physiology of circulation

Cardiac Output, Blood Flow, and Blood Pressure

14-1

www.freelivedoctor.com

Outline

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

14-2www.freelivedoctor.com

Cardiac Output


Is volume of blood pumped/min by each ventricle

Heart Rate (HR) = 70 beats/min Stroke volume (SV) = blood

pumped/beat by each ventricle Average is 70-80 ml/beat

CO = SV x HR Total blood volume is about 5.5L

Cardiac Output (CO)


Regulation of Cardiac Rate

Without neuronal influences, SA node will drive heart at rate of its spontaneous activity

Normally Symp & Parasymp activity influence HR (chronotropic effect) Mechanisms that affect HR: chronotropic

effect Positive increases; negative decreases

Autonomic innervation of SA node is main controller of HR Symp & Parasymp nerve fibers modify

rate of spontaneous depolarization


Regulation of Cardiac Rate continued

NE & 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, slows depolarization & decreasing HR

Fig 14.1


Vagus nerve: Decrease activity: increases heart rate Increased activity: slows heart

Cardiac control center of medulla coordinates activity of autonomic innervation

Sympathetic endings in atria & ventricles can stimulate increased strength of contraction

Regulation of Cardiac Rate continued


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


EDV is workload (preload) on heart prior to contraction SV is directly proportional to preload &

contractility Strength of contraction varies directly with

EDV Total peripheral resistance = afterload

which impedes ejection from ventricle SV is inversely proportional to TPR

Ejection fraction is SV/ EDV (~80ml/130ml=62%) Normally is 60%; useful clinical diagnostic tool

Regulation of Stroke Volume


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 & SV

Fig 14.2


Frank-Starling Law of the Heart continued

(a) is state of myocardial sarcomeres just before filling

Actins overlap, actin-myosin interactions are reduced & contraction would be weak

In (b, c & d) there is increasing interaction of actin & myosin allowing more force to be developed

Fig 14.314-12


At any given EDV, contraction depends upon level of sympathoadrenal activity NE & Epi produce

an increase in HR & contraction (positive inotropic effect)

Due to increased Ca2+ in sarcomeres

Fig 14.414-13


Extrinsic Control of Contractility

Parasympathetic stimulation Negative chronotropic effect

Through innervation of the SA node and myocardial cell

Slower heart rate means increased EDV

Increases SV through Frank-Starling law


Fig 14.5


Venous Return

Is return of blood to heart via veins

Controls EDV & thus SV & CO

Dependent on: Blood volume &

venous pressure Vasoconstriction

caused by Symp Skeletal muscle

pumps Pressure drop during

inhalation Fig 14.7 14-15www.freelivedoctor.com

Venous Return continued

Veins hold most of blood in body (70%) & are thus called capacitance vessels Have thin walls &

stretch easily to accommodate more blood without increased pressure (=higher compliance)

Have only 0-10 mm Hg pressure

Fig 14.6


Blood & Body Fluid Volumes


Blood Volume

Constitutes small fraction of total body fluid

2/3 of body H20 is inside cells (intracellular compartment)

1/3 total body H20 is in extracellular compartment

80% of this is interstitial fluid; 20% is blood plasma

Fig 14.8


Exchange of Fluid between Capillaries & Tissues

Distribution of ECF between blood & 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)


Exchange of Fluid between Capillaries & Tissues

Movement also affected by colloid osmotic pressure = osmotic pressure exerted by proteins

in fluid Difference between osmotic pressures in

& outside of capillaries (oncotic pressure) affects fluid movement

Plasma osmotic pressure = 25 mm Hg; interstitial osmotic pressure = 0 mm Hg


Overall Fluid Movement

Is determined by net filtration pressure & forces opposing it (Starling forces)

Pc + i (fluid out) - Pi + p (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


Fig 14.9


Edema

Normally filtration, osmotic reuptake, & 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


Regulation of Blood Volume by Kidney

Urine formation begins with filtration of plasma in glomerulus

Filtrate passes through & 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


ADH (vasopressin)

ADH released by Post Pit when osmoreceptors detect high osmolality From excess salt

intake or dehydration

Causes thirst Stimulates H20

reabsorption from urine

ADH release inhibited by low osmolality

Fig 14.1114-25


Aldosterone

Is steroid hormone secreted by adrenal cortex

Helps maintain blood volume & pressure through reabsorption & retention of salt & water

Release stimulated by salt deprivation, low blood volume, & pressure


Renin-Angiotension-Aldosterone System

Decreased BP and flow (low blood volume) Kidney secreted Renin (enzyme)

Juxaglomerular apparatus

Angiotensin I to AngiotensinII By angiotensin-converting enzyme (ACE)

Angio II causes a number of effects all aimed at increasing blood pressure:

Vasoconstriction, aldosterone secretion, thirst


Fig 14.12 shows when & how Angio II is produced,

& its effects

Angiotensin II


Atrial Natriuretic Peptide (ANP)

Expanded blood volume is detected by stretch receptors in left atrium & causes release of ANP Inhibits aldosterone, promoting salt

& water excretion to lower blood volume

Promotes vasodilation


Factors Affecting Blood Flow


Vascular Resistance to Blood Flow

Determines how much blood flows through a tissue or organ Vasodilation decreases resistance,

increases blood flow Vasoconstriction does opposite


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) Fig 14.1314-33


Physical Laws Describing Blood Flow

Flow rate is inversely proportional to resistance Flow =P/R Resistance is directly proportional to length of

vessel (L) & 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)


Fig 14.14. Relationshipbetween blood flow, radius & resistance


Sympathoadrenal activation causes increased CO & resistance in periphery & viscera Blood flow to skeletal muscles is

increased Because their arterioles dilate in response

to Epi & their Symp fibers release ACh which also dilates their arterioles

Thus blood is shunted away from visceral & skin to muscles

Extrinsic Regulation of Blood Flow


Parasympathetic effects are vasodilative However, Parasymp only innervates

digestive tract, genitalia, & salivary glands

Thus Parasymp is not as important as Symp

Angiotensin II & ADH (at high levels) cause general vasoconstriction of vascular smooth muscle Which increases resistance & BP

Extrinsic Regulation of Blood Flow continued


Paracrine Regulation of Blood Flow

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


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 & relaxes when not stretched E.g. decreased arterial pressure causes

cerebral vessels to dilate & vice versa


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)

Intrinsic Regulation of Blood Flow (Autoregulation) continued


Aerobic Requirements of the Heart

Heart (& 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 & aerobic

enzymes During systole coronary vessels are

occluded Heart gets around this by having lots of

myoglobin Myoglobin is an 02 storage molecule that releases

02 to heart during systole 14-41www.freelivedoctor.com

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


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


Circulatory Changes During Exercise

At beginning of exercise, Symp activity causes vasodilation via Epi & local ACh release Blood flow is shunted from periphery & visceral to

active skeletal muscles Blood flow to brain stays same

As exercise continues, intrinsic regulation is major vasodilator

Symp effects cause SV & CO to increase HR & ejection fraction increases vascular

resistance


Fig 14.19


Fig 14.20


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


Cerebral Circulation

Is regulated almost exclusively by intrinsic mechanisms When BP increases, cerebral arterioles

constrict; when BP decreases, arterioles dilate (=myogenic regulation)

Arterioles dilate & constrict in response to changes in C02 levels

Arterioles are very sensitive to increases in local neural activity (=metabolic regulation)

Areas of brain with high metabolic activity receive most blood


Fig 14.2114-49


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 & activity of arteriovenous anastomoses which control blood flow through surface capillaries

Symp activity closes surface beds during cold & fight-or-flight, & opens them in heat & exercise

Fig 14.2214-50


Blood Pressure


Blood Pressure (BP)

Arterioles play role in blood distribution & control of BP

Blood flow to capillaries & BP is controlled by aperture of arterioles

Capillary BP is decreased because they are downstream of high resistance arterioles

Fig 14.23


Blood Pressure (BP)

Capillary BP is also low because of large total cross-sectional area

Fig 14.24 14-53


Blood Pressure (BP)

Is controlled mainly by HR, SV, & peripheral resistance An increase in any of these can result in

increased BP Sympathoadrenal activity raises BP via

arteriole vasoconstriction & by increased CO

Kidney plays role in BP by regulating blood volume & thus stroke volume


Baroreceptor Reflex

Is activated by changes in BP Which is detected by baroreceptors (stretch

receptors) located in aortic arch & carotid sinuses

Increase in BP causes walls of these regions to stretch, increasing frequency of APs

Baroreceptors send APs to vasomotor & cardiac control centers in medulla

Is most sensitive to decrease & sudden changes in BP


Fig 14.2614-56


Fig 14.27


Atrial Stretch Receptors

Are activated by increased venous return & act to reduce BP

Stimulate reflex tachycardia (slow HR) Inhibit ADH release & promote secretion

of ANP


Measurement of Blood Pressure

Is 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 & noise as

blood passes constriction during systole & is blocked during diastole

1st Korotkoff sound is heard at pressure that blood is 1st able to pass thru cuff; last occurs when can no long hear systole because cuff pressure = diastolic pressure


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 Fig 14.29


Fig 14.3014-61


Pulse Pressure

Pulse 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


Hypertension


Hypertension

Is blood pressure in excess of normal range for age & gender (> 140/90 mmHg)

Afflicts about 20 % of adults Primary or essential hypertension is

caused by complex & poorly understood processes

Secondary hypertension is caused by known disease processes


Essential Hypertension

Constitutes most of hypertensives Increase in peripheral resistance is universal CO & HR are elevated in many Secretion of renin, Angio II, & aldosterone is

variable Sustained high stress (which increases Symp

activity) & 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 H20


Dangers of Hypertension

Patients are often asymptomatic until substantial vascular damage occurs Contributes to atherosclerosis Increases workload of the heart leading to

ventricular hypertrophy & congestive heart failure

Often damages cerebral blood vessels leading to stroke

These are why it is called the "silent killer"


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, & Angio II-receptor blockers


Circulatory Shock


Circulatory Shock

Occurs when there is inadequate blood flow to, &/or O2 usage by, tissues Cardiovascular system undergoes

compensatory changes Sometimes shock becomes irreversible &

death ensues


Hypovolemic Shock

Is circulatory shock caused by low blood volume E.g. from hemorrhage, dehydration, or burns Characterized by decreased CO & BP

Compensatory responses include sympathoadrenal activation via baroreceptor reflex Results in low BP, rapid pulse, cold clammy

skin, low urine output


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 & resultant low BP Effective treatment includes drugs that inhibit

production of NO

Septic Shock


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


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, & diuretics


physiology of circulation

Documents

increased pressure

hg pressure fig

blood pumpedbeat

volume of blood pumpedmin

blood plasma fig

sv x hr total blood

hr fig

bycolloid osmotic pressure