involuntary (innervated by autonomic nervous system)

3. SMOOTH: unstriated, involuntary (innervated by autonomic nervous system

TOPIC 11

Muscles respond to...

TOPIC 11

Controlled contraction of muscles allow...

1. movement of body or body parts through external environment (walking)

2. manipulation of objects in external environment (writing)

3. propulsion of substances through hollow organs (blood flow, digestion)

4. emptying contents of organs to environment ( e.g. urination, giving birth)

TOPIC 11

MUSCLE:

- the largest group of tissues in the body

- makes up 40 -50% of body mass

TOPIC 11

Organization of an Entire Muscle

A single skeletal muscle is composed of many muscle fibers (a muscle fiber is the same thing as a muscle cell) lying parallel to each other and bundled together by connective tissue

(Fig. 12.1 & 12.2)

A muscle may be innervated by many motor neurons

TOPIC 11

MOTOR UNIT:

1 motor neuron plus all the fibers it innervates (Fig. 11.14)

1. Each motor neuron innervates numerous muscle fibers distributed thoughout the muscle

2. Each muscle fiber is innervated by only one motor neuron

3. When a motor neuron is activated, all fibers that it innervates contract simultaneously

4. One motor unit activation results in a weak contraction of muscle

5. As more motor units recruited (i.e. stimulated) the contraction gets stronger and stronger)

6. Number of muscle fibers per motor unit, and the number of motor units per muscle, vary widely

7. Asynchronous recruitment occurs to prevent fatigue

         a. alternation of motor unit activity, like factory shift 

             work

         b. only possible during submaximal contraction

TOPIC 11

Muscle Fiber Structure

1. Extends the length of the muscle (up to 0.75 meter, or 2.5 feet long)

2. Has multiple nuclei and many mitochondria

3. Composed of many myofibrils, each of which extends the length of the muscle fiber

TOPIC 11

Myofibril Structure:

Composition of a Myofibril

(relaxed Fig. 12.2 & 12.3)

1. thick filaments = 1.6 um long

2. thin filaments = 1.0 um long

TOPIC 11

Myofibril Structure:

A Band

1. Stacked set of thick filaments plus portions of thin filaments that overlap both ends of thick filaments

TOPIC 11

Myofibril Structure:

H Zone

1. light area in A band where thin filaments don't reach

TOPIC 11

Myofibril Structure:

I Band

1. Portion of thin filaments that do not project into A Band

TOPIC 11

Myofibril Structure:

Z Line

1. Cytoskeleton protein that runs vertically through middle of I Band and connects thin filaments of adjoining sarcomeres

TOPIC 11

Myofibril Structure:

Sarcomere

1. Area between two Z Lines

2. Is the functional unit of skeletal muscle, (i.e. smallest component that can perform all the functions of that organ), so sarcomere is smallest contractile unit of muscle

TOPIC 11

Myofibril Structure:

M Line

1. Supporting proteins that hold thick filaments together vertically; extends vertically down the middle of the A Band in the H Zone

TOPIC 11

Myofibril Structure:

Cross Bridges

1. Extend from thick filaments to thin filaments

2. Six thin filaments surround every thick filament; the thick filament projects cross bridges to each of the 6 thin filaments

TOPIC 11

Thick Filament Structure:

Thick Filament Composed of...

1. myosin molecules lying lengthwise parallel to each other

2. half are oriented in one direction

3. half are oriented in another direction

TOPIC 11

Thick Filament Structure:

Myosin Molecule  Structure...

1. Two golf club shaped subunits with tails intertwined and globular heads (myosin heads also called cross bridges!) projecting out at one end

2. Each head contains an actin binding site and a myosin ATPase site

TOPIC 11

Thin Filament Structure:

Actin...

1. molecules are spherical in shape

2. each has a myosin binding site

3. backbone of thin filament formed by two chains of actin molecules wrapped around each other, like two chains of pearls

TOPIC 11

Thin Filament Structure:

Tropomyosin

1. Threadlike proteins that lie end to end along the actin spiral

2. Covers myosin binding site on actin

TOPIC 11

Thin Filament Structure:

Troponin

1. Fastens down each end of the tropomyosin molecules, holding them in place over myosin binding sites

TOPIC 11

Transverse Tubules

(T tubules)

(Fig. 12.2)

1. Part of surface membrane of muscle fiber that dips into fiber at junction of A and I Bands

TOPIC 11

Sarcoplasmic Reticulum

(Fig. 12.2)

1. Modification of endoplasmic reticulum

2. Surrounds each myofibril with separate segments encircling each A and I Band

TOPIC 11

Molecular Basis of Contraction:

The Sliding Filament Model

(Fig. 12.8 & 12.9)

1. Ach released by terminal button of motor neuron and binds to receptors on motor end plate

2. Ach binding on motor end plate causes End Plate Potential which causes an AP to propagate down membrane and down T Tubules into muscle cell

3. AP in the T Tubule causes sarcoplasmic reticulum to realease Ca⁺⁺

4. Released Ca⁺⁺ bind to troponin on actin filaments, which causes tropomyosin to move aside and expose myosin binding sites on the actin molecules

5. Cross Bridge Cycling: myosin cross bridges bind to actin and stroke forward (powered by ATP) pulling actin toward center of sarcomere

6. Ca⁺⁺ actively taken up by SR when no more AP

7. . With Ca⁺⁺ no longer bound to troponin, tropomyosin returns to blocking position over myosin binding site on actin

TOPIC 11

Cross Bridge Cycle in Detail

(Fig. 12.7)

1. ATP broken into ADP and Pi by ATPase on myosin head; the head holds onto the ADP and Pi, and is energized and cocked in the "ready" position

2. In presence of Ca⁺⁺, myosin binding site on actin is uncovered, and myosin head binds to actin

3. On contact of myosin and actin, ADP and Pi released and myosin head strokes forward

4. Fresh ATP binds to myosin, link with actin broken, and return to step 1.

5. This continues, and myosin heads ratchets actin along (Fig. 8-9).

6. When Ca⁺⁺ removed, no more heads are binding to actin, so it slides back into original place = relaxation

TOPIC 11

Changes in Myofibril During Contraction

(Fig. 12.6)

1. sarcomere shortens

2. I Band shortens

3. H Zone gets smaller

4. A Band same width

TOPIC 12

Events in Muscle Contraction

1. Whole muscle is composed of muscle fibers bundled together by connective tissue and attached to bones by tendons

    a. contraction of enough muscle fibers results in movement of bone or limb

2. A single AP produces a brief weak contraction called a twitch

    b. single AP does not normally occur

    c. muscle fibers are organized so they can cooperatively function to produce contractions stronger than a twitch

TOPIC 12

Timing of Contraction:

Latent Period

(Fig. 12.12)

1. time between initiation of stimulation and start of contraction

2. action potential occurs during this time

3. 1-2 milliseconds (msec)

TOPIC 12

Timing of Contraction:

Contraction Time

1. time between onset of contraction and peak tension

2. continues until all Ca⁺⁺ removed

3. 50 msec

TOPIC 12

Timing of Contraction:

Relaxation Time

1. time between peak tension and complete relaxation

2. 50 msec or more

** total contractile response to single AP is 100 msec or more, compared to the 2 msec AP that produced response

TOPIC 12

Factors Influencing Whole Muscle Tension:

Frequency of Stimulation

(voluntary control)

-Twitch Summation-

1. TWITCH SUMMATION (Fig. 12.17)

     a. Single AP: single twitch

         - released Ca⁺⁺ binds to troponin and contraction

           occurs, BUT Ca⁺⁺ is immediately removed and

           contraction stops

     b. Two AP's Close Together: summation of twitch

     c. Multiple AP's Close Together: summation of twitches

         - released Ca⁺⁺ binds to troponin, and then is

            removed, but additional AP release more Ca⁺⁺ so

            that contraction continues, i.e., some contractile

            activity from first AP continues as second AP has its

            effect

TOPIC 12

Factors Influencing Whole Muscle Tension:

Frequency of Stimulation

(voluntary control)

-Tetanus-

Tetanus: many rapid stimuli prevents muscle relaxation

1. is a contraction of maximal strength

2. Increased AP: so much Ca⁺⁺ released that maximum number of cross bridge sites are uncovered = maximal tension

3. all fibers recruited, so asynchronous contracting not possible, fatigue eventually occurs

TOPIC 12

Factors Influencing Whole Muscle Tension:

Number of Muscle Fibers Contracting Within a Muscle

-Motor Unit Recruitment-

(Fig. 12.19)

**Under Voluntary Control

1. external eye muscles: ~ 12 muscle fibers/motor unit

2. leg muscles: ~ 2000 muscle fibers/motor unit

TOPIC 12

Factors Influencing Whole Muscle Tension:

Number of Muscle Fibers Contracting Within a Muscle

-Length of Fiber at Onset of Contraction-

(Fig. 12.18)

1. optimal resting length of muscle gives maximal tension

2. non-optimal resting lengths give sub maximal tension 

TOPIC 12

Factors Influencing Whole Muscle Tension:

Number of Muscle Fibers Contracting Within a Muscle

-Diameter of Muscle-

1. A bigger muscle cell (with more sarcomeres and more crossbridges) can generate more force

TOPIC 12

Muscle Metabolism and Fiber Types:

ATP Required for...

1. energizing of myosin head requires splitting of ATP

2. detachment of myosin cross bridge from actin requires binding (but not splitting) of ATP

3. active transport of Ca⁺⁺ back into SR requires energy of ATP

TOPIC 12

Muscle Metabolism and Fiber Types:

ATP Sources...

-Creatine phosphate is first energy storehouse tapped-

(Fig. 12.11)

1. Creatine phosphate is first energy storehouse tapped

     a. Energy reserves in resting muscle are stored in creatine phosphate (5 times as much in muscle as ATP)

     b. When energy needed for contraction:

         creatine phosphate + ADP <--> creatine + ATP

**(requires activity of enzyme creatine phosphatase)

     c. In resting muscle, creatine phosphate is ready to go, and that's what you use as an ATP source during burst activity (1 min or less)

TOPIC 12

Muscle Metabolism and Fiber Types:

ATP Sources...

-Glycolysis + Krebs Cycle + Oxidative Phosphorylation-

1. Glycolysis + Krebs Cycle + Oxidative Phosphorylation

     a. mitochondria in muscle require oxygen and fuel to produce ATP

     b. can make ~ 38 ATP/glucose this way

     c. But this is slow compared to creatine phosphate

     d. you can do this during aerobic (or endurance) exercise

     e. O₂ is supplied by blood, so during aerobic exercise your body maximizes O₂ delivery to muscles

TOPIC 12

Muscle Metabolism and Fiber Types:

ATP Sources...

-Anaerobic Pathways (glycolysis alone)-

1. can make ATP rapidly

2. but only makes 2 ATP/glucose

3. but rapidly depletes fuel supply (glycogen)

4. but produces lactic acid

     a. May contribute to muscle soreness and fatigue

     b. Will lead to metabolic acidosis (=bad)

5. but contributes to fatigue

6. Bottom line: anaerobic exercise possible for only short time

TOPIC 12

Muscle Metabolism and Fiber Types:

Fatigue...

Muscle Fatigue:

1. asynchronous recruitment of motor units used to limit muscle fatigue (i.e., fibers "take turns" contracting)

2. fatigue occurs when muscle can no longer respond to stimulation with same degree of contractile activity, probably because of lactic acid accumulation and depletion of energy reserves

Neuromuscular Fatigue:

1. motor neurons cannot make Ach fast enough

Central Fatigue:

1. psychological, not well understood

TOPIC 12

Muscle Metabolism and Fiber Types:

Oxygen Consumption Elevated During Recovery from Exercise...

Oxygen Debt:

1. contractile energy debt from nonoxidative ATP sources needs to be repaid during recovery

     a. creatine phosphate resynthesized

     b. lactic acid metabolized

     c. replenish glycogen stores

Recovery from General Metabolic Disturbance:

1. all chem reactions still speeded up

2. still high levels of epi

TOPIC 12

Muscle Metabolism and Fiber Types:

Skeletal Muscle Fiber Types...

1. Three Types: (must see Table 12.1 for characteristics of each)

        a. slow oxidative (type I) fibers

        b. fast oxidative (type IIa) fibers

        c. fast glycolytic (type IIb) fibers

2. Most muscles have all three types

3. A motor unit is composed of all one type of fiber

4. Within a muscle, fast oxidative and fast glycolytic can interconvert over time, depending on how muscle is trained

5. HYPERTROPHY: increase in muscle fiber diameter

6. HYPERPLASIA: increase in muscle fiber number; usually occurs by splitting muscle fibers, rarely happens

TOPIC 12

Control of Motor Movement:

3 Levels of Input Control Motor Unit Neuron Output...

1. Spinal Refelxes

2. Primary motor cortex (in cerebral cortex)

3. Other corical and subcortical regions of the brain (basal nuclei, cerebellum, thalamus, and others) send signals to primary motor cortex and/or brain stem, each of which can then directly control motor neurons

TOPIC 13

Broad Comparisons of Smooth, Cardiac, and Skeletal Muscle:

1. All have contractile system apparatus composed of thin actin filaments that slide past stationary thich myosin filaments in response to increase in Ca⁺⁺

2. All use ATP directly as energy source for cross-bridge cycling

3. But mechanisms of excitation different

4. But coupling of excitation and contraction different

5. But contraction responses different

TOPIC 13

Smooth Muscle Structure:

Structure of Smooth Muscle Cells...

(Fig. 12.33)

1. Found mostly in walls of hollow organs and tubes

     a. contraction causes forward movement of contents of tube

     b. digestive tract and blood vessels

2. Spindle-shaped, have a single nucleus (recall that skeletal muscle cells are multi-nucleated)

3. Smaller than skeletal muscle cells

4. Do not extend full length of muscle as do skeletal muscle cells

5. Groups of smooth muscle cells are typically arranged in sheets

TOPIC 13

Smooth Muscle Structure:

Subcellular Structure of Smooth Muscle...

-3 Types of Smooth Muscle Cell Filaments-

1. Thick Myosin Filaments

      a. longer than in skeletal muscle

2. Thin Filaments Composed of:

      a. actin

      b. tropomyosin

      c. no troponin

        d. 10-15 thin filaments/thick filaments

3. Intermediate filaments only support cell shape

TOPIC 13

Smooth Muscle Structure:

Subcellular Structure of Smooth Muscle...

-continued-

1. Myofibrils are not formed, and here is no sarcomere arrangement

2. No Z Lines:

     a. Smooth muscle doesn have dense bodies made of the same protein that make up Z Lines

     b. Dense bodies are found thoughout cell and are anchored to the cell membrane

     c. actin filaments are anchored to dense bodies

3. NO T Tubules

4. Underdeveloped SR

TOPIC 13

Molecular Basis of Smooth Muscle Contraction

(Fig. 12.34)

1. Ca⁺⁺ channels on smooth muscle membrane open, and Ca⁺⁺ from the ECF diffuses into cell (concentration gradient of Ca⁺⁺is from ECF into ICF)

2. Entering Ca⁺⁺ causes SR to release small amounts of Ca⁺⁺, functionally not very important

     a. Because smooth muscle cells are so much smaller in diameter than skeletal muscle cells, SR & T Tubules are not needed to deliver Ca⁺⁺ deep into the muscle

3. Ca⁺⁺ activates enzyme called calmodulin

4. Activated calmodulin activates enzyme myosin light chain kinase

5. Activated myosin light chain kinase phosphorylates myosin by splitting a phosphate off of ATP

6. Phosphorylated myosin binds with actin and cross bridge cycling begins (contraction)

7. When Ca⁺⁺ removed by active transport out of smooth muscle cell, calmodulin and in turn myosin kinase return to inactive form, and an enzyme called phosphatase removes phosphate from myosin. Hence myosin becomes unphosphorylated and no longer binds to actin, and the muscle cell relaxes

8. Mechanism of stimulation of smooth muscle depends on whether it is multiunit or single unit smooth muscle

TOPIC 13

Multiunit Smooth Muscle (rare):

Organization...

1. Smooth muscle cells within a smooth muscle are organized into different functional units

2. Each unit (i.e., group of smooth muscle cells) separately stimulated by nerves of ANS

     a. such contractions are called neurogenic (nerve produced)

3. Each unit functions independently of other units

     a. similar to skeletal muscle

4. Rare; found in:

     a. walls of large blood vessels

     b. large airways to lungs

     c. eye muscles related to distance vision

     d. iris of eye

     e. base of hair follicles (goose bumps)

TOPIC 13

Single-Unit Smooth Muscle (common)

(Fig. 12.35)

1. Muscle fibers in muscle make up a single unit and contract together

2. Fibers are linked by gap junctions (allows for the contraction of one cell to rapidly spread and cause the contraction of entire muscle), an AP anywhere in the muscle propogates via gap junctions to all fibers, so whole muscle contracts together

      a. EXAMPLE: uterine walls need to contract together to expel baby from uterus

TOPIC 13

Single-Unit Smooth Muscle (common):

Stimulated by...

1. Autonomic Nervous System

2. Myogenic Activity (muscle produced)

      a. Pacemaker Activity (e.g., lymph vessels) [left figure in notes]

           - in a pacemaker cell, the membrane depolarizes on its own because of automatic changes in channel permeability

           - once AP fired in pacemaker, it spreads to rest of smooth muscle cells via gap junctions

      b. Slow wave potential (e.g., intestine) [right figure in notes]

           - gradual alternating hyperpolarizing and depolarizing swings in potential caused by cyclical changes in the rate at which Na⁺ is actively transported across membrane

           - Threshold not always reached, but when it is, a burst of AP's follow

TOPIC 13

Smooth Muscle Mechanics:

Modification of contraction strength in single unit smooth muscle...

1. Fiber tension modified by varying cytosolic Ca⁺⁺concentration

2. As cytosolic Ca⁺⁺ increases, so does number of cycling cross bridges

3. Many single unit smooth muscles maintain low levels of cytocolic Ca⁺⁺, which means low level of contraction always occurring; this is called muscle tone

TOPIC 13

Smooth Muscle Mechanics:

Modification of contraction strength in multiunit smooth muscle...

1. Functional unit recruitment (= motor unit recruitment of skeletal muscle)

2. Varying cytosolic Ca⁺⁺ concentration within a cell

TOPIC 13

Smooth Muscle Mechanics:

Factors that modify cytosolic Ca++ and hence contraction for both single and multiunit smooth muscle...

1. Both branches of autonomic nervous system (symp. & parasymp.)

2. Hormones

3. Metabolics

4. Mechanical stretch

5. Drugs

TOPIC 13

Smooth Muscle Mechanics:

Continued...

1. Considerably stretched smooth muscle can still develop tension

      a. URINARY BLADDER: when full, it is stretched, but you need to develop more tension because you have to contract bladder to empty

2. Can relax even when stretched

      a. probably caused by re-arrangement of cross bridges after stretching

3. Is slow and economical

      a. slow rate of ATP use

      b. cross bridges latch onto thin filaments longer

4. BOTTOM LINE: Smooth muscle is highly specialized to economically maintain tension for long periods without fatigue, and can accommodate variation in contents volume with little change in muscle tension

TOPIC 13

Cardiac Muscle:

Structure...

1. STRIATED: thick and thin filaments highly organized

2. Contains troponin and tropomyosin

3. Clear cut length-tension relationship like skeletal muscle

4. Have T Tubules and pretty good SR

5. Lots of mitochondria like oxidative skeletal muscle fibers

6. Cells are connected by gap junctions

7. Innervated by ANS

8. Fibers are joined in branching network

TOPIC 13

Cardiac Muscle:

Function...

1. Ca⁺⁺ enters cytosol from ECF and SR

2. Some cardiac cells have pacemaker activity like smooth muscle

3. AP's have long duration

TOPIC 14

Introduction to Circulatory System:

Overall function...

1. Need to get nutrients and oxygen to all cells in body

2. Need to remove wastes from all cells in body

3. Blood is transport medium which does this

4. So need to get blood to pass by all cells in body

TOPIC 14

Introduction to Circulatory System:

Circulatory System consists of 3 components...

1. Heart: acts as a pump for blood

2. Blood Vessels: passageways for blood

3. Blood: transport medium

TOPIC 14

Introduction to Circulatory System:

Circulatory System has 2 separate loops...

(Fig. 13.2)

1. Pulmonary: blood movement between heart and lungs (Right atrium/ventricle)

2. Systemic: blood movement between heart and all other parts of body (Left atrium/ventricle)

TOPIC 14

Structure of Heart:

Location in body...

-CD: Anatomy Review 3,4,5,7-

1. Size of clenched fist, located in chest cavity, midway between sternum and backbone

2. Broad base at top of heart, tapers to an apex at bottom

3. Top lies to the right of sternum, apex is to the left of sternum

TOPIC 14

Structure of Heart:

Heart as dual pump...

-Divided into 2 halves separated by muscle wall-

(Fig. 13.2)

1. Divided into 2 halves separated by muscle wall

     a. each half functions as a separate pump

     b. Right side receives blood from systemic circulation and pumps it to pulmonary circulation so that the blood can be oxygenated

     c. Left side receives blood from pulmonary circulation and pumps it to systemic circulation so that the rest of the body gets freshly oxygenated blood

TOPIC 14

Structure of Heart:

Heart as a dual pump...

-Each half divided into 2 chambers-

1. Each half divided into 2 chambers

      a. upper chamber is called atrium (atria is plural) and receives blood returning to heart and transfers it to the...

      b. lower chamber, called the ventricles, which pumps blood out of the heart

TOPIC 14

Structure of Heart:

Heart as a dual pump...

-Blood vessels that return blood to heart are called...-

VEINS:

1. venae cavae brings blood from systemic circulation to heart

2. pulmonary artery carries blood from heart to lungs

TOPIC 14

Structure of Heart:

Heart as a dual pump...

-Blood flow in circulatory systems-

(Fig. 13.3)

1. PULMONARY: all blood flows through the lungs

2. SYSTEMIC: blood divided up among different body systems (i.e., one drop of blood visits only one body tissue/trip, not all tissues/trip)

3. Both sides of heart simultaneously pump equal amounts of blood

        a. Pulmonary circulation is low pressure, low resistance

        b. systemic circulation is high pressure, high resistance

        c. hence the left side of heart performs more work and the heart muscle on the left is much thicker

TOPIC 14

Structure of Heart:

One-way blood flow in heart...

-Blood flow in heart is in one direction-

1. requires valves to prevent backflow

TOPIC 14

Structure of Heart:

One-way blood flow in heart...

-Four one way valves-

(Fig. 13.7 & 13.8)

1. Open and close passively because of pressure differences

      a. forward pressure gradient = opens valves

      b. backward pressure gradient = closes valves

2. 2 atrioventricular (AV) valves

      a. one on each side of heart between atrium and ventricle

3. One aortic valve

      a. junction of left ventricle and aorta

4. One pulmonary valve

      a. junction of right ventricle and pulmonary artery

5. No valves between atria and veins

      a. backflow not a problem because atrial pressure not higher than venous pressure, and entry sites of vein into atria are compressed during atrial contraction

TOPIC 14

Structure of Heart:

Cardiac Muscle: MYOCARDIUM...

-Structure-

1. Cardiac muscle fibers interlaced & arranged spirally around circumference of the heart

2. During ventricular contraction, diameter of chambers reduced, and apex is pulled upwards; wrings blood out of chambers

TOPIC 14

Structure of Heart:

Cardiac Muscle: MYOCARDIUM...

-Interconnections of cardiac muscle cells-

(Fig. 13.9)

1. Adjacent cells joined end to end

2. Joining point, called intercalated discs, composed of:

     a. Gap junctions (allows AP to pass from cell to cell)

            - but no gap junctions between atrial and venticular

              cells; hence APs cannot be passed directly

              between atria and venticles

     b. Desmosomes (good at holding cells together under mechanical stress)

TOPIC 14

Electrical & Contractile Activity of Heart Cells:

Two types of myocardial cells...

-CD: Cardiac Action Potentials-

(Fig. 13.12)

1. 99% are contractile cells which do mechanical work of pumping

2. 1% are autorhythmic cells which are specialized for initiating and conducting APs

TOPIC 14

Electrical & Contractile Activity of Heart Cells:

Autorhythmic cell APs...

(Fig. 13.12)

1. Initial phase of slow depolarization caused by a decrease in passive outward leak of K⁺ by K⁺ channels closing in membrane and an increase in Na⁺ leaking into the cell; inside of cell slowly becomes more positive and drifts toward threshold

2. Eventually a voltage is reached that allows voltage gated Ca⁺⁺ T-Type (transient) channels to open, and Ca⁺⁺ begins to enter the cell, causing it to reach threshold!

3. At threshold, voltage gated Ca⁺⁺ L-Type (long-lasting) channels open (T-Type channels close), and Ca⁺⁺ rushes in, depolarizing the membrane rapidly; this causes an AP

4. Membrane repolarizes by exit of K⁺ from cells as K⁺ channels are opened

TOPIC 14

Electrical & Contractile Activity of Heart Cells:

Contractile cell APs...

(Fig. 13.13)

1. AP in contractile cells are quite different than in cardiac autorhythmic cells

2. When an AP reaches a contractile cardiac cell via a gap junctionm Na⁺ channels open wide and Na⁺ rushes into the cell.

       a. this results in depolarization of membrane. Na⁺ channels then close around +30 mv.

3. Depolarization of membrane causes opening of slow Ca⁺⁺ channels, and Ca⁺⁺ movels slowly into cell.

       a. In addition, depolarization causes K⁺ channels to inactivate

4. These two mechanisms work together to create the plateau phase of the AP. (prevents repolarization from happening rapidly)

5. Repolarization eventually occurs as Ca⁺⁺ channels close, and K⁺channels open and K⁺ moves out of cell

TOPIC 14

Electrical & Contractile Activity of Heart Cells:

Molecular basis of contractile cell contraction...

(Fig. 13.14)

1. AP moves across cell membrane, and Ca⁺⁺ enters cell from ECF (as in smooth muscle)

2. AP also moves down into T tubules and causes release of Ca⁺⁺ from SR (as in skeletal muscle)

    a. All this Ca⁺⁺ entering contributes to plateau phase, as well as to prolonged contraction of cardiac muscle (about 3 times longer than skeletal muscle contraction)

3. Ca⁺⁺ binds to troponin, and tropomyosin moves away from binding sites on actin, allowing cross bridge cycling as in skeletal muscle

4. Ca⁺⁺ eventually removed by active transport, and muscle relaxes

5. Long refractory period of cardiac AP and muscle contraction prevents tetanus of cardiac muscle: tetanus of cardiac muscle would cause death!

TOPIC 14

Electrical Activity of Entire Heart:

(CD: Intrinsic Conduction System 3-6)

Autorhythmic regions of heart...

-Sinoatrial Node-

(Fig. 13.10)

SA Node:

1. in right atrial wall near opening of superior vena cava.

       a. AP/min = 70-80

       b. this is pacemaker of the heart under normal conditions and sets AP pace of whole heart

TOPIC 14

Electrical Activity of Entire Heart:

Autorhythmic regions of heart...

-Atrioventricular Node-

AV Node:

1. at base of right atrium near the septum, just above atria-ventricles junction

       a. AP/min = 40-60

       b. in normal conditions helps spread AP to venticles from right atrium

TOPIC 14

Electrical Activity of Entire Heart:

Autorhythmic regions of heart...

-Bundle of His-

1. Is a tract of specialized cells that originates in AV node and travels around the top of the ventricles

      a. AP/min = 20-40

      b. Under normal conditions helps spread AP to rest of ventricles

TOPIC 14

Electrical Activity of Entire Heart:

Autorhythmic regions of heart...

-Purkinje Fibers-

1. small terminal fibers extending from bundle of His

      a. under normal conditions helps spread AP to rest of ventricles

TOPIC 14

Electrical Activity of Entire Heart:

Spread of AP in Heart...

(Fig. 13.11)

1. SA node in Right atrium initiates an AP

2. AP spreads through both atria via gap junctions between atrial cells. The interatrial pathway extends from SA node to left atrium; the AP moves rapidly through to the left atrium, so that left and right atria contract simultaneously

   **Internodal pathway: pathway of fibers between the AV and SA nodes

3. AP spread to AV node from SA node via the internodal pathway. Because atria are connected to ventricles by non-conducting tissue, AP has to go through AV node to get to ventricles

4. AP travels slowly through the AV node, which allows time for complete ventricular filling. The AV nodal delay is baout 0.1 seconds, which is enough time for atria to contract and empty their contents into ventricles

5. AP goes from AV node through the bundle of His and through Purkinje fibers throughout ventricular myocardium. This rapid conduction of AP to all parts of ventricles allows for a coordinated ventricular contraction to eject blood from ventricles.

TOPIC 14

Electrical Activity of Entire Heart:

Electrocardiograms (ECG or EKG)...

-What an ECG Represents-

1. recoding heart electrical activity that reaches body surface; it is NOT a direct recording of actual heart electrical activity

2. recording of overall spread of electrical activity throughout heart, NOT a single AP in the heart

3. recording represents comparisons in voltage detected by electrodes on 2 different parts of body surface, NOT the actual potential

TOPIC 14

Electrical Activity of Entire Heart:

Electrocardiograms (ECG or EKG)...

-ECG Trace-

(Fig. 13.16)

1. P Wave: atrial depolarization

2. PR Segment: AV nodal delay

3. QRS Complex: ventricular depolarization

       **Note that atrial repolarization occurs at same time

4. ST Segment: ventricles are contracting and emptying

5. T Wave: ventricular repolarization

6. TP Interval: ventricles are relaxing (and passively filling)

TOPIC 15

Mechanical Events in the Cardiac Cycle:

Introduction...

-CD: Cardiac Cycle 5-17-

(Fig. 13.18-13.21) MEMORIZE!!!

1. Systole: Contraction and emptying of the chambers

2. Diastole: Relaxation and filling of the chambers

3. Atria and ventricles go through separate cycle of systole and diastole

4. The contraction status (being in systole or diastole) determines heart chamber pressure which determines whether valves are open or closed.

1. Atria and ventricles are in diastole (i.e., relaxed)

2. Blood flows from veins into atria

3. Atrial pressure > ventricular pressure = AV valve open so...

4. Blood flows from atria directly into ventricles

** ventricular pressure is less than aortic pressure so aortic valve = closed

** volume of blood is increasing in the TP interval

1. SA node reaches threshold and fires

2. Atrial depolarization occurs

3. Atria contract = atrial systole

4. Atrial pressure > ventricular pressure = AV valves open

5. Blood squeezed by atrial contraction from atria into ventricles

**Pressure in aorta is still higher than in the ventricle

1. Atrial pressure > ventricular pressure = AV valves open

2. Blood squeezed from atria into ventricles

3. Electrical impulse enters ventricles from the AV node

4. Ventricles begin to depolarize

5. R peak is the end of ventricular diastole and start of ventricular systole

**pressure in the aorta is still higher than in the ventricle

1. Ventricles begin to contract

2. Atrial pressure < ventricular pressure = AV valves close

3. Atrial contraction and ventricular filling = complete

4. Ventricular pressure still not high enough to open aortic valve

5. Volume of blood in ventricles is called end-diastole volume (EDV) which is ~ 135 mL/ventricle

6. Atria repolarize

1. Ventricular pressure > aortic pressure = aortic valve opens

2. Blood ejected into aorta from ventricles

3. Atria in diastole and filling with blood

1. Repolarization of the ventricles begins

1. Peak of T wave = end of systole and start of diastole

2. Ventricles begin to relax

3. Ventricular pressure < aortic pressure = aortic valve closes

4. No blood can leave ventricles

5. The remaining volume of blood is called End-Systolic Volume (ESV). Typically, about half of the end of diastolic volume remains in the ventricles (about 65 mL/ventricle)

6. Atria in diastole and filling with blood

1. The stroke volume (SV) is equal to EDV-ESV = volume of blood pumped by one ventricle per heart beat.

      a. this averages ~ 70 mL/beat when at rest

1. Much of ventricular filling occurs early in ventricular diastole

2. During times of rapid heart rate, length of ventricular diastole is reduced much more than length of systole

3. However, because most of ventricular filling takes place in early diastole, filling is not seriously impaired during rapid heart rate

1. Classic heart sound description: lub-dub

       a. first sound is turbulent rushing of blood as AV valves are closing

       b. second sound is turbulent rushing of blood as aortic and pulmonary valves are closing

1. Cardiac Output (CO) is the volume of blood pumped by each ventricle/minute

      ** NOT the volume of blood pumped by whole heart

2. Cardiac Output (CO) = heart rate (HR)  multiplied by stroke volume (SV) 

3. Control of cardiac output is accomplished by controlling heart rate and stroke volume!!!!

4. At rest for average individual

       a. HR = 70 beats/min

       b. SV = 70 mL/beat (see above)

       c. CO = 70 beats/min x 70 mL/beat = 4900 mL/min

       d. Because total blood volume in a person is 5 to 5.5 liters, each 1/2 of the heart pumps nearly the whole blood volume each minute at rest

TOPIC 15

Cardiac Output and its Control:

Control of Heart Rate...

-Review-

TOPIC 15

1. Vagus nerve is primary parasympathetic nerve to the heart, supplies the atrium, especially the SA and AV nodes, but has little effect on the ventricles

2. Decreases heart rate by:

           a. decreasing rate of depolarization in SA node

           b. increasing AV node delay

1. Sympathetic cardiac nerves supply the atria, including the SA and AV nodes, and also the ventricles 

2. Increases heart rate by:

           a. increasing rate of depolarization in SA node

           b. reducing AV node delay

           c. speeding up spread of AP through Bundles of His and Purkinje fibers

TOPIC 15

1. longer the fiber at start of contraction, the stronger the contraction

2. more blood that is in chamber, the longer the fiber (i.e. they are stretched) so the stronger the contraction

3. Bottom Line: when venous return of blood to heart is increased (by many factors to be discussed later) the blood volume in heart is increased, which increases fiber length, which increases strength of contraction, which allows pumping of larger volume 

Parasympathetic:

1. shortens APs in atrial contractile cells, which results in weaker contractions

Sympathetic:

1. increases contractile strength of atrial and ventricle cells by increasing Ca⁺⁺ permeability of contractile cells

1. Heart muscle does NOT extract nutrients from blood in chambers

      a. Endocardial lining prevents exchange

      b. Even if exchange could occur, heart walls too thick for effective exchange

2. Coronary Circulation

      a. Coronary arteries branch from aorta just beyond aortic valve

      b. Heart muscle receives most (70%) of nutrient blood supply during diastole because coronary arteries compressed during systole, and entries to these arteries partially blocked during systole

** refer back to notes for diagram & clinical terms on back page

1. mitochondria

2. capillary density

3. max heart rate

4. power of contraction on a per gram basis

Increased blood volume:

1. occurs within a few days

2. can increase up to 15%

3. results in increase in O₂ carrying capacity

4. increased venous return = longer fibers = stronger contraction

Ventricles may increase in size:

1. ... = bigger ventricular chamber

Both contribute to decreased heart rate:

1. ... which in turn allows higher level of ventricular filling

**refer to notes for diagrams

TOPIC 16

(Fig. 14.7)

1. Rapid transit pathways from heart to tissues; offer little resistance to flow

2. Pressure reservoir to provide driving force while heart is relaxing

TOPIC 16

(Fig. 14.5 & 14.10)

1. Branch off of arteries in organs

2. Arterioles contain smooth muscle which can change the radius of the arteriole

3. Changing radii of arterioles is the major way to regulate blood flow to specific organs, and one of the major ways that arterial blood pressure is controlled

    a. Radii of arterioles can be adjusted (independently across arterioles) to...

         - variably distribute cardiac output among organs

         - regulate arterial blood pressure

         - bigger radius = vasodilate

         - smaller radius = vasoconstrict

    b. Convert the pulsing systole-diastole pressure swing into a non-fluctuating pressure       

TOPIC 16

(Fig. 14.12)

Local metabolic changes:

1. Increased metabolic demands of a tissue usually result in vasodilation & increased blood flow

2. Decreased metabolic demands usually result in vasoconstriction & reduced blood flow

Histamine release:

1. Synthesized and stored in special connective tissue

2. When tissue is damaged or during allergic reactions, histamine released in damaged area, and causes vasodilation, which results in increased blood flow and causes swelling etc.

Temperature:

1. local heat application causes vasodilation; local clod application causes vasoconstriction

TOPIC 16

Recall that:

1. alpha receptors bind norepi, cause vasoconstriction in arterioles, and are found in arterioles in most organs

2. beta-2 receptors bind epi preferentially and cause vasodilation of arterioles, found in arterioles mostly in cardiac and skeletal muscle

- At rest there is enough sympathetic activity to maintain tone

- Increased sympathetic activity leads to reduced blood flow to most organs, but increased blood flow to skeletal muscle, heart, and skin (Fig. 14.15)

- Regions of brain responsible for adjusting sympathetic output to arterioles:

      * cardiovascular control center in medulla

      * hypothalamus

Vasopressin and Angiotensin II: are important in fluid balance & are vasoconstrictors (involved with water and salt regulators of the kidneys)

TOPIC 16

1. Site of exchange of materials between blood and tissue

2. Exchange accomplished primarily by diffusion

3. Need to minimize diffusion distance and maximize surface area and time

TOPIC 16

(Fig. 14.19)

1. Composed of a tube of a single layer of flattened endothelial cells (recall that endothelial cells are the lining of other blood vessels)

2. Capillary walls are very thin to minimize diffusion distance

3. Capillary lumen is so narrow that red blood cells must squeeze through single file

4. Water-filled pores between epithelial cells in wall facilitate exchange

TOPIC 16

1. Extensive capillary branching so that all cells in tissues not far from capillaries

2. Large overall surface area

     a. 10 to 40 billion capillaries in your body

     b. Total Surface Area: 600 m²!!!

     c. Volume of blood in capillaries to capillary surface area:

         half pint of paint spread over floor of a high school

         gym

3. Velocity of blood is very slow in capillaries, maximizes time for exchange

     a. Don't confuse flow rate (liters/minute) with velocity (mm/sec)!! Flow rate is always equal to cardiac output in all blood vessels; if blood is pumping 5 liters/minute, then every minute 5 liters of blood passes through arteries, arterioloes, capillaries, and veins

TOPIC 16

1. Most important method of capillary exchange

2. Diffusion occurs between capillaries and interstitial fluid, then between interstitial fluid and cells

     a. RECALL: ECF is composed of plasma (20%) and

                     interstitial fluid (80%)

3. Lipid soluble substances (e.g., O₂ and CO₂) pass through endothelial cells by dissolving in lipid bilayer of membrane

4. Small water soluble substances (ions, glucose, amino acids) pass through water filled pores.

TOPIC 16

1. A volume of protein-free plasma filters out of capillaries, mixes with surrounding interstitial fluid, and is subsequently reabsorbed.

2. Bulk flow does not play a big role in exchange of materials between plasma and interstitial fluid because quantity of solutes moved is relatively small compared to those that move by diffusion

3. IMPORTANCE: distributing ECF between plasma & interstitial fluid

TOPIC 16

1. Capillaries have no smooth muscle & hence cannot regulate blood flow

2. Precapillary sphincters contract & relax & control blood flow into capillaries; these sphincters are regulated by the same local factors that influence arteriolar radius

3. In resting muscle, only about 10% of precapillary sphincters are open

TOPIC 16

- Under normal circumstances, slightly more fluid is filtered out of capillaries during bulk flow than is reabsorbed back into capillaries.

- Need to get this fluid back into cardiovascular system

TOPIC 16

- Extra fluid is picked up by the lymph system...

[an extensive network of one-way vessels that run from tissues to venous system near right atrium...]

... and so is returned to circulatory system

TOPIC 16

1. Return to cardiovascular system excess fluid filtered out of capillaries

a. about 3 liters/day

b. note that plasma volume is only about 2.75 liters

2. Return to cardiovascular system --> protein that got out of capillaries

3. Disease Defense: lymph nodes contain specialized cells to destroy pathogens

TOPIC 16

1. Low resistance passageways to return blood to heart

2. Serve as capacitance (storage) vessels

a. have thin, stretchable but not elastic walls

b. can distend to accommodate lots of blood

c. Under resting conditions, 60% of blood is in veins (Fig. 14.22)

3. A delicate balance exists among capacity of veins, extent of venous return, and cardiac output

TOPIC 16

1. At a constant blood volume, as venous capacity increases, venous return decreases, and lowers effective circulating volume

2. Likewise, at constant blood volume, as venous capacity decreases, effective circulating volume increases (i.e., less blood is being held in veins)

TOPIC 16

1. Driving pressure from cardiac contraction

2. Sympathetic Activity

a. Sympathetic stimulation causes venous vasoconstriction which elevates venous pressure which causes higher venous return

TOPIC 16

1. Skeletal muscle pump:

a. activity increases venous return

b. also counteracts the effects of gravity (Fig. 14.23)

TOPIC 16

1. One way valves in veins prevent backflow of blood away from heart

TOPIC 16

1. Pressure within chest cavity is 5mm Hg less than the rest of the body because of repiratory activity.

2. This adds to pressure gradient difference between limbs and chest cavity

TOPIC 16

1. During ventricular contraction, AV valves are drawn downward, enlarging the atrial cavities and causing atrial pressure to drop below 0 mm Hg, which increases pressure gradient.

[Like a suction pump]

TOPIC 17

1. Plasma (liquid portion of blood)

2. Erythrocytes (RBC's)

3. Leukocytes (WBC's)

4. Platelets (involved in blood clotting)

TOPIC 17

(Table 15.1)

1. 90% water

2. 8% plasma proteins

3. 1% inorganic ions

a. Na⁺ and Cl-

4. 1% nutrients, waste, hormones, etc. 

TOPIC 17

(Fig. 15.1)

(Shaped like a donut with an indentation instead of a hole)

1. Gives a large surface area for diffusion of O₂

2. Thinness allows rapid diffusion of O₂

**main function is to carry oxygen

TOPIC 17

1. Allows cell to take odd shapes and squeeze through narrow openings

TOPIC 17

So full of Hb that it...

1. has no nucleus

2. has no organelles

3. is essentially a sac of Hb

TOPIC 17

1. glycolytic enzymes for energy production

2. carbonic anhydrase which converts CO₂ to bicarbonate for transport back to lungs

TOPIC 17

1. Each erythrocyte lasts about 4 months (very short life)

2. Are replaced at the average rate of 2 to 3 million/second

3. Most old erythrocytes removed by spleen; new are produced by bone marrow

TOPIC 17

(Fig 15.3)

1. Contains 4 globulin chains (protein)

2. Contains 4 iron containing heme groups; each heme group can bind one oxygen atom; hence a Hb molecule can carry 4 oxygen atoms

3. Can also carry CO₂ (transports back to lungs), H⁺ ions (and so acts as a buffer), and CO (poison)

TOPIC 17

(Fig. 15.2)

1. 99% of cells in blood are erythrocytes

2. Packed cell volume after centrifugation is composed almost entirely of erythrocytes; packed cell volume called hematocrit

3. Hematocrit levels average 42% for females, 45% for men

4. Cream colored layer on top of erythrocytes called Buffy Layer, is composed of white blood cells and platelets

TOPIC 17

**Are mobile units of the system:

1. Defend against pathogens

2. Identify and destroy cancer cells

3. Destroy cellular debris in body

** use a seek and destroy approach

** do most of their work in tissues, only use blood as transport

TOPIC 17

1. Small cell fragments from bone marrow-bound cells

2. Contain actin and myosin

3. Do NOT leave blood but can be stored in spleen

4. Are functional for about 10 days

**Involved in blood clotting during injury

TOPIC 17

Hemostasis: the arrest of bleeding from a broken blood vessel

Vascular spasms:

1. reduce blood flow

2. causes broken pieces of vessel to stick together

TOPIC 17

(Fig. 15.6)

1. Under normal conditions, vessel releases prostacyclin, which inhibits platelet aggregation

2. When damage occurs to a vessel, prostacyclin production stops and platelets attach to collagen exposed by damage

3. Attached platelets release two chemicals that causes nearby platelets to get sticky and aggregate together

4. Platelet actin and myosin contract and strengthen aggregate

5. Additional vasoconstrictors released to reduce local blood flow

6. Release additional chemicals needed for coagulation

TOPIC 17

(Fig. 15.9)

Don't worry about details just know the points below

1. Damage and platelet aggregation initiate cascade of clotting factors

2. Eventually fibrinogen (a blood protein) converted to fibrin, which is a loose protein meshwork, and which also activates Factor XIII

3. Factor XIII stabilizes fibrin into a stabilized meshwork, which becomes a clot as blood cells get caught in it

TOPIC 17

F = flow rate = cardiac output

TOPIC 17

/\P = pressure gradient = blood pressure

1. difference in pressure between beginning and end of a blood vessel

2. main driving force for blood flow through cardiovascular system

TOPIC 17

R = resistance

1. Measure of hindrance to blood flow caused by friction between blood and walls of blood vessel

2. The smaller the vessel, the greater the resistance...

a. because in a small vessel a larger volume of the fluid comes into contact with more surface area of the vessel

b. a small change in radius has a huge impact on resistance:

- Res (infinity symbol) 1/radius⁴

- Doubling the radius decreases the resistance 16 times and therefore increases the flow rate 16-fold

TOPIC 17

/\P = FR: Blood pressure = Cardiac Output x Resistance

TOPIC 17

Location of two most important: (Fig. 14.27)

1. Aortic arch

2. Coratid sinus

Usual reflex arch:

1. receptor

2. afferent pathway

3. integrating center (cardiovascular control in medulla)

4. efferent pathway (autonomic nervous system)

5. receptor organ

Baroreceptors constantly fire AP's:

1. When BP goes up, AP frequency increases

2. When BP goes down, AP frequency decreases (Fig. 14.28)

TOPIC 17

1. Exercise raises blood pressure (Fig. 14.33)

2. Chemoreceptors in carotid arch and aortic arteries are sensitive to O₂, CO₂, and acid levels; reflexively increase respiration and BP during exercise

3. Emotions and behaviors (fight or flight, orgasms, blushing)

4. Hypothalamic control over skin arterioles for temperature regulation overrides cardiovascular center control over these arterioles

TOPIC 17

1. Control of plasma volume by left atrial volume receptors and hypothalmic osmoreceptors = control of urine output and thirst

1. When an ATP Binds to a myosin head, a Pi detaches from an ADP which prepares the myosin head into a "cocked" position

2. When the Pi releases from ADP completley, this causes the myosin head to ratchet forward = power stroke

3. After the power stroke, the ADP falls away as the myosin head attaches to the myosin binding site on the actin filament

** Calcium binds to troponin which makes it reveal the binding site

4. When contraction ends (of the muscle), new ATP binds to the myosin head

EXERCISE

&

MUSCLE CRAMPS

Hypothesis 1:

- cold or over exercise causes afferent AP from muscle to spinal cord causing muscle reflex contraction

- the contraction further stimulates afferent AP's to the spinal cord = sets up a positve feedback loop

EXERCISE

&

MUSCLE CRAMPS

Hypothesis 2:

- overexercise without fluid and electrolyte (ion) replacement:

- ion imbalances between ECF and ICF, which changes resting membrane potential

- results in effects of overstimulation, as if lots of AP's are firing

- Binding of ATP causes myosin to release actin

- After you die, membranes in muscle begin to decompose

- Calcium floods muscle cells

- Muscles contract

- No ATP to bind to myosin head to allow muscles to relax

- Eventually muscle proteins begin to decompose and body relaxes

- group of more than 30 genetic diseases

- all affect integrity of muscle membranes

- most common is called Duchenne

1. Pathology:

a. disease characterized by gradual muscle destruction

b. death by heart or respiratory failure

2. Ultimate Cause:

a. sex-linked gene

b. 1 of 3500 boys worldwide affected

3. Mechanistic Cause:

a. Gene makes membrane protein called dystrophin

b. Dystrophin regulates calcium leaks into muscle cells

c. with the disease, no dystrophin and calcium leaks constant

d. high constant of calcium activates proteases that destroy muscle protein

4. Treatment Hopes:

a. cell transplant

b. gene therapy

ABNORMALITIES in CARDIAC FXN

Pacemaker Malfunctions:

SA Node Fails...

- AV node takes over, and sets pace at about 50 bpm

- FIX: artificial pacemaker

ABNORMALITIES in CARDIAC FXN

Pacemaker Malfunctions:

Ectopic Focus...

- An area of the heart (e.g., purkinje fibers) becomes overly excited and depolarizes at a rapid rate

- Pacemaker activity may shift from SA node to teh ectopic focus

- Results in greatly accelerated heart rate

- Associated with heart disease, anxiety, lack of sleep, excess nicotine, caffeine, or alcohol consumption

ISCHEMIC HEART DISEASE

- reduced blood supply to heart

- usually caused by atherosclerosis (arteries filling with plaque) which allows artery to be blocked by blood clot, etc.

- can cause myocardial infraction (heart attack) and cardiac arrhythmias

- leading cause of death in Western Nations

ABNORMALITIES in CARDIAC FXN

Rhythem:

Atrial Flutter...

- rapid but regular atrial depolarizations

- ventricles cannot keep pace; blood output of heart declines

- leads to loss of consciousness and even death

ABNORMALITIES in CARDIAC FXN

Rhythem:

Atrial Fibrillation...

- rapid irregular uncoordinated depolarizations of atria

- some contractions too weak to eject blood, or are so close together that little blood fills ventricles

ABNORMALITIES in CARDIAC FXN

Rhythem:

Ventricular Fibrillation...

- ventricles exhibit uncoordinated chaotic contractions and so are ineffective as pumps

- leads to rapid death (4 min)

SLOW OXIDATIVE..........FAST OXID.........FAST GLYCOLYTIC

high                            high                          low

low                           intermediate                     high

slow                          intermediate                     fast 

small                         intermediate                  large 

RESISTANCE   high                      intermediate                     low

TO FATIGUE