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1. Review the basic physiology of the heart
2. Describe the electrical events involved in the cardiac cycle

CARDIAC CELLS Electrical Cells  Generate and conduct impulses rapidly o o o Muscle Cells  Main function is contraction o Atrial muscle SA and AV node Nodal pathways Interventricular septum  Ventricular muscle Able to conduct electrical impulses o  No contractile properties .


approaches K equilibrium Inward current .takes positive charge out of the cell and hyperpolarizes the membrane potential .brings positive charge into the cell and depolarizes the membrane potential Outward current .determined by conductance to K .CARDIAC ACTION POTENTIAL Resting Membrane Potential .

AP in myocardium differs from AP in skeletal muscle Skeletal muscle Myocardium { .

The origin of different shape of AP curve is in voltage gated L-type calcium channels { .

Excitation-Contraction Coupling    AP spreads from cell membrane to T tubules During plateau phase. Ca conductance increases Ca ion influx influences the strength and duration of myocardial contraction .

Ca entry stimulates release of Ca from sarcoplasmic reticulum Contraction force is dependent on the concentration of Ca in SR Relaxation occurs when Ca is reaccumulated in SR by Ca ATPase pump .

Conducting System of Heart .


Electrocardiogram .

CARDIAC CYCLE  o o 2 components: Diastole – filling of the heart chamber Systole – contraction of the chamber and ejection of blood .

PHASES OF CARDIAC CYCLE 1) Atrial Systole 2) Isovolumetric ventricular contraction 3) Rapid ventricular ejection 4) Reduced ventricular ejection 5) Isovolumetric ventricular relaxation 6) Rapid ventricular filling 7) Reduced ventricular filling (diastasis) .





CARDIAC OUTPUT  the amount of blood ejected from the ventricle in one minute CO = HR X SV   Heart rate – number of cardiac cycles in one minute Stroke volume – amount of blood ejected from the ventricle in one contraction .

affected by venous return ESV: amount of blood remaining in a ventricle after contraction. affected by contractility and afterload Ejection Fraction : % of EDV that is ejected in each SV = SV/EDV   .Stroke Volume   SV = EDV – ESV EDV: amount of blood in a ventricle at end of diastole.

cardiac fibers contract MORE FORCEFULLY when stretched thus ejecting MORE BLOOD (SV) The greater the venous return.Frank-Starling Law  Increases in EDV cause increase in ventricular fiber length which produce an increase in developed tension preload  stretch of muscle  force of contraction  SV   Unlike skeletal fibers. the greater the CO  .

2 m) is achieved. beyond which force and overlap gradually declines to zero (descending limb) The descending limb of the length-tension relationship is prevented by the strong parallel elastic component in cardiac muscle   . and therefore. The maximal force developed at any sarcomere length is determined by the degree of overlap of thick and thin filaments. the number of available crossbridges Force increases linearly until a sarcomere length with maximal overlap (~2.

alterations in cardiac output  VR  EDV and in VR   in EDV  Any  in EDV   in SV Blood loss and extremely rapid HR decrease SV .Frank-Starling Law   Slow HR and exercise increase venous return to the heart. increasing SV  VR changes in response to blood volume.

Factors Involved in Regulation of Cardiac Output .