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Cardiac Function
PittMed: Cardiac Function 1,2,3
| Question | Answer |
|---|---|
| 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
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