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Cardiac Function

PittMed: Cardiac Function 1,2,3

QuestionAnswer
What are the two phases of ventricular systole? Isovolumic contraction and ventricular ejection
What are the two phases of ventricular diastole? isovolumic relaxation and ventricular filling
In an electrocardiogram, the P wave and the QRS complex represent what two depolarizations? P wave = atrial depolarization; QRS = ventricular depolarization
Describe the relative pressures of the left ventricle, the aorta, the left atrium, and the states of the mitrial and pulmonic valves during ventricular filling pressure of LV < aortic pressure and < left atrial pressure; mitrial valve open, aortic valve closed
Describe the relative pressures of the left ventricle, the aorta, the left atrium, and the states of the mitrial and pulmonic valves during isovolumic contraction atrial pressure < pressure of LV < aortic pressure; both valves closed
Describe the relative pressures of the left ventricle, the aorta, the left atrium, and the states of the mitrial and pulmonic valves during ventricular ejection LV pressure > aortic pressure and > LA pressure; mitrial valve closed, aortic valve open
Describe the relative pressures of the left ventricle, the aorta, the left atrium, and the states of the mitrial and pulmonic valves during isovolumic relaxation LV pressure < aortic pressure and > LA pressure; both aortic and mitrial valves open
Describe the cardiac cycle main events Vetricular filling, isovolumic contraction, ventricular ejection, isovolumic relaxation
What are the two components of ventricular filling? Passive filling (blood flows from higher pressure of LA to the lower pressure chamber of LV) and Active filling (atrium contracts during late diastole)
EDV End-diastolic volume: max ventricular volume at time of filling
ESV End-systolic volume: min ventricular volume at the end of ejection
SV Stroke volume: EDV - ESV; the volume ejected from the ventricle
EF Ejection fraction: EF (%) = 100*SV/EDV
Intercalated disks Specialized junctions that connect muscles cells; allow ions and electrical current to pass through without hindrance
Functionally, cardiac muscle is a ___; when one of the cells gets excited, the action potential spreads rapidly to all cells in the latticework syncytium
What is the basic contractile unit of the heart? sarcomere
Describe the composition of the thin filaments of the sarcomere of the heart Actin monomers (G actin) linked in chain structure forming 2 helically arranged polymer strands; troponin and tropomyosin are regulatory proteins that regulate cardiac muscle contraction
Describe the composition of the thick filaments of the sarcomere of the heart made of myosin molecules (dimers), which have long tail and protruding head called cross-bridge; thick filaments have addtional proteins including elastic protein called titin
What interaction is responsible for the main molecular motor of the heart and muscle cells? Actin-myosin interaction
What two main events trigger cardiac contraction? Thin filament activation and actin-myosin interaction
Describe the (4) steps required for thin filament activation (1) Action potential enters from adjacent cell (2) voltage gated Ca++ channels open, Ca++ enters cell (3) Entry of Ca++ triggers release of Ca++ from SR (4) Most of Ca++ comes from SR to bind to troponin (C) to initiate contraction
Describe the steps require for actin-myosin interaction (after Ca++ binds troponin C) (1) myosin head interacts with unblocked actin site (2) unbinding of myosin and actin (3) cocking of the myosin head (4) binding of myosin to actin (5) power stroke (6) rigor/low energy form (7/2) back to step 2
How does myosin become unbound from actin? ATP enters the ATPase site on myosin and causes myosin that is bound to detach
How does the myosin head become cocked? ATP bound on myosin ATPase site hydrolyzed to ADP and Pi (products still bound to myosin); some of the hydrolysis energy capture by myosin, prompting it to go to high energy / cocked state
How does the myosin bind to actin after entering the cocked position? myosin head binds o neighboring actin-->inorganic phosphate is released from myosin ATPase site
How does the myosin complete the power stroke? Release of inorganic phosphate transitions the myosin from the cocked (high energy) position to the low energy state; as it is still bound to actin at this point, the conformational change pulls the actin with it; ADP is released at this point
How does the myosin enter the rigor phase? By the end of the power stroke, myosin has lost ADP and is back to the low energy state; it is still bound to actin
Rigor mortis (explain physiology in terms of the actin-myosin interaction) Stiffening of the body: cross bridge cycle gets stuck in the rigor part in the absence of ATP hydrolysis
The contractile activity originates from the pulling of ____ filaments by the ___ ___ bound to actin and the energy needed for this is derived from ATP hydrolysis by ___ ___ase. thin filaments, myosin heads, myosin-ATPase
What two mechanical components determine the intensity of contraction? number of bound cross-bridges in the post power stroke state and the amount of force generated by each cross-bridge (gennerally assumed constant)
What are the 4 basic ways of augmenting the intensity of contraction of a sarcomere? (1) increase sarcomere length (2) increase cystosolic Ca++ levels (3) increase thin filament activation (4) alter the kinetic rate constants of cross-bridge cycling
How would increasing sarcomere cell length alter the intensity of contraction? Would increase it by altering the overlap between thin and thick filaments-->increased pool of cross bridges for actin myosin interaction and affects myofilaments Ca++ sensitivity
How would increasing cytosolic Ca++ levels alter the intensity of contraction? Higher Ca++ produce greater thin filament activation sites, allowing for greater umber of possible cross-bridges, leading to more intense contractions
How do most ionotropic drugs function? Function by increasing the intracellular levels of Ca++, leading to an increase in thin filament activation, leading to an increase in contractility
How would increasing thin filament activation alter the intensity of contraction? Changes in rate constant associated with Ca++ binding and unbinding to troponin lead to increased activation (more binding results in more available sites for myosin head to form cross bridges-->increased contractility)
How would altering the kinetic rate constants of cross bridge cycling alter the intensity of contraction? Altering the constants such that the number of cross bridges in the post-power stroke increase (i.e. decrease in rate constant of cross-bridge detachment)
Describe the process by which cardiac sarcomeres relax Ca++ unbinds from troponin and is transported back into SR via ATP dependent pump (Ca++ - ATPase); Ca++ removed from cell in exchange for extracellular Na via Na+-Ca++ exchanger in sarcolemmal membrane
When pumping out Ca++ from sarcomere via the Na+/Ca++ exchanger, what additional protein helps maintain the Na+ gradient? The Na+/K+ ATPase on cell membrane (pumps K+ in and Pumps Na+ out)
Created by: karkis77