NROSCI/BIOSC 1070 and MSNBIO 2070 September 18 & 20, 2017 Cardiovascular 3 & 4: Mechanical Actions of the Heart and Determinants of Cardiac Output An essential component for the operation of the heart is the action of the valves. The valves insure that blood moves in only one direction. The opening and closing of the heart valves is controlled simply by the pressure gradients on the two sides of the valves. The two arteriovenous (AV) valves, the tricuspid and mitral valves, are comprised of flaps of connective tissue. On the ventricular side, the valves are attached to collagen cords called the cordae tendinae. The opposite ends of the cords are attached to the moundlike extensions of ventricular muscle called papillary muscles. The cordae tendinae prevent the flaps of the valve from getting stuck against the ventricular wall during ventricular filling and from being forced into the atria during ventricular systole. In contrast, the aortic and pulmonary semilunar valves have three cuplike leaflets that fill with blood, and which snap closed when backward pressure is placed on them. Special tethering such as the chordae tendinae are not required to insure that the semilunar valves close properly. The closing of the heart valves generates vibrations, which result in the heart sounds that physicians often monitor during examinations. The major heart sounds are commonly referred to as “lub-dub”. The softer “lub” is associated with closing of the tricuspid and mitral valves, and the “dub” comes from the closing of the semilunar valves. Careful assessment of the heart sounds can be done using a stethoscope; the procedure is referred to a auscultation. Through careful monitoring, two additional heart sounds are revealed. The third heart sound is associated with turbulent blood flow into the ventricle near the beginning of ventricular filling, and the fourth heart sound is produced by additional turbulent flow into the ventricle during atrial contraction. The heart sounds become abnormal if the valves are diseased. Two general types of abnormal heart sounds can be classified: a murmur and a gallop. Murmurs are heart sounds in addition to the four that are normally present, and gallops are augmented third or fourth heart sounds. Murmurs often occur when valves fail to close properly, producing regurgitation or movement of blood in the wrong direction. For example, if an AV valve does not close properly, blood will move from the ventricle into the atrium during systole. This turbulent movement of blood can be heard as an additional heart sound. Gallops often occur when the AV valves do not open properly or are narrowed (stenosed), resulting in excessive turbulence during movement of blood from the atria into the ventricles. Gallops can also occur when the ventricles are very stiff. 9/18/17 & 9/20/17 Page 1 Cardio 3-4 Clinical Notes: Echocardiography The beating heart can be imaged in real time using echocardiography. This technique employs ultra- sound that is emitted from a piezoelectric crystal. The waves are reflected back to the crystal, and re- sult in the production of electric impulses that are recorded. The characteristics of the reflected waves are dependent on the properties of the tissue that the waves pass through. A computer can interpret the electrical impulses generated by the vibrating pizoelectric crystal, and construct an image from these signals. There are three general placements for the echocardiograph transducer: • Transthoracic echocardiogram (TTE), in which a transducer is moved over dif- ferent locations on the chest or abdomen. • Transesophageal echocardiogram (TEE), in which the transducer is passed down the esophagus to provide clearer pictures of the heart. • Intracardiac echocardiogram, in which the transducer is inserted into the cardiac vessels. The following diagram shows two common planes imaged using transthoracic echocardiography: 9/18/17 & 9/20/17 Page 2 Cardio 3-4 Another way of describing the cardiac cycle is through a pressure-volume graph. Between points A and B in this graph, the ventricles are filling with blood. The AV valves open when the pressure in the atria exceeds that in the ventricles. After the AV valves open, ventricular pressure increases slightly as vol- ume increases. At the end of this part of the cardiac cycle, the atria contract and the ventricles contain the maximal amount of blood that they will have during the cardiac cycle (end diastolic volume, shown at point B). Note that although end diastolic volume is typically about 135 ml, it can be more or less under certain conditions. For example, when heart rate is very high (and filling time is low), end diastolic volume often drops. When cardiac return increases, EDV also increases. In the next phase of the cardiac cycle, the ventricles begin to contract. Very rapidly, pressure in the ventricles exceeds that in the atria and the AV valves close. Subsequently, ventricular pressure increases but ventricular volume stays constant (hence, an isovolumetric contraction). When pressure in the ventricles is great enough, the semilunar valves open and blood is ejected into the aorta and pulmonary arteries (point C). Ventricular pressure continues to increase while ventricular volume drops. Eventually, the ventricles begin to relax, and the semilunar valves close. Note that ventricular volume is not zero at this time, but instead end-systolic volume is about 65 ml. This volume is variable, however, and can decrease if ventricular contractility increases. The ventricle then relaxes, but because the ventricular pressure exceeds atrial pressure the AV valves are closed. This is the isovolumetric relaxation phase of the cardiac cycle. When ventricular pressure drops below atrial pressure, the AV valves open and ventricular filling starts again. Note that if MAP increases, more pressure is needed in the left ventricle to open the aortic valve. Ejection fraction (EF) is defined as the fraction of end diastolic volume that is ejected out of the ventricle during each contraction. EF = SV/EDV If SV=70ml and EDV=135ml Then EF=70/135 or 0.52 9/18/17 & 9/20/17 Page 3 Cardio 3-4 Yet another means of depicting the cardiac cycle is shown above. This diagram includes both electrical and mechanical events that occur in the heart. Such a diagram is called the “Wiggers diagram” after the physiologist who first published it (Carl Wiggers). We have not discussed one pressure tracing in the Wigger’s diagram: a recording of pressure in the left atrium. Three waves are evident: the a, c, and v waves. The a wave is caused by atrial contraction. The c wave is caused by ventricular contraction, and is due to 1) the small backflow of blood from the ventricle to the atrium when the mitral valve closes and 2) the bulging of the closed mitral valve backward into the atrium when ventricle pressure increases. The v wave is due to blood flowing from the veins into the atrium during ventricular contraction, which cannot leave because the mitral valve is shut. When the mitral valve opens, atrial pressure drops, demarking the peak of the v wave. It is important for you to understand the relationships between MAP, aortic valve opening, and end systolic volume. If total peripheral resistance increases, then the pressure in the left ventricle must increase more to open the aortic valve (since MAP is higher [MAP=CO*TPR], and the pressure in the left ventricle must exceed that in the aorta for the valve to open). In addition, the valve closes earlier when the ventricle begins to relax. As a consequence, stroke volume diminishes. 9/18/17 & 9/20/17 Page 4 Cardio 3-4 When stroke volume diminishes, there is more blood left in the ventricle at the end of systole (end systolic volume increases). This increased volume is added to the volume transferred from the left atrium to left ventricle after the mitral valve opens. As a consequence, end diastolic volume increases. Thus, the next ventricular contraction is stronger due to the Frank-Starling effect. In essence, if TPR is high, then the heart must work harder and use more ATP to maintain constant cardiac output. Cardiac output is the amount of blood pumped from the ventricles per unit time. As mentioned in the first lecture, cardiac output at rest is about 5 L/min. This value is derived through the following calculation. The resting heart beats at about 70 times/min, and each ventricular ejection is about 70 ml (EDV-ESV). Thus, 70 beats/min * 0.07 L/beat = 4.9 L/min. You should be familiar with the formula to compute cardiac output, and how cardiac output relates to mean arterial pressure. MAP = CO * TPR MAP=(SV*HR) * TPR SV= Stroke Volume HR=Heart Rate MAP=((EDV-ESV)*HR) * TPR Cardiac output can be changed tremendously during some conditions. For example, during exercise it can rise from 5 L/min to 35 L/min. Let us consider how this happens. Obviously, an increase in stroke volume or heart rate can increase cardiac output. During the last lecture, we noted that intrinsic heart rate is actually 90-100 beats/min, but is tonically suppressed to about 70 beats/minute by the parasympathetic nervous system. Thus, one way of increasing heart rate is by “withdrawing” parasympathetic drive on the heart. Heart rate can be increased further by the actions of the sympathetic nervous system. Recall that binding of NE or EPI to beta receptors on autorhythmic cells increases their firing rate, driving heart rate faster. Furthermore, the catecholamines enhance conduction through the AV node, bundle of His, and Purkinje fibers. However, there is an upward limit on heart rate. If the heart beats too rapidly, there is insufficient time for filling. This condition is calledtachycardia .