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MYOCARDIAL CELLS
THE MYOCARDIUM OF THE HEARTIS COMPOSED OF TWO TYPES
OF CELLS, AUTORHYTHMIC CELLSAND CONTRACTILE CARDIAC
MUSCLE CELLS.
MICROSCOPIC ANATOMY
CONTRACTILE CARDIACMUSCLE CELLS ARECOVERED WITHENDOMYSIUM WHICHATTACHES TO THEFIBROUS SKELETON OFTHE HEART. THEINTERCELLULAR SPACES AREFILLED WITH ENDOMYSIUMAND LARGE NUMBERS OFCAPILLARIES.
MICROSCOPIC ANATOMY
CONTRACTILE CARDIAC MUSCLE CELLS ARE SHORT, HAVE LARGE
DIAMETERS, ARE BRANCHED, AND HAVE INTERCONNECTIONS CALLED
INTERCALATED DISCS.
MICROSCOPIC ANATOMY
CARDIAC MUSCLES HAVE LARGENUMBERS OF MITOCHONDRIA, ABOUT
25% OF THE CELL VOLUME,MYOFIBRILS COMPOSED OF
SARCOMERES, AND A REDUCED AMOUNT OF SARCOPLASMIC RETICULUM WITH LIMITED
TERMINAL CRISTERNAE.
MICROSCOPIC ANATOMY
ENERGY IS PRODUCED BYAEROBIC CELLULAR RESPIRATION.
CONTRACTILE CARDIAC MUSCLE CELLS CAN USE GLUCOSE, FATTY ACIDS AS SUBSTRATES.
AUTORHYTHMIC CELLS
AUTORHYTHMIC CELLS ARE ORGANIZED INTO THE
INTRINSIC CONDUCTIVE SYSTEM OF THE HEART. SEE
MODULE 2 OF THE CARDIOVASCULARSYSTEM FOR INFORMATION
ABOUT THE INTRINSIC CONDUCTIVE SYSTEM.
INTRINSIC CONDUCTIVE SYSTEM OF THE HEART
STRUCTURES
1. SA NODE2. AV NODE3. AV BUNDLE4. R and L BUNDLE BRANCHES5. PURKINJE FIBERS
ECG DEFLECTION WAVE IRREGULARITIES
Prolonged QT Interval =
Repolarization abnormalities increase chances of ventricular arrhythmias.
HEART BLOCKS
Normal ECG
3rd Degree Block
No P waves. Rate determined by autorhythmic cells in ventricles
2nd Degree BlockNot a QRS for each P wave
P
QRS
T
COUPLING OF CELLS
AUTORHYTHMIC CELLS AND CONTRACTILE CARDIAC MUSCLE CELLS ARE “COUPLED”USING GAP JUNCTIONS TO PRODUCE AN ELECTRICAL SYNAPSE. BECAUSE THE CARDIAC CELLS ARE ELECTRICALLY
COUPLED BY THE GAP JUNCTIONS, THE ENTIRE MYOCARDIUM BEHAVES AS A
SINGLE CORRDINATED UNIT, OR FUNCTIONAL SYNCYTIUM.
AUTORHYTHMIC CELLS
SEE MODULE 3 OF THE CARDIOVASCULAR SYSTEM FOR INFORMATION ABOUT THEGENERATION OF AN ACTION
POTENTIAL IN THE AUTORYTHMIC CELLS.
CONTRACTILE MUSCLE CELLS
Fast Na+ VRCP openSlow Ca2+ VRCP begin to open
Fast Na+ VRCP close
Slow Ca2+ VRCP are openK+ permeability membrane decreases
Slow Ca2+ VRCP closeK+ VRCP open
K+ VRCP closeEffects of Na/K and Ca pump
CONTRACTILE MUSCLE CELLS
SEE MODULE 3 OF THE CARDIOVASCULAR SYSTEM FOR INFORMATION ABOUT THEGENERATION OF AN ACTION
POTENTIAL IN THE CONTRACTILE CARDIAC MUSCLE CELLS.
CARDIAC CYCLEAll events associated with a single heart
beat including atrial systole & diastole followed by ventricular systole diastole.
(V. Systole) (V. Diastole)
Systolic BP
Diastolic BP
CARDIAC OUTPUT
CARDIAC OUTPUT IS THE PRODUCT OF CARDIAC
RATE AND STROKE VOLUME.
C.O. = HEART RATE x STROKE VOLUME
THE UNITS WILL BE L/ min.
CONTROL OF HEART RATE
THE MOST IMPORTANT EXTRINIC CONTROL OF HEART RATE IS THEAUTONOMIC NERVOUS SYSTEM.
THE SYMPATHETIC DIVISION INCREASES HEART RATE AND THE
PARASYMPATHETIC DIVISION REDUCES HEART RATE.
AUTONOMIC CONTROL
RECEPTORS1. CAROTID SINUS
2. AORTIC ARCH BARORECEPTORS
3. RIGHT ATRIAL BARORECEPTORS
AUTONOMIC CONTROL
THE CARDIAC REGULATORY CENTERLOCATED IN THE MEDULLA INTERPRETS THE ACTION
POTENTIALS FROM THE SENSORY NERVES.
AUTONOMIC CONTROL
THE CARDIAC REGULATORY CENTERHAS TWO SUB-CENTERS:
THE INHIBITORY CENTER WHICH WILL REDUCE THE HEART RATE, AND THE ACCELERATOR CENTER WHICH WILL INCREASE THE HEART RATE.
AUTONOMIC CONTROL
THE INHIBITORY CENTER USES THE VAGUS NERVE TO REDUCE THE HEART RATE. THE ACCELERATOR CENTER USES THE SYMPATHETIC
DIVISION OF THE A.N.S. TO INCREASE THE HEART RATE.
HEART RATE
OTHER FACTORS WHICH EFFECT HEART RATE:
1. TEMPERATURE2. IONS3. EPINEPHRINE AND NOREPINEPHRINE
FROM THE ADRENAL MEDULLA4. EMOTIONS5. GENDER
STROKE VOLUME
STROKE VOLUME IS THE DIFFERENCE OF THE END-DIASTOTIC
AND THE END-SYSTOLIC.
S.V.= E.D.V. – E.S.V.
END-DIASTOLIC VOLUME
VENTRICULAR FILLING IS THE RESULT OF VENOUS RETURN AND
THE LENGTH OF DIASTOLE. IF ONE OR BOTH OF THESE FACTORS ARE
INCREASED THE END-DIASTOLIC VOLUME WILL INCREASE.
END-SYSTOLIC VOLUME
VENTRICULAR EMPTYING IS THE RESULT OF CONTRACTING
THE VENTRICULES. IF THERE IS AN INCREASE IN EPINEPHRINE,
NOREPINEPHRINE, AND OR Ca2+ IONSTHE STRENGTH OF CONTRACTION
WILL INCREASE.
END-SYSTOLIC VOLUME
THE FRANK-STARLING LAW OF HEART EXPLAINS THE EFFECT
OF STRETCHING CARDIAC MUSCLE. BY STRETCHING CARDIAC MUSCLE,MORE CROSS BRIDGE BONDS CAN
BE FORMED BETWEEN MYOSIN AND ACTIN, AND THE GREATER THE FORCE
OF CONTRACTION WILL BE.