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Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi
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Cardio-vascular Physiology by Dr.Nasreen Abdulrahman Wafi

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  • ECG , CALIBRATION WAVES, DURATION VOLTAGE
  • Transcript

    • 1. Cardiovascular physiology
      • The objectives are to know the following:
      • 1. Functional anatomy of the heart
      • 2. The basics of heart physiology& the origin of heart beat
      • 3. Changes that occur during cardiac cycle
      • 4. Cardiac output & factors affecting it
      • 5. Hemodynamics
      • 6. Physiological abnormalities causing diseases
    • 2. Cardiovascular system
      • Functions of cardiovascular system include:
      • 1. Transport of O 2 , glucose,A.A, F.A, vitamines, drugs & water to the tissues.
      • 2. Rapid washout of metabolic waste products like CO 2 , urea & creatinine
      • 3. CVS is part of a control system in that it distributes hormones to the tissues & even secrete hormones by itself e:g ANP
      • 4. Plays vital role in temperature regulation
    • 3. Cardiovasular system
      • Consists of:
      • Heart: A pump that pumps blood under high pressure
      • A set of blood vessels for conduction of blood from & back to the heart
    • 4. Physiology of heart
      • The heart is a muscular organ. It’s wall consists of three layers:
      • 1.Endocardium
      • 2. Myocardium
      • 3. Pericardium:
      • Visceral ( Epicardium)
      • Parietal:
      • Inner serous layer
      • Outer fibrous layer
    • 5. PERICARDIUM&HEART WALL
    • 6. Three Layers of Heart Wall
      • From the outside-in
        • Epicardium
          • visceral pericardium
        • Myocardium
          • the muscular wall
        • Endocardium
    • 7. Architecture
      • Pericardial cavity
      • Pericardium
        • Viscreal-epicardium-in direct contact with the heart
        • Parietal-surrounds heart, creating pericardial cavity
      • Pericardial cavity contains a small amount of fluid
      • Attached to diaphragm by fibers
    • 8. Location
      • Lies near anterior chest wall, behind sternum
      • Tilted slightly to the left
      • Rotated slightly to the left
      • This causes the anterior surface to consist of the right atria and ventricle
    • 9. Functional anatomy of heart
      • Heart is divided into 2 halves: Rt.& Lt.
      • Each half consists of an atrium & a ventricle
      • Atrium & ventricle of the same side connect through atrioventricular opening.
      • AV opening guarded by presence of a valve
      • [ Atrioventricular valves- AV valves]
      • Mitral valve on Lt.side
      • Tricuspid valve on Rt.side
    • 10. Heart ( functional anatomy)
      • From Lt.ventricle arises the aorta
      • From Rt.ventricle arises The pulmonary artery
      • Openings of the large arteries are guarded by semilunar valves: Aortic & pulmonary valves
      • Valves are passive structures: they open when there is a forward pressure to allow forward flow of blood
      • They close when there is a backward pressure to prevent backward flow of blood
    • 11. Heart functional anatomy
      • Blood reaches Rt. atrium via superior & inferior vena cava
      • Blood reaches Lt. atrium via pulmonary veins
      • Opening of the veins are not guarded by valves
    • 12. Atrial Ventricular
    • 13. Cardiac Muscle
      • Almost totally dependant on aerobic metabolism
      • Each cell connected to its neighbor by intercalated discs
      • Gap junctions connect one cardiac muscle fiber to another,act as functional syncytium
      • In the gap junction there is a channel that allow movement between adjacent m.f
      • Diameter of channel is affected by intracellular calcium concentration
    • 14. FUNCTIONAL SYSCYTIUM
    • 15. Cardiac muscle
      • Striated muscle
      • Arrangement of Actin, Myosin, Troponin & Tropomyosin is similar to those in skeletal muscle.
      • Excitation contraction coupling is similar to skeletal muscle
      • Source of calcium ions: Sarcoplasmic reticulum+I.S.F through calcium channels
    • 16. Cardiac muscle
      • Because of presence of gap junctions, when one cardiac muscle fiber is depolarized the wave of depolaization pass to other cardiac muscle fibers,acting as functional syncytium
      • All or None law applies to the whole cardiac muscle & not to a single muscle fiber as in skeletal muscle.
    • 17.  
    • 18. Sarcomeres are composed of myosin and actin
    • 19. Several proteins mediate the interaction of myosin heads with the actin filament
    • 20. Calcium signaling triggers contraction
    • 21.  
    • 22.  
    • 23. ACTION POTENTIAL IN CARDIAC MUSCLE
      • It is characterized by the presence of action potential plateau ( 0.1-0.3 sec)
      • Plateau keeps the membrane depolarized for longer time than depolarization in skeletal muscle
      • Plateau is due to inward calcium movement through calcium channels
      • Long refractory period
      • No tetanization of cardiac muscle
    • 24.  
    • 25. REFRACTORY PERIOD
    • 26. Conducting System
      • Cardiac cells contract in the absence of neural or hormonal stimulation. This is known as Self excitation or Rhythmicity. automaticity
      • Property of self excitation is obvious in the conducting system of the heart which is made of modified cardiac muscle fibers.
    • 27. Path of the Action Potential
      • Conducting system of heart:
      • SA Node ( Pace maker of the heart)
        • Atrial conducting pathways
      • AV Node
        • Impulse slows down to allow for blood movement and ventricular filling
      • Bundle of His
      • Left and right bundle branches
      • Purkinje fibers
    • 28. Heart Physiology: Sequence of Excitation Figure 18.14a
    • 29. Heart Physiology: Intrinsic Conduction System
      • Autorhythmic cells: Pace maker
        • Initiate action potentials
        • Have unstable resting potentials called pacemaker potentials
        • Use calcium influx (rather than sodium) for rising phase of the action potential
    • 30. Pacemaker and Action Potentials of the Heart Figure 18.13
    • 31.  
    • 32. Conducting system of heart
      • Coducting system perform 2 functions:
      • 1. Generation of impulses
      • 2. Conduction of these impulses
      • Rate of different parts of conductive system:
      • SA node: 70-80/min
      • AV node: 40-60/min
      • Purkinje fibers: 15-40/min
      • SA node dominates because of it ’ s high rate of discharge & is the pace maker of the heart.
      • The other parts function in conducting the impulses.
    • 33. Heart Physiology: Sequence of Excitation
      • Sinoatrial (SA) node generates impulses about 75 times/minute
      • Atrioventricular (AV) node delays the impulse approximately 0.1 second (allow atria to contract before ventricles)
      • Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)
    • 34. Heart Physiology: Sequence of Excitation
      • AV bundle splits into two pathways in the interventricular septum (Rt.& Lt.bundle branches)
        • Bundle branches carry the impulse toward the apex of the heart
        • Purkinje fibers carry the impulse to the heart apex and ventricular walls ( fast conduction allow the ventricle to contract as one unit)
    • 35.  
    • 36. Extrinsic Innervation of the Heart
      • Heart is stimulated by the sympathetic cardioacceleratory center
      • Heart is inhibited by the parasympathetic cardioinhibitory center
      Figure 18.15
    • 37. Cardiac cycle
      • An action potential generated in the SA node,travelling to the atria depolarizing them & bringing contraction of atria.
      • Action potential spreading to the ventricles through AV node,bundle of His & bundle branches depolarizing the ventricles & bringing contraction of the ventrices.
      • Contraction will be followed by relaxation
    • 38. Cardiac Cycle
      • Cardiac cycle refers to all events associated with blood flow through the heart
      • Cardiac cycle consists of systole &diastole
        • Systole – contraction of heart muscle
        • Diastole – relaxation of heart muscle
        • Duration: 0.8 sec if HR 72 ( 60/72)
        • SYS: atrial (0.1sec), ventricular (0.3sec)
        • DIAS: atrial (0.7sec), ventricular (0.5sec)
    • 39. FUNCTIONAL ANATOMY OF HEART
    • 40. Phases of the Cardiac Cycle
      • Ventricular systole
        • Atria relax
      • 1.Isometric ventricular contraction (0.06 sec)
        • Rising ventricular pressure results in closure of AV valves (1 st heart sound)
        • Rising ventricular pressure opens semilunar valves
        • 2.Ventricular ejection phase begins (0.21sec)
    • 41. Phases of the Cardiac Cycle
      • Ventricular diastole
      • 1.Protodiastole (0.02 sec) ends by closure of semilunar valves(2 nd heart sound)
      • 2.Isometric ventricular relaxation (0.05 sec) ends by opening of AV valves
      • 3.Rapid ventricular filling (0.16sec)
      • 4.Slow ventricular filling (0.23sec)
      • 5.Atrial systole (0.1sec) a new wave of depolarization
    • 42. Changes during cardiac cycle
      • 1. PRESSURE CHANGES
      • A. in ventricles
      • Rt ventricle 22/0 mm Hg
      • Lt ventricle 120/0 mm Hg
      • B. Aorta 120/80 mm Hg
      • C. Pulmonary artery 22/8
      • D. Atria Rt.4-6, Lt.7-8 mmHg (a,c,v waves)
    • 43. Changes during cardiac cycle
      • 2.VOLUME CHANGES
      • End Diastolic Volume (120-130ml)
      • Stroke Volume 70 ml
      • End Systolic Volume (50-60ml)
      • EDV- SV= ESV
    • 44. Changes during cardiac cycle
      • 3.HEART SOUNDS
      • First heart sound LUP at beginning of systole
      • Second heart sound DUP at beginning of diastole
      • Third heart sound(some times)-rapid ventricular filling
      • Fourth heart sound( atrial systole)
    • 45. Changes during cardiac cycle
      • 4.ELECTRICAL CHANGES
      • Electrical changes originating in the heart spreads to the surrounding tissue & some reaches the body surface & can be recorded
      • ELECTROCARDIOGRAPHY ECG
    • 46. Phases of the Cardiac Cycle Figure 18.20
    • 47. Electrocardiography
      • Electrical activity is recorded by electrocardiography (ECG)
      • P wave corresponds to depolarization of SA node
      • QRS complex corresponds to ventricular depolarization
      • T wave corresponds to ventricular repolarization
      • Atrial repolarization record is masked by the larger QRS complex
    • 48. Electrocardiography Figure 18.16
    • 49. Action potential in ventricular muscle
    • 50. Heart Excitation Related to ECG Figure 18.17
    • 51. Recording ECG
      • Recording is done by using two types of leads.
      • 1. Bipolar leads: The potential difference between 2 active electrodes is recorded. Also called standard limb leads: Lead I,II,III
      • 2. Unipolar leads: One active electrode called Exploring electrode is put on different points on body surface. The other electrode( indifferent electrode) is kept at zero potential
      • A. Unipolar limb leads( aVR, aVL, aVF)
      • B. Unipolar chest leads( precordial leads): V1,V2,V3,V4,V5,V6
    • 52. Standard limb leads & Einthoven triangle
    • 53. Einthoven law: I + III = II
    • 54. Unipolar chest leads( precordial)
    • 55. Precordial leads
    • 56. Augmented limb leads: waves inverted in aVR
    • 57.  
    • 58. Waves & Intervals
      • P wave: duration:0.1sec,voltage, 0.1-0.3mv
      • P-R interval: 0.12-0.2 sec
      • ORS complex: duration 0.08sec, voltage 0.5-1.5mv
      • T wave: duration 0.27sec, voltage 0.2-0.3mv
      • Q-T interval: 0.35sec
    • 59.  
    • 60.  
    • 61. Most ventricular activity that is recorded is activity in the left ventricle. The same activity gives different shapes in different leads because a wave of depolarization moving toward an electrode will cause an upward deflection on the ECG needle while if depolarization is moving away from an electrode that electrode records a negative wave. Generation of the ECG complexes
    • 62. READING ECG
      • 1. Find heart rate
      • 2. Detection of conduction defects
      • 3. Detection of abnormality in rhythm (arrhythmias)
      • 4. Detection of signs of ischemia
      • 5. Detection of atrial or ventricular hypertrophy
    • 63. Heart rate
      • Is found by dividing 300 by the no. of large squares between 2 successive R waves
      • Normal HR 60-90/min
      • Below 60/min. Bradycardia
      • Above 90/min. Tachycardia
    • 64. Calculation of heart rate
    • 65. CONDUCTION DEFECTS
      • 1.SA node .Sick sinus syndrome ( Stoke ’ s Adam syndrome) :atrial escape.Corrected by artificial pacemaker.
      • 2. AV node,bundle of His. (Heart block)
      • a. Incomplete heart block:
      • 1. 1 st degree HB ( prolongation of P-R interval)
      • 2. 2 nd degree HB ( 2:1 or 3:1 block)
      • b. Complete heart block (3 rd degree HB)
      • ( ventricular escape ventricles beat by their idioventricular rhythm)
      • 3. Bundle branch block ( RBBB, LBBB)
    • 66. Sinoatrial block with AV nodal rhythm
    • 67. First degree heart block
    • 68. Second degree heart block
    • 69. Complete heart block
    • 70. ARRHYTHMIAS
      • 1. SUPRAVENTRICULR
      • a. Sinus ( tachycardia, bradycardia)
      • b. Atrial ( extrasystole, paroxysmal atrial tachycardia, atrial flutter, atrial fibrillation)
      • 2. VENTRICULAR
      • ( extrasystole, tachycardia, fibrillation)
    • 71. Arrhythmias
      • If the irritable ectopic focus discharges once, the result will be a premature beat or extrasystole
      • If the focus discharges repetitively at a rate more rapid than SA node, it produced rapid regular tachycardia
      • A very rapidly & irregularly discharging focus or more likely group of foci can produce fibrillation
    • 72. Sinus tachycardia
    • 73. Sinus bradycardia
    • 74. Supraventricular extrasystole (premature beat)
    • 75. Ventricular extrasystole
    • 76. Paroxysmal atrial tachycardia
    • 77. Paroxysmal ventricular tachycardia
    • 78. Ventricular fibrillation
    • 79. Circus movement
      • A common cause of paroxysmal arrhythmias is a defect in conduction that permits a wave of excitation to propagate continuously within a closed circuit producing circus movement or Re-entry movement
    • 80. Re-entry ( circus movement)
    • 81. Atrial flutter & atrial fibrillation
    • 82. SIGNS OF ISCHEMIA
      • Decreased blood flow to the myocardium
      • Angina pectoris
      • Myocardial infarction
    • 83. Signs of ischemia
    • 84. Atrial hypertrophy
      • Right atrial hypertrophy: Tall & peaked p wave
      • Left atrial hypertrophy: Broad & Bifid p wave
    • 85. Ventricular hypertrophy
      • Estimating the electrical axis of the heart or the main direction of the cardiac vector
      • Estimated from the QRS deflection in 2 standard limb leads usually lead 1 & lead 3
      • Normal electrical axis of the heart +59 degrees [ normal range (-30)-(+110) ]
    • 86. Visualization of the generation of the Left Ventricular portion of the ECG complex in Lead II 1. Septum depolarizes from the inside out and the resulting depolarization wave moves away from the electrode recording Lead II 2. The rest of the ventricle depolarizes counter-clockwise from the inside out and creates the (large arrow) which is essentially, the algebraic sum of all of the small depolarization vectors. This vector is, in a normal heart, almost always moving directly toward Lead II, generating a mostly positive QRS complex main cardac vector Lead II electrode 60 downward rotation angle from the horizontal 0 o o 60 o Note: compared to the left ventricle, the right ventricle is much smaller and contributes little to the overall main vector of depolarization (DEPOLARIATION)
    • 87. Cardiac vector
    • 88. Estimation of electrical axis
    • 89. Electrical axis of different leads
    • 90. Electrical axis estimated from 2 bipolar leads
    • 91. Electrical axis of heart
    • 92. Left axis deviation
    • 93. Right axis deviation
    • 94. Cardiac Output (CO) and Reserve
      • CO is the amount of blood pumped by each ventricle in one minute
      • CO is the product of heart rate (HR) and stroke volume (SV)
      • HR is the number of heart beats per minute
      • SV is the amount of blood pumped out by a ventricle with each beat
      • Cardiac reserve is the difference between resting and maximal CO
    • 95. Cardiac Output: Example
      • CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
      • CO = 5250 ml/min (5.25 L/min)
      • Change in HR or change in SV or change in both of them can change the CO
    • 96. Regulation of Stroke Volume
      • SV = end diastolic volume (EDV) minus end systolic volume (ESV)
      • EDV = amount of blood collected in a ventricle during diastole
      • ESV = amount of blood remaining in a ventricle after contraction
    • 97. Factors Affecting Stroke Volume
      • Preload – amount ventricles are stretched by contained blood[EDV] .increase EDV increases SV
      • Contractility – cardiac cell contractile force due to factors other than EDV
      • Afterload – Is the resistance to ventricular ejection caused by resistance to flow in systemic circulation
      • Increase afterload decreases SV
    • 98. Frank-Starling Law of the Heart
      • Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume. The heart can pump a small or a large volume of blood depending on blood reaching it.
      • Slow heartbeat and exercise increase venous return to the heart, increasing SV
      • Blood loss and extremely rapid heartbeat decrease SV
    • 99.  
    • 100. Venous return to the heart
      • Venous return &EDV increase by:
      • 1. Skeletal muscle contraction
      • 2. Increased negative intrathoracic pressure during inspiration
      • 3. venoconstriction
      • 4. Increased blood volume
    • 101. Venous return
      • Venous return & EDV decrease following:
      • 1. Prolonged standing
      • 2. Excessive bleeding
      • 3.Costrictive pericarditis
    • 102. Preload and Afterload Figure 18.21
    • 103. Contractility of myocarium
      • Contractility is the increase in contractile strength, independent of preload & afterload
      • Increase in contractility comes from:
        • Increased sympathetic stimuli
        • Certain hormones:g Noradrenaline
        • Ca 2+ and some drugs ( sympathomimetic drugs)
    • 104. Contractility and Norepinephrine
      • Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
      Figure 18.22
    • 105. Afterload
      • Resistance offered to ventricular ejection
      • Hypertension, Aortic stenosis
      • Stroke volume is inversely proportional to afterload
    • 106. Regulation of Heart Rate
      • Positive chronotropic factors increase heart rate
      • Negative chronotropic factors decrease heart rate
      • HR is affected by: Nervous & Hormonal factors
    • 107.
      • Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise. Increases HR
      • Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS. Decreases HR
      • PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
      Regulation of Heart Rate: Autonomic Nervous System
    • 108. Atrial (Bainbridge) Reflex
      • Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria
        • Causes stimulation of the SA node
        • Stimulates baroreceptors in the atria, causing increased SNS stimulation
    • 109. Chemical Regulation of the Heart
      • The hormones epinephrine and thyroxine increase heart rate
      • Intra- and extracellular ion concentrations must be maintained for normal heart function
    • 110. Factors Involved in Regulation of Cardiac Output Figure 18.23
    • 111. MEASUREMENT OF CO
      • Clinical exam. Gives a good indication of cardiac function. For example:
      • Skin temperature
      • Capillary refill.
      • Pulse rate & pulse volume.
      • Urine output
      • level of consciousness are reliable markers of CO
    • 112. Measurement of C.O
      • 1. Fick method ( O2 consumption method)
      • Total O2 consumption in one min.
      • C.O=
      • Art.O2 content- Venous O2 content
      • 250ml/min
      • e:g =5L/min
      • 190-140
    • 113. Measurement of C.O
      • 2. Dye dilution method
      • A known amount of dye or radioactive isotope is injected to an arm vein & the concentration of the indicator in serial samples of arterial blood is determined
      • mg dye injected
      • C.O=
      • mean conc. X time from appearance to disappearance of dye
    • 114. Measurement of C.O
      • 3.Doppler method with Echocardiography
      • Pulses of ultrasound are directed at the blood flowing in ascending aorta & reflected back to the probe by red cells in the blood. The velocity of blood in aorta is measured & if the cross sectional area of aorta is measured by echocardiography the stroke volume & C.O can be calculated
    • 115. Effect of various conditions on C.O
      • NO CHANGE:
      • 1. Sleep
      • 2. Moderate change in environmental temp.
    • 116. Increase C.O
      • 1.Anxiety & excitement 50-100%
      • 2.Eating 30%
      • 3.Exercise up to 700%
      • 4.High environmental temp.
      • 5.pregnancy
    • 117. Decrease C.O
      • 1.Sitting or standing from lying position
      • 20-30%
      • 2.rapid arrhythmias
      • 3.Heart disease
    • 118. Oxygen consumption of the heart
      • At rest: 9ml/100gm/min [ normal wt.250-300gm]
      • Increases during exercise & in a no. of different conditions
      • Cardiac muscle obtain energy mainly from metabolism of fatty acids & to a lesser extent from glucose & lactate.
      • Energy expenditure determined by:
      • 1. Heart rate
      • 2. Arterial B.P
      • Energy expenditure can increase when these 2 parameters increase even though the cardiac output is not changed.
    • 119. Vascular system Circulation
    • 120.  
    • 121. Systemic circulation
    • 122. HEMODYNAMICS
      • Include the study of :
      • 1. Mean pressure
      • 2. Type of flow
      • 3. Speed of flow
      • In different parts of the circulation [systemic circulation]
    • 123. Hemodynamics BLOOD VESSELS:   [anatomical & functional classification] A.  Arteries (high pressure vessels) [conducting vessels] 1.  structure             a.  thick-walled              b.  large diameter c.  elastic                      
    • 124. HEMODYNAMICS B.  Arterioles [resistance vessels] [1].  structure           a.  small diameter           b.  smooth muscle in wall            1.  vasoconstriction, vasodilatation   2.  vascular tone [2].  function:  to regulate blood flow to capillary beds     
    • 125. HEMODYNAMICS C.  Capillaries [exchange vessels] 1.  structure        a.  thin-walled;  porous        b.  narrow       c.  Large surface area 2.  function: exchange   3.  capillary blood flow: regulated by presence of     a.  precapillary spincters            
    • 126. HEMODYNAMICS D.  Veins [storage or capacitance vessels] 1.  low pressure vessel 2.  structure      a.  large diameter      b.  distensible   c.  thin-walled d. Valve 3.  function: storage 4.  venous return mechanisms     a.  skeletal muscle pump     b.  sympathetic vasoconstriction c. Thoracic pump                                    
    • 127. Blood Flow
      • Blood flow is defined as the quantity of blood passing a given point in the circulation in a given period and is normally expressed in ml/min
      • Overall blood flow in the total circulation of an adult is about 5000 ml/min … .The cardiac output
    • 128. FORWARD BLOOD FLOW Mechanisms – Movement of Blood 1.Forces imparted by rhythmic contractions of the heart 2.Elastic recoil of arteries following filling by the action of the heart 3.Squeezing of blood vessels during body movements 4.Peristaltic contractions of smooth muscle surrounding blood vessels 5. Negative I.T.pre.during inspiration
    • 129.  
    • 130. FACTORS AFFECTING BLOOD FLOW
    • 131. Forward blood flow
    • 132. Conductance and vessel diameter
      • Slight changes in the diameter of a vessel cause tremendous changes in the vessel's ability to conduct blood when the blood flow is streamlined
      • Although the diameters of these vessels increase only fourfold, the respective flows are 1, 16, and 256 ml/mm, which is a 256-fold increase in flow. Thus, the conductance of the vessel increases in proportion to the fourth power of the diameter
    • 133. Peripheral resistance
      • Blood flow is determined by:
      • 1. Pressure difference between the 2 ends of the vessel
      • 2. Peripheral resistance:
      • A. Vessel diameter: Resistance is inversely proportional to the fourth power of radius
      • B. Blood viscosity: determined by no. of RBC & by plasma proteins
    • 134. HEMODYNAMICS
      • Mean pressure: average pressure during the whole cardiac cycle
      • In the arteries it is obtained by :
      • 1 systolic pressure+2diastoloic pressures
      • 3
      • The mean pressure is important for proper tissue perfusion.
    • 135. MEAN PRESSURE
      • Arteries: 95mmHg
      • Beginning of arterioles: 85mmHg
      • Leaving arterioles: 30mmHg
      • Venular end of capillary: 10mmHg
      • Rt atrium: around zero mmHg
      • All these values are for blood vessels at the level of the heart.
    • 136. MEAN PRESSURE
    • 137. TYPE & SPEED OF FLOW
      • Arteries:Pulsatile flow
      • Capillaries & Veins: Continuous flow
      • Systolic BP-Diastolic BP= Pulse pressure
      • Pulse pressure enables us to feel pulse
      • Arteries: speed of flow 40cm/sec
      • Capillaries: 0.07cm/sec
      • Veins: 10cm/sec
    • 138. LAMINAR & TURBULENT BLOOD FLOW
      • Normally blood flow is laminar flow[silent]
      • If blood passes by an obstruction or rough surface or if it ’ s speed increases , it changes to Turbulent flow[ noisy flow]
    • 139. Modes of flow in vessles
      • Blood flow can either be laminar or turbulent
    • 140. Laminar Flow
      • When blood flows through a long smooth vessel it flows in straight lines, with each layer of blood remaining the same distance from the walls of the vessel throughout its length
      • When laminar flow occurs the different layers flow at different rates creating a parabolic profile
      • The parabolic profile arises because the fluid molecules touching the walls barely move because of adherence to the vessel wall. The next layer slips over these, the third layer slips over the second and so on.
    • 141. LAMINAR or STREAMLINE FLOW P 2 P 1 P 1 > P 2 -Cone Shaped Velocity Profile -Not Audible with a Stethoscope
    • 142. Turbulent flow
      • When the rate of blood flow becomes too great, when it passes by an obstruction in a vessel, when it makes a sharp turn, or when it passes over a rough surface, the flow may then become turbulent
      • Turbulent flow means that the blood flows crosswise in the vessel as well as along the vessel, usually forming whorls in the blood called eddy currents. When eddy currents are present, the blood flows with much greater resistance than when the flow is streamline because eddies add tremendously to the overall friction of flow in the vessel.
    • 143. Turbulent blood flow
      • Turbulent blood flow is a noisy flow
      • It produces sounds that can be heard by a stethoscope
      • The fact that turbulent flow produces sound is used in measurement of arterial blood pressure
      • Sounds produced by turbulence to blood flow during blood pressure measurement are called : Korotkoff sounds
    • 144. BLOOD PRESSURE
      • Arterial blood pressure:
      • It is the force of blood on the wall of arteries.
      • Blood pressure is important because it provides a forward driving force to the flow of blood & it ensures proper blood perfusion to all organs in the body specially the vital organs :
      • [brain, heart, kidneys]
    • 145. Blood pressure
      • Systolic BP: pressure of blood on the wall of arteries during ventricular systole. Normal range is 100-140 mmHg
      • Diastolic BP: pressure of blood on wall of arteries during ventricular diastole. Normal range is 60-90 mmHg
      • Pulse pressure: difference between systolic & diastolic BP
    • 146. BLOOD PRESSURE
      • Factors affecting blood pressure:
      • 1.Cardiac output C.O[ HR, SV]
      • 2.Peripheral resistance
      • [ blood viscosity, diameter of arteriole]
      • 3.Total blood volume
    • 147. Peripheral Resistance
      • Blood viscosity
      • Diameter of arterioles:
      • Vasomotor tone [sympathetic tone]
      • Arterioles are kept in a state of partial vasoconstriction because of activity of VMC through sympathetic NS
      • Increased sympathetic activity= vasoconstriction
      • Decreased sympathetic activity= vasodilatation
      • There is no parasympathetic supply to blood vessels
    • 148. BLOOD PRESSURE
      • B.P = C.O X P.R
      • Changes in C.O affect systolic B.P
      • Changes in P.R affect diastolic B.P
    • 149. Neural regulation of blood pressure
    • 150. Regulation of blood pressure
      • 1. Neural control
      • [ VMC, Sympathetic, Baroreceptors]
      • Baroreceptors found in aortic arch & carotid sinus
      • They are stimulated by increased blood pressure
      • When stimulated they cause inhibition of VMC
      • Inhibition of VMC decrease sympathetic discharge to blood vessels
      • This leads to vasodilatation and decreased peripheral resistance
      • = decreased blood pressure
      • Baroreceptors have a buffering action on blood pressure
    • 151. Aortic & carotid baroreceptors
    • 152. Effect of increased BP on baroreceptor stimulation
    • 153. Regulation of B.P
      • 2. Hormonal regulation
      • A. Epinephrine & Norepinephrine
      • B. Antidiuretic hormone [ ADH] or vasopressin
      • C. Renin-Angiotensin- Aldosterone system
    • 154. The Adrenal Medulla
      • Acts very much like a part of the sympathetic nervous system (fight or flight)
      • Secretes two amines:
        • norepinephrine (20%)
        • epinephrine (80%)
      • Stimulated by preganglionic neurons directly, so controlled by the hypothalamus as if part of the autonomic nervous system.
    • 155. Effects of ADH
    • 156. Renin-Angiotensin – Aldosterone system
      • Decrease in BP or Decrease plasma sodium
      • Stimulates cells in Juxtaglomerular apparatus in the kidney to secrete renin
      • Renin acts on angiotensinogen to form angiotensin I
      • Angiotensin I is activated to Angiotensin II by the Angiotensin converting enzymes( ACE)
    • 157. Angiotensin II
      • Functions:
      • 1. Arteriolar vasoconstriction= increase PR
      • 2. Venoconstriction= increase venous return to heart =Increase CO
      • 3. Stimulates adrenal cortex to secrete Aldosterone which increases sodium reabsorption from renal tubules
    • 158. Regulation of BP by renin-angiotensin
    • 159. Regulation of BP by Renin-angiotensin
    • 160. Blood pressure
      • Effect of gravity on blood pressure:
      • (+) or (-) 0.77mmHg/cm distance from heart level
      • It is (+) for blood vessels below heart level
      • It is ( – )for blood vessels above heart level
      • All values mentioned for mean blood pressure are for blood vessels at level of heart
      • Critical closing pressure:
      • Blood flow stops if the pressure difference between the 2 ends of a vessel is lower than peripheral resistance
    • 161. Effects of gravity on arterial and venous pressures. Each cm of distance produces a 0.77 mmHg change. Sphincters protect capillaries VENOUS PUMP keeps P V < 25 mm Hg Veins Arteries 190 mm Hg 100 mm Hg 0
    • 162. HYPERTENSION
      • Blood pressure levels above the generally accepted normal according to age.
      • 20 year: 140/90mmHg
      • 50 year: 160/95mmHg
      • 70 year: 170/105
      • Exercise,anxiety,discomfort & unfamiliar surrounding can lead to to a transient rise in BP
    • 163. ETIOLOGY OF HYPERTENSION
      • 85-90% : Essential HT
      • 10-15%: Secondary HT ,could be due to:
      • 1. Renal diseases
      • 2. Endocrine disorders& hormone therapy
      • 3. Pregnancy
      • 4. Coarctation of aorta( Ht in upper limb & normal pressure in lower limb)
    • 164. COMPLICATIONS OF H.T.
      • 1. Left ventricular hypertrophy & MI
      • 2. hypertensive encephalopathy & CVA
      • 3. Hypertensive retinopathy
      • 4. Hypertensive nephropathy
      • Treatment aims at decreasing CO, or PR or total blood volume & eventually decreasing BP
    • 165. CAPILLARY CIRCULATION
      • Types of capillaries: Throughfare, True
      • Receives 5% of total CO
      • Thin walled
      • Speed of flow: 0.07cm/sec
      • Exchange: by diffusion ( lipid sol.,water sol.), pinocytosis.
      • Water movement: by Filtration
    • 166.  
    • 167.  
    • 168. Filtration of water
      • Depends on Starling forces:
      • 1. Filtration pressure=
      • Hydrostatic pressure in capillaries-hydrostatic pressure in I.S.F.
      • 2. Osmotic pressure gradient=
      • Colloid osmotic pressure in plasma-colloid osmotic pressure in I.S.F.
    • 169. Filtration
    • 170. Filtration
    • 171. ACTIVE & INACTIVE Capillaries
      • Normally flow is through the throughfare vessels
      • When there is an increased demand for blood flow, blood pass through true capillaries as well.
      • Vasodilator metabolites can cause capillary dilatation.e:g Increased CO2, increased H + , increased lactic acid
      • Decreased sympathetic activity: Vasodilatation & relaxation of precapillary sphincter
    • 172. VENOUS CIRCULATION
      • Function:
      • 1. Storing large quantities of blood(64%) of total C.O
      • 2. Regulating C.O
      • Factors affecting venous flow:
      • 1. Skeletal muscle contraction[ muscle pump]
      • 2. Negative I.T.pre. During inspiration[thoracic pump]
      • 3. Sympathetic venoconstriction
      • 4. Presence of valves in limb veins.
    • 173.  
    • 174. VENOUS PRESSURE
      • Central venous pressure is affected by a balance between:
      • 1. Pumping of blood by heart
      • 2. Venous return
      • Rt.atrial pressure & hence central venous pressure is increased in:
      • 1. Serious HF
      • 2. Following massive transfusion of blood
      • 3. Straining
      • While it decreases in shock
    • 175. VENOUS PRESSURE
      • Effect of gravity on venous pressure is the same as on arterial pressure
      • Veins collapse when their pressure is zero or below zero
      • Measurement of venous pressure:
      • Central venous pressure
      • Peripheral venous pressure
    • 176. LYMPHATIC CIRCULATION
      • Constitute a one way route for the movement of I.S.F to blood
      • Lymphatic system; made of an extensive network of thin vessels resembling veins arise as a group of blind end lymph capillaries permeable to all I.S.F. constituents
    • 177. LYMPH FLOW
      • Assisted by:
      • 1. Pumping action of skeletal muscles
      • 2. Effect of respiration on I.T.Pressure
      • 3. Presence of valves
      • 4. Rhythmic contraction of walls of large lymph ducts
    • 178. Functions of lymphatic system
      • 1. Return of excess fluid from the I.S.compartment
      • 2. Return of proteins [ some capillaries are permeable to protein]
      • 3. Specific transport function for fat
      • 4. lymph nodes & defence
    • 179. Protein content in lymph
      • Source of lymph Protein%
      • Choroid plexus 0
      • Skeletal muscle 2
      • Skin 2
      • Lung 4
      • G.I.T 4.1
      • Heart 4.4
      • Liver 6.2
    • 180. INTERSTITIAL FLUID VOLUME
      • I.S.F volume affected by:
      • 1. Capillary pressure
      • 2. Plasma oncotic pressure
      • 3. Capillary permeability
      • 4. Lymph flow
    • 181. EDEMA
      • Accumulation of fluid in I.S.space
      • Causes:
      • 1. Increased capillary pressure e:g CHF [Increased venous pressure]
      • 2. Hypoproteinemia:
      • a.decreased protein intake
      • b.decreased synthesis by liver
      • c.increased loss through kidney or GIT
      • 3. Increased capillary permeability e:g Kinin,Histamine
      • 4. Lymphatic obstruction e;g Filariasis or Elephantiasis
    • 182. Cardiovascular regulatory mechanisms
      • The aim of these mechanisms is to:
      • 1. Increase blood supply to active tissues.
      • 2. To increase or decrease heat loss from the body by redistributing the blood.
      • 3. In the face of challenges, e:g hemorrhage, they maintain blood flow to vital organs at the expense of the rest of the body.
    • 183. Cardiovascular regulatory mechanisms
      • Cardiovascular adjustments are affected by:
      • 1. Altering the cardiac output.
      • 2. Changing the diameter of resistance vessels
      • 3. Or changing the amount of blood pooled in the capacitance vessels
    • 184. Cardiovascular regulatory mechanisms
      • Diameter of arteiole & amount of blood flow can be regulated by;
      • 1. Systemic regulation [affecting large segment of circulation]
      • 2. local regulation [ Auto-regulation] affecting small segment of circulation
    • 185. Systemic regulation
      • 1. Neural [VMC, Sympathetic N.S]
      • 2. Hormonal: vasodilator or vasocostrictor hormones
      • Vasodilator Vasoconstrictor
      • Kinin Adr & Norad
      • ANP Angiotensin II
      • VIP ADH, Natriuretic F
    • 186. AUTOREGULATION [local]
      • Most tissues have an intrinsic capacity to compensate for moderate changes in perfusion pressure by changes in vascular resistance so that blood flow remains constant.
      • This capacity is well developed in the kidneys,skeletal muscle, brain, liver & myocardium
    • 187. Myogenic theory of autoregulation
    • 188. AUTOREGULATION
      • Local autoregulation could be due to:
      • 1. Accumulation of metabolites:
      • [ metabolic theory of autoregulation]
      • Increase : CO 2 , H + , K + , lactic acid, Adenosine. Or decrease O 2
      • All lead to vasodilatation
    • 189. AUTOREGULATION
      • 2. Substances secreted by endothelium:
      • a. Prostacycline [ vasodilatation]
      • b. Endothelin [ vasoconstriction].Stretching of blood vessels causes the release of endothelin
      • c. EDRF [ Nitric oxide NO ]: vasodilatation
    • 190. Endothelin
      • Endothelin Biosynthesis
      • Endothelin (ET-1) is a 21 amino acid peptide that is produced by the vascular endothelium from a 39 amino acid precursor, through the actions of an endothelin converting enzyme (ECE) found on the endothelial cell membrane. ET-1 formation and release are stimulated by angiotensin II antidiuretic hormone (ADH) , thrombin, cytokines, reactive oxygen species, and shearing forces acting on the vascular endothelium. ET-1 release is inhibited by prostacyclin and atrial natriuretic peptide as well as by nitric oxide .
    • 191. Endothelin
      • Intracellular Mechanisms
      • Once ET-1 is released by the endothelial cell, it binds to receptors on the target tissue (e.g., adjacent vascular smooth muscle). There are two basic types of ET-1 receptors: ET A and ET B . Both of these receptors are coupled to a G-protein and the formation of IP 3 . Increased IP 3 causes calcium release by the sarcoplasmic reticulum, which causes smooth muscle contraction . In blood vessels, the ET A receptor is dominant under normal conditions in terms of ET-1 effects on contraction.
    • 192.  
    • 193. Nitric Oxide in the Muscular System
      • NO was orginally called EDRF (endothelium derived relaxation factor)
      • NO signals inhibition of smooth muscle contraction
        • Ca+2 is released from the vascular lumen activating NOS
        • NO is synthesized from NOS III in vascular endothelial cells
        • This causes guanylyl cyclase to produce cGMP
        • A rise in cGMP causes Ca+2 pumps to be activated, thus reducing Ca+2 concentration in the cell
        • This causes muscle relaxation
    • 194. Nitric Oxide in the Circulatory System
      • NO serves as a vasodilator
        • Released in response to high blood flow rate and signaling molecules (Ach and bradykinin)
        • Highly localized and effects are brief
        • If NO synthesis is inhibited, blood pressure rises
        • During O2 delivery, NO locally dilates blood vessels to aid in gas exchange
    • 195. Nerve cells target the endothelial cells lining of blood vessels Acetylcholine activates NO synthase & production of NO in endothelial cells that surround the smooth muscle cells surround the blood vessel. Role of NO in smooth muscle relaxation of blood vessel walls
    • 196. NO diffuses into smooth muscle, binds to heme group in guanylyl cyclase and activated synthesis of cGMP Nitroglycerin is used to prevent chest pain (angina) because it is rapidly converted to NO
    • 197. Synthesis of Nitric Oxide
      • Nitric oxide is synthesized from L-arginine
      • This reaction is catalyzed by nitric oxide synthase, a 1,294 aa enzyme
      COO- C (CH2)3 NH C H2N H NH2+ +H3N Arginine NOS NADPH + O2 NAD+ COO- C (CH2)3 NH C H +H3N N + H2N H OH N-w-Hydroxyarginine COO- C (CH2)3 NH H +H3N + NO NOS C O NH2 Citrulline
    • 198. Types of NOS
      • NOS I
        • Central and peripheral neuronal cells
        • Ca+2 dependent, used for neuronal communication
      • NOS II
        • Most nucleated cells, particularly macrophages
        • Independent of intracellular Ca+2
        • Inducible in presence of inflammatory cytokines
      • NOS III
        • Vascular endothelial cells
        • Ca+2 dependent
        • Vascular regulation
    • 199. Synthesis & release of nitrous oxide (NO) Nitric oxide synthase (NOS) catalyzes the synthesis of NO from the terminal nitrogen atom of L-arginine in the presence of O2 Once synthesized, NO can freely diffuse across plasma membranes reaching neighboring cells NO acts locally, and has a very short half-life (5-10 secs)
    • 200. PULMONARY CIRCULATION
      • Receives same cardiac output= 5L/min
      • Pulmonary a: Thin [1/3 rd that of aorta]
      • Branches of pulmonary a., smaller a. & arterioles have larger diameter than corresponding systemic vessels.
      • Thinness+ Distensibility= very large compliance which permits the pul.a. to accommodate the C.O. of Rt.ventricle
    • 201. PULMONARY CIRCULATION
      • Pulmonary veins : compliance to similar to those in systemic circulation
      • Bronchial a.[oxygenated blood] : supply connective tissue, septa, large & small bronchi. It empties in pul.vein & enters Lt. atrium.[ decreasing arterial PO 2 =physiological shunt]
    • 202. The pulmonary circulation tissue CO 2 O 2 Pulmonary artery RV LA Pulmonary vein Pulmonary capillaries
    • 203. PULMONARY CIRCULATION
      • Pulmonary pressure= 22/8 mmHg
      • Pulse pressure= 14 mmHg
      • Pulmonary capillary pressure= 7mmHg
      • Mean pressure at Lt.atrium & major pul.veins= 2mmHg
      • Blood volume in the lungs: 450ml[9% of CO]
      • 70 ml of this blood is in the capillaries
      • Remainder in the a. & v.
    • 204. PULMONARY CIRCULATION
      • Blood flow regulation:
      • Local factors [ major role] & autonomic N.S.[minor role]
      • Pul.blood vessels constrict when PO 2 decreases[ in systemic circulation there is vasodilatation when PO2 decreases]
      • Increase Lt.atrial pressure= slows venous return=increased pul. Cap.pre.=pul.edema
    • 205. CIRCULATION THROUGH SPECIAL REGIONS
      • CORONARY CIRCULATION
      • Coronary blood: 5% of resting C.O
      • Major coronary vessels travel in the epicardium & subdivide sending separate branches through the myocardium.
      • During Systole the myocardial wall tension compresses the vessels increasing resistance to flow
    • 206. Coronary arteries
    • 207. Factors affecting coronary blood flow
      • Aortic pressure
      • Coronary arteriolar resistance  myocardial metabolic activity (autoregulation)
      • Extravascular compression
        • importance L > R (lower RV pressures)
        • maximal L flow in early diastole
    • 208. Coronary circulation
      • Maximum flow in left coronary vessels occurs during isometric ventricular relaxation while the arterial pressure is still relatively high & the myocardium is relaxed
      • Control of coronary flow:
      • 1. Autoregulation [ Adenosine]
      • 2. Sympathetic stimulation through ß receptors
    • 209. Coronary blood flow
    • 210. SNS stimulation
      • Receptors:
        •  (vasoconstrictor)
        •  (vasodilator)
      • Direct SNS effect:  vasoconstriction
      • Overcome by vasodilation due to  metabolic activity (local regulation dominant)
    • 211. Coronary circulation
      • Energy obtained mostly through aerobic pathway
      • Normally Hb releases approximately half of it ’ s arterial O 2 content to myocardium in contrast to the remainder of the body [25%]
      • Becomes even higher during exercise or stress
    • 212. Coronary circulation
      • PO 2 % Hb saturation
      • Arterial B 95mmHg 97%
      • Venous B 40mmHg 75%
      • Coronary 25-30mmHg 50%
      • Venous B
      • During exercise cardiac O 2 consumption may increase 5-6 folds in well trained athletes due to:
      • Increase coronary blood flow
      • Widening of arterio-venous O 2 difference
    • 213. Cutaneous circulation
      • Low metabolism
      • Blood flow serves mainly thermoregulatory role
    • 214. Numerous AV anastomoses
      • Thick muscular layer
      • Rich nerve supply
      • No basal tone (can constrict maximally)
      • No metabolic autoregulation
      • Exclusively under SNS control (can close completely)  thermoregulation
    • 215. Skin circulation
    • 216. Effect of changes in environmental temp. on heat conductance from body core to skin surface
    • 217. Cerebral circulation
      • Unique features:
        • contained within rigid structure  inflow/outflow inbalance  pressure
          • Cushing ’ s phenomenon:  systemic BP with  intracranial pressure (e.g. tumor) - by ischemic stimulation of vasopressor center in medulla (helps maintain brain flow)
        • Absolute requirement for adequate flow
          • tissue least tolerant to ischemia
            • 5 sec ischemia  loss of consciousness
            • 3-4 min permenant brain damage
          • glucose-dependent
    • 218. Cerebral circulation
      • Important features:
      • 1. Intracranial pressure [ Cushing reflex]
      • 2. Effect of gravity
      • 3. Blood Brain Barrier [BBB]:
      • A. Protect against changes in ionic composition
      • B. Protection of brain from endogenous & exogenous toxins
      • C. Prevention of escape of neurotransmitters into the general circulation
    • 219. Cushing reflex
    • 220. Neural regulation of brain vessels
      • Minimal importance (local mechanisms predominate)
      • SNS (along carotid & vertebral arteries) - weak vasoconstriction
      • Parasympathetic fibers from facial nerve - weak vasodilation
    • 221. Local regulation of brain vessels
      • Hypoxia
      • Very sensitive to CO 2 (vasodilation via changed pH)
      • H + cannot cross blood-brain barrier  cerebral vasodilation by:
        • local CO 2 /pH changes
        • blood CO 2
        • not blood pH (if = CO 2 )
    • 222. Brain flow auto-regulation
      • Excellent between 60 and 140 mmHg
      • Below 60 mmHg: syncope
      • Above 160 mmHg: cerebral edema
    • 223. Hepatic circulation
      • Hepatic blood flow ~ 25% CO
      • 1/4 of that from hepatic artery
      • 3/4 of that via portal vein
          • little O 2
          • mean pressure ~10 mmHg  small driving pressure gradient
            •  hepatic (and central) venous pressure easily transmit upstream  liver edema  transudation to peritoneal cavity (ascites) (also with  portal resistance due to fibrosis in cirrhosis)
    • 224. Hepatic circulation
    • 225. Regulation of liver circulation
      • Autoregulation
        • not in portal system
        • hepatic arterioles autoregulate
      • SNS
        • constriction of resistance vessels in portal venous & hepatic arterial systems
        • constriction of capacitance vessels more important (blood reservoir)
          • liver contains ~ 15% of all blood
          • 50% of that can be rapidly expelled by SNS
    • 226. FETAL CIRCULATION
      • 2 umbilical arteries[branches of int.iliac] carry blood to placenta
      • Exchange between fetal & maternal blood
      • Return through umbilical vein
      • Some blood pass through liver, remaining through ductus venosus enter inf.vena cava
      • Reach right atrium
      • Go through foramen ovale to left atrium,left ventricle & aorta
      • Remaining go to right ventricle, pulmonary artery
    • 227.  
    • 228. High fetal pulmonary vascular resistance
      • Low O 2  hypoxic vasoconstriction
      • No ventilation  undistended, convoluted vessels
      • Shunts ~90% of CO of right ventricle enters aorta through ductus arteriosus
      • Aorta carries mixed blood to different parts of circulation
    • 229. Birth
      • Umbilical vessels closed by trauma (if not tied)
      • Ductus venosus closes [ligamentum venosum]
      •  CO 2  breathing,expansion of lungs decrease pulmonary resistance
      •  arterial PO 2 constricts ductus arteriosus (via  vasodil. PGs, Bk, also K channels)
      • Closure of placental bed[ increase systemic resistance]
      • Increase afterload closes foramen ovale
    • 230. Heart Failure
      • Physiological definition : Failure of the heart to pump blood normally & to maintain adequate CO
      • Etiology:
      • 1. Ventricular outflow obstructon.e:g Systemic HT, or Pulmonary HT,or aortic & pulmonary stenosis
    • 231. Heart Failure
      • Etiology[cont.]
      • 2. Ventricular inflow obstruction e:g Mitral & Tricuspid stenosis
      • 3. Impaired ventricular function.e:g Myocarditis,Myocardial infarction& subsequent fibrosis.
      • 4. Volume overload.
    • 232. Heart Failure
      • Symptoms:
      • 1. Backward failure e;g edema
      • 2. Forward failure e;g weakness & exercise intolerence
    • 233. Heart Failure
      • Symptoms of Lt.HF:
      • 1. Orthopnoea
      • 2. Paroxysmal nocturnal dyspnoea
      • 3. Crepitation at the base of lung
      • Symptoms of Rt.HF:
      • 1. Raised jugular venous pressure
      • 2. Peripheral edema
    • 234. SHOCK
      • A term used to describe the clinical syndrome that develops when oxygen delivery is inadequate to meet the metabolic needs of the tissues due to some form of acute circulatory failure
    • 235. Clinical features of shock
      • 1. Sweating
      • 2.reduced conscious level:drowsiness
      • 3. Tachypnoea
      • 4. Hypotension
      • 5. Tachycardia with weak pulse
      • 6. Cold skin
      • 7. Oliguria
    • 236. Causes & Types of Shock
      • 1. Fainting [Syncope] or vasovagal attack
      • Caused by pain,stress ,fear ,excessive heat or sight of blood
      • 2. Hypovolemic shock
      • 3. Cardiogenic shock
      • 4. Anaphylactic shock
      • 5. Septic shock

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