How does the arrangement of muscle fiber sheets contribute to maximal contraction in the left ventricle?
The muscle fibers are arranged in a spiral manner so the base "wrings" toward the apex of the heart as it contracts.
What proteins allow the cytoplasms of adjacent cardiac myocytes to contact each other? What function do these serve?
Connexons. These make up gap junctions in intercalated discs that form the functional syncytium. This syncytium allows for electrical and chemical signal communication during action potentials and contraction.
Why are desmosomes critical structures in cardiac tissue?
Cardiac cells are constantly contracting and desmosomes keep linked cardiac myocytes from ripping away from each other during contraction.
What are the critical components of cardiac myocytes that allow them to function the way they need to?
1) T-tubules studded with Ca++ VGCs 2) Sarcoplasmic reticulum that stores Ca++ 3) 35% of cell volume = mitochondria for ATP demand 4) 50% of cell volume = myofilaments
What structure do t-tubules run on top of?
Why does cardiac tissue not contract in the absence of extracellular calcium.
The action potential travels down the t-tubules and stimulates Ca++ release into cell in response to depolarization. Ca++ binds to the ryanodine receptor. This triggers 100 fold increase in cytoplasmic Ca++ and muscle contraction. Without extra cellular Ca++, the ryanodine receptor could not be opened.
How does the initial power stroke take place when a cardiac cell is stimulated to contract?
Ca++ binds to troponin and causes tropomyosin to expose the myosin binding site on actin. Hydrolysis and release of myosin-bound ATP causes the power stroke. Binding of another ATP to myosin resets the process and it continues as long as Ca++ is present.
How is cardiac muscle contraction stopped during diastole?
SERCA (Sarcoplasmic Reticulum Calcium ATPase Pump) pumps intracellular Ca++ back into the SR. There is also an Na-Ca exchange pump that pumps a small portion of Ca++ extracellularly.
What four factors contribute to cardiac performance?
Preload, afterload, contractility and rate/rhythm.
Why does the heart tend to have better contractility when there is greater filling during diastole? What is this concept called.
Filling of the heart causes stretching of the sarcomeres. This exposes more troponin-C that can be bound by Ca++ during systole, producing a stronger contractile force. The filling and stretching to produce better contraction concept is called Preload.
What equation is a function of after load?
Law of La Place where T=tension, P=pressure, r=radius and h=wall thickness. Afterload is the tension in the chamber wall during contraction. The law of La Place comes in because as the ventricle contracts, the wall gets thicker and tension decreases as contraction continues. This means it is easier to eject blood as systole continues.
Is maximizing preload and afterload a good thing?
No. You want to maximize preload to maximize contractile force and minimize afterload to allow maximum expelling of blood from the ventricle.
What is contractility?
The strength of contraction for a given preload and after load. It is entirely dependent on calcium levels.
How do beta-adrenergic receptors increase contractility when they are stimulated?
Stimulation -> G-protein ->Adenylyl Cyclase -> cAMP -> PKA -> phosphorylates and opens Ca2+ channels, allowing Ca2+ to enter and increase contraction. It also increases uptake of Ca2+ by SR, allowing for faster recovery during diastole so the cell is ready to contract again in a shorter period of time.
How does increasing heart rate increase cardiac output?
1) more bpm = more systoles 2) with every systole, more Ca2+ enters the cardiac myocytes and get taken up by the SR (Force Frequency Relationship)