Patho Ch22 obj questions

10. Discuss factors influencing the systemic blood pressure and blood flow.

Blood flow: is the amount of fluid moved per unit of time and is usually expressed in liters per minute (L/min) or milliliters per minute (ml/min), or as cubic centimeters per second (cm3/sec). Flow is regulated by the same physical properties that govern the movement of simple fluids in a closed, rigid system--that is, pressure, resistance, velocity, turbulent versus laminar flow, and compliance. Pressure: Pressure in a liquid system is the force excerted on the liquid per unit area and is expressed as dynes per square centimeter (dynes/cm2) millimeters of mercury (mmHG), or units of pressure (torr). Blood flow depends partly on the difference between pressures in the arterial and venous vessels supplying the organ. Fluid moves from the arterial "side" of the capillaries, a region of greater pressure, to the venous side, a region of lesser pressure. Resistance: Resistance is the opposition to force. In the cardiovascular system, most opposition to blood flow is provided by the diameter and length of the blood vessels themselves. Therefore changes in blood flow through an organ result from changes in the vascular resistance within the organ. Resistance in a vessel is inversely related to blood flow--that is, increased resistance leads to decreased blood flow. Poiseuille law shows the relationship among blood flow, pressure, and resistance: Q=P/R where Q=blood flow, P= pressure difference (P1-P2), and R= resistance. Resistance to flow cannot be measured directly, but it can be calculated if the pressure difference and flow volumes are known. Resistance to blood flow in a single vessel is determined by the radius and length of the blood vessel and by the blood viscosity. The most important factor determining resistance in a single vessel is the radius or diameter of the vessel's lumen. Small changes in the lumen's radius or diameter lead to large changes in vascular resistance. Another important factor is the length of the vessel. Resistance to flow is generally greater in longer tubes because resistance increases with length. Blood flow varies inversely with the viscosity of the fluid. Thick fluids move more slowly and experience greater resistance to flow than thin fluids. For example, blood that contains a high percentage of red cells is more viscous. This relationship is expressed as the the hematocrit-the ratio of the volume of red blood cells to the volume of whole blood. A high hematocrit level reduces flow through the blood vessels, particularly the microcirculation (arterioles, capillaries, venules). Resistance to flow through a system of vessels, or total resistance, depends not only on characteristics of individual vessels but also on whether the vessels are arranged in series or in parallel and on the total cross-sectional area of the system. Vessels arranged in series will generally provide less resistance than vessels arranged in parallel. Blood flowing through the distributing arteries, beginning with branches off the aorta and ending at arterioles in the capillary bed, encounters more resistance than blood flowing through the capillary bed itself, where flow is distributed among many short, tiny branches arranged in parallel (Fig 22-28B) . The total cross-sectional area of the arteriolar system is greater than that of the arterial system, yet the greater number of arterioles arranged in parallel leads to greater resistance to flow in the arteriolar system. In contrast, the capillary system has a larger number of vessels arranged in parallel than the arteriolar system, and the total cross-sectional area is much greater; thus there is lower resistance overall through the capillary system. This, plus the slow velocity of flow in each capillary, promotes optimal capillary-tissue exchange. Blood velocity: Blood velocity is the distance blood travels in a unit of time, usually centimeters per second (cm/sec). It is directly related to blood flow (amount of blood moved per unit of time) and inversely related to the cross sectional area of the vessel in which the blood is flowing. As blood moves from the aorta to the capillaries, the total cross-sectional area of the vessels increases and the velocity of the flow decreases. Laminar vs. Turbulent blood flow: Normally, blood flow through the vessels is laminar (laminar flow), meaning that concentric layers of molecules move "straight ahead." Each concentric layer flows at a different velocity (Fig 22-29). The cohesive attraction between the fluid and the vessel wall prevents the molecules of blood that are in contact with the wall from moving. The next thin layer of blood is able to slide slowly past the stationary layer and so on until, at the center, the blood viscosity is greatest. Large vessels have more room for a large center layer; therefore they have less resistance to flow and greater flow and velocity than smaller vessels. Where flow is obstructed, the vessel turns, or blood flows over rough surfaces, the flow becomes turbulent (turbulent flow), with whorls or eddy currents that produce noise, causing a mumur to be heard on auscultation. Resistance increases with turbulence. Vascular Compliance: Vascular compliance is the increased volume a vessel can accommodate for a given increase in pressure. Compliance depend on the ratio of elastic fibers to muscle fibers in the vessel wall. The elastic arteries are more compliant than the muscular arteries. The veins are more compliant than either type of artery, and they serve as storage areas for the circulatory system. Compliance determines a vessel's response to pressure changes. For example, a large volume of blood can be accommodated by the venous system with only a small increase in pressure. In the less compliant arterial system, even small changes in the volume of blood can cause significant changes in pressure within the arterial vessels. Stiffness is the opposite of compliance. Several conditions and disorders can cause stiffness, with the most common being arteriosclerosis.

8. Compare and contrast the structure and function of arteries, veins, and capillaries.

Blood from the left side of the heart flows through the aorta and into the systemic arteries. The arteries branch into small arterioles, which branch further into the smallest vessels, the capillaries, where nutrient exchange between the blood an tissue occurs. Blood from the capillaries then enters tiny venules that form the larger veins, which return venous blood to the right heart. Read in-between red marks on pg 567-569 Arteries: Arterial walls are composed of elastic connective tissue, fibrous connective tissue, and smooth muscle. (All arteries have a THICKER tunica media and a narrower lumen). Read in-between red marks on pg 569 REFER TO FIG 22-20 Veins: Compared with arteries, veins are thin walled and fibrous and have a larger diameter (see fig 22-20). Veins also are more numerous than arteries. The smallest venules closest to the capillaries have an inner lining composed of the endothelium of the tunica intima and surrounded by fibrous tissue. The largest venules are surrounded by a few smooth muscle fibers constituting a thin tunica media. In veins, the tunica externa has a less elastic tissue than in the arteries, so veins do not recoil after distension as quickly as do arteries. Like arteries, veins receive nourishment from the tiny vasa vasorum. Some veins, most commonly in the lower limbs, contain valves to regulate the one-way flow of blood toward the heart (Fig. 22-26). These valves are folds of the tunica intima and resemble valves of the heart. When a person stands up, contraction of the skeletal muscles of the legs compresses the deep veins of the legs and assists the flow of blood toward the heart. This important mechanism of venous return is called the muscle pump. Capillaries: REFER to green marks on pg.569

4. Describe the function and location of the components of the cardiac conduction system.

Refer to page 557-558 (red marks indicate areas I need to read)

5. Identify the components of an electrocardiogram.

READ Pg. 558-559 in-between green lines The normal electrocardiogram is recorded from electrical activity transmitted by skin electrodes and reflects the sum of all cardiac action potentials. The P wave represents atrial depolarization. The PR interval is a measure of time from the onset of atrial activation to the onset of ventricular activation (normally 0.12 to 0.20 second). The PR interval represents the time necessary for electrical activity to travel from the sinus node through the atrium, AV node, and His-Purkine system to activate ventricular myocardial cells. The QRS complex represents the sum of all ventricular muscle cell depolarization. The configuration and amplitude of the QRS complex vary considerably among individuals. The duration is normally between 0.06 and 0.10 second. During the ST interval, the entire ventricular myocardium is depolarized. The QT interval is sometimes called the "electrical systole" of the ventricles. It lasts about 0.4 second but varies inversely with the heart rate. The T wave represents ventricular repolarization. READ 559-560 in-between blue lines

11. Identify the factors that regulate blood pressure.

READ pg 573-578 thoroughly **need to go over this**

12. Discuss the function of the renin-angiotensin-aldosterone system in regulating blood pressure.

READ pg 574-577

3. Diagram the structures of the heart and location of the great vessels.

(Refer to print out)

9. Describe the critical role of the endothelium for vascular function.

All tissues depend on a blood supply and the blood supply depends on endothelial cells, which form the lining, or endothelium, of the blood vessel. Endothelial cells are really quite remarkable in that they can adjust their number and arrangement to accomodate local requirements. They are a life-support tissue extending and remodeling the network of blood vessels to enable tissue growth, motion, and repair. Vascular endothelial cells produce a number of essential chemicals including vasodilators, vasoconstrictors, anticoagulants, and growth factors. The endothelium performs these vital functions through synthesis and release of vasoactive chemicals: Filtration and permeability: Facilitates transport of large molecules via vesicular transport movement through intercellular junctions. Facilitates transport of small molecules via movement of vesicles, through opening of tight junctions, and across cytoplasm. Vasomotion: Stimulates vascular relaxation through production of nitric oxide, prostacyclin, and other vasodilators. Stimulates vascular constriction through production of endothelin and angiotensin II Clotting: Stimulates clotting by inducing platelet adhesion via production of von Willebrand factor, platelet-activating factor, and others. Prevents clotting through production of endogenous anticoagulants such as heparin sulfate. Promotes fibrinolysis via production of tissue plasminogen activating factor (t-PH) and plasminogen activator inhibitor (PAI-A). Inflammation: Expresses adhesion molecules that allow for monocyte and polymorphonucleocyte margination and diapedis. Expresses receptors for oxidized lipoproteins, allowing them to enter vascular intima.

6. Discuss how factors influencing cardiac output reflect cardiac performance; include ejection fraction, preload, afterload, stroke volume, heart rate, and the neurological and hormonal regulation of the heart rate.

Cardiac output: Cardiac performance can be quantified by measuring cardiac output. Cardiac output is the volume of blood flowing through either the systemic or the pulmonary circuit per minute and is expressed in liters per minute (L/min). To determine cardiac output, heart rate (beats per minute) is multiplied by stroke volume (liters per beat). Normal cardiac output is about 5 L/min for a resting adult. Ejection fraction: The ventricle does not eject all the blood it contains, and the amount ejected per beat is called the ejection fraction. The ejection fraction can be estimated by echocardiography and is the stroke volume divided by end-diastolic volume. The end-diastolic volume of the normal ventricle is about 70 to 80 ml/m2, and the stroke volume is about 40 to 60 ml/beat; thus the normal ejection fraction of the resting heart is about 60% to 75%. The ejection fraction is increased by factors that increase contractility (e.g., sympathetic nervous system activity). A decrease in ejection fraction is a hallmark of ventricular failure. Preload: Preload is the volume and associated pressure generated in the ventricle at the end of diastole (ventricular end-diastolic volume [VEDV] and pressure [VEDP]. Preload is determined by two primary factors: (1) the amount of venous return entering the ventricle during diastole, and (2) the blood left in the ventricle after systole (end-systolic volume). Venous return is dependent on blood volume and flow through the venous system and the atrioventricular valves. End-systolic volume is dependent on the strength of ventricular contraction and the to ventricular emptying. Afterload: Left ventricular afterload is the resistance to ejection of blood from the left ventricle. It is the load the muscle must move after it starts to contract. Aortic systolic pressure is a good index of afterload. Pressure in the ventricle must exceed aortic pressure before blood can be pumped out during systole. Low aortic pressures (decreased afterload) enable the heart to contract more effectively, whereas high aortic pressures (increased afterload) slow contraction and cause higher workloads against which the heart must function so it can eject less blood. Increased aortic pressure is usually the result of increased peripheral vascular resistance (PVR), also called total peripheral resistance (TPR). In individuals with hypertension, increased PVR means that afterload is chronically elevated, resulting in increased ventricular workload and hypertrophy of the myocardium. In some individuals, changes in afterload are the result of aortic valvular disease. Stroke volume: Stoke volume, or the volume of blood ejected per beat during systole, also depends on the force of contraction, which depends on myocardial contractility or the degree of myocardial fiber shortening. Three major factors determine the force of contraction: 1. Changes in the stretching of the ventricular myocardium caused by changes in VEDV (preload). 2. Alterations in the inotropic stimuli of the ventricles (Positive: epinephrine and norepinephrine from sympathetic, thyroid hormone and dopamine. Negative: acetylcholine from vagus nerve). 3. Adequacy of myocardial oxygen supply. Heart rate: As described previously, the activity of the SA node is the primary determinant of the heart rate. The average heart rate in healthy adults is about 70 beats/min. This diminishes by 10 to 20 beats/min during sleep and can accelerate to more than 100 beats/min during muscular activity or emotional excitement. In well-conditioned athletes at rest, the heart rate is normally about 50 to 60 beats/min. In highly trained or elite athletes, the resting heart rate can be below 50 beats/min; these athletes also have a greater stroke volume and lower peripheral resistance in active muscles than they had before training. The control of heart rate includes activity of the central nervous system, autonomic nervous system, neural reflexes, atrial receptors, and hormones. Go look at figure 22-17 and READ pg 565 in-between green marks. Nerolgical and hormonal regulation of the heart rate: Go look at figure 22-17 and READ pg 565 in-between green marks.

1.Diagram the circulatory system (refer to print-out), describing the functions of the heart and the pulmonary and systemic circulatory systems.

Functions: Right heart chambers propel unoxygenated blood through the pulmonary circulation, and the left heart propels oxygenated blood through the systemic circulation. (talk through what happens reffering to page 552)

7. Use the Frank-Starling law to demonstrate the interrelationship between preload, afterload, and contractility.

The Frank-Starling law of the heart describes the length-tension relationship of VEDV (preload) to myocardial contractility (as measured by stroke volume). Muscle fibers have an optimal resting length from which to generate the maximum amount of contractile strength. Within a physiologic range of muscle stretching, increased preload increases stroke volume (and therefore cardiac output and stroke work) LOOK AT FIG. 22-16). Excessive ventricular filling and preload (increased VEDV) stretches the heart muscle beyond optimal length and stroke volume begins to fall. Factors that increase contractility cause the heart to operate on a higher length-tension curve (Figure 22-16,curve A). Factors that decrease contractility (Figure 22-16 curve C) cause the heart to operate at a lower length-tension curve. Figure 22-17 illustrates the relationship between VEDV and stroke volume, cardiac output, and stroke work. Increases in preload (VEDV) not only cause a decline in stroke volume, but also result in VEDP. These changes can lead to heart failure. Increased VEDP causes pressures to "back-up" into the pulmonary or systemic venous circulation, where they force plasma out through vessel walls, causing fluid to accumulate in lung tissues (pulmonary edema) or in peripheral tissues (peripheral edema).

2. Describe the cardiac cycle.

The pumping action of the heart consists of contraction and relaxation of the myocardial layer of the heart wall. Each ventricular contraction and the relaxation that follows it constitute one cardiac cycle. (LOOK AT FIGURE 22-5.) During relaxation, termed diastole, blood fills the ventricles. The ventricles fill rapidly in early diastole and again in late diastole when the atrium contracts. The ventricular contraction that follows, termed systole, propels the blood out of the ventricles and into the circulation. Contraction of the left ventricle is slightly earlier than contraction of the right ventricle. The phases of the cardiac cycle can be identified on initiation of ventricular myocardial contraction (LOOK AT FIGURES 22-6 and 22-7). Expulsion of blood from the ventricles marks the end of one cardiac cycle.