Using the new cardiovascular drug Entresto, relate how the Cardiac action potential arriving at the surface of the sarcolema results in the mobilisation of intracellular calcium and subsequent cellular contraction.
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Using the new cardiovascular drug Entresto, relate how the Cardiac action potential arriving at the surface of the sarcolema results in the mobilisation of intracellular calcium and subsequent cellular contraction.
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- Describe the main theories for the termination of calcium sparks in the cardiac muscle excitation contraction-coupling processA 65-year old man with heart failure is unable to climb a flight of stairs without experiencing dyspnea. After several years of therapy with carvedilol, captopril and furosemide, the therapeutic plan probably needs to change now. You empirically add digoxin to improve cardiac muscle contractility. Within 4 week he has a marked improvement in his symptoms. Which of the following best describes the main cellular action of digoxin that accounts for its ability to improve his cardiovascular function? Activates beta1-adrenergic receptors Facilitates GTP binding to specific proteins Increases mitochondrial calcium (Ca++) release Inhibits sarcolemmal Na/K-ATP-aseUnlike skeletal muscle, cardiac muscle doesn’t undergo tetany. Explain how this is achieved and why is this necessary?
- Answer ALL parts of this question. In terms of heart failure there is a decrease in cardiac output. This is due to a contractile deficit in the individual cardiac myocytes. (a) Explain how this contractile deficit occurs. (b) What common cardiac problem is often associated with the changes in calcium handling often seen in cardiac cells of heart failure patients? Explain how this problem arises. (c) Describe the mechanism of action of levosimendan in the treatment of heart failure.Describe the functional significance of the skeletal muscle pump and illustrate the action ofvenous valves.Concisely describe the path of depolarization in the heart, include where the signal for contraction starts and explain why it is functionally important that there is a delay between where depolarization starts in the atria and depolarization in the ventricles.
- Consider the ventricular cardiomyocyte action potential shown below: a) Which phase of the cardiac myocyte action potential would be most significantly affected by the L-type calcium channel blocker nifedipine? b) Draw the predicted effects of nifedipine on the cardiac myocyte action potential.Briefly describe the events of excitation-contraction coupling in cardiac muscle cells.Caffeine lowers the heart rate by increasing rates of depolarization at the SA node True False Nicotine raises the heart rate because it stimulates the activity of the sympathetic neurons in medulla oblongata True False The Frank-Starling Law of the Heart states that the force of heart contraction is directly proportional to the initial length of the muscle fiber, within optimal limits of length True False If the sarcomeres stretched beyond the optimal length, the force of contraction would go down, but that can potentially happen only during open heart surgery when the heart is not constrained by the pericardium, lungs, ribs and diaphragm. True False It is the Na+ channel-driven spontaneous depolarization that is affected by sympathetic and parasympathetic inputs to speed up or slow down the firing rate of the SA node and other conductive cells. True False
- Discuss TWO (2) body surface electrodes that can record the bioelectric potential of the heart activity.Cells in the body have the ability to undergo a transiet depolarization and repolarization. A. Plot the action potential of non-pacemaker cardiac myocyte and indicate what kinds of ion channels involved in each phase and compare ion movement during a myocardial cell's action potential to ion movement of a neuron's action potential. B.Explain why contractions in the cardiac muscle cells are different to skeletal muscle cells.The pressure in the aorta changes throughout the cardiac cycle. During systole, as the heart contracts, the outflux of blood into the aorta causes an increase in pressure, whereas during diastole the pressure decreases as the heart relaxes. A simple model for the aortic pressure waveform is given by the Windkessel effect described by the image below. In this model, the heart is considered a pressure generating pump which is directly connected to an elastic compartment (the aorta), which in turn is connected to a rigid set of peripheral vessels (the hose of the firefighter). 5 Pump Heart Air Windkessel Elastic arteries In order to find the aortic pressure waveform from the Windkessel model, a mass balance formulation around the aorta must be formulated. Coming into the aorta from the heart we have the flowrate Q(t). According to conservation of mass, this inflow rate Q(t) must be equal to the outflow rate into the peripheral vessels and the change in volume of the aorta. To find these…
