Cardiovascular 5 Flashcards
Sympathetic modulation of contraction (SV): 4 steps
- Phosphorylation of CA2+ channels increases calcium conductance during an AP
- Phosphorylation of ryanodine receptors enhances sensitivity to Ca2+, increasing release of Ca2+ from SR
- Increases rate of myosin ATPase (binds faster)
- Phosphorylation of SERCA increases speed of CA2+ reuptake, increasing Ca2+ storage
-that can be used for next contraction
Increasing sarcomere length increases
Force of Contraction (SV)
2 Reasons why increasing sarcomere length will increase force of contraction
- Increases the Ca2+ sensitivity of Myofilaments
-a stretched sarcomere has a decreased diameter, can reduce distance Ca2+ needs to diffuse
-increases probability of cross bridging - Additional tension on stretch activated Ca2+ channels
-increases Ca2+ entry from extracellular space
-increasing Ca2+ induced Ca2+ release
-increases tension
The degree of myocardial stretch prior to contraction is known as
The preload on the heard
-load on ventricles before contraction
Increase preload= increase contractility
Frank- Starling Law of the Heart
Stroke volume increases with increasing EDV
The amount of force developed by cardiac muscle of ventricle (SV) depends on the initial stretch oof the ventricle walls (ventricular filling)
How is EDV determined
Normally by Venous return
-increased venous return increase venous pressure
-results in increased atrial filling and leading to increased ventricle filling
Factors affecting Venous Return: (3)
- Skeletal Muscle Pump
- Respiratory Pump
- Sympathetic Constriction of Veins
How does the Skeletal Muscle Pump affect venous Return
Skeletal muscle activity compresses veins in the extremities, pushing blood back to the heart
-increased muscle activity of the extremities can increase venous return
-through one way valves it returns
-pressure in veins usually low at rest
How does the Respiratory Pump affect Venous Return
During inspiration, the chest expands and diaphragm moves down
-creates a subatmoshperic pressure in the thoracic cavity
-draws blood into the vena cava that exist within
Basically makes thoracic cavity bigger and creates a negative reassure to stretch internal viscosities more
-also during inspiration veins in the abdomen are compressed -forces blood back to the heart
How does sympathetic constriction of veins affect Venous Return
-decreases their volume squeezing blood back towards the heart
-Fromm norepinephrine -pressurized blood to increase return
What is after load
The end load against which the heart contracts to eject blood
3 factors that affect SV of the heart
Preload. After load, COntractility
How is afterload determined
By the combination of the EDV and the pressure in the outflow artery, prior to contraction
Afterload can be increased how
Increased arterial blood pressure, decreased aortic compliance, chronic hypertension, echocardiography, altered ejection fraction
Hypertrophy in the Ventricles means
The muscle around it (wall) gets thicker
-this causes the ventricles to lose elasticity and compress the coronary arteries
-results in a lower SV as the ventricle can’t stretch to fill
Heart rate is determined by
The rate of depolarization in autorhytmic cells
Cardiac Output is determined by:
Heart rate and Stroke volume
-about 5L/min
Heart rate decreases due to
Parasympathetic innervation
Heart rate increases due to
Sympathetic innervation and epinephrine