Individual muscle cells are able to modify the muscle force development due to the different characteristics, they posses different length, size, diameter and even the composition of the contractile proteins. A muscle fibre contract maximally when the sarcomere is at its normal length, when it is stretch to a higher length, a higher resting tension develops before contraction due to the elastic force of the elastic tissue in the sarcolemma, but the tension during contraction decreases with increase in the muscle initial length.
The load on the heart muscle also have an effect on the tension generation: increase in load will reduces the velocity of contraction (Guyton and Hall 2000). B] Three main sources are available to the muscle cell to replenish the used up ATP. The first one is the phosphocreatine- which carries a high energy phosphate bond. When it is cleaved the released energy will be use to reform ATP from the bonding between ADP and phosphate ion. It is available only for a very short period of time.
The second source is the glycogen that has been stored by the cell; this glycogen is broken down to pyruvic acid and lactic acid to yield energy that is used to convert ADP to ATP. It is also available for a short time during the muscular contraction. The last one is the employment of oxidative metabolism by using oxygen to oxidize various food stuffs to liberate ATP. This is the most widely use during long term muscle contraction. C] No, due to the differences in the make up of the muscle fibres, they cannot utilize these sources equally. They are different in terms of their size, length and diameter.
Some muscle react rapidly while some react very slowly. D] The contraction of the smooth muscle is slightly different from that of the skeletal and cardiac muscle. Though both involve interaction between the contractile elements actin and myosin, but smooth muscle does not possess troponin complex. Initiation of contraction in smooth muscle is as a result of increase in calcium in the cell, this calcium will bind with calmodulin protein and the calmodulin-calcium complex will now activate the myosin kinase and the contraction of muscle starts.
The stimulus for calcium entrance can be hormonal, nerve stimulus or changes in the environment of the muscle fibre. The contraction in smooth muscle is prolonged i. e. very large absolute refractive period, so there is no room for tetanic fade during the contraction. 2A] The electrocardiograph shows that there is complete heart block, in which impulses from the atria does not reach the ventricle. This result in the P wave being completely dissociated form the QRS wave (Guyton and Hall 2000).
Numerous P wave are seen, depicting that the atria is beating rapidly but since the connection between the atria and ventricle have been lost, the ventricle beats at its own natural rate which is slower. This effect is commonly caused by ischemia of the AV bundles as a result of coronary insufficiency; it can also be cause by compression of the bundle of His by scar tissue that was caused by the insufficient arterial supply to the part o the heart. B] The elevated potassium ion surrounding the cardiac cells will cause an increase in irritability of the cardiac muscle which will result into fibrillation.
The build up of potassium ion in the fluid will result in the repolarization refractive period of the myocardial cell. Action potential will be caused by increase in the movement of sodium ion into the cell and movement of potassium ion out of the cell. Build up of potassium in the interstitial space will make the muscle cell membrane to be more susceptible to the incoming depolarization wave even during an ongoing action potential. C] TRUE: insufficient blood supply to the heart will make the heart muscle to be weak, and result into less ability to pump blood in to arterial tree.
This will effect a sympathetic response which will cause an increase in the slope of the depolarising wave of the SA node. 3A] Nitroglycerin is a antiangina drug that is applied sublingually to reduce the effect of the liver on it, it function mainly to dilate and relax the blood vessels which will allow blood flow to the heart to increase and reduces the workload on the heart. B] B1 adrenergic receptor located on the heart is blocked by the B-blockers to reduce the effect of the sympathetic stimulation on the heart. They are very important for the treatment of prinzmetal type of angina pectoris
C] Ca channel blockers act by reducing the heart work through arteriolar vasodilatation and after-load reduction and cause more blood to flow to the heart muscles. They also act to block the entry of calcium ion into the cardiac cell thereby reducing the rate of contraction of the heart muscle 4] Circulatory shock is a situation whereby reduce or no blood is getting to the tissue, this has resulted in the tissue toxicity due to the build up of the toxic waste product that were not carried by the blood out of the tissue.
The shock may be related to low cardiac output of there can be adequate cardiac output and yet the tissues will still be experiencing shock. Shock is divided into 3 stages in order of their chronic effects namely; a] non progressive stage: this stage can be reverse even without external interference, by the inherent compensatory mechanism of the cells. b] Progressive stage: the shock progressively becomes worst if untreated. c] Irreversible stage: in this stage, most of the cardiac cells are gone, so there is no remedy for the patient as all the therapy will be futile.
Shock can be cause by decreased venous return to the heart causing reduction in the cardiac output or excessive body metabolism in which the normal cardiac output is inadequate. There are about four types of shock namely: hypovolemic shock, caused majorly by haemorrhage and fluid loss, anaphylactic shock, caused by the release of histamine and other autacoids into the blood vessels, septic shock which is caused by bacteria infections and neurogenic shock resulting from the increased dilatation of the vessels.
Both shocks are interrelated. Though there are some differences between the shocks that happen to the student and the shock that happen to the patient in emergency situation. There is a sudden vasoconstriction in the student’s blood supply to the brain which resulted into fainting, but the patient’s shock was because of the blood loss, which decreases blood supply to all the vital organs of the man.
Guyton AC and Hall JE (2000): Textbook of Medical Physiology, Membrane Physiology, Nerve and Muscle, 10TH Edition. Pages 71-76. Guyton AC and Hall JE (2000): Textbook of Medical Physiology, The Heart, 10TH Edition. Pages 134-138. Nitroglycerin-sublingual (2005) www. medicinenet . com/nitroglycerin-sublingual/article. htm. Date of retrieval 12th March 2008 from www. medicinenet . com/nitroglycerin-sublingual/article. htm. Rang HP, Dale MM, Ritter JM, Moore PK (2003): Pharmacology, The Heart. 5th Edition Pages 271-272. .