1. CARDIOVASCULAR PHYSIOLOGY of the HEART

2. HEART THE HEART IS PART OF THE CARDIOVASCULAR SYSTEM. THE FUNCTION OF THE HEART IS TO PUMP BLOOD.

3. HEART WALL THE HEART WALL CONSISTS OF 3 LAYERS 1. EPICARDIUM 2. MYOCARDIUM 3. ENDOCARDIUM

4. MICROSCOPIC ANATOMY

5. MYOCARDIAL CELLS THE MYOCARDIUM OF THE HEART IS COMPOSED OF TWO TYPES OF CELLS, AUTORHYTHMIC CELLS AND CONTRACTILE CARDIAC MUSCLE CELLS.

6. MICROSCOPIC ANATOMY CONTRACTILE CARDIAC MUSCLE CELLS ARE COVERED WITH ENDOMYSIUM WHICH ATTACHES TO THE FIBROUS SKELETON OF THE HEART. THE INTERCELLULAR SPACES ARE FILLED WITH ENDOMYSIUM AND LARGE NUMBERS OF CAPILLARIES.

7. MICROSCOPIC ANATOMY CONTRACTILE CARDIAC MUSCLE CELLS ARE SHORT, HAVE LARGE DIAMETERS, ARE BRANCHED, AND HAVE INTERCONNECTIONS CALLED INTERCALATED DISCS.

8. MICROSCOPIC ANATOMY

9. INTERCALATED DISCS CONTAIN ACHORING DESMOSOMES AND GAP JUNCTIONS.

10. MICROSCOPIC ANATOMY CARDIAC MUSCLES HAVE LARGE NUMBERS OF MITOCHONDRIA, ABOUT 25% OF THE CELL VOLUME, MYOFIBRILS COMPOSED OF SARCOMERES, AND A REDUCED AMOUNT OF SARCOPLASMIC RETICULUM WITH LIMITED TERMINAL CRISTERNAE.

11. MICROSCOPIC ANATOMY ENERGY IS PRODUCED BY AEROBIC CELLULAR RESPIRATION. CONTRACTILE CARDIAC MUSCLE CELLS CAN USE GLUCOSE, FATTY ACIDS AS SUBSTRATES.

12. AUTORHYTHMIC CELLS AUTORHYTHMIC CELLS ARE ORGANIZED INTO THE INTRINSIC CONDUCTIVE SYSTEM OF THE HEART. SEE MODULE 2 OF THE CARDIOVASCULAR SYSTEM FOR INFORMATION ABOUT THE INTRINSIC CONDUCTIVE SYSTEM.

13. AUTORHYTHMIC CELLS

14. INTRINSIC CONDUCTIVE SYSTEM OF THE HEART STRUCTURES 1.SA NODE 2.AV NODE 3.AV BUNDLE 4.R and L BUNDLE BRANCHES 5.PURKINJE FIBERS

15. AUTORHYTHMIC CELLS

16. ECG DEFLECTION WAVES (Pacemaker) Atrial repolarization

17. ECG DEFLECTION WAVES 60 seconds ÷ 0.8 seconds = resting heart rate of 75 beats/minute

18. ECG DEFLECTION WAVES 1st Degree Heart Block = P-Q interval longer than 0.2 seconds.

19. ECG DEFLECTION WAVE IRREGULARITIES Enlarged QRS = Hypertrophy of ventricles

20. ECG DEFLECTION WAVE IRREGULARITIES Prolonged QT Interval = Repolarization abnormalities increase chances of ventricular arrhythmias.

21. ECG DEFLECTION WAVE IRREGULARITIES Elevated T wave : Hyperkalemia

22. ECG DEFLECTION WAVE IRREGULARITIES Flat T wave : Hypokalemia or ischemia

23. HEART BLOCKS Normal ECG 3rd Degree Block No P waves. Rate determined by autorhythmic cells in ventricles 2nd Degree Block Not a QRS for each P wave P QRS T

24. 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.

25. AUTORHYTHMIC CELLS SEE MODULE 3 OF THE CARDIOVASCULAR SYSTEM FOR INFORMATION ABOUT THE GENERATION OF AN ACTION POTENTIAL IN THE AUTORYTHMIC CELLS.

26. CONTRACTILE MUSCLE CELLS

27. Fast Na + VRCP open Slow Ca 2+ VRCP begin to open Fast Na + VRCP close Slow Ca 2+ VRCP are open K + permeability membrane decreases Slow Ca 2+ VRCP close K + VRCP open K + VRCP close Effects of Na/K and Ca pump

28. CONTRACTILE MUSCLE CELLS SEE MODULE 3 OF THE CARDIOVASCULAR SYSTEM FOR INFORMATION ABOUT THE GENERATION OF AN ACTION POTENTIAL IN THE CONTRACTILE CARDIAC MUSCLE CELLS.

29. CARDIAC CYCLE All events associated with a single heart beat including atrial systole & diastole followed by ventricular systole diastole. (V. Systole)(V. Diastole) Systolic BP Diastolic BP

30. CARDIAC CYCLE SEE CLASS HAND OUT FOR INFORMATION ABOUT THE CARDIAC CYCLE.

31. 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.

32. CONTROL OF HEART RATE THE MOST IMPORTANT EXTRINIC CONTROL OF HEART RATE IS THE AUTONOMIC NERVOUS SYSTEM. THE SYMPATHETIC DIVISION INCREASES HEART RATE AND THE PARASYMPATHETIC DIVISION REDUCES HEART RATE.

33. HEART RATE

34. AUTONOMIC CONTROL RECEPTORS 1. CAROTID SINUS 2. AORTIC ARCH BARORECEPTORS 3. RIGHT ATRIAL BARORECEPTORS

35. AUTONOMIC CONTROL SENSORY NERVES 1. CRANIAL NERVE IX 2. and 3. CRANIAL NERVE X

36. AUTONOMIC CONTROL THE CARDIAC REGULATORY CENTER LOCATED IN THE MEDULLA INTERPRETS THE ACTION POTENTIALS FROM THE SENSORY NERVES.

37. AUTONOMIC CONTROL THE CARDIAC REGULATORY CENTER HAS TWO SUB-CENTERS: THE INHIBITORY CENTER WHICH WILL REDUCE THE HEART RATE, AND THE ACCELERATOR CENTER WHICH WILL INCREASE THE HEART RATE.

38. 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.

39. HEART RATE OTHER FACTORS WHICH EFFECT HEART RATE: 1. TEMPERATURE 2. IONS 3. EPINEPHRINE AND NOREPINEPHRINE FROM THE ADRENAL MEDULLA 4. EMOTIONS 5. GENDER

40. STROKE VOLUME STROKE VOLUME IS THE DIFFERENCE OF THE END-DIASTOTIC AND THE END-SYSTOLIC. S.V.= E.D.V. – E.S.V.

41. STROKE VOLUME FACTORS WHICH EFFECT STROKE VOLUME: 1. END-DIASTOLIC VOLUME 2. END-SYSTOLIC VOLUME

42. 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.

43. END-SYSTOLIC VOLUME VENTRICULAR EMPTYING IS THE RESULT OF CONTRACTING THE VENTRICULES. IF THERE IS AN INCREASE IN EPINEPHRINE, NOREPINEPHRINE, AND OR Ca 2+ IONS THE STRENGTH OF CONTRACTION WILL INCREASE.

44. 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.

45. FRANK STARLING LAW

46. CARDIAC OUTPUT SEE CLASS HAND OUT FOR MORE INFORMATION ABOUT THE CARDIAC OUPUT.