Outline the Effects of the Sympathetic Nerves on the Heart

Outline the effects of the sympathetic nerves on the heart?

Sympathetic nerves act as part of the reaction to the ‘fight, fright or flight’ scenario. The nerves are distributed not only to the sinoatrial and atrioventricular nodes but also to the cardiac muscle of both ventricles and atria. The effects of sympathetic innervation can be broken down into increasing the heart’s rate of pumping and also increasing the heart’s strength of contraction. The sympathetic nerves release noradrenaline at their junctions. Sympathetic activity also causes adrenaline to be released from the adrenal medulla. Both these neurotransmitters bind to β1 adrenoreceptors in the SA node. This process increases cAMP levels in the cell and results in a faster increase in sodium and calcium permeability during the pacemaker stage of the potential and thus producing early action potentials. Hence more action potentials can occur in a set time and the rate of firing of the SA node determines the rate of contraction in the heart and so this increases as well. Sympathetic fibers also innervate the atria, AV node, Purkinje fibers and ventricular muscle. Their effect here is mostly to increase the speed of conduction. The AV node delay is decreased and the action potential duration itself is shortened. This shorter cycle is caused by sarcolemmal increases in permeability to potassium and calcium ions and a more rapid uptake of calcium ions in to the sarcoplasmic reticulum. The other effect of the sympathetic innervation in increasing contractile strength and ejection velocity is explained by the increased permeability to calcium ions which are essential for the contraction process. In this way cardiac output can be increased by up to 100%. Under normal conditions the sympathetic stimulation has the heart pumping at about 30% of a higher rate than it would do without stimulation.

Explain the effects of parasympathetic nerve activity on heart rate.

The parasympathetic nerve system is associated with energy conservation and the normal activity of the body. Parasympathetic activity decreases the heart rate. Both sympathetic and parasympathetic systems are tonically active in the heart but the latter is more active in humans at rest and reduces the rate from about 100 to 70 beats per minute. Since the vagus transmits the parasympathetic fibers, the heart is described as having vagotonic tone. The vagus has fibers distributed to the AV and SA nodes as well as the atria. The system releases acetylcholine at its junctions and this acts on muscarinic cholinoceptors in the SA node to hyperpolarize and slow the rate of pacemaker potential depolarization. The hyperpolarization is achieved by a decrease in cAMP activity which is triggered by the muscarinic receptors which inhibit adenylate cyclase via the G protein. This decrease in cAMP causes additional potassium channels to open, and reductions in the permeability to calcium and sodium ions reduces the slope of the pacemaker potential. This response is faster to occur than sympathetic stimulation. Parasympathetic fibers also innervate the atria and the AV node where it increases the AV node delay. The action potential duration itself is lengthened by parasympathetic activity. Although parasympathetic innervation via the muscarinic receptors decreases atrial contractility it does not affect ventricular contractility. This reinforces the notion that the main effect of parasympathetic innervation is to reduce heart rate and hence cardiac output.

Discuss the mechanisms used by the body to increase cardiac output.

Cardiac output is the volume of blood pumped per minute by each ventricle. It is the product of stroke volume and heart rate. Thus to increase the cardiac output, one must increase either of these two elements. To increase, heart rate, sympathetic stimulation can increase the rate of firing in the SA node and also the rate of conduction of action potentials in the heart’s conducting system and this increases the heart rate. On the other hand, stroke volume is subject to intrinsic and extrinsic control. Intrinsic control causes the heart to respond with a greater force of contraction, ejecting a larger stroke volume when end diastolic volume increases according to Starling’s law of the heart. EDV can be altered by events in the chest and changes in blood volume or venous capacity. More negative intrathoracic pressure than normal such as occurs on large inspirations will increase EDV. An increased venous return when one changes from standing to reclining will do the same. A moderate increase in heart rate increases end-diastolic volume due to an increase in atrial contractility. Very high heart rates are more complicated. A very high heart rate reduces the time available for filling and so end diastolic volume has a tendency to fall. The increase in myocardial contractility increases the rate of ventricular relaxation and this increases the rapid phase of ventricular filling. On balance the end diastolic volume remains about the same and so cardiac output increases. Increased volumes in the ventricle produce stronger contractions as the cardiac muscle fibers are normally at a less than optimal state before contractions. Increased volumes bring the fibers closer to the optimal position and thus contractile strength increases. This control is limited as the ventricle can only stretch to a limit before one exceeds the optimal position. Extrinsic control is dependent on sympathetic controlled calcium entry into muscle fibers which enhances myocardial contractility and ejection velocity.

Draw an ECG trace and briefly explain the origin of each wave.

The first wave in an ECG is the P wave. This is caused by atrial depolarization. The SA node produces action potentials which spread throughout the atrial muscle which then depolarizes as a synctium. The action potential causes the opening of fast sodium channels and slower calcium channels with a decrease in permeability to potassium ions which depolarizes the membrane. The inside of the cell thus becomes positive and the outside is also reversed to become negative. The P wave is soon followed by atrial contraction. The next wave is the QRS complex. This is the product of depolarization of the ventricles. The complex hides the repolarization of the atrium which happens almost simultaneously. Thus while the atria are relaxing the ventricles start to contract. The Q and S parts are negative because their vectors are directed to the right. The S wave is directed upwards and to the right because the last part of the myocardium to be depolarized is the base. The T wave then corresponds to the ventricular repolarization due to the action of slow acting potassium channels which leak potassium ions out of the cell and cause it to repolarize. The PQ interval is the time taken for excitation to spread through the atria, AV node and bundle of His. The QT and PS intervals are measurements of the duration of ventricular and atrial action potentials. The reason for the dip before the spike in the QRS complex is because as ventricular depolarization begins at the IV septum which depolarizes from left to right, it gives a vector directed downwards to the right.

How do myocardial autorhythmic cells generate spontaneous depolarizations?

The resting membrane potential of the cells of the SA node is between -55 to -60 mV which is less than normal. The lower negativity is caused by the leaky nature of the membrane of there cells which allow sodium and calcium ions to enter and thus reduce the negativity of the cell interior. Although most of the fast sodium channels are closed, the leaky membrane and the high sodium concentration outside the cell causes further sodium entry and when the membrane depolarizes to about -40mV, the sodium-calcium channels open. Thus the depolarization process quickens up until potassium channels open and cause repolarization as positive potassium ions leave the cell. At the same time as the opening of the potassium channels the sodium-calcium channels close. Thus a state of hyperpolarization is obtained but the potassium channels gradually close and the leaky membrane lets the sodium and calcium ions in again until the threshold is again reached and another action potential is released. The rate of action potentials in the SA node is higher than in the other autorythmic cells and so it is referred to as the pacemaker of the heart.

Explain how heart sounds are generated during a cardiac cycle.

Heart sounds are caused by the closure of valves in the heart. The first heart sounds are caused by the closure of the AV valves, the bicuspid or mitral and tricuspid valves respectively. These are opened by the pressure building in the atria as they fill with blood to allow filling of the ventricle. When the ventricle is filled, however, the ventricular muscle begins to contract and an effect of the rising pressure in the ventricle is the closure of the AV valves. This produces the first heart sound. After this blood is ejected through a second set of valves, the semilunar valves of the pulmonary trunk and aorta. However when the blood is ejected, the pressure in the ventricle begins to fall rapidly as the muscle relaxes. For a moment, the pressure in the aorta and pulmonary trunk is higher than that in the respective ventricle and thus a reflux of blood occurs in the direction of the heart. This causes the semilunar valves to collect the blood into their sinuses and they close. This causes the second heart sound, which is shorter due to the more rapid closure.

Describe the responses of the cardiovascular and respiratory systems to exercise.

What property of the sino-atrial node makes it the normal pacemaker of the heart?

The slope of the pacemaker potential in the SA node is steeper than in the AV node. Therefore the SA node triggers its action potential first and is the pacemaker from which the heart beat originates. The action potential arrives in the AV node well before the pacemaker in the AV node has reached its threshold and thus is triggered to activation by the AV’s rate of pulsation.

With the aid of a diagram, clearly indicate the pressure changes that occur in the right side of the heart during a cardiac cycle.

The right atrium has a negative pressure at the end of its ejection of slightly below zero. This allows a pressure difference for venous blood return from the capillaries and veins which drain the tissues. It rises to about 2mmHg due to blood from the veins accumulating behind a closed AV valve. This is signified by the v wave on the diagram. When right ventricular pressure drops to below this, the AV valve opens and the blood enters the ventricle. This corresponds to the y descent in the graph. Atrial contraction in response to depolarization occurs in late diastole and this contributes the final 20% to ventricular filling. This is signified by the a wave in the graph. Soon after this the ventricle starts to contract. When it reaches a greater pressure than the right atrium, the tricuspid valve is forced to close. The bulging of the AV valve back into the atrium causes its pressure to rise to about 5mmHg, known as the c wave. Then, after the isovolumetric contraction period, when ventricular pressure exceeds pulmonary pressure the pulmonary valve opens and blood is ejected. The pressure recorded in the pulmonary trunk is 8mmHg in diastole and 25mmHg in systole. The AV fibrous rings are pulled down during this ejection and this leads to the x descent in the atria. The ventricles soon relax again and pressure drops leading to the closure of the pulmonary valve and the opening of the AV valve again.

Explain the changes that occur in each of the following when sympathetic nerves to the heart are activated:

(a) R-R interval This refers to the time taken for one full cycle in the ECG to occur. The interval is reduced as the rate of firing in the SA node increases due to noradrenaline activating a cAMP second messenger system in the cells which increases the cells permeability of sodium and calcium ions. Thus a higher firing rate increases the number of ECGs recorded in a set time. The length of the ECGs themselves also decreases due to the increased conduction speeds and shorter action potentials in the electrical conduction system of the heart, in the AV node and purkinje fibers etc. Thus the interval between two R waves is reduced by both these effects.

(b) P-R interval This refers to the time taken for depolarization to spread from the atria to the ventricles. This time is shortened because the conduction speeds of the atria and the AV nodes as well as the purkinje fibers and the ventricles are all increased under the influence of sympathetic innervation. The action potential time itself and the AV node delay are both reduced and so the time between atrial and ventricular depolarizations is reduced.

(c) duration of systole Systole refers to the contraction of the ventricles and their emptying of blood into the aorta and pulmonary vessels. The length of contraction is dependent on the time between ventricular depolarization and repolarization. This time interval would decrease because of the increased permeability to potassium and calcium in the sarcolemma.

Outline the changes that occur in the cardiovascular system when one changes from a supine to an upright position.

When this change occurs, the blood pools in the legs and so venous return is reduced to the heart. Venous return determines end diastolic volume and this in turn determines stroke volume. Hence if blood pools in the legs, cardiac output via stroke volume is reduced.

Discuss the factors that can aid venous return to the heart.