Chapter 6: The Cardiovascular System and Its Control

Transcription

1 Part II: Cardiovascular and Respiratory Function (6 th Edition) Why do we need cardiorespiratory systems? As organisms became more complex, lost touch with the environment---beyond simple diffusion! Chapter 6: The Cardiovascular System and Its Control Function of the cardiovascular system-reaches every cell in the body Delivery-O 2 and nutrients Removal-CO 2 and metabolic wastes Transports-hormones Thermoregulation Maintenance-body s ph via blood buffering & overall body fluid balance Immune function Structure and Function of the Cardiovascular System Any system of circulation requires: 1-a pump (heart), 2-a system of channels (blood vessels), and 3-fluid medium (blood) Primary goal is to meet the metabolic demand of the tissues I. The Heart Basic Anatomy (example of structure/function, i.e. size of chambers, thickness of walls, valves insure unidirectional flow)[fig 6.1] A. Blood Flow through the heart 1. By this point in your career you should be able to easily trace a drop of blood from left ventricle back to the left atrium identifying any major structure (vessels, chambers and valves) 2. Mitral valve prolapse-example of retrograde flow of blood 3. Heart Murmur B. The Myocardium (collective name of cardiac muscle) 1. Cardiac muscle fibers (striation is similar to skeletal muscle [Figs ]) are anatomically interconnected end-to-end by facilitates spread of action potential so all fibers contract with each beat-why? a. Receives nutrients and has waste products removed by the coronary circulation (Fig 6.4) (1) Right coronary supplies the right side of the heart; divides into two primary branches, the and artery (2) Left coronary artery supplies the left side of the heart; divides into two major branches, the and the (LAD) b. Where do the right and left coronary artery originate? Does this have any effect of coronary blood flow? 2. Cardiac muscle contraction (Fig 6.2) a. calcium-induced calcium release (1) During the action potential, calcium enters the sacolemema of the heart cell by the dihydropyridine receptors in the. (2) This calcium binds to the ryanodine receptor on the, causing release of the calcium that is stored in the SR 3. Strength of contraction is controlled by concentration of intracellular Ca ++ [i.e., that stored in the SR](unlike skeletal muscle that is all-or-none and contracts maximally and controls tension by recruitment and frequency of MU firing and thus relies on increasing the total number of fibers contracting.). Remember, all cardiac muscles contract with each beat! WHY? Because it would not be effective in pumping blood is only some of the Page -1-

2 fibers contracted-just thing if only the fibers in the base of the ventricle would contract it would propel some of the blood toward the valve and some retrogradely back towards the apex. a. Amount of Ca ++ entering cell depends on the magnitude of the AP and thus the neural/hormonal activation that effects the AP and/or calcium channels. (Fig 6.2) b. As noted above, entering the myocardium does not bind to Troponin-C, but instead stimulates the release of SR Ca ++.(Which in not stored in the larger volumes that is seen in skeletal muscle SR). (1) The above mentioned Ca ++, if not removed from the cell, is then taken up by the SR for release on the subsequent beat(s) (a) Thus, the amount of Ca ++ entering the myocyte has the potential to alter the number of cross-bridges, and thus force of contraction!!!!!!!!! (2) If experimentally, or pathologically, there is a decrease if extracellular Ca ++, then less Ca ++ will enter the cell, less will be taken up by the SR, and therefore the subsequent force of contraction will be decreased because fewer cross-bridges will be formed (3) So, to summarize: ALL cardiac cells contract with each beat of the heart. As such, increasing the number of cardiac cells contracting is NOT a mechanism to increase the strength of contraction that in needed during exercise. To increase the strength of contraction, more Ca++ is needed in the SR. One way this is accomplished is by, for example, epinephrine, which binds to Beta receptors opening Ca++ channels and permitting more CA++ to enter the cell (SR). Then, in subsequent beats, more Ca++ is released from the SR and thus saturates more Tropin-C eventually leading to increased cross-bridge formation and thus increased tension (strength) development of the myocardium. Keep in mind two things eventually more Ca++ leaves the cell than enters the cell (and thus returns the strength of contraction to resting conditions. And, there is a price to pay for this increased tension development more need for oxygen!!!!! (Think supply-demand balance). In your very healthy hearts, this increase in demand is easily met by an increase in coronary blood flow. BUT, in a person with CAD, the increased demand is not met by an increase in flow, and can result in a myocardial infarction. (Oxygen demand < supply). To prevent this imbalance from occurring, physicians sometime try to keep oxygen demand from increasing; that is, they prescribe the patient either a Beta blocker, or a calcium channel blocker. And so, demand remains limited a good thing. BUT..the flip side is that these individuals are incapable of doing very strenuous work because either their HR will not increase above approximately 120 bpm (think about the Fick equation and thus how this drastically reduce VO2) as in the case of Ca++ blockers, or in the case of Beta blockers, HR is reduced some and so is LV contractility thus resulting in a decreased stoke volume; again, think about this in terms of the Fick equation c. A plot of tension (Y axis) vs LV volume (x axis) is called a curve a.k.a. - Law (1) The ascending limb is due to: (a) More optimal alignment of the myosin and actin, and thus increasing the # of cross-bridges (b) Better diffusion for Ca ++ (2) An up-ward (leftward) of a normal or resting Starling curve indicates greater contractility whereas a downward (rightward) shift indicates a decrease in contractility. C. The Cardiac Conduction System: (Fig6.5) 1. node determines intrinsic heart rate (typically 60-80bpm), called the sinus rhythm: impulses (action potential) originate (are generated) here. 2. node conducts the impulse from the atria into the ventricles after delaying impulse ~0.13 sec allowing maximal filling of ventricles (because of atrial contraction) Page -2-

3 3. AV bundles (bundles of His) travel along septum and then sends branches into both ventricles and terminates into branches called the fibers. D. Extrinsic Control of Heart Activity (Fig 6.6) 1. Parasympathetic nervous system-acts on the heart through the nerve (cranial nerve X) which releases (acts as brake):slows HR via release of Ach near SA node and decreases strength of contraction-via release of ACh in LV myocardium. Resting vagal tone. (What would happen to HR if we cut the vagus?) 2. Sympathetic nervous system- acts via sympathetic innervation (nerves) to heart via release of NE or by circulation EPI and NE: increases HR (via NE released near SA node) and strength of contraction (circulating EPI/NE acting on Beta receptors in myocardium) * normal resting HR 60-85bpm: w/et, can decrease resting HR to ~35bpm ( vagus tone)! E. Electrocardiogram (Fig 6.7) 1. The ECG Three components of the ECG represent distinct aspects of cardiac function: a. -wave: represents atrial depolarization and occurs when the electrical impulse travels from the SA node through the atria to the AV node. b. complex: represents ventricular depolarization c. T-wave: represents ventricular repolarization 2. Cardiac Arrhythmias (irregular heart rhythm) a. means slow heart <60 bpm b. means fast heart >100 bpm c. Premature ventricular contractions (PVCs) successive ventricular contractions; usually caused by irritable or ectopic focus within the ventricle d. : atria contract at rates of 200 to 400 bpm e. : rapid an uncoordinated contractions f. uncoordinated contraction of the ventricular tissue (1) NO BLOOD IS PUMPED!!!! (2) How can this be reversed? F. Terminology of Cardiac Function - KNOW the Wiggers Diagram (Fig 6.8)!!!! 1. Cardiac Cycle: all events occurring between 2 consecutive heartbeats: in mechanical terms, all chambers undergo a relaxation phase (diastole) and a contraction phase (systole) a. chambers fill with blood (1) *diastole is longer than systole (at rest, approximately % of time in diastole - WHY??? Functionally significant?? ) a. ventricles contract and expel their contents b. From examining a Wiggers diagram, you should be able to: (1) Determine diastolic blood pressure (2) Determine systolic blood pressure (3) Determine stoke volume (4) Determine ejection fraction c. Also, from this diagram we can lean how important DIASTOLIC blood pressure is correct? That is, during isovolumic contraction, blood does not leave the left ventricle (SV) until the LV develops a pressure greater than the diastolic blood pressure, which is holding the aortic valve closed. And so, if DBP is high, the LV spends more time, and ENERGY, in the isovolumic phase. The result is a reduced SV (because the LV can only develop pressure for a finite time period, and, over time, lead to a hypertrophied left ventricle (pathologically hypertrophied). In summary, an chronically elevated diastolic blood pressure, increases afterload, resulting in a decreased SV and morphological changes to the LV wall that leads to problems. 2. Stroke volume (SV): volume of blood ejected from LV during systole. (Fig 6.9) a. At the end of diastole, just before contractions, the volume of blood is called end- volume (EDV) e.g., 100ml b. At the end of systole, just after contraction, the volume of blood remaining in the LV is called the end- volume (ESV) e.g., 40ml c. *Therefore: SV= EDV - ESV e.g.: SV = 100ml - 40ml so that SV = 60ml Page -3-

4 d. Stroke Volume: major determinant of CR endurance: determined by: (1) Volume of venous blood returned to the heart (preload) (2) Ventricular distensibility or capacity to enlarge the ventricle (a) 1&2 influence filling capacity; how much available to be pumped (think Frank-Starling Law ) (3) Ventricular contractility (4) Aortic pressure (afterload) (pressure against which the ventricle must contract) (a) 3&4 influence the ventricle s ability to empty i) note that there a drop in total peripheral resistance during exercise, due to vasodilitation in skeletal muscle. This helps keep aortic pressure, and thus afterload, from increasing facilitating SV. 3. Fraction: proportion of the blood pumped out of the LV with each beat a. Determined by SV/EDV e.g. 60ml/100ml ~60% at rest 4. Cardiac output (Q): is the total volume of blood pumped by the ventricle per minute: Q = HR * SV e.g.: 70bpm X 60ml = 4,200ml/min (Fig 6.9) *Average adult has ~5L of blood, and thus, ~ all of our blood is pumped (circulated) every minute II. The Vascular System [Parallel system! - think STRUCTURE/FUNCTION!!!!!!!] A. Vessels: 1. A s largest, most muscular and most elastic vessels that carry blood away from the heart: Volume and pressure storers a. The heart is an intermittent pump! And yet, blood flows constantly. How is this accomplished? The reason for this is because of a transient imbalance between the blood entering the large arteries, and that leaving. During systole, more blood enters the arteries than leaves. This results in a buildup of blood volume and thus pressure. And so during diastole, when no blood is entering the arteries, the pressure (systolic BP) that is built up drives the blood (the stored volume ) resulting in a continuous flow. And of course, as this volume leaves the arteries in a greater volume that is entering (zero increase during diastole) resulting in a decreased arterial volume and hence decreased pressure (diastolic BP). 2. A s -controls the distribution (flow) of blood!!! (and thus indirectly the pressure) a. These vessels control the rate at which the volume of blood in the arteries leaves the arterial side of the system. This is accomplished by varying the diameter of the arterioles and hence resistance, often known as total peripheral resistance (TPR). So we saw that stoke volume accounts for the inflow into the larger arteries, and now we learn that the arterioles control the outflow. And hence, as stated earlier, arterial BP is very dependent upon TPR as well as SV. b. And of course, as will be seen, changing the resistance (arteriole diameter) in different tissue/organ beds results also in changes of distribution of the CO!!!! 3. Capillaries exchange vessels 4. Venules Veins provide a low pressure storage system for blood. At rest, ~ % of blood volume is in this system. 6. Coronary Arteries: supply the vascular requirements of the heart. Originate from the as it leaves the heart. During LV ejection, valve blocks the entrances to the coronaries: coronary Q is only during.(thus capillaries don t see the high systolic pressure.) B. Blood Pressure: is the pressure exerted by the blood on the vessel walls. BP = CO * TPR 1. Pressure: the highest pressure in the artery and corresponds to ventricular systole (increase pressure places greater demands on the heart and can also lead to blood vessel damage) 2. Pressure: represents the lowest pressure in the artery and corresponds to ventricular diastole (Insidious nature of BP; increased pressure lead to LV hypertrophy!!!) 3. Pressure: represents the average pressure driving blood flow. Is approximately equal to: DP +[0.333( - )] This is NOT an average of the two WHY? Page -4-

5 4. Pressure-rate product [HR * SP] determines myocardial e demand!!!!!!! (gauge of how hard the heart is working!) 5. Blood flow: Blood flow = Change in Pressure / Resistance C. General Hemodynamics 1. Why does blood flow? a. Because of a pressure gradient (Fig 6.10) 2. How do blood vessels provide resistance? a. Resistance = [çl/r 4 ] where ç -= viscosity; L = length of vessel; r = r of the vessel (1) Thus, changes in vascular resistance are largely due to changes in blood vessel radius (vasoconstriction or vasodilation) (primarily the arterioles!) (a) Provides an effective mode to divert blood flow to areas of greatest need b. Resistance also is an effect method to maintain arterial BP what happens when too many arterioles vasodilate? D. Distribution of Blood:[At rest; Fig 6.11] At rest, the most metabolically active tissues receive the greatest blood supply (liver and kidneys combined receive almost half the blood being circulated)[fig 6.11] Resting skeletal muscle receives only about to %: however, during heavy exercise, skeletal muscle receives about to % of available blood!!! [Fig 6.11] Brain receives ~same absolute amount of flow during rest and heavy exercise (~1L/min) 1. Intrinsic Control of Blood Flow a. Autoregulation: the control (vessel diameter) of arterioles and thus blood distribution. Self-regulation of tissues flow depending upon demands. (Fig 6.12) (1) metabolic stimuli: This is mediated by local chemical environment: O 2 will cause dilation as well as CO 2, H +, K +, lactic acid. (2) Vasodialators include endothelium-derived substances such as: Nitric Oxide (NO), prostaglandins, endothelium-derived hyperpolarizing factor (EDHF) (3) Pressure changes within the vessel can also cause changes in the vessel s diameter 2. Extrinsic Control a. control: -redistribution of blood flow (via changes in resistance) at the system or body level.(alteration in vasomotor tone less constriction, not via direct vasodilatation) 3. Distribution of Venous Blood: At rest, the majority of blood volume ~ %, is located in the venous system. (Fig. 6.13) With sympathetic stimulation of the venues and veins, blood is redistributed from peripheral venous circulation, to the heart, and then to those areas that are most metabolically active i.e. skeletal muscle.(thus, heart is allowed to see more blood) 4. Integrative Control of Blood Pressure a. - pressure sensors (sense stretch ) in the aortic arch and carotid arteries. Work to maintain homeostasis! HOW? (1) Any implications for taking HR? 5. Return of blood to the heart: ******The heart can only pump what is sees. Venous return is the main determinant of CO, not the contractile state of the heart!!!!!!!!! a. The pumping action of the muscles prevent pooling in the large veins of the lower extremities. (The heart can only pump what is returned, so that large amount of pooling causes venous return to decrease, and subsequently, SV and BP to decrease!)[fig 6.14] b. Valves in veins c. Respiratory pump (due to changes in thoracic cavity during respiration) B. The Blood: primary functions are: Transport, temperature and acid-base (ph) regulation 1. Blood Volume and Composition Page -5-

6 a. Generally 5-6 L men and 4-5 L women b. Composition [Fig 6.15]: (1) -( is about 55-60% of blood volume) primarily water (90%) and some protein (7%) and remaining 3% is cellular nutrients, electrolytes, enzymes, hormones and antibodies and wastes. (2) elements ~40-45% of total blood volume: consists of RBC, WBC and platelets; RBC =~99% of formed element volume (3) The percentage of the total blood volume composed of red blood cells is referred to as, which typically varies between 40 and 45%. (White blood cells and platelets account for <1%.) c. Red Blood Cells (Erythrocytes) (1) Production and Regulation of Production of RBCs (a) Produced in the bone marrow. (After age 20, membranous bones, e.g., vertebrae, sternum, ribs and ilia) (b) decrease in tissue oxygenation (low blood volume, anemia, low hemoglobin, poor blood flow, pulmonary disease, cardiac failure, high altitude) stimulates increased production (c), (90% formed in kidney, 10% in liver) is the principle stimulant of RBC production i) Epinephrine and norepinephrine also stimulate erythropoietin production ii) Utilized to help in anemia, abused to gain an advantage in endurance events (2) Can be destroyed during exercise from the wear and tear associated with exercise-the constant pounding of the sole of the foot during distance running can increase fragility and destruction of RBCs (3) Transport oxygen, primarily bound to (a) ~15 g of hemoglobin per 100 ml of blood i) Heme contains iron, which binds oxygen ii) each gram of hemoglobin can combine w/~1.34 ml of O 2 : ~20ml of O 2 can be bound to each 100ml of blood (15g X 1.34ml O 2 per g = ~20 ml of O 2 per 100ml of blood iii) Anemia: RBC = O 2 carrying capacity d. Blood viscosity-resistance to flow (about 2X viscosity of water). It is not until hematocrit reaches 60% or more, that this becomes a problem to flow. (1) No problem with RBC with training as long as it is accompanied by in plasma volume e. Donating Blood (1) removal of one unit (~500ml) represent ~ an 8-10% reduction in both the total blood volume and in the number of circulating RBCs. Plasma volume (primarily water) returns to normal in hrs, 6-8 wks to return to same number of RBCs. Can greatly compromise endurance performance. 2. Sickle Cell Anemia a. Genetic Disease resulting in RBCs that become stiff and oblong in shape (crescent like a sickle) (1) Inefficient at carrying oxygen (2) Can adhere to vessel walls slowing or blocking flow (3) (4) Sickle Cell Trait (a) Increased risk of exercise related pathologies Page -6-