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A heart physiology

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  • Transcript

    • 1. The Heart
    • 2. Chambers of the Heart
    • 3. Cardiac Cycle Ventricular systole - isovolumic contraction - ejection Ventricular diastole - isovolumic relaxation - rapid filling - atrial contraction
    • 4. 4) Ventricular Filling 5) Atrial Contraction
      • Isovolumic
      • Ventricular Contraction
      2) Ventricular Ejection 3) Isovolumic Ventricular Relaxation
    • 5. Can the heart beat by itself ?
    • 6.  
    • 7. Autorhythm The heart can beat on its own without the need for exogenous commands.
    • 8. Skeletal muscle Motor nerve Conclusion ? The heart generates electricity.
    • 9.  
    • 10.
      • TERMINOLOGY
      • Excitation
      • - definition: generation of action potentials
      • - different from contraction
      • Contraction
        • - definition: shortening of muscle cells
        • - triggered by excitation
    • 11. Excitation -Contraction coupling Excitation Contraction [ Ca ++ ] i (Action Potentials) (shortening)
    • 12. Sinus-Atrial node (SA node) Atria Atrial-ventricular node (AV node) Ventricles Sequence of excitation
    • 13. SA node - located in the right atrial wall, just inferior to the entrance of the superior vena cava. Original Impulses from S-A Node The electrical impulses are normally generated by a group of specialized pacemaker cells at sinoatrial (SA) node.
    • 14. Conduction of Electrical Impulses in the Heart
    • 15.  
    • 16.   Conduction of Action Potentials from Cell to Cell
        • through gap junctions in intercalated discs
        • (electrical synapses)
    • 17. Conduction in Atria The electrical impulses from SA node spread through the entire right and left atrial muscle mass, triggering contraction of the right and left atrium.
    • 18. Delay at A-V Node - The impulses from S-A node travel to atrioventricular (A-V) node . - A-V node is located in lower end of the interatrial septum near the tricuspid valve. A-V node
    • 19. Delay at A-V Node - A-V node is the only normal route that impulses from SA node are transmitted into ventricles. - Conduction speed in A-V node is slow (delay). - This delay allows time for the atria to finish contraction and empty their contents into the ventricles before ventricles start to contract.
    • 20.
      • From AV node to Ventricles
      • His bundle
        • left branch (anterior/posterior division)
        • - right branch
      His bundle
    • 21.
      • 1) Purkinje fibers
        • located in the subendocardial layer
        • - fastest conduction (4 m/s)
      • 2) Ordinary ventricular myocardial cells
        • able to conduct AP at a slower speed
      After the delay at A-V node, the impulses rapidly spread to the ventricles via specialized fibers, Purkinje fibers . Rapid Conduction in Ventricles
    • 22. Rapid conduction in the ventricles simultaneous excitation of the ventricles functional syncytium
    • 23. NNote : - Each electrical impulse can trigger cardiac muscle contraction normally only once. - A normal heart generates 60 to 100 impulses in 1 minute at resting state. 1 1
    • 24. Excitation Contraction [ Ca ++ ] i (Action Potentials) (shortening) Properties of Cardiac Muscle Excitation of the heart is triggered by electrical impulse rather than neural transmitters. Contraction of the heart is triggered by elevation of intracellular calcium influx.
    • 25. Properties of Cardiac Muscle - Myocytes depend heavily on oxygen and blood supply. - Not fatigue - Excitability Cycle The myocytes have Long refractory period during which they do not respond to any electrical impulses.
    • 26. RRole of a Long Refractory Period – 1 prevent ventricles from contracting at too high rates so that enough time is allowed for refill of the ventricles
    • 27. Role of Long refractory period - 2 Prevent retrograde excitation
    • 28. ELECTROCARDIOGRAPHY (ECG)
    • 29. EELECTROCARDIOGRAPHY ((ECG) the recording of electrical activities of the heart via electrodes placed on body surface.
    • 30.
          • Applications of ECG
              • 1)   measure automaticity
              • HR, rhythmicity, pacemaker
              • 2)   measure conductivity
              • pathway, reentry, block
              • 3)   reveal hypertrophy
              • 4)   reveal ischemic damages
              • location, size, and progress
    • 31. Waves and Intervals of ECG P wave : atrial depolarization QRS complex : ventricular depolarization T wave : ventricular repolarization
    • 32. PR Interval
    • 33. Disorders of the Cardiac Conduction System ---- Arrhythmias - refers to abnormal initiation or conduction of electrical impulses in the heart. - caused by ischemia, fibrosis, inflammation, or drugs.
    • 34.
        • Bradycardia
      • slow heart rate ( < 60 beats/min)
      •  
        • Tachycardia
      • fast heart rate ( > 100 beats/min)
    • 35. - contract uncoordinatedly and extremely rapidly. - Ventricular fibrillation is lethal. Atrial or Ventricular Flutter and Fibrillation
    • 36. is when the heart beat is triggered by ectopic pacemakers (cells other than SA node). Premature contraction
    • 37. Conduction Block
    • 38. Artificial Pacemaker Application: sinus abnormality, complete AV or ventricular block Function: - generate electric pulses - sensing - antitachyarrhythmia
    • 39. Heart Sounds Four heart sounds can be recorded via phonocardiography, but normally only two, the first and the second heart sounds, are audible through a stethoscope.
    • 40.
      • First heart sound :
      • occurs when the atrioventricular (AV) valves close at the beginning of ventricular contraction.
      • generated by the vibration of the blood and the ventricular wall
      • is louder, longer, more resonant than the second heart sound.
    • 41. - occurs when aortic and pulmonary semilunar valves close at the beginning of ventricular dilation - generated by the vibration of the blood and the aorta - Aortic valve closes slightly before pulmonary valve. Second heart sound
    • 42. Heart Murmur - abnormal heart sound - occur in valvular diseases and septal defects
    • 43. Two Basic Types of Valvular Diseases 1) valvular stenosis , a narrowing of the valve 2) valvular insufficiency (incompetence). A valve is unable to close fully; so there is some backflow (regurgitation) of blood.
    • 44. MECHANICAL PROPERTIES OF THE HEART
      • CONTENT
          • Heart Rate
          • Stroke volume
          • Cardiac Output (CO)
          • Ejection Fraction
          • Preload
          • Afterload
          • Contractility
          • Frank-Starling Mechanism
          • Factors on Cardiac Output
    • 45.   Heart Rate the number of heart beats in 1 minute. Normal value: 60-100/min Stroke volume the volume of blood pumped out by each ventricle per each contraction. SV
    • 46. Cardiac Output (CO) the amount of blood pumped out by each ventricle in 1 minute. Cardiac output = stroke volume x heart rate Example: 70 ml x 75 beat/min = 5,250 ml/min 70 75 beat/min ml
    • 47. Ejection Fraction = stroke volume  end-diastolic ventricular volume 70 ml  130 ml = 54% 60 ml End of diastole 130 ml 70 ml End of systole SV =
    • 48. End of diastole 133 ml 120 ml End of systole SV = Ejection Fraction 120 ml  133 ml = 90% increases during exercise
    • 49.
      • Preload
          • the force that stretches the muscle before contraction.
      • Afterload
          • the force that stretches muscle during contraction.
      preload afterload
    • 50. Preload to ventricles = ventricular end diastolic pressure - the degree of stretch of the ventricular muscle cells just before they contract. - determined by ventricular filling.
    • 51. Afterload to left ventricle: aortic arterial pressure Afterload to right ventricle: pulmonary arterial pressure Afterload to the left ventricle is greater than that to the right ventricle. Aortic arterial pressure
    • 52. Contractility - the intrinsic strength of cardiac muscles.
    • 53.
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
      • 2) Afterload :  
      • 3) Contractility :
      •  
      • 4) Heart Rate :
    • 54.
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
       Preload   cardiac output (Starling-Frank Mechanism)
    • 55. More in More out
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
       Preload   cardiac output (Starling-Frank Mechanism)
    • 56.
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
      • 2) Afterload :  
       afterload   CO R
    • 57.
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
      • 2) Afterload :  
      • 3) Contractility :
       contractility   CO
    • 58.
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
      • 2) Afterload :  
      • 3) Contractility :
      •  
      • 4) Heart Rate :
      dual effects  CO =  Heart Rate x Stroke Volume
    • 59. less in less out
      • Factors on Cardiac Output
      •  
      • Preload :
      •  
      • 2) Afterload :  
      • 3) Contractility :
      •  
      • 4) Heart Rate :
      dual effects Heart Rate Stoke Volume  CO =  Heart Rate x  Stroke Volume 300% 400%
    • 60. REGULATION OF THE HEART FUNCTION
    • 61. Regulation of the Cardiac Function
      • 1) Nervous control
        • Sympathetic control
        • Parasympathetic control
        • Higher centers
        • Reflexes
      • 2) Hormonal Control
      • 3) Autoregulation
      • 4) Other factors
    • 62. Regulation of the Cardiac Function
      • 1) Nervous control
        • Sympathetic control
        • Parasympathetic control
    • 63.
      • Sympathetic Nervous System
        • - controls all components of the heart.
        • - release Norepinephrine (NE).
        • - increases heart rate (positive chronotropic) and contractility (positive inotropic) .
      Cell  1
    • 64. Cell m
      • Parasympathetic Nervous System (PNS)
        • - controls SA node and AV node.
        • releases Acetylcholine (Ach).
        • - decreases heart rate (negative chronotropic).
        • - prolongs delay at AV node.
        • - has little effect on contractility.
    • 65.
        • Higher Centers of Autonomic Nervous System
          • - Medulla Oblongata
          • - Hypothalamus, Thalamus, Cerebral cortex
    • 66. Centers in Medulla Oblongata Sympathetic center: distinct accelerator and augmentor Parasympathetic center: Nucleus vagus and nucleus ambiguus
    • 67. Hypothalamus, Thalamus, Cerebral cortex Involved in the cardiac response to environmental temperature changes, exercise , or during excitement , anxiety , and other emotional states
    • 68. Neural Control via Reflexes
    • 69. Baroreceptors
    • 70. 1) Baroreceptor Reflex - stimulated by increase in arterial pressure (stretch) - Effect: negative chronotropic and inotropic - regulate the heart when BP increases or drops - involved in short term regulation of BP
    • 71. 2) Chemoreceptor Reflex
    • 72. Chemoreceptors Chemoreceptors Chemoreceptors
    • 73. 2) Chemoreceptor Reflex - stimulated by  oxygen ,  pH , or  CO 2 - overall effect: positive choronotropic and inotropic. - less important in regulating cardiac function
    • 74. 3) Proprioceptor Reflex - Stimulated by muscle and joint movement - Effects: increase heart rate during exercise
    • 75. Regulation by Hormones
      • Epinephrine
        • - released from adrenal gland.
        • - increases heart rate and contractility.
      • Thyroxin
        • - released from thyroid gland.
        • - increases heart rate.
      •  
    • 76. Autoregulation of the Heart Stroke volume is autoregulated by ventricular filling ( Frank-Starling law ). SV More in More out
    • 77.
      • 4) Other Factors
      • - Blood level of ionic calcium, sodium, and potassium
      • Hypercalcemia (high plasma Ca ++ ):
          • positive inotropic
          • Hypernatremia (high plasma Na + ):
          • negative chronotropic
          • Hyperkalemia (high plasma K + ):
          • negative chronotropic
          • used in lethal injection
      - Age, gender, exercise, and body temperature
    • 78. Blood Supply to Cardiac Muscles
    • 79. Can cardiac muscles get nutrients from the blood in heart chambers?
    • 80. The cardiac muscles get nutrients from coronary circulation. Anterior view Posterior view
    • 81. Coronary arterial anastomosis
    • 82. Coronary venous blood is emptied into the right atrium through cardiac veins and coronary sinus. coronary sinus Posterior view
    • 83. Blockade of coronary artery causes myocardial infarction , or heart attack .
    • 84. Coronary Atherosclerosis
    • 85. dull white and slightly elevated fibrous plaque ( atheroma ) on coronary arterial lumen. Typical lesion of Coronary Atherosclerosis
    • 86.  composed of lipid, smooth muscle, macrophages, and connective tissues.  cause stenosis of coronary arteries Histology of the plaque    occlude arterial lumen when combined with internal hemorrhage, thrombosis, and arterial spasm
    • 87.    occur often at arterial branching points
    • 88. Surgical Therapies 1)
    • 89. 2) Coronary angioplasty
    • 90. 3) Stenting