Heart As A Pump 1 Flashcards
Whaat are the 3 major types cardiac muscle?
- Atrial muscle
- Ventricular muscle
- Specialized excitatory and conductive muscle fibers
Summarize how cardiac muscle contracts
The atrial and ventricular types of muscle contract like skeletal muscle except, the duration of contraction is much longer.
The specialized excitatory and conductive fibers exhibit either automatic rhythmic electrical discharge in the form of action potentials or conduction of the action potentials through the heart. This is the excitatory system that controls the rhythmical beating of the heart. This conducting system is be discussed in the cardiac action potential lecture.
Contrast cardiac and skeletal muscle
- Form branching network of cells (separated by intercalated discs)
- Low resistance gap junctions which allow action potentials to spread from cell to cell
- Tetanic contractions are not possible because of long refractory period of cardiac action potentials
This features identified allows the contracting cardiac muscle to function as a synctium, thus allowing it to operate as a pump
What are determinants of myocardial performance?
- preload
- afterload
- Contractility
Explain preload
The degree of tension or load on the ventricular muscle when it begins to contract/at the end of diastole. It cannot be measured directly. Instead indices such as left ventricular end-diastolic volume and left ventricular end-diastolic pressure are measured directly. The preload can be explained on the basis of change in sarcomere length.
Explain after load
The load that the heart must eject blood against. It is the pressure in the aorta leading from the ventricle. The afterload of the ventricle corresponds to the systolic pressure described by the phase III curve of the volume-pressure diagram. The best ‘marker’ of afterload is systemic vascular resistance also called peripheral resistance
Explain what is contractility
Change in performance at a given preload or afterload. Change in force of contraction at any given sarcomere length. Acute changes in intracellular calcium and drugs can alter the contractility. Contractility affects the rate at which a muscle can develop active tension. Ejection fraction is the best index of contractility.
Describe the mechanics of cardiac muscle contraction
Cross bridge contraction enables a muscle to develop force (isometric contraction) or to shorten (isotonic contraction). Which one it does depends on the phase of the cardiac cycle.
During Isovolumetric phase (inlet and outlet valves are closed) contraction is isometric and ventricle develops a force (tension ) but there is little or no shortening of the muscle fibers
Once aortic valves are open, contraction becomes isotonic and ventricles shorten and eject blood
Summarize isometric contractions mechanisms
- Stretching myocardial muscle fibers will increase the active tension it can develop-up to a point.
- Lmax is the optimum muscle length at which maximum tension can occur. Cardiac muscles operate around 50% Lmax
- small changes in myocardial muscle fiber length—> large changes in active tension
- Cardiac muscle is much stiffer than skeletal muscle (resting tension is much greater)
- Good thing that cardiac muscle is not too distensible otherwise it may distend too much
What is resting tension ?
Force required to stretch a resting muscle to different lengths
What is active tension?
When a muscle is stimulated to contract whilst it’s length it’s held constant, it develops an additional force called active tension
What is peak isometric tension?
The total tension developed(active and passive)
The amount of active tension developed by a cardiac muscle during an isometric contraction depends on the initial myocardial muscle length. Stretching the resting myocardial muscle fiber before it contracts will increase the amount of tension it can develop
How do we calculate total tension?
Peak isometric tension/ total tension= resting tension + active tension
Summarize isometric contraction
- As the resting muscle fiber is stretched, tension developed increases—> increases force of contraction
- Length-dependent change in sensitivity of the myofilaments to calcium. (As muscle length is increased ability of TN-C to bind Ca is increased) Results in optimal overlap between actin and myosin filaments (as in skeletal muscle)
- Resting muscle fiber length is increased by increasing the load on the muscle (before it contracts). This load-termed preload
- Increased preload—>. Increased force of contraction
How would changes in contractility affect isometric tension?
Increased contractility
-At a particular muscle length, NE makes the myocardium contract with a greater force. This is described as an increase in contractility or a positive inotropic effect
What is inotropism?
Inotropism (contractility) is a change in active force development in the absence of a change in preload (I.e. resting muscle length)
Summarize sympathetic effects on inotropic actions
Increasing the resting length of a myocardial fiber will increase the tension developed when the fiber contracts. Length-tension relationship
-Sympathetic activity via NE and B1 activation increases the contractility of the myocardium I.e. in the presence of NE the myocardial fibers develop a greater tension from the same myocardial muscle fiber length
Common confusion- the term contractility refers to how efficiently the myocardium contracts from a given myocardial muscle length. NE increases contractility and is therefore described as having positive inotropic actions
Describe length-tension relationships in isotonic contractions
In this type of contraction, muscle fibers contract against an “afterload” . Initially the fibers need to develop an isometric tension (force) that is equal to the afterload, and once that is achieved the muscle can then shorten. When the muscle actually shortens the tension in the muscle doesn’t change (i.e. isotonic)
What are the effects of increasing contractility with Norepinephrine in isotonic contractions?
Sympathetic activity via NE & B activation shifts the peak isometric tension curve up and to the left. When the heart now contracts isotonically it is able to shorten more in the presence of NE.
Positive inotropes shift the isometric length-tension curve to the left (and up) thereby increasing the extent of shortening of muscle at any given set of preload and afterload
The smaller the afterload…
The faster the shortening velocity
If the muscle is stretched(increased preload)…
The velocity of shortening is greater
Describe velocity relationships effects changing preload on velocity shortening
A positive inotrope allows cardiac muscle, at any given length (preload) to move a heavier load faster than that possible with normal myocardium at the same preload
Vmax represents max rate of Crossbridge cycling
Note: increasing contractility in cardiac muscle will increase Vmax. So Vmax in cardiac muscle is NOT constant (unlike skm)
Positive inotropes increase Vmax, negative inotropes decreased Vmax
Give a brief overview of the Frank-sterling experiment
Investigated pressure and volume changes in the whole isolated heart in the early 1900s
Pressure changes is equivalent to tension changes in the myocardium
Volume changes results in changes in length of myocardial fibers
What are the results of Frank starlings results?
The intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called the Frank Starling mechanism of the heart
This led to Starling’s heart: As EDV, increasesstroke volume increases
