Chapter 14

Cardiac Output, Blood Flow, and Blood Pressure

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Chapter 14 Outline
Cardiac

Output Blood and Body Fluid Volumes Factors Affecting Blood Flow Blood Pressure Hypertension Circulatory Shock

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Cardiac Output

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Cardiac Output (CO)

Is

volume of blood pumped/min by each ventricle Stroke volume (SV) = blood pumped/beat by each ventricle CO = SV x HR Total blood volume is about 5.5L

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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

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Regulation of Cardiac Rate continued

NE

and Epi stimulate opening of pacemaker HCN channels This depolarizes SA faster, increasing HR ACH promotes opening of K+ channels The resultant K+ outflow counters Na+ influx, slowing depolarization and decreasing HR
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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

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Stroke Volume

Is

determined by 3 variables: End diastolic volume (EDV) = volume of blood in ventricles at end of diastole Total peripheral resistance (TPR) = impedance to blood flow in arteries Contractility = strength of ventricular contraction

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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

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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
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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

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Extrinsic Control of Contractility

At

any given EDV, contraction depends upon level of sympathoadrenal activity NE and Epi produce an increase in HR and contraction (positive inotropic effect) Due to increased Ca2+ in sarcomeres
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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
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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
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Blood and Body Fluid Volumes

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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

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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)

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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

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Overall Fluid Movement

Is

determined by net filtration pressure and forces opposing it (Starling forces)

Pc

+ Pi (fluid out) - Pi + Pp (fluid in)

Pc

= Hydrostatic pressure in capillary Pi = Colloid osmotic pressure of interstitial fluid Pi = Hydrostatic pressure in interstitial fluid Pp = Colloid osmotic pressure of blood plasma

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Edema
Normally

filtration, osmotic reuptake, and lymphatic drainage maintain proper ECF levels Edema is excessive accumulation of ECF resulting from: High blood pressure Venous obstruction Leakage of plasma proteins into ECF Myxedema (excess production of glycoproteins in extracellular matrix) from hypothyroidism Low plasma protein levels resulting from liver disease Obstruction of lymphatic drainage

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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

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ADH (vasopressin)
ADH

released by Post Pit when osmoreceptors detect high osmolality From excess salt intake or dehydration Causes thirst Stimulates H2O reabsorption from urine ADH release inhibited by low osmolality

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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

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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

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Angiotensin II

Fig

14.12 shows when and how Angio II is produced, and its effects

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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

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Atrial Natriuretic Peptide (ANP) continued

ANP,

together with decreased ADH, acts in a negative feedback system to lower blood volume

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Factors Affecting Blood Flow

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Vascular Resistance to Blood Flow

Determines

how much blood flows through a tissue or

organ Vasodilation decreases resistance, increases blood flow Vasoconstriction does opposite

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Physical Laws Describing Blood Flow

Blood

flows through vascular system when there is pressure difference (DP) at its two ends Flow rate is directly proportional to difference (DP = P 1 - P2)

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Physical Laws Describing Blood Flow continued

Flow

rate is inversely proportional to resistance Flow = DP/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 = DPr4( ) L(8)

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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

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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

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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

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Extrinsic Regulation of Blood Flow continued

Parasympathetic

effects are vasodilative 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

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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
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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

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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 (= active hyperemia)

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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
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Regulation of Coronary Blood Flow

Blood

flow to heart is affected by Symp activity NE causes vasoconstriction; Epi causes vasodilation Dilation accompanying exercise is due mostly to intrinsic regulation

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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

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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
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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

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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
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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
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Blood Pressure

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Blood Pressure (BP)

Arterioles

play role in blood distribution and control of BP Blood flow to capillaries and BP is controlled by aperture of arterioles Capillary BP is decreased because they are downstream of high resistance arterioles

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Blood Pressure (BP)

Capillary

BP is also low because of large total crosssectional area

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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

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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 APs Baroreceptors send APs to vasomotor and cardiac control centers in medulla Is most sensitive to decrease and sudden changes in BP

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Atrial Stretch Receptors

Are

activated by increased venous return and act to reduce BP Stimulate reflex tachycardia (slow HR) Inhibit ADH release and promote secretion of ANP

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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
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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

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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

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Hypertension

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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

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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
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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"

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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

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Circulatory Shock

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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

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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

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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

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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

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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

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