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Chapter 14 Lecture Outline Copyright © The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Chapter 14 Outline Cardiac Output Blood Volumes Vascular Resistance to Blood Flow Blood Flow to the Heart and Skeletal Muscles Blood Flow to the Brain and Skin Blood Pressure Hypertension, Shock, and Congestive Heart Failure 14-2 Cardiac Output 14-3 Cardiac Output (CO) Is volume of blood pumped/min by each ventricle Stroke volume (SV) = blood pumped/beat by each ventricle Heart rate (HR) = the number of beats/minute CO = SV x HR Total blood volume is about 5.5L 14-4 Regulation of Cardiac Rate Without neuronal influences, SA node will drive heart at rate of its spontaneous activity Normally Symp and Parasymp activity influence HR (chronotropic effect) Autonomic innervation of SA node is main controller of HR Symp and Parasymp nerve fibers modify rate of spontaneous depolarization 14-5 Regulation of Cardiac Rate continued Norepinephrine and epinephrine stimulate opening of pacemaker HCN channels This depolarizes SA node faster, increasing HR ACh promotes opening of K+ channels The resultant K+ outflow counters Na+ influx, slowing depolarization and decreasing HR 14-6 Regulation of Cardiac Rate continued Cardiac control center of medulla coordinates activity of autonomic innervation Sympathetic endings in atria and ventricles can stimulate increased strength of contraction 14-7 14-8 Stroke Volume Is determined by 3 variables: End diastolic volume (EDV) = volume of blood in ventricles at end of diastole Total peripheral resistance (TPR) = resistance to blood flow in arteries Contractility = strength of ventricular contraction 14-9 Regulation of Stroke Volume EDV is workload (preload) on heart prior to contraction SV is directly proportional to preload and contractility Strength of contraction varies directly with EDV Total peripheral resistance = afterload which impedes ejection from ventricle Ejection fraction is SV/ EDV Normally is 60%; useful clinical diagnostic tool 14-10 Frank-Starling Law of the Heart States that strength of ventricular contraction varies directly with EDV Is an intrinsic property of myocardium As EDV increases, myocardium is stretched more, causing greater contraction and SV 14-11 Frank-Starling Law of the Heart continued (a) is state of myocardial sarcomeres just before filling Actins overlap, actin-myosin interactions are reduced and contraction would be weak In (b, c and d) there is increasing interaction of actin and myosin allowing more force to be developed 14-12 Extrinsic Control of Contractility At any given EDV, contraction depends upon level of sympathoadrenal activity Norepi. and Epi. produce an increase in HR and contraction (positive inotropic effect) Due to increased Ca2+ in sarcomeres 14-13 14-14 Venous Return Is return of blood to heart via veins Controls EDV and thus SV and CO Dependent on: Blood volume and venous pressure Vasoconstriction caused by Symp Skeletal muscle pumps Pressure drop during inhalation 14-15 Venous Return continued Veins hold most of blood in body (~70%) and are thus called capacitance vessels Have thin walls and stretch easily to accommodate more blood without increased pressure (=higher compliance) Have only 010 mm Hg pressure 14-16 Blood Volume 14-17 Blood Volume Constitutes small fraction of total body fluid 2/3 of body H2O is inside cells (intracellular compartment) 1/3 total body H2O is in extracellular compartment 80% of this is interstitial fluid; 20% is blood plasma 14-18 Exchange of Fluid between Capillaries and Tissues Distribution of ECF between blood and interstitial compartments is in state of dynamic equilibrium Movement out of capillaries is driven by hydrostatic pressure exerted against capillary wall Promotes formation of tissue fluid Net filtration pressure= hydrostatic pressure in capillary (17-37 mm Hg) - hydrostatic pressure of ECF (1 mm Hg) 14-19 Exchange of Fluid between Capillaries and Tissues Movement also affected by colloid osmotic pressure = osmotic pressure exerted by proteins in fluid Difference between osmotic pressures in and outside of capillaries (oncotic pressure) affects fluid movement Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure = 0 mm Hg 14-20 Overall Fluid Movement Is determined by net filtration pressure and forces opposing it (Starling forces) + I)– (Pi + p) [fluid out] – [fluid in] Pc = Hydrostatic pressure in capillary i = Colloid osmotic pressure of interstitial fluid Pi = Hydrostatic pressure in interstitial fluid p = Colloid osmotic pressure of blood plasma (Pc 14-21 14-22 Edema Normally filtration, osmotic reuptake, and lymphatic drainage maintain proper ECF levels Edema is excessive accumulation of fluid resulting from: High arterial blood pressure Venous obstruction Leakage of plasma proteins into interstitial fluid Myxedema (excess production of glycoproteins in extracellular matrix) from hypothyroidism Low plasma protein levels resulting from liver disease Obstruction of lymphatic drainage 14-23 Regulation of Blood Volume by Kidney Urine formation begins with filtration of plasma in glomerulus Filtrate passes through and is modified by nephron Volume of urine excreted can be varied by changes in reabsorption of filtrate Adjusted according to needs of body by action of hormones 14-24 ADH (vasopressin) ADH released by Post Pit when osmoreceptors in hypothalamus detect high osmolality From excess salt intake or dehydration Causes thirst Stimulates H2O reabsorption from urine Homeostasis maintained by these countermeasures 14-25 Aldosterone Is steroid hormone secreted by adrenal cortex Helps maintain blood volume and pressure through reabsorption and retention of salt and water Release stimulated by salt deprivation, low blood volume, and pressure 14-26 Renin-Angiotension-Aldosterone System When there is a salt deficit, low blood volume, or pressure, angiotensin II is produced Angio II causes a number of effects all aimed at increasing blood pressure: Vasoconstriction, aldosterone secretion, thirst 14-27 Angiotensin II Fig 14.12 shows when and how Angio II is produced, and its effects 14-28 Atrial Natriuretic Peptide (ANP) Expanded blood volume is detected by stretch receptors in left atrium and causes release of ANP ANP inhibits aldosterone, promoting salt and water excretion to lower blood volume And promotes vasodilation 14-29 Atrial Natriuretic Peptide (ANP) continued ANP, together with decreased ADH, acts in a negative feedback system to lower blood volume and venous return 14-30 Vascular Resistance to Blood Flow 14-31 Vascular Resistance to Blood Flow Determines how much blood flows through a tissue or organ Vasodilation decreases resistance, increases blood flow Vasoconstriction does opposite 14-32 14-33 Physical Laws Describing Blood Flow Blood flows through vascular system when there is pressure difference (P) at its two ends Flow rate is directly proportional to difference (P = P1 - P2) 14-34 Physical Laws Describing Blood Flow continued Flow rate is inversely proportional to resistance Flow = P/R Resistance is directly proportional to length of vessel (L) and viscosity of blood () Inversely proportional to 4th power of radius So diameter of vessel is very important for resistance Poiseuille's Law describes factors affecting blood flow Blood flow = Pr4() L(8) 14-35 14-36 Physical Laws Describing Blood Flow continued Mean arterial pressure and vascular resistance are the 2 major factors regulating blood flow Blood is shunted from one organ to another by degree of constriction of their arterioles 14-37 Total Peripheral Resistance Sum of all vascular resistances within the systemic circulation is total peripheral resistance Arteries supply tissues and organs in parallel circuits Changes in resistance in these circuits determines relative blood flow 14-38 Extrinsic Regulation of Blood Flow Sympathoadrenal activation causes increased CO and resistance in periphery and viscera Blood flow to skeletal muscles is increased Because their arterioles dilate in response to Epi and their Symp fibers release ACh which also dilates their arterioles Thus blood is shunted away from visceral and skin to muscles 14-39 Extrinsic Regulation of Blood Flow continued Parasympathetic effects cause vasodilation However, Parasymp only innervates digestive tract, genitalia, and salivary glands Thus Parasymp is not as important as Symp Angiotenin II and ADH (at high levels) cause general vasoconstriction of vascular smooth muscle Which increases resistance and BP 14-40 Paracrine Regulation of Blood Flow The endothelium produces several paracrine regulators that promote relaxation: Nitric oxide (NO), bradykinin, prostacyclin NO is involved in setting resting “tone” of vessels Levels are increased by Parasymp activity Vasodilator drugs such as nitroglycerin or Viagra act thru NO Endothelin 1 is vasoconstrictor produced by endothelium 14-41 Intrinsic Regulation of Blood Flow (Autoregulation) Maintains fairly constant blood flow despite BP variation Myogenic control mechanisms occur in some tissues because vascular smooth muscle contracts when stretched and relaxes when not stretched e.g. decreased arterial pressure causes cerebral vessels to dilate and vice versa 14-42 Intrinsic Regulation of Blood Flow (Autoregulation) continued Metabolic control mechanism matches blood flow to local tissue needs Low O2 or pH or high CO2, adenosine, or K+ from high metabolism cause vasodilation which increases blood flow causing the tissue to appear red=reactive hyperemia A similar inc. in blood flow occurs in sk. Muscle and other organs as a result of inc. metabolism=active hyperemia 14-43 Aerobic Requirements of the Heart Heart (and brain) must receive adequate blood supply at all times Heart is most aerobic tissue--each myocardial cell is within 10 m of capillary Contains lots of mitochondria and aerobic enzymes During systole, coronary vessels are occluded Heart gets around this by having lots of myoglobin Myoglobin is an O2 storage molecule that releases O2 to heart during systole 14-44 Regulation of Coronary Blood Flow Blood flow to heart is affected by Symp activity Norep. causes vasoconstriction; Epi causes vasodilation Dilation accompanying exercise is due mostly to intrinsic regulation 14-45 Regulation of Blood Flow Through Skeletal Muscles At rest, flow through skeletal muscles is low because of tonic sympathetic activity Flow through muscles is decreased during contraction because vessels are constricted 14-46 Circulatory Changes During Exercise At beginning of exercise, Symp activity causes vasodilation via Epi and local ACh release Blood flow is shunted from periphery and visceral to active skeletal muscles Blood flow to brain stays same As exercise continues, intrinsic regulation is major vasodilator Symp effects cause SV and CO to increase HR and ejection fraction increases vascular resistance 14-47 14-48 14-49 Cerebral Circulation Gets about 15% of total resting CO Held constant (750ml/min) over varying conditions Because loss of consciousness occurs after few secs. of interrupted flow Is not normally influenced by sympathetic activity 14-50 Cerebral Circulation Regulated almost exclusively by intrinsic mechanisms When BP increases, cerebral arterioles constrict; when BP decreases, arterioles dilate (=myogenic regulation) Arterioles dilate and constrict in response to changes in CO2 levels Arterioles are very sensitive to increases in local neural activity (=metabolic regulation) Areas of brain with high metabolic activity receive most blood 14-51 Changing patterns of blood flow in the brain. 14-52 Cutaneous Blood Flow Skin serves as a heat exchanger for thermoregulation Skin blood flow is adjusted to keep deep-body at 37oC By arterial dilation or constriction and activity of arteriovenous anastomoses which control blood flow through surface capillaries Symp activity closes surface beds during cold and fight-or-flight, and opens them in heat and exercise 14-53 Blood Pressure 14-54 Blood Pressure (BP) Arterioles play role in blood distribution and control of BP Blood flow to capillaries and BP is controlled by diameter of arterioles Capillary BP is decreased because they are downstream of high resistance arterioles 14-55 Blood Pressure (BP) Capillary BP is also low because of large total crosssectional area 14-56 Blood Pressure (BP) Is controlled mainly by HR, SV, and peripheral resistance An increase in any of these can result in increased BP Sympathoadrenal activity raises BP via arteriole vasoconstriction and by increased CO Kidney plays role in BP by regulating blood volume and thus stroke volume 14-57 Baroreceptor Reflex Is activated by changes in BP Which is detected by baroreceptors (stretch receptors) located in aortic arch and carotid sinuses Increase in BP causes walls of these regions to stretch, increasing frequency of Act. Pot. Baroreceptors send Act. Pot. to vasomotor and cardiac control centers in medulla Is most sensitive to decrease and sudden changes in BP 14-58 14-59 14-60 Atrial Stretch Receptors Are activated by increased venous return and act to reduce BP and in response: Stimulate reflex tachycardia (slow HR) Inhibit ADH release and promote secretion of ANP 14-61 Measurement of Blood Pressure Via auscultation (to examine by listening) No sound is heard during laminar flow (normal, quiet, smooth blood flow) Korotkoff sounds can be heard when sphygmomanometer cuff pressure is greater than diastolic but lower than systolic pressure Cuff constricts artery creating turbulent flow and noise as blood passes constriction during systole and is blocked during diastole 1st Korotkoff sound is heard at pressure that blood is 1st able to pass thru cuff; last occurs when one can no long hear systole because cuff pressure = diastolic pressure 14-62 Measurement of Blood Pressure continued Blood pressure cuff is inflated above systolic pressure, occluding artery As cuff pressure is lowered, blood flows only when systolic pressure is above cuff pressure, producing Korotkoff sounds Sounds are heard until cuff pressure equals diastolic pressure, causing sounds to disappear 14-63 The indirect, or auscultatory, method of blood pressure measurement: 14-64 Pulse Pressure pressure = (systolic pressure) – (diastolic pressure) Mean arterial pressure (MAP) represents average arterial pressure during cardiac cycle Has to be approximated because period of diastole is longer than period of systole MAP = diastolic pressure + 1/3 pulse pressure Pulse 14-65 Hypertension, Shock, and Congestive Heart Failure 14-66 Hypertension Blood pressure in excess of normal range for age and gender (> 140/90 mmHg) Afflicts about 20% of adults Most common type is primary or essential hypertension Caused by complex and poorly understood processes Secondary hypertension is caused by known disease processes 14-67 Essential Hypertension Increase in peripheral resistance is universal CO and HR are elevated in many Secretion of renin, Angio II, and aldosterone is variable Sustained high stress (which increases Symp activity) and high salt intake act synergistically in development of hypertension Prolonged high BP causes thickening of arterial walls, resulting in atherosclerosis Kidneys appear to be unable to properly excrete Na+ and H2O 14-68 Dangers of Hypertension Patients are often asymptomatic until substantial vascular damage occurs Contributes to atherosclerosis Increases workload of the heart leading to ventricular hypertrophy and congestive heart failure Often damages cerebral blood vessels leading to stroke These are why it is called the "silent killer" 14-69 Treatment of Hypertension Often includes lifestyle changes such as cessation of smoking, moderation in alcohol intake, weight reduction, exercise, reduced Na+ intake, increased K+ intake Drug treatments include diuretics to reduce fluid volume, beta-blockers to decrease HR, calcium blockers, ACE inhibitors to inhibit formation of Angio II, and Angio II-receptor blockers 14-70 Possible Causes of Secondary Hypertension Kidney disease—kidney disease; renal artery disease Endocrine disorder—excess catecholamines; excess aldosterone Nervous system disorder—inc. intracranial pressure; damage to vasomotor center Cardiovascular disorder—complete heart block; arteriosclerosis of aorta Circulatory Shock Occurs when there is inadequate blood flow to, and/or O2 usage by, tissues Cardiovascular system undergoes compensatory changes Sometimes shock becomes irreversible and death ensues 14-72 Hypovolemic Shock Is circulatory shock caused by low blood volume e.g. from hemorrhage, dehydration, or burns Characterized by decreased CO and BP Compensatory responses include sympathoadrenal activation via baroreceptor reflex Results in low BP, rapid pulse, cold clammy skin, low urine output 14-73 Septic Shock Refers to dangerously low blood pressure resulting from sepsis (infection) Mortality rate is high (50-70%) Often occurs as a result of endotoxin release from bacteria Endotoxin induces NO production causing vasodilation and resultant low BP Effective treatment includes drugs that inhibit production of NO 14-74 Other Causes of Circulatory Shock Severe allergic reaction can cause a rapid fall in BP called anaphylactic shock Due to generalized release of histamine causing vasodilation Rapid fall in BP called neurogenic shock can result from decrease in Symp tone following spinal cord damage or anesthesia Cardiogenic shock is common following cardiac failure resulting from infarction that causes significant myocardial loss 14-75 Congestive Heart Failure Occurs when CO is insufficient to maintain blood flow required by body Caused by MI (most common), congenital defects, hypertension, aortic valve stenosis, disturbances in electrolyte levels Compensatory responses are similar to those of hypovolemic shock Treated with digitalis, vasodilators, and diuretics 14-76