6.3: Cardiovascular Mechanics Flashcards
Single ventricular cell structure
100 µm long and 15 µm wide
T-tubules on cell surface
Structure of T-tubule openings
Openings up to 200nm diameter
Spaced so that T-tubule lies alongside each Z-line of every myofinril
Carry surface depolarisation deep into the cell
Ventricular cell structure composition
Myofibrils 46%
Mitochondria 36%
Sarcoplasmic reticulum 4%
Nucleus 2%
Excitation-contraction coupling in the heart
1) SAN depolarises
2) Action potential travels down t-tubules
3)Ca2+ enters cell and binds to ryanodine receptor
4) Ca2+ enters cytoplasm from cytoplasmic reticulum and brings to troponin C
5) myosin heads bind to actin
6) Muscle fibres shorten
The relationship between force production and intercellular Ca2+
Sigmoidal curve, more Ca2+ greater attraction
As muscle length increases passive force
Increases continuously
What 4 things affect preload
Increased adrenaline secretion during fight or flight response
Decreased ventricular compliance
Decreased central venous pressure
Right atrial pressure
Two forms of heart contraction
Isometric and isotonic
In isometric contraction
Muscle fibres do not change length, but exert force so pressures increase in both ventricles
In isotonic contraction
Shortening of fibres and blood is ejected from ventricles
In vivo correlates of preload
Blood fills heart during diastole, stretching resting ventricular walls
Stretch determines the preload on the ventricles before ejection
Preload is dependent on venous return
Measures of preload include end-diastolic volume, end diastolic pressure and right atrial pressure
In vivo correlates of afterload
Afterload is the load against which the left ventricle ejects blood after opening of aortic valve
Any increase in afterload decreases the amount of isotonic shortening
Measures of afterload include diastolic blood pressure
Definition of the Frank-Starling relationship [F-S]
Increased diastolic fibre length increases ventricular contraction
Consequence of the Frank-Starling relationship [F-S]
Ventricles pump greater stroke volume so that, at equilibrium, cardiac output exactly balances the augmented venous return
Two factors the F-S relationship is thought to be caused by
Changes in the number of myofilament cross bridges that interact
Changes in the Ca2+ sensitivity of myofilaments
How do changes in the number of myofilament cross bridges that interact affect the F-S relationship
At shorter lengths than optimal the actin filaments overlap on themselves so reducing the number of myosin cross bridges that can be made
How do changes in Ca2+ sensitivity of myofilaments affect the F-S relationship
Ca2+ required for myofilament activation
Troponin C (TnC) is think filament protein that binds Ca2+
TnC regulates formation of cross bridges between actin and myosin
At longer sarcomere lengths, the affinity of TnC for Ca2+ is increased due to conformational change in protein
Less Ca2+ required for same amount of force
Definition of stroke work
Work done by the heart to eject blood under pressure into aorta and pulmonary artery
Equation for stroke work
SW= SV x P
SV- volume of blood ejected during each stroke
P- pressure at which blood is ejected
Law of LaPlace
When the pressure within a cylinder is held constant, the tension in its walls increases with increasing radius
Wall tension equation
Wall tension = pressure in vessel x Radius of vessel
T= P x R
Law of LaPlace in humans
Radius of curvature of walls of LV less than that of RV allowing LV to generate higher pressures with similar wall stress
How is the law of LaPlace affected during heart failure
Heart becomes dilated, increasing wall stress
What is the communication interface
Sarcoplasmic reticulum and ryanodine
What is a huge intracellular calcium store in muscles
Sarcoplasmic reticulum
What is heart contraction like
Concentric in the heart
Preload is
The initial stretching of the heart muscle during diastolic filling
Afterload is
The pressure against which the heart must eject to allow systolic ejection e.g ciastoliny blond pressure
What is the law of LaPlace applicable to
Ventricles and blood vessels
What does the law of LaPlace describe doesn’t happen
Heart doesn’t rip given high internal pressures it creates
