CARDIOVASCULAR PHYSIOLOGY of the HEART

HEART

THE HEART IS PART OF THE CARDIOVASCULAR SYSTEM.

THE FUNCTION OF THE HEARTIS TO PUMP BLOOD.

HEART WALL

THE HEART WALL CONSISTS OF 3 LAYERS

1. EPICARDIUM

2. MYOCARDIUM

3. ENDOCARDIUM

MICROSCOPIC ANATOMY

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

MICROSCOPIC ANATOMY

INTERCALATED DISCS CONTAIN ACHORING DESMOSOMES AND

GAP JUNCTIONS.

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.

AUTORHYTHMIC CELLS

INTRINSIC CONDUCTIVE SYSTEM OF THE HEART

STRUCTURES

1. SA NODE2. AV NODE3. AV BUNDLE4. R and L BUNDLE BRANCHES5. PURKINJE FIBERS

AUTORHYTHMIC CELLS

ECG DEFLECTION WAVES

(Pacemaker) Atrial repolarization

ECG DEFLECTION WAVES60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute

ECG DEFLECTION WAVES

1st Degree Heart Block = P-Q interval longer than 0.2 seconds.

ECG DEFLECTION WAVE IRREGULARITIES

Enlarged QRS =

Hypertrophy of ventricles

ECG DEFLECTION WAVE IRREGULARITIES

Prolonged QT Interval =

Repolarization abnormalities increase chances of ventricular arrhythmias.

ECG DEFLECTION WAVE IRREGULARITIES

Elevated T wave :

Hyperkalemia

ECG DEFLECTION WAVE IRREGULARITIES

Flat T wave :

Hypokalemia or ischemia

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

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 CYCLE

SEE CLASS HAND OUT FORINFORMATION ABOUTTHE CARDIAC CYCLE.

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.

HEART RATE

AUTONOMIC CONTROL

RECEPTORS1. CAROTID SINUS

2. AORTIC ARCH BARORECEPTORS

3. RIGHT ATRIAL BARORECEPTORS

AUTONOMIC CONTROL

SENSORY NERVES

1. CRANIAL NERVE IX

2. and 3. CRANIAL NERVE X

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.

STROKE VOLUME

FACTORS WHICH EFFECT STROKEVOLUME:

1. END-DIASTOLIC VOLUME

2. END-SYSTOLIC VOLUME

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.

FRANK STARLING LAW

CARDIAC OUTPUT

SEE CLASS HAND OUT FOR MORE INFORMATION ABOUT

THE CARDIAC OUPUT.